SWINE DISEASE

MANUAL

Fifth Edition

Edited by:
E.J. Neumann, A. Ramirez, and K.J. Schwartz
ISBN 978-0-9843503-1-5

COPYRIGHT © 2020 American Association of Swine Purchase online: http://ecom.aasv.org/sdm

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DISCLAIMER: Information in this manual comes
from many sources and may contain errors. In Copyediting and proofreading
particular, information on drugs, chemicals, antibiotics, Karen Richardson
anthelmintics, parasiticides, feed additives, vaccines and Sue Schulteis
any other agents used to prevent or treat swine diseases
may contain errors and inaccuracies. Veterinarians and Text formatting and cover design
all others using those products are advised to use their Barbara Molnár-Smith
own independent, best judgment, based on the most Tina Smith
recent and authoritative information provided by those
producing the product. Also, management changes and
management practices mentioned in the manual are to be
used at the discretion of the owner(s) of the swine or the
person(s) charged with those responsibilities. Neither the
authors nor universities nor diagnostic laboratories they
represent shall be liable for damage caused by reliance on
information in this manual.

Cover photo credits

Front cover photo courtesy of
Tina Smith
Front cover histopathological
images courtesy of Iowa State
University Veterinary
Diagnostic Laboratory

Back cover photo courtesy of

Ashley Schwartz
A
B C
Histopathological image descriptions
A. Alveolar macrophages of lung have positive staining for PRRSV by immunohistochemistry (IHC). Pig.
B. Intestinal enterocytes have positive staining for PEDV by immunohistochemistry (IHC). Neonatal pig.
C. Spiral-shaped bacteria (Brachyspira hyodysenteriae) present in colon by in situ hybridization (ISH). Pig.
 PREFACE

This manual was written primarily for veterinary students and those who teach swine diseases. It also
may be of interest to veterinary practitioners, veterinary technicians, and others interested in swine
diseases in production systems. This manual attempts to update, condense and simplify the great
mass of information available. Only basic material appropriate for students is included. More detailed
information is available via an array of texts, websites, and scientific publications.
Disease topics are listed as individual entities. The student should be reminded that in reality, the
occurrence and severity of disease outbreaks are strongly influenced by production practices, housing,
environment, nutrition, and genetics. Diseases may occur concurrently in modern production systems
with large populations of animals; for example, porcine respiratory disease complex (PRDC) is usually a
co-infection with Mycoplasma hyopneumoniae and/or other bacteria or viruses. Diagnostic methods for
disease complexes are usually more complicated than finding a single agent. Likewise, control of disease
frequently involves not only specific intervention, but also modification of environment, husbandry,
and production practices. For this reason, the prevention and control sections in this manual refer to
specific agents but are not always appropriate or complete in terms of control of disease complexes.
Swine practitioners expend considerable effort in diagnosis, herd investigation, and understanding the
interactions of risk factors before implementing cost-effective control strategies. These activities are
beyond the scope of this manual but our vision is that this manual will serve as a foundation on which to
build a better understanding of the complexities of disease in swine populations.
Familiarity with the organization of the manual will make it more useful. The table of contents lists the
diseases and conditions of swine covered in this manual. Most sections are based on the nature of the
etiologic agent, and each section is preceded by its own table of contents. The time-saving index at the
back of the book lists each major disease by name, often cross-referenced with a synonymous name.
Several tables are included. Some are designed to help in differential diagnosis. Others list major diseases
of a single body system and permit a rapid overview of diseases of that system. The tables may be of
special value in preparing for board exams.
Comments on the manual and how it can be made more useful are encouraged and appreciated. They
can be mailed to Dr. Alex Ramirez, 2231 Lloyd Veterinary Medical Center, 1809 S Riverside Drive,
Iowa State University, Ames, Iowa 50011 or e-mailed to ramireza@iastate.edu.
 TABLE OF CONTENTS

Table of Contents
Abbreviations .....................................................................................................................................................................................1
Swine industry terminology............................................................................................................................................................3

SECTION I: Diseases caused by bacteria, mycoplasmas, and spirochetes..................................7

Actinobacillus pleuropneumoniae.....................................................................................................................................................9
Actinobacillus suis............................................................................................................................................................................ 12
Anthrax............................................................................................................................................................................................. 14
Atrophic rhinitis............................................................................................................................................................................. 16
Clostridial diarrhea......................................................................................................................................................................... 18
Colibacillosis.................................................................................................................................................................................... 21
Erysipelas.......................................................................................................................................................................................... 25
Greasy pig disease............................................................................................................................................................................ 27
Haemophilus parasuis .................................................................................................................................................................... 29
Ileitis.................................................................................................................................................................................................. 32
Leptospirosis.................................................................................................................................................................................... 35
Mycoplasma suis .............................................................................................................................................................................. 37
Mycoplasmal arthritis.................................................................................................................................................................... 39
Mycoplasmal pneumonia ............................................................................................................................................................. 41
Pneumonic pasteurellosis.............................................................................................................................................................. 44
Salmonellosis................................................................................................................................................................................... 46
Streptococcus suis.............................................................................................................................................................................. 50
Swine brucellosis............................................................................................................................................................................. 53
Swine dysentery and spirochetal colitis...................................................................................................................................... 55
Tuberculosis..................................................................................................................................................................................... 58

SECTION II: Diseases caused by viruses ........................................................................... 61

African swine fever ........................................................................................................................................................................ 63
Blue eye disease................................................................................................................................................................................ 65
Classical swine fever....................................................................................................................................................................... 67
Encephalomyocarditis virus.......................................................................................................................................................... 70
Foot-and-mouth disease ............................................................................................................................................................... 72
Hemagglutinating encephalomyelitis......................................................................................................................................... 74

i
 SWINE DISEASE MANUAL

Inclusion body rhinitis................................................................................................................................................................... 76

Influenza .......................................................................................................................................................................................... 78
Japanese encephalitis...................................................................................................................................................................... 81
Parvovirus......................................................................................................................................................................................... 83
Porcine circovirus associated diseases......................................................................................................................................... 85
Porcine picornaviruses................................................................................................................................................................... 88
Porcine reproductive and respiratory syndrome...................................................................................................................... 92
Porcine respiratory coronavirus................................................................................................................................................... 96
Pseudorabies .................................................................................................................................................................................... 98
Rotavirus.........................................................................................................................................................................................101
Senecavirus A.................................................................................................................................................................................103
Swine enteric coronavirus diseases............................................................................................................................................105
Swine vesicular disease.................................................................................................................................................................108
Swinepox.........................................................................................................................................................................................110
Vesicular exanthema ....................................................................................................................................................................111
Vesicular stomatitis ......................................................................................................................................................................112

SECTION III: Emerging viruses .......................................................................................115

Filoviruses (Ebola virus and Marburg virus), Hepatitis E virus ...............................................................................................117
Paramyxoviruses (Menangle and Nipah viruses), Pestivirus F (Bungowannah virus) .........................................................118
Porcine adenovirus, Porcine astrovirus, Porcine bocavirus ..................................................................................................119
Porcine parainfluenza virus type 1, Porcine sapovirus..........................................................................................................120
Torque teno virus, West Nile virus (Kunjin virus) ................................................................................................................121

SECTION IV: Diseases caused by parasites ....................................................................123

Coccidiosis.....................................................................................................................................................................................125
Cysticercosis...................................................................................................................................................................................127
Lice...................................................................................................................................................................................................129
Lungworm......................................................................................................................................................................................130
Mange..............................................................................................................................................................................................132
Minor intestinal nematodes: Kidney worm, Nodular worm, Thorny-headed worm, Threadworm...........................134
Roundworm...................................................................................................................................................................................137
Trichinellosis..................................................................................................................................................................................139
Whipworm.....................................................................................................................................................................................141

ii
 TABLE OF CONTENTS

SECTION V: Miscellaneous ...............................................................................................143

Atresia ani, Aural hematoma, Congenital tremors, Cystitis and pyelonephritis, Dermatosis vegetans......................145
Ectopic ossification, Epitheliogenesis imperfects, Gastric ulcer ........................................................................................146
Hemorrhagic bowel syndrome, Hernias, Hydronephrosis, Hypogalactia and MMA...................................................148
Hypoglycemia, Megacolon, Mulberry heart disease and related conditions...................................................................149
Osteochondrosis, Pityriasis rosea, Porcine stress syndrome................................................................................................151
Prolapses, Pustular dermatitis, Rabies, Ringworm.................................................................................................................152
Shoulder ulcers in sows, Skin necrosis of piglets, Splayleg (spraddleleg), Sunburn and photosensitization.............153
Torsion and volvulus, Vestibular syndrome, Vices (tail biting, ear biting, flank biting, navel sucking).....................154

SECTION VI: Nutritional diseases, toxicoses, and poisonings .......................................155

Mycotoxicoses................................................................................................................................................................................157
Nutritional deficiencies and excesses........................................................................................................................................159
Toxins (plants, feed additives, chemicals, and gases).............................................................................................................162

SECTION VII: Tables .........................................................................................................165

Anthelmintics and parasiticides for swine...............................................................................................................................167
Arthritis in neonatal and growing swine..................................................................................................................................168
Central nervous system (CNS) diseases in swine: comparative approach to diagnosis.................................................169
Diarrheal diseases common at various ages.............................................................................................................................171
Diarrheal diseases in swine: comparative approach to diagnosis........................................................................................172
Internal parasites...........................................................................................................................................................................175
Intestinal hemorrhage: differential diagnosis..........................................................................................................................177
Mycoplasma-related diseases......................................................................................................................................................179
Reproduction: causes of low farrowing rate............................................................................................................................180
Reproductive failure: infectious causes ...................................................................................................................................181
Respiratory disease in swine: comparative approach to diagnosis......................................................................................183
Skin lesions: differential diagnosis............................................................................................................................................186
Vesiculating viral diseases............................................................................................................................................................189
Zoonotic agents found in swine and humans.........................................................................................................................190

INDEX ........................................................................................................................................... 193

iii
iv
 ABBREVIATIONS

Abbreviations
AASV American Association of Swine Veterinarians FDA US Food and Drug Administration
AAVLD American Association of Veterinary FE Feed efficiency
Laboratory Diagnosticians
FMD Foot-and-mouth disease
AD Aujeszky’s disease (pseudorabies)
FSIS Food Safety Inspection Service
ADFI Average daily feed intake
HA Hemagglutination assay
ADG Average daily gain
HACCP Hazard analysis critical control point
AI Artificial insemination
HE Hemagglutinating encephalomyelitis
AIAO All-in all-out
HEV Hepatitis E virus
AMDUCA Animal Medicinal Drug Use Clarification Act
HI Hemagglutination inhibition
APHIS Animal and Plant Health Inspection Service
HPS Haemophilus parasuis
APP Actinobacillus pleuropneumoniae
IAV-S Influenza A virus of swine
AR Atrophic rhinitis
IBR Inclusion body rhinitis
ASF African swine fever
IF Immunofluorescence
BED Blue eye disease
IFA Immunofluorescent antibody
BVD Bovine viral diarrhea
IHA Indirect hemagglutination
CF Complement fixation
IHC Immunohistochemistry
CNS Central nervous system
ISH In situ hybridization
CPE Cytopathic effect
JE Japanese encephalitis
CSF Classical swine fever
JSHAP Journal of Swine Health and Production
CVM Center for Veterinary Medicine
LPS Lipopolysaccharides
DIVA Differentiate infected from vaccinated animals
MARV Marburg virus
DON Deoxynivalenol
MEW Medicated early weaning
EBOV Ebola virus
MHP Mycoplasma hyopneumoniae
ED Edema disease
MHR Mycoplasma hyorhinis
ELISA Enzyme-linked immunosorbent assay
MHS Mycoplasma hyosynoviae
EM Electron microscopy
MLVA Multiple-locus variable number tandem
EMC Encephalomyocarditis repeat analysis
EP Enzootic pneumonia MLST Multi-locus sequence typing
EPG Eggs per gram MMA Mastitis, metritis, agalactia
ET Embryo transfer MMEW Modified medicated early weaning
FA Fluorescent antibody MPS Mycoplasmal pneumonia of swine
FAT Fluorescent antibody test MRSA Methicillin-resistant Staphylococcus aureus
FADDL Foreign animal disease diagnostic laboratory NAD Nicotinamide adenine dinucleotide
FCR Feed conversion ratio NADC National Animal Disease Center
ABBREVIATIONS 1
SWINE DISEASE MANUAL

NPB National Pork Board PSY Pigs weaned per sow per year
NPPC National Pork Producers Council PWM Preweaning mortality
NRC National Research Council RFLP Restriction fragment length polymorphism
OA Osteoarthritis SAHO State animal health official
OCD Osteochondrosis SD Swine dysentery
PAdV Porcine adenovirus SECD Swine enteric coronavirus diseases
PAR Progressive atrophic rhinitis SEW Segregated early weaning
PAstV Porcine astrovirus SIV Swine influenza virus (archaic; see IAV-S)
PBoV Porcine bocavirus SMEDI Stillbirth, mummification, embryonic death,
infertility
PCMV Porcine cytomegalovirus
SMSLV San Miguel sea lion virus
PCR Polymerase chain reaction
SN Serum neutralization
PCV Porcine circovirus
SPF Specific pathogen free
PCVAD Porcine circovirus associated disease
SVA Senecavirus A
PCVD Porcine circovirus disease
SVV Seneca Valley virus (see SVA)
PDCoV Porcine deltacoronavirus
SwPV Swinepox virus
PDNS Porcine dermatitis and nephropathy syndrome
TB Tuberculosis
PED Porcine epidemic diarrhea
TGE Transmissible gastroenteritis
PHE Porcine hemorrhagic enteropathy
USAHA United States Animal Health Association
PIA Porcine intestinal adenomatosis
USDA United States Department of Agriculture
PMWS Postweaning multisystemic wasting syndrome
VE Vesicular exanthema
PPE Porcine proliferative enteropathy
VES Vesicular exanthema of swine
PPV Porcine parvovirus
VFD Veterinary Feed Directive
PQA Pork Quality Assurance
VI Virus isolation
PRCV Porcine respiratory coronavirus
VN Virus neutralization
PRDC Porcine respiratory disease complex
VS Vesicular stomatitis
PRRS Porcine reproductive and respiratory syndrome
WNV West Nile virus
PRV Pseudorabies virus
PSS Porcine stress syndrome

2 ABBREVIATIONS
 SWINE INDUSTRY TERMINOLOGY

Swine industry terminology

Following are some terms used in the swine industry. Although
many of the terms have never been defined precisely, the defini-
tions give some idea as to their meaning.
Acclimatization Type of swine farm where the main intention is to raise pigs for
A period for new breeding stock to become immune to disease
organisms on the farm. This is usually accomplished by isolating
new animals prior to their entry into the herd, while intentionally
exposing them to potential pathogens on the recipient farm, such
as by commingling with culls. The goal is for incoming breeding
stock to become immune to and cease shedding endemic disease
agents. Acclimatization is often performed at the same time as the
period of isolation.
Average daily gain (ADG)
The average amount of weight a pig gains per day.
Adjusted farrowing rate or nearly so, or where a facility is not completely depopulated
The number of sows farrowed, divided by (the number of sows
serviced minus the number of sows that were culled for non-re-
productive reasons).
All-in all-out (AIAO) Special feed fed to piglets prior to weaning.
A production method where there are no additions to a group of
pigs following their placement into a room, barn, or location. All
pigs are removed before any subsequent groups of pigs are placed.
Usually, pigs in a group are born in as brief a period as possible (1
to 2 weeks), started, raised, and sold together. Each subsequent
group is separated physically and has separate air space. The
facilities are totally depopulated, cleaned, and disinfected before
the next group of pigs enters. There are many disease control
advantages of AIAO because there is only one age group of pigs
in a location.
Back pressure test
Applying pressure to the back of a sow to determine if she is
exhibiting estrus.
Barrow ing the facilities, and then repopulating the farm with pigs free of
Castrated male pig.
Carcass yield
Percent of the live body weight in the eviscerated carcass.
Commercial herd
slaughter. These herds make the final cross between “terminal”
sires and “maternal” females to produce fast-growing, lean, effi-
cient pigs for slaughter. Commercial herds are also referred to
as “parent” herds; they receive replacement gilts from multiplier
herds and send offspring to slaughter.
Conception rate
The number of sows detected pregnant divided by the total num-
ber of sows serviced (bred).
Continuous flow
Any rearing system under which the pigs use facilities continuously
before more pigs are added. Often the pigs are not started, raised,
or sold together, which is the opposite of the AIAO system.
Creep feed
Cross-fostering
Moving pigs from one sow to another to balance the size or num-
ber of pigs per litter.
Cryptorchid
A male pig with one testicle retained in the body cavity.
Cull rate
The number of sows removed from a herd annually, divided by
the total number of sows in the herd.
Depopulation/Repopulation
Removing all animals on the entire farm, cleaning and disinfect-
specific diseases.

Boar Down time

Intact male pig. Time during which there are no animals in a barn, which facili-
tates cleaning and disinfecting.
Boar taint
The characteristic smell and taste that is often detectable in pork Farrow
derived from sexually mature boars. To give birth to piglets.

Carcass index
An index used to establish the value of a carcass based on body
weight and backfat measurement.

SWINE INDUSTRY TERMINOLOGY 3

SWINE DISEASE MANUAL

Farrow-to-finish Induced farrowing

A swine production system where all stages of production The use of chemicals to trigger parturition and enable a producer
(breeding, gestation, farrowing, nursery, and finishing) are on to attend farrowings.
the same site, often housed together or in immediately adjacent
buildings. The buildings may be subdivided or partitioned into Isolation
sections for each stage of production. Animals (eg, new breeding stock) that have a risk of introducing
a disease into a breeding herd are placed in a location that is iso-
Farrowing rate lated from the rest of the herd. There they are observed and tested
The number of sows that farrowed divided by the number of sows
for disease exposure before being allowed to enter the breeding
serviced (bred).
herd. Often, isolation and acclimatization occur simultaneously.
Feed conversion ratio (FCR) Lactogenic immunity
The amount of feed used divided by the total weight gained; also
Antibodies (especially IgA) passed from the sow to the piglet via
referred to as feed efficiency or feed to gain (F:G).
the milk.
Feed wastage Market hog
Feed that is fed but is not eaten.
Market weight pig; usually greater than 220 pounds (100 kilo-
grams) in the US.
Feeder pig
A pig moved or sold from a nursery at approximately 50 pounds
(23 kilograms).
Medicated early weaning (MEW)
A system of raising pigs under which piglets are weaned very
young, as early as 4 to 5 days of age, and are aggressively medicated
Finisher from birth until they are 10 to 20 days old. The system is used to
Stage of production after the grower phase, starting at around reduce or eliminate pathogens that might be transmitted to piglets
150 pounds (68 kilograms) and continuing to market weight of from the dams. Modified medicated early weaning (MMEW) is
250 to 290 pounds (114 to 132 kilograms). a variant of MEW where pigs are weaned later than a specified
age (eg, 17 days of age). The specific weaning age and medication
Floor feeding depend on the disease(s) in the source herd to be controlled.
Putting the pigs’ feed directly on the floor, rather than in a feeder.
Multiple mating
Genetic pyramid Mating or inseminating a sow more than once during a single
System by which animals of highest genetic value are used to pro- estrus cycle.
duce offspring that will be used to populate commercial farms. The
“nucleus” herd supplies genetically superior animals to “multiplier” Multiplier herd
herds that produce the gilts that will populate commercial farms. Herd of purebred animals that are crossed to produce replace-
ment gilts for use in commercial herds. Multiplier herds receive
Gilt gilts from nucleus herds and send their offspring to commercial
A young female pig that has not given birth. farms. Multiplier herds are also called “grandparent” farms.

Gilt pool Multi-site production

The group of gilts selected for the breeding herd but not yet bred.
Grower is the facility where weaners are placed in a nursery, and site 3 is
Stage of production after the nursery phase, when a pig weighs
between 50 and 150 pounds (23 and 68 kilograms).
Hybrid vigor
The improved production due to heterosis; the combination of
two purebreds.
A system of raising pigs in well-separated facilities. In a 3-site
system, site 1 includes breeding, gestation, and farrowing, site 2
a grower/finisher facility. All sites operate as AIAO. Some pro-
ducers prefer to combine sites 2 and 3, and the operation is then
referred to as a 2-site system.
Not in pig (NIP)
A sow that is assumed to be pregnant at the end of gestation but
found not pregnant just prior to farrowing.

4 SWINE INDUSTRY TERMINOLOGY

 SWINE INDUSTRY TERMINOLOGY

Nucleus herd Seasonal infertility

A herd at the top of a genetic pyramid, usually composed only Decreased production associated with breeding sows during the
of purebred stock of superior quality and housed in highly spe- summer months.
cialized, biosecure farms called “nucleus” farms. Improvement
at this level is obtained by selecting superior individuals within Segregated early weaning (SEW)
each breed. From these pure lines, individuals are selected for Weaning all piglets under a specified age, often approximately
particular characteristics such as growth rate, backfat, or litter 17 days of age, usually as part of a short-term disease control
size. The best individuals from this population will go to multi- strategy.
plier herds for crossbreeding. Nucleus farms are also referred to as
“great grandparent” farms. Service
One or more mating events that occur during a single estrus cycle
Nursery pigs constitute a service.
Pigs from weaning to 50 to 75 lbs (23 to 34 kilograms).
Specific pathogen free (SPF)
Parity A method of obtaining pigs free of specified pathogens by raising
The number of litters that a sow has farrowed. surgically derived piglets apart from their dam, usually in an
isolated facility or by a foster sow in the recipient herd. A strategy
Parity 0 used for genetic improvement, disease elimination, or starting a
A gilt that has been bred but has not yet farrowed. new, disease-free herd.

Partial depopulation Split suckle

Depopulating one area of a barn or phase of production to create Management technique where the more robust or first-farrowed
a physical “gap” in the production flow; part of some disease pigs of a large litter are removed for one to two hours to allow
control strategies. smaller, later-born pigs to suckle to ensure all piglets receive an
adequate dose of colostrum.
Pig density
The number of pigs per square area (foot or meter) of floor space. Split wean
Weaning the biggest pigs in a litter 2 to 3 days before the others
Pigs marketed per sow per year in order to increase weaning weight of the remaining piglets and
The number of pigs marketed per year divided by the number of decrease weaning-to-breeding interval.
sows in the herd.
Sow
Pigs weaned per sow per year (PSY) A female pig that has been bred and given birth.
The number of pigs weaned per year divided by the number of
sows in the herd. Starter feed
First specialized diet fed to newly weaned pigs.
Preweaning mortality (PWM)
Total number of pigs that die after birth but before weaning Weaner (weaner pigs)
(number of pigs born alive minus number of pigs weaned) Term describing pigs when they are removed from the sow and the
divided by total number of pigs born alive. early growing, ie, nursery, phase for up to 8 weeks after weaning.

Return to estrus Weaning-to-breeding interval

Sow that comes back into heat after breeding and before farrow- Number of days between weaning and breeding a sow.
ing, indicative of a failed conception or loss of pregnancy.
Wean-to-removal interval
Savaging Time between weaning and culling a sow.
When a sow or gilt is aggressive to her newborn piglets, usually
by biting or eating them. The cause of the condition is poorly Zero wean
understood. Weaning a sow the day that she farrows.

Scour
Common term for diarrhea.

SWINE INDUSTRY TERMINOLOGY 5

6
 BACTERIA
Section I

Diseases caused by bacteria,

mycoplasmas, and spirochetes

Actinobacillus pleuropneumoniae ....................................................................................................................................................9

Actinobacillus suis............................................................................................................................................................................ 12
Anthrax............................................................................................................................................................................................. 14
Atrophic rhinitis............................................................................................................................................................................. 16
Clostridial diarrhea ........................................................................................................................................................................ 18
Colibacillosis ................................................................................................................................................................................... 21
Erysipelas.......................................................................................................................................................................................... 25
Greasy pig disease ........................................................................................................................................................................... 27
Haemophilus parasuis .................................................................................................................................................................... 29
Ileitis.................................................................................................................................................................................................. 32
Leptospirosis.................................................................................................................................................................................... 35
Mycoplasma suis .............................................................................................................................................................................. 37
Mycoplasmal arthritis.................................................................................................................................................................... 39
Mycoplasmal pneumonia ............................................................................................................................................................. 41
Pneumonic pasteurellosis.............................................................................................................................................................. 44
Salmonellosis................................................................................................................................................................................... 46
Streptococcus suis.............................................................................................................................................................................. 50
Swine brucellosis............................................................................................................................................................................. 53
Swine dysentery and spirochetal colitis ..................................................................................................................................... 55
Tuberculosis..................................................................................................................................................................................... 58

7
 8
BACTERIA
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Actinobacillus pleuropneumoniae
Alternate names and abbreviations
APP, porcine pleuropneumonia, Haemophilus pleuropneumoniae
or HPP (archaic)
Definition
This organism causes severe pleuropneumonia and is a highly
contagious disease of swine often characterized by sudden onset,
short clinical course, high morbidity, and high mortality.
Occurrence
Porcine pleuropneumonia caused by Actinobacillus pleuropneumo-
niae (APP) is widely distributed throughout major swine-raising
countries and is one of the most important bacterial respiratory
pathogens globally. The host range of APP is restricted to swine.
Most virulent strains can cause rapidly fatal pneumonia, with
abrupt and severe outbreaks not uncommon. In naïve herds, APP
occurs in all age groups, but it is most frequently seen in pigs 6 to
20 weeks of age. Actinobacillus suis can cause similar disease and
lesions but is not as contagious as APP.
Historical information
In the US, APP was first reported in 1957. It was reported
frequently in the 1960’s and 1970’s. The frequency of outbreaks
increased with the industrialization of swine production. The
disease and its epidemiology are well researched through exper-
imental studies and field experiences. Because of the economic
consequences of mortality and cost of control of this disease,
most producers strive to eliminate the more virulent serotypes of
APP from herds.
Etiology
The APP organism is a hemolytic, Gram-negative, encapsulated,
coccobacillary rod that is highly host-specific for swine and
fragile outside the host. Strains denoted by serotype vary in vir-
ulence and pathogenicity. There are 2 biotypes, whereby biotype
I is dependent on an exogenous source of NAD (nicotinamide
adenine dinucleotide) in culture and biotype II is not. NAD is
usually supplied by a Staphylococcus nurse streak, which allows the
“satellite” growth of APP biotype I on blood agar. Biotype 1 has
14 serotypes (1-12, 15, 16) and biotype II is composed of 2 sero-
types (13, 14) that are usually considered to be less virulent than
biotype I serotypes. However, because genetic variation, serologi-
cal cross-reaction, and different classification schemes are utilized,
categorical classification of isolates can sometimes be confusing if
not daunting. Serotype prevalence varies considerably across the
globe and by region.
The APP organisms secrete one or more of 4 exotoxins: ApxI,
ApxII, ApxIII, and ApxIV, together called RTX toxins. Actino-
bacillus pleuropneumoniae also produces abundant endotoxin.
The RTX toxins are cytotoxic and/or hemolytic. The types and
BACTERIA
quantities of exotoxins produced vary among the 16 serotypes.
Antibodies to the specific exotoxins probably are important in
protective immunity.
Actinobacillus suis is closely related to APP, and some strains pro-
duce one or more of the RTX toxins as well. The two organisms
may cross-react on some serological tests; polymerase chain reac-
tion (PCR) tests must also be interpreted with care.
Epidemiology
Actinobacillus pleuropneumoniae is usually transmitted within and
between herds by direct contact via nasal secretions and fomites,
but transmission via aerosol for short distances (eg, 100 meters)
has been reported. Fomites, including boots and coveralls, can
spread the organism but are infectious for only a short time since
APP is fragile outside the host. APP does not persist in the envi-
ronment but can survive several days to several weeks in mucus
exudates in moist organic matter. Routine hygienic practices with
disinfection are effective for environmental elimination.
Transmission from dam to offspring in positive herds probably
occurs late in the suckling phase (“late colonizer” of nasopharynx
and tonsil), making APP elimination from populations possible
by medicated early weaning techniques. Subclinical carriage of
APP in tonsils occurs for long (indefinite) periods in both healthy
animals as well as in survivors of clinical outbreaks. The likelihood
of disease expression is strongly influenced by the virulence cassette
of the particular serotype present, the status of passive or active spe-
cific immunity, and the presence of both infectious and non-infec-
tious risk factors. Overstocking, inadequate ventilation, coinfection
with other respiratory pathogens, or unusual stress may facilitate
transmission or precipitate outbreaks.
Pathogenesis
Although carriage of organisms by asymptomatic carriers can be
for indefinite periods, when finally introduced into the deep lung
(alveoli), disease onset is rapid with fatal pleuropneumonia pos-
sible within hours. This suggests that other risk factors can facili-
tate or initiate outbreaks in colonized populations of pigs. Once
introduced to the deep lung tissue, hemolysins, Apx toxins, and
other proteins produced by APP affect the function of endothe-
lial cells and pulmonary alveolar macrophages. There is variation
in the hemolytic and cytotoxic effects of ApxI, ApxII, and ApxII,
which impacts virulence. Severe damage to endothelial cells,
pneumocytes, and inflammatory cells from Apx cytotoxins occurs
rapidly and leads to ischemic necrosis and endotoxic shock. These
peracute cases typically present as cases of sudden deaths. In acute
and subacute cases, inflammation and thrombosis is followed by
infarction and sequestration of infarcts in the lungs.
Pathogenesis involves both variation in host resistance and
variation in virulence among serotypes. Generally, serotypes 1
ACTINOBACILLUS PLEUROPNEUMONIAE 9
 SWINE DISEASE MANUAL
BACTERIA
and 5 are considered more virulent than 7 or 3, but all can cause
significant disease and any of these may be present subclinically in
populations of pigs.
Other pathogens (eg, Mycoplasma hyopneumoniae, influenza A
virus in swine, and porcine reproductive and respiratory syndrome
virus), commingling, or environmental factors that affect pulmo-
nary clearance in the lung may influence onset and course of the
disease. Colostral immunity in young pigs confers some resistance
to infection and permits gradual development of active immunity
in many exposed, growing pigs. Naïve pigs suddenly exposed to
APP are more likely to develop fulminating clinical signs.
Clinical signs
Signs vary considerably between peracute and chronic forms
of APP. With peracute disease, individual pigs are either found
dead or have high fever, lethargy, anorexia, and may vomit. Pigs
rapidly become recumbent, cyanotic, dyspneic, and die with
foamy blood-tinged discharge from the nose. With acute disease,
more pigs are affected, with slower progression of similar signs,
and the outcome is not necessarily fatal. Pigs may have a shallow
cough, and pigs medicated at this stage may respond to antimi-
crobial intervention. In less severely affected pigs, chronic disease
can result and is seen as intermittent cough, reduced gain, and
ill-thrift with signs of undifferentiated pneumonia because of the
pleural adhesion and pulmonary abscesses that are likely present.
Morbidity and mortality in growing swine vary but can become
high. Peak mortality usually occurs in pigs 10 to 16 weeks old.
Mortality can reach 20% to 80% in fattening pigs. Abortions may
occur in acutely infected pregnant females.
Lesions
Lesions of APP are usually restricted to the lungs. Characteristic
lesions include locally extensive areas of pulmonary necrosis
and hemorrhage that are quite firmly consolidated, dark red in
color, and are nearly always accompanied by fibrinous pleuritis.
The thoracic cavity often contains blood-tinged fluid. The classic
lesion of APP consists of large areas of hemorrhage and necrosis
in the dorsal portion of one or both diaphragmatic lobes accom-
panied by severe fibrinous pleuritis. These lesions develop as a
result of APP gaining access to alveoli (through inhalation) and
causing large areas of infarction overlaid with fibrinous pleuritis.
Bloody froth often fills larger airways and there may be interlobu-
lar edema along with congestion in the remainder of lung. Fibrin-
ous pleuritis almost always overlays pneumonic areas and extends
to adjacent costal pleura. Occasionally there may be serofibrinous
pericarditis. Even less frequent is necrotic or ulcerative pharyngi-
tis and polyarthritis.
Chronic cases often have large, sequestered or encapsulated nod-
ules of necrosis in the lungs that incompletely resolve as abscesses.
Lung lesions are often attached to the rib cage by fibrous adhe-
sions, leading to condemnations at slaughter.
10 ACTINOBACILLUS PLEUROPNEUMONIAE
Accurate differentiation of APP and A suis based on gross lesions
is difficult, perhaps impossible. Because A suis infection is more
often accompanied by septicemia, bacterial culture is an import-
ant tool in establishing a diagnosis. This differential is important
with less virulent strains of APP where disease is sporadic and less
severe.
Diagnosis
The sudden onset of an acute, rapidly spreading, respiratory dis-
ease associated with high morbidity and mortality is suggestive of
APP. Observation of dark red infarcts and pleuritis in the lungs
of acutely affected cases, sequestered nodules in lungs of chronic
cases, and a high incidence of pleuritis in the herd are also highly
suggestive for APP involvement. Virulent serotypes of APP exist
within both biotype I (NAD dependent) and biotype II (NAD
independent). Isolation and identification of APP is commonly
practiced in order to confirm the diagnosis. Detection by molec-
ular testing (PCR) is also confirmatory and may allow immediate
genotyping to predict serotype. Histopathology is useful to
confirm typical lesions as well as to elucidate whether other insult
types are present. Acute outbreaks of APP must be differentiated
from other respiratory diseases, especially A suis infection, classi-
cal swine fever, pneumonic pasteurellosis, pneumonic salmonello-
sis, influenza, and mycoplasmal pneumonia.
Serotyping is commonly performed on isolates confirmed as
APP to characterize expected virulence, aid in epidemiology, or
predict immune cross-protection by natural or vaccinal exposure.
However, cross-reactions are problematic for some isolates. Use
of monoclonal antibodies improves accuracy but some isolates
still cannot be differentiated by serological tests. Advancement in
molecular techniques, particularly PCR, for predicting serotype,
is providing less uncertainty for some of the more troubling sero-
types and likely will improve over the next few years. PCR toxin
typing does not provide serotype information but can determine
which Apx toxin genes are present in a particular isolate.
To eliminate APP from a herd, accurate detection of inapparent
carriers can be very helpful. Immunomagnetic separation and cul-
ture of tonsil samples has been useful but is quite technical and
laborious with limited availability. PCR performed on tonsils,
tonsil biopsies or tonsil scrapings is quite sensitive, particularly if
performed after selective enrichment culture, but is not capable
of differentiating APP serotypes. Detection of inapparent carriers
with 100% sensitivity should not be expected with either culture
or molecular techniques.
Serology is useful for APP surveillance and probably the most
useful tool for detection of subclinical infections. Enzyme-linked
immunosorbent assay (ELISA) tests can target Apx antigens,
with a commercially available ELISA for detection of ApxIV
antibodies shown to be quite sensitive for detection of subclinical
carriers or previously infected pigs. As with all diagnostic tests,
communication with experts at the diagnostic laboratory is essen-
tial for sample selection, preservation, test type(s) requested, and
interpretation of results.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Control
Herds free of APP should be managed as closed herds since
introduced swine may be carriers. Breeding stock and pigs that
must be introduced should originate from APP-free herds. They
should be introduced only after testing both before and after a
quarantine period of at least 30 days.
Introduction of naïve animals to an APP-positive herd requires
careful planning. Usually, animals to be introduced are vacci-
nated, perhaps multiple times, with a homologous bacterin-tox-
oid. They are monitored closely when commingled with resident
animals and, should some sicken, be treated parenterally as indi-
viduals or by affected pen.
Usually, control of APP in endemically infected herds requires
a combination of medication, improved husbandry, and vacci-
nation. Because antibiotic therapy is only effective early in the
course of this rapidly progressing disease, outbreaks of pleuro-
pneumonia should be treated aggressively to decrease mortality
and mitigate lung damage in survivors. Acute outbreaks demand
immediate parenteral antimicrobial treatment of entire pens con-
taining affected pigs as well as those in adjacent pens because of
the rapid nose-to-nose spread. Depending on the situation, anti-
biotics administered via the water supply may be a useful adjunct
during outbreaks to suppress new cases in those pigs that are still
willing to drink. However, water medication should not be relied
on for treatment of pigs that are sick.
Feed medication in pulse doses or continuously has been used for
prevention and on-going control in groups of pigs. This combi-
nation of injectable antibiotic augmented with medicated feed
or water for a few weeks can reduce mortality and decrease the
impact of chronic disease. Antimicrobials do not eliminate the
infection from a group; outbreaks can still occur after the medica-
tion has been removed.
Management factors of importance in prevention include all-in,
all-out, age-segregated production with careful cleaning and
disinfection between groups, avoiding overstocking, assuring
ventilation systems are functioning properly, and eliminating or
controlling other predisposing diseases.
The use of vaccines, usually in the form of killed bacterin-toxoids
or subunit toxin-based products, is important for the prevention
of APP. Bacterins are usually serotype-specific and are sometimes
produced as autogenous products. Bacterins may induce pro-
duction of antibodies to surface antigens of APP. However, the
appearance of antibodies after vaccination may not relate to the
level of protection provided by the vaccination. Newer types of
subunit or toxin-based vaccines may produce limited cross-pro-
tection against multiple serotypes. Some of these products are
“fortified” with other components of APP such as outer mem-
brane proteins. Their use should not interfere with the serological
tests that are based on detection of antibodies to capsular or
lipopolysaccharides (LPS).
BACTERIA
The efficacy of various vaccines can be difficult to quantify. Gen-
eration of antibodies or the level of serum antibodies to various
components in the vaccine (eg, LPS, capsule, outer membrane
proteins, Apx toxins) may not be an accurate predictor of the
level of protection.
Most commonly, vaccines are used to increase immunity in the
sow herd, and the practice of vaccinating the sow may have the
benefit of delaying the colonization of her piglets. However,
routine practice of sow-herd vaccination remains controversial
because the resulting high level of maternal antibodies that occurs
in these piglets means that piglet vaccination must be delayed
until piglets are perhaps as much as 7 weeks old before the mater-
nally derived antibodies have declined to low enough levels to
permit effective vaccination. Vaccination tends not to eliminate a
carrier state from developing.
In some cases, particularly those associated with serotypes of high
virulence, all efforts to control the disease effectively fail and the
cost of long-term control becomes unacceptably high. At this
point, eradication of APP becomes a consideration, and in fact
is achievable, though it requires careful planning, commitment,
and effort. Complete depopulation followed by repopulation
with APP-free animals is an effective but costly method of erad-
ication. Depopulation must be followed by thorough cleaning
and disinfection of all facilities and leaving them vacant for a few
weeks, then restocking using APP-free swine. An alternative to
depopulation is medicated early weaning with age segregation,
perhaps augmented by vaccination, medication, culling, and
repopulation. This option can result in weaning of APP-negative
piglets, even though the breeding herd remains APP positive.
Each farm and each serotype have different nuances, hence
careful review of necessary biosecurity, vaccination, colostrum
management, facility limitations, interventions, procedures, and
costs are warranted before attempting elimination.
ACTINOBACILLUS PLEUROPNEUMONIAE 11
 SWINE DISEASE MANUAL
BACTERIA
Actinobacillus suis
Alternate names and abbreviations
None
Definition
An infectious disease caused by Actinobacillus suis characterized
by septicemia, with hemorrhages and embolic lesions at multiple
sites, more obviously in the lungs. Necrotizing bronchopneumo-
nia with pleuritis is common, often with serous or serofibrinous
exudates in the thorax, pericardium or abdomen.
Occurrence
Outbreaks occur sporadically as various manifestations of acute
sepsis in pigs of all ages, with serositis in young pigs, acute pneu-
monia in grower pigs, and acute septicemia in adults as the most
common presentations. Most outbreaks are in recently weaned
pigs or in grow-finish pigs, usually with acute illness and death of
individual pigs while the remainder of the cohort remains clini-
cally normal.
Historical information
There have been reports of the disease since 1962. In the 1980’s,
after management techniques were introduced that minimized
exposure of neonates to many endemic pathogens, the incidence
of A suis infections appeared to increase in the US industry.
Misdiagnosis of the disease as Actinobacillus pleuropneumoniae
(APP) infection or other bacterial septicemias likely contributed
to under-reporting of the true prevalence of the disease.
Etiology
Actinobacillus suis is a Gram-negative, nicotinamide adenine
dinucleotide (NAD)-dependent, non-motile coccobacillus. It can
be aerobic or facultatively anaerobic. All isolates appear to be very
similar based on biochemical characteristics, restriction fragment
length polymorphism (RFLP), and toxin analysis. Antibodies to
A suis and APP may cross-react on some serological tests.
Epidemiology
The epidemiology is not completely understood but carrier pigs
probably introduce A suis into herds. The organism appears to
be widespread in swine populations and can be isolated from
the nasal cavity and tonsils of many healthy pigs as well as the
reproductive tract of healthy sows. It is believed to be an “early
colonizer” of neonates. Less than optimal environmental con-
ditions or concurrent diseases may increase the ability of A suis
to cause disease. Prevalence of the disease seems to be greater in
newly populated herds or high health herds, presumably due to
an absence of herd immunity.
12 ACTINOBACILLUS SUIS
Pathogenesis
Invasion probably occurs through the tonsil with the organism
then spreading through the bloodstream. This is suggested by the
presence of the organism in emboli within small blood vessels
at many lesion sites. The agent’s pathogenic effect is probably
a result of production of hemolysin and Apx toxins, similar to
those produced by APP. The organism has genes that code for
ApxI and ApxII, similar to APP, but appears to produce less of
those toxins. Other virulence factors are suspected to be pro-
duced by A suis but are not well characterized.
Clinical signs
The first signs of an outbreak may include sudden death of young
pigs with lesions attributed to a bacterial septicemia. Sick piglets
are febrile, breathe rapidly, and may have congested or cyanotic
extremities. Cyanosis, arthritis, enteritis, and rarely necrosis
of the feet, tail, and ears have been reported and are similar to
other causes (streptococcal infection, erysipelas, Salmonella) of
bacterial septicemia, particularly in suckling piglets and weaners.
Occasionally, infected pigs may show central nervous system
signs including tremors, shaking, or paddling. Mortality within
affected litters can be high, up to 50%.
Older growing pigs and adults can have similar signs but may also
have signs of acute respiratory distress. Lethargy or depression,
anorexia, and rarely irregular reddened skin lesions that resemble
those of erysipelas may be observed. Pregnant sows may abort.
Lesions
Lesions are similar in pigs of all age groups but vary considerably
between pigs and include petechial and ecchymotic hemorrhages
in many organs. Frequently, lesions are present in the lungs as
disseminated foci of hemorrhagic to necrotizing pneumonia, the
latter more marked in older piglets and growers and often with
fibrinous pleuritis. A consistent lesion in all age groups is serous
or serofibrinous exudate in the abdominal and thoracic cavities.
Polyarthritis may occur in piglets and grow-finish pigs.
Microscopic lesions occur in many major organs. These develop
around small colonies of A suis within the vascular emboli or
thrombi. Occasionally there are eosinophilic clubs surrounding
the colony. Both gross and microscopic lesions are typical of
embolic, bacterial septicemias.
Diagnosis
History, signs and lesions are suggestive of the diagnosis, but it
should be confirmed by culture of A suis from multiple organs.
PCR tests are available to detect A suis and differentiate it from
APP. Serological diagnosis is unreliable because antibodies to
A suis and APP may sometimes cross-react. Laboratory testing for
A suis is not routinely available.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES

BACTERIA
Control
Autogenous vaccines have been used but have not been evaluated
critically. Because there are multiple types of lipopolysaccharides
(LPS) in A suis, the LPS profile of the vaccine strain must match
that of the pathogen. Bacterin-toxoids containing ApxI and
ApxII are available.
Actinobacillus suis is sensitive to many antibiotics. Sick pigs
should be treated parenterally as soon as possible. The exposed
group can be treated by medicating the water.

ACTINOBACILLUS SUIS 13
 SWINE DISEASE MANUAL
BACTERIA
Anthrax
Alternate names and abbreviations
None
Definition
Bacillus anthracis can cause an acute bacterial disease in most
warm-blooded animals, including swine and man.
Occurrence
In swine, anthrax is relatively rare except when large numbers
of anthrax organisms are ingested. Although anthrax occurs
throughout the world, incidence in swine in the US is low.
Anthrax in grazing animals other than swine tends to occur in
certain geographic areas and is not seasonal. Swine, however, are
rather resistant to anthrax.
Historical information
Although there are many historical reports of anthrax in species
other than swine, most reports on the disease in swine have
occurred since 1952 to 1953 when a major epidemic occurred in
several Midwestern states. The outbreak was caused by imported,
contaminated bone meal used in preparing feed for swine. The
feed was widely distributed before anthrax was finally diagnosed.
In 1989 to 1990, an outbreak lasting over 14 weeks in a 500-
sow operation was reported. Reports of this outbreak serve to
emphasize the great difficulties and expense in depopulating,
cleaning, and disinfecting a large contaminated confinement
facility or slaughterhouse.
Etiology
Anthrax is caused by infection with B anthracis, a large, aerobic,
Gram-positive rod. The organism is easy to culture, and colonies
start to appear on blood agar within 12 hours. After 24 hours, the
colonies will be non-hemolytic and have irregular borders giving
them a “ground glass” appearance; they are sticky when touched
with a bacteriologic loop. Under suitable aerobic conditions,
spores are formed that are quite resistant to heat, desiccation, and
many disinfectants. Spores can persist in the environment for over
50 years.
In tissue, the organisms have a well-developed capsule and grow
in short chains. They have square ends when found in contact
with others in the same chain.
Epidemiology
Decaying, anthrax-infected carcasses and their fluids contaminate
the soil with resistant spores which then serve as a source of infec-
tion for grazing animals for months to years. Swine, however, are
rather resistant to anthrax and are seldom infected while grazing.
Infection of swine usually occurs when they have fed on an
anthrax-infected carcass, or when feeds containing large numbers
of spores are fed to them. The source in contaminated feeds is
14 ANTHRAX
the animal source component (eg, bone meal, tankage, or meat
scraps). Direct pig-to-pig transmission is rare. Biting flies and
mosquitoes have been shown to transmit anthrax.
Pathogenesis
During infection, the anthrax bacilli produce a complex
exotoxin. In experimental settings, a lethal factor in the exotoxin
is responsible for the death of the animal. Lethal factor causes
depression of the central nervous system and has a harmful effect
on mitochondria.
Invasion of the anthrax bacilli is usually through defects in the
pharyngeal mucosa or the tonsils. Invasion is often followed by
lymphangitis and localization of B anthracis in tonsils and/or cer-
vical lymph nodes. Alternatively, there can be focal or multifocal
localization in the intestine followed by spread to one or more
mesenteric lymph nodes. Localizations tend to be necrotizing.
Frequently, both pharyngeal and intestinal lesions develop. There
seldom is a septicemic form of anthrax in swine.
Clinical signs
Sudden, unexpected deaths may be the first signs of anthrax
following a highly variable incubation phase (1 to 8 days). Signs
depend upon the site of localization of lesions. Three forms of
anthrax, based on site of localization have been described: pha-
ryngeal anthrax, intestinal anthrax, and septicemic anthrax. Swine
with pharyngeal anthrax, the most common form, show marked
cervical swelling and dyspnea; they may die from suffocation.
Other signs include fever, depression, and inappetence, perhaps
vomiting. Swine with intestinal anthrax have similar signs, except
that cervical edema and dyspnea may not be apparent. Also, there
may be blood in the feces. Both pharyngeal and intestinal forms
can occur in the same animal. Swine are quite resistant to anthrax
and spontaneous recovery from cases with localized lesions is com-
mon. The rare septicemic cases that do occur have a short course
and may result in sudden death.
Lesions
A necropsy should not be performed on any animal suspected of
having died from anthrax; spores will be formed when the carcass is
opened and the organism is exposed to oxygen; these spores can per-
sist at the site for years. Necropsy will also expose humans to anthrax.
In anthrax-infected cadavers, rigor mortis may be weak or absent.
The blood may fail to clot and may be discharged from nose,
mouth, or anus. Many animals have no visible external lesions
other than pharyngeal swelling. Animals with pharyngeal anthrax
usually have a gelatinous cervical edema and markedly enlarged,
hemorrhagic, cervical lymph nodes. Tonsils are often covered
with fibrinous exudates. There may be a marked pharyngitis. In
chronic cases, necrotic lesions in nodes or tonsils may be gray-
ish-yellow and circumscribed.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Swine with intestinal anthrax usually have peritonitis with
excessive, bloody peritoneal fluid. Fibrin may be present in the
fluid and overlay the serosa of affected segments of intestine.
The mesentery attached to affected intestine (ileum and spiral
colon) is edematous and may contain reddened streaks around
the vasculature. There are focal or multifocal areas of severe, often
diphtheritic, enteritis. Regional lymph nodes draining the area
are enlarged and reddened. Animals with intestinal anthrax often
have pharyngeal lesions.
In septicemic anthrax, carcasses may appear pale and dehydrated.
There is bloodstained peritoneal fluid and scattered petechiation.
Diagnosis
Although bacteremia and septicemia are unusual findings in
swine infected with anthrax, it is advisable to take a peripheral
blood sample aseptically for smears and culture. Smears can be
fixed in Zenker’s solution and stained with polychrome methy-
lene blue. Anthrax bacilli will appear as long, square-ended, blue
rods with a pinkish capsule. Alternatively, smears can be stained
with Gram stain. The large Gram-positive, rod-shaped organisms
have a “boxcar” appearance that is presumptive but not definitive
of anthrax. Sometimes it may be necessary to biopsy or excise
an affected lymph node for culture using sterile technique. Any
necessary cut on a suspected cadaver should be disinfected or
plugged with a mass of cotton saturated with 10% formaldehyde.
BACTERIA
Bacillus anthracis can also be identified via polymerase chain
reaction or be cultured on blood agar and identified from colo-
nies that soon develop. Caution must be used when growing B
anthracis due to the zoonotic potential of this pathogen. Anthrax
must be differentiated from pharyngeal malignant edema, acute
erysipelas, and classical swine fever.
All cultures, contaminated materials, disposable equipment, and
infected experimental animals and their feces should be inciner-
ated. For carcass disposal, deep burial (greater than 4 feet deep)
followed by covering with lime is recommended. Any known or
suspected areas of contamination should be disinfected. Ten per-
cent sodium hydroxide, 5% formaldehyde, and 2% glutaraldehyde
are among the better disinfectants for B anthracis.
Control
An attenuated live vaccine against anthrax has been used for
prevention in some species but is seldom used for swine since they
have enough natural resistance to withstand considerable exposure.
Prevention in swine is usually by avoidance of heavy exposures
that might occur through ingestion of anthrax-infected carcasses
or contaminated feeds. Laws now exist that prevent importation
of raw bone meal. Some states have laws that regulate the use of
animal-origin products in feeds.
Treatment of infected animals can be effective if given early. Both
penicillin and oxytetracycline have been used effectively. Infection
can persist for up to 21 days.
ANTHRAX 15
 SWINE DISEASE MANUAL
BACTERIA
Atrophic rhinitis
Alternate names and abbreviations
Progressive atrophic rhinitis, PAR, AR, rhinitis
Definition
An infectious disease characterized in its early stages by sneez-
ing, snorting, and perhaps nosebleed. Advanced cases will prog-
ress to include atrophy and distortion of the nasal turbinates of
affected pigs.
Occurrence
Atrophic rhinitis (AR) occurs globally and only occurs in swine,
although a similar disease has been described in dogs and goats.
Signs and lesions can occur in any age group. In the US, AR has
decreased in prevalence in most areas due to routine use of early
weaning and age segregation, which, when combined with all-in,
all-out flow, will result in elimination of the disease from most
farms.
Historical information
Atrophic rhinitis was described first in 1830 but not actually
reported in the US until 1944. The condition rapidly increased
in frequency with expansion and intensification of swine pro-
duction and stimulated a great amount of research; AR has a
complex etiology.
Etiology
Toxigenic strains of Bordetella bronchiseptica and Pasteurella mul-
tocida (usually type D), may cause AR. Both organisms are aero-
bic, Gram-negative rods that readily colonize the nasal passages
of swine, and non-toxigenic strains are often widely distributed
in the swine population. Along with its association with AR, B
bronchiseptica can cause or contribute to bronchopneumonia in
suckling pigs or weaned pigs up to 8 weeks of age. Widespread
endemic P multocida infections are more likely to be opportun-
ists, contributing to bronchopneumonia in pigs of any age. Both
organisms have been isolated from many species other than swine
(dogs, cats, rodents, rabbits, wildlife); however, most of those
strains are not believed to play a role in causing AR in swine.
Colonization of nasal passages with toxigenic B bronchiseptica
can cause mild turbinate atrophy in pigs 1 to 6 weeks of age.
Lesions from B bronchiseptica tend to be mild and can usually
be resolved by the host, therefore not leading to progressive AR.
However, this insult or other sources of irritation to nasal mucosa
can enhance colonization with P multocida.
Pasteurella multocida is a ubiquitous early colonizer of pigs,
commonly isolated from nasal cavity, tonsils, and lungs of pigs
without signs or lesions of AR. However, toxigenic strains of
P multocida type D associated with AR are less widespread in
the swine population. Colonization with toxigenic P multocida
type D alone can cause AR, but disease is enhanced when
the P multocida type D is associated with B bronchiseptica.
Toxigenic P multocida type D produces several toxins, the
16 ATROPHIC RHINITIS
most important being a dermonecrotizing toxin. Atrophic
rhinitis can be reproduced experimentally by exposure of pigs to
dermonecrotizing toxin, even in the absence of the P multocida
organism.
Management and husbandry factors have long been suspected
of being important predisposing or contributing factors to AR.
Dust, ammonia, endotoxin from bacteria, and other organic or
chemical irritants may increase incidence and severity of AR.
Epidemiology
Transmission of toxigenic B bronchiseptica and P multocida is
through direct contact or short distance aerosolization between
infected (sometimes inapparent) and uninfected pigs. Carrier
sows expose their piglets to the organisms very early in lactation
and when these infected piglets are mingled with others, the
agents can be transmitted horizontally. Immune sows do provide
their piglets with some colostral immunity, but this immunity
wanes soon after weaning, leaving young pigs susceptible to
infection. Older sows may provide more colostral immunity to
their piglets than do gilts and may also shed fewer organisms.
Management or environmental factors, particularly inadequate
ventilation, increase the susceptibility of pigs to AR. Other con-
tributing factors include high concentrations of dust or ammonia,
overstocking, substandard housing or sanitation, and continu-
ous-flow production.
Pathogenesis
The initial requirement for development of AR is colonization
of the nasal passages by toxigenic strains of B bronchiseptica or P
multocida. Bordetella bronchiseptica adheres to the nasal mucosa,
probably by attaching to the ciliated epithelial cells. The toxin
elaborated by the organisms diffuses into the turbinates and is
responsible for osteopathy and hypoplastic rhinitis. Later, after
the disease becomes more quiescent, some degree of regeneration
and repair can occur. The term “nonprogressive atrophic rhinitis”
is sometimes used for this form of AR. However, when toxigenic
P multocida colonizes the nasal mucosa, usually after mild rhinitis
has been established by B bronchiseptica, other agents, or envi-
ronmental irritants, the organism produces a potent toxin that
causes a rhinitis with progressive osteopathy of facial and turbinate
bones. The term “progressive atrophic rhinitis” (PAR) is some-
times used to indicate this form of AR.
Clinical signs
Signs may appear in pigs as young as 1 week old but more often
appear shortly after weaning. Sneezing, snorting, and develop-
ment of a serous or mucopurulent nasal discharge are early signs
of AR. Rhinitis obstructs the flow of tears through the infraor-
bital ducts. Tears therefore travel from the medial canthus of the
eyes along the skin. The dirty and discolored hair and skin result-
ing from this is commonly known as “tear-staining.” Signs caused
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
by B bronchiseptica alone tend to peak after a few weeks and then
diminish. Signs related to toxigenic P multocida often appear
in 4- to 8-week-old pigs and may persist for weeks or months.
Signs occasionally include nosebleed, and growth retardation
may become apparent. Occasional pigs develop secondary bron-
chitis, bronchiolitis, or pneumonia as an indirect effect of AR. A
variable number of pigs develop lateral or dorsal deviation of the
snout. Dorsal deviation often results in shortening of the snout
or wrinkling of the skin over the snout. Marked snout deviation
in many pigs is usually associated with toxigenic P multocida.
Lesions
Lesions are usually restricted to turbinates, nasal septum, and
nasal and facial bones, and these lesions can be most easily
observed by sawing transversely across the snout at the level of
the second premolar (first cheek tooth in pigs less than 6 months
of age), typically located at the commissure of the lips. Lesions
vary in severity and are usually graded on a scale of 0 to 5. Minor
lesions must be differentiated from normal variations in anatomy
and breed character. Mild lesions usually result in atrophy of the
ventral scroll of the ventral turbinates; severe cases are more likely
to involve the dorsal turbinate scrolls. In extreme cases, the dorsal
and ventral turbinates may be almost completely destroyed and
there may be atrophy of ethmoid turbinates. Deviation of the
nasal septum is more common in severe cases. Nasal and facial
bones may be thinned or distorted. Mucoid or mucopurulent
exudate is often present on blanched mucous membranes and
in adjacent sinuses. Microscopic study usually reveals fibrous
replacement of the bony plates of conchae that remain.
Diagnosis
History, signs, and lesions are often adequate to make a clinical
diagnosis of AR, with confirmation to follow by isolation and
identification of the etiologic agent(s). Bacterial cultures made
from nasal swabs from live or sacrificed pigs are most rewarding
during the early course of infection (first few weeks post-weaning).
Toxigenic P multocida can be determined by genotyping with
polymerase chain reaction (PCR) to confirm if the isolate has the
ability to elaborate dermonecrotizing toxin. Most toxigenic strains
will be P multocida type D, whereas P multocida type A organisms
are more likely to be isolated from bronchopneumonia. Both
organisms are common residents of the nasopharynx.
Differential diagnosis should exclude other diseases or irritants
that can cause rhinitis, such as porcine reproductive and respira-
tory syndrome virus, pseudorabies virus, inclusion body rhinitis,
or excessive dust or ammonia.
BACTERIA
Control
After AR has been diagnosed, the source of infection confirmed,
additional risk factors identified, and the extent of losses consid-
ered, a decision should be made to either attempt to control the
disease or to initiate some type of elimination program.
If the decision is made to control rather than eradicate AR,
control measures fall into 3 major categories. The first control
measure is improvement of husbandry, management, housing,
and ventilation. The second measure is initiation of a vaccination
program for the breeding stock, pigs, or both. Vaccination of
the sows may be most cost-effective. Sows are often vaccinated
twice at about 4 and 2 weeks prior to parturition. Bacterin-toxoid
vaccines provide some protection and historically have been
widely used. The third control measure involves administration of
antibiotics to sows and piglets around the time of farrowing and
again at weaning in an effort to limit the extent of colonization in
the young pigs. The value of antibiotic therapy to control AR in
growing swine is questionable.
Eradication of toxigenic P multocida from a herd or system has
been successfully achieved. One method for elimination involves
total herd depopulation, thorough clean up and disinfection of
facilities, and restocking with swine known to be free of AR. This
method is expensive. The second method does not require depopu-
lation and involves staged use of several control strategies. First, the
herd should be closed to gilt introductions. Second, an intensive
period of medication and pre-farrowing vaccination of sows should
be implemented. Finally, piglets are medicated and weaned early
to avoid colonization. Concurrently, nasal swabs for P multocida
and toxin testing by PCR can be used to identify the remaining
infected animals, which can then be culled (test and removal).
Progress in control of AR should be evaluated by repeatedly
examining nasal swabs from a large number of pigs submitted for
slaughter for the presence of the offending agent(s). In addition,
routine scoring of the severity of nasal and turbinate lesions from
snouts collected at slaughter may also be a useful monitoring tool.
ATROPHIC RHINITIS 17
 SWINE DISEASE MANUAL
BACTERIA
Clostridial diarrhea
Alternate names and abbreviations
Sometimes referred to as enterotoxemia, clostridial enteritis,
Clostridium difficile associated disease, CDAD
Definition
Disease associated with Clostridium perfringens and other clos-
tridia occurs in many different animal species. Systemic disease,
including myositis, cellulitis, and gangrene, is uncommon in pigs,
but described with opportunists such as C chauvoei, C septicum,
and C sordelli.
In swine, diarrhea is caused by enterotoxemia associated with
C perfringens type C, which affects neonates and suckling pigs
and causes sudden deaths, bloody diarrhea, or necrotic enteritis
with high mortality. Neonatal diarrhea associated with C per-
fringens type A is reported with moderate morbidity and low
mortality. Clostridium difficile causes necrotizing typhlocolitis in
suckling piglets with variable morbidity and mortality.
Occurrence
Although most outbreaks of C perfringens type C are acute and
occur in piglets less than 1 week old, chronic cases may occur in
pigs up to several weeks of age. The disease is reported globally
but incidence varies greatly, depending on local geography and
management practices. Type C clostridial enteritis also occurs
in young lambs, calves, foals, and poultry, but less often in adult
sheep, cattle, and goats. Diarrhea associated with C perfringens
type A or C difficile is sporadic, but both are recognized con-
tributors to diarrhea in young pigs on farms around the world.
Clostridium difficile also causes antibiotic-induced typhlocolitis
in humans and other species. Evidence to implicate pigs or pork
products as sources of these human infections is generally lacking.
Historical information
Enterotoxemia in piglets associated with C perfringens type C was
reported, experimentally reproduced, and researched in the
1960’s. Many early reports on C perfringens type C enteritis are
from species other than swine. The application of molecular tech-
nologies allows further characterization of toxins produced by
Clostridium species and facilitates study and diagnosis of C per-
fringens type A and C difficile, with particular emphasis on identi-
fying the presence of genes associated with toxin production.
Etiology
Clostridium perfringens and C difficile are large, anaerobic,
Gram-positive bacilli with both vegetative and sporulated forms
common in the intestine, colon, feces, and soil that have been in
contact with livestock. Both C perfringens and C difficile are “early
colonizers” of newborn piglets, achieving high numbers within 1
to 2 days of birth.
18 CLOSTRIDIAL DIARRHEA
Five toxigenic types of C perfringens (A, B, C, D, E) are distin-
guished by the major toxins they produce (alpha, beta, epsilon, or
iota). By definition, all C perfringens produce alpha toxin. Use of
polymerase chain reaction (PCR) to detect the genes coding spe-
cific toxins has simplified their identification. Type C organisms
produce beta toxin, which cause the severe necrotizing enteritis.
Clostridium perfringens type A can produce a beta2 toxin and
perhaps other less characterized toxins which may contribute to a
much milder diarrhea than C perfringens type C. Virulent strains
of C difficile produce an enterotoxin (TcdA) and a cytotoxin
(TcdB), which are associated with systemic illness in piglets as
well as localized typhlocolitis and mesocolonic edema.
Epidemiology
Feces from carrier sows contain pathogenic clostridial organisms
and, coupled with a contaminated farrowing environment, are the
likely source of exposure for piglets. The bacteria and its spores
survive in soil and can be carried on shoes, boots, or other fomites.
Each outbreak renews the supply of organisms and spores in the
farrowing environment to infect the next litter of susceptible pig-
lets. Most piglets are colonized with C perfringens and C difficile
within hours of birth, usually with no adverse clinical outcomes.
Although other species of animals have C perfringens type C infec-
tion, there are very few reports of interspecies transmission.
The magnitude of the dose and level of active or passive immu-
nity play a large role in disease occurrence. Immune dams (from
natural exposure, perhaps augmented by vaccination) likely pro-
vide antitoxin antibodies via colostrum to offspring. In contrast
to C perfringens, antibodies against C difficile toxins are not pres-
ent in colostrum. Sanitation in farrowing rooms between groups
decreases the infectious dose in the environment.
Pathogenesis
Clostridium perfringens and C difficile are ubiquitous early
colonizers of the gastrointestinal tract and normally achieve
high populations (greater than 10 million organisms per gram
feces) in the intestine and colon within 24 to 48 hours of birth.
Conditions that favor proliferation include absence of acid in the
stomach and the presence of antitrypsin factor.
Pathogenic C perfringens type C can attach to epithelial cells
of the proximal small intestine, proliferate, then elaborate
necrotizing beta toxin which causes acute and severe necrosis
and desquamation of epithelial cells. This is accompanied by
hemorrhage and severe suppurative inflammation. Fermentation
produces gas that accumulates in the lumen and/or wall (intes-
tinal emphysema) of necrotic sections of intestine. Death results
from mucosal necrosis and the systemic effect of toxins on other
organs. In older suckling piglets, clostridial colonization may be
secondary to other agents of enteritis, most notably coccidiosis,
thus contributing to necrotic enteritis.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Pathogenesis is less clear with C perfringens type A, as disease has
not been successfully reproduced experimentally. Novel toxins
(eg, beta2 toxin, NetB, or NetF) may have a role in initiating
diarrhea but presently no clear mechanisms or virulence factors
for C perfringens type A have confirmed roles in neonatal pigs.
Diarrhea is most often associated with exotoxins produced by C
perfringens and is less commonly a result of the endotoxins which
may also be present.
Similar to C perfringens type C and C perfringens type A, C dif-
ficile colonizes neonates very quickly after birth, and under
ill-defined circumstances or at high doses, toxigenic strains can
produce TcdA or TcdB toxins causing lesions in the cecum and
colon. Mesocolonic edema and multifocal necrosis of epithelium
with a flux of neutrophils spewing onto the mucosal surface
(“volcano lesion”) is the classic microscopic lesion. Nontoxigenic
strains of C difficile are widespread and are commonly found in
colonic contents in the absence of any clinical signs or lesions.
Although C difficile typhlocolitis is a common sequel to oral anti-
biotic therapy in humans, disease in piglets does not appear to be
associated with misuse or overuse of antimicrobials.
Clinical signs
Clinical signs produced by C perfringens type C vary depending
on infectious dose, virulence, and quantity of antitoxin provided
via colostral immunity. Susceptible neonates can become ill in
just a few hours after exposure to virulent C perfringens type C
and may be found dead in as little as 4 to 8 hours after birth, prior
to onset of diarrhea (peracute form). Sick piglets soon become
weak, prostrate, and moribund; weakened piglets have a higher
risk of being crushed by the dam. Piglets able to survive infection
for a few days may have bloody diarrhea. Occasionally, piglets
may live several weeks and develop a yellow or gray, mucoid diar-
rhea, then tend to remain unthrifty with a chronic form of the
disease; fibrinonecrotic enteritis is a common lesion in these pigs.
Morbidity is variable, but mortality can be high, up to 100%, in
susceptible litters.
In reports of uncomplicated cases of C perfringens type C or
C difficile, clinical signs include mild, non-watery diarrhea and
compromised growth rate. Morbidity is variable to high, but
mortality is generally low. Diarrhea produced by C difficile may
be indistinguishable from that of C perfringens type A or neo-
natal colibacillosis. Morbidity is variable with all three agents,
with some litters more severely affected than others. Mortality is
expected with C perfringens type C but not C perfringens type A.
Gross lesions are expected with C perfringens type C and C diffi-
cile but are not often grossly apparent with C perfringens type A.
Lesions
Necropsy of piglets with C perfringens type C infection may
reveal cyanosis or darkening of the abdominal skin. The peri-
toneal and pleural cavities may contain excessive, blood-tinged
fluid. Typical acute cases have a dark red, segmental, or diffuse,
BACTERIA
necrohemorrhagic small intestine with lesions most commonly
found in the proximal half of small intestine, though lesions can
be observed occasionally in the lower intestine, cecum, or colon.
Gas and bloody fluid may be present in the intestinal lumen and
wall of the intestine with fibrinous adhesion between intestinal
loops. Piglets that live a few days may have a necrotic pseudo-
membrane lining the mucosa of affected intestine. Microscopy
reveals acute necrosis with severe suppurative inflammation and
robust rod-shaped bacteria in close association with or end-on
attachment to enterocytes.
Piglets with diarrhea associated with C perfringens type A rarely
present with any gross lesions. The small intestine may be thin-
walled and fluid-filled or contain milky content. Colonic content
is usually creamy. Microscopic lesions are quite mild. Accumula-
tions of neutrophils at villus tips, perhaps with focal enterocyte
necrosis or sloughing of apical enterocytes, is described from nat-
urally occurring cases, but experimental reproduction of specific
microscopic lesions has not been reported. Occasionally, sporu-
lating rods are detected in close association with enterocytes.
Lesions of C difficile are usually confined to the cecum and colon and
include moderate to severe mesocolonic edema and watery or creamy
colonic contents. Microscopically there is erosion of the colonic
epithelium with infiltration and exudation of neutrophils (“volcano
lesions”) as a common and nearly pathognomonic finding.
Diagnosis
Acute C perfringens type C cases manifest with an acute, rapid
clinical course with variable-to-high morbidity, high mortality,
and typical gross lesions in neonatal piglets. Demonstration
of a large population of Gram-positive, rod-shaped bacteria in
mucosal smears is supportive of the diagnosis, which is confirmed
by typical microscopic lesions that are nearly pathognomonic for
C perfringens type C. Samples should be selected from acutely
affected, non-medicated pigs early in the course of disease. Con-
firming C perfringens type C in lesions by isolation, PCR, and
toxin detection is useful.
Criteria for diagnosis of disease associated with C perfringens
type A are less clear. Diarrhea is usually mild, mortality low, and
only mild non-specific gross and microscopic lesions are typically
present. High populations of C perfringens can be isolated from
intestine and colon of normal suckling piglets. Detection by
isolation or PCR is not sufficient to confirm a diagnosis of C
perfringens type A.
Diagnosis of C difficile is often made by observing typical diarrhea
at 3 to 7 days of age, the presence of gross lesions of mesocolonic
edema, and observation of typical microscopic lesions in cecum
and colon. Detection of TcdA and TcdB in colon contents or
feces by enzyme-linked immunosorbent assay is helpful. Isolation
of organisms can be helpful for confirmation and/or additional
characterization.
Anaerobic culture and isolation of Clostridium species or detec-
tion by PCR are not particularly useful for diagnosis since these
CLOSTRIDIAL DIARRHEA 19
 SWINE DISEASE MANUAL
BACTERIA
agents are early colonizers of many healthy neonatal pigs. How-
ever, isolates and molecular techniques can be useful for further
characterization of the organism once a diagnosis has been made.
A number of laboratory techniques are available to detect either
toxins or toxin genes in intestinal contents isolates from typical
cases. PCR techniques are generally available to detect and dif-
ferentiate clostridial toxins of various species. Clostridial enteritis
must be differentiated from other neonatal diarrheal diseases,
particularly coccidiosis, colibacillosis, or viral insults.
Control
With outbreaks of C perfringens type C, immediate passive
immunity can be provided by administering immune antiserum
(antitoxin) orally or parenterally within 2 hours of birth. Pigs
acutely affected with C perfringens type C often do not respond
to treatment. Treatment of milder cases with antimicrobials is
commonly practiced. Prophylactic antimicrobials for C perfrin-
gens type C, C difficile, and C perfringens type A can be an aid
in reducing severity or prevalence of the disease. Some studies
suggest administration of oral probiotics shortly after birth may
help in preventing cases of clostridial diarrhea, but studies docu-
menting efficacy for this treatment are lacking.
Ensuring maternal passive immune protection for piglets via
colostrum and milk is a preferred method to prevent disease
20 CLOSTRIDIAL DIARRHEA
caused by infection with C perfringens. Assuring adequate intake
of colostrum and milk is essential to prevent endemic diarrheal
diseases. Natural exposure via proper gilt acclimatization aug-
mented by vaccination of dams with bacterin-toxoids is generally
helpful in enhancing maternal immunity. Commercial vaccines are
available for C perfringens type A and C, and autogenous products
are sometimes used for C difficile and C perfringens type A as well as
C perfringens type C. Two doses of vaccine, given at around 6 and
2 weeks prior to farrowing is a common practice in gilts. A single
booster vaccination given to sows a few weeks prior to subsequent
farrowings is often recommended in problem herds.
Hygiene and management are critical control points in the
farrowing facility. Attention to details of management, environ-
ment, temperature, drafts, and hygienic practices is a constant
requirement. Breaking cycles of infection with all-in, all-out
farrowing and thorough washing and disinfection of the facility
between groups is often sufficient to reduce the occurrence of
diarrhea in neonates.
Antimicrobials fed to sows prior to farrowing is sometimes rec-
ommended by veterinarians to decrease shedding of clostridia
in feces from sows but credible data to support this practice is
generally lacking.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Colibacillosis
Alternate names and abbreviations
Escherichia coli (E coli) diarrhea, neonatal scours, post-weaning
diarrhea, edema disease (ED), gut edema
Definition
The focus of this chapter is the colonization of intestine and
colon by different pathotypes of E coli, resulting in 3 primary
disease manifestations: diarrhea in neonates (neonatal colibacil-
losis), diarrhea after weaning (post-weaning colibacillosis), and
enterotoxemia (also known as edema disease or ED). The latter
is an acute, often fatal enterotoxemia of recently weaned pigs
characterized by tissue edema, sudden deaths, and occasionally by
neurologic signs related to lesions in the brain.
Important but not discussed here are sporadic outbreaks of septice-
mia and polyserositis caused by E coli in young pigs, as well as coli-
form mastitis and urinary tract infections of sows and older pigs.
Occurrence
Colibacillosis and ED affect pigs in all major swine-raising coun-
tries. There are many different strains of E coli, each of which
may possess several of many potential virulence factors. Neonatal
colibacillosis occurs from 1 to 7 days of age. Post-weaning coli-
bacillosis and ED tend to occur in older pigs from 3 to 7 weeks
of age. Risk factors and strain variation are often involved in out-
breaks of what are usually endemic infections with potentially
pathogenic E coli. Genotype, nutritional factors, environmental
stress, management type, herd immune status, and the presence
or combination of specific virulence factors of E coli account for
the wide variation in the age of pigs that are affected as well as
the significance of clinical signs that are expressed.
Historical information
Colibacillosis has been recognized for nearly a century as an
important diarrheal disease of pigs; ED is a unique form of coli-
bacillosis first reported in 1938. For many years, treatment and
control were largely empirical. Recurring losses, as well as the
importance of E coli in other species including humans, stimulated
research on the disease. Advances in molecular biology have sim-
plified identification of different pathogenic E coli, based on the
presence of virulence genes as well as differences in surface antigens.
Escherichia coli strain O157:H7 is an important foodborne zoo-
nosis in humans, however these strains in people do not appear to
cause disease in swine, nor is this serotype common in swine.
Etiology
Pathogenic strains of E coli are Gram-negative, flagellated bacilli
easily isolated from non-medicated animals. Most pathogenic
strains form smooth to mucoid colonies on agar plates, many but
not all of which are beta-hemolytic on blood agar. Numerous
virulence factors include variations of fimbria (pili), enterotoxins
BACTERIA
(exotoxins), endotoxins, and capsules. Fimbria are hair-like
processes on the bacterial surface that allow attachment to genet-
ically determined receptors on the surface of mucosal enterocytes
(colonization). Pathogenic strains also produce one or more
enterotoxins, which are exotoxins elaborated locally in the small
intestine with either local or systemic effects. These pathogenic
strains are termed enterotoxigenic E coli (ETEC). There are mul-
tiple schemes in use for classifying E coli:
Serotype: Based on the formula of the surface O (somatic or
polysaccharide), K (capsular or microcapsular), H (flagellar),
and F (fimbrial) antigens that are present.
Pathotype: Based on virulence mechanisms, such as enterotoxi-
genic E coli (ETEC), Shiga-toxin producing E coli (STEC),
enterohemorrhagic E coli (EHEC), attaching and effacing
E coli (AEEC), enteropathogenic E coli (EPEC), and extrain-
testinal E coli (ExPEC).
Pilus type: Based on presence of antigenically distinct pilus
types, including F4 (K88, archaic), F5 (K99, archaic), F41,
F6 (987P, archaic) and F18. The first 4 pilus types mediate
adhesion in neonates, while F18 and F4 are much more
common in post-weaning colibacillosis.
Toxin type: Based on the type of enterotoxins that are elabo-
rated. Toxins elaborated by ETEC strains include labile toxin
(LT), heat stable toxin A (StA), heat stable toxin B (StB),
and shiga-like toxin (referred to variably as SLT, STx2e, vero-
toxin, edema disease principal, neurotoxin, or vasotoxin).
The first 3 toxins act locally causing hypersecretion of fluid
from the intestine while shiga-like toxins are responsible for
the systemic vascular effects of ED.
There are many strains and types of E coli present in swine and
their environment. Enteropathogenic E coli have fimbria-me-
diated adhesion to enterocytes as well as elaborate one or more
toxins. Other forms of colibacillosis may be caused by some of the
same pilus types that cause ED but have different pathogenesis
due to differences in the enterotoxins that are elaborated. Excep-
tions and variation like this are common with E coli.
Epidemiology
Potentially pathogenic E coli are global in distribution, present
in the intestinal tract and feces of many normal swine, and are
generally able to survive for long periods of time in the environ-
ment. Transmission is usually through ingestion of feces directly
or from fomites. Airborne dust containing E coli can transmit
the organism over short distances.
Neonates are most often infected by ingestion of E coli shed from
immune carrier dams or the environment; very high populations
of the organism can be established in the intestine and colon
within hours of birth. The dominant strain(s) of E coli in a pig
can change rapidly over time and with age. Continuous farrowing
accompanied by poor sanitation or chilling increases the risk of
colibacillosis. Piglets lacking passive immunity from colostrum
and milk are likely to be the first pigs in a litter to become ill from
COLIBACILLOSIS 21
 SWINE DISEASE MANUAL
BACTERIA
colibacillosis. The dose of pathogenic coliforms is magnified by
shedding from infected pigs to littermates. Disease occurrence
and its severity are related to the infectious dose and the occur-
rence of other risk factors and is mitigated by the presence of
effective passive or active immunity.
Similar risk factors for neonatal colibacillosis (presence of carrier
pigs, high levels of environmental contamination, infectious
dose, pig genotype, weaning age, and environmental stress) also
influence the occurrence of post-weaning diarrhea and ED. In
addition, nutrition and feeding management often play a role
in post-weaning colibacillosis and ED. Increase in the rate of
enterocyte turnover can lead to increased expression of receptors
post-weaning which is favorable for colonization with entero-
pathogenic E coli. Other contributors favoring colonization
include viral infections (eg, rotavirus) or diet (ration formu-
lation, processing type, high protein content, certain dietary
constituents) as well as poor hygiene and environmental control.
Disease-causing E coli tends to persist on farms that do not
provide adequate attention to good management of sanitation,
husbandry, and other risk factors.
Pathogenesis
Pili of ingested pathogenic E coli allow adherence to genetically
determined receptors on microvilli of enterocytes in the jejunum
and ileum (and sometimes in the colon) where they then colo-
nize, proliferate, and elaborate various enterotoxins that cause the
clinical signs.
Clinical diarrhea in neonates or post-weaning pigs is the result of
toxin-mediated hypersecretion of water and electrolytes by crypt
epithelial cells. This can result in up to 40% loss of the piglet’s
bodyweight over a few hours to days. Death is usually the result
of dehydration and metabolic acidosis, perhaps with terminal sep-
sis and endotoxemia. Some of the enterotoxins, endotoxin, and/
or adhesins may damage the microvilli and enterocytes, which
can reduce the absorptive capacity of the intestine and contribute
to even more severe diarrhea. In some cases, the large intestine
can be affected similarly to the small intestine, further compro-
mising the pig’s ability to resorb water from the gut. Damage to
gut epithelial cells sometimes leads to septicemia, and death is
usually the result of dehydration and metabolic acidosis or from
terminal septicemia.
Pathogenesis of ED is similar to that of neonatal diarrhea caused
by E coli but infection with F18 pilus is much more common
in ED (in the US) than with the F4 typically seen in neonatal
diarrhea. In Canada, ED is more commonly associated with F4
than with F18 types. The shiga-like toxin produced locally in the
intestine is absorbed and has systemic effects on the endothe-
lium of blood vessels of multiple tissues, most notably areas of
the brain, eyelid, stomach wall, and mesentery.
Whether piglets develop colibacillosis or ED depends on a balance
between dose, specific virulence factors of the organism, the pig’s
innate and acquired resistance to the disease, and environmental
22 COLIBACILLOSIS
factors (effective temperature, humidity, sanitation, etc). Neo-
natal piglets have immature immune systems and limited innate
resistance, and therefore are largely dependent on passive immu-
nity acquired from colostrum and milk. Purchased breeding stock
may not have immunity to specific resident E coli and may have
increased risk for disease in newborns because their colostrum
and milk may not contain enough antibodies to protect their
piglets. Chilling of piglets and weaners impairs intestinal motility
and lowers resistance to infection. Massive exposure dose can
overwhelm resistance. During the early nursery phase of recently
weaned pigs, the absence of milk antibodies, transition to a plant
protein-based diet, cool or damp environmental stresses, weaning
stress, commingling, and other risk factors may contribute to out-
breaks of colibacillosis or ED.
Clinical signs
Colibacillosis is usually signaled by the appearance of watery diar-
rhea, with piglets from gilts usually more severely affected than
piglets from multiparous sows. The severity of the diarrhea within
and between litters can vary. The hypersecretory diarrhea associ-
ated with colibacillosis usually has an alkaline pH and varies from
clear and watery to white or yellow; the color is influenced by
type of ingesta and duration of the disease and is neither pathog-
nomonic for the occurrence of colibacillosis nor an indicator of
disease severity. Vomiting is not as prominent as with coronavirus
infections. There is progressive dehydration and the hair coat
becomes roughened. Body temperature is often subnormal.
Shivering is often noted unless an adequate supplementary heat
source is available. Signs are similar in post-weaned pigs. Death
losses can be severe if husbandry and environmental conditions
are poor. Diarrhea tends to persist until successful intervention is
achieved.
Edema disease usually occurs 1 to 2 weeks post-weaning, often
signaled by finding a few acutely dead pigs that were previously
known to be in excellent health. Morbidity is usually low, but
mortality is high in pigs that show signs. Signs include anorexia,
ataxia, stupor, and recumbency, often accompanied by paddling
and running movements. When caught, affected pigs may
respond with an abnormal squeal, a consequence of laryngeal
edema. Diarrhea is not usually present in pigs with typical ED
but may be present in other pigs in the same group. Swelling
of the face and eyelids may or may not be present. Sick pigs die
within a few hours or days. The few that survive often have neu-
rologic deficits. The course of ED in a herd is usually around 2
weeks. However, the disease may reappear when other batches of
pigs reach the age group at risk.
Escherichia coli is one of the most common causes of neonatal
septicemia and polyserositis. Often, strains associated with septi-
cemia are not enteropathogenic.
Lesions
With colibacillosis, dehydration is severe. The small intestine
and colon may contain excess watery fluid or may be distended
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
and gas-filled. There may be mild reddening and congestion
of the stomach. Lesions are often surprisingly mild, especially
in very young piglets. However, in outbreaks caused by certain
pathogenic strains (usually in older post-weaned pigs), there can
be marked congestion in the gastrointestinal tract. Microscopy
of the mucosa of the small intestine will reveal high numbers of
coliforms adhered to microvilli of intestinal epithelial cells. Villi
and enterocytes are usually intact. With some strains of E coli,
there may be necrosis of some villi and microvascular thrombosis
in the lamina propria.
Lesions of ED vary between individuals. In pigs found dead,
visceral congestion may be prominent. Usually, some will have evi-
dence of subcutaneous edema of the face or eyelids, gastric submu-
cosa, or in the mesentery of the spiral colon. There may be slightly
increased volumes of clear fluid in the peritoneal cavity, chest, or
pericardial sac. Occasionally, there are hemorrhages under the epi-
cardium or endocardium. In subacutely or chronically affected pigs,
microscopic degenerative changes can be found in small arteries
and arterioles at many sites. The changes are sometimes apparent
in vessels supplying the brain. Histologic sections of brain stem
and basal ganglia may confirm suspected areas of hemorrhage and
malacia, but these lesions are not consistently present.
Escherichia coli is a common cause of septicemia in neonates,
characterized by fibrinous polyserositis and arthritis.
Diagnosis
The typical clinical signs, dehydration, and subtle lesions
described above are useful for diagnosing colibacillosis but are
not definitive. The isolation of a uniform and high population of
smooth, mucoid, or hemolytic E coli from the small intestine is
suggestive of colibacillosis or ED in typically affected neonates
and post-weaned pigs, with the hemolytic colony type more
likely in post-weaned pigs. As E coli are commonly found in the
small intestine of both normal and diseased pigs, microscopic
examination of sections of small intestinae is very useful in deter-
mining the significance of the infection. Dense colonization
of the brush border with adherent E coli should be expected in
most cases of colibacillosis, with additional erosive or congestive
changes present depending on the toxins that have been elab-
orated. Tissue samples should be immediately collected from
acutely affected, non-medicated, euthanized pigs and preserved
in formalin.
Polymerase chain reaction (PCR) assays are available to identify
the presence of pathogenic E coli. Genotyping by multiplex PCR
is widely practiced in order to identify specific pilus and toxin
genes present in the isolate. Colibacillosis must be differentiated
from other diarrheal diseases of young pigs. Important differ-
entials include transmissible gastroenteritis, porcine rotavirus,
coccidiosis, and Strongyloides parasitism. Starvation is also a major
differential diagnosis.
With ED, the history, signs, and lesions are often sufficient for
establishing a presumptive diagnosis. Bacterial culture of the
BACTERIA
small intestine from a non-medicated, typically affected pig
will yield high populations of hemolytic colonies of E coli. It is
useful to genotype the isolate for confirmation of the presence
of genes that determine pilus type and potential for production
of shiga-like toxin Stx2e. Typical microscopic vascular lesions
help confirm diagnosis. Edema disease must be differentiated
from other causes of neurologic signs (eg, pseudorabies, water
deprivation, and organic arsenical poisoning) and septicemia and
meningoencephalitis caused by Streptococcus suis, Haemophilus
parasuis, and others.
Investigation of outbreaks of colibacillosis should include iden-
tification of any risk factors such as chilling, poor sanitation, or
starvation that may be contributing to the disease. These must be
corrected if prevention or treatment is to be successful.
Control
Escherichia coli that cause clinical colibacillosis or ED are often
endemic on farms, with disease expression most influenced by
changes to the occurrence of non-infectious risk factors. For coli-
bacillosis, the use of all-in, all-out (AIAO) systems of farrowing
and raising piglets is recommended. Farrowing should occur in a
facility that has been thoroughly cleaned, disinfected, and dried
between farrowing groups, along with an on-going sanitation
program and internal biosecurity measures that prevent pathogen
build-up. The farrowing facility should be designed to provide
a dry, comfortable, draft-free environment for piglets as well as
accommodate dam comfort. This requires lower temperatures
(approximately 70°F [21°C]) for sows, areas warmed (up to
approximately 90°F [31°C]) for small piglets, and the use of hus-
bandry practices that minimize stress.
It is wise to obtain breeding stock from a single source that does
not have a historical problem with colibacillosis. Dams should
be acclimatized together for 3 to 6 weeks prior to breeding so
they can develop immunity to endemic potential pathogens that
exist on the farm. This will encourage production of high-quality
colostrum that contains an adequate concentration of specific
antibodies directed at the E coli present on that farm. Enhance-
ment of sow immunity is effective with commercially available
vaccines made from bacterial pili, or toxins, or both. Pregnant
gilts are usually vaccinated twice at 2- to 3-week intervals prior
to farrowing; sows need a single booster vaccination 2 to 3 weeks
prior to farrowing. Immediate treatment of piglets is warranted
should signs of colibacillosis appear. Antimicrobials can be
administered to neonates orally or by injection. Because the
disease is contagious and sick piglets shed high numbers of organ-
isms, it is wise to treat all pigs in the litter at the same time.
For post-weaning colibacillosis and ED, attention to details of
husbandry and management is essential. No prevention method
is universally accepted or successful, because the erratic occur-
rence of colibacillosis and ED makes intervention strategies hard
to assess. General strategies to consider include:
COLIBACILLOSIS 23
 SWINE DISEASE MANUAL
BACTERIA
1. Minimizing environmental stress (eg, temperature variation,
drafts, damp conditions), limiting commingling, and using
AIAO flow with scrupulous sanitation and disinfection
between groups.
2. Nutritional considerations include the use of creep feed-
ing, restricted feeding, multiple feedings (small quantities
fed 3 to 6 times per day) after weaning, increasing fiber in
the rations, adding acidifiers to feed or water, and adding
zinc oxide or plasma proteins to the ration. Probiotics are
perceived by some to have benefit during the transition to
grain-based diets. Avoid abrupt dietary changes, including
ingredient changes, and use step-wise transition diets when
making changes.
3. Passive or active immunoprophylaxis can be very helpful on
farms known to have a colibacillosis problem. Oral products
specifically formulated to contain high levels of antibody
(milk, plasma protein, egg powder) can help to prevent
colonization and disease. Active immunity can be induced
against specific adhesins or toxins. Oral vaccination with live
or killed cultures that contain F18 or F4 pili (but lacking
genes for toxin production) have been used successfully on
some farms. Toxoids prepared from Stx2e have also been
demonstrated to be effective against ED but are not commer-
cially available. While effective as a vaccination for pregnant
sows, administration of killed bacterins to newborn, nursing,
or post-weaning pigs has been much less effective.
4. Competitive exclusion may be an effective mechanism
whereby receptors for pathogenic E coli are occupied by
avirulent agents with products fashioned similar to avirulent
live vaccines.
24 COLIBACILLOSIS
5. Routine administration of antimicrobials in feed or water is
often practiced but not desirable, as the practice is expensive
and can contribute to development of antimicrobial resistance.
6. Natural resistance to colibacillosis and ED is possible in pigs
genetically lacking receptors for F18 and/or F4 pili. Genet-
ically resistant pigs have been developed. In herds negative
for ED, it is prudent to prevent introduction of the disease
by careful scrutiny of the disease history of breeding stock
that are being considered for purchase. Elimination of the
clinical disease may be possible by using depopulation and
disinfection.
7. Should diarrhea occur, weanlings may be given antibiotics in
water with the antimicrobial selection based on sensitivity
data. Oral electrolyte replacement solutions are sometimes
used to help treat dehydration and acidosis. Treatment of
pigs affected with ED can be frustrating since toxin pro-
duction (and clinical signs) is generally too far advanced for
effective treatment by the time clinical signs become visible.
During an outbreak of colibacillosis or ED, control efforts
are better directed toward reducing the incidence of infec-
tion in the remainder of the population at risk by adminis-
tering antimicrobials to the unaffected pigs and including
acidifiers in the feed or water. In severe outbreaks, removal
of the existing feed with replacement by a ration containing
less protein, a lower percentage of soybean meal, or higher
proportion of fiber may be beneficial.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Erysipelas
Alternate names and abbreviations
Swine erysipelas, diamond skin disease, human erysipeloid
Definition
Erysipelas is an infectious disease that can affect swine of any age,
though it is most common in growing or adult swine. Infection
may result in acute sepsis, chronic arthritis, endocarditis, condem-
nations at slaughter, or be subclinical.
Occurrence
Erysipelas occurs in swine, lambs, turkeys, occasionally in
other poultry and wild birds, and sporadically in most kinds
of livestock, wild mammals, reptiles, and amphibians. Seasonal
distribution is suspected, with losses greater during warm summer
months. Occasionally, people who work with infected animals,
poultry, fish, or animal by-products can become infected through
skin wounds and develop a localized skin condition referred to as
an erysipeloid rash though an identical condition can be caused
by other infections as well.
In humans, the condition referred to as “erysipelas” is actually
caused by a streptococcal infection.
Historical information
In 1885, Dr. Theobald Smith isolated an organism from swine in
the US that was similar to one Pasteur had isolated 3 years earlier
from swine affected by a condition called rouget du porc; both were
eventually identified as Erysipelothrix rhusiopathiae, the causative
agent of swine erysipelas. Some of the earliest recognized outbreaks
of erysipelas were reported from South Dakota in 1928 and led to
greater awareness, increased recognition of the disease, and devel-
opment of bacterins. However, erysipelas remains a constant threat
in both confinement and outdoor swine farms.
Etiology
Erysipelothrix rhusiopathiae is a Gram-positive, aerobic, slightly
bent, thin bacillus. It is resistant to many environmental condi-
tions and survives for months in meat, cured hams, fish meal,
and decaying animal carcasses. There are at least 28 serotypes of
E rhusiopathiae, of which swine are susceptible to at least 15. In
the US, most isolates from sick pigs are serotype 1a, followed
by 2, 5, and 1b. Non-pathogenic species (E tonsillarum) are fre-
quently isolated from normal swine. The organism is sensitive to
penicillin and usually to tetracyclines. It resists many antibiotics
and sulfonamides. It is susceptible to most disinfectants.
Epidemiology
Worldwide in distribution, E rhusiopathiae is assumed to be spread
by inapparent carriers within and between herds. It has been
estimated that over half of healthy swine are carriers of pathogenic
and/or non-pathogenic Erysipelothrix species and can dissemi-
nate the organism through their feces and oronasal secretions.
BACTERIA
In addition to these inapparent carriers, affected pigs also shed
large numbers of organisms that further contaminate feed, water,
soil, and bedding. Contaminated soil probably does not remain
infective for more than 35 days, but organisms can flow in surface
water to adjacent premises, and a wide range of wild mammals,
poultry, wild birds, and pets can then further disseminate the
bacteria. There is empirical evidence that biting flies and ticks
can sometimes transmit erysipelas between swine, though it is
unlikely they transmit the infection between farms. Erysipelas
tends to have a seasonal occurrence with spikes during the hot
summer months. Eradication of erysipelas from a herd is unlikely.
Pathogenesis
Variation in virulence between isolates of E rhusiopathiae is
attributable to the presence and expression of various virulence
factors. In general, ingestion of contaminated feed and water
allows E rhusiopathiae to gain access to the body, probably
through the tonsils or other lymphoid tissue of the digestive
tract. Less often, contaminated skin wounds may permit organ-
ism entry. Bacteremia and sepsis results in localization of E rhu-
siopathiae at various sites throughout the body.
The precise mechanisms by which E rhusiopathiae causes disease
are speculative. The organism wall and capsule along with several
proteins it produces, appear to mediate the widespread vascular
damage that accompanies erysipelas and allow for persistence
in tissues. Vascular damage leads to thrombosis and interference
with microcirculation in capillaries and venules.
In chronic proliferative arthritic cases, there is a vasculitis with
exudation of fibrin into perivascular tissues and joints, causing
marked villous proliferation of the synovial membrane. Con-
nective tissue forms around joints, accompanied by perivascular
fibrin and thickening of the joint capsule. Pannus may develop,
accompanied by destruction of articular cartilage and ankylosis of
adjacent bones. Persistence of inflammation around an affected
joint may be from a few living bacteria in the joint or it may be
the result of hypersensitivity to remaining bacterial antigens.
Vegetative valvular endocarditis is another chronic lesion asso-
ciated with erysipelas. Emboli of E rhusiopathiae may cause
inflammation of blood vessels within heart valves. During the
inflammatory process, the endocardium is breached and bacterial
colonies are established at the site. Exuded fibrin deposits are
slowly organized to form nodular vegetations. Emboli that arise
from vegetations can cause sudden deaths. Vegetative endocarditis
can occur without clinical signs.
Susceptibility to infection is not well understood. Many swine
that are exposed to organisms do not develop disease. Lactogenic
immunity protects young piglets for several weeks. In older,
susceptible swine, various stresses (heat, aflatoxin, poor nutrition)
are suspected to play a role in precipitating outbreaks.
ERYSIPELAS 25
 SWINE DISEASE MANUAL
BACTERIA

Clinical signs sloughed. Vegetative valvular endocarditis of chronic cases usually

Clinical signs of erysipelas may be acute, subacute, chronic, or
inapparent. Acute outbreaks of erysipelas are manifestations of
sepsis, high fever (up to 42°C/108°F), and vascular damage in
various tissues. Clinically, there may be acute deaths. Affected
pigs have fever, cyanosis, stilted gait due to painful joints, and
often vocalize in pain when moved. These signs may be accompa-
nied by the classic skin lesions which are pink-to-purple, raised,
and rhomboid or diamond-shaped. Young pigs (2 to 8 weeks of
age) may have profound cyanosis of ears, snout, and extremities.
Pregnant sows may abort from the effects of acute sepsis or from
transplacental fetal infection.
The subacute form of disease is viewed as simply a less severe
illness than the acute form. The classic cutaneous diamond skin
lesions may be observed on pigs that are otherwise clinically
normal. Cutaneous lesions may coalesce over the rump, back, or
shoulders, and occasionally patches of affected skin may become
necrotic. Sloughing of the tip of the tail or tips of the ears can
occur with erysipelas but these lesions can also have other causes.
The chronic forms of erysipelas may either follow acute and sub-
acute forms or develop insidiously. Chronic erysipelas is manifested
usually as either chronic arthritis or chronic vegetative valvular
endocarditis. With the former, there little mortality but rather a
gradual enlargement of leg joints, most noticeable in the hock and
carpus, observed in an increasing number of pigs; affected pigs tend
to become unthrifty as the disease persists. With chronic vegetative
valvular endocarditis, pigs often present few signs. However, when
these pigs are exerted they may show signs of acute respiratory dis-
tress which occasionally triggers collapse and sudden death.
Lesions
Pigs that die of acute erysipelas may present as sudden deaths
without the appearance of any gross lesions. Cyanosis or dia-
mond-shaped skin lesions may be apparent. Necropsy may reveal
congested or edematous lymph nodes and perhaps subcapsular
hemorrhage if the animal lived a few days after onset. Petechial
hemorrhages may be present on the kidneys, epicardium, and
endocardium. The liver is often swollen and lungs may be con-
gested and edematous. The spleen may be enlarged, especially in
cases that survive beyond a few days; it may occasionally contain
infarcts. Microscopic lesions include vasculitis in capillaries and
venules at many lesion sites, including glomerular tufts, pulmo-
nary alveolar walls, and skin. Bacteria may be apparent within
microthrombi in blood vessels.
With chronic joint disease, there is arthritis with proliferative,
villous synovitis in one or more swollen joints. Synovial fluid
is viscous and only modestly increased in amount. The joint
capsule may be visibly thickened. An organized inflammatory
exudate (pannus) may be present in affected joints, sometimes
with ulceration of the articular cartilage or ankylosis of adja-
cent bony surfaces. Chronic cutaneous lesions may appear as
one or more patches of dry, necrotic skin. Sometimes there are
granulating, healing areas where patches of necrotic skin have
affects the mitral valve and may appear as irregular masses of con-
siderable size. Such cases often have infarcts in the spleen, kidneys,
or other sites as a result of embolism from valvular lesions.
Diagnosis
Clinical diagnosis is based on the appearance of typical clinical
signs and lesions in multiple pigs; favorable response of acute
cases to high doses of penicillin and/or hyperimmune serum also
helps to confirm a presumptive diagnosis of erysipelas. Acute
cases usually have exceptionally high temperatures, evidence of
marked pain in multiple joints, and typical diamond-shaped skin
lesions. Diagnosis can be confirmed by bacterial culture or poly-
merase chain reaction of kidney, spleen, skin, lung, lymph nodes,
blood, or other tissues. Isolation of E rhusiopathiae is more likely
from acute cases; failure to recover the organism should not rule
out a diagnosis of erysipelas. Acute erysipelas must be differenti-
ated from classical swine fever, other causes of acute septicemia
(eg, salmonellosis, streptococcal infection), and other causes of
dermatitis. Actinobacillus suis is reported to cause rhomboid cuta-
neous lesions that resemble those of acute erysipelas.
Chronic erysipelas can be challenging to diagnose. Culture of
multiple joints or valvular endocarditis lesions does not often
result in isolation of E rhusiopathiae. However, in situations
where these lesions are occurring in appreciable numbers, careful
examination of the rest of the pigs in the herd will likely result
in identification of at least a few pigs periodically showing more
acute clinical signs and/or diamond-shaped skin lesions. This
is often accompanied by a history of change (or absence) of
vaccination for erysipelas. It is important to remember that both
arthritis and vegetative, valvular endocarditis can be caused by
many different organisms, most notably Streptococcus suis.
Control
Acute outbreaks of erysipelas can usually be controlled by injec-
tions of penicillin and/or erysipelas antiserum into affected pigs
with simultaneous administration of appropriate antimicrobials
via the drinking water. Vaccination in the face of an outbreak has
merit in reducing future cases.
A vaccination program is advisable for farms on which outbreaks
have occurred previously or where exposure is expected. Killed
or attenuated live vaccines are available. Most now have a dura-
tion of immunity of 26 weeks and are efficacious across a broad
spectrum of serotypes. Killed vaccines are given by injection
whereas attenuated live vaccines are given either by injection or
oral administration. Two doses of bacterin will usually protect
growing pigs to market weight. Boosters may be necessary in
some herds, especially those with a history of repeated exposure
to the organism. Erysipelas rhusiopathiae is a common constitu-
ent of pre-breeding vaccines that also include porcine parvovirus
and Leptospira. A combination of regular vaccination, good
sanitation, the elimination of carriers with lesions, and appropri-
ate quarantine measures for purchased stock will usually aid in
control of erysipelas.

26 ERYSIPELAS
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Greasy pig disease
Alternate names and abbreviations
Exudative epidermitis
Definition
An acute, exudative dermatitis affecting pigs from a few days to
about 8 weeks of age, characterized by variable to high morbid-
ity and variable mortality. The causative organism can contribute
to skin infections in older pigs as well as sporadic cases of sepsis
in pigs of any age.
Occurrence
Exudative epidermitis occurs in most major swine-raising coun-
tries. It is a sporadic disease that is occasionally seen by most
swine practitioners. Although acute exudative epidermitis usually
occurs in pigs less than 8 weeks old, the disease also occurs in a
less severe form in older pigs. It seldom occurs in adult swine.
Historical information
Exudative epidermitis was described over 150 years ago and
Staphylococcus hyicus, the etiologic agent, was first identified
1965. Despite research, the complete etiology of exudative epi-
dermitis is unclear.
Etiology
Staphylococcus hyicus is a hardy, Gram-positive coccus. Staphy-
lococcus hyicus may normally be present at many sites, including
skin, nasal mucosa, vagina, and prepuce. At least 6 serotypes have
been identified. Experimentally, inoculation of pigs with cultures
of certain strains of S hyicus, as well as bacteria-free culture super-
natant, is able to induce exudative epidermitis in pigs. At least 6
exfoliative exotoxins have been identified but not all are present
in every isolate; these toxins target cells of the stratum granulosum
in the epidermis.
Epidemiology
Most herds (and pigs) are endemically infected with S hyicus, but
exudative epidermitis seems to occur only as a sporadic, opportun-
ist disease in individual pigs. However, on occasion exudative epi-
dermitis can occur as an epidemic within certain age cohort groups.
Vertical transmission of the organism occurs within 24 hours of
birth, with further lateral transmission occurring from pig to pig.
Maternal immunity is likely important in preventing the disease
in pigs less than 8 weeks of age. When they occur, outbreaks of
exudative epidermitis are usually self-limiting within 3 months as
a function of herd immunity developing.
Under experimental conditions, only certain strains of S hyicus
can colonize the skin and cause disease. The epidemic form of
exudative epidermitis tends to occur in start-up herds or follow-
ing introductions of new breeding stock to a herd, suggesting that
BACTERIA
differences in strain virulence or variations in animal immune
status are important in the epidemiology of the disease. However,
some outbreaks do occur that are not related to introduction of
new animals, suggesting that other risk factors are likely involved.
The organism is hardy and may persist in facilities, particularly
those with poor hygiene and high humidity. Important risk
factors for exudative epidermitis include management practices
or environmental conditions that are associated with frequent
breaches to the skin epithelium. Sources of skin trauma and
abrasions are numerous and include frequent commingling
events, large litter sizes (or cross-fostering techniques) that create
competition for nipples, facility design or maintenance issues
that result in cuts or abrasions, and the use of caustic compounds
or disinfectants that cause skin irritation. Other possible factors
for exudative epidermitis expression include: viruses causing
transient vesicles (eg, certain strains of parvovirus, poxvirus, or
members of Picornaviridae), nutritional deficiencies (eg, zinc or
vitamins), ringworm, pityriasis rosea, parasitism (including lice
infestation), lack of competing bacterial flora on the skin, and
genetic susceptibility.
Bacteremia and sepsis that may occur along with exudative
epidermitis may occasionally cause polyarthritis and serositis in
young pigs or abortion in sows.
Pathogenesis
Initial skin lesions are likely toxin mediated, resulting in desmo-
some lysis and focal erosions in the stratum granulosum that often
form intracorneal pustules laden with bacteria. Lesions extend
into hair follicles as suppurative folliculitis. Sebaceous glands
secrete excessive amounts of sebaceous, greasy exudates that accu-
mulate over the dermatitis lesions. Severe epidermal erosion and
ulceration follow with formation of surface cracks, fissures, and
ulcers that enlarge and may coalesce. Systemic effects of dehydra-
tion with loss of serum proteins and electrolytes occur.
Clinical signs
Listlessness and anorexia in some or all piglets in a litter, in the
absence of fever, are early warning signs of the disease. The skin in
the axilla and groin is often reddened and non-pruritic, but these
lesions may not be noticed until brownish spots (starting as 1 to
2 centimeter in diameter) covered by serum and exudate appear
on the skin of the face or head. In some cases, the lesions will be
resolved without treatment but in most cases, the lesions enlarge
and coalesce then spread posteriorly with a generalized dermatitis
becoming apparent in as few as 24 to 48 hours. Although initial
lesions usually affect haired areas, ulcers may develop on the
tongue or in the mouth.
Young pigs can die within 3 to 5 days. Overall morbidity and
mortality are usually high in younger pigs. Pigs older than about
GREASY PIG DISEASE 27
 SWINE DISEASE MANUAL
BACTERIA
8 weeks may have only a few lesions and these may be mostly
confined to the head. These older pigs often survive but tend to
gain weight slowly. Adult swine occasionally have a few brown
exudative lesions on the back and flanks but infections in this age
group are uncommon and often unrelated to known outbreaks in
younger pigs. The adult lesions can easily be confused with focal
areas of ringworm.
Lesions
Affected pigs are usually dehydrated and malodorous, with exten-
sive gross lesions on the skin. Fissured dark crusts involve most
haired areas, with the head and neck most often affected, though
feet, body, and occasionally the mouth and tongue may also be
affected. Peripheral lymph nodes draining areas of infected skin
are swollen. Microscopically, there is a pustular dermatitis largely
in the stratum corneum and a suppurative folliculitis; suppurative
lymphadenitis may occur in enlarged peripheral lymph nodes.
Diagnosis
Clinical signs and gross lesions are adequate for diagnosis, with
confirmation by isolation of S hyicus or by histopathology. Mild
cases require differential testing for other skin diseases.
Control
Consistently efficacious therapies have not been reported,
although injectable antimicrobials are considered beneficial
28 GREASY PIG DISEASE
during the very early stages of the disease. As much of the pathol-
ogy is related to the effect of bacterial toxins rather than simply
bacterial colonization, antibiotic therapy often has little effect in
advanced cases. Topical application of antimicrobials or solutions
(as approved in specific countries) such as 10% bleach, chlor-
hexidine, Virkon, or dilute tamed iodine have been utilized to
some effect. Affected litters or individual pigs should be isolated
immediately and commingling of pigs should be avoided if an
outbreak has occurred. If an outbreak is well established in small
pigs before diagnosis, it may be prudent to euthanize those with
advanced lesions. Any that recover will gain weight inefficiently.
Prevention of exudative epidermitis starts with providing a high
standard of sanitation for pregnant sows, especially in farrowing;
washing of sows prior to entry into the farrowing house is a good
practice.
Control of exudative epidermitis is largely dependent on pre-
venting trauma to the skin and improving environmental hygiene
through good ventilation, cleaning, drying, and disinfection
between groups, all-in, all-out pig flow, low humidity, and
avoidance of high stocking densities. Vaccination with an autoge-
nous bacterin of S hyicus has been reported, but there is little
information regarding the efficacy of this procedure. In addition,
outbreaks of exudative epidermitis often develop so rapidly that
an autogenous bacterin cannot be prepared and administered in
time to have any beneficial effect.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Haemophilus parasuis
Alternate names and abbreviations
HPS, Glässer’s disease, Glaesserella parasuis
Definition
A common acute infectious disease of pigs, characterized by
various combinations of meningoencephalitis, polyserositis, and
polyarthritis as well as a contributor to bacterial pneumonia.
Occurrence
Glässer’s disease is caused by Haemophilus parasuis and occurs
sporadically among swine, usually in pigs between 3 weeks and
4 months of age. It often occurs subsequent to stressful events
such as weaning, environmental stressors, commingling, or as a
coinfection with other disease agents. Glässer’s disease is present
in all major swine-raising countries and is common in modern
age-segregated production systems.
Historical information
In 1910, Glässer observed a unique swine disease that was associ-
ated with a small, Gram-negative rod. In 1931, an organism was
isolated from pigs with influenza and was named Haemophilus
influenzae suis. By 1943, it was clear that the organism was a
pathogen in its own right and not the cause of influenza in swine
and therefore the name was shortened to Haemophilus suis. By
1976, taxonomic studies had been completed that resulted in the
organism’s present name, Haemophilus parasuis. The importance
of Glässer’s disease has increased with expansion of the swine
raising industry.
Etiology
Haemophilus parasuis is a small, pleomorphic, fastidious,
Gram-negative rod of the family Pasteurellaceae. It grows on
blood agar as “satellite” colonies near a streak of Staphylococcus
organisms, an alternative source of nicotinamide adenine dinu-
cleotide (NAD), or on enriched chocolate agar. Haemophilus
parasuis is a common inhabitant of the nasopharynx in healthy
pigs. It causes disease when it becomes septic or when it infects
lung tissue, the latter frequently as a coinfection with other dis-
ease processes. As a septicemia, H parasuis has predilection for
colonization of serosal surfaces (peritoneum, pleura, epicardium),
synovium, and/or meninges.
At least 15 major serovars have been identified with many addi-
tional serovars, including untypeable strains, also common. Herds,
groups of pigs, and even individual animals often harbor several
different serovars of H parasuis simultaneously. Serovars 4, 5, 13,
and 14 are the most prevalent in North America. Cross-protection
may occur among serotypes but is incomplete. Molecular charac-
teristics of isolates differ, depending on whether they have been
isolated from systemic sites or from the respiratory tract. Prediction
of virulence or cross-protection based on genotyping information
BACTERIA
is not reliable despite descriptions of at least 48 putative virulence
factors. Virulence appears to be related to capsular antigens but is
not necessarily related to immunogenicity.
Epidemiology
Haemophilus parasuis is widely distributed in swine populations
throughout the world; the host range is limited to swine. The
organism is considered part of the normal respiratory microbiota,
often with multiple strains being present simultaneously in a herd
and in individual pigs. Some, but not all, suckling piglets are nat-
urally exposed from the dam and will become colonized within
days of birth.
Colostral antibodies usually protect pigs from disease during
the period of time required for the colonized pigs to develop an
active immunity, usually by 7 to 8 weeks of age. However, piglets
colonized later in life, perhaps during commingling events or
with different strains, may not have sufficient or specific passive
protection at this point. Therefore, some pigs in a group will tend
to become infected through this horizontal transmission and
develop fulminating disease. Unusual stresses such as weaning,
prolonged transport, or the occurrence of other diseases may
predispose to outbreaks.
Haemophilus parasuis is quite labile outside of the pig and does
not persist in the environment, particularly with modern hygiene
practices such as all-in, all-out pig flow.
Pathogenesis
Intranasal inoculation of susceptible pigs with virulent strains
results in colonization and suppurative rhinitis. Haemophilus
parasuis can then be picked up by macrophages and/or through
lymph drainage and be distributed systemically (septicemia) to a
variety of internal organs and epithelial surfaces. Highly virulent
stains can persist in blood and resist clearance by macrophages,
thereby enabling them to access and colonize serosal surfaces,
synovium, and meninges. The resulting tissue colonization and
local tissue damage results in classic Glässer’s disease with severe
inflammation and exudation.
Haemophilus parasuis has a predilection for the leptomeninges
and brain, and often localizes there. This commonly stimulates a
severe inflammatory reaction in the meninges. Damage to endo-
thelium probably facilitates formation of inflammatory exudate
and increased synovial fluid in joints as well.
Haemophilus parasuis can also colonize lower respiratory tract
and when armed with the necessary virulence factors, can survive
destruction by pulmonary alveolar macrophages and contribute
substantially to suppurative bronchopneumonia that may have
been initiated by other pathogens.
The severity of disease expressed depends on virulence factors
contained in the particular strain of H parasuis, the immune
status of the pig, the presence of other pathogens, and myriad risk
HAEMOPHILUS PARASUIS 29
 SWINE DISEASE MANUAL
BACTERIA
factors or stressors. Haemophilus parasuis can be a primary patho-
gen acting alone. However, disease often occurs in conjunction
with other diseases such as porcine reproductive and respiratory
syndrome virus (PRRSV), porcine circovirus type 2 or influenza
A virus. The lesions or stress associated with concurrent diseases
likely enhances access of the organism to the blood or compro-
mises innate or acquired immune mechanisms, thus allowing
disease expression.
Clinical signs
Onset of typical Glässer’s disease is usually sudden, often affecting
the most robust pigs in a group first. They may be found dead or
die after a disease course of less than 2 days. The sudden deaths
may occur in any age group and sometimes there are signs sugges-
tive of septicemia or myositis.
Clinical signs depend upon where the organisms localize. Signs
of central nervous system disturbance often predominate as a
consequence of localization of H parasuis in the brain, meninges,
and spinal cord. Signs may then include tremors, incoordination,
posterior paresis, or lateral recumbency. In most cases, there is
an initial, marked rise in temperature, along with anorexia and
depression. In some outbreaks, swollen leg joints, fever, reluctance
to move, and lameness are common and may even predominate.
Less frequent signs include rhinitis, dyspnea, reddening of the
conjunctiva, cyanosis of the extremities, and edema of the eyelids
or ears. Morbidity is usually low, but mortality is high among
those pigs left untreated.
Haemophilus parasuis infection that manifests as a respiratory
disease may involve serotypes that are different from those
causing septicemias and classic Glässer’s disease. Compromised
growth or stunting may be apparent in a portion of pigs, partic-
ularly those where fibrinous serositis resolves with fibrosis and
serosal adhesions.
Lesions
External examination may reveal cyanosis of the skin, swollen
joints, or conjunctivitis. Lesions will vary with each pig, but those
of classic Glässer’s disease often have copious serofibrinous or
fibrinopurulent exudate in the peritoneal cavity, the pericardial
sac, within meninges, and/or on pleura in the thorax. Pleuritis
is a common lesion and may be present with or without obvious
pneumonia. Lesions in the lungs are often red, multifocal, dis-
seminated, and are suggestive of septicemia and hematogenous
spread. Haemophilus parasuis may also contribute to typical bron-
chopneumonias caused by other agents.
One or more major leg joints are often swollen, perhaps in combi-
nation with lesions at other sites, and there may be fibrin within
the joint capsule along with reddened and swollen synovium.
Exudate in joints is often fibrinous and gray to green in color.
Occasionally, some peracutely affected pigs will contain no readily
visible gross lesions. However, in many of these cases if the brain is
removed, a fibrinopurulent exudate may be visible on the ventral
30 HAEMOPHILUS PARASUIS
aspect of the brain. In advanced cases, the exudates may be present
over the cerebellum or cerebrum. The atlanto-occipital joint is
frequently affected.
Less common and less specific findings of Glässer’s disease
include congestion of the fundus of the stomach and petechial
hemorrhages on the kidneys. Microscopic lesions are usually
acute, suppurative to fibrinopurulent, with suppurative infiltrates
in meninges, pleura, serosa, and synovium common findings. Vas-
culitis and vascular thrombi are occasionally recognized.
Diagnosis
A presumptive diagnosis can often be made on the basis of his-
tory, clinical signs, and the appearance of typical gross lesions.
The diagnosis should be confirmed, however, by demonstrating
the presence of H parasuis within lesions. Samples of choice for
culture include systemic locations, while avoiding the nasophar-
ynx and lung. Samples from these sites may include fibrin or
swabs from serous membranes, meninges, synovium, cerebro-
spinal fluid, or other affected tissues. Detection of the organism
can be achieved by culture or polymerase chain reaction. Culture
has the advantage of being able to determine the antibiotic
susceptibility on the resulting isolate. In addition, the isolate is
also then available for further characterization or production of
autogenous bacterins. Isolates must be differentiated from other
Haemophilus-like organisms, especially Actinobacillus suis.
Concurrent infections with Streptococcus suis or Mycoplasma
hyorhinis are not uncommon. Brain, visceral pleura and other sero-
sal exudates are preferred culture sites since those are most likely
to have virulent H parasuis present. Because it is a common inhab-
itant of the nasopharynx in healthy pigs, detection of H parasuis
from the nasopharynx, lung parenchyma, or oral fluids has no
value in confirmation of Glässer’s disease. Serology is of little value
in diagnosis of disease.
Because of the multisystemic nature of Glässer’s disease, numer-
ous other causes of sudden deaths, respiratory distress, sepsis,
polyserositis, lameness, arthritis, and central nervous system dis-
eases should be included in the list of differential diagnoses.
In complicated cases of Glässer’s disease, histopathology is
extremely useful to confirm the presence of typical Glässer’s
lesions and to implicate roles for other disease agents. Molecular
techniques are well described for identifying H parasuis from
clinical specimens, as well as for characterizing the organism and
for carrying out epidemiological studies.
Control
The course of the disease is often short and many of the sick ani-
mals die if left untreated. For that reason, sick animals should be
promptly treated parenterally with an appropriate antimicrobial.
If numerous pigs are affected, it may be advisable to mass medi-
cate. Haemophilus parasuis is sensitive to many antibiotics but the
sensitivity pattern of isolates from individual farms may vary over
time so antimicrobial sensitivity testing is warranted.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Prevention of Glässer’s disease may involve changes to manage-
ment procedures, including improvements to husbandry and
environment, control of primary diseases such as PRRSV, admin-
istration of prophylactic antimicrobials, or vaccination. Since
H parasuis colonizes relatively early in the piglet’s life (less than
10 days of age), segregated rearing has not been uniformly suc-
cessful in preventing transmission to piglets or the downstream
spread of infection and disease. Achieving herd immunity to the
agent is helpful and is augmented by proper acclimatization and
perhaps vaccination of breeding stock. Minimizing stressors asso-
ciated with weaning, commingling, and the nursery environment
should be emphasized as well.
Killed bacterins as well as avirulent live vaccines are available and
can be effective for prophylaxis. Unfortunately, protection against
one serovar of H parasuis does not ensure good protection against
all serovars; cross-protection is difficult to predict even with
molecular technologies. Limited research suggests that piglets
from dams that have been vaccinated against H parasuis prior to
BACTERIA
farrowing, or piglets vaccinated when 1 to 3 weeks of age, have
resistance to disease caused by the same (homologous) serovar.
Colostral immunity in the piglets may sometimes interfere with
very early vaccination against H parasuis infection.
The natural process of herd immunity probably involves coloni-
zation of young pigs while in the presence of maternal immunity.
This prevents expression of clinical disease, yet allows induction
of active immunity to the agent, rendering pigs resistant to
subsequent challenge with homologous strains. One innovative
approach to control of the disease is based on purposefully man-
aging controlled exposure of nursing piglets to live H parasuis
endemic to the farm. The objective of this strategy is to permit
successful infection and development of active immunity in all
pigs, while disease expression is suppressed by maternal immu-
nity. This concept attempts to mimic the natural ecology of
organism and host. However, this technique may not be appro-
priate on large farms with multisite production that tend to have
multiple strains of H parasuis at any given time.
HAEMOPHILUS PARASUIS 31
 SWINE DISEASE MANUAL
BACTERIA
Ileitis
Alternate names and abbreviations
Porcine proliferative enteritis (PPE), porcine intestinal adeno-
matosis (PIA), porcine hemorrhagic enteropathy (PHE), regional
ileitis, garden-hose gut
Definition
Porcine proliferative enteritis, commonly known as ileitis, is a
bacterial enteric disease caused by Lawsonia intracellularis and
is characterized by hyperplasia of crypt enterocytes and mucosal
thickening, with inflammation and sometimes ulceration or hem-
orrhage of the intestine and/or colon. Clinical signs vary con-
siderably between individual pigs as does gross lesion location,
extent, and duration.
Occurrence
Lawsonia intracellularis and its associated disease is distributed
worldwide with disease expression having become more common
as production systems have become more modern. Disease is
categorized pathologically as either acute porcine hemorrhagic
enteropathy (most typical in older pigs and young adults) or as a
chronic, proliferative, and/or necrotic form that is more common
and usually occurs during the grow-finish phase.
Disease occurs most frequently in pigs 8 to 20 weeks of age, but
may also occur in pigs as young as 3 weeks of age (especially in
antibiotic free or organic farms), in market-weight pigs, replace-
ment gilts, or in adult swine. Disease occurrence often appears to
be more severe and at an increased incidence in age-segregated
“high-health” herds. Natural infection with similar signs and
lesions has been reported in other mammals, including horses,
hamsters, ferrets, guinea pigs, foxes, lambs, rabbits, rats, dogs,
white-tailed deer, and emus. Irrespective of the source, no sub-
stantial differences have been detected in the genotype of the
L intracellularis agent. Hamsters have been used in research and
are readily infected by the porcine organism.
Historical information
Lesions of ileitis were first reported as adenomatosis in 1931
due to the characteristic severe crypt enterocyte hyperplasia that
was associated with the disease. The name “regional ileitis” was
applied because of the propensity for lesions to be seen in the
ileum. Ileitis was recognized as a sporadic disease over the next
40 years. It was not until the 1970’s that rising mortality and
performance losses from ileitis on large, modern farms stimulated
specific research efforts on the disease. Several bacteria were
erroneously implicated as causal over the next 20 years. However,
in 1993 L intracellularis was isolated in tissue culture, and subse-
quent experimental infection studies confirmed it as the cause of
all forms of ileitis.
32 ILEITIS
Etiology
Early microscopic reports of lesions of ileitis identified the
presence of curved, rod-shaped, Gram-negative bacilli in the
apical cytoplasm of proliferative crypt enterocytes. In 1993, the
offending fastidious causal bacteria was finally cultivated in vitro
in tissue culture. Isolation of L intracellularis is laborious and
quite technical; only a few laboratories routinely attempt to iso-
late the organism from field samples. As an obligate intracellular
bacterium, tissue culture (eg, rat enterocyte) is still required for
organism propagation. Experimental inoculation of susceptible
pigs with a pure culture of L intracellularis consistently repro-
duces ileitis, which has greatly augmented study of the organism
and disease. All L intracellularis isolates examined from various
host species or different geographical locations appear to be
quite similar genetically. With multiple passages in tissue culture,
L intracellularis becomes attenuated; the technique has been used
to develop a commercially available vaccine.
Despite rigorous investigation, virulence factors and protective
epitopes of L intracellularis are not well understood. Polymerase
chain reaction (PCR) has been useful for detection of the agent
and continuing investigation of sequence data is being used in
attempts to characterize epidemiologically important attributes of
L intracellularis.
Epidemiology
Lawsonia intracellularis is endemic globally and is found in most
domestic swine herds. Carrier dams have been shown to infect
their litters as early as 6 days of age, a likely reason for failure of
segregated early weaning techniques to control disease. Passive
immunity may prevent infection in some pigs, hence transmis-
sion from pig to pig within groups probably continues for several
months. This is supported by the gradual seroconversion that
occurs in groups of pigs over weeks to months during the growing
phase. It follows that clinical impact may be present for weeks
to months, if no interventions are applied. Research has demon-
strated that L intracellularis recovered from experimentally
infected pigs spreads to naïve sentinel pigs penned with them
or penned separately in the same enclosed area. The incubation,
recovery, and carrier phase of L intracellularis infection can be
quite long in some pigs, probably months. There undoubtedly are
carrier swine that disseminate L intracellularis to susceptible pigs
through their feces by the fecal-oral route or via feces-contam-
inated fomites. Although other animal species may be infected
with L intracellularis, there is little evidence suggesting direct
interspecies transmission. However, mice have been demon-
strated to harbor and shed L intracellularis in feces and hence
may have a role in introduction or maintenance of L intracellu-
laris in swine herds.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Infectious dose is low and fecal excretion from clinically affected
pigs is high. The severity of disease tends to be proportional to
the infecting dose. The incubation period for expression of the
disease is at least 2 weeks. The L intracellularis organism has been
shown to survive at least 2 weeks in organic material, a feature
which also helps to assure its continuous maintenance on a
farm premises.
Ileitis may occur explosively, particularly when naïve older ani-
mals are exposed to L intracellularis through commingling with
infected animals or when they are placed under stress in an envi-
ronment in which L intracellularis is present in high numbers.
Common examples of these situations occur when naïve gilts
enter a sow farm or when carrier gilts enter a naïve sow popula-
tion. It is also common to have acute outbreaks of ileitis occur
just after some, but not all pigs, are sorted from the group then
removed for transport to slaughter.
Outbreaks in endemic populations have often been associated
with a variety of stressors. Infections in these circumstances are
often subclinical yet may have substantial impact on growth and
performance. Vaccines for L intracellularis are very effective in
preventing clinical signs and lesions, but do not prevent coloniza-
tion or stimulate sterilizing immunity.
Pathogenesis
Lawsonia intracellularis infects enterocytes within hours after
ingestion and survives intracellularly, free in cytoplasm. When
enterocytes undergo mitosis, each cell retains some of the
bacteria. However, these infected enterocytes fail to mature.
This results in the hallmark lesion of proliferative enteritis - the
proliferation of immature enterocytes. Whether the organism
stimulates greater proliferation, retards maturation, or both is not
known. Microscopically, organisms are visible within the apex of
crypt epithelial cells. Although much is known regarding patho-
genesis, some details remain speculative, particularly the existence
and role of specific virulence factors and mechanisms.
Infection results in crypt epithelial hyperplasia, crypt elongation,
degeneration and necrosis of enterocytes, fewer goblet cells,
and an inflammatory response. There are often degenerative
changes, cell necrosis, inflammation, and repair simultaneously
present. The variations in the reported clinical and pathological
syndromes may correlate with different stages in lesion develop-
ment, variation in immune modulation, or different individual
pig responses to infection via variations in predisposing factors,
stresses, microbiome, or presence of other saprophytes.
Seroconversion usually occurs 2 to 4 weeks after infection,
although detectable lesions may not develop until 3 weeks
post-infection. The protected, intracellular environment in which
the organism lives probably means that a cell-mediated response
is required to eliminate infection.
Resolution of lesions starts approximately 3 to 4 weeks after
infection, but shedding may continue for months.
BACTERIA
Clinical signs
There has been much confusion related to nomenclature,
lesions, and clinical signs of ileitis, primarily due to the variation
that exists in clinical signs, age of pigs affected, gross lesions,
and clinical impact. Three clinical forms of ileitis are commonly
recognized.
The acute hemorrhagic form (PHE) is characterized by the
appearance of acute bloody diarrhea with blood clots and the
sudden death of previously healthy pigs. This form of the dis-
ease is most common in pigs greater than 20 weeks of age (late
grow-finish or young adults). Feces in PHE-affected pigs may be
dark or black from blood loss, and affected animals may be pale
from anemia. This clinical presentation must be differentiated
from bleeding gastric ulcers and hemorrhagic bowel syndrome.
The chronic clinical form is most frequent in pigs from 6 to 20
weeks of age. Affected animals lose body condition and have
persistent or intermittent, liquid, gray feces. Salmonellosis, swine
dysentery, whipworm infestation, and some enteric coronaviruses
are common clinical differentials. Morbidity and mortality with
both the acute and chronic presentation are quite variable.
Some pigs may have severe proliferation of the mucosa of the
terminal small intestine yet can be clinically asymptomatic. These
pigs fall into the third clinical form of ileitis referred to as the
subclinical form. Affected pigs are without visible or obvious
clinical signs but have compromised growth performance that
may only be measurable through production data recorded at a
herd level. These pigs have lesions that are identifiable at a micro-
scopic level that are not grossly visible at necropsy. Understanding
whether L intracellularis is present and its relative importance is
critical whenever groups of pigs have intermittent diarrhea with
visible variation in growth.
Lesions
Ileitis lesions correspond to the clinical forms described above.
Regardless of form, the lesions vary between pigs based on the
duration, severity, extent, and location of the infection. However,
lesions that include gross thickening of a portion of the mucosa
of the small and/or large intestine virtually always occur. In the
acute form, there are often bloody intestinal contents associated
with grossly thickened small intestine. Clotted blood in the small
intestine is highly indicative of PHE.
Lesions are more variable in the chronic form. The small intestine
is commonly affected with a hose-like, palpable thickening of
the mucosa of the ileum. The serosal surface of affected loops
of thickened intestine has a unique wrinkled appearance due to
mucosal thickening and the presence of exudates. Peyer’s patches
may be hyperplastic. Lesions can be found in the small or large
intestine, or both.
In the cecum or colon, the mucosa is thrown into thick folds,
plaques, or polyps, and it may be covered by inflammatory exudate
ILEITIS 33
 SWINE DISEASE MANUAL
BACTERIA
and vaguely resemble lesions of swine dysentery, trichuriasis,
salmonellosis or even porcine circovirus type 2-associated disease.
Healing lesions of ileitis and ileal thickening in pigs at slaughter
suggest that some affected swine may show few or no signs and
recover spontaneously.
Histopathology is useful to confirm the nearly pathognomonic
lesions of ileitis, which usually include easily identifiable intracellu-
lar L intracellularis organisms. Multiple sections should be exam-
ined in mild cases, lesions may be microscopic and segmental. The
hallmark lesion of crypt enterocyte hyperplasia should be accom-
panied by demonstration of intracellular organisms via immuno-
histochemistry (IHC), in situ hybridization (ISH), or silver stains,
irrespective of the clinical or pathologic form of disease. Crypt
hyperplasia alone is not sufficient to make the diagnosis of ileitis
since some crypt regeneration (proliferation) is not uncommon in
subacute or chronic stages of other enteric diseases.
Diagnosis
A presumptive diagnosis is best made by observation of charac-
teristic gross lesions at necropsy. Clinical signs are helpful but
often not specific. Confirmation of diagnosis is by observation
of typical microscopic lesions and demonstrating the presence
of intracellular curved L intracellularis in enterocyte apical cyto-
plasm by IHC, ISH, fluorescent antibody test (FAT), or silver
stains; IHC is considered the gold standard test for visualizing
the organism on histopathologic examination. Lesions may be
segmental; histopathology should therefore be performed on
multiple carefully selected and preserved sections of intestine and
colon. Polymerase chain reaction (PCR) testing on samples of
affected feces, oral fluids, or mucosa is useful to confirm presence
of L intracellularis, but results should be interpreted with care
because of the high prevalence of L intracellularis in most farms,
regardless of whether signs of ileitis are being expressed.
The detection of L intracellularis does not confirm presence of
the disease. Quantitative PCR performed on samples from clin-
ically affected pigs may be suggestive of ileitis, but the diagnosis
is not definitive without a complete diagnostic workup. Demon-
strating L intracellularis presence by PCR may be coincidental
with other enteric diseases such as salmonellosis, trichuriasis,
swine dysentery, coronaviruses, circovirus insult, or gastric ulcers.
Negative PCR tests do not rule out carrier status.
34 ILEITIS
Serology has limited availability and, similar to PCR testing,
requires understanding of both the test and immunopathogen-
esis of L intracellularis. Antibody specific for L intracellularis
can be detected within 2 weeks of infection. The magnitude and
duration of antibody response is proportional to disease severity.
When applied in a systematic manner on a herd basis through
sequential or cross-section sampling, serology can confirm that
L intracellularis is present in a herd, the age when infection likely
occurs, and the prevalence.
Control
Outbreaks of ileitis require antimicrobial intervention to prevent
mortality. Affected pigs are usually injected with an appropriate
antimicrobial while the rest of the group may be medicated via
water or feed for several days. Pulse doses of antimicrobials are
sometimes used for ongoing control or prevention, particularly
during or after periods of stress, or during outbreaks. Because of
the 2- to 3-week long incubation period, pulse doses are thought
to allow colonization and initiation of immunity while prevent-
ing the occurrence of clinical disease. Medication failures can
occur in limit-fed breeding stock where animals are not fed ad
libitum. In small herds that practice continuous-flow production
and/or late weaning, clinical disease may be mitigated by herd
immunity. Presumably, passively acquired maternal antibody
allows infection and active immunity to develop but prevents
overt disease. Control of ileitis has been a major reason for use of
feed-grade antimicrobials in grow-finish swine.
Vaccination for ileitis is widely practiced. Both avirulent live vac-
cines and killed vaccines are widely available and have very good
efficacy when properly administered. Vaccination of growing pigs,
as well as breeding gilts during acclimatization, has been very suc-
cessful in reducing or eliminating clinical signs of ileitis. In some
herds, vaccination has allowed the elimination of continuous
administration of feed-grade antimicrobials.
Elimination of L intracellularis from populations of pigs is cur-
rently impractical because exposure of swine to L intracellularis is
currently unavoidable. Segregated rearing has not been successful
and may even increase the likelihood of fulminating acute ileitis
occurring in “high-health” herds where normal herd immunity
mechanisms are often purposefully disrupted as part of control
programs for other diseases.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Leptospirosis
Alternate names and abbreviations
Lepto
Definition
Leptospirosis is a contagious disease of swine (and many animals,
including humans) caused by any one of a large group of Lepto-
spira bacteria. Disease expression in swine varies with the partic-
ular species and serovar that is involved; swine are susceptible to
many different serovars.
Occurrence
Leptospirosis occurs in swine in all parts of the world where
environmental conditions are favorable for the survival of Lep-
tospira. The occurrence of any one serovar of Leptospira in an
area depends on the presence of maintenance hosts in which the
infection can persist or the presence of incidental hosts. In both
instances, Leptospira can be effectively disseminated to swine. The
disease occurs more frequently where the hosts are numerous,
concentrated, or in frequent contact with swine.
Historical information
Early reports of “swine herder’s disease” in Europe described a
disease among caretakers of swine that probably was leptospirosis.
In the US, leptospirosis was recognized as an important disease
of swine in the 1940s and 1950’. The disease continues to be
endemic in areas where environmental conditions are favorable
for Leptospira. However, losses have been reduced through rou-
tine use of confinement housing, good sanitation, management
changes, vaccination, and the use of antibiotics. Exposure to Lep-
tospira, and consequently the occurrence of clinical leptospirosis,
is now relatively uncommon in modern swine production.
Etiology
Leptospira are motile spirochetes, 6 to 12 microns long, and
0.1 µm in diameter. They are usually hooked on both ends and
can be stained by Giemsa stain or in tissue, by silver stains. In the
laboratory, they are often studied under darkfield microscopy.
In laboratory media, they are difficult to culture and grow very
slowly (12 to 26 weeks). Many pathogenic strains can survive in
the environment for long periods of time under moist conditions
with a slightly alkaline pH. Most cannot withstand desiccation
and are destroyed by common disinfectants.
Taxonomy of Leptospira remains confusing. Under the most
current classification, the family Leptospiraceae contains 8 patho-
genic species, of which three are of most importance to swine:
Leptospira interrogans (serovars pomona, icterohaemorrhagiae,
canicola, and bratislava), Leptospira borgpetersenii (serovars sejroe
and tarassovi), and Leptospira kirschneri (serovar grippotyphosa).
Serovars pomona and bratislava are uniquely adapted to swine;
others are maintained in other species but sometimes infect
BACTERIA
swine. Serovar L hardjo is the most important serovar of bovines
and has been reported to infect pigs kept in close contact with
cattle. Leptospira bratislava is reported to be the most common
strain in swine, although the role of this serotype as a cause of
disease is debatable.
Epidemiology
Many of the pathogenic Leptospira serovars, including L pomona,
have a predilection for the kidneys where they tend to persist.
Both maintenance and incidental hosts pass large numbers of
Leptospira in their urine, with shedding often lasting for weeks
to months after clinical signs have concluded. Infection is usu-
ally introduced into a herd by infected, shedding swine (often
replacement gilts or boars), by direct or indirect contact with
incidental hosts (rats, mice, skunks, raccoons, foxes, opossums,
etc), or through Leptospira-contaminated water, soil, or effluent.
Outbreaks have been reported in herds using untreated surface
water for drinking.
Under ideal conditions, Leptospira survives in water and damp
soil, remaining a persistent threat to a wide range of animals
including swine and humans. Incidental hosts can be infected or
merely act as passive transport hosts that carry Leptospira to other
premises. Carnivores that consume dead pigs may be underesti-
mated as transmitters of Leptospira.
Fetuses infected in utero may survive as infected piglets and
become adult carriers, eventually transmitting Leptospira via
urine to cohorts, offspring, or other farms, or acting as a source of
contamination for vectors or the environment. Some Leptospira
serovars, especially L bratislava, have a predilection for the genitalia
of both male and female swine and can be transmitted venereally as
well as through urine.
Pathogenesis
Leptospira penetrate mucous membranes (eyes, mouth, nose,
or vagina), wounds, abrasions, and perhaps water-softened skin
of the host. A leptospiremia then develops and organisms may
affect many major organs. Many Leptospira species localize in the
kidney or in the uterus during the last half of gestation. Leptospira
bratislava can localize in the oviduct and uterus of non-pregnant
sows and in the genital tract of boars. The exact way in which
Leptospira produce their pathogenic effect is not known but
capillary damage is a major feature. Localization in the kidney,
first in the interstitium and later in the tubules, results in vascular
damage and at least temporary damage to tubules. Interstitial
nephritis, if extensive, can lead to kidney failure and uremia.
The liver may also be affected. In addition, Leptospira produce
hemolysins which result in the hemolysis of erythrocytes and
causes hemoglobinuria and hemolytic anemia. The severe effects
of hemolytic anemia occur mostly in very young piglets, perhaps
fetuses, and may trigger abortions.
LEPTOSPIROSIS 35
 SWINE DISEASE MANUAL
BACTERIA
Clinical signs
The acute phase of leptospirosis largely coincides with an initial
stage of leptospiremia as well as virulence of the particular serovar
involved. Signs often go unnoticed in mature, non-pregnant
swine and in growing pigs. A careful observer might notice
mild fever and inappetence for a few days. In very young piglets,
however, there may be fever, anorexia, hemolytic anemia, hemo-
globinuria, icterus, convulsions in occasional pigs, and a failure to
grow and gain weight.
Chronic infection in dams is usually apparent only as various forms
of reproductive failure, including poor conception rates. Pregnant,
infected animals often abort in late gestation. In many cases, fetuses
are carried almost full term but may be mummified, dead, or weak
at birth. Although many infected neonatal pigs die within a few
days, some often survive. The dams usually recover promptly. They
often conceive again and carry their litters to term.
Lesions
Lesions have seldom been described in sows since most infected
adults recover. Grow-finish swine may have scattered foci of
interstitial nephritis or generalized kidney scarring that may only
be noticed at slaughter as white-spotted kidneys. Lesions in small
piglets include patchy areas of hepatic necrosis, excessive fluid
and fibrin in the peritoneal cavity, and evidence of inflammation
in multiple organs. Microscopically, there is a marked focal, dis-
seminated, interstitial nephritis; tubules and glomeruli often have
degeneration and inflammation. Occasionally, a non-suppurative
meningitis can be observed. Placental lesions are seldom marked
or significant but may include edema and scattered hemorrhages.
Diagnosis
A history of abortions in late gestation along with lesions in
neonates may suggest leptospirosis, but mere observation is inad-
equate for accurate diagnosis. Demonstration of organisms in
tissues or fluids by polymerase chain reaction can confirm infec-
tion but may not identify the particular serotype. Histopathology
with immunohistochemistry or fluorescent antibody test on
kidney or liver is quite definitive. Silver stains of tissue smears or
urine can reveal organisms with compatible morphology, as can
darkfield or phase-contrast microscopy, but may not be specific or
sensitive enough to detect some infections. Isolation and identifi-
cation of Leptospira is both tedious and laborious.
36 LEPTOSPIROSIS
Diagnosis of outbreaks is often based on serological herd testing
using the microscopic agglutination test. Serum samples from
both affected and unaffected animals should be tested. High
antibody titers are usually present at the time of abortion or
farrowing, but paired samples may sometimes be required to
correctly interpret titer levels. Microscopic agglutination testing
is serovar specific, so the use of multiple assays may be required to
arrive at a diagnosis. Breeding animals are commonly vaccinated
against multiple Leptospira serovars, so interpretation of serolog-
ical results must also consider vaccination history of the animal.
Titers from infection are usually much higher than those induced
by vaccination.
Control
Control is usually attempted by prevention of exposure, immu-
nization through vaccination, and/or the use of antibiotics. Pre-
vention of exposure is difficult to achieve because so many species
can act as carriers of Leptospira. These include infected swine,
rodents (especially mice and rats), and many kinds of wildlife.
Once Leptospira are introduced into a favorable wet environ-
ment, they often persist there as a continuing source of infection.
Nonetheless, leptospirosis can be effectively controlled (perhaps
even eradicated) from swine populations raised under confine-
ment conditions using a combination of medication, vaccination,
vector control, and providing a treated or non-contaminated
drinking water source.
Immunization through the use of bacterins, widely practiced in
breeding herds, will usually reduce the prevalence of infection
and abortions. The bacterin must be appropriate for the serovar
of Leptospira causing the disease on the farm. Many bacterins
are multivalent. The level of immunity obtained and its duration
may not always be satisfactory, meaning sows may need to be
vaccinated 2 or 3 times per year to maintain protection. Also,
bacterins will not usually eliminate infection in carriers.
Antibiotics used judiciously may reduce the impact of leptospi-
rosis. It is doubtful that all carriers can be eliminated through
the use of antibiotics. Research suggests that oxytetracycline,
tylosin, and erythromycin are among the most effective agents
for treating leptospirosis.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Mycoplasma suis
Alternate names and abbreviations
Eperythrozoon suis (previously), epy, eperythrozoonosis
Definition
A sporadic disease usually observed in young growing pigs, char-
acterized by listlessness, fever, anorexia, hemolytic anemia, and
(in severe cases) icterus. Occasionally, dysgalactia has also been
associated with infection in sows.
Occurrence
Mycoplasma suis is a bacterial infection that can occur in all age
groups of swine but is seldom clinically apparent except in young,
growing pigs. Distribution is worldwide, with infection common
but actual disease outbreaks rather uncommon.
Historical information
Icteroanemia in growing swine was described in the US in 1943
and was investigated in the 1950s. Recognition that there were
many carriers came after development of an antibody test in
1975. Research with this organism has been sporadic, but with
the advent of polymerase chain reaction (PCR) testing for the
organism, the disease has garnered renewed interest.
Etiology
Mycoplasma suis organisms are obligate, intracellular bacteria
lacking cell walls. The organism is usually from 0.2 to 1.0 µm in
diameter but may be larger during the acute stages of infection. It
is usually coccoid-shaped but may appear rod or ring-shaped when
adhered to an erythrocyte’s cell membrane. The organism has not
been cultured in cell-free media.
Epidemiology
Herd prevalence is quite variable, with some countries reporting
up to 90% of herds infected, with herd prevalence of 10% to
20%. There are likely numerous subclinical M suis carriers in the
swine population. In utero transmission has been demonstrated
experimentally. Since the disease occurs more frequently in the
summer and fall, it is suspected that mosquitoes and biting flies as
well as the hog louse (Haematopinus suis) may play a role in trans-
mission. The use of contaminated surgical instruments, including
castration knives and needles used repeatedly during vaccination,
is also believed to transmit the organism. Ongoing infectious and
parasitic diseases are believed to play an important role in precip-
itating outbreaks.
Pathogenesis
Much of the information on pathogenesis is based on the study
of experimental infection in splenectomized pigs. In those pigs,
the clinical and pathologic aspects resemble reports of natural
infections. Once M suis is introduced into the blood, a fever
BACTERIA
occurs after about 7 to 8 days, which is during the acute phase of
the disease and the time when organisms are most numerous on
the surface of erythrocytes. Infected pigs become hypoglycemic
and gradually develop hemolytic anemia. Hemoglobinuria does
not occur because hemolysis is extravascular. However, icterus
can occur in some cases.
The number of platelets, the packed cell volume, and hemoglobin
values decrease. Most affected animals recover in the absence of
additional stressors but some do remain as carriers. The organism
was thought to reside in the cell membrane, but M suis is now
known to transmigrate to the interior of the red blood cells. In
most situations, M suis rarely causes substantial death loss. Rather,
it is recognized as an occasional cause of anemia or icterus in
young pigs or as a contributor to compromised reproductive or
lactation performance in sows.
Clinical signs
In young growing pigs, signs may include anorexia, listlessness,
weakness, pale mucous membranes, and sometimes icterus. Body
temperature is initially raised during infection but is often sub-
normal by the time the pigs are examined. In chronic cases, there
is often marked icterus, and deaths may occur. Signs in breeding
stock are similar but are less obvious and often go unnoticed. In
breeding herds, M suis infection has been associated serologi-
cally with various reproductive problems, including dysgalactia.
However, proof that these reproductive effects are caused by the
disease is still lacking.
Lesions
Lesions at necropsy depend somewhat on the duration of illness
and the age of the animals. In younger pigs, there may be pallor
and watery blood compatible with anemia, and perhaps modest
enlargement of the spleen. In cold climates, there may be necro-
sis of extremities. External parasites (such as lice), their ova, or
insect bites may be present. In older pigs, the same hematology
findings and spleen lesions are apparent at necropsy but splenic
enlargement is more noticeable. There is often icterus (more
obvious internally) that may be marked. The bone marrow is
red, suggestive of hyperplasia. The liver often has a brownish cast
from hemosiderosis. There are often suffusions in the abdomen,
thorax, and pericardial sac. Lymph nodes are edematous and
swollen. The heart is often thin-walled and flabby. Careful exam-
ination often reveals lesions of concurrent diseases or parasitism.
Diagnosis
Mycoplasma suis is not a major cause of disease, nor are outbreaks
spectacular. The history, signs, and gross lesions are often subtle
or vague, yet are of value in diagnosis. Confirmation of the
diagnosis is made by demonstrating the presence of organisms by
microscopy, PCR, or indirectly by serology. Organisms can be
MYCOPLASMA SUIS 37
 SWINE DISEASE MANUAL
BACTERIA

visualized on the surface of erythrocytes in blood smears or on Control

impression smears from spleen tissues that have been stained with
Wright-Giemsa or Diff-Quick stains. Blood with anticoagulant
(eg, citrate, heparin, or EDTA) should be collected from pigs in
the acute stage of disease. Another reported technique for diag-
nosis is mixing equal parts of blood with 10% formalin, and then
staining a smear of the material with acridine orange. Diagnostic
laboratories now usually prefer to confirm the presence of M suis
in blood or spleen by PCR.
Serological tests (indirect hemagglutination [IHA] or enzyme-
linked immunosorbent assay) may be available to confirm M suis as
a problem in a herd, although these tests have limited availability.
Infected pigs less than 3 months old seldom react on IHA. Differ-
ential diagnoses for M suis include systemic salmonellosis, porcine
circovirus associated disease, mycotoxicosis, hepatotoxicosis, iron
deficiency anemia, and autoimmune hemolytic anemia.
Tetracyclines are used with success for treatment of M suis infec-
tions. Intracellular organisms may not be responsive to single tetra-
cycline treatments so treatment may need to be repeated. Affected
pigs can be treated individually with injectable oxytetracycline.
Where available, serology may be useful as a screening test prior to
the purchase of breeding stock or to identify herd infection.
There are no vaccines for the prevention of M suis. In modern pro-
duction systems, clinical infections with M suis are unusual. Since
signs are sometimes vague, diagnostic investigations may need to be
expanded to assure other agents or risk factors are not contributing.

38 MYCOPLASMA SUIS
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Mycoplasmal arthritis
Alternate names and abbreviations
Mycoplasma hyosynoviae (MHS), Mycoplasma hyorhinis (MHR)
Definition
Mycoplasma hyorhinis and M hyosynoviae are considered com-
mensal bacteria in swine but are also known to be important
causes of arthritis on some farms. Mycoplasma hyorhinis usually
affects younger pigs up to 10 weeks of age. In addition to arthri-
tis, it can also cause polyserositis, otitis, pneumonia, and sporadic
abortions in sows. Mycoplasma hyosynoviae usually causes arthritis
in older (greater than 10 weeks of age) grow-finish pigs and
young adults.
Occurrence
It is suspected that both bacteria have a worldwide presence,
but published data on regional prevalence are lacking. Even in
herds where Mycoplasma hyopneumoniae has been eradicated,
M hyorhinis and M hyosynoviae are still present. In some areas,
there are perceptions that disease associated with these organ-
isms has increased, particularly in “high health” herds. In recent
years, diagnostic laboratories have reported increased frequency
of detection of these organisms, which may be associated with
increased testing, improved diagnostic capabilities, or an increase
in the clinical impact of these agents in some herds.
Historical information
Mycoplasma lack a cell wall and are the smallest and simplest
known self-replicating organisms. Mycoplasma hyorhinis was
initially described by Switzer in 1955. In 1970, Ross and Karmon
first described M hyosynoviae. In recent years, M hyorhinis and
M hyosynoviae have been increasingly recognized as swine patho-
gens from both an economic as well as an animal welfare perspec-
tive, especially in herds with higher health status.
Etiology
The small genome of both organisms and their inability to rapidly
synthesize ribosomes results in relatively slow replication rates
compared to most bacterial pathogens. As with most Myco-
plasma, they attach to and replicate on epithelial cells.
Both M hyorhinis and M hyosynoviae are known to infect swine
only. Both bacteria are easier to isolate and cultivate in vitro than
M hyopneumoniae, but each still requires unique special enriched
media as well as several days to a week for isolation or propagation.
The complex system of membrane lipoproteins of M hyorhinis
creates remarkable membrane lipoprotein diversity with variable
protein expression and size which is suspected to be important
in pathogenesis and immune evasion. Typing methods such as
multi-locus sequence (MLST) and multiple-locus variable num-
ber tandem repeat analysis (MLVA) have been developed recently
to better characterize this diversity.
BACTERIA
Epidemiology
Mycoplasma hyorhinis and M hyosynoviae are considered commen-
sals, colonizing the tonsils and respiratory epithelium of the nasal
cavity and conducting airways. A majority of colonized pigs have
no apparent clinical disease. Transmission is suspected to be pri-
marily via nasal secretions by direct contact or close proximity with
the dam (M hyorhinis) or penmates (M hyorhinis and M hyosyno-
viae). Prevalence of M hyorhinis is high at or shortly after weaning.
Prevalence of M hyosynoviae is low at weaning and slowly increases,
peaking around 10 to 16 weeks of age. The conditions or risk fac-
tors that trigger systemic spread of these tonsillar and respiratory
tract commensals are unknown. However, evidence suggests that
the dam is an important source of both organisms, leading to early
colonization of piglets and making the likelihood of eradication of
either organism from a farm very unlikely.
Pathogenesis
Both bacteria bind to the ciliated respiratory epithelium of the
nasal cavity and conducting airways. Systemic invasion from these
commensal sites is well documented, but mechanisms of invasion
and spread are still unknown. Both bacteria can be detected in
the blood of asymptomatic pigs for short periods of time. In
some, the organisms are able to localize and colonize systemic
sites, stimulating inflammation and disease expression. With
M hyosynoviae, systemic colonization is usually limited to syno-
via, with disease and lesions referable to synovitis. On the other
hand, M hyorhinis can colonize serosal surfaces of heart, pleura,
peritoneum, or synovium, causing inflammation and fibrinous
exudates at any or all of those locations. In a challenge study,
M hyosynoviae was found in multiple joints at the same time,
supporting the role of bacteremia as a prerequisite to disease
expression.
Detection of either or both organisms in lungs of healthy pigs
by polymerase chain reaction (PCR) is common and does not
appear to correlate with coughing or pneumonic lesions, nor do
the organisms appear to contribute to porcine respiratory disease
complex. Sporadic abortions reported with M hyorhinis are rare,
presumably a result of transplacental infection as sequel to bactere-
mia in young dams.
Clinical signs
Clinical signs of arthritis are similar for M hyorhinis and
M hyosynoviae, but the age of pigs affected is usually 3 to 10
weeks for the former, compared to 3 to 5 months for the latter.
Joint swelling can occur in single or multiple joints, manifested as
a painful lameness. Lameness may be transient (just a few days) or
last for an extended time, especially when complicated by other
health or environmental conditions. Affected pigs generally are
off feed and reluctant to move, with older pigs sometimes pre-
ferring a “dog-sitting” posture. This is accompanied by reduced
MYCOPLASMAL ARTHRITIS 39
 SWINE DISEASE MANUAL
BACTERIA
weight gain and loss of body condition. If not rapidly resolved,
pigs spend more time in recumbency, are more likely to have joint
calluses or chronic lameness, and are more likely to be culled.
Experimental studies confirm that pigs inoculated with M hyorhinis
can develop polyserositis and/or arthritis approximately 3 to 10 days
post-inoculation. Labored breathing and dyspnea can be observed in
pigs with pleuritis. Studies have shown that after experimental infec-
tion with M hyosynoviae, lameness can occur in up to 30% of pigs
within 4 to 10 days after experimental inoculation.
Lesions
Gross lesions associated with M hyorhinis most commonly
include polyserositis (involving pleura, pericardium and/or peri-
toneum) and/or fibrinous synovitis. Microscopic lesions include
infiltration of lymphocytes, plasma cells, and macrophages in
serosal connective tissues. Synovia are edematous with fibrino-
suppurative exudates and expansion of the synovial stroma by
infiltrates of lymphocytes, plasma cells, macrophages, and fewer
neutrophils. Co-inoculation of M hyorhinis with porcine repro-
ductive and respiratory syndrome virus or porcine circovirus type
2 has resulted in more severe lesions.
Mycoplasma hyosynoviae causes lesions in one or more joints
without specific tropism to any one joint. Grossly, affected joints
often have increased amounts of red-tinged synovial fluid with
decreased viscosity and very moist, swollen synovia. Microscop-
ically, the synovial stroma is expanded by serofibrinous effusion
and sparse aggregates of lymphocytes and plasma cells. As lesions
become subacute to chronic and the fibrin and neutrophilic
infiltrates resolve, large numbers of lymphocytes and plasma cells
expand the synovial stroma. The result is proliferation of synov-
iocytes and supporting connective tissue, resulting in grossly
visible villous proliferation of the synovium.
Diagnosis
Clinical signs and gross lesions are not usually sufficient for diagno-
sis of mycoplasmal arthritis or serositis. The age of the pigs affected
is an important consideration to clinically differentiate the acute
arthritis caused by these two mycoplasmas. Pigs greater than 10
weeks of age are more likely to be afflicted with M hyosynoviae,
whereas M hyorhinis is more likely to affect pigs less than 10 weeks
of age. A rapid and favorable response of acutely affected pigs to the
injection of an appropriate antimicrobial can support a diagnosis of
M hyosynoviae involvement but is not confirmatory.
40 MYCOPLASMAL ARTHRITIS
Samples for confirmation of disease include fibrin or swabs col-
lected from joints with lesions (M hyorhinis and M hyosynoviae),
or fibrin or fluid from the pleural, pericardial, and peritoneal
cavities where lesions are present (M hyorhinis). PCR assays are
the usual means for detection. It is important to remember that
as commensals, both organisms can commonly be detected in
nasal and respiratory tracts of normal pigs, hence PCR for disease
diagnosis should be performed only on suspected lesions such as
fibrinous exudates, synovium, or synovial fluid.
Molecular characterization of M hyorhinis has been performed
with MLST and MLVA typing although epidemiological inter-
pretation of these results is currently being investigated.
Both M hyorhinis and M hyosynoviae can be grown in their
respective culture media but primary isolation attempts are easily
overgrown by other bacteria unless samples are aseptically col-
lected from lesions present in acutely affected, unmedicated pigs.
Serological enzyme-linked immunosorbent assays are not widely
available and are currently under development or investigation to
better interpret their results.
There are many other causes of polyserositis and arthritis that can
present with similar clinical signs and gross lesions, including Strep-
tococcus suis, Haemophilus parasuis, Actinobacillus suis, and Erysip-
elothrix rhusiopathiae. Other potential contributors to lameness
or joint lesions include non-infectious causes and risk factors such
as trauma, commingling, nutritional diseases, and environmental
(flooring and housing) and management factors. Osteochondrosis
can be a differential for M hyosynoviae in older pigs.
Control
The widespread commensal occurrence of both of these patho-
gens, along with the current limited knowledge on strain variabil-
ity, strain virulence, and epidemiology, makes them difficult to
prevent or control. Current efforts in prevention are focused on
the use of vaccines. The effectiveness of autogenous vaccines has
not been documented.
Treatment of outbreaks of arthritis with antimicrobials is often
practiced. Early detection of lameness and rapid implementation
of specific antimicrobial therapy, often by injection of acutely
affected pigs, is critical for successful treatment.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Mycoplasmal pneumonia
Alternate names and abbreviations
Enzootic pneumonia (EP), mycoplasmal pneumonia of swine
(MPS), Mycoplasma hyopneumoniae (MHP)
Definition
A widespread, chronic respiratory disease of swine characterized
by coughing, growth retardation, and reduced feed efficiency.
Occurrence
Mycoplasmal pneumonia of swine is a common, widely dis-
tributed disease that occurs throughout the year. It is restricted
to swine and occurs in all major swine-raising countries except
possibly Switzerland, where a national eradication program
appears to have been mostly successful. Chronic MPS is often
more apparent on farms where there is continuous-flow produc-
tion and management, and where husbandry and environmental
conditions are poor. The disease may cause acute and severe
disease in immunologically naïve pigs in age-segregated systems.
It may affect pigs early after weaning, when passive immunity has
waned, but more commonly occurs in grow-finish pigs from 3 to
6 months of age. Mycoplasmal pneumonia often interacts with or
contributes to other respiratory diseases and is considered to have
a central role in porcine respiratory disease complex (PRDC).
Secondary bacterial infections are common.
Historical information
Chronic pneumonia in swine, part of which was probably myco-
plasmal pneumonia, has been recognized for at least a century.
Mycoplasmal pneumonia was once believed to be caused by a
virus and was misnamed viral pig pneumonia. However, clear
distinction of mycoplasmal pneumonia from influenza A and
recognition of it as a specific disease began in 1948. Mycoplasmal
pneumonia was first reproduced experimentally in the US and
England in 1965. Subsequently, it was reported in most major
swine-raising countries. Mycoplasmal pneumonia is recognized as
a very costly, widespread disease of swine due to its negative effects
on growth rate and feed efficiency, its very high prevalence in
infected herds, and its role in PRDC.
Etiology
Mycoplasma hyopneumoniae, the etiologic agent of mycoplasmal
pneumonia, is difficult to isolate and grows slowly in the labo-
ratory. It is a small, filterable bacteria, survives only a short time
in swine housing environments, and can be destroyed by most
disinfectants. Mycoplasma hyopneumoniae is frequently found in
association with other respiratory pathogens, including bacteria
and viruses, the resulting combination of which is often termed
PRDC. In pigs with pneumonia, it may be difficult to determine
which agent is the primary pathogen. Evidence suggests that
M hyopneumoniae increases the severity of several other infec-
tions, including porcine reproductive and respiratory syndrome
BACTERIA
virus (PRRSV), influenza, porcine circovirus type 2, Actinoba-
cillus pleuropneumoniae, and Pasteurella multocida. Mycoplasma
hyopneumoniae is quite capable of acting as a significant primary
pathogen on its own.
Three other pathogenic mycoplasmas are recognized in swine.
Mycoplasma hyosynoviae is a sporadic cause of epidemic synovitis
in growing swine. Mycoplasma hyorhinis infection is common in
swine and can cause fibrinous polyserositis in young pigs. Both of
these agents are of increasing concern in modern commercial pro-
duction systems. Mycoplasma suis (previously known as Eperyth-
rozoon suis) infects red blood cells and can cause anemia in pigs.
Epidemiology
Carrier swine are the most common source of infection. Since
M hyopneumoniae does not survive for long in the environment,
carriers are essential for its maintenance in populations. The
organism persists for 7 to 8 months in the lungs of infected, often
asymptomatic pigs, including young breeding stock. There is no
evidence to implicate infection or carriage in other species. Pigs are
infected by M hyopneumoniae transmitted from dams, cohorts, or
exposure to other, usually older, pigs. The organism can be detected
in nasal secretions, so transmission by nose-to-nose contact and
coughing are likely. The organisms also appear to be transmitted by
aerosol; empirical evidence suggests that aerosol spread can occur
over several miles. A mycoplasma-free herd status can be difficult to
maintain in areas with high pig density.
Pathogenesis
Mycoplasma hyopneumoniae can be observed microscopically on
the ciliary epithelium of trachea, bronchi, and bronchioles. The
distribution of pulmonary lesions suggests bronchogenic distri-
bution with settling of exudate cranioventrally because of the
compromised mucociliary apparatus. Virulence factors derived
from M hyopneumoniae outer membrane proteins damage several
respiratory defense mechanisms and facilitate infection. The cell
membrane presents a mosaic of epitopes that camouflage pro-
tective antigens, rendering the immune response inefficient. The
immune response by macrophages and neutrophils also appears
to be compromised. Poor air quality (dust or noxious gases) can
irritate airways and increase susceptibility.
The initial lesions are bronchitis and bronchiolitis. There is
hyperplasia of the mucus-secreting cells in the mucosa and a loss
of cilia from many epithelial cells of airways. The inflammatory
reaction spreads into surrounding alveoli causing alveolar exu-
dates, pneumonia, airway obstruction, and atelectasis. Over time,
there is a marked hyperplasia of lymphoid tissue around airways
and adjacent blood vessels, often described as lymphocytic
peribronchiolitis or hyperplasia of bronchiolar-associated lym-
phoid tissue. Increased mucus in airways, ciliostasis, and pressure
of surrounding lymphoid tissue interfere with the lung clearance
MYCOPLASMAL PNEUMONIA 41
 SWINE DISEASE MANUAL
BACTERIA
of mucus and exudate. Secondary bacterial infections, most
notably with Pasteurella multocida but also others, contribute
substantially and are the usual cause of severe bronchopneumonia
and deaths.
Clinical signs
The principal clinical sign is chronic, persistent, non-productive
cough. In naïve animals, onset often occurs about 2 to 3 weeks
after exposure and is usually gradual in a herd. Coughing may
persist for weeks to months. Excessive dust, irritating gases, or
concurrent infections result in more severe coughing and pneu-
monia. As pneumonia develops in some pigs, dyspnea becomes
more marked. Growth is retarded, and feed efficiency decreases
in the face of near-normal appetites. Morbidity is high. Mortality
is low, except when the disease is complicated by other viral and
aggressive bacterial infections or when proper treatment and
interventions are not instituted.
Lesions
In affected pigs, pneumonic lesions are generally well-demarcated
and cranioventral in distribution. Gross lesions are not pathogno-
monic and usually involve apical, intermediate, and cardiac lobes
but may extend into diaphragmatic lobes in severe cases. Chronic
lesions are usually reduced in volume (atelectasis) and dark gray
in color. More recent lesions tend to be reddish brown or a lighter
gray, with edema, mucus, and inflammatory cells apparent in
the airways. Raised areas adjacent to pneumonic areas are often
emphysematous and lighter pink than normal lung. On the cut
surface of pneumonic areas, mucopurulent exudate can often be
squeezed from airways. Secondary infection with other respira-
tory pathogens is common and may modify the appearance of
mycoplasma-initiated lesions.
Typical microscopic lesions, although not pathognomonic, reveal
lymphohistiocytic peribronchiolar cuffing, mucocellular exu-
dates, and atelectasis.
Neither gross nor microscopic lesions are pathognomonic
for M hyopneumoniae. Cranioventral, bronchogenic, clearly
demarcated consolidation of lungs is a characteristic of the bron-
chopneumonia that is produced by M hyopneumoniae and can
be present even when the pneumonia is complicated by other
bacterial and viral agents.
Diagnosis
History, clinical signs, and gross and microscopic lesions are
suggestive of M hyopneumoniae, but laboratory assistance is
necessary to confirm a role for M hyopneumoniae in a given pig.
Isolation is slow, laborious, difficult, and generally not routinely
available. Detection of M hyopneumoniae in lung samples taken
at necropsy is usually done by polymerase chain reaction (PCR),
in situ hybridization (ISH), immunohistochemistry (IHC), or
fluorescent antibody (FA) techniques (listed in decreasing order
of sensitivity). Since many pigs may carry M hyopneumoniae
asymptomatically in lung tissue, PCR may detect the presence
42 MYCOPLASMAL PNEUMONIA
of the organism but PCR alone probably should not be used to
confirm a role for M hyopneumoniae in disease causation. Histo-
pathology, ISH, IHC, and FA are preferred methods to confirm
a role for M hyopneumoniae in the pneumonia process. Moreover,
histopathology can help rule out other contributors.
Serological tests including complement fixation and enzyme-
linked immunosorbent assay can be useful on a herd basis, but
interpretation must be made with care and knowledge of the
herd, the particular age and individuals sampled, and their vac-
cination status. Antibody tests on individual animals have little
value because many pigs without active disease have antibodies
to M hyopneumoniae or other cross-reacting Mycoplasma species
(especially M flocculare). Antibody levels develop slowly in many
infected animals. In vaccinated animals, the detection of antibod-
ies in serum can be quite variable (ranging from 30% to 100%) as
can the duration of antibody detection (1 to 3 months), depend-
ing on the vaccine used and the assay used for detection.
PCR technology can be used to determine herd status in some
situations. Sample types, in decreasing order of sensitivity, include
tracheobronchial swabs and lavages, lung tissue, laryngeal swabs,
tonsil swabs, nasal swabs, and oral fluids. The sensitivity of the
different sample types is quite variable. For example, oral fluids
have low sensitivity for detection of carriers but can detect
M hyopneumoniae quite efficiently in pigs with clinical disease.
Detection of the organism by PCR confirms the presence of the
organism but does not confirm its role in disease.
The value of slaughter checks to evaluate the impact of mycoplas-
mal pneumonia is questionable, since gross lesions may be healed
by the time pigs reach market weight and lesions from other bac-
terial and viral agents may mimic those of M hyopneumoniae.
Control
Many methods of control for mycoplasmal pneumonia are in use,
and many herds supplying genetic stock are maintained negative
for M hyopneumoniae. Such herds obviously must have scrupu-
lous isolation, acclimatization, testing, and biosecurity protocols
in place to assure the organism is not reintroduced.
Most M hyopneumoniae-negative herds have been created as a
result of depopulation and repopulation with negative breeding
stock. In some cases, herds have become negative through one or
more management techniques, including strict medicated or seg-
regated early weaning, other minimal disease programs, or closing
the breeding herd to introductions of new animals for at least
6 to 7 months.
Historically, specific pathogen free herds were established with
pigs delivered via hysterectomy or cesarean section and raised in
isolation on colostrum-free diets. Those animals were then used
to repopulate previously depopulated farms.
Maintaining commercial herds free of M hyopneumoniae infec-
tion when located in swine-dense regions has not been successful
long term. A strategy referred to as “Swiss depopulation” is based
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES

BACTERIA
on the hypothesis that most adult swine raised on an endemically for minimizing the impact of the disease. Despite reports of many
infected farm are exposed to M hyopneumoniae early in life with methods to eliminate or control M hyopneumoniae, it remains
subsequent recovery (and presumably robust immunity with a significant economic problem, particularly when PRRSV or
limited carrier status) by 10 months of age. Swiss depopulation influenza A virus is also endemically present in the herd.
involves implementation of a period of intensive vaccination of
Vaccines are generally thought to be efficacious in mitigating
all breeding animals on a farm followed by removal of all animals
losses due to M hyopneumoniae by reducing the prevalence and
less than 10 months of age. This is coupled with cessation of
severity of lung lesions and improving growth performance.
farrowing for at least 3 weeks while applying aggressive antimi-
However, vaccines do not prevent colonization or transmission
crobial therapy to eliminate any remaining M hyopneumoniae
of M hyopneumoniae from sow to piglet or between pigs. In most
that may be residing in carrier animals. Removal of all susceptible
herds, maternal antibodies do not seem to interfere with piglet
swine combined with vaccination and/or medication programs
vaccination, meaning that piglets on most farms can be success-
generally results in a significant decrease in the disease for up
fully vaccinated at or before weaning, with a booster dose given
to 2 years, with true eradication of the organism from the farm
around 3 weeks later.
reported in some instances. Modifications to these procedures
continue. Antibiotics may augment management and vaccination programs
but should not be considered as a cost-effective, long-term con-
Other measures to aid in control, but not elimination, of M hyo-
trol strategy. Antimicrobials can be strategically administered in
pneumoniae include early weaning or various forms of medicated
the feed or water, or by injection. Many antibiotics and chemo-
early weaning. Early weaning (7 to 10 days of age) may prevent
therapeutic agents have been used in feed or water for prevention
transmission of M hyopneumoniae (and other organisms) from
or treatment of mycoplasmal pneumonia, often with inconsistent
dams to piglets before they are weaned and moved to a separate,
results. The efficacy of antimicrobials in controlling M hyopneu-
clean nursery or grow-finish facility. Age-segregated rearing and
moniae losses may be related either to anti-mycoplasmal activity
the use of all-in, all-out systems of management with cleaning and
or by suppression of other bacterial infections.
disinfection of facilities between batches of pigs is widely used
and believed to be one of the more practical and useful measures

MYCOPLASMAL PNEUMONIA 43
 SWINE DISEASE MANUAL
BACTERIA
Pneumonic pasteurellosis
Alternate names and abbreviations
Pasteurellosis; also see chapter on Atrophic rhinitis
Definition
Pneumonic pasteurellosis is usually secondary to other infectious
diseases or environmental factors that impair pulmonary func-
tion. Both primary and secondary forms of disease occur.
Occurrence
Pneumonic pasteurellosis occurs throughout the world. Second-
ary pasteurellosis is seen in association with several other diseases,
especially mycoplasmal pneumonia, Actinobacillus pleuropneu-
moniae, and viral lung infections, or it can accompany or follow
environmental or other stresses. Pasteurellosis occurs in many
other species of domestic and wild animals. Primary pasteurellosis
occurs occasionally as a septicemic disease in piglets, but this
rarely occurs in older or adult swine. Secondary pasteurellosis
occurs very frequently as a contributor to bronchopneumonia.
Historical information
Louis Pasteur experimented with a disease of poultry (fowl chol-
era) caused by a bacterium now known as Pasteurella multocida.
Subsequent research implicated P multocida as both a primary
and secondary pathogen in many species, including swine.
Etiology
Pasteurella multocida is a Gram-negative coccobacillus easily
grown in the laboratory. There are both toxigenic and non-toxi-
genic strains. The organism is a common inhabitant of the
pig’s nasal passages and can be isolated from most swine herds.
There are 5 capsular serotypes (A, B, D, E, and F) and at least 16
somatic serotypes. In the US, pasteurellosis of swine is caused by
serotypes A and D.
Epidemiology
Ubiquitous in swine, P multocida is probably introduced into
most herds by carrier swine, with subsequent vertical and lateral
transmission to other pigs. Transmission from dam to offspring
occurs early in lactation, and lateral transmission is via nose-to-
nose contact. Although many other species harbor P multocida,
there is little evidence of interspecies transfer of pathogenic P
multocida to swine.
Pathogenesis
Healthy pigs are highly resistant to development of pasteurellosis
when experimentally inoculated with only P multocida. Many
normal swine carry P multocida in their nasopharynx. Chronic,
progressive pneumonia occurs when pulmonary immune func-
tion has been comprised, allowing the organism to colonize
deeper portions of the lung.
44 PNEUMONIC PASTEURELLOSIS
Pathogenic strains damage endothelium and microvasculature
in the lung. This leads to the formation of fibrinous thrombi in
alveolar capillaries and fibrinous alveolitis accompanied by sup-
puration. The lesion may slowly organize into fibrous connective
tissue or form abscesses as a consequence of infarction or necrosis
from toxin associated with the bacteria and inflammation; only
occasionally does fibrinous pleuritis or pericarditis occur. When
present, fibrinous pleuritis, serositis, and/or fibrous adhesions are
much more likely due to prior effects of Actinobacillus or Strep-
tococcus infections than as a direct result of P multocida. In acute
cases, septicemia can occur as a result of the infection; deaths are
believed to be caused by endotoxic shock and respiratory failure.
Clinical signs
Signs vary in severity and are similar to those seen with other
types of bronchopneumonia: coughing, dyspnea, fever, and pros-
tration. Chronic cases tend to have less fever, a persistent cough,
and a more marked dyspnea. Swine with well-developed pneumo-
nia or extensive adhesions between the lungs and rib cage often
have a marked expiratory diaphragmatic lift or “thump.”
Lesions
Lesions are those of bronchopneumonia, with firmly consol-
idated areas affecting the cranioventral lobes of the lungs and
often extending to adjacent parts of the diaphragmatic lobes.
Pneumonic areas are remarkable for their firmness and density.
The pleura over the lesions may be granular; scant fibrin may be
visible on the surface. Regional lymph nodes are usually enlarged.
Microscopic lesions include suppurative bronchopneumonia
with fibrin and neutrophils, with bacteria sometimes noticeable
in affected alveoli and airways. Other reported but rare lesions
include acute necrotizing pharyngitis, fibrinous polyarthritis
without joint swelling, meningitis, and/or meningoencephalitis.
Diagnosis
History, signs, and remarkable pulmonary lesions may be sugges-
tive of pasteurellosis, but culture of lung lesions from a non-med-
icated pig is required for confirmation. Histopathology can con-
firm typical microscopic lesions and can implicate or rule out roles
for common primary pathogens. Pasteurellosis is often secondary
to one or more of a host of primary infectious lung diseases. Since
the agent is common, easily isolated, contributes to lesion severity,
and persists in lesions, P multocida is frequently isolated from
lungs at the same time as other primary agents of pneumonia
(Mycoplasma hyopneumoniae, Actinobacillus, influenza A, and
porcine reproductive and respiratory syndrome virus [PRRSV]).
Serology and isolation of P multocida from nasal swabs are of little
diagnostic value. Non-pathogenic commensals are common and,
in contrast to the use of polymerase chain reaction for toxins asso-
ciated with progressive atrophic rhinitis, tests are not available to
be able to predict P multocida pathogenicity in lung.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Environmental factors such as dusty or overcrowded conditions,
excessive ammonia gas, or poor ventilation may be important
predisposing factors for pasteurellosis. Only when all other pos-
sible causes have been eliminated should there be a diagnosis of
primary pasteurellosis. Nevertheless, P multocida can cause severe
disease and is an important component of respiratory disease
when present with typical lesions.
Control
Individual acutely affected pigs require immediate antimicrobial
intervention, usually by injection. Basic therapeutic caveats of
early diagnosis, appropriate choice of antimicrobial, and appro-
priate dose with sufficient duration of therapy are particularly
important for success. Many different antibiotics are available for
injection or water medication at therapeutic levels. Mass medi-
cation may be warranted while identifying and controlling the
primary initiators of the pasteurellosis.
BACTERIA
Control methods include all of the biosecurity measures that might
prevent introduction of a new strain of P multocida into a herd.
Herd additions should be quarantined for at least a few weeks
before entry into a herd. Management practices including use of
all-in, all-out production with age segregation that minimizes
commingling will reduce the likelihood of pasteurellosis occurring.
Mixing and sorting of pigs should be minimized. Importantly,
implementing control of other respiratory pathogens (eg, M
hyopneumoniae, influenza A, PRRSV, Actinobacillus pleuropneumo-
niae) is critical to prevent outbreaks of pasteurellosis. Identification
and elimination of other diseases, environmental or air quality
concerns, and other stress factors that might lower resistance are
also critical components of a control program.
Bacterins for P multocida are available, but their efficacy in
preventing or minimizing the severity of respiratory disease is
questionable.
PNEUMONIC PASTEURELLOSIS 45
 SWINE DISEASE MANUAL
BACTERIA
Salmonellosis
Alternate names and abbreviations
None
Definition
Salmonellosis is the disease caused by infection with any of more
than 2000 Salmonella serotypes. In swine, only a few serotypes
are primary causes of disease. Disease may be manifested as
enterocolitis or septicemia with localization of infection at
various tissue sites. Asymptomatic Salmonella infections are
common. Swine may serve as a source of Salmonella infection to
humans via contamination of pork products.
Occurrence
Infection of swine and most vertebrates with a broad range of
Salmonella serotypes is common and occurs worldwide. Clinical
disease is much less common than infection and occurs through-
out the year in all major swine-raising countries. All age groups
are susceptible, but the disease usually occurs in newly weaned
or grow-finish pigs. Many other species, including humans, are
susceptible to salmonellosis caused by some of the Salmonella
serotypes that infect swine. Contaminated pork products are not
a primary source of food-borne salmonellosis outbreaks in peo-
ple, but efforts to reduce Salmonella in the pork food chain are a
high priority for the swine industry.
Historical information
In 1884, the organism now known as Salmonella enterica ser
Choleraesuis was isolated and erroneously reported to cause clas-
sical swine fever. After the viral etiology for classical swine fever
was identified, salmonellae were considered only as secondary
pathogens. However, some Salmonella serotypes frequently act
as primary pathogens causing septicemia and/or enterocolitis in
swine. Species-adapted Salmonella serotypes are relatively infre-
quent but cause severe typhoid or typhoid-like disease in host
species. Most serotypes, including Salmonella ser Typhimurium
and its serological variants (eg, S. 1,4,[5],12:i:-), are capable of
infecting a broad range of vertebrates.
Outbreaks of salmonellosis in people are often food-borne from
products of animal origin, including pork. Both animal and
human health could be improved if Salmonella could be effec-
tively controlled across animal production and food processing
systems. Salmonella reduction programs at farm level constitute
a logical step in minimizing the occurrence of outbreaks in
humans. Swine industry-led national Salmonella control pro-
grams in North America and Europe are an effort to understand
what management strategies are most likely to minimize the
impact of the organism on both human and animal health.
46 SALMONELLOSIS
Etiology
Salmonellae are small, hardy, ubiquitous, Gram-negative bacilli
which contain endotoxin and are capable of elaborating a variety
of other toxins. Isolation and propagation on a variety of culture
media have been well-described.
Two species of Salmonella are recognized: S enterica and Salmo-
nella bongori. Salmonella enterica is the type species and is further
divided into 6 subspecies that include over 2600 serotypes which
are serologically clustered into serogroups (Table). Further iden-
tification to serotype usually has to be done by reference laborato-
ries though some large veterinary laboratories are equipped to do
serotyping for a limited number of strains.
Primary pathogenic serotypes for swine are relatively few, with
most outbreaks caused by S Typhimurium, S Choleraesuis, or
Salmonella ser Heidelberg. The serotypes that most commonly
cause disease in both people and swine include serotypes S Typh-
imurium and its serologic variants (eg, S 1,4,[5],12:i:-), S Heidel-
berg, Salmonella ser Agona, and Salmonella ser Infantis. Salmo-
nella Choleraesuis and Salmonella ser Typhisuis are host-adapted
to swine and are rarely isolated from sources other than swine.
Salmonellae readily survive in many swine environments but can
be inactivated by chlorine, iodine and phenol-based disinfectants.
Epidemiology
Host-adapted S Choleraesuis is the cause of swine paratyphoid, a
severe systemic disease of pigs; this was the major manifestation
of the disease caused by Salmonella throughout the 20th century.
Since the 1990’s, cases of paratyphoid have decreased precipi-
tously in modern swine industries as a result of elimination of
the serotype from breeding herds, better hygiene, adoption of
multisite, age-segregated production systems, improved biose-
curity, and some use of effective vaccines. However, salmonel-
losis has not gone away in modern industries but has instead
been replaced by S Typhimurium and its serological variants
(eg, S 1,4,[5],12:i:-); the reasons for this are unknown.
Salmonellae are commonly found in intestinal tracts of most
warm and cold-blooded vertebrates. Fecal contamination of
premises, feed, or fomites from any species is a possible source of
Salmonella introduction to a herd. However, it appears that most
introductions of the disease are a result of the introduction of
asymptomatic carrier pigs. Clinically normal pigs are inapparent
carriers of a variety of serotypes of Salmonella infections which
persist in their tonsils, intestine, lymph nodes, or gall bladder.
Individual carrier pigs may regularly or occasionally shed Sal-
monella in their feces and are a major source of exposure to sus-
ceptible cohorts. A variety of stressors can exacerbate shedding,
including weaning, abrupt feed changes, transportation, com-
mingling, and environmental stresses all of which may precipitate
outbreaks of salmonellosis. Once introduced, salmonellae are
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES

BACTERIA
Table: Common serotypes of Salmonella enterica within serogroups B, C1, C2, D and E isolated from US pigs.

Group B Group C1 Group C2 Group D Group E

Abortus-equi Choleraesuis Hadar Dublin Anatum
Agona Infantis Kentucky Enteritidis Meleagridis
Brandenburg Lille Litchfield Miami Muenster
Bredeney Mbandaka Manhattan Riefild New Brunswick
California Montevideo Muechen Orien
Derby Tennessee
Heidelberg Newport
Saint Paul
Schwarzengrund
Typhimurium
Thompson
Senftenberg
Uganda

spread by the fecal-oral route, in contaminated feed and water,
and sometimes by short distance aerosol. Exposed pigs may
either develop clinical signs of salmonellosis or be colonized and
remain healthy. Although individual pigs may eventually clear the
infection, any pig exposed to Salmonella should subsequently be
considered as a possible carrier of the organism.
Salmonella-contaminated buildings and pens can remain infectious
for weeks if not thoroughly cleaned and disinfected. Although feed
is a common source of many serotypes of Salmonella, a notable
exception is S Choleraesuis, which has not been reported in feed.
Most serotypes are capable of infecting a broad range of hosts, so
livestock, poultry, wild birds and mice (as well as feces-contaminated
feedstuffs) are believed to be important disseminators of Salmonella.
Salmonellosis often appears during or following stressful events
(eg, prolonged transport, drought, overcrowding, change of
rations, parturition, prolonged treatment with drugs or antibi-
otics) or secondary to an outbreak of another disease in a herd.
Stressful events can lower immune resistance and/or increase the
magnitude of Salmonella shedding and therefore precipitate out-
breaks. A balance of virulence, dose, and resistance exists between
swine and the Salmonella they carry.
Salmonella contamination of pork products as a source of food-
borne salmonellosis in humans is a global concern. Market pigs
exposed to new serotypes of Salmonella can be rapidly colonized,
with high numbers of organisms detected in intestinal contents
and regional lymph nodes within hours of exposure occurring
during the transport or lairage processes. The marketing chain
provides many potential sources of Salmonella contamination,
including transportation and feed withdrawal stresses that
increase shedding by inapparent carriers, contamination at swine
concentration points and in transportation vehicles, and com-
mingling of pigs in holding pens at an abattoir. Efforts to decrease
the prevalence of inapparent carriers and prevent exposures from
occurring during the marketing chain are major areas of focus in
food-borne Salmonella reduction programs.
Pathogenesis
Salmonella vary considerably in virulence, depending on which
of more than 200 known genetically or plasmid-determined vir-
ulence cassettes and pathogenicity genetic elements they possess.
In enteric salmonellosis, mucosal damage and necrosis are the
result of mucosal ischemia caused by vasculitis and microvascular
thrombosis. Vasculitis is present in all forms of salmonellosis.
Diarrhea is attributed to tissue fluids leaking from damaged
mucosa and compromise of mucosal absorption. An enterotoxin
similar to that produced by enterotoxigenic E coli (causing cyclic
AMP-mediated hypersecretion of fluids and salts from entero-
cytes) has been described for S Heidelberg.
Transient bacteremia can occur with a variety of serovars but the
host-adapted S Choleraesuis is an exceptional example that causes
septicemia. Following ingestion or inhalation of this serotype,
S Choleraesuis invades the tonsil and/or intestinal mucosa and
spreads to regional lymph nodes. Other Salmonella serotypes usu-
ally remain confined to the intestine and occasionally the adjacent
lymph nodes, producing only a transient septicemia. Host-adapted
S Choleraesuis organisms, however, are phagocytized, survive
within macrophages and neutrophils, and then are transported
to other sites (eg, lungs, liver, meninges, joints, and lymph nodes)
where they localize and cause further severe tissue damage.
SALMONELLOSIS 47
 SWINE DISEASE MANUAL
BACTERIA
Clinical signs
Salmonellosis presenting as diarrhea with enterocolitis is
usually caused by S Typhimurium and its serological variants
(eg, S 1,4,[5],12:i:-) and less often by S Heidelberg or other sero-
types. Enteric salmonellosis mostly occurs in pigs from weaning
to about 5months of age. Initial signs include moderate anorexia
and diarrhea that may be watery, yellow, and intermittent. Ini-
tially, animals are moderately febrile, but temperatures usually
decrease as diarrhea continues. As the disease progresses, there
may be mucus, fibrin, and blood in the feces, although blood is
not a prominent feature of enteric salmonellosis. Over time, mor-
bidity is high and mortality is moderate. Surviving animals often
become emaciated or gain weight slowly.
Historically, septicemic salmonellosis is caused by host-adapted
S Choleraesuis. It is most commonly seen in pigs from weaning to
about 180 pounds, although the disease can occur in all ages. Lac-
togenic immunity is usually protective. The onset of an outbreak
may be signaled by finding a pig dead within a group of appar-
ently thrifty pigs. Within a few days, the disease spreads to other
pigs in the group. Morbidity is usually low to moderate, but mor-
tality is high among those that become ill. Clinical signs include
inappetence, depression, huddling, weakness, temperatures up to
107°F (42°C), and red to purple discoloration of the skin of the
extremities (cyanosis). Diarrhea is not present initially but fre-
quently occurs after a few days of illness. The length of course is
variable, both in individual animals and in the herd. Localization
of S Choleraesuis in the lungs, brain, meninges, lymph nodes,
or - less commonly - joints can lead to mild pneumonia with dys-
pnea, lameness with reluctance to move, or vague central nervous
system signs.
Lesions
With enteric salmonellosis, the large intestine and the lower small
intestine are heavy, edematous, and the wall is thickened. There
may be excess peritoneal fluid and strands of fibrin on the serosa.
The ileocolic and mesenteric lymph nodes are usually markedly
enlarged, congested, and edematous. There are usually focal, mul-
tifocal, or diffuse areas of mucosal necrosis with fibrinonecrotic
exudates in colon, cecum, and/or small intestine. In chronic
cases there may be raised, circular lesions in the colon referred to
as button ulcers. Dry gangrene may occur on the ears or tail of
survivors.
With septicemic salmonellosis, gross lesions include red to
purplish discoloration of the extremities, marked enlargement
of the spleen, moderate swelling of the liver (perhaps with slight
icterus), severe pulmonary congestion and edema, and swollen
and edematous lymph nodes. Frequently there will be petechial
hemorrhages in skin, larynx, lungs, heart, bladder, and kidneys.
The liver may or may not contain small, white to yellow foci of
necrosis (paratyphoid nodules). Less frequently observed is syno-
vitis in joints or fibrinopurulent meningitis. Intestinal lesions vary
in severity, largely related to duration of illness. At onset there
48 SALMONELLOSIS
may be only congestion with superficial fibrinous inflammation
in cecum, colon, or ileum. In long-standing cases, the intestinal
lesions resemble those of the enterocolitic form of salmonellosis.
Diagnosis
History, clinical signs, and typical gross lesions may be adequate
for a presumptive diagnosis. Diagnosis should be confirmed by
laboratory culture and identification of Salmonella, especially
if the disease is new on the premises. Sero-grouping is readily
available and can aid in determining potential serotypes involved
(Table 1). Serotyping is available in some reference laboratories
and is sometimes useful in understanding the epidemiology of an
outbreak.
There are several serological assays for investigating or diagnosing
outbreaks of Salmonella. Most are based on enzyme-linked
immunosorbent assay and typically exploit known differences in
the lipopolysaccharides or other surface antigens to detect the
different serotypes. These assays are used on a herd basis only as
they lack sensitivity and specificity for individual animal use.
Necropsy and sampling of typical, untreated, acutely affected pigs
for bacteriologic culture and histopathologic study is usually war-
ranted. Microscopic examination of tissues will help identify typ-
ical lesions and differentiate them from those of other enteric and
septicemic diseases that are commonly present and may be pri-
mary risk factors for salmonellosis expression. Common agents of
post-weaning diarrhea, notably coronaviruses, rotaviruses, E coli,
dysbacteriosis, or dietary hypersensitivities often have secondary
or concurrent infections with Salmonella. Other differentials
include ileitis, whipworms, and swine dysentery, the latter two of
which are restricted to the large intestine. Host-adapted S Chol-
eraesuis causes rather unique paratyphoid nodules in the liver.
Septicemic salmonellosis must be differentiated carefully from
classical swine fever, erysipelas, and other septicemias, as well as
other causes of interstitial pneumonia.
Control
Although prevention is preferred, outbreaks of clinical salmonel-
losis do occur and proper treatment with appropriate antimicro-
bials is warranted. The objective is to decrease mortality, reduce
the duration and severity of production losses, and to decrease
shedding in order to minimize transmission of the organism to
other pigs or cohort groups.
Numerous antibiotics and chemotherapeutic agents have been
used for prevention and/or treatment. Visibly sick pigs may be
injected with an appropriate, approved, systemic antibiotic, par-
ticularly if there is clinical evidence of septicemia. This treatment
is usually augmented by concurrent mass medication through
water, usually with an aminoglycoside. There is no evidence that
treating infected pigs with antimicrobials increases the likelihood
of inducing a Salmonella carrier status as has been suggested in
humans. Prophylactic use of antimicrobials in the feed is widely
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
practiced but not preferred because of eventual antimicrobial
resistance.
Prevention relies on sound management that is properly and
consistently executed. Breeding stock should be acquired only
from suppliers with no history of salmonellosis. If feasible, all
breeding stock should be from a single source. Essential addi-
tions to the herd should be made only after a quarantine period
of 30 to 60 days.
Ideally, only pigs from a single source and of similar age should be
raised together in a closed, all-in, all-out system. Buildings should
be cleaned and disinfected carefully between batches. All possible
carriers, including rodents, birds, pets, and wildlife should be
eliminated or excluded from contact with pigs. Unusual stresses
should be avoided insofar as possible. Perhaps the most import-
ant approach to control of salmonellosis involves provision of
comfortable, dry housing, maintaining proper stocking density,
managing the ventilation system, and implementing a high stan-
BACTERIA
dard of sanitation. Early weaning followed by removal of piglets
to a separate, clean site has been successful in minimizing trans-
mission of S Choleraesuis from breeding populations to their
offspring.
There are several efficacious avirulent live vaccines for control of
S Choleraesuis and S Typhimurium. Killed Salmonella bacterins
and mutant-derived endotoxin vaccines are available but thought
to be less effective. All vaccination programs should be coupled
with proper sanitation, husbandry, and pig flow.
Successful reduction of Salmonella infections in swine herds has
been reported in Europe and the US. The programs are based
largely on serological testing of breeding stock, culture of sam-
ples taken at slaughter, establishment of measures that reduce
contamination of carcasses at slaughter, and controlling risks that
are likely to result in the introduction of Salmonella through
feed or drinking water. The hazard analysis critical control point
(HACCP) programs instituted by US abattoirs have adopted
many of these measures. 
SALMONELLOSIS 49
 SWINE DISEASE MANUAL
BACTERIA
Streptococcus suis
Alternate names and abbreviations
Strep, Strep encephalitis
Definition
The predominant streptococcal disease of swine is caused by
Streptococcus suis. Streptococcus suis is the most important strepto-
coccal infection of pigs and is usually seen in nursing or recently
weaned piglets. The disease is usually characterized by septicemia
with tissue localizations, which can present as acute meningitis,
polyarthritis, polyserositis, or bronchopneumonia.
Other less common, largely sporadic, streptococcal infections
also occur in pigs. Sporadic infections are occasionally caused by
Streptococcus dysgalactiae subspecies equisimilis. This beta-hemo-
lytic Streptococcus and a few others are endemic opportunists that
sometimes cause arthritis, septicemia, or meningitis in young pigs,
complicate other disease processes, and may contribute to cases of
vegetative valvular endocarditis in older grow-finish pigs. These
organisms are indigenous on the skin (including the vagina), and
it has been shown that most piglets become infected at the time
of birth. Cases in young pigs are a result of navel infection, breaks
in the integument due to knee abrasions, or infection of skin
wounds, including those caused by tail docking, ear notching, or
clipping of needle teeth.
Streptococcus porcinus is the same as Lancefield group E Strepto-
coccus and is associated with jowl abscess (feeder boils) in swine.
This disease was once quite prevalent but is now rare, presumably
because of improvements in husbandry and feeder design. It is
occasionally isolated from pigs with septicemia or abscesses.
Streptococcus durans has been associated with enteritis in suck-
ling pigs. Additional streptococci are sporadic opportunists
isolated from the respiratory tract, mammary glands, localized
skin lesions, subcutaneous abscesses, the reproductive tract of
aborting sows, and sows with fertility problems or agalactia.
Their role in these conditions is not clear but probably driven by
other risk factors.
Occurrence
Although S. suis infection occurs primarily in nursing or
recently weaned pigs, it can affect pigs of all age groups. The
disease is found in all major swine-raising countries. It is rel-
atively common, occurs throughout the year, and is prevalent
in confinement-raised swine. Streptococcus suis infection also
occurs sporadically in several domestic animals (cattle, sheep,
goats, horses, dogs). It is zoonotic and occurs occasionally in
people who work with pigs or handle meats (butchers, farmers,
and veterinarians), causing localized infections, arthritis, septi-
cemia, and sometimes death.
50 STREPTOCOCCUS SUIS
Historical information
Outbreaks of streptococcal infection in swine occurred many
years before the organism S. suis was identified in 1987. Out-
breaks of S suis infection now are reported frequently. Because
S suis colonizes piglets at birth, neither segregated early weaning
nor medicated early weaning programs are able to prevent S suis
transmission to piglets.
There has been much research on S suis. Early research was largely
focused on the study of capsular serotypes and comparison of
signs and lesions produced by different serotypes; identification
of virulence factors has been the focus of more recent research.
Experimental infection models vary widely and likely contribute
to the lack of agreement in findings reported in published studies.
Etiology
Streptococcus suis is Gram-positive, alpha-hemolytic, and easily
grown on blood agar. Identification is based on biochemical
reactions and capsular serotyping. There are about 35 capsular
serotypes. Their prevalence varies in different geographic regions
of the US, with types 2, 3, 4 and 7 predominating in the Midwest.
Type 2 may be most prevalent worldwide and is the most likely to
express virulence. Virulence factors are not well understood, but
capsular polysaccharide and 2 proteins, muramidase released pro-
tein and extracellular factor, are thought to play important roles
in the severity of disease caused by infection with type 2.
Many species of Streptococcus can be isolated from normal swine.
There is no single, consistent predictor of virulence, immunity,
or cross-protection. Environmental or other predisposing fac-
tors may influence pathogenicity. Most Streptococcus are readily
destroyed by common disinfectants such as phenol, quaternary
ammonium, formaldehyde, hypochlorite, chlorhexidine, and 3%
iodine.
Epidemiology
Streptococcus suis survives in dust and feces in the usual swine
environment. It can be isolated from the nasal cavity, palatine
tonsils, and genitalia of many normal pigs. It is present in the
feces and nasal secretions of carriers. Transmission may be
through ingestion, inhalation or nose-to-nose contact. Flies and
rodents may play a role in mechanical spread. Streptococcus suis
can survive on flies for at least 5 days.
Sows infect piglets with the bacterium during the birthing pro-
cess or shortly thereafter. Contaminated secretions, excretions,
and the skin of infected pigs serve to expose other pigs to the
organism. These factors make early weaning programs, with or
without medication, ineffective in preventing transmission to at
least some piglets that may then serve as sources of infection for
the rest of their cohort during lactation and nursery phases.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Wounds also are a common route of entry for S suis. Once a few
piglets are infected, they are able to disseminate the bacteria to
other litters or commingled pigs. Close contact favors spread.
The role of fomites and insects has been demonstrated but their
importance remains uncertain.
Multiple serotypes or genotypes may exist on the same farm.
Control of one particular type of S suis may lead to emergence of
another serotype, frustrating long-term control strategies.
Pathogenesis
Pathogenesis is somewhat speculative and may differ among
serotypes. Management and husbandry stresses may predispose
piglets to outbreaks. Also, preexisting injury to respiratory epi-
thelium, especially rhinitis, may predispose to infection. Known
causes of rhinitis include ammonia fumes, infection with Borde-
tella bronchiseptica and Pasteurella multocida, and inclusion body
rhinitis. Interaction of S suis with viruses (eg, porcine reproduc-
tive and respiratory syndrome [PRRS], pseudorabies, and influ-
enza A) may trigger outbreaks. Overcrowding, poor ventilation,
and high humidity also favor disease expression.
After oral or respiratory exposure, streptococci can be found in
crypts of the palatine tonsils or in nasal mucosa. From there, the
organism can become systemic, spreading through the blood
stream to multiple organ systems. Some organisms may survive
within phagocytes and gain access to the cerebrospinal fluid,
brain, meninges, lungs, and joints where they localize and cause
meningoencephalitis, arthritis, or pneumonia. In pneumonic
lungs, S suis can be either a primary or secondary pathogen.
Clinical signs
Signs and lesions are similar in all S suis infections, regardless of
serotype. Signs usually suggest septicemia and/or localization of
systemic infection. High rectal temperatures (greater than 105°F
[41°C]) are common early in the course of infection. Pigs with
septicemia die after a short, acute course and are sometimes sim-
ply found dead without having ever been observed as sick. Young
piglets with central nervous system lesions are often found in
lateral recumbency and paddling. Older pigs have a wider variety
of central nervous system signs that include ataxia, opisthotonus,
incoordination, tremors, convulsions, blindness, deafness, or
vestibular syndromes. Pigs with polyarthritis have swollen joints
and are lame. In some outbreaks, respiratory signs associated with
pneumonia may occur. Both morbidity and mortality vary widely
and are affected by treatment. Streptococcus suis, much like Pasteu-
rella multocida, is ubiquitous in swine and a frequent secondary
contributor to pneumonia.
Lesions
There is often reddening of the skin and modest enlargement of
lymph nodes. Pigs that die suddenly often have fibrinopurulent
BACTERIA
meningitis microscopically, seen grossly as visible clouding of
the leptomeninges of the brain. In septicemic cases there may be
slight enlargement of the spleen and petechial hemorrhages on
the kidneys or other organs. With polyarthritis there is enlarge-
ment of joints that contain turbid synovial fluid.
Streptococcus suis pneumonia, often secondary, has a broncho-
genic cranioventral distribution pattern of firm consolidation
in lung. Predominance of any one of these lesions varies in
outbreaks. Polyserositis is quite common. Other lesions seen in
chronic cases include endocarditis (usually on the mitral valve),
myocarditis, and fibrinopurulent to fibrous pericarditis.
Diagnosis
A presumptive diagnosis can often be made on the basis of his-
tory, signs, lesions, and the demonstration of Gram-positive cocci
in the lesions. Confirmation should be made through culture
and identification of the Streptococcus. Both pathogenic and
non-pathogenic strains can be recovered from pigs on most farms,
so demonstrating organisms from systemic locations (brain, joint,
fibrinous exudates) with typical gross and microscopic lesions, in
addition to a typical clinical picture, is important in establishing
the correct diagnosis. If convenient, the capsular type should be
determined since that can assist in selecting an appropriate vac-
cine. The predominate capsular type may change over time within
a farm, so periodic typing of S suis organisms recovered from
affected pigs may have value as an epidemiologic tool. Outbreaks
are frequently associated with a variety of infectious and non-in-
fectious risk factors, so a complete diagnostic evaluation of agents
as well as risk factors in the environment is usually warranted.
Control
At present there are no highly effective measures for control of S suis.
Elimination of stresses, particularly overcrowding, poor ventila-
tion, high humidity, and inadequate sanitation, should be part of
the strategy. The all-in, all-out system with emphasis on age seg-
regation, multi-site rearing, and strict sanitation of facilities and
instruments used in processing piglets may be beneficial. The con-
trol of primary diseases (PRRS, influenza A, pseudorabies, Myco-
plasma  hyopneumoniae, etc) that interact with S suis is important.
It may reduce incidence and improve response to treatment.
Affected pigs should be treated individually as early as possible
with injectable antibiotics. Systemically available antibiotics are
sometimes pulsed strategically for a few days in feed or water to
groups experiencing high morbidity. Some strains of S suis are
resistant to many antibiotics (particularly tetracyclines), so sensi-
tivity tests are helpful in selecting a therapeutic agent. Because the
type of S suis may differ in consecutive outbreaks, sensitivity tests
often need to be repeated.
Vaccines and commercial antisera, when available, may be of
value as management tools. The capsular type of the product
being used should be the same as the type causing the disease.
STREPTOCOCCUS SUIS 51
 SWINE DISEASE MANUAL
BACTERIA

Not all vaccines have been effective, however, perhaps because

the product used was not appropriate for the serotype causing
the problem, because of a shift to another predominant serotype
within the herd, or because of a failure to address underlying risk
factors. Proper acclimatization of gilts and perhaps vaccination of
sows prior to farrowing may be helpful for control in suckling pig-
lets but is of less value for control of post-weaning streptococcosis.
Streptococcus suis can be an important zoonotic pathogen, with
spread generally thought to be a result of direct inoculation
through skin wounds. A large outbreak of S suis type 2 infection
in humans was reported from China in 2005 that included a case
fatality rate of approximately 18%.

52 STREPTOCOCCUS SUIS
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Swine brucellosis
Alternate names and abbreviations
None
Definition
An infectious disease of swine characterized by reproductive
impairment or failure, and often by localization of Brucella suis in
bones and joints of breeding stock.
Occurrence
Swine brucellosis occurs primarily in domesticated and feral
swine; wild hares have been proposed as a reservoir of infection
in some countries. The disease occurs in many countries where
domestic or feral swine are present in large numbers.
Swine brucellosis once was common in the US, but due to rig-
orous control measures the disease is now very uncommon. The
porcine type of brucellosis occurs as a serious zoonosis, primarily
among abattoir workers, farmers, and veterinarians.
Historical information
Brucellosis was first identified as a disease of swine in 1914 but
was believed to be a form of bovine brucellosis caused by Brucella
abortus. In 1919, the porcine organism was named as a separate
species (B suis). Swine brucellosis increased in importance as
swine production intensified and because of the severe disease
caused in people. A cooperative, 3-stage, state-federal-industry
eradication program was initiated with a goal of eradication of
brucellosis. This goal is nearly accomplished in domestic herds,
but feral swine remain a reservoir in the US.
Etiology
Under the present classification scheme, B suis is the organism
that causes most brucellosis in swine. There are 5 biotypes of B
suis. Biotypes 1 and 3 cause generalized infections that result in
reproductive failure.
Brucella suis organisms are moderately resistant to environmental
influences. Survival time of organisms in the environment decreases
as temperatures rise. However, the bacteria often survive desicca-
tion and can survive freezing and near-freezing temperatures for
over 2 years. Pasteurization of milk kills B suis. Most commonly
used disinfectants, as well as ultraviolet light, kill the organism.
Epidemiology
Brucella suis is usually transmitted to susceptible swine through
direct contact with infected swine. The route of exposure is
ordinarily through the alimentary or genital tract. Pigs are often
infected by ingesting aborted fetuses, fetal membranes, or fluids
discharged at the time of abortion. The organisms are also trans-
mitted in infectious semen during natural breeding and artificial
insemination. Transmission through abraded skin, conjunctiva,
and nasal mucous membranes is possible.
BACTERIA
Cattle can be infected naturally with B suis. Milk and aborted
fetuses can transmit the organisms to swine. Milk-borne epidem-
ics have occurred in people and swine. Infected feral swine, if in
contact with domestic swine, are another source of exposure.
The bacteremia that occurs during infection of swine often results
in infectious carcasses. Abattoir workers can be infected by
handling infectious carcasses or cuts of meat. Farmers and veteri-
narians may be exposed while assisting sows at farrowing or when
handling infectious placentas or newborn infected piglets.
The prolonged survival of B suis in pastures and farrowing houses
is probably a significant factor in the spread of infection, espe-
cially in colder climates or seasons on farms where management
and sanitation are poor. Swine moved into infectious lots or
buildings can be infected by surviving B suis.
Pathogenesis
Penetration of mucous membranes by B suis results in the coloni-
zation of regional lymph nodes, which is followed by long, con-
tinuous, or intermittent periods of bacteremia. The bacteria then
infect and persist in many other organs, including lymph nodes,
placenta, mammary gland, joint fluids, bone, and the testicles or
accessory genital organs of boars.
A large percentage of swine, especially females, recover after
several months. The recovery rate in boars is low, perhaps never
more than 50%. Enough animals remain infected in a herd to
perpetuate the disease. Surprisingly, most piglets in infected herds
are free of infection at the time of weaning.
Clinical signs
Most owners of B suis-infected herds notice no signs of infection
prior to evidence of infertility in the herd. In dams infected at
breeding, disease is first suspected when numerous sows or gilts
return to heat 30 to 45 days after breeding. Females first exposed
during late gestation have abortions or dead and weak pigs. Early
abortions often go undetected.
Sows and gilts usually recover promptly after aborting, success-
fully re-breed, then deliver live pigs. Infected boars present few
signs of infection, although their fertility may be below normal.
They may or may not show lack of sexual drive.
In growing pigs, lameness may occur due to joint and bone
infection with B suis. In mature boars, orchitis, epididymitis, and
infertility are common.
Lesions
In dams, gross lesions are limited except in chronic cases. At the
time of abortion, there may be some degree of endometritis.
Occasionally, some of the fetal membranes are retained. Infected
placentas may not have grossly visible lesions, or may be con-
gested, edematous, and have small hemorrhages. Infected fetuses
may have subcutaneous edema, especially around the umbilicus,
and there may be effusions in body cavities.
SWINE BRUCELLOSIS 53
 SWINE DISEASE MANUAL
BACTERIA

In intact males, reproductive organs with multiple granulomas
are occasionally accompanied by fibrinopurulent or hemorrhagic
periorchitis, often resulting in enlarged testes that can become
atrophied with time. Calcified foci may also be in the testes and
accessory sex glands.
Chronic infections in growing pigs and breeding stock may man-
ifest as fibrinous or fibrinopurulent arthritis. These lesions often
affect the large joints of the legs. Osteomyelitis may be apparent
within vertebrae, especially the lumbar vertebrae, sometimes with
paralumbar abscesses present.
Microscopic lesions include small granulomas in the liver during
the bacteremic phase of acute infection. Small, focal areas of
inflammation or microabscesses may be found at many sites,
including the bone marrow adjacent to the epiphyses of long
bones. The microscopic lesions are suggestive of brucellosis but
not specific.
Diagnosis
Diagnosis is usually made on the basis of serological testing. The
buffered, acidified plate antigen test and the standard card test
have been used extensively as presumptive tests. For confirmation,
either the standard tube test or the particle concentration fluores-
cence immunoassay is used. Serological testing is very useful as a
herd test but is not infallible on individual animals.
All testing for swine brucellosis has limitations. Swine may be
infected for 6 to 8 weeks before developing antibodies that will
result in a positive test. In uninfected herds, occasional animals that
test positive will later test negative. Infections with several other
genera of bacteria may result in positive brucellosis tests. In particu-
lar, infection of swine with Yersinia enterocolitica has led to positive
tests for brucellosis. The limitations of testing may justify the use of
a slaughter program in the later stages of an eradication effort.
Direct culture is probably the most accurate and sensitive method
of diagnosis of acute cases but is usually less practical than sero-
logical testing. Specimens include lymph nodes from slaughter,
blood, semen, castrated testicles, infected joints, vaginal swabs, or
aborted materials from suspect cases. The bacteriologist should be
alerted if brucellosis is suspected since colonies are slow-growing
and easily missed in routine diagnostic investigations.
Control
Prevention is best accomplished by focusing on implementation
of those measures that are most likely to prevent exposure. No
animals should be added to a herd without having originated
from a negative herd. Those animals should test negative initially,
be quarantined for at least 30 days, then again test negative before
being added to the herd. No effective vaccines are available for
immunization of swine.
Infected herds can be handled in 2 different ways. If the herd has
many reactors, as is often the case, the premises should be depop-
ulated and allowed to stand idle for at least 2 to 3 months before
restocking. This is often the least expensive way. Depopulation
with slaughter of infected herds is often used in the final efforts at
eradication. If a herd test reveals only one or a few reactors, those
can be removed, and the herd retested periodically.
In some cases where valuable bloodlines must be saved, weaned
pigs, usually negative when tested at weaning, can be moved to
separate, clean premises. They must be retested at least once prior
to breeding them to tested, clean boars.

54 SWINE BRUCELLOSIS
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Swine dysentery and spirochetal colitis
Alternate names and abbreviations
Brachyspira (previously Serpulina or Treponema), swine dysen-
tery, SD, porcine intestinal spirochetosis
Definition
Swine dysentery is a severe infectious disease caused by strongly
beta-hemolytic Brachyspira organisms, characterized by muco-
hemorrhagic diarrhea and lesions of marked inflammation that
are limited to the large intestine. Porcine intestinal spirochetosis
causes milder mucoid colitis in young pigs and is associated with
a variety of weakly beta-hemolytic Brachyspira organisms, most
notably B pilosicoli.
Occurrence
Swine dysentery occurs only in swine and is a very important
disease causing significant economic and production losses world-
wide. Other animal species can be transiently infected and shed
or harbor pathogenic Brachyspira. Swine dysentery can occur in
any age pig but is most prevalent from 6 weeks of age through
adult. The prevalence of dysentery in the US has decreased
because of successful eradication programs and through wide-
spread adoption of swine buildings that have fully-perforated
flooring, minimizing the recycling of the causative agent between
pigs and between subsequent groups. Outbreaks occur through-
out the year.
With an increased interest in niche pork production in the US
(eg, organic, antibiotic-free, and free-range systems), there is the
potential for a resurgence in swine dysentery.
Spirochetal colitis, associated with B pilosicoli, also has worldwide
distribution but is associated with a milder, non-hemorrhagic,
mucoid colitis. Several other Brachyspira species may contribute
to mild mucoid colitis as well.
Historical information
Swine dysentery was first reported in 1921 and was subsequently
described in many swine-raising countries throughout the world.
The etiology remained unknown until the isolation of Brachyspira
hyodysenteriae in 1971, which allowed characterization and more
focused research during the 1970s and 1980s. With the advent of
genetic sequencing, additional strongly beta-hemolytic Brachy-
spira species (B hampsonii and B suanatina) have been associated
with swine dysentery. Spirochetal colitis associated with B pilosi-
coli was described in the late 1980s.
Prior to the discovery of organic arsenicals and effective antimi-
crobials as treatments and preventatives, dysentery caused disas-
trous losses among swine herds. Improved methods of control
and elimination have markedly reduced losses in the US, but
dysentery remains a very important disease globally. Methods of
elimination of dysentery from individual swine herds have been
well described. Although national eradication programs have
BACTERIA
been considered, the lack of sensitive monitoring tests precludes
this effort at a national or regional level. Antimicrobial resistance
is common.
Etiology
Brachyspira are short, slender, spiral-shaped bacteria with axial
filaments that provide serpentine locomotion. The organisms are
Gram-negative, oxygen-tolerant anaerobes, and the strains that
can cause bloody diarrhea (dysentery) are strongly beta-hemolytic
on blood agar, notably B hyodysenteriae and, more recently, B
hampsonii and B suanatina.
Hemolysin activity of Brachyspira is an important virulence
factor and pathogenicity is seemingly proportional to hemolytic
activity, with dysentery caused only by strongly beta-hemolytic
isolates. Isolation of strongly beta-hemolytic Brachyspira colonies
on blood agar is probably the most accurate and sensitive method
to confirm that the presence of organisms capable of causing
mucohemorrhagic colitis typical of dysentery. Properly validated
polymerase chain reaction (PCR) tests are useful for screening
and speciation but may lack sensitivity to detect all pathogenic
variants. Attempts to classify Brachyspira using a variety of other
techniques have shown genotypic and phenotypic variation, but
have not proven useful to predict virulence, pathogenicity, immu-
nogenicity, or immune cross-protection.
Brachyspira pilosicoli and other weakly beta-hemolytic Brachyspira
species, including B murdochii, B intermedia, and B innocens, are
common in swine and can be isolated and/or detected by specific
PCR testing. These agents are common inhabitants of swine
colons and may cause or exacerbate other causes of colitis in
young and growing swine, but they do not cause swine dysentery.
Epidemiology
Transmission of Brachyspira occurs by the fecal-oral route. Feces
or any materials soiled with feces are sources of infection, along
with carrier swine or other animal species capable of harboring
organisms. Brachyspira persist in lagoon water and moist feces
for at least 2 months and soil for 3 weeks. Mice can shed strongly
beta-hemolytic Brachyspira for at least 180 days and dogs can
shed for at least 13 days. Birds, waterfowl, flies, and fomites can
harbor and transmit organisms as well. Asymptomatic carrier
swine can transmit the agent for at least 90 days. The introduc-
tion of inapparent carriers, including breeding stock, is often the
source of initial exposure. Contaminated transport vehicles are
frequently implicated as well. Carrier sows can intermittently
transmit Brachyspira to their piglets. Infected mice on the prem-
ises may also be an ongoing source of infection, something to
keep in mind when considering elimination strategies.
Brachyspira survive under a wide range of environmental con-
ditions but are susceptible to heat, ultraviolet light, desiccation,
soaps, most disinfectants, and alkaline environments.
SWINE DYSENTERY AND SPIROCHETAL COLITIS 55
 SWINE DISEASE MANUAL
BACTERIA
Pathogenesis
After ingestion of pathogenic Brachyspira, clinical signs of
diarrhea can develop in 5 to 21 days (or more). The incubation
period is dependent upon dose, herd immunity, and individual
pig susceptibility, but the infective dose is quite small. Diet can
influence prevailing microflora to facilitate or ameliorate colo-
nization and lesion formation. The organism reaches the large
intestine, colonizes, proliferates, penetrates the mucus layer,
becomes closely associated with epithelial cells, and causes a flux
of mucus. This is followed by superficial epithelial erosion and
hemorrhage. Invasion may not be essential for lesion production.
The exact mechanisms of tissue destruction are not known, but
toxins, hemolysin, and lipopolysaccharides are probably involved.
In typical lesions, organisms are present within crypts, epithelial
cells, and occasionally in the lamina propria. The lack of lesions
at other sites suggests the entire pathogenesis occurs locally
within the large intestine. Systemic effects of the disease include
dehydration, acidosis, and electrolyte imbalance caused by colitis.
Colonic inflammation can be severe and prolonged.
Clinical signs
Disease is most common in pigs from 6 weeks of age to market
but can occur in any pig from 3 weeks of age through adults. The
appearance of gray to yellow, mucoid diarrhea is often one of the
first signs of the disease. With dysentery, diarrhea continues and
quickly becomes mucohemorrhagic with excess mucus and fresh
blood apparent. In a small proportion of pigs, diarrhea may be
preceded by tail twitching or a humped, gaunt appearance. Fresh
red blood in mucus-containing feces is often profuse with abun-
dant perineal staining. Prolonged diarrhea leads to dehydration,
electrolyte imbalance and acidosis, sunken eyes, marked weak-
ness, hollow flanks, and weight loss. Anorexia is common, but
affected animals usually continue to drink. Morbidity is greater
than 50% and mortality can approach 50% in untreated herds;
affected pigs may remain stunted even after successful treatment.
Spirochetal colitis is generally seen as a mild diarrhea accompa-
nied by excess mucus. Affected pigs may be less thrifty, but effects
on growth performance may not be overtly obvious.
Lesions
Lesions associated with Brachyspira are limited to the large intes-
tine. With dysentery, the mesentery and serosa are edematous
and hyperemic. In acute cases, the mucosa of the affected large
intestine is diffusely reddened, edematous, and swollen. There
may be only small amounts of fibrin but copious mucus. Any or
all parts of the large intestine may be affected. As lesions progress,
the colon wall thickens with inflammation, congestion, and
edema and the mucosa becomes hyperemic with excess mucus
and flecks of blood. Further progression leads to the mucosa
becoming covered, diffusely or in patches, with layers of fibrin,
necrotic debris, mucus, and blood. Pigs that die suddenly may be
in surprisingly good body condition but have extensive lesions in
the large intestine.
56 SWINE DYSENTERY AND SPIROCHETAL COLITIS
Microscopy reveals moderate, non-suppurative colitis and typhli-
tis, mucus metaplasia, crypts dilated with mucus and organisms,
mucosal congestion and edema, and superficial epithelial necro-
sis. Spiral-shaped organisms are demonstrable using silver or
immunohistochemistry staining.
Brachyspira pilosicoli appears to exert its pathogenic effect by
attachment to enterocytes and creating microerosions in the
epithelium. Lesions of spirochetal colitis are milder that those seen
with dysentery, with mild mucosal hyperemia and excess mucus
observed on the mucosa of large intestine. Microscopically, there
may be abundant spiral-shaped organisms colonizing epithelium,
accompanied by mild non-suppurative inflammation.
Diagnosis
A field diagnosis of dysentery is based on clinical signs, necropsy
findings, and typical gross lesions that are limited to the large
intestine. Demonstrating high numbers of spirochetes in smears
made from colonic scrapings or feces using crystal violet or Vic-
toria blue stains adds confidence to the field diagnosis. However,
other Brachyspira species are common flora in some herds and
are morphologically indistinguishable from B hyodysenteriae, B
hampsonii or B suanatina on a smear.
Laboratory confirmation is usually warranted, especially if the
outbreak is new, its impact is high, or there is doubt about the
true cause of the clinical signs. Tissues should be collected for
culture and histopathology from acutely affected non-medicated
pigs. Culture of a strongly beta-hemolytic Brachyspira from
colonic scrapings is the most accurate and sensitive way to con-
firm diagnosis. Biochemical differentiation of pathogenic and
non-pathogenic strains is not consistent. Polymerase chain reac-
tion techniques are available for detection of some Brachyspira
and can provide differentiation to the species level, but specificity
limitations of molecular technologies can lead to false negative or
false positive tests, especially when only feces are tested.
Several diseases can mimic or occur simultaneously with dysen-
tery: ileitis, whipworms, salmonellosis, gastric ulcers, and intes-
tinal accidents. Severe whipworm infestations can very closely
mimic the gross lesions associated with dysentery, particularly as
the worms may not be grossly visible until perhaps 3 to 4 weeks
after exposure to the whipworm ova. Lesions of salmonellosis
extend deeper into the mucosa than those seen with dysentery
and tend to present as small ulcers, which may be multifocal in
distribution and have much less mucus and fresh blood than dys-
entery. Salmonellosis lesions are not usually confined to the large
intestine. Though ileitis typically affects the small intestine, some
cases seem to have a predilection to cause lesions only in the large
intestine; in these cases, histopathology can easily differentiate
the disease from dysentery.
Spirochetal colitis is best diagnosed by necropsy of acutely
affected pigs, followed by histopathology on affected tissues,
isolation of the weakly beta-hemolytic causative organism, and
definitive identification by biochemical tests or PCR.
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
Control
Preventing the introduction of pathogenic Brachyspira to nega-
tive herds through strict biosecurity measures is a high priority.
Additions to the herd should be made only from herds known to
be historically free of dysentery and only after a quarantine period
of 30 to 60 days.
Elimination of dysentery from farms can be successful with
scrupulous attention to the details of a well-designed plan. One
method of elimination commonly used in the US relies on the
use of a medicated early weaning protocol, whereby piglets are
weaned to a clean site concurrent with implementation of an
intensive off-site breeding program. While the infected sow
farm is depopulated and the facilities cleaned and disinfected, an
off-site breeding program establishes a disease-free population
of sows that can eventually be relocated back to the site that was
previously depopulated. Variations of this program exist and have
also been quite successful in eliminating dysentery. A second
elimination method relies more heavily on use of antibacterial
medication and is generally only applicable to the breeding herd
population in a multi-site production system. In this method,
the herd population is reduced as far as practical to decrease
medication cost. An intensive oral medication regimen of all
animals then follows. Debilitated animals must be culled before
the eradication program since they may not consume enough
medicated feed or water to eliminate the infection. Few antimi-
crobials are effective at complete elimination of the organism, so
product selection should be made with care and directions for its
use should be followed carefully. Often, improvements to farm
biosecurity are implemented at the same time as the medication
program. A third method for elimination is through complete
depopulation of the farm; this is most useful on farms where age
segregation, biosecurity, and sanitation are difficult to implement.
Depopulation should be done during warm, dry weather. During
depopulation, all facilities and equipment should be thoroughly
cleaned, disinfected, and idled. During periods of warm, dry
weather, Brachyspira will not usually survive for more than 2
weeks in soil or grass pens. Obviously, significant investment
should be made in confirming that depopulation is followed only
by repopulation with swine known to be free of dysentery.
BACTERIA
Any effort to eradicate dysentery requires an initial accurate
diagnosis of dysentery, a high level of commitment from the
owners and workers, and an agreement to consistently execute
the herd-specific protocol with ongoing veterinary supervision.
Successful implementation of a dysentery elimination project
requires exquisite attention to and compliance with the details
laid out in the implementation plan. The eradication effort
should be made during the warmest time of the year. A profes-
sionally managed rodent control program is an essential part
of any eradication program. Eradication must be coordinated
with pig flow so that thorough cleaning and disinfection can
be accomplished when the premises is vacant or the population
minimal. If infected animals must be retained during the effort,
a barrier system must be set up to separate clean from potentially
contaminated areas. In contrast to the diagnosis of disease in
overtly affected animals, detection of non-clinical carriers can be
difficult. Repeated sampling of non-medicated pigs over time is
often required.
Producers trying to control endemic dysentery generally rely
on the use of preventive and therapeutic levels of antibiotics
administered in the feed and/or water. Pulse-dosing or contin-
uous administration, coupled with good sanitation and manure
removal, can be effective but is costly. Development of antimicro-
bial resistance is common, making control programs (as opposed
to elimination) a poor long-term strategy. Vaccination has not
proved to be reliably effective in control or elimination programs.
Some dietary considerations (highly digestible, low insoluble
fiber) may be useful in controlling dysentery when coupled with
consistent sanitation and manure removal strategies.
Control of B pilosicoli should follow the same principals of sanita-
tion and husbandry as described for dysentery. The disease usually
responds favorably to the antimicrobials listed for swine dysentery.
SWINE DYSENTERY AND SPIROCHETAL COLITIS 57
 SWINE DISEASE MANUAL
BACTERIA
Tuberculosis
Alternate names and abbreviations
TB
Definition
Tuberculosis is a chronic, granulomatous disease of swine, poul-
try, wild birds, many domestic and wild animals, and people.
Occurrence
Tuberculosis occurs frequently in humans, domestic and wild
animals, poultry, and wild birds. It occurs in almost all vertebrates
and in some cold-blooded animals. The disease is present world-
wide throughout the year.
The incidence of tuberculosis condemnations in over 100 million
swine slaughtered in federally inspected abattoirs of the US was
0.003% in 1995 and has remained stable at this low incidence.
Historical information
In the US, tuberculosis was once a common disease of poultry,
cattle, swine, and people. A major effort to eradicate tuberculosis
from cattle and in people markedly reduced incidence of the
classic, severe disease caused by infection with Mycobacterium
tuberculosis, M bovis, and closely related subspecies, now referred
to as Mycobacterium tuberculosis complex. Swine and poultry are
susceptible to M tuberculosis complex but are now rarely exposed
to or infected with it. Infection with granulomatous lesions in
swine and poultry is usually caused by M avium and related sub-
species, referred to as Mycobacterium avium complex.
Changes in the poultry industry leading to the establishment of
large, integrated production systems largely eliminated the raising
of poultry as a private commercial enterprise for small farmers,
which traditionally had been the source of exposure for swine. As a
consequence, the incidence of tuberculosis in swine has decreased
substantially. Reductions were achieved without an eradication
program directed specifically at swine or poultry tuberculosis.
An increasing prevalence of tuberculosis in immunocompro-
mised people, coupled with resistance of tuberculosis to many
therapeutic agents, continues to be a public health concern for
much of the world.
Etiology
There are at least 177 species of Mycobacterium, many of which
are soil saprophytes. Tuberculosis in bovines and humans refers
specifically to disease caused by M tuberculosis complex organ-
isms. Swine and poultry can be infected and can develop lesions
with M tuberculosis complex but are much more likely to be
infected with M avium complex. This latter group causes gran-
ulomatous lesions that resemble classic tuberculosis of humans
and bovine and are a public health concern for immunocompro-
mised humans.
58
As a genus, Mycobacteria are Gram-positive, acid-fast bacilli. They
are highly resistant to most environmental factors, many disin-
fectants, and an increasing number of antibiotics. Mycobacterium
avium complex organisms have survived for more than 4 years in
poultry lot soil, in cages, and in sawdust used as litter.
Epidemiology
The marked resistance of Mycobacterium to environmental factors
makes contaminated premises a long-term threat to swine. The
tuberculosis organisms are usually spread to swine by tubercu-
losis-infected poultry, wild birds, cattle or people, or by soil or
bedding materials contaminated by them. The route of exposure
is usually by ingestion, although spread by inhalation occasionally
occurs. Infectious feeds that have spread tuberculosis bacilli to
swine include offal from infected poultry and cattle, uncooked
garbage, and unpasteurized milk and dairy products. Exposure of
swine to lots contaminated by the feces of tuberculosis-infected
poultry has often led to their infection by M avium complex.
Other less common but proven routes of exposure include expo-
sure to serovars of avian type contained in sawdust or wood shav-
ings used as bedding, congenital exposure of fetuses of infected,
pregnant sows, and animal-to-animal exposure among swine.
Rarely, infected swine have tuberculosis lesions in their tonsils or
intestine and shed the organisms in their feces.
Pathogenesis
The complex lipid nature of the organisms may explain the diffi-
culty the body defenses have in destroying mycobacteria though
phagocytosis and oxidative killing. In mononuclear phagocytes,
toxic lipids in the mycobacteria, or factors released by them,
appear to interfere with phagolysosome formation or to inacti-
vate lysosomal enzymes. If macrophages fail to destroy ingested
mycobacteria, they can carry them to other sites. There, the bacte-
ria are liberated upon death of the macrophages, and the released
organisms set up new foci of infection.
In swine, tuberculosis bacilli appear to initially infect the tonsils
and intestinal mucosa and then spread to the regional lymph
nodes, especially those of the cervical area and less often to
mesenteric nodes. Lesions in the nodes tend to develop slowly
and, in most cases, the bacilli are successfully walled off. Most M
avium complex infections are asymptomatic, with granulomatous
lymphadenitis the predominant outcome.
Clinical signs
In swine with localized tuberculosis infections, there are usually
no signs. Since most swine are slaughtered at an early age, there is
little time for generalization of infection and the appearance of
signs. Condemnation of carcasses at slaughter is the usual presen-
tation. In older breeding stock, tuberculosis generalization does
 DISEASES CAUSED BY BACTERIA, MYCOPLASMAS, AND SPIROCHETES
occur occasionally. Affected animals tend to waste away despite
adequate feed. They eventually become emaciated and may die
from tuberculosis.  of history, study of gross and microscopic lesions, and the
Lesions
In localized tuberculosis, grossly visible lesions are usually
apparent only in cervical, submaxillary, or mesenteric lymph
nodes. Lesions vary considerably in appearance, depending on
the type of infection. Localized avian and human type infections
tend to produce enlarged, firm nodes with no discrete purulent
foci. Calcification is seldom apparent and lesions are not easily
enucleated. Nodes affected by M tuberculosis complex organisms
(specifically M bovis) tend to be well encapsulated, relatively easy
to enucleate, and there is often marked calcification in the lesions.
On rare occasions where disease is caused by M tuberculosis com-
plex organisms, the infection is much more likely to generalize
than tuberculosis caused by M avium complex organisms. Lesions
in the organs vary considerably. Initially, the lesions are miliary
and widely distributed. Those in the lungs tend to develop along
pleural and septal lymphatics and resemble dewdrops. Those in
the liver tend to have caseated or liquefied centers. Splenic lesions
commonly occur and, when well developed, often protrude.
Serous membranes are seldom affected.
BACTERIA
Diagnosis
A presumptive diagnosis can often be made on the basis
presence of acid-fast bacteria within discrete granulomas or
granulomatous tissue. A confirmed diagnosis can be made
only after isolation, identification, and typing of the bacteria.
Polymerase chain reaction and immunohistochemistry are
increasingly useful for confirmation.
Antemortem diagnosis is possible but rarely done in pigs.
Control
Prevention is by avoiding exposure of swine to tuberculosis
bacilli. Swine are quite susceptible to M tuberculosis complex
organisms, which are usually acquired from exposure to offal or
unpasteurized milk and dairy products from tuberculous cows.
Fortunately, exposure is rare in modern agriculture production;
however, it remains a real threat where bovine tuberculosis is still
endemic and the feeding of waste food or milk is common.
Mycobacterium avium complex infections of swine occur with
some frequency. Raising either swine or poultry in confinement
can reduce the most common exposure of swine to infection.
Conversely, close confinement of swine with careless exposure
to wild birds or poultry can provide an opportunity for greater
exposure. All swine, as well as all bedding, should be protected
from domestic and wild birds. Phenol-based disinfectants are
preferred for environmental disinfection.
TUBERCULOSIS 59
 60
BACTERIA
 Section II

Diseases caused by viruses

VIRUSES
African swine fever ........................................................................................................................................................................ 63
Blue eye disease................................................................................................................................................................................ 65
Classical swine fever....................................................................................................................................................................... 67
Encephalomyocarditis virus.......................................................................................................................................................... 70
Foot-and-mouth disease ............................................................................................................................................................... 72
Hemagglutinating encephalomyelitis......................................................................................................................................... 74
Inclusion body rhinitis................................................................................................................................................................... 76
Influenza .......................................................................................................................................................................................... 78
Japanese encephalitis...................................................................................................................................................................... 81
Parvovirus......................................................................................................................................................................................... 83
Porcine circovirus associated diseases......................................................................................................................................... 85
Porcine picornaviruses................................................................................................................................................................... 88
Porcine reproductive and respiratory syndrome...................................................................................................................... 92
Porcine respiratory coronavirus................................................................................................................................................... 96
Pseudorabies .................................................................................................................................................................................... 98
Rotavirus.........................................................................................................................................................................................101
Senecavirus A.................................................................................................................................................................................103
Swine enteric coronavirus diseases............................................................................................................................................105
Swine vesicular disease.................................................................................................................................................................108
Swinepox.........................................................................................................................................................................................110
Vesicular exanthema ....................................................................................................................................................................111
Vesicular stomatitis ......................................................................................................................................................................112

61
 62
VIRUSES

African swine fever
Alternate names and abbreviations
ASF, ASFV
Definition
A highly contagious, viral disease with signs, lesions, and other
features that closely resemble classical swine fever. The disease is
exotic to the US There is no evidence that African swine fever
(ASF) virus infects humans.
Occurrence
African swine fever occurs naturally in wild, feral, and domestic
swine (Suidae). At present, ASF does not occur in the western
hemisphere. It is endemic in several African countries, and an
outbreak of the disease has been occurring across multiple coun-
tries in Asia and Europe since 2007, with recent (2018) epidemic
status reported from China and Southeast Asia. Its distribution
among countries changes, depending on new infections, reinfec-
tions, and the success of eradication programs.
Historical information
African swine fever has been a serious problem in many African
countries since the disease was first reported in 1921. In 1957,
the disease occurred in Portugal, the first non-African country
to be infected. Additional outbreaks have since occurred in Asia,
Europe, the Caribbean, and South America. Although many of
these outbreaks were eradicated at significant cost, the risk of
re-introduction remains. In 2007, ASF was introduced into the
Caucasus region of Eurasia, where it then spread to wild boars
and domesticated pigs in several member countries of the Euro-
pean Union. In 2018, this outbreak extended into China.
Prohibiting the importation of swine and pork from infected
countries and eliminating or regulating the practice of waste-food
feeding to pigs are fundamental to most successful eradication
programs. The existence of a feral reservoir, widespread tick vec-
tors, and the high cost of eradication make worldwide eradication
unlikely. The US has never experienced an outbreak, although
ASF has occurred several times in nearby Caribbean islands.
Etiology
African swine fever virus is a DNA virus and is currently the only
member of a family called Asfarviridae. More than 20 genotypes of
ASF virus have been identified, most from wildlife cycles in Africa.
Isolates differ greatly in virulence, ranging from highly pathogenic
viruses that kill most pigs to strains that result only in seroconversion.
Epidemiology
In general terms, 4 transmission cycles have been described to
explain the transmission and maintenance of ASF virus in pigs.
The first cycle describes a sylvatic relationship between sub-
Saharan warthogs and the tick Ornithodoros porcinus porcinus,
DISEASES CAUSED BY VIRUSES
in which neither species develops significant clinical disease
from the infection despite high levels of viremia during the acute
stage of infection. The second cycle describes the relationship
between domestic pigs (truly domestic pigs, but also the Eurasian
wild boar, and feral pigs or free-living pigs that are a result of
VIRUSES
escaped or released domestic pigs) and any of several argasid ticks
including but not limited to O porcinus porcinus. The third cycle
describes those situations whereby the infection can persistent
within populations of truly domestic pigs without any need for
a tick vector (ie, direct pig-to-pig transmission). In this third
cycle, ASF virus is thought to be primarily transmitted via direct
contact with excreted virus in oral and nasal secretions, feces,
and perhaps short distance aerosols. The US has ticks which
could potentially act as vectors for ASF virus. The fourth cycle,
described as the “wild boar - habitat cycle,” is characterized both
by direct transmission between infected and susceptible wild
boars and, importantly, by indirect transmission to wild boars
through their contact with carcasses of wild boars that have
recently succumbed to ASF. This fourth cycle was described to
explain the persistence of the highly virulent ASF virus associated
with the ongoing Eurasian wild boar population in the apparent
absence of an endemic tick vector.
While both sylvatic and pig-to-pig transmission models can
explain the persistence of ASF virus in populations of domestic
or wild pigs, it appears that the most important means of trans-
mitting the virus over long distances is through the movement of
infected pigs and the feeding of pigs on swill containing infected
pork products. Feeding of contaminated swill is particularly
important, as it is considered to be one of the most likely routes
for introduction of the virus into ASF-free countries that do not
share a contiguous border with countries having populations of
wild pigs known to be infected.
Pigs that 1) have died acutely from ASF, 2) have died in a more
chronic stage of the disease, or 3) are wild Suids living in an area
known to be endemically affected by ASF, all present a risk of
virus transmission to other pigs. As omnivores, pigs that come
across the carcass of a dead pig are likely to interact with, if not
actively feed on, the carcass. Given the propensity of the virus to
remain infectious for days to weeks in a protein-rich substrate
such as meat, tissue or blood, oral exposure to a contaminated
carcass is likely to lead to transmission of the virus.
African swine fever virus is stable across a wide range of pH and
temperatures, particularly when stored in the presence of pro-
tein. Virus has been shown to remain infectious for more than
400 days when stored in filtered serum at room temperature, at
least 6 years in a cold room, and for at least 16 days in putrefy-
ing blood. The virus can remain infectious for years at freezing
temperatures. The virus can also survive in feedstuffs. The
stability of this virus in a variety of matrices is a major threat for
spread of this disease globally.
AFRICAN SWINE FEVER 63
 SWINE DISEASE MANUAL
Phenol disinfectants, in particular 1-Stroke Environ®, appear to
be most effective in inactivating the virus from surfaces, although
extended contact time (greater than 1 hour) may be required.
Pathogenesis
The primary infection usually starts in the tonsils and mandibular
lymph nodes. Virus then spreads in lymph and blood to secondary
VIRUSES
replication sites (bone marrow, lung, spleen, and kidney). A
persistent viremia begins about 1 week after infection. The main
target cells of the virus include monocytes, macrophages, cells of
the reticuloendothelial system, endothelial cells, and platelets.
Destruction of antigen processing cells in lymph nodes, spleen,
and bone marrow apparently interferes with formation of pro-
tective antibodies. Destruction of endothelial cells and vascular
damage is responsible for hemorrhages, edema, and transudate
formation. The virus also causes a meningoencephalitis which can
lead to ataxia in affected pigs. The virus affects multiple organs of
fetuses and causes fetal deaths.
Clinical signs
Clinical signs appear 5 to 15 days after infection. Signs vary
greatly, depending on the virulence of the virus, and can range
from inapparent or subclinical to peracute with sudden death.
Many initial outbreaks closely resemble outbreaks of acute classi-
cal swine fever.
In acute outbreaks, signs include anorexia, high temperatures,
listlessness, incoordination, leukopenia, cutaneous hyperemia,
hemorrhages on the skin (especially on ears and flanks), and
hyperpnea. Vomiting, diarrhea, dehydration, and ocular dis-
charge may occur. Morbidity and mortality are high and can
approach 100%. Death usually occurs in 4 to 7 days. In subacute
or chronic cases, signs include abnormal respiration, abortion,
and low mortality.
Lesions
The lesions are similar to those of classical swine fever. There
are petechial and ecchymotic hemorrhages at many sites (skin,
kidneys, lymph nodes, serosal and mucosal surfaces, epicardium,
endocardium, larynx, bladder, gall bladder, and lung), edema,
hydrothorax, hydropericardium, and ascites. The liver and spleen
are congested. The spleen is often enlarged, friable, and may have
infarcts. There is often congestion of the meninges and brain.
Lesions that are often present with ASF, but seldom with classical
64 AFRICAN SWINE FEVER
swine fever, include hydrothorax, hydropericardium, ascites, and
pulmonary edema. Hemorrhages and edema are usually more
severe in ASF than with classical swine fever.
Gross lesions in chronic cases of ASF include fibrinous peri-
carditis and pleuritis, spleen and lymph node enlargement, and
caseous lobular consolidation of areas in the lungs, possibly
with mineralization.
Histologic lesions of ASF include meningoencephalitis, peripor-
tal hepatitis, extensive necrosis with karyorrhexis (cell nucleus
rupture) in lymphoid tissues, and degeneration and necrosis of
endothelial cells and cells of the mononuclear-phagocytic system.
Diagnosis
Diagnosis can be confirmed by detecting ASF virus, viral anti-
gen, viral genes, or antibodies to the virus. Virus isolation and
identification using available tests (eg, hemadsorption, immuno-
fluorescence, and polymerase chain reaction [PCR]) confirm the
presence of ASF virus. Several techniques have been developed to
identify ASF virus antigen in paraffin-embedded tissue sections
(eg, immunohistochemistry) or frozen sections (eg, indirect
immunofluorescence). PCR assays on tissue or blood detect viral
genes and are in common use globally. Viral DNA can also be
detected in tissue sections by in situ hybridization. A number
of tests are used to identify ASF antibodies, including indirect
immunofluorescence, enzyme-linked immunosorbent assay, com-
plement fixation, immunoblotting, and radioimmunoassay.
Control
Control in most countries is limited to preventing entry of the
virus. Early diagnosis of suspected cases is important. State and
federal disease control authorities should be informed imme-
diately if an ASF or classical swine fever outbreak is suspected.
If ASF should gain entrance, early quarantine and restriction
of movement of animals in the area are important. Vaccines are
unsatisfactory, both for control of clinical signs and for preven-
tion of infection.
Massive amounts of virus are found in many tissues, especially
blood. Care must be taken when performing necropsies to
prevent substantial environmental contamination. Feeding pigs
waste food that has not been heat treated is illegal in the US and
most other countries; good compliance with waste food feeding
regulations is a critical step in preventing an incursion of ASF
into a country.

Blue eye disease
Alternate names and abbreviations
BED, Porcine rubulavirus, porcine paramyxovirus, La Piedad
Michoacan virus
Definition
Blue eye disease is the common name for a disease caused by a
porcine rubulavirus that is characterized clinically in nursing or
growing pigs by the occurrence of central nervous system (CNS)
signs and corneal opacity. Signs in sows and boars include various
forms of reproductive failure and corneal opacity.
Occurrence
Blue eye disease is only known to occur in swine. In Mexico
(the only country that has reported the disease), blue eye disease
occurs throughout the year but is more common during hotter,
drier months. Swine diseases caused by other paramyxoviruses
have occurred in several countries (Australia, Canada, Israel,
Japan, and the US), but the diseases they cause are sporadic, rare,
and distinctly different from blue eye disease, usually manifesting
as transient outbreaks of pneumonia, encephalitis, or reproduc-
tive disease.
Historical information
Blue eye disease first occurred in 1980 in a large swine-raising
operation in central Mexico, and within a short time it had
spread to at least half of the Mexican states. It is currently consid-
ered to be an economically important disease in that country. The
first outbreaks occurred mainly in unweaned piglets less than 30
days old, frequently in piglets less than 2 weeks old. After 1983,
severe outbreaks tended to occur in larger pigs (33 to 99 lb [15
to 45 kg]). Signs of reproductive failure were also observed in
mature sows and boars.
Etiology
The agent that causes blue eye disease is officially named porcine
rubulavirus and is a member of the Paramyxoviridae family of
RNA viruses. Other members of this family include Hendra heni-
pavirus (Hendra virus disease), Menangle rubulavirus (Menangle
virus disease), and Nipah henipavirus (Nipah virus disease), each
of which are emerging as important zoonotic agents in other
parts of the world. Although no wildlife reservoir has been iden-
tified for blue eye disease virus, pteropid fruit bats are known to
be the reservoir for the other viruses listed above and are critically
important in the epidemiology of those diseases.
Epidemiology
Both direct contact and short distance aerosolization are import-
ant routes of transmission for blue eye disease virus. Direct
contact is not required for transmission. Infectious virus has also
been found in urine and semen, and the virus can be transmitted
DISEASES CAUSED BY VIRUSES
to the fetus in utero. In recovered pigs, porcine rubulavirus has
been isolated intermittently from semen for up to 7 weeks after
experimental inoculation, and from the testes and epididymis for
as long as 20 weeks.
VIRUSES
While infectious virus is not routinely isolated from tissues in pigs
after recovery from the acute illness, viral RNA has been detected
in numerous organs for as long as 13 months, suggesting the virus
may persist in at least some pigs for an extended period of time.
Paramyxoviruses are readily destroyed by light, heat, and drying,
and they are normally short-lived in the environment. In general,
members of Paramyxoviridae are susceptible to many common
disinfectants including sodium hypochlorite, sodium hydroxide,
aldehydes, iodine, chlorhexidine, detergents, oxidizing agents,
and low pH.
Pathogenesis
Natural infection is thought to occur by inhalation, based on
experimental exposures where intratracheal and intranasal expo-
sure reproduced the disease. The initial site of viral replication is
unknown but may be in the nasal mucosa or tonsils. Virus soon
spreads to the brain, lung and many other organs, suggesting that
viremia occurs. Reproductive problems in dams suggest that the
virus crosses the placenta and infects the fetuses.
Corneal opacities (blue eye) sometimes occur late in the course of
the disease. The opacities disappear spontaneously, presumably as
inflammatory edema resolves. The opacities are perhaps the result
of an immunologic reaction accompanied by inflammation. Virus
may replicate in the eyes, since inclusion bodies have been demon-
strated there.
Experimentally infected piglets developed clinical signs 3 to 5
days after exposure.
Clinical signs
Signs vary somewhat with the age groups affected but are mainly
related to encephalomyelitis in both young and growing pigs. In
young piglets, onset is sudden with prostration and fever. Other
signs include ataxia, weakness, muscle tremors, rigidity, nystagmus,
abnormal postures, hyperexcitability, squealing, and paddling
movements; occasionally there is blindness. Often there is conjunc-
tivitis with adherence of the eyelids. Corneal opacity may occur
in 1% to 10% of young piglets and may be seen in the absence of
other signs. Twenty to 65% of litters can be affected. Morbidity
within litters is between 20% to 50%; mortality in affected pigs can
reach 90%. Piglets affected early in an outbreak often die within 48
hours. Those affected later in life usually die after a course of 4 to 6
days. Mortality occurs over a 2- to 9-week period.
In pigs greater than 30 days old, signs are more moderate and
transient. They include fever, sneezing, coughing, and anorexia.
BLUE EYE DISEASE 65
 SWINE DISEASE MANUAL
Central nervous system signs include listlessness, ataxia, and cir-
cling. Less than 5% of the pigs are affected and mortality usually
is low. However, in pigs weighing 35 to 45 lb (16 to 20 kg), out-
breaks with 20% mortality and up to 30% corneal opacity have
occurred. Adult animals occasionally develop corneal opacities.
In pregnant swine, returns to estrus may occur and persist in the
herd for 6 to 8 months. There is also an increase in stillbirths and
VIRUSES
mummified fetuses, and occasional abortions. In affected boars,
there is a reduction in fertility and an increase in testicular size,
usually unilateral, followed by atrophy.
Lesions
Gross lesions are limited and nonspecific. They may include
mild anteroventral pneumonia, tonsillitis, and mild ascites with
some fibrin. Brain congestion and an increase in the amount of
cerebrospinal fluid may be present. There is conjunctivitis and
perhaps corneal opacity in one or both eyes. Pericardial and renal
hemorrhages have also been reported. In affected boars there is
orchitis, epididymitis, and testicular atrophy.
Microscopic lesions include a nonsuppurative encephalomyelitis
affecting mainly the gray matter of the midbrain, thalamus, and
cerebral cortex. Intracytoplasmic inclusions in neurons have been
reported. Affected eyes have corneal edema and anterior uveitis,
perhaps with exudate in the anterior chamber. Intracytoplasmic
inclusions may be present in epithelial cells near the drainage
angle of the corneoscleral junction.
66 BLUE EYE DISEASE
Diagnosis
Clinical signs of encephalomyelitis as described and the presence
of corneal opacity, particularly in suckling pigs, suggest a diagno-
sis of blue eye disease. These clinical signs in sows or boars may be
followed by prolonged or ongoing reproductive failure, including
increased mummies, small litters, and infertility. Microscopic
lesions of encephalomyelitis and the presence of intracytoplasmic
inclusion bodies in neurons or eyes strongly suggest blue eye
disease.
The hemagglutinating virus can usually be isolated from the
brain, tonsil, serum, and many other tissues using PK-15 or Vero
cells. Serological assays have been developed and include hemag-
glutination inhibition, virus neutralization, and enzyme-linked
immunosorbent assay. Blue eye disease must be differentiated
from other causes of CNS disease, especially pseudorabies.
Control
A rigorous health control program to prevent introduction of the
virus is the best preventive measure. Maintaining a closed herd
and use of the all-in, all-out system of production may be helpful.
Essential replacement stock should be added only after negative
serological tests and a period of quarantine. Commercial vaccines
have been produced but there is little information available
regarding their efficacy.
Blue eye disease has been eliminated from infected sites by dis-
posing of infected animals, cleaning and disinfecting the site, and
using sentinel pigs to confirm elimination of infection. There is
no satisfactory treatment of blue eye disease: pigs that develop
CNS signs usually die. Pigs having only corneal opacities fre-
quently recover without treatment.

Classical swine fever
Alternate names and abbreviations
CSF, CSFV, hog cholera, swine fever
Definition
Classical swine fever (CSF) is a highly contagious, viral disease of
swine that in its most virulent form causes morbidity and mortality
approaching 100%. Viral strains of low to moderate virulence cause
infections with a gradient of severity, some clinically inapparent.
Occurrence
Classical swine fever occurs only in swine, and all age groups are
susceptible. The disease occurs in most major swine-raising coun-
tries where eradication programs have not been successfully imple-
mented. In the US, CSF was once a frequent occurrence but was
eradicated in 1976. Classical swine fever currently exists in many
countries, including areas of Central and South America, Asia, the
Caribbean, and in localized feral pig populations in Europe. Since
1997, sporadic epidemics of CSF have been reported in many
European countries, including Germany, Italy, The Netherlands,
and Spain, suggesting the disease is an ongoing threat for countries
with modern, commercial pork production industries.
Historical information
The historical record does not clearly indicate where CSF
originated, but a disease with clinical signs similar to CSF was
reported from the eastern US in the early 1800s. Until organized
efforts to control the disease began in the 1960s, the US routinely
experienced significant regional outbreaks of CSF. The earliest
efforts to minimize losses from CSF were first achieved through
the administration of CSF antiserum as either a prophylaxis
or for treatment of the disease. When properly performed on
healthy swine, it resulted in strong immunity. However, there
were many cases when serum administration triggered outbreaks
of other diseases (in addition to CSF), as the serum preparation
was not well regulated - meaning it could contain live viruses
or other disease-causing organisms. Serum administration was
eventually prohibited when a national CSF eradication program
began in 1962. Improvements in CSF vaccine, farm biosecurity,
and coordinated industry actions resulted in the eradication of
CSF in 1976. Eradication was a remarkable achievement, con-
sidering the highly infectious nature of virus and the extensive,
poorly regulated commerce in pigs and pork products at the time.
Etiology
Classical swine fever is a pestivirus related to the viruses that
cause bovine virus diarrhea and border disease. Classical swine
fever virus is closely related to these ruminant pestiviruses which
can also occasionally infect pigs, causing serological reactions
that may be mistaken for CSF. Strains of CSF vary greatly in
antigenicity and virulence. Virulence can increase during a single
DISEASES CAUSED BY VIRUSES
passage through pigs. Strains of high virulence cause classic out-
breaks with high morbidity and mortality. Strains of moderate
virulence cause subacute or chronic infections. Strains of low
virulence can cause mild or inapparent infection, reproductive
failure, or neonatal losses.
VIRUSES
New strains of CSF have emerged in Asia in the last few years.
Their clinical presentation does not appear to be substantially
different than those produced by classical strains of the virus but
immunologic cross-protection (by natural exposure or vaccina-
tion) is limited.
Classical swine fever virus can persist for days to weeks in pig
facilities, excreta, and bedding, depending upon temperature.
The virus survives some curing processes as well as in frozen pork
for months to years, and in chilled meats for months. The virus is
inactivated by 2% sodium hydroxide or by lipid solvents.
There is no evidence that classical swine fever virus can be trans-
mitted to humans.
Epidemiology
Pigs are infected with classical swine fever virus mainly by direct
contact with other infected pigs through the oral or oronasal
routes. However, the virus may also be transmitted through natu-
ral mating or artificial insemination.
Pigs with acute infection shed large amounts of virus before they
are visibly ill, during illness, and after recovery. The virus is shed
in most body fluids, including saliva, urine, feces, and semen.
Shedding can begin before the onset of clinical signs. Classical
swine fever virus can persist in blood and tissues after death,
explaining why an important route of transmission is related to
the feeding of uncooked waste food that contains tissues from
infected pigs.
Aerosol transmission has been demonstrated experimentally with
some strains but is probably not a significant means of moving
virus between farms.
Other methods of viral spread include fomites (farm equipment,
wagons, trucks, tractors, machinery) and personnel (farmers and
staff, farm visitors, veterinarians).
Pathogenesis
After ingestion, the virus infects epithelial cells in the crypts of
tonsils, spreads to adjacent lymph nodes and produces viremia
within 24 hours. Tonsils are the initial site of viral replication.
Replication also occurs at other sites, especially in lymphoid tis-
sues (spleen, Peyer’s patches, lymph nodes, and thymus), endothe-
lial cells, bone marrow, and circulating leukocytes. Within 3 to 4
days, the virus spreads to many epithelial-type cells and is present
in excretions and secretions.
CLASSICAL SWINE FEVER 67
 SWINE DISEASE MANUAL
The virus causes lymphoid depletion, making affected swine more
susceptible to other infections. Bone marrow damage leads to
leukopenia and thrombocytopenia. Thrombocytopenia, along
with endothelial cell damage, results in petechial and ecchymotic
hemorrhages at many sites. Swine with chronic CSF infection
may develop glomerulonephritis from antigen-antibody com-
plexes that damage glomeruli.
VIRUSES
In pregnant sows and gilts, the virus may cross the placenta and
infect some or all of the fetuses. The effect depends on the stage
of pregnancy and can include abortion or production of mummi-
fied fetuses, stillborn piglets, or persistently infected live piglets.
Fetal anomalies may result from in utero infection; a remarkable
anomaly is hypomyelinogenesis, a syndrome that results in shak-
ing piglets (myoclonia congenita).
Clinical signs
In typical acute outbreaks, clinical signs are nonspecific and
include depression (a hunched posture with drooping head and
a straight-hanging tail), anorexia, high fevers (106°F [41°C]),
conjunctivitis, and a strong desire to lie down and huddle or pile
with other affected pigs. There may be diarrhea or constipation,
and perhaps vomiting. Signs caused by central nervous system
lesions are often apparent and may include reeling when forced
to walk, hindquarter paresis or paralysis, and occasional tonic/
clonic convulsions in young growing pigs. Most affected pigs die
within 3 weeks of onset.
Outbreaks with less virulent virus or chronic cases seldom present
with typical signs but often have conjunctivitis, diarrhea or con-
stipation, and some degree of emaciation. Mildly virulent strains
of the virus seem to be becoming more prevalent worldwide and
present a significant opportunity for misdiagnosis by veterinar-
ians and producers unfamiliar with the disease. Pigs infected as
fetuses or neonates may present no signs.
Lesions
In typical acute CSF, lesions include petechial and ecchymotic
hemorrhages at several common sites, including the epiglottis,
bladder mucosa, cortex and pelvis of the kidneys, gall bladder
mucosa, on the lungs and heart, at the ileocecal junction, and
in the skin. Lesions sometimes considered of special value in
diagnosis include single or multiple infarcts along the border of
a spleen of normal size, subcapsular hemorrhage in many lymph
nodes, and hemorrhages on the cortices of the kidneys and on the
lungs. There usually is some degree of congestion in the fundus
of the stomach and small intestine. Small foci of necrosis may be
present in the tonsils.
Peracute cases may have no lesions. In chronic cases, ulcers with
raised edges (“button ulcers”) are often present in the cecum and/
or colon. Grossly visible fetal lesions include ascites, hepatic nod-
ularity, pulmonary hypoplasia, petechiation of the skin, microen-
cephaly, hydrocephalus, and cerebellar hypoplasia.
68 CLASSICAL SWINE FEVER
Microscopically, there is a panencephalitis that is most apparent in
the medulla, pons, midbrain, or thalamus. Glial cell nodules often
cluster around destroyed capillaries. Vascular lesions are present at
many sites, perhaps more pronounced in splenic follicular arteries.
Diagnosis
Typical acute CSF should be suspected on the basis of history,
clinical signs, body temperature, and gross lesions. Numerous
postmortem examinations will increase the accuracy of diagnosis.
Leucopenia in multiple affected pigs is suggestive of CSF. The
lesions of typical acute cholera closely resemble and must be
carefully differentiated from those of African swine fever, acute
salmonellosis, and acute swine erysipelas. Lesions sometimes
resemble those of other septicemic diseases, including strepto-
coccosis and Glasser’s disease. Infection with mildly virulent
strains may be indistinguishable from many endemic systemic or
respiratory pathogens. Diagnostic testing is imperative whenever
the combination of gross pathology, clinical signs, and lack of
response to antimicrobial therapy suggest that CSF should be on
the list of possible etiologies.
Suspected outbreaks should be reported immediately to author-
ities to confirm the diagnosis. Three laboratory procedures com-
monly used in confirming a diagnosis include: 1) demonstration
of CSF viral antigen in frozen tissue sections by immunofluo-
rescence with preferred tissues being tonsil, pharyngeal lymph
nodes, spleen, kidney and distal ileum; 2) isolation of virus in
cell culture and identification of viral antigen in the culture by
the fluorescent antibody test; and 3) identification of antibodies
to CSF virus (CSFV) by virus neutralization tests. Regardless of
the procedure used, it may still be necessary to differentiate CSF
from bovine viral diarrhea. Virus isolation and polymerase chain
reaction assays for CSFV are available.
Control
Control of CSF is possible through prevention of exposure,
vaccination, or eradication. In most countries, a cornerstone for
prevention of the disease is a ban or strict control on the impor-
tation of live pigs, fresh pork, insufficiently heated pork products,
and other possible sources of virus (imported swine semen and
embryos, and biologicals produced with porcine serum or prod-
ucts), and prohibiting the feeding of uncooked waste food. Most
developed countries have strict regulations that prohibit disposal
of garbage from international vessels (planes and ships) without
heat treatment.
In countries where the virus is endemic, attenuated vaccines are
often used for preventing or reducing the prevalence of infection
and minimizing the severity of clinical disease. Effective commer-
cial vaccines are available, although some countries rely on gov-
ernment-produced vaccines that have unknown efficacy. In the
final stages of an eradication program that has relied on CSF vac-
cination, vaccine use may be stopped as ongoing use of modified
live vaccines will prevent true disease freedom from occurring.
 DISEASES CAUSED BY VIRUSES

Bovine viral diarrhea (BVD) virus and

border disease (BD) virus of sheep
These two pestiviruses and CSF virus are closely related. Natu-
rally occurring infections with bovine viral diarrhea and border
disease have occurred in swine. Their major importance in swine
is that they both induce antibodies that can lead to serological
misdiagnosis of CSF. This can cause confusion in countries trying

VIRUSES
to eradicate CSF or maintain a CSF-free status. This confusion
can be avoided if specific laboratory methods of CSF diagnosis
are used.
Clinically apparent outbreaks of bovine viral diarrhea and bor-
der disease in swine are uncommon. Outbreaks that have been
suspected are manifested in breeding herds as reproductive prob-
lems, such as poor conception rates, small litters, abortions, and
an excessive number of dead and mummified fetuses. In infected
live piglets, the signs are expected to be similar to those of con-
genital bovine viral diarrhea and border disease, including deaths
in piglets less than 5 weeks old, anemia, unthriftiness, congenital
tremors, and convulsions.

CLASSICAL SWINE FEVER 69

 SWINE DISEASE MANUAL
Encephalomyocarditis virus
Alternate names and abbreviations
EMC, EMCV
Definition
Encephalomyocarditis (EMC) is a disease caused by infection with
VIRUSES
EMC virus. Encephalomyocarditis virus commonly infects suscep-
tible species; clinical disease is unusual in domestic animals.
Occurrence
Susceptible species include humans, primates, many species of
rodents, marsupials, mongoose species, and several species of
birds. In zoos, rapidly fatal infections have been reported in
elephants, primates, and artiodactyls. Horses, cattle, swine, dogs,
and cats are susceptible to infection, but except for swine there is
no clear evidence that encephalomyocarditis viruses are signifi-
cant pathogens of domesticated species.
Historical information
In 1940, Columbia SK virus was the first strain of encephalo-
myocarditis virus identified. At the time, it was postulated to be
a strain of poliovirus, but this was later shown not to be the case.
Infection in swine was not reported until outbreaks occurred
in Panama (1958) and Florida (1960). Subsequently, clinical
encephalomyocarditis was reported in Australia, Brazil, Cuba,
Greece, New Zealand, and North America.
Research on the encephalomyocarditis viruses in swine was
conducted in the early 1990s because of an erroneous association
with “mystery swine disease,” which was later proven to be caused
by porcine reproductive and respiratory syndrome (PRRS) virus.
At present in the US, encephalomyocarditis may be a sporadic
pathogen of dubious clinical significance as a swine pathogen.
Etiology
The encephalomyocarditis group of viruses is classified in the
genus Cardiovirus in the Picornaviridae family. They are non-en-
veloped, single-stranded RNA viruses. These hemagglutinating
viruses are stable in many environments and can be grown in cell
culture. Areas contaminated with encephalomyocarditis viruses
can be disinfected with iodine-based disinfectants or 0.5 ppm
residual chlorine.
Epidemiology
The encephalomyocarditis group of viruses is present throughout
the world. Infection is common but clinical disease is rare in
domestic animals and humans. Rats and mice are considered to
be the principal reservoirs of the virus, although the experimental
evidence to support this is weak. Transmission of encephalomyo-
carditis virus among rodent species is difficult to achieve and a
chronic intestinal carrier state, a key epidemiologic feature in
closely related picornaviruses (ie, polioviruses or enteroviruses),
70 ENCEPHALOMYOCARDITIS VIRUS
does not occur. Infected rodents excrete virus and their diseased
carcasses contain large amounts of virus. Presumably, swine are
infected by ingesting feed or water contaminated by rats, mice,
or the carcasses of animals that died from encephalomyocarditis.
Infected swine excrete virus for about 9 days, but it is not clear
that they play an important role in transmission to other pigs.
Virus has been isolated from certain tick and mosquito species,
but vector competency studies have not shown transmission from
infected arthropods.
Pathogenesis
Following experimental oral infection of piglets, viremia occurs.
Lymphoid tissues contain virus and are probably the major sites
of virus replication. The highest titers of virus occur in damaged
heart muscle. Most deaths are related to right-sided heart failure.
Transplacental infections can occur in fetuses near full-term and
fetuses may develop myocardial lesions. Pigs that survive develop
antibodies that persist for long periods.
Clinical signs
Infection in swine is usually subclinical, but in rare cases it
produces myocarditis and high mortality in nursing pigs and/
or reproductive failure in dams. For unknown reasons, clinical
outbreaks in swine generally occur in tropical or semi-tropical
climates. Clinical disease in young piglets is often characterized
by an acute course and sudden death. Less acute cases have respi-
ratory signs with dyspnea, fever, anorexia, depression, trembling,
staggering, and paralysis. Mortality may approach 100% in neo-
natal and nursing pigs. Older pigs and adults usually have subclin-
ical infection, but some mortality may occur, even among adults.
In pregnant sows and gilts, there are mid- to near-term abortions
with an increase in stillbirths and mummified fetuses.
Lesions
In young piglets there are changes compatible with right-sided
heart failure, including hepatomegaly, hydropericardium,
hydrothorax, pulmonary edema, and ascites. The heart may be
enlarged, flabby, and pale red with subepicardial, petechial hem-
orrhages. Lesions are most marked in the right ventricle where
there may be discrete yellow or white foci, or diffuse, pale areas
of myocardial necrosis. Similar myocardial lesions may be visible
in the heart of aborted fetuses. Microscopic lesions include focal
nonsuppurative interstitial myocarditis and myocardial necrosis;
infiltration of small numbers of neutrophils may be evident.
Occasionally, this finding is accompanied by a nonsuppurative
meningoencephalitis.
Diagnosis
Disease associated with encephalomyocarditis is rare but
should be considered in cases where there is marked dyspnea

and sudden deaths in pre-weaning age piglets, high preweaning
mortality, an increase in late-term abortions, or gross and/
or microscopic myocardial lesions. Myocardial lesions must be
differentiated from those of PRRS, mulberry heart disease, toxo-
plasmosis, bacterial septicemia, and cardiac infarcts.
Definitive diagnosis requires demonstration of virus associated
with compatible gross and microscopic lesions. The virus can be
isolated from the myocardium or spleen of acute cases in young
piglets. Polymerase chain reaction assays are available to detect
the presence of the virus.
A number of serological assays have been developed. A serum
neutralization assay is widely available and has been shown to be
specific for antibodies against encephalomyocarditis virus. Serum
neutralizing antibodies may persist for an extended period of
time, so serological evidence of recent infection requires demon-
strating a 4-fold increase in neutralizing antibody titers in conva-
lescent versus acute sera.
DISEASES CAUSED BY VIRUSES
Control
Until encephalomyocarditis is demonstrated to be a significant
cause of disease, one should interpret any positive diagnostic test
results with caution to ensure that other more likely agents are
not involved.
Elimination or reduction of feral rodent populations is recom-
VIRUSES
mended in order to minimize environmental contamination with
virus. Feeds from all sources should be properly stored and kept
free of contamination by rodents. Pigs from farms known to have
encephalomyocarditis should not be added to known negative
herds. Pigs, rodents, and other animals that have died should
be removed promptly to avoid transmission through ingestion.
Basic hygienic and sanitary practices should be followed. An
inactivated vaccine is commercially available, but its use should be
clearly justified. There is no specific treatment.
ENCEPHALOMYOCARDITIS VIRUS 71
 SWINE DISEASE MANUAL
Foot-and-mouth disease
Alternate names and abbreviations
FMD, FMDV
Definition
Foot-and-mouth disease (FMD) is a highly contagious viral
VIRUSES
disease of many wild and domestic cloven-footed mammals, and
many other animals. In swine, the disease is characterized by vesi-
cles on the feet, snout, and in the mouth.
Occurrence
Many wild and domestic animals, especially cloven-footed mam-
mals, are susceptible to FMD virus. Important livestock hosts
include cattle, pigs, sheep, and goats, as well as water buffalo and
yaks in Asian countries. Cattle can act as important maintenance
hosts as some individuals will harbor virus for many months after
clinical disease has resolved. Some strains of FMD virus are host-
adapted to cattle, sheep, or pigs, but one should consider all species
to be at risk, regardless of the strain responsible for an outbreak.
Other susceptible species include wild and farmed cervids (deer,
moose, caribou, elk, etc), llamas, and alpacas. Experiments suggest
that Bactrian camels can develop FMD, but dromedary camels
appear to be resistant to infection.
Horses are uniformly resistant to infection with FMD virus, a
fact that can be very useful in formulating a list of differential
diagnoses in the early phase of an outbreak. The disease occurs
in most countries that have large livestock populations unless the
country has made specific efforts to eradicate it. All age groups
are susceptible. In the absence of farmed susceptible livestock,
FMD is generally unable to sustain itself in populations of wild
susceptible animals.
Historical information
Foot-and-mouth disease is an ancient disease. A description of
a disease observed in 1546 probably was a description of FMD,
and the disease has continued to cause major losses in livestock
throughout the world. Losses have been greater from loss of pro-
ductivity than from mortality.
Nine outbreaks of FMD have occurred in the US with the last one
occurring in 1929. All 9 outbreaks were followed by eradication,
often at great expense. A new outbreak of FMD could cause great
losses in the US, as it is likely that the disease would become wide-
spread before it was recognized, due to the frequent long-distance
transportation of livestock in the cattle and swine industries.
Recent outbreaks of FMD in Japan, South Korea, and other
countries with modern livestock sectors have demonstrated the
devastation and frustration wrought by FMD. In addition to the
cost of the national disease response, these outbreaks resulted
in the immediate restriction of meat and livestock exports, mass
72 FOOT-AND-MOUTH DISEASE
culling, and production losses to farmers. The outbreaks also
had substantial effects on the national economies due to reduced
tourism, a temporary decline in meat consumption, and flow-on
effects to related agribusinesses.
Outbreaks of all vesicular diseases of swine are of concern because
the lesions cannot be distinguished from those of FMD except
by laboratory means. Swine are of special concern because they
are susceptible to more vesicular diseases than other species of
livestock and they often play a major role in the spread of FMD
by producing large, infectious aerosols of virus.
Etiology
Foot-and-mouth disease virus is a member of the genus Aphthovi-
rus in the family Picornaviridae. There are 7 major viral serotypes:
O, A, C, South African Territories type 1 (SAT1), South African
Territories type 2 (SAT2), South African Territories type 3
(SAT3), and Asia 1. Serotype O is the most common serotype
worldwide. Among the 7 types, one particular antigen (virus
infection-associated antigen or “VIA”) is group reactive and use-
ful in serological diagnosis of FMD infection.
Over 60 subtypes of virus have been identified and new subtypes
continue to develop. Many differ enough antigenically to require
preparation of subtype vaccines for their control. The antigenic
variation of the virus and the limited cross-protection among
strains has made it impossible to prepare a single vaccine that
protects satisfactorily against all strains. Effective disinfectants
of FMD virus include sodium hydroxide, acetic acid, sodium
carbonate, and Virkon™.
Epidemiology
Virus transmission occurs through respiratory aerosols and direct
or indirect contact with infected animals. Aerosol transmission
of FMD virus over distances as great as 30 miles is believed to
occur under certain weather conditions. For some virus subtypes,
infected swine can act as exceptional disseminators of virus and
are capable of producing aerosols with greater virus concentration
than those produced by cattle or sheep.
Infected animals disseminate virus in their excretions and secre-
tions. Food products containing infectious pork can also spread
FMD virus. Virus persists for long periods of time in frozen meat
products. In several notable FMD outbreaks, the index case has
been associated with pigs consuming uncooked waste food con-
taining infectious meat scraps. Contaminated biologics, including
vaccines, have also been responsible for outbreaks. People with
residual FMD virus in their respiratory tract can transmit the
virus to livestock for a short time.
Some species of animals, particularly cattle, recover from FMD and
remain carriers for weeks, months, and possibly years. Occasionally,

they disseminate virus that initiates new outbreaks. Swine are not
believed to be long-term carriers of FMD virus.
The incubation period for FMD can vary with the species of
animal, the dose of virus, the viral strain, and the route of inocu-
lation. It is reported to be 2 to 4 days in pigs (with some experi-
ments reporting clinical signs in as little as 18 to 24 hours).
Pathogenesis
Foot-and-mouth disease virus adheres to the mucosa of the
respiratory tract, the usual site of virus entry. Macrophages are
believed to transport the virus to secondary sites that include
epithelium, mucosa, and myocardium. In secondary sites, the
virus replicates, a marked viremia develops, and then the virus
infects epithelium at many other sites. Within a few days, vesicles
develop, usually at sites of mechanical stress. In swine, common
vesicle sites include the snout, mouth, tongue, and especially the
feet. In cattle, FMD virus affects the mammary gland epithelium
and the virus is shed in milk for a prolonged period of time.
Although unproven, similar shedding may occur in swine.
The lesions of the major vesiculating viral diseases are similar. Ves-
icles develop in the epidermis and then the epithelium over the
vesicle soon sloughs. Enough of the stratum basale is preserved to
regenerate the epidermis unless there is secondary infection of the
lesions. Secondary infection occurs on the feet of some swine and
leads to chronic lameness.
Foot-and-mouth disease can cause severe myocardial necrosis in
neonatal and young pigs which often leads to sudden deaths from
myocardial failure. The mottled myocardial lesions are sometimes
referred to as “tiger-heart” lesions and are useful in diagnosis.
Clinical signs
Lameness is often the first clinical sign of FMD infection. There
is an initial acute rise in temperature; slobbering and chomping
are common signs. Pregnant sows may abort or deliver stillborn,
infected piglets. Sudden deaths may occur in neonatal pigs, some-
times before signs or lesions are apparent in the sow. The early
stages of lesions appear as blanched, small foci in the skin on the
snout, soft tissues of the feet, and perhaps the teats of lactating
sows. By the time signs are readily apparent, there are usually
cutaneous vesicles or bullae. Signs develop rapidly, and morbidity
rapidly increases. Mortality is usually less than 5% but there can
be higher mortality in young pigs.
Lesions
Well-developed vesicles and bullae are soon apparent. They are
frequently present on the snout, behind the rim of the snout, in
the nares, on the tongue and lips, and on the soft tissues of the
feet including the coronary band, the bulbs of the toes, and inter-
digital clefts. Lesions are probably more common on the feet than
in the mouth. Less often, the lesions are on the vulva, the teats of
lactating sows, or the scrotum of boars. Extensive lesions on the
coronary band may lead to sloughing of the hoof and lameness.
DISEASES CAUSED BY VIRUSES
Foot lesions may involve one or more of the feet. Vesicles usually
rupture within 24 hours and the superficial epidermis sloughs to
reveal hyperemia and hemorrhage on underlying tissue. Uncom-
plicated lesions usually heal within 2 weeks. In a virulent form
of FMD, young pigs and sometimes older animals may have
extensive mottled areas of myocardial necrosis on ventricles and
in papillary muscles.
VIRUSES
Diagnosis
A diagnosis cannot be reliably made on the basis of clinical signs
and lesions, since they are similar in all of the vesicular viral dis-
eases of swine. The state animal health official (SAHO or state
veterinarian) or a USDA-APHIS Assistant District Director
(ADD, previously called the Area Veterinarian in Charge or
AVIC) should be contacted immediately if an outbreak is sus-
pected. Differential diagnosis of vesicular viral diseases should
only be completed in specifically designated laboratories having
facilities to safely handle exotic disease organisms. Plans must be
made for collecting and mailing specimens. The Foreign Animal
Disease Diagnostic Laboratory in Plum Island, New York, often
does the diagnostic work.
Diagnostic techniques include serological tests to identify FMD
virus infection-associated antigens, complement fixation and
enzyme-linked immunosorbent assay (ELISA) to detect FMD
virus antigen, virus isolation, virus neutralization, electron micros-
copy, and animal inoculation studies. Polymerase chain reaction
tests have been developed and are frequently utilized. Foot-and-
mouth disease must be differentiated from all other vesicular viral
diseases and from other diseases that cause erosive or ulcerative
lesions in the oral cavity. Positive diagnoses usually require less time
than negative diagnoses. An ELISA is available that can differen-
tiate antibody titers from infected versus vaccinated animals but is
not yet officially recognized by many countries.
Control
In the US, prevention of FMD depends on regulations that govern
the importation of animals, animal products, semen, and embryos,
and on regulations related to the safety of vaccines and other bio-
logic products. There are special regulations on both cooking and
disposal of waste food to prevent spread of the virus. Reliance on
the vigilance of veterinary practitioners and diagnostic laboratory
personnel is important in early detection of outbreaks.
In countries where FMD has not been eradicated, vaccines are
used for prevention. The recently developed subunit vaccines
have been of value in preventing some types and subtypes of
FMD infection but have not provided consistent protection
for type O infection, the most prevalent form of FMD. In the
event of an outbreak in the US, vaccine use will be considered.
The disease will be managed through quarantine, restriction of
movement of animals in quarantined areas, slaughter followed
by burial or incineration of infected and exposed animals, and
disinfection of production sites. Eradication is considered to be
less costly than living with FMD.
FOOT-AND-MOUTH DISEASE 73
 SWINE DISEASE MANUAL
Hemagglutinating encephalomyelitis
Alternate names and abbreviations
HE, HEV, vomiting and wasting disease
Definition
A disease seen in pigs less than 4 weeks old, characterized by vom-
VIRUSES
iting, wasting, and perhaps neurologic signs.
Occurrence
Hemagglutinating encephalomyelitis occurs only in swine. The
disease occurs in most major swine-raising countries but tends to
be quite sporadic. Infection is clinically silent except in piglets less
than 4 weeks old. The disease occurs as an acute outbreak affect-
ing most piglets in litters of non-immune dams.
Historical information
In 1959 an encephalomyelitis of suckling pigs was reported
in Ontario, Canada. In 1962, other investigators reported a
hemagglutinating virus producing encephalomyelitis in piglets.
In 1969, vomiting and wasting disease, similar in many respects
to the encephalomyelitis reported in Canada, was reported in
England. Viruses from the outbreaks later were proven to be
similar or identical.
Much of the research on hemagglutinating encephalomyelitis
infection in swine was completed in the 1970s and 1980s. Epi-
demiologic studies have shown the virus to be widespread in the
US. However, clinical outbreaks seldom occur, and the disease is
of modest economic importance.
Etiology
Porcine hemagglutinating encephalomyelitis virus is a sin-
gle-stranded, positive-sense RNA virus in the family Coronavi-
ridae, genus Betacoronavirus. The virus can be grown in several
porcine cell culture systems and hemagglutinates erythrocytes
from several kinds of animals. Only one serotype of the virus is
recognized. Differences in strain virulence, along with differences
in susceptibility are responsible for 2 clinical syndromes.
Epidemiology
Only pigs are susceptible to infection with hemagglutinating
encephalomyelitis virus. While the virus can infect naïve pigs of
any age, clinical signs including vomiting and wasting or enceph-
alomyelitis, are generally seen only in piglets less than 4 weeks
of age. Transmission of virus is presumably through actively
infected or carrier swine. Exposure is probably through infectious
nasal secretions or aerosol. Most large breeding herds in major
swine-raising countries are endemically infected.
In most swine herds, immune sows provide colostral antibody
that protects their piglets for 4 to 18 weeks. Passive immunity in
the growing pigs is replaced by active immunity as a consequence
74 HEMAGGLUTINATING ENCEPHALOMYELITIS
of exposure to virus in the environment followed by subclinical
infection. Clinically apparent disease develops only when young
piglets from non-immune sows are exposed.
Pathogenesis
The virus replicates in the nasal epithelial mucosa, tonsils, lungs,
and small intestine and spreads via the peripheral nervous system
to the central nervous system. Viremia is probably of little signifi-
cance in spread. In the central nervous system, virus localizes first
in nuclei of the medulla oblongata but later moves to the brain
stem, spinal cord, and sometimes to the cerebrum and cerebel-
lum. The virus produces lesions in a variety of nuclei, ganglia, and
plexi (trigeminal ganglion, vagal sensory nuclei, some brain stem
nuclei, and intramural plexi of the stomach). Clinical signs vary,
depending upon which nuclei are affected by the virus. Death
occurs whenever a vital nucleus ceases to function.
Clinical signs
Two similar clinical syndromes are caused by infection with hem-
agglutinating encephalomyelitis virus.
Vomiting and wasting syndrome
Sneezing and coughing may occur at onset. Within a few days,
vomiting of milk and retching are prominent signs. The young
pigs dehydrate rapidly and often grind their teeth. When water
is supplied, piglets mouth it but drink little, presumably because
of pharyngeal paralysis. After a few days they exhibit dyspnea,
cyanosis, coma, and die. Pigs in older litters survive longer but
continue to vomit occasionally. The anterior abdomen of some
of them may become distended, presumably from impaired emp-
tying and accumulation of gas. Most affected piglets waste away
over a few weeks and die. The few that survive remain unthrifty.
Morbidity and mortality can approach 100% in affected litters.
Encephalomyelitis syndrome
Initial signs are similar to those in the above syndrome. Vomiting
and retching occur less often and lead to less dehydration. In 1
to 3 days, any of a variety of signs of encephalomyelitis appear.
These may include stilted gait, muscle tremors, nystagmus, blind-
ness, opisthotonus, convulsions, and progressive paresis leading
to recumbency with paddling of the legs. Occasional pigs walk
backwards and assume a dog-sitting position. Affected pigs soon
weaken, pass into coma and die. In some litters of older pigs, there
may be only transient posterior paresis followed by recovery.
Lesions
Lesions are similar in the two syndromes. Chronically infected
pigs have cachexia and there may be distension of the anterior
abdomen by excessive gas in the stomach.

Microscopic lesions include a nonsuppurative encephalitis affect-
ing the gray matter of the medulla and brain stem. The frequency
of lesions at specific sites may vary in the two syndromes. There
is inflammation of the trigeminal, paravertebral, and autonomic
ganglia. Also, ganglia in the stomach wall, mostly in the pyloric
area, may show degeneration.
Diagnosis
The history, signs, and age group affected may support a diag-
nosis of hemagglutinating encephalomyelitis. However, for
definitive diagnosis, the virus should be isolated from affected
pigs, demonstrated present within lesions using antigen-based
stains, or detected by polymerase chain reaction. Virus isolation
can best be made from the brainstem of piglets showing signs for
less than 2 days.
DISEASES CAUSED BY VIRUSES
Paired early and late serum samples can sometimes be used to
show a rise in antibody titer against the infection. The first blood
samples should be taken early in the course of the disease since
antibody levels rise quickly. There does not appear to be serologi-
cal cross-reaction with other porcine coronaviruses.
Once the virus is introduced, it persists in the herd until all
breeding stock (including replacement females) have been
VIRUSES
exposed. Development of an active immunity against the virus
allows for development of adequate passive lactogenic immunity
for their piglets.
There is no effective treatment for affected individuals.
HEMAGGLUTINATING ENCEPHALOMYELITIS 75
 SWINE DISEASE MANUAL
Inclusion body rhinitis
Alternate names and abbreviations
Porcine cytomegalovirus, PCM, PCMV, IBR, nonprogressive
rhinitis
Definition
VIRUSES
A common viral infection but sporadic cause of disease. Nursing
or newly weaned piglets may have rhinitis and conjunctivitis
accompanied by sneezing and nasal discharge.
Occurrence
Porcine cytomegalovirus, sometimes referred to as inclusion body
rhinitis, occurs in all age groups of previously uninfected swine,
including developing fetuses. Inclusion body rhinitis occurs only
in pigs and is found in all major swine-raising countries. Infection
is common but is often inapparent when herd immunity is pres-
ent or when pigs are over 6 weeks old.
Historical information
Rhinitis accompanied by inclusion bodies was described in pigs
in 1955 and was identified as a transplacental infection of fetal
pigs in 1961. Over the next 20 years, research reports provided
details on the disease and its manifestations in all ages of swine,
as well as characteristics of the virus. There are proposed rela-
tionships between infection with porcine cytomegalovirus and
reproductive failure in dams, neonatal losses, and as a predispos-
ing factor for other swine respiratory diseases, but evidence to
support these associations is lacking. Losses from inclusion body
rhinitis are small; both the disease and the infection are largely
ignored by farmers.
Etiology
Porcine cytomegalovirus is a beta-herpesvirus related to human
herpesviruses 6 and 7. It has many of the characteristics of herpes-
viruses, including the ability to induce latent infection in carriers
that can later be reactivated by stress. Porcine cytomegaloviruses
can be propagated in cell culture. In several epithelial type cells of
swine, the virus causes marked cell enlargement and formation of
large intranuclear inclusion bodies.
Epidemiology
Serological testing has shown that most herds are antibody posi-
tive to porcine cytomegalovirus. The presence of the virus within
a herd is often unrecognized because many sows are immune,
show no signs of infection, and colostral antibodies protect
piglets from lesions after they become infected. In endemically
infected herds, piglets 3 to 8 weeks old tend to become infected
and shed virus for around 30 days in nasal and ocular secretions,
urine, cervical fluid, and the aerosol created by sneezing and
coughing. Transmission of virus is oronasal. Recovered ani-
mals may carry virus as a latent infection, becoming shedders
76 INCLUSION BODY RHINITIS
if severely stressed. These carriers then disseminate virus when
mixed with susceptible swine. By both experimental and natural
routes, the porcine cytomegalovirus can sometimes cross the
placenta to infect developing fetuses, which may result in dead or
mummified fetuses, or infected, weak piglets. Infected piglets can
then spread virus to susceptible piglets.
Pathogenesis
The primary site of virus replication is in the nasal mucous
glands, and lachrymal or Harderian glands. Destruction of these
cells results in a marked rhinitis and conjunctivitis, sometimes
accompanied by fibrinopurulent exudates from bacterial coin-
fections. Viremia follows mucosal replication. The virus localizes
in epithelial and endothelial cells at many sites as well as within
macrophages and reticuloendothelial cells, with occasional inclu-
sions visible in affected tissues such as kidney. In fetuses and neo-
nates, capillary endothelium and sinusoids of lymphoid tissue are
infected. Congenitally infected fetuses excrete virus indefinitely.
Bone marrow damage is suspected of causing anemia in neonates.
Widespread damage caused by the virus or secondary infections
can lead to death.
Clinical signs
When disease is expressed, it is usually observed in 1- to 5-week-
old pigs. In suckling pigs, especially pigs less than 3 weeks old,
signs include mucopurulent rhinitis accompanied by violent
sneezing, respiratory distress, conjunctivitis, shivering, and
mouth-breathing. Although unusual, mortality can be high in
pigs born to naïve gilts or sows, or if the inclusion body rhinitis
is complicated by other diseases. Infected neonatal piglets appear
weak, anemic, or stunted, and there may be edema around the
throat and tarsal joints. Signs in older pigs or dams with viremia
may include listlessness and mild anorexia but infection in these
animals is often inapparent. Porcine cytomegalovirus is capable
of causing fetal mummification, stillbirths, neonatal deaths, and
cause failure of piglets to thrive when associated with infection
of naïve, pregnant sows but reproductive manifestations of the
disease appear to be rare.
Lesions
In nursing piglets, the most commonly recognized gross lesion
is production of mucopurulent nasal exudate that can often
partially obstruct the nasal passages. Complications sometimes
include sinusitis, otitis media, or pneumonia. In neonatal pigs,
petechial hemorrhages can be seen on the subcutis, serosal
surfaces, and nasal turbinates, and subcutaneous edema can
occur. Effusions in the thorax, abdomen, and pericardial sac,
and edema of the lungs are often present. Microscopically, baso-
philic intranuclear viral inclusions can usually be found in nasal
mucous glands, Harderian glands, and lachrymal glands of
nursing pigs. They may be present in renal glomeruli and tubu-
lar epithelium, liver, capillary endothelium, choroid plexus,

glial cells, and in various epithelial type cells. Focal gliosis is
common throughout the central nervous system. Inclusions can
sometimes be found at several sites in fetuses.
Diagnosis
The disease is usually diagnosed after finding microscopic, baso-
philic intranuclear inclusions in the tissues of a typical infected
piglet. Where available, polymerase chain reaction can demon-
strate specific viral genetic material in affected tissues. Alterna-
tively, an enzyme-linked immunosorbent assay or an immunoflu-
orescence assay test on serum samples can be used to confirm the
presence of porcine cytomegalovirus in a herd..
DISEASES CAUSED BY VIRUSES
Control
Because the disease is seldom recognized as a cause of severe loss,
control measures are often ignored. Growing pigs are usually pro-
tected from large losses by antibodies provided by their immune
dams. As piglets grow, they are exposed to virus in the environ-
ment and respond by producing their own antibodies.
VIRUSES
Environmental conditions, if poor, should be improved. Herd
immunity via acclimatization of breeding stock is commonly
practiced. There is no known effective treatment or medication.
Antibiotics may be useful to control concurrent diseases or sec-
ondary bacterial infections.
INCLUSION BODY RHINITIS 77
 SWINE DISEASE MANUAL
Influenza
Alternate names and abbreviations
Influenza A virus of swine, IAV-S, influenza A, flu, swine influ-
enza (archaic), SIV (archaic), swine flu (archaic)
Definition
VIRUSES
Influenza A in swine is a rapidly spreading viral disease character-
ized by sudden onset of fever, oculonasal discharge, prostration,
and weakness, followed by paroxysmal coughing over a relatively
short course of 5 to 7 days, and relatively low mortality in uncom-
plicated outbreaks.
Several overlapping systems of nomenclature exist for influenza
viruses. With the complexity of the virus origins and the public
health consequences of nomenclature, use of the terms swine flu,
swine influenza, and SIV is discouraged, because these terms impli-
cate swine as the origin of the virus. For this chapter, we will refer
to the typical viruses that infect swine as “influenza type A viruses
of swine” or IAV-S. The clinical expression of the disease caused by
infection with IAV-S will be referred to as “influenza A.”
Occurrence
In the US, IAV-S is common and widespread. Serological surveys
show that nearly all herds in the US have antibodies to IAV-S.
Influenza A occurs in swine of all ages and is present in most
major swine-raising countries.
Historical information
The first influenza virus to be recognized in pigs was an H1N1
virus known as the classical influenza A virus. Pigs are thought
to have acquired this virus in 1918, at the same time as the severe
Spanish flu pandemic in humans. H1N1 viruses circulated in
both species after this time but diverged genetically in the two
host populations.
In 2009, a novel H1N1 virus emerged in human populations. It
contained genetic components from swine, avian, and human
influenza viruses. This virus caused a human pandemic from
2009 to 2010, and then became established as a seasonal human
influenza virus. It is currently the predominant H1N1 virus cir-
culating in people and has been found sporadically in pigs since
its emergence.
While influenza A has always been a significant public health
concern, the emergence of the pandemic H1N1 strain in 2009
has resulted in increased research on the disease and coordinated
surveillance activities among veterinary, public health, and wild-
life sectors. There is clear evidence of interspecies transmission
of influenza viruses among swine, chickens, ducks, turkeys, wild
birds, equines, companion animals, and people. When concur-
rent infection with more than one virus occurs in any of the spe-
cies, the potential for genetic reassortment between the viruses
occurs which can result in development of new viral strains (ie,
genetic shift).
78 INFLUENZA
Etiology
Influenza viruses (eg, IAV-S) belong to the species Influenza A
virus, genus Influenzavirus A, and family Orthomyxoviridae.
Serological and virological evidence indicates that influenza B
and C viruses from humans can occasionally infect pigs but this
appears to be rare and not often associated with significant clin-
ical signs. A novel cattle-associated influenza C-like virus, with
the proposed designation “influenza D” has been found in some
pigs with respiratory signs, although pigs are not thought to be
reservoir hosts.
Influenza A viruses have glycoprotein “spikes” on their surface
that act as major surface antigens. There are at least 16 hemag-
glutinin (H) and 9 neuraminidase (N) surface glycoproteins that
are numbered to help identify virus strains. Influenza A viruses
are very diverse and two viruses that share H and N types may
not be closely related. This high variability is the result of two
processes: mutation and genetic reassortment. Mutations cause
gradual changes in the H or N proteins of the virus, a process
called antigenic drift. Genetic reassortment can cause more rapid
changes. The influenza A genome consists of 8 individual gene
segments; when two different viruses infect the same cell, gene
segments from both viruses may be packaged into a single, new
virus. An important aspect of reassortment is that it can generate
viruses containing either a new H, a new N, or both. Such abrupt
changes are called antigenic shifts. There is often poor cross-pro-
tection between IAV-S subtypes because of the considerable
genetic and antigenic variation among IAV-S viruses.
The classic subtype in swine, H1N1, has been the predominant
subtype in swine in the US since 1918. H3N2 viruses acquired
from humans were also detected during this period. However,
they did not become established as stable, widespread lineages
in pigs until more recently. Around 1998, “triple reassortant”
H3N2 viruses first emerged in North America and soon spread
to other regions. These viruses contain H and N proteins derived
from human influenza viruses, and internal proteins from
the classical influenza A virus, an avian influenza virus, and a
human influenza virus. The particular combination of internal
genes carried by these viruses is known as the triple reassortant
internal gene (TRIG) cassette. Viruses that contain this cassette
seem to be prone to increased antigenic drift. They also seem to
readily acquire new H and N genes, which has resulted in new
TRIG-containing viruses with various combinations of H1, H3,
N1, or N2 from additional human influenza viruses, and/or H1
and N1 from the classical influenza A virus.
Epidemiology
In pigs, influenza viruses are transmitted in droplets and aerosols
created by coughing and sneezing, and by contact with nasal dis-
charges, either directly or on fomites. Viremia is not a feature and
there is no evidence that transplacental transmission of influenza

A viruses occurs in pigs. Asymptomatic carrier status was not
thought to occur, but recent evidence from persistent outbreaks
in herds not having any known ongoing risk of exposure is
changing the conventional thinking on the topic. The presence of
antibody (maternal or active) will mitigate the severity of disease
and influence the rapidity of spread through a population. Thus,
influenza A can become an endemic disease in populations that
use continuous pig flows.
Virus shedding can begin within 1 to 3 days after a pig becomes
infected and typically continues for 4 to 10 days. There is some
evidence that aerosol transmission might be possible, at least
within densely populated pig barns and possibly over longer
distances in swine-dense regions. Influenza A viruses of swine
have been isolated from air samples inside barns and immediately
outside exhaust fans.
Both human-to-pig and pig-to-human transmission of IAV-S
viruses have been documented to occur. As a result of increased
surveillance since the 2009 pandemic, transmission events
between pigs and people at livestock exhibitions are detected by
public health systems most years in the US.
Influenza A virus probably does not survive more than 2 weeks
outside the host and can be inactivated by many disinfectants.
Pathogenesis
The IAV-S virus gains access by the nasopharyngeal route with
receptor-mediated entry into respiratory epithelium, where it
causes inflammation with widespread degeneration and necro-
sis of cells lining bronchi and bronchioles. Also, virus can be
demonstrated in interalveolar septa, sometimes in turbinate
epithelium, and in mediastinal lymph nodes. In the lung, alveolar
type 2 pneumocytes are affected and produce less surfactant. This
impairs phagocytosis of secondary microorganisms by alveolar
macrophages. Epithelial necrosis compromises the mucociliary
escalator, compromising the removal of cellular debris and bacte-
ria. The inflammatory exudates in the smaller airways sometimes
block them, leading to atelectasis, emphysema, and bronchoint-
erstitial pneumonia. In most cases, epithelial damage is repaired,
and the lesions resolve in 7 to 10 days if the infection is uncom-
plicated. The severity of the effect of infection is mitigated by the
quantity of homologous circulating antibody (maternal or active).
Most of the mortality associated with IAV-S virus infection is the
result of secondary bacterial infections or concurrent infections
with other primary agents of pneumonia.
Clinical signs
In a typical outbreak, there is a sudden onset of a marked respira-
tory illness affecting most pigs in the herd. Depending on the herd,
clinical signs may be seen only in certain age groups, while other
animals remain asymptomatic. The clinical signs may include fever,
lethargy, anorexia, weight loss, coughing, sneezing, nasal and ocular
discharge, conjunctivitis, and labored breathing (“thumping”), but
all of these signs do not occur in all infected animals. The cough
DISEASES CAUSED BY VIRUSES
usually develops after a few days, at which time the fever has often
started to diminish. Recovery begins about the sixth day and the
herd is largely recovered in 1 to 2 weeks. Morbidity is high; mor-
tality is low in most uncomplicated outbreaks.
Uncomplicated influenza A usually causes little death loss, but
losses of weight and body condition can be significant, as can
the cost of medication and an increase in the incidence of gastric
VIRUSES
ulcers. Concurrent infections with other respiratory diseases can
greatly increase mortality and culls.
Reproductive problems occasionally associated with IAV-S are
likely incidental to the systemic effects of acute illness experi-
enced by sows. Acute illness during pregnancy may result in abor-
tion and, sometimes, small, weak litters.
Lesions
The gross lesions include lobular distribution of congestion,
firmness, atelectasis, emphysema, and perhaps pneumonia. Gross
lesions are often restricted to the apical and cardiac lobes but may
affect entire lungs. Areas of atelectasis are irregular, darkened, and
firm. Lesions often appear as distinct, scattered lobules. Airways
may contain blood-tinged exudate. Regional lymph nodes are
moderately enlarged. Microscopic lesions include degeneration and
necrosis of portions of airway epithelium and obstruction of air-
ways with exudate. There may be bronchointerstitial pneumonia.
Marked edema and congestion of the entire lung may be present in
severe cases. Necrotizing bronchiolitis is highly suggestive of IAV-S.
Diagnosis
A history of sudden onset of a severe respiratory illness in many
animals, along with typical signs and lesions, is often adequate
for a field diagnosis. It is useful to confirm the diagnosis since
the disease may reappear and go unrecognized in a less typical,
subacute form.
Confirmation of the diagnosis can be made in several ways, but
detection of the virus or its components is most successful from
acutely affected (febrile) pigs. The virus can be identified by
fluorescent antibody test on fresh lung sections or by immunohis-
tochemistry staining on formalin-fixed lung sections from acutely
affected, euthanized pigs. A polymerase chain reaction (PCR)
test is often used to detect virus in nasal swabs or lungs and has
the advantage that the subtype can be immediately determined,
and the product can be sequenced for epidemiologic purposes.
The IAV-S virus can be isolated from nasal swabs or lung tissue
in chick embryos. There are commercially available influenza A
antigen detection kits that can be used to detect IAV-S on nasal
swabs. Hemagglutination inhibition (HI) assays have been used
to evaluate titer levels but knowledge of the virus subtype respon-
sible for the infection is required for accurate test results. In some
cases, paired serum samples taken early and late in an outbreak
can be used to demonstrate a rising serotype-specific antibody
titer to IAV-S. Serological testing is complicated by the fact that
INFLUENZA 79
 SWINE DISEASE MANUAL
several subtypes of IAV-S can be present in a group of pigs and
most serological tests do not sufficiently cross-react to detect anti-
bodies of all IAV-S subtypes.
Because there are multiple subtypes of IAV-S in swine popula-
tions, mere detection of IAV-S is not sufficient to warrant imple-
mentation of specific control strategies. The offending IAV-S can
be subtyped by some laboratories using PCR genetic sequencing
VIRUSES
or serological methods (HI assays with multiple virus subtypes).
This allows for more accurate vaccine selection and application.
It is quite common to have other viral, bacterial, mycoplasmal,
and parasitic diseases in association with IAV-S, especially in out-
breaks with considerable mortality.
Reproductive failure associated with influenza is due to the
effects of acute disease in sows. The virus cannot be detected in
aborted fetuses but can be detected in acutely affected, febrile
sows. Serology is not a reliable method of diagnosis of reproduc-
tive failure since most sow herds will be serologically positive
from previous exposure to the agent.
Control
There are no specific therapeutics for IAV-S infection. Often,
antimicrobials are used to control or prevent secondary bacterial
infections. Aspirin or other anti-inflammatory agents may offer
relief to severely affected pigs. Treatment should emphasize pro-
viding a comfortable environment and ready access to fresh feed
and water.
Prevention has depended largely on maintaining a closed herd
to avoid introducing infected pigs. Inactivated vaccines are
widely used in Europe and the US. Several types of commercial
vaccines are available and autogenous products are commonly
80 INFLUENZA
used. Directions provided with the vaccine should be followed
carefully. Cross-protection between subtypes should not be
expected in most situations.
In modern production system units, control of influenza A in
recently weaned pigs usually requires stabilization of the breeding
herd by acclimatization or vaccination. Vaccination prior to far-
rowing to stimulate colostral protection for the young piglets is
sometimes practiced. New additions to the breeding herd should
be vaccinated during their isolation period.
Successful control of influenza A in the grow-finish phase of
known IAV-S positive herds can be difficult. Nursery pigs can be
vaccinated prior to moving them to the finisher. However, mater-
nal antibody interference with vaccination is a major concern in
timing of vaccination since antibody levels are highly variable in
populations and even low levels of antibody may interfere with
immune response. There is little cross-protection between sub-
types, making vaccine selection challenging. Often, the offending
virus must be subtyped to aid in selection of the correct antigen.
On infected premises, all-in, all-out pig flow with cleaning and
disinfection of facilities between groups helps prevent virus
carryover, as does vaccination of the breeding herd to stabilize
the infection to prevent virus transmission to offspring. Depopu-
lation of continuous flow nurseries or finishers may be necessary
to stop virus circulation. Implementing consistent and effective
control strategies for other respiratory insults that may be con-
currently present in the herd (eg, bacteria, viruses, parasites, air
quality, and poor ventilation) can also decrease the severity of
IAV-S outbreaks.

Japanese encephalitis
Alternate names and abbreviations
JE, JEV, Japanese B encephalitis (archaic)
Definition
Japanese encephalitis is a mosquito-borne disease affecting many
animals, including wild birds, horses, swine, and people. In swine,
the only evidence of disease may be reproductive failure. Japanese
encephalitis is one of the most prevalent causes of encephalitis in
humans in Asia; pigs are an important amplifying host for the virus
in areas where people, pigs, and the mosquito vector overlap.
Occurrence
Japanese encephalitis occurs in most domestic animals and also
in wild birds, reptiles, perhaps chickens, and people. Swine can
be infected, and all ages are susceptible. Major epidemics have
occurred in horses, donkeys, and people.
Japanese encephalitis is confined largely to southeastern Asia,
Indonesia, and major Pacific islands. At least 20 countries have
reported occurrence of the disease. In many locales, epidemics
correlate with the mosquito season.
Historical information
Japanese encephalitis was first described in 1933. Major epi-
demics in people have been reported from India, Japan, Korea,
and Nepal. The disease has not been reported in the western
hemisphere, although the range seems to be increasing due to
the expanding range of suitable mosquito vectors. Abortion
in women and encephalitis in children are caused by Japanese
encephalitis and the virus is recognized as an important zoonosis.
Etiology
Japanese encephalitis virus is an arbovirus, meaning it is transmit-
ted to mammalian hosts through an arthropod vector. The virus
is a member of the genus Flavivirus and family Flaviviridae and is
related to other zoonotic arboviruses including West Nile virus,
Murray Valley encephalitis virus, and St Louis encephalitis virus.
It does not persist in the environment and is easily inactivated by
many disinfectants.
Epidemiology
Mosquitoes become infected by feeding on viremic hosts: usually
pigs, horses and other equids, and birds. The virus is then trans-
mitted through the mosquitoes’ saliva when they subsequently
feed on uninfected people or animals. The virus is transmitted
mainly by mosquitoes of the genus Culex, although some Aedes
and Anopheles can also act as vectors; the virus can be transmitted
transovarially in some species of mosquitoes.
DISEASES CAUSED BY VIRUSES
Although humans and most domesticated animals can develop
clinical signs after becoming infected with Japanese encephalitis
virus, they are considered to be incidental hosts as they typically
produce low levels of viremia and are not thought to be signifi-
cant in further virus transmission. In contrast, birds and pigs can
VIRUSES
amplify Japanese encephalitis virus and are therefore important
in the epidemiology of transmission of the virus. Domesticated
pigs are considered to be particularly efficient amplifying hosts, as
large numbers of susceptible young swine are produced each year,
often in close proximity to people. In addition, boars are report-
edly able to transmit the virus in semen.
Pathogenesis
After an incubation period of around 3 days, infected pigs remain
viremic for several days. In porcine fetuses, the virus often causes
the development of anomalies in the brain as well as encephalitis
and degenerative neuronal changes.
Transplacental infection in swine sometimes occurs. The effect
of the virus depends on whether the fetuses are immunologically
competent. When dams are infected between 40 to 60 days in
gestation, fetuses are often killed, and some are mummified.
There may be no effect on fetuses if dams are 85 or more days in
gestation. Fetal deaths are believed to be caused by destruction of
vital stem cells.
Clinical signs
Mature swine seldom show signs of infection other than those of
reproductive failure. Signs may occur in fetuses or piglets if their
dam was infected during pregnancy. Signs include stillborn and
mummified fetuses or weak pigs that may have signs of central
nervous system disease. Subcutaneous edema and hydrocephalus
may be present in stillborn pigs. Abortions seldom occur. Infected
boars may have orchitis, reduced libido, and disturbance of sper-
matogenesis. Young, susceptible pigs occasionally contract Japanese
encephalitis and show signs of central nervous system lesions.
Lesions
Gross lesions in stillborn or infected neonatal piglets include
hydrocephalus, subcutaneous edema, ascites, hydrothorax, hem-
orrhages on serous membranes, congestion of lymph nodes, and
necrotic foci in the liver and spleen. Other lesions may include
congested meninges, hypoplastic areas in the cerebral cortex,
hypoplasia of the cerebellum, or spinal hypomyelinogenesis.
Histologically, in infected fetuses or piglets there is diffuse
nonsuppurative encephalitis and neuronal degeneration and
necrosis in the cerebrum and cerebellum. In mature boars, there is
excessive fluid in the tunica vaginalis, orchitis, epididymitis, and
degenerative changes in seminiferous epithelium.
JAPANESE ENCEPHALITIS 81
 SWINE DISEASE MANUAL

Diagnosis
A definitive diagnosis is often based on isolation and identifica-
tion of the virus from fetuses or infected piglets. Virus is usually
isolated from brain extracts inoculated into suckling mice or cell
cultures. Virus can be identified by neutralization tests in suckling
mice or cell culture. Alternatively, viral antigen in tissues from
infected fetuses or stillborn pigs can be identified by fluorescent
VIRUSES
Control
It may be possible to break the cycle of infection by controlling
mosquito populations, but this is often impractical. The disease
can be controlled by vaccinating the breeding stock; vaccines are
common in parts of Asia. Young gilts and boars are vaccinated
twice at 2- to 3-week intervals prior to the mosquito season.
Growing pigs are also vaccinated in endemic areas.

antibody or immunohistochemistry staining of formalin-fixed

tissues. In suspected outbreaks, serial serum samples from pigs
sometimes are used to show a rising titer against Japanese enceph-
alitis virus. Serological tests that reveal antibody in fetuses are also
useful in diagnosis. Polymerase chain reaction assays have been
developed to identify the virus in tissues and serum.

82 JAPANESE ENCEPHALITIS

Parvovirus
Alternate names and abbreviations
PPV, parvo, SMEDI (stillbirth, mummification, embryonic
death, and infertility)
Definition
Porcine parvovirus can cause reproductive failure in naïve dams. It
is characterized by the occurrence of large numbers of mummified
fetuses, an increase in the number of returns to estrus, small litters,
failures to farrow, decreased farrowing rate, and, rarely, abortion.
Many manifestations of reproductive failure seen with porcine
parvovirus accompany other reproductive diseases of swine. The
many manifestations of reproductive failure should not be con-
sidered pathognomonic for porcine parvovirus.
Occurrence
Porcine parvoviral infection is endemic in most swine herds. It is
usually subclinical and is a very common infection. Prior to the
emergence of porcine reproductive and respiratory syndrome
(PRRS), porcine parvovirus was probably the most commonly
diagnosed infectious cause of reproductive failure in swine. Repro-
ductive failure is much more likely to occur in gilts than in sows,
since lifelong immunity is induced after active infection. Porcine
parvovirus occurs worldwide in major swine-raising countries.
Historical information
The earliest publication about porcine parvovirus occurred in
1965, when the agent was identified as a cell-culture contami-
nant. Further investigation over the next decade confirmed por-
cine parvovirus as a major cause of reproductive failure in pigs. To
this day, vaccines developed during that period remain effective at
preventing losses from porcine parvovirus.
Etiology
Porcine parvovirus is a single-stranded DNA virus. The strain of
porcine parvovirus typically identified in cases of reproductive
failure is the serotype designated as porcine parvovirus 1. All por-
cine parvovirus 1 isolates are similar antigenically. At least 6 other
parvoviruses have been detected in swine (porcine parvovirus 2,
3, 4, 5, 6, and 7), as well as a closely related virus called porcine
bocavirus. However, none of these appear to be pathogenic in
swine and they are therefore considered to be commensals. Por-
cine parvovirus is quite resistant to environmental degradation
and many disinfectants; it can persist for at least 4 months on
contaminated premises. Porcine parvovirus hemagglutinates
many kinds of erythrocytes, a feature useful in its laboratory iden-
tification. Porcine parvovirus does not cause diarrhea in swine
although related parvoviruses do so in several other species.
Epidemiology
Parvoviral infection is endemic in most swine herds. Following
infection, virus is shed in the secretions and excretions from
the animal for approximately 2 weeks. An infected dam will
DISEASES CAUSED BY VIRUSES
disseminate virus in feces and fluids, including placental fluids
and mummified fetuses. Fetuses infected during gestation can be
born as infected immunotolerant piglets that can pass the virus
intermittently or continuously, but the significance or likelihood
of this phenomenon is unknown. Because parvovirus is quite
VIRUSES
resistant to environmental influences, contaminated facilities are
an important source of ongoing exposure.
Oronasal transmission can occur among susceptible swine of all
ages. However, serological surveys show that many herds with
endemic infection contain at least some animals that are suscepti-
ble. Transplacental infection of embryos and fetuses is the result of
dams failing to develop an active systemic immunity prior to preg-
nancy. Passive immunity persists in some gilts beyond the time they
are old enough to be bred and this maternal antibody can interfere
with their development of an active immune response to natural
or vaccine exposure. Active immunity usually develops following
exposure of gilts to parvovirus in the environment as passive immu-
nity wanes. Gilts with little or no immunity can become infected
during their first pregnancy. If infected during pregnancy, virus may
cross the placenta and infect some or all of their embryos or fetuses.
Porcine parvovirus can be found in semen of naturally infected
boars, hence it can likely be transmitted mechanically through nat-
ural breeding or artificial insemination.
Pathogenesis
Only porcine parvovirus 1 is known to cause reproductive failure
or disease. Pregnant, infected dams develop a viremia during the
acute phase of porcine parvovirus 1 infection. Virus then may
cross some or all of the separate placentas of developing embryos
or fetuses. Fetal infection during the first 35 days of gestation
causes death and resorption of embryos, resulting in irregular
returns to estrus or reduced litter size. Infection between 35 and
70 days of gestation results in fetal death and mummification.
Since fetuses become immunologically competent by about the
70th day of gestation, fetuses older than that may successfully
resist the effects of becoming infected and survive to full term.
After one embryo or young fetus is infected, the virus may slowly
spread through the uterus and infect some or all of the others.
The direct effect of porcine parvovirus 1 on the uterus may also
contribute to reproductive failure.
The death of embryos and fetuses is attributed to the direct
destructive effect of porcine parvovirus on their organs and tis-
sues. Many kinds of cells are affected, especially mitotically active
capillary endothelium and neurons. Extensive endothelial cell
damage may be reflected in damage to many organs.
Clinical signs
In most swine, a transient leukopenia occurs within 10 days of
infection with porcine parvovirus 1. However, this and any other
PARVOVIRUS 83
 SWINE DISEASE MANUAL
indication of infection are inapparent in all swine except develop-
ing fetuses. Infection of a naïve herd of pregnant females results
in irregular return of bred animals to estrus, increased numbers
of mummified fetuses, smaller litter sizes, increases in animals
checked positive for pregnancy that fail to farrow, and prolonged
gestation lengths. The increase in mummified fetuses after a
normal gestation period is the hallmark of porcine parvovirus 1.
VIRUSES
Abortions attributable to this virus are rare.
Lesions
Gross lesions are not apparent in the dams. The most important
gross observation with porcine parvovirus 1 infection is mum-
mified fetuses. In experimentally infected dams, nonspecific
microscopic and gross lesions are described but are not often of
diagnostic value.
Diagnosis
The lack of illness in the dams, coupled with increased mummies,
irregular return to estrus, decreased litter size, or pseudopregnancy
occurring primarily in gilts is suggestive of porcine parvovirus 1
infection. A presumptive diagnosis can be confirmed by demon-
strating porcine parvovirus 1 antigen in the tissues (lungs, hearts,
and thoracic fluids) of several truly mummified (died before 70
days of gestation showing severe in utero dehydration) fetuses using
polymerase chain reaction or immunofluorescent antibody (IFA)
testing. The preferred specimen for diagnosis by IFA testing is the
lung tissue from several mummified fetuses less than 16 cm long.
Larger fetuses are not satisfactory since their tissues may contain
antibody that interferes with the procedure.
Sometimes antibody can be demonstrated in fluids or sera from
stillborn pigs or from pre-suckle neonatal live pigs. While this may
be an indirect indication of intrauterine infection with porcine par-
vovirus 1, there is considerable likelihood of false positive serologi-
cal reaction from these specimens. Serology from breeding animals
84 PARVOVIRUS
may be difficult to interpret since cross-sectional sampling will
often reveal a wide range of titers. Demonstration of serocon-
version in many gilts and sows with paired serology may be used
for a positive diagnosis but acute samples are often not available.
Conversely, the absence of titers may aid in exclusion of porcine
parvovirus 1 as the cause. If mummies are not available for evalua-
tion, efforts should concentrate on gilt serology, comparing titers
from unmated gilts to those exhibiting signs of infertility. There
are likely other viruses that can infect unborn fetuses, particularly
in litters of naïve pregnant gilts; some of these may be present
concurrently with porcine parvovirus 1 and should be considered
as differentials. Examples include PRRS, porcine circovirus type
2, porcine circovirus type 3, members of Picornaviridae (enterovi-
ruses, Teschovirus, Sapelovirus), and Astrovirus, among others.
Control
There is no effective treatment for porcine parvovirus infection.
Probably the best way to prevent porcine parvovirus infection is
to vaccinate all susceptible breeding stock twice at 2- to 3-week
intervals with the second dose administered at least 3 weeks before
breeding. Killed vaccines are available and effective. Pre-breeding
boosters are recommended in herds of unknown status. Vacci-
nation of susceptible breeding stock lacking maternal antibody
should stimulate an active immunity that will protect the devel-
oping fetuses. It is important to note that virus circulation within
a population cannot be completely prevented by vaccination. The
virus will continue to circulate in the face of vaccination programs;
hence eradication is not likely and continued vaccination should be
an ongoing part of the herd vaccination program.
Another control alternative is to expose seronegative stock to
animals or environmental materials from seropositive older stock.
In this situation, animals should be used for breeding only after
demonstrated seroconversion.

Porcine circovirus associated diseases
Alternate names and abbreviations
Porcine circovirus disease, PCVD, PCVAD, postweaning multisys-
temic wasting syndrome, PMWS, porcine dermatitis and nephrop-
athy syndrome, PDNS, circovirus, circo, PCV, PCV2, PCV3
Definition
Porcine circovirus is a common virus of pigs, found throughout
the world. It was originally described as an adventitious virus of
porcine tissue culture cells (now known to be porcine circovirus
type 1). The detection and emergence of a novel porcine circo-
virus (porcine circovirus type 2; PCV2) in the 1990s coincided
with the occurrence of new clinical syndromes in swine referred
to as postweaning multisystemic wasting syndrome or porcine
circovirus associated disease. Since its appearance, PCV2 and
disease associated with its presence has become widely distributed
in most developed swine industries around the world. The term
porcine circovirus associated disease (PCVAD) is now used in
North America to refer to the different disease manifestations
associated with PCV2. In Europe, the term porcine circovirus
disease (PCVD) is used preferentially to the US term PCVAD.
Circoviruses are also thought to be one of the causes of an
immune-mediated condition called porcine dermatitis and
nephropathy syndrome (PDNS) in swine.
Recently, another type of circovirus, porcine circovirus type 3
(PCV3), has been detected in swine herds around the world.
Fetal deaths, porcine dermatitis and nephropathy syndrome, and
systemic post-natal infections have recently been associated with
the presence of this virus; definitive studies of causation, patho-
genesis, and immunity are in progress.
Occurrence
Infections and disease associated with PCV2 are reported
from nearly every country with a significant commercial swine
industry. Porcine circovirus type 2 is strongly associated with
the occurrence of postweaning multisystemic wasting syndrome,
porcine circovirus associated disease, porcine respiratory disease
complex, and is occasionally associated with reproductive failure.
The number of reported cases of porcine circovirus associated
disease increased dramatically in the first decade of this century.
Porcine circovirus associated disease is widespread in Asia,
Europe, and the US, and has been reported from virtually all
swine-producing areas of the world. As an apparent immune-me-
diated sequel to viral infection, PDNS is sporadically reported
associated with circovirus infections.
Fetal infections with PCV2 and PCV3 may be inapparent or can
be associated with reproductive failure, fetal deaths, mummifica-
tion, or abortion. Both viruses are common in swine populations,
and other viral agents or risk factors for reproductive failure are
frequently present, so disease associations with PCV2 and PCV3
are sometimes difficult to prove.
DISEASES CAUSED BY VIRUSES
Historical information
Circoviruses infect other species of mammals and avians. They
cause psittacine beak and feather disease in chickens as well as
lethal infections in pigeons, canaries, and finches. Porcine circovi-
VIRUSES
rus type 2 infection of pigs was reported in North America starting
around 1994. Over the next decade, similar outbreaks occurred in
Europe and most swine-rearing areas of the world and were consis-
tently associated with PCV2 infection. Genomic sequencing and
restriction fragment length polymorphism techniques have defined
several distinct genotypes within PCV2, but the clinical relevance
of these distinctions has not been demonstrated.
In 2016, PCV3 emerged and has been increasingly detected in
swine, sometimes associated with cases of PDNS, fetal infection,
or postnatal systemic insult.
Etiology
Circovirus is a non-enveloped, single-stranded DNA virus unique
for its small size (approximately 1800 bp), circular genome, and
hardiness within the environment. Circovirus is sensitive to most
disinfectants, but chlorhexidine, ethanol, and iodine tend to be less
effective than other commercial products. Three types of PCV have
been described in swine: porcine circovirus types 1, 2 and 3.
Multiple genotypes of PCV2 have been described (eg, PCV2a,
PCV2b, PCV2c, PCV2d, and PCV2e). The prevalence of each
genotype has varied over time, but all are considered to be of the
same type and there is little evidence to suggest significant differ-
ences in pathogenicity, antigenicity, or cross-protection between
these genotypes.
Recently characterized PCV3 appears to have distinct genetic and
antigenic differences from PCV2, but the clinical and epidemiolog-
ical significance of these differences is unknown at this time.
Epidemiology
Only swine are known to be susceptible to PCV 2 or 3 infection.
Globally, nearly all commercial swine herds are seropositive for
PCV2. Seroconversion usually occurs by 2 to 4 months of age,
irrespective of whether clinical signs of porcine circovirus asso-
ciated disease are observed. Preliminary studies suggest PCV3 is
detectable in a high percentage of herds globally as well. Oronasal
transmission through direct contact is the most likely and the
most efficient mode of transmission. Porcine circovirus type 2
or type 3 is found in most secretions and can persist for weeks in
contaminated organic matter. Experimentally, infection of preg-
nant susceptible dams with PCV2 can result in transplacental
infection of fetuses and fetal deaths or long-term virus carriers
within survivors; PCV3 can be expected to behave similarly.
PORCINE CIRCOVIRUS ASSOCIATED DISEASES 85
 SWINE DISEASE MANUAL
Pathogenesis
Pigs infected with PCV2 develop viremia of variable duration,
with replication and persistence most extensive in macrophages
and monocytes of lymphoid organs and lung, and in epithelial
cells in various organs. Characteristic microscopic lesions include
lymphoid depletion at multiple sites, chronic lymphohistiocytic
to granulomatous inflammation, and an erosive bronchiolitis
VIRUSES
with fibrosis.
Reproduction of typical lesions by inoculation with PCV2 has
been inconsistent, but there is general agreement that PCV2 is
a necessary (although perhaps not sufficient) cause of porcine
multisystemic wasting syndrome and porcine circovirus associated
disease expression. Mechanisms that allow disease expression and/
or immunity remain obscure but are related to macrophage activa-
tion with compromised antigen processing and presentation thus
thwarting an effective immune response. Studies demonstrate that
PCV2 infections have immunosuppressive characteristics, which
can exacerbate the impact of other pathogens in a herd. The role of
PCV 2 or 3 in occurrence of PDNS, and the circumstances under
which that syndrome is expressed, is even less clear. The blotchy
purple skin lesions and nephropathy of this syndrome are suspected
to be an immune-mediated sequel to viral infection and are not
necessarily specific for either PCV 2 or 3 infections.
Clinical signs
Subclinical infections are common, as many herds are infected
with PCV 2 or 3 with no apparent clinical signs. When disease
occurs, multiple body systems can be affected, with considerable
variation in morbidity and mortality. Few infectious agents have
more variation in signs, tissues affected, or in individual and herd
impact than PCV2.
The effects of porcine circovirus associated disease in growing
pigs varies from severe disease with high mortality to only mild
clinical disease. Disease is now usually referred to simply as differ-
ent expressions of porcine circovirus associated disease.
In severe forms of the disease, pigs between 2 and 4 months of
age sicken and rapidly waste away while cohorts seem to grow
normally. Morbidity varies from 2% to 30% but case fatality can
be high, approaching 80% in unvaccinated herds. The severity of
clinical signs varies between individuals and includes gradual or
rapid wasting, unthriftiness, rough hair coat, polypnea, dyspnea,
pallor, diarrhea, and occasionally icterus. Many affected pigs and
clinical survivors are severely stunted. Less affected pigs continue
to grow but contribute to variation in production efficiencies and
market weights, whereas non-clinical pigs in the same groups per-
form quite well. Both signs and lesions vary considerably among
affected herds. Because clinical signs are not specific, a diagnosis
of porcine circovirus associated disease requires compatible
lesions and demonstrable PCV2 within typical lesions.
Porcine dermatitis and nephropathy syndrome is suspected of
being a sequel to infection by one of several different viruses,
86 PORCINE CIRCOVIRUS ASSOCIATED DISEASES
including PCV 2 or 3. In this condition, individual pigs, usually
from 8 to 18 weeks of age, develop small red-purple blotches on
the skin, sometimes slightly raised, and most obvious on the hind
legs and perineum. Focal lesions can expand and coalesce, extend
over the abdomen, and eventually cover the whole body. Most
pigs with PDNS eventually die.
Clinical signs of transplacental infections with PCV 2 or 3 mimic
those of other viruses which cause in utero death of fetuses less
than 70 days gestation (eg, porcine parvovirus). This is usually
manifested as increases in mummies, small litters, sows that fail
to farrow with overall decreased farrowing rate or litter size, with
occasional abortions also reported.
Lesions
Gross lesions of porcine circovirus associated disease may include
pallor, marked enlargement of all lymph nodes and perhaps
spleen, interstitial pattern of pneumonia in lungs, and occasion-
ally multiple foci of pallor within swollen kidneys. Less often
present are icterus, a fluid-filled intestine, atrophy of the liver,
and ulceration of the pars esophagea of the stomach. Microscopy
reveals depletion of germinal centers in lymphoid tissues with
replacement by histiocytes and multinucleated giant cells. Baso-
philic intracytoplasmic inclusion bodies can sometimes be seen in
macrophages in lymph nodes, tonsils, spleen, and Peyer’s patches.
Lymphohistiocytic to granulomatous inflammation can be pres-
ent in any organ, typically lungs and/or lymphoid tissues, and
PCV2 antigen is abundantly present within characteristic lesions
when examined by immunohistochemistry or in situ hybridiza-
tion assays. Erosive bronchiolitis and fibrosis of airways are also a
common finding.
With PDNS, there are small, circumscribed circular to irreg-
ular, deep-purple discolorations of skin that become apparent
on the hindquarters, perineum, and flanks. Over the course of
several days, the skin discolorations either resolve or expand and
coalesce. Kidneys are usually swollen with foci of pallor and/
or hemorrhage in parenchyma. Microscopically, there is non-
suppurative vasculitis in the affected areas of the skin. Kidneys
often have swollen glomerular tufts, inflammation, and protein in
tubules. Multifocal nonsuppurative interstitial nephritis can also
be a feature. The lesions are thought to be due to immune-me-
diated (immune complex) vasculitis. Lesions of PDNS are not
specific for porcine circovirus.
Diagnosis
Diagnosis of porcine circovirus associated disease is based on
clinical features and gross lesions and confirmed by finding typi-
cal microscopic lesions and demonstrating PCV2 within lesions.
Microscopic lesions are quite characteristic and virus inclusion
bodies can sometimes be identified in depleted lymph nodes,
spleen, tonsils, or Peyer’s patches. Polymerase chain reaction
(PCR) will confirm the presence of virus but does not confirm
the presence of disease. However, demonstration of high virus

load with quantitative PCR techniques along with typical signs
and lesions can implicate PCV2 in the disease process. Similarly,
isolation and identification of PCV2 is not useful for diagnosis
since asymptomatic infection is widespread in swine populations.
Serological testing for PCV2 has been developed to confirm
infection but finding antibodies to circovirus in the herd is not
diagnostic for disease, since most herds are positive without
discernible disease. Porcine circovirus associated disease must be
differentiated from other bacterial or viral diseases, especially por-
cine reproductive and respiratory syndrome (PRRS), which has
similarities in clinical signs and lesions. Concurrent coinfections
and diseases are common.
Diagnosis of PDNS is by observing typical clinical signs, gross
lesions, and by histopathology. Demonstration of PCV 2 or 3
antigen in the lesions is not consistent.
In cases where reproductive failure (evidenced by mummification,
low farrowing rate, stillbirths, and abortions) is due to infection
with PCV2, the virus should be demonstrable in fetal hearts as
well as other tissues.
Porcine circovirus type 2 can contribute to porcine respiratory
disease complex in some herds. Experimental coinfection stud-
ies as well as anecdotal evidence suggest that PCV2 is likely
to increase the severity of pneumonia caused by Mycoplasma
hyopneumoniae, influenza A virus of swine, PRRS virus, and
others. In addition, many, but not all, field cases of PCVAD have
concurrent viral infections or some other evidence of immune
stimulation that seems to allow replication and pathologic
effects of PCV2 in swine. Risk factors and coinfections should
be thoroughly investigated. Herds that are endemically infected
with other significant pathogens, are operated on a continuous
flow basis, are in swine dense areas, or practice poor biosecurity
have been shown to be more likely to experience an outbreak of
porcine circovirus associated disease.
At the present, PCV3 diagnosis relies on detection and identifica-
tion of the virus by PCR or genomic sequencing.
DISEASES CAUSED BY VIRUSES
Control
There is no specific treatment for pigs infected with PCV type 2
or type 3. Anti-inflammatory agents and/or antimicrobials are
sometimes used in groups of pigs experiencing outbreaks of por-
cine circovirus associated disease to assist in managing secondary
infections. The use of all-in, all-out pig flow, thorough cleaning
and disinfection between batches of pigs, and early segregation
VIRUSES
and euthanasia of severely affected pigs are measures that may
help control the disease.
Vaccines that were developed for PCV2 shortly after the virus
emerged do not prevent infection but are efficacious in prevent-
ing most clinical signs of PCVAD. The timing of vaccination
and the selection of the appropriate population to be immunized
(ie, breeding herds, replacement stock, neonatal pigs, or growing
pigs) vary between farms, depending on the characteristics of
the affected populations and the physical layout of the farm. It is
common to vaccinate gilts at the time of selection or before first
breeding. Ongoing vaccination of sow herds is not consistently
practiced. However, booster vaccination of sow herds may be war-
ranted when the virus is determined to be circulating in gestating
animals or suckling piglets despite having a vaccination program
in place. Vaccination of offspring is usually performed at weaning,
perhaps followed by booster vaccination at least 3 weeks later.
Although a few studies have shown that that PCV2 can be eradi-
cated from an affected farm by total depopulation, the ubiquitous
nature of the virus makes it unlikely that commercial farms can
be maintained free of the virus over time. Until the epidemiology,
transmission, and virulence factors relating to PCV2 are further
understood, the use of total depopulation as a control strategy is
not recommended.
Porcine circovirus type 2 and type 3 have been identified in the
semen of acutely affected boars. However, the role of semen as
a source of these infections on sow farms remains unknown.
Booster vaccination of boars prior to entry into boar studs is
probably warranted.
Currently, there is no commercial vaccine for PCV3. The extent of
cross-protection afforded by existing PCV2 vaccines is unknown.
PORCINE CIRCOVIRUS ASSOCIATED DISEASES 87
 SWINE DISEASE MANUAL
Porcine picornaviruses
Alternate names and abbreviations
Enteroviruses, Teschen disease, Talfan disease, Sapelovirus
Definition
VIRUSES
Members of the family Picornaviridae can occasionally cause
diverse disease syndromes in swine. At least 10 genera have been
detected in swine. Changes in the nomenclature and classification
of these viruses can be a source of confusion. Foot-and-mouth
disease (genus Aphthovirus), Senecavirus A (genus Senecavirus),
and encephalomyocarditis (genus Cardiovirus) are discussed
in separate chapters within this manual. This chapter briefly
describes 6 additional genera, including Teschovirus, Sapelovirus,
Enterovirus (with special mention of swine vesicular disease
caused by Enterovirus B, formerly Coxsackie virus), Pasivirus,
Parechovirus, Kobuvirus, and an unassigned virus.
Although most infections with these agents are asymptomatic in
commercial swine production, the diseases associated with several
of these viruses can include polioencephalomyelitis, fetal infec-
tions, fetal death seen as reproductive disorders, skin lesions or
vesicles, myocarditis and pericarditis, pneumonia, or diarrhea.
Occurrence
Porcine picornaviruses are widespread, if not ubiquitous, in con-
ventional and commercial swine herds. They occur only in swine,
and most infections are asymptomatic. Sporadic disease can occur
in susceptible herds, ranging from polioencephalomyelitis (most
notably teschovirus and sapelovirus) to reproductive disorders
(formerly referred to as SMEDI: the acronym for stillbirths,
mummification, embryonic death, infertility) to sporadic out-
breaks of mild transient skin eruptions, myocarditis, pneumonia,
or diarrhea.
Historical information
Teschen disease was first reported as a cause of severe polioen-
cephalomalacia in Czechoslovakia over 75 years ago; the disease
has been limited to parts of Europe and Africa. Talfan disease,
described as a milder form of Teschen disease, was reported
nearly 60 years ago. Both diseases remain well-controlled and
geographically confined. Other members of Picornaviridae can
also occasionally cause polioencephalomyelitis.
Swine vesicular disease is an important differential for vesicular
diseases in swine caused by the species Enterovirus B. This disease
was first reported from Italy in 1966 with limited reports also from
other countries in Europe and Asia; reports of disease with this
virus are relatively infrequent. The western hemisphere is consid-
ered free of the virus. Neither swine vesicular disease nor vesicular
exanthema has been reported in the US for many years, but both
remain very important differentials for foot-and-mouth disease.
88 PORCINE PICORNAVIRUSES
In the 1960s, Dr. Howard Dunne coined the term “SMEDI” to
refer to symptoms of reproductive failure (specifically stillbirths,
mummification, embryonic death, and infertility) that did not
include abortion. Eventually, picornaviruses or “enteroviruses”
were implicated in several of these cases. Even though picorna-
viruses can cause this syndrome, they are currently considered
much less important than other known viral causes of reproduc-
tive failure (particularly parvovirus) on most farms.
Picornaviruses occasionally contribute to the development of
lesions or signs associated with other disease agents (including
skin vesicles, myocarditis, pericarditis, pneumonia, and diarrhea),
but this appears to be a relatively infrequent event that seldom
results in severe losses.
More recently, Sapelovirus has been demonstrated as a sporadic
cause of outbreaks of polioencephalomalacia, usually manifested
as paresis and paralysis. It has also been implicated as a rare and
minor cause of fetal wastage.
Many of the picornaviruses, particularly those currently classified
as true enteroviruses appear to be very common in the feces of
healthy pigs and are rarely associated with disease. Additional
enteroviruses not associated or confirmed to cause disease in
swine are likely to continue to be detected in swine.
Etiology
Picornaviruses are spherical, non-enveloped, single-stranded
RNA viruses. Most can be readily grown in cell cultures of
porcine origin. The current nomenclature of the most common
porcine picornaviruses is summarized in the table on page 89.
Picornaviruses are relatively stable and highly resistant to envi-
ronmental influences and many disinfectants. Many can maintain
infectivity in processed meats. There is considerable variability in
their susceptibility to disinfectants, but all can be inactivated by
sodium hypochlorite.
Epidemiology
All picornaviruses are assumed to have similar epidemiology. All
ages of swine are susceptible if they have not previously encoun-
tered a particular picornavirus species or strain. The viruses are
commonly and extensively shed in the feces; transmission is usu-
ally fecal-oral. Spread of the virus is usually by direct or indirect
contact with infected pigs. Neonates infected in utero but born
alive are sometimes a source of viral exposure of other pigs. Con-
taminated fomites can easily be a mechanism to transmit picorna-
viruses within and between farms as the virus family is relatively
stable in the environment.
Less virulent strains of the virus are endemic in most herds, with
disease expression mitigated by the presence of established herd
 DISEASES CAUSED BY VIRUSES

Table: Current nomenclature of porcine picornaviruses detected in swine.

Genus Species, virus name, and/or disease Skin CNS Fetal Other
Foot-and-mouth disease virus
Aphthovirus + + + Heart
Foot-and-mouth disease

VIRUSES
Cardiovirus A
Cardiovirus + + + Heart
Encephalomyocarditis virus (EMCV)
Cosavirus Cosavirus A No disease confirmed or implicated
Enterovirus B
Swine vesicular disease virus + +
Enterovirus (serotype is Coxsackie)
Enterovirus G
+ +
(formerly porcine enterovirus B)
Aichivirus C
Kobuvirus No disease confirmed or implicated
Porcine kobuvirus 1
Pasivirus Pasivirus A No disease confirmed or implicated
Parechovirus Parechovirus A No disease confirmed or implicated
Sapelovirus A
Sapelovirus + +
(formerly enterovirus A)
Senecavirus A
Senecavirus + Neonatal death
Seneca Valley virus
Teschovirus A
Teschovirus + + Heart, lung
Porcine teschovirus
Unassigned Porcine picornavirus Japan (unassigned) No disease confirmed or implicated
CNS = central nervous system; + = present

immunity. Alterations in production and management, including
segregated rearing, introduction of breeding stock or contam-
inated semen, failure to properly acclimate incoming breeding
stock, commingling, as well as other risk factors may change the
ecology or serve as a source for the introduction of new viruses.
Pathogenesis
Picornaviruses are ingested and then replicate in the tonsil, intes-
tinal tract, and probably in lymphoid tissue in the lamina propria.
The milder strains usually remain confined to the intestinal tract,
although transient viremia is not unusual. Epithelial cell destruc-
tion is not a feature of most picornaviral infections. With the
more virulent strains, viremia occurs, and the virus may spread to
the central nervous system (CNS) or other sites such as lymphoid
organs, heart, lung, or placenta. When the placenta of the preg-
nant uterus becomes infected, it commonly leads to infection of
the developing fetuses, which may then lead to sequential death of
fetuses. Occasionally, mild skin eruptions, rashes, or glossitis are
associated with acute infection with some of the picornaviruses.
Infections of the CNS vary in extent and severity and may affect
different portions of that system from the olfactory bulbs to the
lumbar cord. Most often, the lesions occur in the region between
the hypothalamus and the medulla. In prolonged cases, there may
be lymphocytic meningitis, particularly in the cerebellum and
brain stem. Spinal cord lesions are largely confined to the gray
matter of the ventral horns. There is a gradient in the severity
of lesions; the outcome in an infected pig depends on location,
severity, and extent of the lesions.
Clinical signs
For more virulent disease manifestations such as Teschen, Talfan,
or when the virus infects a naïve population, all age groups may
be affected. Morbidity and mortality are expected to be high.
Early signs include anorexia, listlessness, and fever that are soon
PORCINE PICORNAVIRUSES 89
 SWINE DISEASE MANUAL
followed by ataxia, abnormal postures, and recumbency. There
may be opisthotonus, convulsions, nystagmus, and coma. Death
occurs within a few days. Occasional cases survive but may have
residual paralysis and require euthanasia. Talfan disease is less
severe than Teschen disease but presents similarly.
Talfan disease, other strains of teschoviruses, sapelovirus, and
some enteroviruses can produce ataxia and paresis in infected
VIRUSES
pigs. Often the paresis does not progress to paralysis and most
pigs recover with overall morbidity of 5% to 15% and mortality
of less than 3%. However, some outbreaks caused by strains that
induce CNS signs can have mortality that approaches 10%.
Reproductive disorders caused by these viruses are usually man-
ifested by increased mummification rates, decreased farrowing
rate, variable litter size, and increased stillbirths; all have been
reproduced experimentally by inoculation with various members
of the Picornaviridae. Although still infrequent and sporadic,
the occurrence of these SMEDI-like syndromes not explained
by infection with porcine parvovirus (which therefore may be
caused by picornaviruses) appears to be increasing in some high
health herds.
Unique or new picornaviruses are occasionally detected in cases
of diarrhea or pneumonia, particularly as part of larger surveys,
but generally do not appear to have a primary role in disease in
the surveyed farms. Efforts should be made to rule out more
likely causes of disease (or lesions) before attributing them to a
“new enterovirus” that has been detected.
Lesions
There are no specific gross or microscopic lesions caused only
by this group of picornaviruses. Any clinical presentation that
involves skin lesions such as vesicles on lips, snout, or coronary
bands should be aggressively investigated to rule out exotic vesic-
ular diseases. With Teschen, Talfan, and other sporadic picornavi-
ral diseases having a similar presentation related to brain or spinal
cord dysfunction, there will typically be prominent nonsuppura-
tive inflammation in the gray matter of the brain stem, cerebel-
lum, and spinal cord (polioencephalomyelitis). In affected areas,
many neurons will be degenerated or necrotic. In prolonged cases,
there may be lymphocytic meningitis affecting the cerebellum,
brain stem, or spinal cord. Lesions tend to be more marked and
extensive with Teschen or Talfan disease than in cases caused by
less virulent picornaviruses such as sapelovirus.
With reproductive disorders, lesions are unusual. Some fetuses
occasionally have nonsuppurative myocarditis or encephalitis
seen on microscopic examination.
Other lesions rarely observed or described include cutaneous ves-
icles, nonsuppurative myocarditis, mild interstitial pneumonia,
and mild lymphadenitis. These lesions are most likely to be seen
in young pigs. Increased edema in the mesentery or subcutis of
neonates and fetuses is also reported yet uncommon.
90 PORCINE PICORNAVIRUSES
Diagnosis
The presence of ataxia and posterior paresis in the absence of
gross lesions is not sufficiently specific to diagnose picornaviral
infection. There are many differential diagnoses, including
nutritional deficiencies, toxicities, and other infectious diseases.
Therefore, diagnosis is contingent on the observation of compati-
ble microscopic lesions in the brain and/or spinal cord. Typically,
the lesions that are present will be suggestive of viral infection but
not pathognomonic for a particular agent.
Detection of virus in aseptically collected neural tissue (brain,
spinal cord) or heart by polymerase chain reaction (PCR), in
situ hybridization, immunohistochemistry, fluorescent antibody
staining, or by virus isolation is highly suggestive, if not confirma-
tory, of diagnosis. Many nonpathogenic strains can be routinely
recovered from enteric tissues of both normal and clinically ill
pigs. However, any virus detected within nervous tissue and
accompanied by characteristic pathology in the tissue should be
considered a significant finding. Neurotropic picornaviral dis-
eases must be differentiated from other diseases associated with
CNS disease.
Paired serum samples taken at least 2 weeks apart may show a
rising titer in serum neutralization or complement fixation tests
but seroconversion to endemic viral agents may be coincidental
to disease expression.
Confirmation of reproductive disorder associated with members
of Picornaviridae can be challenging. Nucleic acid from a viral
infection is sometimes harbored in tissues of mummified or dead
fetuses such that detection by PCR from aseptically collected
samples can be highly suggestive for diagnosis. Samples should
be collected carefully to prevent fecal contamination, a common
cause of false positive PCR test results for picornaviruses.
Control
Most herds develop effective immunity to endemic on-farm
picornavirus infections. In herds where picornaviruses have his-
torically caused reproductive or other problems, new breeding
stock should be introduced into the herd at least a month before
breeding begins and be exposed to the endemic picornaviruses
prior to mating. This will provide sufficient time for recovery
and development of active immunity before pregnancy. It may
be preferable to expose new stock to a composite sample of feces
or reproductive materials from the herd to which they are to be
added.
In Europe, Teschen disease and Talfan disease have been con-
trolled by slaughter and ring vaccination around farms or areas
where outbreaks have occurred. Both live-attenuated and inac-
tivated vaccines have been used to control outbreaks in addition
to traditional control strategies such as restricting animal move-
ments out of infected areas.

In the US, occasional outbreaks of neurologic disease associated
with picornaviruses occur in nursery and grower stages. Most
of the outbreaks have been transient and limited to individual
groups of pigs or production sites, but losses can be significant. As
with many endemic agents, establishment of good herd immunity
is fundamental for long-term control of the agent. However, age
segregation, multi-site production, and frequent commingling
can make herd immunity difficult to achieve. Vaccination with
autogenous products has not been consistently effective.
DISEASES CAUSED BY VIRUSES
Outbreaks of disease (poliomyelitis, vesicular lesions) of unusual
severity or suspected of being caused by any of the virulent types
of picornaviruses should be reported immediately to animal
disease control authorities. Thus far, import regulations on swine
and pork products have kept the US free of most highly virulent
porcine picornaviruses including Teschen, Talfan, and foot-and-
mouth disease virus.
VIRUSES
PORCINE PICORNAVIRUSES 91
 SWINE DISEASE MANUAL
Porcine reproductive and respiratory syndrome
Alternate names and abbreviations
PRRS, PRRSV, mystery pig disease (archaic)
Definition
Porcine reproductive and respiratory syndrome (PRRS) is a viral
VIRUSES
disease characterized by two overlapping clinical presentations,
namely reproductive failure in breeding animals and/or respira-
tory disease affecting pigs of all ages. Porcine reproductive and
respiratory syndrome is the most economically significant infec-
tious disease in the US and most areas where it is present.
Occurrence
Porcine reproductive and respiratory syndrome occurs in all age
groups. Reproductive impairment or failure primarily affects sows
or gilts, but it also can affect boar health and fertility. The respira-
tory syndrome affects pigs of any age but is more severe in young
growing pigs. Porcine reproductive and respiratory syndrome
exists in all major swine-raising countries except Australia, New
Zealand, Norway, Sweden, and Switzerland.
Historical information
The clinical disease was first described in 1987 and 1988 in the
US, with reports of the disease occurring in multiple states by
1990. During the 1990s, PRRS spread rapidly in both Europe
and North America. By the end of 1992, the disease was reported
in Canada, Great Britain, and several European countries. Two
distinct strains of virus, one in Europe and one in the US, were
isolated and characterized and found to be genetically different
but clinically similar in most respects. Both strains are now in the
US, along with a multitude of viral variants.
Porcine reproductive and respiratory syndrome was first
described as a syndrome and was confused initially with several
other diseases. It was referred to as swine mystery disease or swine
infertility and respiratory syndrome before PRRS became the
generally agreed upon name. Considerable research efforts over
the past 30 years have revealed much about the virus, the disease,
and its transmission. However, details related to control of the
disease for all types of swine-raising operations are far from com-
plete. The consolidation of the swine industry over the past 25
years has led to entire production systems being designed around
strategies for preventing, controlling, or eliminating this disease.
Etiology
Porcine reproductive and respiratory syndrome virus is an
enveloped RNA virus in the genus Arterivirus in the family
Arteriviridae. The prototype US strain (porcine reproductive
and respiratory syndrome 2, or the “North American” strain) is
related to, but distinct from, the first European isolate (porcine
reproductive and respiratory syndrome 1, or the “European” or
“Lelystad” strain) that was first identified in the Netherlands.
There are significant genetic and antigenic differences between
92 PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME
these type 1 and type 2 viruses, but both are able to produce
similar clinical signs.
Because of the broad array of viral variants, there is considerable
difficulty grouping PRRS virus (PRRSV) into species, hence it
is often considered to exist in an animal (and in a population of
animals) as a “quasispecies.” There is considerable heterogeneity
in the genome, virulence, and antigenicity of PRRSV because of
inherent errors common in the transcription of RNA viruses.
Protective epitopes on the virus surface are not well known nor
can they be predicted from genomic analysis. Although much
is known about the genetic organization of PRRSV, the biolog-
ical properties of isolates are highly variable within countries,
geographical areas, and even a single farm. This variation often
translates to a lack of immunologic cross-protection, posing a
continuous challenge to control of the disease.
The virus has a predilection for cells of the immune system, includ-
ing pulmonary intravascular macrophages and pulmonary alveolar
macrophages, and it replicates extensively in the latter. Porcine
reproductive and respiratory syndrome virus is only moderately
resistant to environmental degradation. The virus is easily inacti-
vated by phenol, formaldehyde, and most common disinfectants.
Epidemiology
Pigs (and peccaries) are the only species known to be susceptible
to PRRSV infection. Pigs shed virus in oral and nasal secretions,
urine, semen, milk, and feces. An important feature of the virus is
its ability to persist for extended periods (greater than 200 days)
in carrier pigs. Porcine reproductive and respiratory syndrome
virus can be shed in boar semen for more than 3 months.
The infective dose varies by route of exposure. For example, the
oronasal route requires 10,000 virions to cause infection com-
pared to as few as 10 to 20 virions for infection by parenteral
exposure or skin scarification. Infected dams experience viremia,
which allows transplacental transmission to fetuses, particularly
during the last trimester of pregnancy.
Shedding by asymptomatic carrier pigs, contaminated transport
vehicles, and fomites are probably the most common means of
virus introduction to a herd or population of pigs.
Semen is a major concern as a route of viral introduction into sow
herds. Infection of sows can occur through natural breeding or
artificial insemination.
The virus spreads readily by direct contact, and aerosol spread
between farms is known to occur over several kilometers depend-
ing on local geography and weather conditions.
Despite the potential for long-term carriage, field observations
suggest that most, but not all, infected pigs eventually become
immune to homologous virus and cease viral shedding by 60 days
postinfection, although some may remain carriers for more than

200 days. Immune clearance of the virus is accompanied by a
steady decline in antibody titers over a period of 4 to 8 months.
In some cases, infection of a herd with PRRSV is manifested as an
epidemic. In other cases, herd infection results in a more insidious
increase in respiratory disease or reproductive failure. Although
debate continues as to the relative importance of vertical, hori-
zontal, and lateral (from a source external to the farm) routes of
transmission, genetic sequencing of the offending PRRSV can be
quite useful in helping to determine the source of infection and
the epidemiology of an outbreak.
Sows infected while pregnant may deliver viremic, persistently
infected piglets. The infection can then cycle between young
pigs well into the nursery phase. Older infected pigs held back
in nurseries or cross-fostered in the farrowing house are often a
source of virus for younger pigs.
Research suggests that the virus is unlikely to be spread to pigs
by birds or rodents. There are no known replication-competent
insect vectors, but mosquitoes and house flies are capable of act-
ing as fomites with the potential to spread the virus mechanically.
Pathogenesis
Once transmission of virus to the tonsil or upper respiratory sys-
tem has occurred, primary replication occurs in lymphoid tissues.
Viremia follows and may persist for 3 to 4 weeks ensuring virus
access to a variety of organs, including the uterus and placenta of
pregnant sows. The virus has a predilection for lymphoid tissues
(spleen, thymus, tonsils, lymph nodes, and Peyer’s patches).
Porcine reproductive and respiratory syndrome virus infects and
compromises the function of pulmonary alveolar macrophages
and pulmonary intravascular macrophages, resulting in intersti-
tial pneumonia as a primary component of respiratory disease.
Besides the direct effects of interstitial pneumonia, the virus com-
promises pulmonary clearance mechanisms and also has other
systemic effects that include fever, lymphadenitis, and fever. As a
consequence, infected pigs have increased susceptibility to other
disease agents. Such coinfections often magnify the severity of
both PRRS and the co-infecting agent.
Porcine reproductive and respiratory syndrome virus is known to
cross the placenta with great efficiency, particularly in late gestation
(after 70 days), and may reach a high titer in fetuses. Recently, a
porcine cell receptor (CD163) present on macrophages was found
to be an important factor, if not a prerequisite, for PRRSV infec-
tion. It is thought that the number of permissive cells containing
the CD163 receptor is greater in older fetuses. Consequently, the
probability that transplacental infection will kill all or some of the
fetuses in later gestation is greater than when infection occurs prior
to 70 days. The common outcome of infection of pregnant dams
is late-term abortion, the result of either the effects of acute disease
and fever in sows, or the effects of infection and death of fetuses.
Recovered sows are resistant to reinfection when exposed to a
homologous strain of the virus but are likely to show clinical signs
again if a heterologous strain is encountered.
DISEASES CAUSED BY VIRUSES
Clinical signs
Where present, PRRS is probably the most important swine
disease to emerge in the last half-century. Serological testing has
revealed there are many infected herds in which significant clinical
signs are not apparent. Where signs are apparent, they vary and are
influenced by the virulence of the isolate, whether it is an initial
infection of naïve animals or an on-going herd challenge, the age
VIRUSES
group affected, the presence of other disease-causing agents present
in the population, the herd size, and management practices.
In breeding-age gilts, sows, and boars, clinical signs may include a
period of anorexia, fever, lethargy, depression, and perhaps respi-
ratory distress or vomiting. Mild cyanosis of the ears, abdomen
and vulva has been reported in some outbreaks. Reproductive
problems, often the most obvious signs, include a decrease in the
number of dams that conceive or a decrease in farrowing rate.
There is usually an increase in premature farrowings, late term
abortions, stillborn or weak piglets, and mummified fetuses.
Pre-weaning mortality is very high. Nursing pigs may have dys-
pnea, fever, ill-thrift, diarrhea, or increased susceptibility to other
bacterial infections. Reproductive signs will persist in a breeding
herd for at least 2 to 3 months until a degree of herd immunity
is established; a slow improvement in reproductive performance
then begins. In larger operations, clinical signs may continue to
cycle, especially if naïve gilts or sows continue to be introduced
into the herd.
Suckling piglets in farrowing rooms often propagate virus and
serve as an important ongoing source of reinfection for the rest
of the herd, particularly when internal biosecurity measures are
not practiced. Importantly, herds may be infected simultaneously
with multiple, heterologous strains of PRRSV that are not com-
pletely cross-protective. This situation substantially decreases the
odds of establishing herd immunity, and clinical signs are likely to
continue. In boars, clinical signs are similar to those in sows and
are usually accompanied by a transient decrease in semen quality.
The primary clinical signs in young, grow-finish pigs are fever,
depression, lethargy, stunting due to systemic disease, and pneu-
monia. Sneezing, fever, and lethargy are followed by expiratory
dyspnea and stunting. The peak age for respiratory disease is 4 to
10 weeks, but signs can occur at any age. Postweaning mortality is
often markedly increased. Bacterial infections, particularly those
capable of sepsis (eg, Streptococcus suis), are usually increased
along with the ever-present concurrent or secondary bacterial and
viral infections.
Lesions
Porcine reproductive and respiratory syndrome virus infection
generally results in mild to severe lesions in lungs and lymph
nodes. The interstitial pneumonia varies from multifocal to lob-
ular to diffuse in distribution. Lungs appear mottled and tan, but
lesions are highly variable in extent. Lymph nodes are generally
swollen, tan, and edematous or cystic. Microscopic lesions may
include nonsuppurative interstitial pneumonia, mild nonsuppu-
PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME 93
 SWINE DISEASE MANUAL
rative encephalitis, myocarditis, rhinitis, and perhaps depletion of
germinal centers of lymph nodes.
Most fetuses and stillborn pigs with uncomplicated PRRS have
no discernible lesions but some may have umbilical cord arteritis
and hemorrhage, patchy distribution of slightly firm lungs (inter-
stitial pneumonia), enlargement of lymph nodes, hemorrhages
in the skin, edema of various tissues, and dehydration with
VIRUSES
prominence of the vertebral column. Sows with acute PRRS have
typical lung and systemic lesions. Endometritis, myometritis, and
placental lesions have been reported but are generally mild.
Diagnosis
Clinical signs and history are often enough to suggest a diag-
nosis of PRRS, especially in acute outbreaks. Characteristic
microscopic lesions in lungs and several other tissues also are
suggestive but not pathognomonic. Any presumptive clinical
diagnosis should be confirmed by detection of the virus. Histo-
logic examination is very useful to rule out roles for other agents
and confirm that any PRRSV that is detected is associated with
compatible lesions. A number of antigen tests including culture,
polymerase chain reaction (PCR), immunohistochemistry, and
in situ hybridization are widely available for detection of virus in
most tissues. Serological tests are also widely available but only
provide indirect evidence of infection; additional information is
required to determine if PRRSV is truly the cause of the clinical
disease being investigated.
To diagnose an involvement of PRRSV in respiratory disease of
postnatal pigs, growing pigs, or adults, samples should be collected
from acutely affected pigs with typical clinical signs. Detection of
the virus in serum by PCR would be highly suggestive for active
infection, but its role in disease cannot be fully elucidated and so it
is important to perform a complete diagnostic examination to rule
out other primary agents of pneumonia. The presence of PRRS
viral antigen in pneumonic lesions is significant.
Porcine reproductive and respiratory syndrome virus can cause
reproductive failure in two general ways. First, acute disease in
dams causing fever and anorexia can induce acute abortion of
fresh, non-mummified fetuses. In this case, dams will be viremic
at the time of abortion and the virus will be readily detectable in
the dam’s serum, but the virus is not likely to be in their aborted
fetuses since transplacental infection will not yet have occurred.
Second, dams may be subacutely infected several days to weeks
previously but not abort their litter (or farrow early). Over time,
the virus in these cases will cross the placenta and infect fetuses,
which will result in their eventual death. Abortion may not occur
until a sufficient number of fetuses have become infected and die,
which typically does not happen until later in gestation (100 to
110 days of gestation). Weak pigs, stillbirths, and occasionally
increased mummies may be present in litters that are delivered
at term. Sows in this situation are generally not sick at the time
of abortion and are usually not viremic but will usually have high
antibody levels in serum. Aborted, mummified, or stillborn pigs are
94 PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME
useful for diagnosis in this situation as there is a reasonable chance
that one or more of the fetuses will contain detectable levels of
virus. In general, submission of serum from acutely affected dams
and at least 3 fetuses from each of at least 3 aborted litters should
be sufficient to confirm a role for PRRSV in reproductive failure.
Other suitable samples to confirm a PRRS outbreak are tissues
(bronchoalveolar lavage, serum, lung, lymph nodes, tonsil, and
spleen) from weak neonates and clinically affected nursing piglets.
Techniques for differentiating viral isolates are available and
include restriction enzymes and RNA fragment analysis, and
genetic sequencing of some or all of the viral genome. Both
techniques can deliver epidemiologically useful information, but
neither is well suited for predicting virulence, antigenicity, or
the likelihood of cross-protective epitopes amongst virus strains.
Sequencing is helpful in documenting the various strains and/
or the changes that occur in the circulating virus population in
endemically infected herds, with data often presented in the form
of a dendrogram or phylogenetic tree.
Serology may be helpful in confirming the presence and perhaps
how recently PRRSV infection occurred in a non-vaccinated
herd. A cross-sectional sample of blood from various ages of pigs
on a farm is useful for determining the kinetics of virus circu-
lation and therefore helps to inform control strategies. Several
different tests for PRRS virus antibody are available, including
immunofluorescence antibody, serum neutralization, and
enzyme-linked immunosorbent assay (most common); some have
the ability to discriminate antibodies from European and North
American strains of virus. Maternally derived antibody may be
detectable up to 6 to 8 weeks of age.
Control
Herds that are negative for PRRSV should make every effort
to avoid becoming infected. Biosecurity protocols surrounding
animal introductions, transportation processes, truck disinfec-
tion, and staff movements need to be properly executed every
day. Because airborne transmission can occur (particularly in
pig-dense areas), air is sometimes filtered to prevent airborne
introduction of the virus. Expenses associated with extreme
biosecurity measures, such as air filtering, farmer-owned truck
washes, and staff biosecurity procedures, can be substantial, but
the economic impact of PRRS often warrants these measures.
Should an outbreak occur, a control program should be tailored
to fit the individual farm situation.
Due to differences in virus strain biology, biosecurity constraints
for individual farms, concurrent disease challenges, incomplete
knowledge of virus transmission and epidemiology, and diffi-
culties establishing cross-protective immunity, there is no single
successful strategy for control of the disease
An accurate diagnosis is essential to confirm the presence of the dis-
ease and understand the epidemiology of the disease on a particular
farm. This usually requires disease characterization (demonstration

of the disease agents and lesions) at each stage of production or
site within the flow using a combination of serological testing and
virus identification and characterization. Combinations of testing
strategies on statistically significant numbers of serum, oral fluid, or
environmental samples can determine status in post-weaned pigs.
Initial assessments should indicate the stage (acute or chronic) of
infection in the herd as well as where and how the virus is being
spread within the herd.
Once the herd epidemiology has been characterized, the first
steps in development of a PRRS control program usually occur
at the sow farm, with a strategy developed to achieve one of two
objectives: 1) elimination of the virus from the breeding herd,
or 2) long-term management of the virus. For either objective,
the initial goal is to manage the breeding herd in such a way that
batches of weaned pigs that are free of the virus are consistently
being weaned. Breeding herds can be considered as:
• Naïve (never infected)
• Actively infected (virus is detectable in sows or weaner pigs)
• Previously infected but currently stable (herd is antibody
positive, but no virus is detected in the sows or weaners by
routine testing)
Although the naïve status is preferred, the reality is that, long-
term, most herds will need to be brought to and managed in the
stable status.
The status of sow herds can be monitored in part by routine testing
of weaners. Naïve farms can be monitored by routine testing for anti-
body. Asymptomatic but positive sow farms are usually monitored by
PCR testing using pooled samples of serum or oral fluids at weaning
and/or tissue fluids collected at the time of piglet processing.
Breeding herd stability is achieved by establishing a high level of
herd immunity, which dramatically decreases the likelihood of
transmission of virus from dams to fetuses or neonates. When
coupled with segregated rearing of offspring in this situation,
the clinical effects of infection can be minimized or eliminated.
Breeding herd stabilization can be accomplished by vaccination,
by intentional whole-herd infection with the resident live virus,
by aggressive acclimatization of replacement breeding stock, by
closing the herd to additions of animals for 6 to 10 months, or by
a combination of these strategies.
Consideration needs to be given on how one will limit the fre-
quency of seed stock introductions to the sow herd, and to ensure
that the replacement gilts will be well acclimatized to the virus cur-
rently resident in the sow herd prior to their entry and first mating.
Replacement gilts can be exposed to virus either by vaccination or
through exposure to field virus; in either case they must be given
at least 60 days to recover and stop shedding virus before they are
introduced into the sow herd. If boars are to be introduced, they
should be handled in a manner similar to the replacement gilts. If
using artificial insemination, semen should be sourced only from
PRRS-negative studs that have comprehensive PRRSV monitoring
programs in place.
DISEASES CAUSED BY VIRUSES
There are killed and avirulent live commercial vaccines as well as
autogenous killed vaccines available for control of PRRS. Killed
vaccines are generally considered less efficacious than avirulent
live vaccines; all suffer from having only a moderate ability to
provide protection across the entire spectrum of genetically
diverse isolates.
Herds that have successfully stabilized will produce offspring, the
VIRUSES
vast majority of which will be virus free. Once reaching this stage,
it is necessary to evaluate the nursery, grower, and finisher phases
of production to determine what measures (depopulating, clean-
ing, disinfecting, vaccinating, etc) are necessary to maximize the
chance for the weaned pigs to remain virus free for the duration
of their grow-out.
Some producers with sow herds that consistently produce negative
offspring may attempt to eliminate PRRSV from the sow herd. At
this point, all subsequent replacement seed stock should be naïve for
PRRSV infection and any residual infected sows in the herd should
be eliminated. The latter is accomplished by testing (serology and/or
PCR) and removal, or in some cases by normal attrition.
In some operations, it may be economically feasible to depopulate
the site, clean and disinfect the facilities, and after a few weeks
repopulate with stock free of PRRSV and other major diseases.
Another means to stabilize and eliminate the virus is to close the
herd to all new animal introductions for at least 200 days. Herd
closure requires that all weaned pigs be moved off-site and that
no internal replacement animals are allowed to be kept on-site.
Most breeding stock companies today are able to provide PRRS-
free seed stock, thereby eliminating which was once a major
limitation to producers’ control strategies.
Before embarking on a PRRS control or elimination strategy,
one should honestly assess risk factors for reinfection of the herd
as well as the level of biosecurity that can be maintained by the
producer. Herds located in swine-dense areas are at great risk for
reinfection.
There is no specific treatment for PRRSV infection. Broad-spec-
trum antibiotics may be useful in controlling secondary bacterial
infections. Anti-inflammatory products are commonly adminis-
tered during acute disease to mitigate fever and encourage appe-
tite. Other helpful techniques may include early weaning and
isolation of piglets and various PRRS vaccination protocols.
The challenge of achieving consistently effective immunologic
control of PRRSV has proven insurmountable. Recent reports that
pigs may be bred for genetic resistance to PRRSV infection are
encouraging. Pigs lacking CD163 receptor on their cells are resis-
tant to many strains of PRRSV infection. Commercial application
of this finding offers some optimism for the future control of this
devastating disease. In the meantime, since PRRSV strains vary,
control strategies will also vary to accommodate needs specific to
the farm. It is imperative that experienced practitioners, diagnos-
ticians, and research workers continue to objectively expand their
knowledge to better control and eventually eliminate this disease.
PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME 95
 SWINE DISEASE MANUAL
Porcine respiratory coronavirus
Alternate names and abbreviations
PRCV
Definition
A viral disease of pigs that can cause a mild pneumonia in sus-
VIRUSES
ceptible pigs but often occurs without producing any clinical
signs. Porcine respiratory coronavirus (PRCV) is closely related
to transmissible gastroenteritis (TGE) virus, and immunity gen-
erated as a result of infection with PRCV can provide substantial
cross-protection against TGE virus.
Porcine respiratory coronavirus is not zoonotic and infects only
swine.
Occurrence
Porcine respiratory coronavirus was first identified in Europe in
1986 and spread widely across the rest of the continent in the
space of a few years. In 1990, the same virus appeared on a farm
in the US, with infections subsequently reported across the rest
of the country and Canada. Parts of Asia also began reporting the
appearance PRCV at about the same time.
There is no mandatory international reporting of PRCV outbreaks
to the World Organization for Animal Health, so little has been
documented about the presence of the virus in specific countries.
However, the virus is assumed to be endemic in much of the world,
with the possible exceptions of Australia and New Zealand.
Historical information
In Europe during the early and mid-1980s, veterinarians and
researchers began to report an unexplained decline in the occur-
rence of clinical outbreaks of both TGE and porcine epidemic
diarrhea (PED). During this period in Britain, a large number of
herds appeared to be seroconverting to TGE virus in the absence
of any of the normally severe enteric signs typically associated
with that disease. In 1986, investigation of one of these herds
led to the identification of a viral agent that cross-reacted sero-
logically with TGE virus and was designated as TLM83. During
the late 1980s in the US, a similar phenomenon was recognized;
eventually a virus identical to TLM83 was identified and came to
be known as porcine respiratory coronavirus.
Etiology
Porcine respiratory coronavirus is a member of the Coronaviridae
family of enveloped, positive-sense, single-stranded RNA viruses.
The virus is in the sub-family Coronavirinae, genus Alphacorona-
virus along with other porcine viruses including TGE virus and
PED virus.
Porcine respiratory coronavirus is believed to have arisen as a
mutant of TGE virus and is antigenically related to that virus.
Compared to TGE virus, PRCV has a large deletion in the S gene
96 PORCINE RESPIRATORY CORONAVIRUS
and additional smaller deletions in ORF 3; the deletion in the
S gene is believed to play a role in the change of tropism from
an enteric infection with TGE virus to a pneumonic infection
with PRCV.
Epidemiology
Porcine respiratory coronavirus is spread primarily by short-dis-
tance aerosols and direct contact between pigs. Most commercial
herds are endemically infected with the virus, and young pigs are
assumed to be infected by their dams or horizontally from other
pigs between 4 and 10 weeks of age when maternally derived
antibody-mediated protection declines.
Porcine respiratory coronavirus is generally a subclinical infec-
tion, although mild respiratory signs may occur in some herds;
severe disease has been described in experimentally infected pigs,
but this seems to be a very rare occurrence in field settings. In
either situation, mortality is rare though morbidity can often
approach 100%.
Pathogenesis
Despite its genetic similarity to TGE virus, infection with PRCV
does not cause any pathology to the enteric system.
The virus replicates in the upper and lower respiratory tract (alveo-
lar cells, nasal mucosa, tracheal, bronchial, and bronchiolar epithe-
lium, alveolar macrophages, and tonsils). Limited replication of the
virus in some cells of the intestine has been shown in experimen-
tally infected animals, but this finding is probably not significant
in disease development, although it could perhaps be related to the
eventual cross-protection afforded against TGE virus.
Viremia may occur as early as 2 days postinfection and last for 10
to 14 days.
Clinical signs
Infection with the virus does not generally result in any signifi-
cant clinical signs, although in naïve pigs or in some experimen-
tal work, dyspnea, tachypnea, sneezing, coughing, fever, and
anorexia can be seen. Severe disease or death is rare. Clinical signs
occur between around 4 and 10 days postinfection.
Lesions
Gross lesions of infection with PRCV are not typically seen
because the subclinical nature of the disease means that few pigs
are actually examined by postmortem. However, experimentally,
lesions including multifocal to coalescing areas of consolidation
and interlobular pulmonary edema may be present.
Microscopic lesions are similar to other viral pneumonias though
less severe: thickening of interstitial septa, lymphoplasmacytic
and histiocytic bronchiolar and alveolar exudate, hypertrophy

and proliferation of type II pneumocytes, airway epithelial necro-
sis, squamous metaplasia, dysplasia, and proliferation in all sizes
of airways. Infections complicated by secondary bacterial patho-
gens can result in bronchopneumonia.
Diagnosis
Porcine respiratory coronavirus is easily isolated from nasal
swabs or lung tissue following inoculation onto appropriate cell
culture, with confirmation by virus neutralization or immuno-
fluorescence. More commonly, polymerase chain reaction is used
to identify this virus from lung tissue. In situ hybridization and
immunohistochemistry tests are also available to identify the
virus in tissues.
DISEASES CAUSED BY VIRUSES
An enzyme-linked immunosorbent assay can discriminate anti-
bodies produced by infection with TGE virus from those pro-
duced by infection with PRCV. The test is not sufficiently specific
enough to use on an individual-pig basis but can be used as part
of a herd-based monitoring program.
Other serological tests have been described for PRCV, but the
user is cautioned of the need to investigate the extent to which
VIRUSES
each might cross-react against TGE virus. If not specifically
stated, one can assume significant cross-reaction will occur.
Control
In most situations, little is done to prevent or control infection
with PRCV, since the protection that is afforded against TGE sub-
stantially outweighs the cost of disease primarily caused by PRCV.
PORCINE RESPIRATORY CORONAVIRUS 97
 SWINE DISEASE MANUAL
Pseudorabies
Alternate names and abbreviations
Aujeszky’s disease, AD, ADV, PRV, SuHV-1, mad itch
Definition
Pseudorabies is a highly contagious and significant disease of pigs.
VIRUSES
This viral infection tends to cause central nervous system (CNS)
signs in young animals, respiratory illness in older pigs, and repro-
ductive losses in sows. Pseudorabies can result in trade restrictions
and economic losses in countries where it is endemic and remains
a significant problem among domesticated pigs in countries that
have not eradicated it.
Occurrence
Among domestic animals, swine are the only natural host of
pseudorabies virus. All age groups not previously exposed or vac-
cinated are susceptible. The disease was eradicated from the US
commercial pig industry in 2004 but remains in some feral swine
populations. The disease remains common in many other major
swine-raising countries. Most domestic animals (cattle, sheep,
dogs, cats, and goats, but not horses) and many wild animals (rats,
mice, raccoons, opossums, rabbits, and several other fur-bearing
mammals) are susceptible to the virus, but transmission occurs
only when these species are kept in close contact with acutely
infected swine; death is the usual outcome in these aberrant
hosts. Pseudorabies occurs with some frequency in both cattle
and sheep, especially those in close contact with swine. The dis-
ease cannot be transmitted to humans.
Historical information
The disease is named after the Hungarian veterinarian Dr Aladar
Aujeszky who linked the disease in cattle, dogs, and cats in 1902.
Pseudorabies was not identified as a viral disease in swine until 1909.
Prior to 1960, the disease in swine was important in Eastern
Europe but major outbreaks did not occur in the US until the
mid-1970s. Incidence of the disease increased with the widespread
introduction of purchased breeding stock, total confinement, and
continuous farrowing during this period. Active pseudorabies erad-
ication programs exist in many countries and have been successful,
in large part due to efficacious vaccination programs.
In 1989, the US embarked on a 5-stage federal/state/industry
program for eradication of pseudorabies in swine. Eradication of
pseudorabies from the commercial industry was achieved in 2004.
However, feral pigs remain infected in some parts of the country.
Etiology
Pseudorabies is caused by infection with suid herpesvirus 1
(SuHV-1); the virus is commonly known as Aujeszky’s disease
virus in most of the world and as pseudorabies virus in North
America. This virus is a member of the genus Varicellovirus
98 PSEUDORABIES
and family Herpesviridae (subfamily Alphaherpesvirinae).
Viral variants that emerged in China in 2011 have significant
genetic differences from other pseudorabies strains that circulate
worldwide. In addition, different pseudorabies strains are
maintained in feral swine, although the clinical disease caused
by these strains is identical to that caused by strains found in
domesticated pigs.
Like many other herpesviruses, pseudorabies virus can persist
in a latent state in recovered animals (usually in the trigeminal
ganglia). The virus does not survive well outside the host, with
survival depending largely on environmental factors. Except
during cold weather, the virus probably does not survive more
than 2 weeks outside the pig. Under exceptional conditions it
may survive longer in infected fetuses, dried tissue, and buildings.
The virus can be destroyed by many disinfectants, including
ortho-phenylphenol, quaternary ammonium, iodine compounds,
and 5% sodium hydroxide.
Genetic engineering has been used to create highly effective vac-
cines by deleting one or more of the surface glycoproteins of the
virus. Antibodies to these gene-deleted vaccines differ sufficiently
from antibodies generated by exposure to wild virus such that
serological tests can differentiate infected from vaccinated ani-
mals (DIVA). Protection induced by these pseudorabies vaccines
appears to be effective against all wild types of the virus.
Epidemiology
Pseudorabies virus is spread and persists by several mechanisms.
Swine that recover from pseudorabies excrete large amounts of
virus in saliva and nasal secretions, and perhaps in urine and feces,
for up to 2 weeks. Virus can persist in the tonsils of carrier swine
for at least several weeks. Latent virus can persist in the CNS
for many months. Recrudescence of the virus often occurs after
stress. Inapparent shedders are frequently the means of introduc-
tion of the virus into susceptible herds. Once introduced, the
virus spreads by nose-to-nose contact, through feed and water
contaminated by oral secretions, and by aerosols coughed into the
air. The virus can be shed in the semen of acutely infected boars,
resulting in infection by venereal spread or artificial insemination.
The virus can be transmitted transplacentally and cause fetal
deaths, abortions, and viremic pigs at birth. In a farrowing house,
aborted fetuses or live piglets born infected with or incubating
the disease soon contaminate the house. The virus may survive
long enough to infect piglets of the next farrowing.
Feral swine remain a possible source of infection to domestic
swine. Other pseudorabies-infected animals (eg, rats, mice, dogs,
cats, raccoons, and opossums) are considered dead-end hosts and
will shed pseudorabies for only a short time. They may, however,
visit swine facilities and either shed virus that contaminates the
facility, or die and be eaten by swine. The possible role of flies or
birds in transmission is dubious.

Experimental and field evidence from outbreaks in the US and
Europe suggest that aerosolized virus can travel several kilometers
between farms under ideal conditions.
The incubation period in pigs is usually 2 to 6 days.
Pathogenesis
Pathogenesis is variable, depending on virulence of the viral strain,
age of the pig, and the route and severity of exposure. Experimen-
tally, pigs can be infected by many routes of inoculation. Under
field conditions the oral-nasal route of exposure is probably most
common. Virus often localizes in the epithelium of the tonsils.
The primary site of replication is epithelium of tonsils, nasophar-
ynx, and upper respiratory tract. With highly virulent strains of
virus there may be a short period of viremia with dissemination to
many tissues. Most viral strains have a tropism for the CNS and
upper respiratory tract.
The virus can also spread along nerves from a primary site of
infection to the CNS, then to the spinal cord, where it spreads
centrifugally along nerve trunks. The virus often localizes in gan-
glia (eg, the trigeminal nerve ganglia and paravertebral ganglia)
and may become latent there. It may be reactivated later by stress.
In many areas of localization, including respiratory epithelium,
the virus causes inflammation and necrosis of tissue. In some
organs and tissues, necrotic areas are often large enough to be
grossly visible. Virus may cross the placenta to infect some or all
fetuses. In the reproductive tract, the virus causes endometritis,
vaginitis, and necrotic placentitis. Lesions and virus may be
present in infected fetuses. Intranuclear inclusion bodies are pro-
duced in a variety of cells in swine of all ages, including fetuses.
Clinical signs
Signs vary, depending largely on the immune status of the dam
and the age of the pigs affected. In general, younger pigs are more
severely affected and become more resistant as they age. Neonatal
pigs born to naïve dams are highly susceptible to infection; piglets
become ill 2 to 4 days after exposure. Very young neonates may die
without signs having even been noticed. Nursing pigs usually show
signs of neurologic involvement. Signs may include high fever,
depression, anorexia, tremors, incoordination, dog-sitting position,
vomiting, foaming at the mouth, blindness, paddling, coma, and
convulsions. Death often occurs within 1 to 3 days. Morbidity
and mortality may approach 100% in neonates, especially in naïve
herds. Piglets nursing recovered or vaccinated dams are well pro-
tected from clinical signs and infection with the virus.
Weaned pigs (3 to 9 weeks of age) have similar signs but mor-
tality is usually much lower. Respiratory signs often occur in
the older pigs of this age group. They include sneezing, nasal
discharge, coughing, and labored breathing. Most of the pigs
survive, provided they do not succumb to secondary infections,
especially bacterial pneumonia.
DISEASES CAUSED BY VIRUSES
In susceptible, grow-finish swine (10 weeks of age to market
weight), respiratory signs predominate, and morbidity is high.
Signs include a febrile response, depression, anorexia, sneezing,
coughing, and nasal discharge. Central nervous system signs
occur in occasional pigs and vary in severity from tremors to con-
vulsions. Most pigs recover in about 7 to 10 days.
In breeding herds, clinical signs may not be apparent except
VIRUSES
during the period of initial infection. These signs are primarily
respiratory, and most animals will recover. In pregnant sows or
gilts, reproductive failure sometimes occurs. Dams infected in the
first trimester may absorb their fetuses and return to estrus. Those
in the second or third trimester may abort or have mummified,
stillborn, or weak-born pigs. Those infected close to term may
deliver infected piglets that die within a few days.
Lesions
Neonates that die acutely after infection may have no gross
lesions. In piglets showing CNS signs, congestion of the menin-
ges is often visible. In those showing respiratory signs, there may
be a rhinitis with patchy epithelial necrosis. The rhinitis can be
seen after splitting the skull and nasal bones midsagittally. The
inflammation and necrosis often extend into the fauces and
larynx, and occasionally into the trachea or esophagus. Other
gross lesions may include keratoconjunctivitis and necrosis of the
tonsils. Gross and/or microscopic white foci of necrosis may be
seen in the liver, spleen, lungs, adrenals, and lymph nodes. Similar
foci are sometimes present in aborted fetuses.
Gross lesions are often subtle, absent, or difficult to find in
postweaning pigs. Some pigs will have serous or fibrinonecrotic
rhinitis, pharyngitis, and tracheitis visible at necropsy. Pulmonary
edema, congestion, or consolidation is sometimes present, and
secondary bacterial pneumonia can result in more obvious gross
lesions. The lymph nodes may be congested and contain small
hemorrhages. Affected pigs may also have necrotic tonsillitis or
pharyngitis which is almost pathognomonic for the disease.
Microscopic lesions often include a panencephalitis, ganglioneu-
ritis at multiple sites, and perhaps nonsuppurative meningitis. The
most severe lesions in the brain are usually in the cerebral cortex
and often include neuronal degeneration and necrosis. In the
lungs there may be bronchitis, bronchiolitis, and alveolitis with
hemorrhagic foci of necrosis, but lung lesions are generally neither
severe nor specific. Intranuclear inclusion bodies may be found at
many sites, often within neurons, astrocytes, oligodendroglia, and
respiratory epithelium.
In dams that have infected fetuses or abort, the uterine wall may
be thickened by inflammatory edema. Necrotic placentitis may be
apparent in the placenta of infected fetuses and neonatal piglets.
PSEUDORABIES 99
 SWINE DISEASE MANUAL

Diagnosis farms can occur. Occasionally, acute central nervous disease,

Diagnosis can often be made based on knowledge of endemic fever, and rapid death in hunting dogs or animals consuming feral
circulation of pseudorabies virus in the area combined with history, pig offal will be the first indication of pseudorabies in pigs.
clinical signs, gross and microscopic lesions, and serological testing.
Control
White necrotic foci (1 to 2 mm in diameter) in the liver, tonsil,
Pseudorabies is currently considered an exotic viral disease in the
and spleen of suckling piglets is highly suggestive but should be
US since its eradication in 2004. In countries where the disease
VIRUSES

confirmed as pseudorabies by appropriate testing. Tests applicable

remains endemic, it may be possible to prevent exposure of a neg-
for all ages include fluorescent antibody testing on tissue sections,
ative herd to pseudorabies through strict testing, quarantine, and
immunohistochemistry or in situ hybridization on formalin-fixed
isolation procedures. Only seronegative animals should be added
tissues, and polymerase chain reaction or virus isolation per-
as necessary to a herd. Additions should be made only after a quar-
formed on brain, tonsils, and spleen, along with histopathology
antine period of at least one month and negative serological tests
to confirm typical microscopic lesions.
before and after quarantine. Cats, dogs, rats, mice, and all wildlife
Available serological tests include serum neutralization, latex should be prevented from coming into contact with swine.
agglutination, and enzyme-linked immunosorbent assay. Serum
Pseudorabies DIVA vaccines are essential in the control and erad-
neutralization is the standard regulatory test in the US, but the
ication of the disease. These highly efficacious vaccines increase
other test platforms are widely used as screening tests. Serological
resistance to infection, virtually eliminate clinical signs associated
testing is widely used for herd diagnosis. Accurate serological
with infection, and minimize the amount of viral shedding that
tests that can differentiate vaccine antibody from wild type (ie,
ensues if infection does occur. The incidence of latency and the
DIVA) are widely available and are commonly used as part of
frequency of recrudescence of virus in latently infected swine are
national disease control programs.
also decreased in vaccinated swine. Some sow farms have elimi-
Importantly, the clinical signs associated with acute pseudorabies nated pseudorabies through aggressive vaccination programs that
virus infection in postweaning pigs can be indistinguishable from follow a strict elimination plan that includes test and removal of
other common causes of respiratory disease. Remember that the dams seropositive to wild-type virus.
expanding US feral pig population remains infected with pseu-
dorabies virus; periodic incursions of the virus into commercial

100 PSEUDORABIES

Rotavirus
Alternate names and abbreviations
None
Definition
Rotaviruses cause diarrhea in nursing and post-weaned pigs and
affect primarily the small intestine. If uncomplicated, the usual
outcome of infection is high morbidity with low mortality.
Occurrence
Rotaviruses are ubiquitous in swine populations throughout
the world. Rotavirus infections are common in most avian and
mammal species, including humans. Although all rotaviruses are
related, porcine rotaviruses infect only swine.
Historical information
In 1969, rotaviruses were identified in calves and subsequently
detected in other species, including swine and humans. Rotavi-
ruses are important, common, and reduce productivity.
Etiology
There are at least 7 antigenically distinct serogroups of rotaviruses
(A, B, C, D, E, F, and G) within the family Reoviridae, of which
4 (A, B, C, and E) are known to infect swine. There are also anti-
genically dissimilar subgroups within each of the major groups.
Group A rotaviruses have been the most researched, but group B
and C appear to be becoming more common on farms. Rotavirus
B and C and are also associated with outbreaks of diarrhea, par-
ticularly in suckling piglets. Immunity is generally not cross-pro-
tective between serogroups.
Epidemiology
Rotaviruses are ubiquitous; all pigs in the US are assumed to
eventually become infected with one or more rotaviruses. Neonatal
and susceptible young growing pigs are exposed to virus shed from
carriers, including sows and older pigs, or as a result of coming into
contact with virus present in their environment. Herd immunity
more or less mitigates what would otherwise be a severe viral
enteritis characterized by profuse diarrhea, similar to that pro-
duced by infection with swine enteric coronaviruses. Infected pigs
may develop clinical or subclinical disease, but most pigs recover
uneventfully, with a proportion of pigs becoming carriers. Interspe-
cies transmission of rotaviruses has not been documented.
A major reason for the ubiquity of rotaviruses is that they are
very stable in the environment, assuring their survival in swine
populations and facilities. Rotaviruses are very resistant to
temperature changes, many chemicals, various pH levels, and
many disinfectants, allowing them to persist in environments
for weeks or months. Recommended disinfectants for cleaned
surfaces include formaldehyde and chlorine-based disinfectants,
DISEASES CAUSED BY VIRUSES
including Clorox®. Rotavirus infections can occur concurrently
with or predispose pigs to other diarrheal diseases of young pigs,
particularly colibacillosis or salmonellosis. Combined infections
with other agents cause more severe clinical signs and lead to
higher mortality.
VIRUSES
Pathogenesis
The pathogenesis of rotavirus infections in pigs is similar to
that of coronaviruses or other agents that infect enterocytes of
the small intestine. Transmitted mainly by the fecal-oral route,
rotaviruses reach the small intestine and attach, enter, replicate,
and destroy enterocytes in segments of the ileum, jejunum, and
duodenum. The pathology results in villus fusion, blunting, and
atrophy, all of which contribute to the development of a malab-
sorptive diarrhea.
Lesions can be subtle, segmental, or severe. Villus fusion and
the destruction of villus epithelium result in impaired intestinal
function, reduced disaccharidase activity, and the accumulation
of osmotically active products in the intestine. The osmotically
active products promote the movement of water into the intestinal
lumen. A non-structural protein, NSP4, mediates hypersecretion
which, along with malabsorption, leads to diarrhea. IgA antibody
effectively mitigates severity while multiple factors including
malnutrition, dehydration, imbalance of electrolytes, and cardiac
failure can ultimately cause death. However, death is an unusual
outcome. The pathogenesis of all porcine rotavirus types (A, B, C
and E) is likely to be similar.
Clinical signs
The onset and severity of signs depend on the dose of virus that
has been ingested, the amount of protective antibody in the
dam’s colostrum and milk, and the presence (or absence) on the
intestinal wall of IgA immunoglobulins secreted within the intes-
tine by active immune processes. Outbreaks on specific premises
often occur repeatedly when the piglets reach an age at which
lactogenic immunity is no longer adequate to protect against the
degree of exposure.
Diarrhea, usually white to yellow in color, commences and gen-
erally continues for a few days until the pig develops an active
immunity. There is usually moderate accompanying dehydration.
Vomiting occurs but is not a major clinical sign. Morbidity is
variable, but mortality is usually low when good housing and
husbandry are present. Severity of clinical signs, morbidity, and
mortality will be increased if there is concurrent disease, poor
husbandry, exposure to cold, or continuous exposure to high
doses of virus. Sanitation is paramount in mitigating the dose.
ROTAVIRUS 101
 SWINE DISEASE MANUAL
Lesions
Pigs that die or are euthanized are dehydrated and may have
abundant fecal staining of the perineal area. The intestinal wall
will be thin, flaccid, and rather transparent. The small intestine
and colon contain yellow or gray fluid and debris. Microscopic
lesions are largely confined to villi of the jejunum and ileum, with
necrosis of apical enterocytes. This acute change is rapidly fol-
VIRUSES
lowed by squamous and cuboidal metaplasia of epithelium, and
villus fusion and blunting, with crypt hyperplasia as enterocytes
regenerate and lesions resolve.
Diagnosis
History, clinical signs, and gross lesions are helpful in establishing
a presumptive diagnosis but need to be confirmed by labora-
tory testing. Histopathology is quite important to confirm the
presence of typical viral lesions, since the simple detection of
rotaviruses is not unexpected, given that it is a ubiquitous endemic
agent. Typical lesions are described above but are not specific for
rotavirus insult. With compatible lesions, the demonstration of
rotavirus in the lesion by immunohistochemistry, fluorescent anti-
body, polymerase chain reaction (PCR), or electron microscopy is
considered confirmatory.
Not all techniques are widely available to differentiate or identify
the specific rotavirus that is present. A multiplex PCR test for
rotavirus A, B, and C coupled with histopathology is usually
sufficient for diagnosis.
Virus shedding is much greater and lesions are more definitive
during the early stages of the disease, therefore samples should
be obtained from acutely affected pigs. Demonstrating abundant
rotavirus by laboratory testing of feces from acutely affected
pigs with an antigen-based test suggests a role for rotavirus but
does not rule out the possibility of other diseases such as enteric
coronavirus disease, colibacillosis, salmonellosis, or coccidiosis.
Because lesions are not pathognomonic and coinfections are
common, it is wise to rule out coinfections with a thorough diag-
nostic investigation.
Control
There are no proven specific therapies for rotavirus infection in
young piglets. Good husbandry and supportive therapy, includ-
ing electrolytes in drinking water, can be of value. A dry, warm
environment and good nutrition are important in reducing the
102 ROTAVIRUS
severity of outbreaks. Antibiotics are not effective for rotaviral
infections but may be indicated for concurrent bacterial diseases.
All-in, all-out pig flow with thorough cleaning and disinfection
between farrowing groups reduces the exposure of piglets to
rotavirus. Limiting the age spread of piglets within a farrowing
room minimizes the potential transmission of virus from older to
younger pigs. If rotavirus is determined to be a consistent cause
of diarrhea in post-weaned pigs, sanitation and environmental
management of both the farrowing and nursery facilities should
be investigated. Decreasing the dose through good hygiene is a
priority for breaking the cycle of rotavirus disease.
Both modified-live virus and killed rotavirus vaccines are avail-
able, although they are mostly focused on rotavirus type A. Dams
can be vaccinated at intervals prior to farrowing to stimulate
them to produce higher levels of antibody in their colostrum and
milk. This passive antibody protection should provide time for
their piglets to develop their own immunity prior to complete
loss of lactogenic antibody protection. Booster vaccinations to
sows are generally given several weeks before each subsequent
farrowing to maximize the concentration of immunoglobulins in
colostrum and milk. Although widely practiced, the efficacy of
various vaccination strategies has not been consistent, and it can
be difficult to prove their benefit on some farms.
Acclimatization of incoming breeding stock is often practiced
for rotavirus, as well as a variety of other endemic pathogens in a
herd. This is generally accomplished by intentional exposure of
new breeding stock to resident stock and/or biofeedback materi-
als from the herd, prior to their first mating. In this way, the new
breeding stock can develop active immunity to indigenous rota-
viruses (and other endemic potential pathogens) that are being
shed by older stock on the farm or are present in the materials
used for biofeedback.
Some sow farms attempt to booster sow immunity through
intentional exposure by feeding feces-laden material from the
farrowing areas or intestinal contents from acutely affected piglets
back to sows in late gestation. Although commonly practiced, the
efficacy of this procedure is not proven.

Senecavirus A
Alternate names and abbreviations
Senecavirus, SVA, Seneca Valley virus, SVV
Definition
Senecavirus A (formerly Seneca Valley virus) can cause vesicular
lesions in all ages of swine. The lesions are indistinguishable from
those of other vesiculating diseases such as foot-and-mouth dis-
ease (FMD). Increased mortality in suckling piglets is reported
during the acute phase of herd outbreaks with Senecavirus A.
Occurrence
Swine are considered the natural and only host for Senecavirus
infections. Senecavirus A has been reported throughout the west-
ern hemisphere, Asia, and Europe and is one of many members of
the viral family Picornaviridae that can cause vesicular lesions and
reproductive losses in swine.
Historical information
Senecavirus was first isolated in the US as a tissue culture contam-
inant in a laboratory located in Gaithersburg, Massachusetts near
Seneca Creek State Park. Although first thought to be nonpatho-
genic in pigs, it is now clear from field experience and experimen-
tal inoculations that some strains of Senecavirus can cause vesicu-
lar lesions indistinguishable from those of FMD, swine vesicular
disease, vesicular stomatitis, and vesicular exanthema of swine.
Etiology
The genus Senecavirus and species Senecavirus A are found within
the family Picornaviridae. Senecaviruses are small, spherical, sin-
gle-stranded RNA viruses that have 4 structural proteins forming
the capsid. This virus was first isolated as a cell culture contami-
nant in 2002.
Epidemiology
Senecaviruses have circulated in swine in the US and other parts
of the world since at least 1988 with sporadic reports of vesicular
disease reported since that time. Recent, increasing numbers of
outbreaks of the disease have fostered more in-depth investi-
gations and research on the virus. Genetic analysis suggests all
Senecaviruses are closely related yet have different propensity to
cause lesions.
Although other species of animals have occasionally been found
to have antibodies against Senecaviruses, pigs are thought to be
the only host; no wildlife or avian species appear to act as a reser-
voir for Senecavirus A. Morbidity associated with Senecavirus A
infections can be extremely variable, but mortality is rare except
in neonates. In growing pigs and sows, clinical signs may be
absent or exceed 50%. Morbidity in suckling piglets can also be
quite high, with mortality ranging from 5% to 60%.
DISEASES CAUSED BY VIRUSES
The virus is likely spread by the fecal-oral route or through
breaches in the skin, but vertical transmission is also suspected.
The duration of shedding is not known but thought to be at least
10 to 14 days; some reports suggest the virus may be detected
in pigs for at least 28 days. Senecaviruses are susceptible to most
VIRUSES
modern disinfectants but because of their potential to be mis-
taken for exotic vesicular diseases, protocols effective for FMD
should generally be followed.
Pathogenesis
Experimental inoculation of susceptible pigs with Senecavirus A
will cause formation of vesicles on the snout, lips, coronary bands,
and interdigital spaces within 3 to 4 days after infection. Rup-
tured vesicles generally heal within a week but may persist longer,
especially if complicated with secondary bacterial infections.
Neonates infected with Senecavirus A may have lethargy, weak-
ness, and often fail to nurse, with diarrhea and death developing
as a consequence. The morbidity may be high. Outbreaks tend to
resolve quickly, usually running their course in 5 to 10 days. Mor-
tality in neonates can be quite high during the short, acute phase
of a herd outbreak.
Viral shedding in feces and oral or nasal secretions is detectable
for up to 28 days, but viremia is relatively short, starting around
3 days postinfection and resolving within a week. Immunity
appears to be rapid and long lasting, based on clinical observa-
tions and serological antibody assays.
Clinical signs
In acute outbreaks, clinical signs are generally of short duration,
lasting no more than 2 weeks. Sows are not usually systemically
ill; they have mild clinical signs, the most common of which are
the presence of vesicular lesions on snouts, lips, coronary bands,
and interdigital spaces. Transient mild lameness can be associated
with vesicular lesions on the feet. Increased mortality in neonates
is often seen in acute outbreaks, but vesicles are not usually
observed on piglets. Outbreaks in this group of pigs generally
have a short course (5 to 7 days), but up to 50% of piglets less
than a week of age can develop diarrhea, weakness, and lethargy,
leading to death.
Vesicles in sows may not be noticed until investigation of
decreased piglet livability is undertaken by the farmer; vesicles
can be easily overlooked without careful examination of multiple
individual animals. Along with the typical vesicular lesions, grow-
ing pigs may have acute lameness that can affect up to 80% of a
group; signs in this age group tend to be present for the relatively
short time of 2 to 10 days.
SENECAVIRUS A 103
 SWINE DISEASE MANUAL
Lesions
Grossly visible vesicles approximately 0.2 to 2 cm in diameter
form rapidly on snouts and coronary bands of growing or adult
animals and are apparent within 2 to 3 days of infection. The
vesicles rupture within 24 hours of emergence, form a superficial
ulcer, and then heal over a 1- to 2-week period. In acutely affected
neonates, gross lesions are usually absent, although increased mes-
VIRUSES
enteric and subcutaneous edema has been reported.
In experimental challenge studies of growing or adult swine,
characteristic histologic lesions are generally limited to skin,
although nonspecific inflammatory changes can be seen in some
other tissues. In neonates, microscopic changes may include mild
nonsuppurative infiltrates in lung, kidney, brain, or heart. Focal
ulcerative glossitis has also been observed.
104 SENECAVIRUS A
Diagnosis
History, clinical signs, and the appearance of vesicles on the snout
or feet should prompt an aggressive diagnostic investigation
to rule out FMD and to confirm Senecavirus A as the cause of
the lesions. Confirmation is usually made by polymerase chain
reaction performed on vesicle fluids, lesions, or oral fluids. Immu-
nohistochemistry, in situ hybridization, and fluorescent antibody
tests are also available for detection of the agent in lesions. The
virus can also be isolated from vesicular fluids or swabs from
acute lesions using tissue culture. Serology tests such as enzyme-
linked immunosorbent assay can indirectly implicate previous
infection but should not be relied on for diagnostic confirmation.
Control
Most outbreaks of Senecavirus A resolve fairly quickly as a result
of the development of herd immunity. There are no effective
treatments, immunoprophylaxis methods, or vaccines available to
prevent Senecavirus A infection. Prevention is through scrupu-
lous attention to details of external biosecurity, particularly those
involving transportation vehicles used for moving pigs to slaughter.

Swine enteric coronavirus diseases
Alternate names and abbreviations
SECD, transmissible gastroenteritis, TGE, TGEV, porcine epi-
demic diarrhea, PED, PEDV, porcine deltacoronavirus, PDCoV
Definition
Swine enteric coronavirus diseases (SECD) are a group of dis-
eases in swine caused by infection with one of several members
of the Coronaviridae family of viruses including transmissible
gastroenteritis (TGE) virus, porcine epidemic diarrhea (PED)
virus, and porcine deltacoronavirus (PDCoV). Swine enteric
coronavirus diseases are characterized by acute, rapidly spreading,
epidemic diarrhea in pigs of all ages. The severity of the disease
is generally related to the age of the pig, with younger pigs being
more severely affected. The World Organization for Animal
Health lists only TGE as an internationally reportable disease.
Occurrence
Enteric coronaviruses of pigs are found in most countries in the
world that have significant commercial pork industries. Exposure
to these viruses has been detected in some feral pig populations,
although prevalence appears to be at a low level and there is no
indication that feral pigs serve as a reservoir species. Viruses asso-
ciated with SECD are not zoonotic.
Historical information
Transmissible gastroenteritis was first described in 1946 in the
US, after which time the disease became endemic throughout
the US and other countries. Porcine epidemic diarrhea emerged
in England in the early 1970s and spread to other parts of Asia
and Europe over the next 30 years. In 2013, an epidemic of PED
occurred in the US that was associated with a highly virulent strain
of the virus circulating in Asia at the same time; the epidemic
eventually spread to include countries in Asia, Central and South
America, and Europe, where the infection remains in an endemic
state. In 2014, an emerging PDCoV first reported in Hong Kong
in 2012 was also discovered in the US. For purposes of regulatory
control during the US PED epidemic, the US Department of Agri-
culture began referring to all infections associated with TGE, PED,
or PDCoV as SECD. The term SECD has now come into common
usage in the US but less so in other countries.
Etiology
Coronaviridae is a family of enveloped, positive-sense, sin-
gle-stranded RNA viruses with a viral genome ranging from
approximately 26 to 32 kilobase (kb) pairs in length. Virions
are spherical, 120 to 160 nm across and are typically covered
with large approximately 20 nm club- or petal-shaped surface
projections referred to as spikes, which in electron micrographs
of spherical particles create an image reminiscent of the solar
corona, hence the more familiar name of coronaviruses.
DISEASES CAUSED BY VIRUSES
The virus family Coronaviridae is in the order Nidovirales. In the
sub-family Coronavirinae, there are 4 genera: Alphacoronavirus,
Betacoronavirus, Deltacoronavirus, and Gammacoronavirus.
Transmissible gastroenteritis virus, PED virus, and porcine respi-
ratory coronavirus are members of Alphacoronavirus. Betacorona-
VIRUSES
virus includes porcine hemagglutinating encephalomyelitis virus
and a number of human pathogens, most notably severe acute
respiratory syndrome-related coronavirus and Middle Eastern
respiratory coronavirus. Deltacoronavirus is relatively undescribed
and includes PDCoV.
Epidemiology
Infected pigs excrete SECD viruses in their feces for 2 to 3 weeks
postinfection with some reports of shedding for up 8 weeks. Typ-
ically, the viruses can be found in intestinal tissue for much longer
than in feces, with some reports describing recovery of the virus
from intestinal tissue for several months.
Contact with feces of infected pigs has been repeatedly shown to
be the most critical risk factor for transmission of SECD viruses.
Direct contact between pigs and indirect contact with the virus
through fomites is sufficient to cause infection. The role of con-
taminated livestock trucks in transmitting PED virus between
farms has recently been investigated. In this study, environmental
samples were collected from the inside floor of 575 livestock trail-
ers before and after pigs were unloaded into holding pens at 6 US
commercial slaughter facilities over several days. Before unload-
ing, 6.6% of the trailers were PED virus positive. Of trailers that
were negative at the time of arrival to the slaughter facility, 5.2%
were contaminated by the time the unloading process was com-
pleted. Despite biosecurity recommendations to the contrary, all
truck drivers were observed to have stepped into the slaughter
facility at least once during the unloading process, leading to
high rates of unintentional contact between abattoir staff and the
driver (or trailer).
Several studies have implicated large herd size as a risk factor
for the occurrence of SECD. These studies suggested that larger
herds tend to have continuous (weekly) farrowing, have regular
input of replacement gilts, utilize off-site contracted grow-finish
facilitates, are more likely to commingle postweaning pigs, and
utilize large (greater than 1000 head) grower pig facilities, all of
which increase the likelihood of bringing naïve pigs into contact
with infected pigs.
The potential for aerosol transmission of TGE and PED virus
over distances of a few meters has been established under exper-
imental conditions. However, the significance of this mode of
transmission in the spread of SECD viruses between farms under
field conditions is considered to be low. Although TGE and PED
viruses have been identified in common house flies (Musca domes-
tica), flies are not considered to act as a significant biological or
mechanical vector.
SWINE ENTERIC CORONAVIRUS DISEASES 105
 SWINE DISEASE MANUAL
Porcine-origin ingredients are routinely used as a part of the
commercial diets fed to pigs in many parts of the world. Their
risk as a possible vector for a number of pathogens has been
previously described and will not be reviewed here. However, the
potential for these ingredients to be a vector for PED virus was
raised specifically as part of investigations into the introduction
of PED virus into Canada in 2014 and the spread of PED virus
VIRUSES
within the US during the same period. Studies since this time
have shown that feed contaminated with virus (as a result of the
inclusion of porcine-origin products or as a result of cross-con-
tamination from other sources) has the potential to introduce
SECD viruses into farms or countries.
Milk from sows recently infected with TGE or PED virus has been
shown to contain infectious virus and is capable of infecting neo-
natal pigs that consume the milk. However, the significance of this
finding is questionable, given the multiple sources of virus a nursing
piglet would be exposed to if its dam was recently infected.
Pathogenesis
Infection with an SECD virus typically occurs through oral
exposure. All parts of the small intestine are capable of replicating
SECD viruses and their generation time is around 6 to 12 hours.
After exposure to the virus, clinical signs of diarrhea and vomiting
usually occur within 18 to 24 hours in young pigs, although older
animals may not show clinical signs until 2 to 3 days after expo-
sure. Although these viruses have been reported from nonenteric
tissues on occasion, the viruses replicate exclusively in enterocytes
of the small intestine. Virus can be shed for several days after
diarrhea has resolved.
Once infected, enterocytes rapidly cause severe damage to the
microvilli structure of the small intestine, which results in a
malabsorptive diarrhea. Younger pigs are more severely affected
than older pigs for two reasons: a larger proportion of the small
intestine tends to be affected in younger pigs, and the regen-
eration time of new enterocytes is slower in younger pigs, thus
efforts to repair damage to the intestinal mucosa are ineffective in
controlling the clinical disease.
Clinical signs
For the purposes of this chapter, clinical signs and pathology of
SECD (TGE virus, PED virus, and PDCoV) will be considered
as a single entity, based on the occurrence of essentially identical
syndromes among the diseases.
The clinical signs of epidemic outbreaks of SECD at both an
individual and herd level have changed little since the first report
of TGE in 1946 when the authors described:
... a disease characterized by diarrhea, vomiting in
some cases, rapid loss of weight, and a high death
rate in baby pigs…losses limited largely to pigs only
a few days old … recovery was prompt in older
106 SWINE ENTERIC CORONAVIRUS DISEASES
animals and the death loss was usually very small …
disease was observed affecting nearly entire herds of
shoats when there were no baby pigs on the farm ...
A number of observational or experimental studies describing
similar findings have been published since that time and summa-
rized by other authors; one should consider that TGE, PED, and
PDCoV are virtually indistinguishable in clinical presentation
and epidemiology.
When introduced into a susceptible herd, the disease usually
spreads rapidly with some degree of appetite loss and diarrhea
in most animals, with vomiting occurring in some animals. The
occurrence of SECD in a herd where most of the pigs are naïve is
referred to as epidemic or epizootic SECD. In this situation, most
pigs within a space (barn, room, or pasture) are affected within
a 2- to 5-day period. Transmission of the infection to adjoining
spaces is generally inevitable through movement of clinical or
subclinical pigs, contact with contaminated inanimate vectors, or
through short-distance aerosols. The incubation period is 18 to
72 hours. In piglets under approximately 2 weeks of age, infection
leads to vomiting and profuse, nonhemorrhagic diarrhea often
associated with a characteristic foul smell. Virtually 100% of pigs
less than 1 week of age will die within 2 to 7 days of the onset of
clinical signs. While morbidity in piglets over 1 week of age will
still approach 100%, mortality declines with age at onset, such
that most pigs infected at greater than 3 weeks of age will survive.
Older growing pigs and adults will have diarrhea, with vomiting,
and inappetence occurring less predictably. A sow acutely affected
during lactation may produce less milk, contributing to an even
more rapid decline in her affected litter.
Lesions
Gross lesions of SECD virus infection in acutely affected
neonatal piglets include dehydration, focal hemorrhages in
the submucosa of the stomach, highly fluid intestinal contents
having a yellow-green color, thinning of the small intestine wall,
engorged mesenteric blood vessels, and some evidence (paleness)
of degeneration in the kidney. Frequently, piglets of this age will
present with excessive amounts of curdled milk in the stomach
and an absence of chyle in mesenteric lymphatics. Virus does not
replicate, nor has it been identified, in peritoneal fluid, spleen,
kidney, pancreas, thymus, lung, or stomach. The most significant
lesions are confined to the small intestine and include congestion,
edema, and necrosis of intestinal villi.
Microscopically, lesions can vary based on the age of the pig,
stage of infection, and dose of virus. The key pathological feature
is villus atrophy, the speed and severity of which is mostly asso-
ciated with pig age. Virus can commonly be recovered from the
intestinal mucosa for 1 to 2 weeks postinfection. Desquamation
of enterocytes accompanied by villus blunting is apparent by 12
to 18 hours postinfection. By 24 hours, sloughed cells are begin-
ning to be replaced by enterocytes migrating upwards from the
crypt region.

Diagnosis
The typical coronavirus morphology of SECD viruses has been
described by electron microscopy. The virus is pleomorphic and
ranges in diameter from 95 to 190 nm, including the length of the
surface projections which are approximately 15 to 20 nm in length.
Isolation of SEDC viruses can be challenging. Most field strains
are difficult to grow in cell culture, generally requiring that other
methods be used to identify the viruses.
While serological testing as part of a diagnostic plan can be useful
in some circumstances, cross-reaction between various members
of the family has been described for at least 40 years and can
complicate interpretation. Few commercial serological tests are
available for routine diagnostic use, particularly for differentiating
exposure to the various porcine coronaviruses.
A number of techniques have been described for detection of
SECD viruses in tissue samples. The fluorescent antibody tech-
nique is a simple method and has been an important tool in con-
firming infection in field cases or experimental studies for many
decades. The technique is frequently used as a rapid and accurate
diagnostic test on frozen intestinal tissues from clinical specimens
for PED and TGE. False negative reactions can be a common
occurrence on acute or sub-acute samples if intestinal epithelial
cells have been severely denuded. Immunohistochemistry and in
situ hybridization assays have also been developed.
Increasingly, polymerase chain reaction assays capable of detec-
tion and differentiation of the SECD viruses are being used for
diagnosis as well as for environmental monitoring.
The following diseases should be considered in a differential
diagnosis of SECD based on clinical signs, lesions, or diagnostic
test cross-reaction: colibacillosis, coccidiosis, hemagglutinating
encephalomyelitis, porcine rotavirus infection, Clostridium per-
fringens type A or type C infection, swine dysentery, salmonello-
sis, ileitis, classical swine fever, and African swine fever.
Control
The porcine enteric coronaviruses are problematic for the
immune system to control because in an acute outbreak, the
pigs that are most severely affected (neonates) are faced with a
significant challenge dose of the virus almost immediately after
birth, are born with no pre-existing humoral defense specific to
the virus, have the maximum number of susceptible enterocytes
in their small intestine, and need to manage an infection caused
by a virus having a replication time of only 6 to 8 hours. In effect,
there is not sufficient time available for a neonatal piglet to
generate an active response to the infection before mortality is
likely to occur. Therefore, in this population of pigs, a ready and
ongoing supply of colostral and lactogenic immunoglobulin from
an immune dam is imperative in combating the infection.
In pigs older than 3 to 4 weeks, the pig is inherently less likely to
have severe clinical signs because the population of enterocytes
DISEASES CAUSED BY VIRUSES
is more resistant to infection with the viruses and those entero-
cytes that do become infected can be regenerated more quickly.
This situation tends to lead to only a transient diarrhea that is
self-limiting in 3 to 6 days, with little measurable effect on growth
or mortality. Given this clinical situation, much of the research
emphasis has been on developing methods to generate high-qual-
ity active immunity in breeding sows so that neonatal pigs born
VIRUSES
into a contaminated environment will be protected.
The primary means of controlling an acute outbreak of SECD
in a breeding herd is through rapid, intentional, and controlled
exposure of all sows in the herd to live virus; the technique has
been used for many diseases since the early 1950s. Prescriptive
step-by-step instructions for implementing this process of
“auto-vaccination” or “biofeedback” are not widely available, but
the objectives of all intentional exposure programs are the same:
to establish effective sow herd immunity to the virus as quickly as
possible in order that high-levels of colostral and lactogenic anti-
bodies are produced, thus protecting neonatal pigs from infec-
tion. Done correctly, this process will create an immune breeding
herd concurrent with a fully protected population of neonatal
pigs that can then be weaned into cleaned and disinfected facil-
ities. These two outcomes effectively eliminate the potential for
virus to come in contact with susceptible pigs, and eventual elimi-
nation of the virus from the farm will result. Intentional exposure
is done by collecting feces and digesta from acutely infected
neonates and then individually exposing each breeding sow to the
material via the oral route. Intentional exposure programs will
typically bring a return to normal farm productivity in approxi-
mately 4 to 6 weeks.
In acute outbreaks of these diseases in isolated herds of growing
pigs greater than 3 weeks of age, the infections are self-limiting
and will resolve without intervention beyond supportive care.
Critically, no new animals should be introduced into the popula-
tion for at least 60 days after cessation of clinical signs.
Vaccines are available for TGE and PED, although not for
PDCoV. In general, these vaccines do not generate immunity suf-
ficient to stop infection from occurring, eliminate clinical signs,
or limit ongoing transmission. However, some veterinarians have
found their use helpful as part of a whole-herd program to eradi-
cate the virus from particularly intractable infections.
There are no specific effective treatments for pigs affected by an
enteric coronavirus, although supportive care may have some
minor benefits in neonates.
SWINE ENTERIC CORONAVIRUS DISEASES 107
 SWINE DISEASE MANUAL
Swine vesicular disease
Alternate names and abbreviations
SVD, SVDV
Definition
A viral disease manifested by vesicles on the feet (coronary
VIRUSES
bands), snout, mouth, and teats. Clinical course is mild and short
in duration with the primary concern being the need to differen-
tiate it from foot-and-mouth disease (FMD).
Occurrence
The virus is reported as endemic in Italy, with sporadic reports
of disease outbreaks in other parts of Europe and Asia. Because
the disease is mild, it may be subclinical or not noticed. Some
countries employ active serological surveillance to monitor for
infection in swine populations.
Swine are the only known natural hosts for swine vesicular disease
virus. The virus is not considered zoonotic, although there are
rare, historic reports of transient infection of humans working
with the virus in a laboratory setting; however, none with recent
circulating strains.
Historical information
First identified in Italy in 1966, swine vesicular disease has been
reported throughout Europe and Asia. It has been eliminated
from most swine-rearing regions but is still occasionally reported
from Italy and Portugal with rare sporadic outbreaks in other
parts of Europe. This disease is no longer listed by the World
Organization for Animal Health because improved diagnostic
testing allows it to be readily detected and differentiated from
FMD and the virus does not cause significant economic losses.
Etiology
Swine vesicular disease virus is a member of the genus Enterovi-
rus within the family Picornaviridae. It is closely related to and
thought to be derived from a coxsackievirus serotype of human
enterovirus B.
Picornaviruses are non-enveloped, single-stranded RNA viruses
that tend to be quite hardy in the environment. All strains of
swine vesicular disease virus are considered as the same serotype.
Epidemiology
Pigs are the only natural host for swine vesicular disease virus,
although there is a report of sheep that were held in close contact
to affected pigs seroconverting to the virus. The primary method
of transmission between pigs is through direct contact with
affected pigs, exudates, lesions, or feces. Other methods of trans-
mission include orally through feeding of uncooked waste food,
contact with contaminated fomites, and through transport in
contaminated vehicles.
108 SWINE VESICULAR DISEASE
Pigs shed virus in nasal secretions, oral fluids, feces, urine, and
serum, with shedding possible for up to 2 days prior to the
appearance of clinical signs. Most pigs clear the virus within 2 to
3 weeks, although a few may harbor the virus for longer periods
of time.
The virus is quite hardy and survives over a broad pH range of
2.5 to 12. It survives in environment, manure, slurry, or organic
substrates for months and has been shown to remain viable in
processed meats for up to 2 years; this resistance to environ-
mental extremes helps to account for the importance of indirect
methods of transmitting the virus between pigs or farms. Swine
vesicular disease virus is fairly resistant to disinfectants. Disinfec-
tion protocols developed for use in foot-and-mouth elimination
programs are also used for swine vesicular disease virus.
Pathogenesis
Virus enters via the skin, mucus membranes, or digestive tract,
with viremia occurring within 1 to 2 days. The period between
infection and the appearance of clinical signs can vary from 2 to
7 days, with viral shedding occurring before lesions or clinical
signs are observed. The virus can be found in high titers within
vesicles of the skin, epithelial tissues, and occasionally myocar-
dium or brain.
Clinical signs
The predominant clinical signs of infection with swine vesicular
disease virus are the vesicular lesions that develop on the coronary
bands or interdigital spaces of feet, and epithelium of the lips,
mouth, snout, tongue, and occasionally the teats of lactating
sows. Clinical signs can develop within 1 to 2 days and become
apparent at about the same time lesions develop. In mild cases of
lameness, the lesions may easily go unnoticed.
Lesions
Any vesicular lesions of coronary bands, feet, lips, snout, mouth,
or teats should be thoroughly investigated, since the lesions of
swine vesicular disease are indistinguishable from those of FMD.
Lesions of swine vesicular disease are most common around cor-
onary bands and the skin of the foot, and less prominent on the
snout, lips, or tongue. Lesions start as small vesicles that rupture
within 24 hours, leaving a red scab. Lesions usually heal within
7 days, with complete recovery occurring over 2 weeks. Histo-
pathology of the skin lesions is typical of other vesicular diseases
and is devoid of any particularly distinguishing features. Occa-
sionally, affected pigs may have mild nonsuppurative myocarditis
or encephalitis, but this is usually of no clinical impact.
Diagnosis
The investigation of swine vesicular disease often begins with
examination of a recumbent pig suffering from acute lameness.
Examination of peracutely and acutely affected pigs will identify
areas of blanching on the coronary band that will be followed

by vesicle development (and perhaps rupture) within 24 hours.
During this acute phase, ulcers may be observed in and around
the mouth as well. However, confirmation of diagnosis must be
made by laboratory testing.
Confirmation of acute cases is through demonstration of the
virus in tissues with lesions, lesion scrapings, or vesicular fluids.
Polymerase chain reaction, antigen-capture enzyme-linked
immunosorbent assay (ELISA), and immuno-stains are available
to assist in identifying the presence of the virus in lesions. Virus
isolation is possible but usually done only to assist in resolving
other equivocal test results. Other viruses, including other strains
or members of Picornaviridae, can cause lesions similar to swine
vesicular disease. Care is necessary for proper sampling, process-
ing, and testing to ensure an accurate diagnosis.
DISEASES CAUSED BY VIRUSES
Feces and serum can be used for monitoring disease occurrence
at a herd level in endemic regions. Serology is usually done by
ELISA and should be used only for monitoring or surveillance
and not relied upon for diagnosis of acute disease. Because
the goal of control is elimination, serological surveillance is an
important component of control.
VIRUSES
Control
There is no treatment for this disease. In most instances, the usual
objective after detection of an outbreak is to eradicate the virus by
stamping out positive herds, followed by disinfection.
Countries and regions that are free of the disease should strive to
remain so by screening the introduction of new stock, restricting
pork products from areas that have infection, and eliminating
waste food feeding.
SWINE VESICULAR DISEASE 109
 SWINE DISEASE MANUAL
Swinepox
Alternate names and abbreviations
Pox, congenital swine pox, congenital pox, SwPV
Definition
A viral disease caused by swinepox virus that is characterized by
VIRUSES
the acute appearance of round to oval cutaneous lesions that heal
in 3 to 4 weeks.
Occurrence
Swinepox occurs only in swine. All age groups are susceptible, but
most outbreaks are encountered in young growing pigs. It occa-
sionally occurs congenitally and in neonates. Swinepox occurs
worldwide in the major swine-raising countries. It occurs more
often where the insect vectors of swinepox virus are not con-
trolled. Modern swine raised free of lice rarely exhibit the disease.
Historical information
Swinepox was first reported in Europe in 1842 and in the US in
1929. The disease persisted and was relatively common, perhaps
because it caused little obvious economic loss to swine produc-
ers. Outbreaks were once caused by 2 viruses: vaccinia virus (a
laboratory strain) and swinepox virus. Vaccinia virus is no longer
used to vaccinate people against smallpox and hence it no longer
spreads to pigs. Only swinepox virus now causes the disease.
Etiology
Swinepox virus, a member of the genus Suipoxvirus within the
Poxviridae family, is the etiologic agent. The virus is rather resis-
tant to environmental degradation; it persists in scabs for up to a
year. Microscopically, the virus is visible as large intracytoplasmic
inclusions in infected cells.
Epidemiology
Persistent virus within desquamated scabs can be transmitted
to other pigs when introduced into skin abrasions. The virus
can also spread horizontally from nasal and oral secretions from
infected pigs. Once a few virus-containing lesions appear, the
virus can be transmitted mechanically by the bites of vectors that
have recently fed in pox lesion areas. Common vectors include
the hog louse (Haematopinus suis), mosquitoes, and biting flies.
Once introduced, infected swine or virus-carrying biting insects
can initiate outbreaks in susceptible herds. There is evidence of
transplacental infection of neonatal pigs.
110 SWINEPOX
Pathogenesis
Virus introduced into abrasions replicates in cells of the stratum
spinosum causing typical skin lesions to develop. The lesions go
through the stages of macules, papules, vesicles, pustules, and
crusts. All but the vesicle stage are easily identified. As lesions
mature and heal, crusts containing virus desquamate and leave
white macules.
A viremic stage of the disease has not been demonstrated. How-
ever, it must occur in some animals since transplacental infection
of neonatal piglets has been reported. Antibody to swinepox
virus is formed as a consequence of infection and immunity is
long-lasting.
Clinical signs and lesions
Systemic clinical signs of disease are seldom observed, but the
skin lesions are easily seen. Initial lesions usually occur along the
ventral aspect of the abdomen, inside the legs, and in inguinal
areas; all of these areas are favorite feeding sites of lice. However,
lesions have been observed at many cutaneous sites, so most of
the skin appears to be susceptible. Initially, there are small vesicles
that are largely unnoticed. The papules that result occur as 1 to 3
mm circular red spots. As lesions mature, crusts form that even-
tually heal uneventfully. In severe infections, lesions may occur in
upper respiratory and digestive tracts. This is particularly true of
congenitally acquired pox where piglets are born with or develop
lesions over the entire body shortly after birth. Exudative epider-
mitis and secondary bacterial dermatitis occasionally occur as a
sequel to swinepox. Swinepox does not appear to cause a pruritic
response in affected pigs.
Diagnosis
Swinepox is easily diagnosed by identifying the lesions. Lesions
are round to oval and are usually less than 1 cm in diameter. The
brown to black crusts are easily seen, but the vesicle stage can
seldom be identified grossly. If confirmation is needed, histologic
diagnosis can be made by identifying typical large intracytoplas-
mic inclusion bodies in cutaneous lesions. Pox lesions should
be differentiated from those of other vesiculating viral diseases,
pityriasis rosea, dermatosis vegetans, streptococcal dermatitis,
ringworm, and exudative epidermitis.
Control
Control of swine pox relies on the establishment of herd immu-
nity and prevention of transmission. Swinepox is seldom a
problem if the usual vectors of the virus, especially hog lice, are
controlled by insecticides or elimination. Congenital swinepox is
generally a sporadic, self-limiting event. There are no treatments.

Vesicular exanthema
Alternate names and abbreviations
VE, VEV, vesicular exanthema of swine virus, VES, VESV, San
Miguel sea lion disease, SMSL
Definition
An acute, rare, contagious disease of swine characterized by
vesicles on the feet, snout, mucous membranes of the mouth and
tongue, and non-haired skin. The disease in sea lions causes vesi-
cles on the flippers.
Occurrence
Of the domestic animals, vesicular exanthema occurs only in
swine. The disease has never been reported from any country
other than the US. Vesicular exanthema has not recurred in
domestic swine since it was eradicated in 1956.
San Miguel sea lion virus disease occurs in sea lions, fur seals, ele-
phant seals, opal-eye fish, and several other marine animals off the
western coast of the US.
Historical information
The disease has only occurred in the US, and the historical
record is incomplete. The disease was apparently first reported
in California around 1932, presenting with lesions that closely
resembled those of foot-and-mouth disease. The 1932 outbreak
was linked to feeding of uncooked garbage and fish scraps to pigs.
During the 1950s, infection spread more generally across the US
and the principle route of transmission was thought to be a result
of feeding untreated contaminated garbage, although direct
transmission from infected pigs was also possible. As a result of
an organized and vigorous campaign, vesicular exanthema was
eradicated in 1959 and declared to be an exotic disease.
Beginning in 1973, caliciviruses indistinguishable from the virus
that causes vesicular exanthema were isolated from sea lions,
northern elephant seals, fur seals, and certain kinds of fish. Each
of the viruses can produce lesions in swine and certain sea mam-
mals. Research continues with these viruses and new serotypes are
being identified.
Vesicular exanthema of swine virus and some recent serotypes of
San Miguel sea lion virus have occasionally been isolated from
humans with blisters. However, the virus is not considered to be a
serious public health threat.
Etiology
Vesicular exanthema of swine virus is a non-enveloped RNA
virus in the family Caliciviridae. The calicivirus that causes
vesicular exanthema and San Miguel sea lion disease is believed
DISEASES CAUSED BY VIRUSES
to be the same. Caliciviruses have a cup-shaped morphology
from which they are named. The calicivirus that causes vesicular
exanthema is sensitive to many common disinfectants, includ-
ing 2% sodium hydroxide.
VIRUSES
Epidemiology
The opal-eye fish (Girella nigricans) now is believed to be the
primary host of the calicivirus that may be passed to pinnipeds
and swine. The method of spread of the virus among sea lions and
other sea mammals is speculative. It could be through ingestion
of infected fish or small marine life, by coastal contamination, or
direct contact.
Swine are usually exposed to the vesicular exanthema calicivirus
by eating uncooked garbage containing infectious meat scraps
from swine or certain fish. Although unproven, some marine-ori-
gin feed supplements for swine may contain calicivirus. Vesicular
exanthema is quite contagious among swine and spreads by direct
contact and fomites. Neither long-term carriers nor aerosol
spread have been demonstrated.
Pathogenesis
In swine, historical outbreaks of vesicular exanthema were usually
related to feeding of uncooked food waste. Virus enters the epi-
thelium through abrasions and multiplies in the basal layer of the
epidermis. Intracellular and intercellular edema and coalescence
of disintegrating cells lead to vesicle formation. Virus spreads cell
to cell as lesions develop. A low-grade viremia occurs and leads to
secondary lesions at other sites. Extensive lymphocyte destruction
occurs in regional lymph nodes. Since much of the basal layer of
the epidermis survives, regeneration of epithelium in swine usually
occurs within 1 to 2 weeks. Lesions in sea lions closely resemble
those seen in swine.
Experimentally, it requires much more virus by oral exposure
to produce vesicular exanthema than is required by intradermal
injection. This suggests that the virus can be spread more readily
through abrasions on the skin. Most swine infected with vesic-
ular exanthema will recover if allowed to do so. However, it is
anticipated that USDA-APHIS would require that infected pigs
be destroyed as a precaution to prevent the surreptitious entry of
foot-and-mouth disease.
Diagnosis
Vesicular exanthema of swine virus can be grown in cell culture.
In addition, electron microscopy and polymerase chain reaction
assays can be used to assist in identifying the virus in tissue or
blood. Available serological tests include complement fixation,
virus neutralization, and enzyme-linked immunosorbent assay.
VESICULAR EXANTHEMA 111
 SWINE DISEASE MANUAL
Vesicular stomatitis
Alternate names and abbreviations
VS, VSV
Definition
A vesicular viral disease capable of infecting cattle, horses, swine,
VIRUSES
people, and many kinds of wildlife.
Occurrence
Vesicular stomatitis is endemic in various regions of North, Cen-
tral, and South America. Widespread epidemics usually occur
about every 10 years. The virus is endemic in areas of the south-
western US, but it has not spread to swine. Most outbreaks of vesic-
ular stomatitis affect horses and cattle, less often swine. Infection
also occurs in deer, bobcats, raccoons, feral swine, and rodents.
Historical information
Vesicular stomatitis was first recognized in horses during the Civil
War. In 1943, infection occurred in swine stemming from the use
of vesicular stomatitis virus-contaminated hog cholera serum. The
endemic nature of vesicular stomatitis in limited geographic areas
and its epidemic nature in other areas remain unexplained by
epidemiologists. The close resemblance of vesicular stomatitis to
foot-and-mouth disease and other exotic vesicular diseases con-
tinues to compel interest in the disease by animal health officials.
Etiology
Vesicular stomatitis is caused by one of four named viruses in the
genus Vesiculovirus of the family Rhabdoviridae: vesicular sto-
matitis New Jersey virus (VSV-NJ), vesicular stomatitis Indiana
virus (VSV-IN), vesicular stomatitis Alagoas virus (VSVAV),
and Cocal virus. The VSV-NJ and VSV-IN appear to be most
common in pigs and other livestock in the US. There is little
immunological cross-protection after infection with one of the
viruses. Vesicular stomatitis virus is not considered to be highly
contagious among domestic animals.
Epidemiology
Livestock are not able to maintain vesicular stomatitis viruses
long-term and the reservoir or amplifying hosts are unknown.
Deer mice (Peromyscus species) can become viremic. These and
other small rodents have been proposed as possible reservoir
hosts; however, the complete epidemiology of vesicular stomatitis
is not fully understood.
Vesicular stomatitis viruses are endemic in southern Mexico,
Central America, and northern South America but VSV-NJ and
VSV-IN regularly cause localized outbreaks in southern regions
of the US. There may be unknown reservoirs and vectors of the
virus, including insects. The disease remains endemic in certain
river basins and coastal areas. In temperate zones, the appearance
112 VESICULAR STOMATITIS
of vesicular stomatitis usually coincides with the appearance of
warm weather and ceases with the first frosts. This suggests that
the virus is transmitted by insects, especially to horses and cattle,
which are frequently infected while on pasture. However, insect
transmission does not appear to be essential, as contact transmis-
sion between horses has occasionally been observed.
Vesicular stomatitis virus has been isolated from both biting and
nonbiting insects. Insect vectors are thought to introduce vesic-
ular stomatitis virus into populations of domesticated animals.
Sand flies, blackflies, and Culicoides midges can act as biolog-
ical vectors; however, studies have not supported their role in
long-distance transmission between farms or between geographic
regions. Once animals develop lesions, insects may become
infected by feeding on viruses in the lesions or in contaminated
secretions; these insects then pass the infection to a susceptible
animal at the next feeding.
Fomites associated with recent outbreaks have been shown to
play a role in the spread of vesicular stomatitis to swine.
Pathogenesis
Virus appears to require introduction into epithelium through
insect bites or abrasions of the skin. However, transmission may
occur through the respiratory tract. After an incubation period
of 3 to 7 days, lesions appear initially as small, blanched papules.
Lesions first develop in cells of the stratum spinosum and vesicles
form. Epithelial cells above the stratum basale separate in about
30% of the cases. Loss of fluid through the stratum corneum
results in inspissation (thickening by dehydration) of many
lesions. The devitalized epithelium over vesicles soon erodes to
leave shallow craters that fill with serum and erythrocytes. Since
the basal layer of epidermis usually remains intact, most lesions
soon heal. Gross and microscopic lesions of the vesicular diseases
of swine are similar to those of other species, and their morphol-
ogy is not an adequate basis for differential diagnosis.
Clinical signs and lesions
Clinical signs are similar in all of the vesicular viral diseases of
most domestic species, but there are a few differences peculiar to
species and in the location of most lesions. Infection with vesic-
ular stomatitis virus stimulates a sharp rise in temperature that
usually regresses after onset.
In swine, vesicles on the feet are common. Lameness is often the
first sign that is noticed. Vesicles that form and coalesce around
the coronary band may lead to loss of hooves, foot deformity,
and persistent lameness. Vesicles frequently occur on the snout
and may extend into the nares. If lesions develop on the lips or
in the mouth, there may be excessive salivation, slobbering, and
chomping. Lesions are occasionally seen on the vulva or scrotum.
In nursing sows, vesicles may occur on the teats. Vesicles often
develop at points of abrasion.

Vesicles usually rupture within 24 hours and the overlying
epithelium detaches to leave shallow erosions with reddened or
hemorrhagic surfaces. Lesions usually heal within 2 weeks unless
secondarily infected with bacteria.
Pregnant sows may abort as a consequence of fever but none of
the vesicular viruses have been reported to affect fetuses. The
morbidity rate for vesicular stomatitis is highly variable and
ranges from 5% to more than 90%. Some reports suggest that
only 10% to 20% of the animals in a herd may become symptom-
atic even though nearly all may seroconvert to the virus.
Diagnosis
Because signs and lesions of the vesicular viral diseases are similar,
a variety of laboratory techniques have been developed for dif-
ferential diagnosis. In the US, the Federal Animal Disease Diag-
nostic Laboratory at Plum Island, New York, will usually have
responsibility for confirming a diagnosis of vesicular stomatitis. If
signs or lesions consistent with vesicular stomatitis are observed,
state animal disease control offices should be contacted and will
help make necessary arrangements for sample testing.
Epithelial and vesicular fluid samples can be tested using com-
plement fixation or enzyme-linked immunosorbent assay tests to
identify viral antigen. Heparinized and clotted blood should be
collected for virus isolation and identification, and for serological
DISEASES CAUSED BY VIRUSES
testing, respectively. Virus isolation and polymerase chain reac-
tion assays are readily available for vesicular stomatitis diagnosis.
A full set of tissues should be taken for histologic evaluation.
Foot-and-mouth disease is of primary concern in differential
diagnosis. If horses are affected, it is useful to know that horses
are susceptible to vesicular stomatitis but are not susceptible to
the other exotic vesicular viral diseases.
VIRUSES
Control
During outbreaks of vesicular stomatitis, uninfected livestock
should be kept away from any animals that could be infected.
Quarantines and animal movement restrictions can help reduce
virus spread.
There should be no movement of animals from a quarantined
property for at least 21 days after all lesions are healed. Isolating
symptomatic animals may also be helpful in controlling spread
within a herd. Potential fomites should be cleaned and disin-
fected to prevent spread of the virus.
Emergency measures for control of outbreaks of vesicular diseases
in swine require quarantine, identification of the disease, and
slaughter of all infected and exposed swine. This is followed by a
thorough cleaning and disinfection of the premises.
VESICULAR STOMATITIS 113
VIRUSES

114 VESICULAR STOMATITIS

 Section III

Emerging viruses

Filoviruses (Ebola virus and Marburg virus), Hepatitis E virus ...............................................................................................117

Paramyxoviruses (Menangle and Nipah viruses), Pestivirus F (Bungowannah virus) .........................................................118

EMERGING
Porcine adenovirus, Porcine astrovirus, Porcine bocavirus ..................................................................................................119
Porcine parainfluenza virus type 1, Porcine sapovirus..........................................................................................................120
Torque teno virus, West Nile virus (Kunjin virus) ................................................................................................................121

115
 116
EMERGING

Filoviruses (Ebola virus and Marburg virus)
Ebola virus (EBOV) and the closely related Marburg virus
(MARV) belong to the family Filoviridae. They are enveloped,
filamentous, negative-sense RNA viruses and may be associated
with severe zoonotic disease in humans. Currently four species of
EBOV have been reported: Zaire ebolavirus (ZEBOV), Sudan
ebolavirus (SEBOV), Ivory Coast ebolavirus, and Reston ebola-
virus (REBOV). A fifth species, Bundibugyo ebolavirus, has been
proposed. Filoviruses occur mainly in regions of Africa; bats are
thought to be the primary reservoir hosts. Four species of EBOV
have caused fatal disease in humans, with mortality rates of 50%
to 90%, depending on virus strain. In contrast, REBOV has never
been identified as the cause of disease in people, though there are
some reports of seroconversion occurring.
Reston virus has been detected in pigs that were suffering from
porcine reproductive and respiratory syndrome in China and the
Philippines. Subsequently, several pig farmers were found to be
seropositive for REBOV antibodies, providing a strong indica-
tion that they acquired the virus from infected pigs. Experimen-
tally, infection of pigs with both REBOV and EBOV has been
successfully achieved.
Hepatitis E virus
Hepatitis E virus (HEV) is a non-enveloped RNA virus in the
genus Orthohepevirus in the family Hepeviridae. There is a single
HEV serotype, but the genus Orthohepevirus contains 4 subgen-
era based on species affected. Within the subgenus Orthohepevi-
rus A, there are at least 7 different genotypes. Hepatitis E virus-3
and HEV-4 are zoonotic with swine serving as the reservoir host.
Little is known about virus survival outside the host. However,
HEV is thought to be stable in the environment since feces are
an important source of infection. Heating pork products to an
internal temperature of 160°F (71°C) for 20 minutes is required
to completely inactivate HEV.
Hepatitis E virus can be isolated from many different species,
including pigs, and is zoonotic. The severity of infection in
humans varies from subclinical to causing fulminant hepatitis and
occasionally reproductive disease. Pigs are the most important
animal reservoir for genotypes capable of infecting people.
EMERGING VIRUSES
A 2-part study was undertaken to determine the effect of REBOV
on pigs. For each study, 8 pathogen-free pigs were kept in 2 groups
of 4. In study 1, REBOV genome was detected in nasopharyngeal
secretions of pigs from 2 to 8 days following exposure by the
oronasal route. Neither genome nor virus was found in rectal
swabs, urine, or blood of these animals at any time. Tissue samples
collected at euthanasia on day 28 after infection were negative by
polymerase chain reaction (PCR) for REBOV. In study 2, REBOV
genome was found in nasopharyngeal secretions, rectal swabs,
blood, skeletal muscle, and most other organs and tissues that were
sampled 1 to 2 weeks after inoculation.
In experimentally infected 3- to 6-week-old piglets, ZEBOV
EMERGING
caused mostly respiratory signs with no hematologic abnormali-
ties. Experimentally infected pigs were able to transmit the infec-
tion to in-contact pigs and indirectly to non-human primates.
Until recently, validated serologic tests have not been available to
determine the significance, if any, of wild pigs as a vector or reser-
voir species for EBOV in West Africa. In Sierra Leone, 400 sera
from village pigs were analyzed for the presence of EBOV-specific
antibodies. Three samples reacted with antibody to EBOV nucle-
oprotein but had no neutralizing antibodies.
The virus can be found in nearly every region in the world. Geno-
typic niches occur, with HEV-3 and HEV-4 mainly occurring
in the US. Eighty to 100% of commercial swine farms in the US
show evidence of infection with HEV. Most pigs acquire HEV
via the fecal-oral route, and HEV infections in swine are usually
asymptomatic. Hepatitis E virus is not cultivatable in cell culture.
Hepatitis E infection of people in both developed and developing
countries appears to be on the rise. A number of recent review
articles are available describing important risk factors for infec-
tion with human or environmental genotypes of the virus as well
as zoonotic infections arising from contact with pigs, their waste,
or pork products (usually undercooked liver or pates). Several
hundred papers are published each year on this disease in people;
far fewer papers deal with the disease directly in pigs.
Hepatitis E virus infection of people caused either by environ-
mental or swine-origin viruses appears to be increasing globally.
FILOVIRUSES; HEPATITIS E VIRUS 117
 SWINE DISEASE MANUAL
Paramyxoviruses (Menangle and Nipah viruses)
Menangle and Nipah viruses are members of the family
Paramyxoviridae, which also includes a number of other viruses
that have emerged following transmission to a new host species.
For example, measles virus emerged in humans around 10,000
years ago from an undetermined host, which also appeared to be
a common ancestor of the ruminant viruses Rinderpest and peste
des petits. Also, canine distemper virus has recently emerged in
lions, various marine mammals, and ferrets, presumably as a result
of a jump from its domestic dog host. Pteropid fruit bats are the
reservoir host for Menangle and Nipah viruses.
Nipah virus emerged in pigs in Malaysia and Singapore in
1999. In a dramatic, multi-site outbreak, pigs were exhibiting
EMERGING
respiratory and neurological signs. Morbidity was high in these
outbreaks, but mortality was only moderate. Concurrently, some
pig-farm workers were also showing signs of severe pneumonia
as a result of direct contact with pigs or through short-distance
aerosols; pigs are thought to act as amplifying hosts for the
virus. An extensive epidemiological workup involving both
veterinarians and public health workers was conducted around
the outbreak. To eradicate the outbreak, approximately 1,000,000
pigs were euthanized over approximately 6 months. An estimated
265 people were infected with Nipah virus, of which 105
died - a case fatality rate of nearly 40%. Though this outbreak
was contained, smaller outbreaks have continued to appear in
the region including Bangladesh, India, parts of South Asia,
and Oceania. These outbreaks have primarily involved people
(including human-to-human transmission) and ruminants.
Nipah virus is closely related to Hendra virus, which to date has
only been found in Australia. Hendra virus shares similar features
to Nipah, but thus far infection has been limited to pteropid bats,
horses, and humans.
Pestivirus F (Bungowannah virus)
In June 2003, an outbreak of disease was reported on a pig farm
in New South Wales, Australia. The outbreak initially presented
as sudden death in 2- to 3-week-old piglets around the time
of weaning, but soon after the onset, deaths were observed in
younger pigs and there was a marked increase in the birth of
stillborn piglets, with a slight increase in the occurrence of mum-
mified piglets. Cumulative losses in some weeks exceeded 50%
of piglets born, and estimates for losses to production from the
outbreak were as high as 50,000 pigs.
Gross lesions at necropsy included hydropericardium, excess
pleural and pericardial fluid, and a dilated heart. Some affected
118 PARAMYXOVIRUSES; PESTIVIRUS F
Menangle virus, like Nipah and Hendra viruses, circulates among
flying foxes. It has only been identified in Australia. The virus
does not cause disease in bats; however, in the single outbreak
in pigs that occurred in New South Wales, Australia in 1997,
reproductive disease was apparent. During this outbreak, infected
sows gave birth to litters with mummified or stillborn piglets,
some with congenital defects of the skeleton and central nervous
system. No clinical disease was otherwise noted in the sows or
in other pigs on the farm. There is no evidence that Menangle
virus continues to circulate in Australian pigs, but sporadically,
individual pigs have been found to be antibody positive to the
virus. Menangle virus is zoonotic, as evidenced by two farm
workers who were in close contact with infected pigs on the New
South Wales outbreak farm becoming ill with severe but self-
limiting influenza-like disease; the workers were later determined
to be antibody positive for Menangle.
After experimental inoculation, 6-week-old pigs were found to
shed Menangle virus in nasal and oral secretions, urine, and feces,
and could transmit the infection to in-contact pigs. Though pigs
remained asymptomatic throughout the study, virus shedding in
the urine of some pigs continued for nearly 3 weeks, but there
was no evidence that pigs become persistently infected beyond
this period. No efforts have been made to reproduce the disease in
pregnant sows.
Pteropid bats have featured significantly in the last 10 to 15 years
as a source of emerging viral diseases in humans and livestock. It
is assumed that human effects (deforestation, increasingly inten-
sified livestock production near bat habit, climate change, etc) on
the bat’s normal habitat are placing bats, livestock, and humans
in greater contact than ever before and therefore increasing the
opportunity for interspecies disease transfer.
stillborns had a distinctive subcutaneous edema over the head
and thorax. Pathological changes in affected animals consisted
almost exclusively of a multifocal non-suppurative myocarditis,
with myonecrosis observed in some cases. The clinical presenta-
tion was referred to as the porcine myocarditis syndrome. The
virus was initially named Bungowannah virus and was recently
renamed Pestivirus F.
To date, the virus has only been detected in a limited number
of farms in Australia. Other countries, including the US, have
undertaken limited surveillance for the agent but it has not been
detected outside Australia.

Porcine adenovirus
Porcine adenovirus (PAdV) is a non-enveloped DNA virus in the
genus Mastadenovirus, family Adenoviridae. There are currently
3 porcine species and 5 serotypes recognized: PAdV-A (serotypes
1-3), PAdV-B (serotype 4), and PAdV-C (serotype 5). Adeno-
viruses are relatively host-specific, and pigs are the only known
hosts for PAdV.
The geographic distribution of PAdVs is not fully known,
although the virus is suspected to be widespread in domestic
swine populations. Serological surveys from Canada and England
in the 1960s and 1970s indicated that up to 60% of swine test
positive for anti-PAdV antibodies; additional countries in Europe
and South America have since reported presence of the virus and
it is assumed the virus is distributed globally. However, current
seroprevalence data is lacking.
Porcine astrovirus
Porcine astrovirus (PAstV) is a non-enveloped RNA virus in the
family Astroviridae. There are 5 known lineages, each having sub-
stantial genetic variability. Astrovirus (AstV) is resistant to heat
and requires very acidic pH for inactivation; it can survive for a
long time in the environment.
Astroviruses affect a wide variety of species and are mostly asso-
ciated with gastrointestinal disease. Porcine astrovirus was first
isolated from the feces of pigs in 1980. Astroviruses have also
been linked to neurological disease in humans, mink, cattle, and
sheep. Recently, PAstV-associated polioencephalomyelitis has
been reported in pigs in Hungary and the US. Porcine astrovirus
has previously been found in pigs with congenital tremors but the
significance of this is unknown.
The zoonotic potential of AstV is unclear; porcine-human AstV
recombinants have been documented and human-to-pig trans-
mission is suspected. Porcine astrovirus has been isolated from
pigs worldwide. Human AstV infections are most common in the
Porcine bocavirus
Porcine bocavirus (PBoV) is a non-enveloped, single-stranded
DNA virus in the family Parvoviridae, genus Bocavirus. Although
bocaviruses (BoVs) have been recognized in veterinary medicine
since the early 1960s, PBoV was not isolated until 2009 in Swe-
den, where the virus was found in the lymph nodes of pigs with
post-weaning multisystemic wasting syndrome.
Currently there are seven known PBoV genotypes, divided into
three distinct groups based on the sequence of the VP1 gene:
PBoV G1, PBoV G2, and PBoV G3.
PORCINE ADENOVIRUS; PORCINE ASTROVIRUS; PORCINE BOCAVIRUS 119
EMERGING VIRUSES
Porcine adenovirus generally causes subclinical infections and
is commonly isolated from the gastrointestinal tract of normal
swine. However, PAdV has been sporadically associated with
enteritis, encephalitis, nephritis, respiratory disease, conjunctivi-
tis, and reproductive disorders, though other concurrent diseases
or causes of immune suppression are frequently reported in these
instances.
Porcine adenovirus has been detected on pork carcasses after
bleeding, dehairing, pasteurization, and evisceration, and on
some retail pork samples. Most evidence suggests adenovirus in
these locations is due to fecal or wash-water contamination rather
than a primary infection of the carcass or tissue.
EMERGING
Adenovirus-based products have been developed for use as vec-
tors in both human and animal vaccines.
winter, but there is little information about seasonal incidence of
AstV infection in pigs.
Prevalence of PAstV in swine feces can be very high. However,
viral co-infection with other enteric pathogens (eg, rotavirus,
transmissible gastroenteritis virus, porcine circovirus 2, and por-
cine hemagglutinating encephalitis virus) is often observed. Case
fatality rates for PAstV-associated neurological disease on affected
US swine farms have been reported between 75% and 100%.
Transmission of PAstV is thought to be fecal-oral. Porcine astro-
viruses are thought to cause mild, self-limiting secretory diarrhea.
Young pigs are most affected. Viral co-infections may contribute to
observed clinical signs. Reported neurological signs associated with
PAstV include hind limb weakness, posterior paraplegia, quadri-
plegia, convulsions, loss of consciousness, and flaccid paralysis of
muscles. Congenital tremors may be related to PAstV infection in
in piglets, but this is unclear.
Survival of PBoV in the environment has not been reported. In
general, parvoviruses are very resistant to dry heat, requiring
158°F (70°C) for 10 minutes to become inactivated. In
addition to infecting pigs, BoVs have been linked to respiratory
disease, gastrointestinal disease, and reproductive loss in cattle.
No cases of PBoV have been reported in humans. However,
PBoVs and human strains are antigenically cross-reactive. Viral
recombination has also been documented in both human and
porcine BoVs, raising the possibility of cross-species transmission.
 SWINE DISEASE MANUAL
Porcine bocaviruses have been identified in Africa, Asia, Eastern
Europe, North America, and the United Kingdom. Reported
PBoV prevalence in sick pigs in China is around 11%, while US
studies have documented prevalence rates in sick pigs of approxi-
mately 43% and 59%.
Infection occurs most commonly in weaned piglets. Transmission
routes of PBoV remain unclear. Viral DNA can be detected in a
range of tissues, including lymph nodes, serum, lung, oral fluids,
Porcine parainfluenza virus type 1
Porcine parainfluenza virus type 1 (PPIV-1; species porcine
respirovirus 1) was first identified in 2013 from nasopharyngeal
EMERGING
samples collected from deceased slaughterhouse pigs in Hong
Kong, China. The PPIV-1 genome was reported at that time to
be a novel paramyxovirus with highest genetic similarity to Sen-
dai virus and human parainfluenza virus type 1.
Porcine respirovirus type 1 is a member of the genus Respirovirus
in the Paramyxoviridae family and is an enveloped, single-stranded,
negative sense RNA virus. Porcine respirovirus-1 is widespread in
the US and has been detected by PCR in all ages of swine but more
commonly in nursery and grow-finish pigs. The virus has been
detected in respiratory samples, including lung tissues, nasal swabs,
and oral fluids.
Viral infection has been associated with respiratory disease in
pigs, with clinical signs that may include coughing, minor sneez-
ing, and serous nasal discharge. It has been suggested that PPIV-1
Porcine sapovirus
Porcine sapovirus (PSaV) is a non-enveloped RNA virus in the
family Caliciviridae. Different strains of porcine sapovirus (PSaV)
can simultaneously circulate within swine farms or herds; PSaV
was previously known as porcine enteric calicivirus.
Porcine sapovirus is stable at temperatures of 127°F (56°C) and
at pH 3 to 8. Recombination events between human and porcine
sapoviruses seem likely.
Porcine sapovirus has been isolated from pigs in Belgium, Brazil,
China, Denmark, Finland, Hungary, Italy, Japan, Slovenia, South
Korea, Spain, the US, and Venezuela, but human sapoviruses are
found worldwide. A surveillance study among pig farms in Europe
found PSaV on 44.3% of farms and in 7.6% of all pigs, with the
highest prevalence in piglets aged 2 to 8 weeks. Porcine sapovi-
ruses were detected by PCR in 62% of fecal samples collected
from 3 states in the US from swine of all ages. Post-weaning pigs
had the highest prevalence, while the lowest prevalence was in
nursing pigs (20% to 21%).
120 PORCINE PARAINFLUENZA VIRUS TYPE 1; PORCINE SAPOVIRUS
and feces. The pathogenesis of PBoV and its ability to induce
clinical signs are not well understood. Viral coinfections are com-
mon in PBoV-positive pigs. To date, PBoVs have been reported
in pigs with porcine circovirus associated disease (PCVAD),
respiratory disease, diarrhea, and in asymptomatic swine. Repro-
ductive failure may also occur. A single case of PBoV-associated
encephalitis has been reported. It does not appear that any studies
of experimental PBoV infection have been conducted in pigs.
may play a role in the porcine respiratory disease complex. How-
ever, the pathogenesis of PPIV-1 has not been fully elucidated
and the causal links between PPIV-1 and disease have not been
established.
Porcine parainfluenza virus type 1 is distinctly different than
parainfluenza virus 5 which has recently been isolated from
diarrhea-affected piglets in China. Parainfluenza virus 5 is a
negative-sense, non-segmented, single-stranded RNA virus that
belongs to the genus Rubulavirus in the family Paramyxoviri-
dae. This virus was present in intestinal tissue samples collected
from diarrhea-affected piglets in 4 provinces and municipalities
of the country, but little additional information exists at this
time regarding pathogenesis or its association with other enteric
pathogens.
Canadian investigators identified porcine enteric calicivirus
(assumed to be PSaV) in 18 of 88 (20.5%) Canadian finishing
farms that were tested, confirming its widespread occurrence
in that industry. Similarly, researchers in Brazil investigated the
occurrence of the virus on pig farms. Fecal samples of asymp-
tomatic pigs aged 9 to 24 weeks old were collected from 16
grow-finish herds and evaluated for porcine norovirus (assumed
to be PSaV) presence by PCR. Porcine norovirus was detected in
58 (51.8 %) of the 112 fecal samples and in 14 (87.5 %) of the 16
herds evaluated.
There have been no reports of PSaV-related fatalities in pigs.
Transmission of enteric caliciviruses is thought to be fecal-oral.
Experimentally infected piglets typically develop diarrhea.
Vomiting and diarrhea were noted in a 2008 outbreak in pigs in
China; both signs were reproduced experimentally in 10-day-old
piglets after feedback of feces from infected pigs. Subclinical
infection also seems to occur.

Torque teno virus
Torque teno viruses are small, non-enveloped viruses with a
circular, single-stranded DNA genome belonging to the newly
created family Anelloviridae. In pigs, the genus Iotatorquevirus
is composed of 2 species, TTSuV1a (formerly TTSuV1) and
TTSuV1b (formerly TTSuV2), and the genus Kappatorquevirus
also includes 2 species, Torque teno sus virus k2a and k2b.
The Torque teno viruses have been identified in tissue and feces
of pigs from many countries around the world. Transmission of
the viruses among pigs is horizontal and mainly via the fecal-oral
route. It is unknown whether they are a primary cause of disease,
but many authors seem to agree that they are most likely found as
part of a co-infection with other pathogens and that in these situ-
ations, their presence might promote increased disease severity or
virulence. Little evidence to date supports their role as a significant
pathogen in pigs.
West Nile virus (Kunjin virus)
West Nile virus (WNV) is a mosquito-borne virus that circulates
among birds but can also affect other species, particularly humans
and horses, and until the 1990s, tended to circulate only in parts
of Africa. Most human infections were asymptomatic. Since that
time, this picture has changed, with West Nile virus emerging as
a significant human and veterinary pathogen in the Americas,
Europe, the Middle East, and other areas. The disease became
established in the US in 1999, and while approximately 80% of
the people infected with these strains were asymptomatic, 20%
had flu-like signs and a small but significant percentage (<1%)
developed neurological disease. Although the introduction of an
equine vaccine has helped control the disease in horses, there is
currently no vaccine for humans. Recent experiences suggest that
human outbreaks may continue to occur in North America at
unpredictable intervals.
West Nile virus is an arbovirus in the Flavivirus genus of the
family Flaviviridae. It belongs to the Japanese encephalitis virus
complex or serogroup. The strain that entered the US in 1999 is
called NY99 and is among the most pathogenic strains. Kunjin
virus is a subtype of West Nile Virus found in Australia.
Wild birds are the main reservoir hosts for WNV; passeri-
formes (perching birds) are important in virus amplification.
In endemic regions, the virus is maintained in a cycle between
mosquitoes and birds. When environmental conditions favor
EMERGING VIRUSES
One study found that in pigs suffering from PCVAD, the levels
of TTSuV2 had higher viral DNA titers but lower anti-TTSuV2
antibody levels than healthy animals. In another study of natu-
rally infected pigs from 5 weeks of age up to 24 weeks of age, the
virus was present in a number of tissues (brain, lung, mediastinal
lymph node, heart, spleen, kidney, mesenteric lymph node, and
bone marrow) with medium to high DNA loads.
While Anelloviruses are considered to be highly species-specific,
one study showed porcine anelloviruses were detected in 5 out of
21 (24%) human fecal samples from volunteers eating pork meat
between 2 and 7 times per week, though there was no evidence
that tissue infection actually occurred in the humans.
EMERGING
high viral amplification, significant numbers of “bridge vector”
mosquitoes (mosquitoes that feed on both birds and mammals)
become infected in the late summer and then are able to trans-
mit the virus to humans, horses, and other incidental hosts. In
some birds, viremia can persist for more than 3 months, possibly
contributing to the overwintering of the virus.
Among mammals, disease occurs mainly in equids (horses, don-
keys, and mules), and an efficacious vaccine has been developed
for use in these species.
Little work has been done with West Nile virus in pigs. However,
several seroprevalence studies in feral pigs have been published,
including one from the US in which 222 samples were collected
from 2001 to 2004. The overall seroprevalence was 22.5%, with
individual rates in Florida, Georgia, and Texas reported as 17.2%,
26.3%, and 20.5% respectively. Young adult and weaner pigs
were experimentally challenged with the NY99 strain of the virus
through the bite of infected mosquitoes. While each of the adult
pigs seroconverted to the virus, virus could only be isolated from
the serum of one pig. In the weaner pigs, however, 3 of 5 devel-
oped a viremia. No clinical signs attributable to WNV infection
were observed in any of these animals. The authors concluded
that pigs are unlikely to play a significant role as amplifying hosts
of West Nile virus.
TORQUE TENO VIRUS; WEST NILE VIRUS 121
 122
EMERGING
 Section IV

Diseases caused by parasites

Coccidiosis.....................................................................................................................................................................................125
Cysticercosis...................................................................................................................................................................................127
Lice...................................................................................................................................................................................................129
Lungworm......................................................................................................................................................................................130
Mange..............................................................................................................................................................................................132
Minor intestinal nematodes: Kidney worm, Nodular worm, Thorny-headed worm, Threadworm...........................134
Roundworm...................................................................................................................................................................................137
Trichinellosis..................................................................................................................................................................................139

PARASITES
Whipworm.....................................................................................................................................................................................141

123
 124
PARASITES

Coccidiosis
Alternate names and abbreviations
Isosporosis (archaic), Isospora (archaic), cystoisosporosis,
Cystoisospora, Eimeria
Definition
Coccidiosis is the enteric disease caused by infestation with
variety of coccidia, usually manifested as diarrhea in suckling or
recently weaned pigs. The disease is usually caused by Cystoisos-
pora (previously Isospora) suis in suckling piglets and by Eimeria
species in older pigs.
Occurrence
Neonatal coccidiosis caused by C suis usually occurs in con-
finement-raised nursing piglets that are more than 5 days old;
it is less frequent and less severe in older, recently weaned pigs.
Coccidiosis occurs in all countries where confinement rearing
and continuous farrowing are practiced, with outbreaks tending
to be more common in warmer months. Several coccidia of the
genus Eimeria, particularly E spinosum, commonly infect 1- to
3-month-old swine and can be a primary cause of enterocolitis
when previously unexposed pigs are placed in highly contami-
nated environments, including unsanitary nurseries, grow-finish
facilities, or boar studs.
Historical information
Although first associated with enteric disease in 1934, the
coccidia found in pigs were considered as common endemic pro-
tozoans of little consequence until the 1970s. The prevalence of
disease increased with the adoption of confinement rearing and
continuous farrowing, particularly in inadequately disinfected
farrowing crates located over solid floors in a warm environment.
These conditions facilitated rapid completion of the life cycle of
C suis, resulting in the continuous presence of high numbers of
infective oocysts in farrowing crates. Fortunately, prevalence of
the disease decreased with improvements in perforated flooring
materials and hygiene, but the disease remains a problem for
some farrowing and nursery operations even when dedicated
efforts are made to eliminate the infection. Eimeria species are
also a common infection but cause disease only when naïve pigs
are exposed to high environmental doses.
Etiology
Cystoisospora suis goes through repeated cycles of sporogeny,
excystation, and endogenous development within intestinal
villus epithelium more rapidly than most Eimeria. Development
usually occurs in the small intestine, especially in the jejunum and
ileum but less often in the duodenum, cecum, and colon. Oocysts
may be shed in as little as 5 days postinfestation with C suis.
Oocysts shed from piglets rapidly become infective within about
12 hours when held in temperatures between 68° and 97°F (20°
DISEASES CAUSED BY PARASITES
and 36°C), which is well within the range maintained in nearly
all confinement farrowing facilities. Fully sporulated oocysts
of C suis have 2 sporocysts and each of these has 4 sporozoites.
Because of the rapid generation of high numbers of oocysts and
the rapid onset of infectivity, Cystoisospora suis is the usual cause
of coccidiosis in very young, confinement-raised pigs. Eimeria
species are quite similar but have a longer (18 day) life cycle and
therefore are much less likely to cause disease in neonates. Eime-
ria outbreaks are more likely to occur in the nursery phase as a
result of environmental contamination by oocysts from previous
groups of pigs.
Epidemiology
Sporulated coccidia are very resistant to cleaning and disin-
fectants, which explains their ubiquitous distribution. Disease
results when naïve piglets or weanlings are exposed to high
doses of infective oocysts. Coccidia are initially introduced into
farrowing facilities by carrier sows, but the dose in the envi-
ronment is then magnified over time by the accumulated fecal
contamination from previous litters and/or infected littermates.
Sporulation is required for infectivity and this occurs in as little
PARASITES
as 12 hours in warm environments. Parasitized piglets produce
very large numbers of oocysts that survive extremely well on
surfaces in the farrowing environment. Once sporulated, these
oocysts become a major source of infection for littermates and
subsequent litters. When infected with an identical dose, piglets
infected at 1 to 3 days of age have much more severe disease than
those infected beyond 3 weeks of age (ie, disease is more severe
in younger piglets). High doses of oocysts are required to cause
clinical disease, but high doses occur frequently as a result of the
environmental buildup of oocysts in farrowing facilities. Inade-
quate sanitary practices between farrowing groups undoubtedly
facilitate this buildup.
Pathogenesis
All stages of the development of coccidia occur in intestinal
villus enterocytes. This results in death and desquamation of
enterocytes, especially those on the distal tips of villi. The severity
of lesions is related to the number of oocysts ingested. Bacteria
in the intestine, including Clostridium species, may contribute
secondarily to the overall severity of the lesions. When many
coccidia are ingested, lesions are severe. In serious infections, the
erosion of villous epithelium results in loss of fluid and failure of
surviving epithelium to absorb nutrients and fluids. This leads to
diarrhea, dehydration, and loss of electrolytes, perhaps death.
Since regeneration of villous epithelium occurs more slowly in
neonates, they are more severely affected. If piglets ingest only
small numbers of oocysts, they survive and develop effective
immunity unless they are in a stressful environment or compro-
mised by secondary infections. In a warm, moist environment,
COCCIDIOSIS 125
 SWINE DISEASE MANUAL
oocysts in feces-contaminated farrowing rooms and crates soon
become infective. They are ingested when piglets first nurse or
when they ingest feed, water, or feces in the farrowing crate. The
sporozoites within the oocysts mature and are released to pene-
trate enterocytes. Many enterocytes are destroyed by the develop-
ing coccidia. Released oocysts are passed in the feces.
Clinical signs
With C suis, diarrhea can occur as early as 5 days after birth but
is more commonly seen in piglets from 1 to 3 weeks of age. Signs
include yellowish, pasty to clear, watery diarrhea, followed by
dehydration, rough hair coat, and failure to gain weight. The
clinical disease within a litter can appear in two waves. The first
wave (5 to 6 days of age) is the result of some piglets in the litter
becoming infected shortly after birth, developing diarrhea, and
then subsequently heavily contaminating the farrowing crate. The
second wave occurs 4 to 8 days later, after the rest of the litter
becomes infected as a result of the first wave of infection.
Piglets usually continue to nurse when affected by coccidiosis
but may vomit milk. Morbidity is high, but mortality is variable,
often low or moderate. Until becoming familiar with coccidiosis,
producers may report the disease as an outbreak of colibacillosis
that fails to respond to the usual antibiotic therapy.
PARASITES
With Eimeria, nonspecific but persistent diarrhea occurs in the
nursery phase. Acute enterocolitis has also been reported in naïve
high-health boars placed in unsanitary boar studs. Fecal blood is
not a feature of coccidiosis from C suis or Eimeria species.
Lesions
Lesions are proportional to the dose of oocytes ingested and
the age of pigs at the time of infection. The lesions are usually
restricted to the intestinal tract, especially the lower jejunum
and ileum. In mild infections, the intestine tends to be turgid.
Mild fibrinous enteritis may be visible in short segments of the
lower small intestine. In severe infections, there may be extensive
fibrinonecrotic enteritis of the terminal third of small intestine
and occasionally colon. Segmental necrotic enteritis in pigs 1 to
4 weeks of age is fairly common with severe C suis insults. Gross
lesions with Eimeria species tend to be subtle.
Microscopically, there is necrosis and later, atrophy and fusion of
some mucosal villi along with hyperplasia of cryptal epithelium,
elongation of mucosal crypts, and nonsuppurative infiltrates in
the lamina propria. Shortened villi may be covered by cuboidal or
flattened epithelial cells. Various stages of Cystoisospora or Eime-
ria are apparent in parasitized cells. If adequate time has elapsed
since initial infection, there may be oocysts in the feces.
126 COCCIDIOSIS
Diagnosis
Diagnosis of disease states is most accurate by identifying the coc-
cidia in histologic sections. The presence of paired type 1 mero-
zoites is considered diagnostic for C suis. Several areas of infected
mucosa should be examined in order to maximize sensitivity of
the histological examination, as the distribution of microscopic
lesions and merozoites is unpredictable.
Diagnosis by fecal examinations may be possible but is thought
to be much less sensitive than examination of affected small
intestinal tissue. In fecal samples, either “hazy bodies” between
the oocyst wall and the sporont, or oocysts in the 2-cell stage,
are diagnostic for C suis. For Eimeria species, detection of high
numbers of oocysts in feces and absence of other pathogens are
indicative of infestation. Coccidiosis can occur concurrently
with other diseases, so it is often necessary to eliminate them as
additional causes of the diarrhea. These include viruses (rotavirus,
swine enteric coronavirus diseases), colibacillosis, parasitism by
Strongyloides ransomi, and infection with Clostridium perfringens
type A or type C.
Control
For control of coccidiosis in suckling pigs, a vigorous, effective
sanitation program, including careful cleaning and disinfection
of farrowing crates between farrowings, is essential. Strong bleach
or ammonium compounds can be used for disinfection after
thorough cleaning of the crates. Steam cleaning of the entire far-
rowing facility may be necessary. Sealing all surfaces with paint or
a water sealant may be an option to break the cycle of infection.
Wooden and concrete surfaces are particularly difficult to clean
effectively. Installation of perforated metal or plastic flooring in
the crates is essential for long-term control of coccidiosis and
other neonatal enteric diseases.
On farms known to be affected by coccidiosis, routine treatment
of all piglets with toltrazuril in the first 1 to 2 days after birth has
been used to minimize the severity of coccidiosis. There is no
proven, widely accepted anticoccidial or drug for use in dams that
is effective at controlling the disease in neonates.
Most cases of coccidiosis associated with Eimeria species are the
result of the introduction of naïve pigs into a heavily contami-
nated environment. Control is based on minimizing the dose of
oocysts ingested. Scrupulous sanitation between groups of pigs
is usually sufficient to prevent disease. Amprolium is effective for
treatment of Eimeria outbreaks but not Cystoisospora.

Cysticercosis
Alternate names and abbreviations
Taenia, taeniasis, taeniosis, pork measles
Definition
Cysticercosis occurs as a result of pigs consuming eggs of the
human tapeworm, Taenia solium. The larvae of the parasite
migrate to skeletal and cardiac muscles where they form cysticerci
and remain as an important source of infection for a subsequent
human host that consumes raw or undercooked pork. Infected
pigs are generally asymptomatic.
The terms taeniasis or taeniosis refer to intestinal infection of the
definitive host (humans) with the adult tapeworm. Cysticercosis
refers to extra-intestinal infection of the intermediate host (pigs)
with the encysted larval stage of the parasite in muscle tissue.
Humans can also develop cysticercosis after ingesting T solium
eggs through contact with human sewage and thus can act both
as a direct or intermediate host. Cysticerci in humans often occur
in the central nervous system, causing a condition known as neu-
rocysticercosis.
Taenia saginata is a related, but different, species of human tape-
worm that causes cysticercosis in cattle.
Occurrence
Taenia solium is considered to be endemic in parts of Asia,
South and Central America, and sub-Saharan Africa. In Europe
and North America, modern pig rearing systems that minimize
contact between pigs and human sewage, in combination with
long-term commitments to meat inspection and improvements
to public health and sanitation, are believed to have eliminated
autochthonous infections. However, human cases still occur in
these regions related to international travel or migratory move-
ments towards and from endemic countries.
Taeniasis and human cysticercosis are not notifiable in most coun-
tries; therefore it is difficult to assess the true prevalence of human
infection in various parts of the world. Porcine cysticercosis must
be reported to the World Organization for Animal Health, but
there is no mandatory reporting for bovine cysticercosis.
Historical information
Human taeniasis and porcine and human cysticercosis are ancient
diseases and almost certainly part of the basis for certain societal and
religious biases against pigs and pork. In the third book of the Bible
(Leviticus, 11:7-8), it is written:
And the pig, though it has a divided hoof, does not chew
the cud; it is unclean for you. You must not eat their
meat or touch their carcasses; they are unclean for you.
DISEASES CAUSED BY PARASITES
The ancient Greeks were also familiar with the disease. In Aris-
tophanes’ (c 448 to 385 BC) comedic play “The Knights,” one of
the supporting characters aids the local sausage-maker in berating
the play’s protagonist by suggesting they:
set his mouth open with a wooden stick as the cooks do with
pigs; we will tear out his tongue, and looking down his gaping
throat, will see whether his inside has any pimples,
a clear reference to the practice of slicing the tongue of pigs
during slaughter to check for the presence of cysticerci. Aristotle
(c 384 to 322 BC) described in detail the presence of cysts in
pig muscles that were similar to hailstones. Pigs were considered
impure in ancient Greece; it is possible that this belief induced
Muhammad (570 to 632 AD) to prohibit the consumption of
pork when the Quran was written.
Taeniasis remains an important zoonotic disease today. An out-
break of neurocysticercosis was identified among members of a
non-pork-eating Orthodox Jewish community of New York City
in 1990 to 1991. Investigation of the outbreak concluded that the
source of the infection was most likely a result of incidental con-
tact between domestic staff (recent migrants from Latin America,
subsequently determined to be actively infected with the para-
PARASITES
site) and family members. The outbreak highlighted the fact that
contact with pigs is not required to explain the occurrence of
taeniasis and neurocysticercosis in people and served to increase
research and awareness of the disease over the last 25 years.
Neurocysticercosis is the most common parasitic infection of the
brain and is an endemic condition in many developing countries
of Africa, Asia, Central America, and South America. It has
been estimated that in these areas, 25% to 40% of patients with
new-onset epilepsy have evidence of neurocysticercosis. At the
same time, reported cases of neurocysticercosis are increasing in
the US (especially in southwestern states) and other developed
countries, especially among immigrants from endemic areas.
Etiology
Taenia solium belongs to the family Taeniidae, which includes
3 parasites affecting humans: T solium (the pork tapeworm),
Taenia saginata (the beef tapeworm), and Taenia asiatica (a tape-
worm that is morphologically similar to T saginata but biologi-
cally analogous to T solium).
Epidemiology
The major risk factor for cysticercosis in pigs is exposure to con-
taminated human sewage through a water or feed source. Pigs
can potentially become infected by consuming the carcass of an
infected, deceased pig but this route of transmission does not
appear to feature significantly in the epidemiology of the disease.
Infected pigs are generally not infectious to other pigs.
CYSTICERCOSIS 127
 SWINE DISEASE MANUAL

Pathogenesis Taeniasis in humans is usually asymptomatic except for the passage

The life cycle of the human tapeworm T solium normally requires
the pig as an intermediate host, although humans do occasionally
develop neurocysticercosis after ingesting T solium eggs directly,
as described above.
Adult tapeworms in the human consist of a scolex and numer-
ous body segments called proglottids. The terminal proglottid
contains thousands of eggs that are shed in carriers’ stools. Cys-
ticercosis in pigs is a result of pigs ingesting these T solium eggs,
usually as a result of consuming water, food, or soil contaminated
with untreated human sewage.
When pigs ingest these eggs, oncospheres (larvae or embryos)
hatch in the intestine and, after invading the intestinal wall, are
disseminated to other organs (usually muscle) where they mature
into cysts (cysticerci) over several weeks. Cysticerci consist of
a membranous wall filled with fluid and an invaginated scolex
(head). Humans who eat undercooked pork that contains cys-
ticerci can then develop a tapeworm infection (taeniasis) and
complete the life cycle of the parasite.
Human ingestion of cysticerci-infected pork typically leads only
to intestinal tapeworm infection and not neurocysticercosis. Neu-
rocysticercosis is generally a result of humans ingesting T solium
PARASITES
of proglottids in the stool.
Lesions
Cysticerci in pork are clear, translucent, or white; they are round
to ovoid in shape. Cysts are usually around 1 centimeter or less in
diameter and surrounded by a fibrous capsule. Each fluid-filled
vesicle contains a single invaginated protoscolex which usually
appears as a single dense white body. An organ may contain one
to hundreds of cysticerci. When larvae die, the cyst degenerates
and eventually becomes filled with greenish or yellow caseous
material. In pigs, most T solium cysticerci are found in the skeletal
or cardiac muscles, brain, liver, or heart.
Diagnosis
Antemortem diagnosis of cysticercosis in live pigs is difficult.
Some serological tests have been described but are not in com-
mon use. Cysticercosis is usually diagnosed postmortem during
meat inspection, which is why a series of sagittal slices is often
made across the tongue of butchered pigs.
Control
In theory, cysticercosis may be treated with anthelmintic drugs

such as albendazole and praziquantel. More practically, the

eggs or larvae, with the larvae then moving to extraintestinal
disease is managed by controlling risk factors and exposure to T
sites in a manner similar to what occurs in pigs. Humans affected
solium eggs. Free-ranging pigs, particularly those with potential
by taeniasis are at very high risk of autoinfection and resultant
exposure to human sewage and untreated surface water are at
neurocysticercosis if they ingest tapeworm eggs through failures
highest risk of contracting the infection. Farm workers should
of their own personal hygiene; they are also a significant source of
use toilet facilities that ensure human feces do not come into
infection to others in their household. Humans with neurocystic-
contact with pigs; handwashing after using the toilet is a practice
ercosis are dead-end hosts and do not transmit the disease further.
that should obviously be encouraged. Those who travel to parts of
Taenia solium in humans reach the adult stage in 5 to 12 weeks the world where taeniasis is endemic should be advised to avoid
after ingestion of contaminated pork. Adult T solium are 2 to becoming infected through consumption of undercooked pork
7 meters long and may live for up to 25 years. Although up to or through contact with human sewage. Most taeniasis is asymp-
25 tapeworms have been recorded in a single person, there is tomatic; therefore, fecal examination or prophylactic treatment
usually only 1. Taenia solium eggs can survive in the environment may be advised in people known to have a high risk of exposure.
for a few weeks or months. Experimentally, pork can become
infectious to humans in as little as a few weeks after a pig ingests
T solium eggs. More typically, 2 to 3 months are required for
pork to become infectious to humans.

Clinical signs
Cysticercosis in pigs is usually asymptomatic during both the
larval migration and the establishment of cysts. Cysticerci can
induce some symptoms when the encysted larvae die or if a cyst
becomes large enough to interfere with the function of vital
organs.

128 CYSTICERCOSIS

Lice
Alternate names and abbreviations
Haematopinus, pediculosis, hog louse
Definition
Infestation with the louse Haematopinus suis.
Occurrence
Infestation with Haematopinus suis is common where husbandry
and management are poor or efficacious insecticides are not
available. These lice live only on swine, although they may tem-
porarily infest people handling swine. All age groups of swine are
susceptible to infestation, with greater infestations when there
are many pigs in close contact. Infestation is more severe in the
winter although it persists throughout the year. Presumably, the
parasitism occurs worldwide wherever swine are raised.
Historical information
Prior to the development of good parasiticides, pediculosis in
swine was very common. It was a common practice to use waste
oil or diesel fuel as a topical spray on swine to reduce the number
of lice, but the efficacy of this treatment was poor. The relatively
recent development of many effective parasiticides has made it
possible for a producer to completely eradicate lice. Products that
control both internal and external parasites, including lice, have
made control of lice even more convenient.
Etiology
Haematopinus suis is one of the largest species of lice, up to 6 mm
long. Haematopinus suis is a sucking louse that obtains blood
meals from the host through its penetrating mouth parts. The
louse spends its entire life on the host. It can survive off the host
for only a few days. The female louse lives about 23 to 30 days,
lays 3 to 4 eggs (nits) per day, and attaches them to hair shafts
near their base. Eggs are 1 to 2 mm long and light cream to gray
in color. They hatch in 12 to 20 days.
Epidemiology
Hog lice are host specific. They usually spread among swine when
the pigs are in close contact, as when they crowd together for
warmth, shade, or comfort. Also, lice can spread to pigs moved into
quarters recently vacated by lousy animals. Infested animals added
to a clean herd often introduce lice.
Lice living on a pig have certain preferred sites because they prefer
to feed on thin-skinned areas. Favorite sites include the neck, jowl,
flank, the inner side of the legs, and ears. In the ears, they often
reside in nests. Similar nests often are found on the abdomen,
sometimes within the circles of pityriasis rosea lesions. Location
within the ear offers lice protection from parasiticides because it is
difficult to thoroughly wet the inner surface of the ear.
DISEASES CAUSED BY PARASITES
Pathogenesis
Lice annoy swine when they pierce the skin to take a blood meal.
Dermatitis develops and leads to rubbing, scratching, and some
loss of hair. Loss of blood is not severe in older pigs, but neonates
and nursery pigs can exhibit anemia if heavily infested. Parasit-
ized pigs are restless. They may lose weight and utilize feed less
efficiently.
Lice are known vectors of agents that cause swinepox, African
swine fever, Mycoplasma suis, and quite likely other blood-borne
pathogens as well.
Clinical signs
Persistent rubbing and scratching, patchy alopecia, and pallor
from anemia are clinical signs of pediculosis. Similar signs are
seen with sarcoptic mange. Pediculosis and sarcoptic mange often
occur concurrently and must be differentiated. Hog lots and
facilities with many rubbing sites also suggest that lice or mange
are present.
Diagnosis
Lesions include a rough, dull hair coat, often with patchy alo-
PARASITES
pecia. A thorough examination of infested pigs will often result
in seeing the lice with the naked eye. Examination of the inner
aspect of the ears often reveals the lice; this area is also a preferred
location to look for sarcoptic mange lesions.
It is a good practice to occasionally pick up a few small and grow-
ing pigs, turn them over, and examine their undersides. Lice, as
well as lesions of several other diseases, are often readily apparent
on the posterior abdomen or on the inside surface of the legs.
After the dehairing process at slaughter plants, the punctate cuta-
neous lesions caused by feeding lice are easily visible, especially in
white-skinned hogs.
Control
If they are not from a source that has been confirmed negative for
lice and mange, animals that are introduced into a herd should
always be treated with a parasiticide while in an isolation area.
A minimum of 2 treatments, at 18- to 21-day intervals while in
isolation prior to introduction to the herd, is required for elim-
ination of lice and mange. Many effective parasiticides are now
available. The repeated treatments facilitate the killing of juvenile
lice that emerge from eggs 12 to 20 days after an initial treatment.
Several parasiticides control external parasites other than lice
(flies, mites, and ticks). Injectable avermectins have been very
effective in controlling both lice and mange; programs have been
devised for eradicating both. Directions for use should be fol-
lowed carefully. Some parasiticides require withholding periods
prior to marketing.
LICE 129
 SWINE DISEASE MANUAL
Lungworm
Alternate names and abbreviations
Metastrongylus, metastrongylosis
Definition
Infection with any one or more of 3 species of metastrongyle
nematodes.
Occurrence
Swine can be infected by any of 3 species of metastrongyles. All
ages of swine are susceptible, but heavy infections occur mostly
in young pigs over 6 weeks of age. Infection is common in areas
where pigs are raised outdoors with access to soil. Lungworms
likely occur in all countries where swine and the intermediate
host (the earthworm) are present.
Historical information
Historically, lungworm infection was a major problem in US
swine production. With the development of confinement
housing and subsequent lack of access to soil (and earthworms),
lungworm infection has decreased in prevalence. However, where
pigs are raised in the outdoors, lungworm infection can still be a
PARASITES
serious problem. Parasiticides effective in controlling lungworms,
as well as many other parasites, have improved control. At one
time, lungworms were erroneously believed to be important in
the transmission of influenza virus to swine.
Etiology
Lungworms that infect swine include Metastrongylus elongatus
(apri), M pudendotectus, and M salmi, with the former most
common; infection with more than one species can occur. Lung-
worms usually have an indirect life cycle through earthworms, but
a direct cycle has been reported. Adult lungworms vary in length
from 14 to 66 mm. They are white, threadlike, and easily visible at
necropsy. Lungworm ova are larvated, thick-shelled, about 40 by
50 µm in size, and are passed in feces.
Epidemiology
First-stage lungworm larvae hatch from eggs in swine feces and
survive in feces or moist soil for long periods of time. In some
regions of the country, the first-stage larvae can survive over win-
ter. After being ingested by earthworms, larvae are able to develop
to the third infective stage in about 10 days. They then remain
quiescent in the earthworm for up to 18 months. Thousands of
larvae can accumulate in a single earthworm, apparently without
harm to the earthworm. Pigs on pastures with soft or moist soils
root for earthworms, ingest the parasitized earthworms, and are
then infected by the larvae within the earthworms. The lungworm
larvae penetrate the intestinal mucosa, migrate through lymphatics
and venous blood, and reach the lungs. There they localize, grow to
maturity, and produce larvated ova about 25 days after ingestion.
130 LUNGWORM
Infection becomes patent in about 4 weeks. The larvated ova are
coughed into the pharynx where they are swallowed and passed
out through the feces.
Survival of lungworms depends largely on the survival of infective
larvae in earthworms for long periods of time as well as the ability
of first-stage larvae to survive for long periods in swine feces.
Breeding stock and other older pigs can remain infected for long
periods, and lungworm eggs in their feces continue to contami-
nate the environment.
Pathogenesis
Third-stage larvae penetrate the small intestine mucosa and pass
in lymph and blood to the liver and lungs. Some larvae migrate in
the liver and cause gray to white areas of scarring, similar to those
caused by ascarid migration. Larvae that reach the lungs break
into alveoli where they mature, extending into terminal bronchi-
oles. The parasites preferentially localize along the caudodorsal
border of the diaphragmatic lobes. Their presence results in alve-
olitis and bronchiolitis, which leads to coughing. Exudate that
forms around lungworms and their ova partially or completely
obstructs airways, resulting in alveolar emphysema and/or atelec-
tasis. Secondary bronchopneumonia is a common sequel.
Clinical signs
Common clinical signs include chronic, sometimes paroxysmal,
coughing that eventually leads to generalized unthriftiness. If
secondary pneumonia occurs, there may be dyspnea and perhaps
an abdominal type respiration (“thumping”). Signs are similar to
those caused by ascarid migration in the lungs. The two parasit-
isms often occur concurrently where pastures are heavily contami-
nated by both ascarids and lungworms.
Lesions
Pigs with many lungworms are unthrifty, have a rough hair coat,
and are small for their age. Pulmonary lesions often occur on the
caudodorsal border of diaphragmatic lobes. When viewed from
the dorsal aspect, the lesions often have a roughly triangular,
wedge-like shape and appear as recessed darker areas of atelectasis
or raised, lightly colored, emphysematous areas; both types of
lesions can be present in the same pig. If the distal border of the
lobe is trimmed and lesion areas squeezed, adult worms can be
expelled. The bronchial tree should always be opened as lesions
along the border are not always present. When this is done,
inflammatory exudate and lungworms may be found in terminal
airways. Scattered 1- to 2-cm areas of gray to white scarring may
be visible in the liver.
 DISEASES CAUSED BY PARASITES

Diagnosis
Diagnosis is made by postmortem examination of a few typical,
affected pigs. Also, laboratory fecal examinations will usually
reveal the embryonated eggs of lungworms. Postmortem exam-
inations often require less time and have the advantage of permit-
ting examination for other parasites and diseases.

Control
Prevention of heavy infection is possible by preventing access of
pigs to soil that contains larvae or earthworms. Consequently,
most confinement-raised pigs are free of lungworms.
Pigs raised outdoors can often avoid heavy infection if they are
farrowed and raised on clean pastures. Pasture rotation is helpful
but sometimes fails to prevent infection as lungworm larvae
persist in earthworms for long periods of time. Using an effective
anthelmintic on sows prior to farrowing and then moving them
to clean pasture is helpful.

PARASITES

LUNGWORM 131
 SWINE DISEASE MANUAL
Mange
Alternate names and abbreviations
Sarcoptes, sarcoptic mange, acariasis, scabies
Definition
A skin disease caused by the sarcoptic mange mite, characterized
by marked pruritis and papules.
Occurrence
Sarcoptic mange occurs in all age groups but is inapparent in
suckling pigs until signs and lesions have had time to develop.
Mange is present in all countries where pigs are raised in large
numbers. Sarcoptic mange is the most important ectoparasitic
disease of swine. Sarcoptic mange occurs in many other species
but the mite Sarcoptes scabiei var suis is specific only for swine.
Historical information
Sarcoptic mange, first reported about 100 years ago, was largely
ignored because it was widely believed that scratching was a
natural and normal behavior for pigs. Also, the economic loss
caused by the disease was not widely appreciated. Intensification
of production after World War II and the economics of produc-
PARASITES
tion focused attention on the avoidable losses caused by sarcoptic
mange. Development of better and more convenient acaricides
has greatly improved control.
Etiology
The mite Sarcoptes scabiei var suis causes most mange in swine.
The mite is about 0.5 mm in length, gray to white, and just visible
to the naked eye when on a black background. All stages of the
mite (ova, larvae, nymphs, and adults) develop in the epidermis.
The life cycle is completed in about 10 to l5 days. Depending on
temperature, humidity, and environment, mites and ova can sur-
vive off the host for up to 15 days.
Demodectic mange, caused by the mite Demodex phylloides, is
unrelated to sarcoptic mange and relatively unimportant in swine.
It is mentioned here because it occasionally causes dermatitis over
the snout, inside the thighs, and over the flanks. Occasionally, it
involves the whole body and leads to excessive trimming or con-
demnation at slaughter. Nodules caused by D phylloides have been
mistaken for swine pox.
Epidemiology
Mange in a herd usually develops after introduction of asymptom-
atic swine carriers. Sarcoptes scabiei var suis is rarely if ever, trans-
mitted from other species. If swine are moved immediately into
quarters recently vacated by infested pigs, they are likely to become
infested. Spread is usually by direct body contact, often the result of
pigs crowding together for warmth or shade. Mites from the dam
often invade neonatal piglets within a few hours of birth.
132 MANGE
Pathogenesis
Mites spread among pigs in close contact and invade the skin.
They burrow through the epidermis where eggs are laid. The
mites are a strong irritant to the skin and initiate severe scratching
and rubbing. In about 2 to 3 weeks, an allergic hypersensitivity
develops in many pigs causing them to rub and scratch even more
vigorously, further traumatizing the skin.
Mites tend to first colonize the skin of the inner surface of the ear.
From this site, they spread out over the body, tail, and legs. Ear
lesions first appear as small encrustations. These enlarge to form
plaque-like lesions. Constant rubbing and scratching irritate the
skin at many sites on the body and promote hyperkeratosis and
proliferation of connective tissue in the dermis. These lead to
thickening, wrinkling, and folding of the skin. Hyperkeratotic,
gray to white patches often form on the irritated skin. Reddened
macules and papules that develop on the skin of young growing
pigs are thought to be related to hypersensitivity.
Clinical signs
Frequent rubbing and scratching are the usual signs and are often
more marked when the skin is warmed, presumably the result
of increased mite activity. Equipment or facilities often have
polished surfaces from rubbing pigs. Decreased rate of growth,
inefficient use of feed, and low sow productivity follow. Although
morbidity is high, mortality from mange alone is unusual.
Lesions
Young pigs that have developed hypersensitivity to mange mites
display reddened macules or papules, especially over the rump,
flanks, and abdomen. Chronic mange affects relatively few older
animals in the herd and is less pruritic. Lesions vary in extent,
covering much of the body in advanced cases. In some cases, lesions
may be confined mostly to the inner surface of the ears, where
hyperkeratotic areas often develop a brownish-red discoloration.
Diagnosis
Clinical signs and skin lesions are suggestive of mange; marked
pruritis often helps differentiate mange from other diseases of
the skin. Diagnosis is confirmed by identifying the mites in skin
scrapings or in exudates from the external auditory canal. Scrap-
ings from the inner surface of the ear usually reveal more mites
than scrapings from other sites. Scrapings can be wetted with
10% potassium hydroxide, cover-slipped, and examined under
low-power magnification. A simple technique is to place the
scrapings on a piece of black paper for a few minutes, carefully
blow off the superficial debris and examine the site on the paper
for the small, light colored mites. Diseases that must be differ-
entiated from mange include parakeratosis, dermatomycosis,
exudative epidermitis, pityriasis rosea, and photosensitization or
sunburn. Inspection of carcasses at slaughter may be useful both

in diagnosis and in evaluating the efficacy of a mange control pro-
gram. An enzyme-linked immunosorbent assay for serological diag-
nosis of mange is available in some countries for herd diagnosis.
Control
Control programs should focus first on the breeding herd, which
- if infected - inevitably transmits mites to the piglets. These pro-
grams usually involve treatment of dams with external acaricide
sprays or with an injectable avermectin a few days prior to enter-
ing the farrowing facility. Many farms using this control strategy
find it necessary to also treat growing pigs at 8 to 10 weeks of age.
Initiating an eradication program usually starts with culling of all
severely infested breeding stock. Immediately following this, 2
consecutive doses of an injectable avermectin, 18 to 21 days apart,
DISEASES CAUSED BY PARASITES
are administered to every pig on the farm (adults, neonates, and
growing pigs). Removal of bedding material, if present, and appli-
cation of an effective acaricide to environmental surfaces is often
recommended at the same time injections are given. While erad-
ication can be an expensive task in the short term, it is reliably
efficacious and requires only standard biosecurity procedures to
keep the mite from returning to the farm. Eradication of mange is
achievable in most production settings.
The avermectin class of parasiticides controls many external and
internal parasites. One should carefully follow the directions that
come with any product, as some require a lengthy withholding
period following their use.
PARASITES
MANGE 133
 SWINE DISEASE MANUAL
Minor intestinal nematodes: Kidney worm, Nodular
worm,Thorny-headed worm, and Threadworm
Kidney worm
Definition, occurrence, and historical information
The nematode Stephanurus dentatus is known as the kidney
worm, occurs only in swine, and affects all age groups, includ-
ing fetuses. Pigs raised on moist, shaded pastures in tropical or
subtropical areas such as the southeastern US are most often
infected. Once the life cycle was determined, control became pos-
sible via facility management and the availability of more effective
parasiticides. However, kidney worms have not been eradicated
from the US and are maintained in feral pigs and anywhere there
are suitable outdoor habitats.
Etiology, pathogenesis, and epidemiology
Adult kidney worms are 20 to 45 mm long and about 2 mm in
diameter. They have black and white mottling related to inter-
nal organs and their contents. Their life cycle is lengthy, with a
prepatent period of 9 to 12 months, meaning the eggs are not
shed from pigs that have not yet reached breeding age (ie, adults).
Once a patent infection is established, ova are shed continuously
PARASITES
in the urine. Ova are thin walled, morulated, and measure 120
by 70 µm. In a warm, moist, shaded environment, ova can hatch
in 1 to 2 days; larvae are infective in 3 to 5 days. Under favorable
conditions, the larvae can survive in the environment for several
months.
Infection can occur by larval invasion prenatally across the pla-
centa, by skin penetration, by ingestion in feed, and perhaps by
ingestion of earthworms. Ingestion is probably the most common
route of infection. Larvae complete 5 developmental stages (L1-
L5) to reach maturity. Ingested or penetrating L3 larvae migrate
from the small or large intestine to various sites. Many larvae
travel via mesenteric lymphatics or by portal venous blood to the
liver where they migrate extensively for 2 to 4 months. The larvae
penetrate the liver capsule, cross the peritoneal cavity, and then
encyst in perirenal fat or near ureters. Here they establish fistu-
lous connections with the renal pelvis or ureters. When mature,
they discharge their ova into the urine after a 9- to 12-month
prepatent period.
Most swine are marketed before patency can occur but affected
pigs will be unthrifty. Migrating larvae cause phlebitis, interstitial
hepatitis, and fibrosis in various tissues. Liver condemnations are
frequent in infested slaughter-age swine.
Diagnosis and control
Diagnosis is usually made at necropsy by observation of the
abscesses and parasites at sites of localization. The extensively
scarred, enlarged liver seen with severe infestations is rather
unique in swine. Diagnosis can be made in the live animal or at
134 MINOR INTESTINAL NEMATODES
necropsy by identifying ova in the urine. The first urine passed in
the morning often contains many ova.
Control is possible through a breeding program that utilizes
only gilts and young boars. These are slaughtered after producing
one litter. This usually precludes their living long enough for
ova of S dentatus to be passed in their urine. Eradication has
been achieved on some production sites by this program and
by adopting management practices that preclude swine coming
into contact with the parasite on pasture. Placing feeding and
watering equipment on concrete (rather than on dirt) in a sunny,
well-drained location is a simple management practice that has
value in controlling the parasite as does the use of confinement
housing. Treating sows with an anthelminthic a few weeks prior
to farrowing will usually prevent transplacental transmission of
the parasite to fetuses.
Nodular worm
Definition, occurrence, and historical information
Oesophagostomum are frequently associated with disease in swine,
sheep, and cattle but only with host-specific species. Oesopha-
gostomum species, most commonly O dentatum and O quadrisp-
inulatum, are distributed worldwide but clinical parasitism
usually occurs only in pigs raised in open lots or pasture. All age
groups of pigs are susceptible but pigs over 3 months of age may
be more so.
Etiology, pathogenesis, and epidemiology
Adult Oesophagostomum worms are white to gray, 1 to 2 cm long,
and have slightly curved bodies. Ova are morulated, thin-shelled,
and about 70 by 40 µm. Ingested L3 larvae penetrate the mucosa
of the cecum and colon, encyst for 6 to 20 days and molt to L4
larvae before returning to the intestinal lumen. Some L3 pene-
trate deeply and cause marked inflammatory and fibrotic nodules
visible on the serosa, with possible serosal adhesions and peritoni-
tis the result. Repeated invasions and concurrent hypersensitivity
reactions can contribute to severity.
Severely infested pigs may have ill-thrift or diarrhea, but most
infestations are asymptomatic. Adult worms reside in the intesti-
nal lumen and become patent as early as 3 weeks after ingestion of
the L3. Large numbers of ova are passed in the feces. Under favor-
able conditions, the nonparasitic L1 and L2 stages can persist
on pastures for up to a year. Increased numbers of ova are passed
during the periparturient and lactation period, almost ensuring
that some of an infected sow’s piglets will be infected. Necropsy
of affected pigs will reveal inflammatory nodules or necrotic
debris present in the cecum and colon with nodules up to 20 mm
in diameter scattered in the mucosa and submucosa as well as
some apparent on the serosa. The lesions are easily confused with

dilated lymphoglandular complexes, which are common in the
colon of pigs with chronic bacterial enteritis. Oesophagostomum
infestations are uncommon in most production systems.
Diagnosis and control
Diagnosis is usually made on postmortem examination. Nodules
in and on the large intestine and the presence of adult parasites in
the lumen can easily be recognized. Lesions must be differentiated
from abscessed lymphoglandular complexes, which tend to be very
common in chronic colitis from various causes. Fecal examination
is also useful for diagnosis. The eggs must be differentiated from
grain mite eggs and ova of other Strongyloididae; differentiation
from Hyostrongylus rubidus may require larval culture.
Nodular worm infection is usually controlled by the use of
anthelmintics. Deworming sows prior to farrowing will reduce
exposure of the nursing piglets. In confinement operations, fre-
quent removal of feces and good sanitation also reduce exposure
of piglets. In outdoor operations, lots and pastures that are heav-
ily contaminated should be avoided. Pasture rotation, with tillage
of land when not pastured, is helpful. Many anthelmintics are
available for control.
Thorny-headed worm
Definition, occurrence, and historical information
Macracanthorhynchus hirudinaceus, literally the “thorny-headed
blood-sucking” worm, is limited to pigs and usually occurs in
grow-finish pigs old enough to have had an opportunity to root
and forage, thus having access to the larval stages of beetles that
serve as an intermediate host for the parasite. Infection is rela-
tively common in pigs raised outdoors in southern states but can
occur elsewhere sporadically.
Macracanthorhynchus hirudinaceus has an elongated, sac-like
body with no internal alimentary canal. It has a protrusible pro-
boscis armed with about 6 rows of spiny hooks for attachment
deeply into the intestinal wall. The worms are 10 to 40 cm long,
up to 9 mm wide, and are transversely wrinkled, slightly curved,
light pink in color and attenuated posteriorly. The brown ova are
large, up to 110 by 65 µm, have a 3-layered shell, and are resistant
to environmental degradation.
The eggs are passed in swine feces and ingested by beetles, grubs,
or other arthropods that act as intermediate hosts. Swine then
ingest these intermediate hosts. The eggs hatch in the intestinal
tract of the pig and the worms attach there, usually in the ileum.
The parasites develop by absorbing nutrients from the ingesta.
Pigs with many parasites tend to become unthrifty from loss of
blood, localized inflammation at sites of attachment, the effect of
many localized lesions, and impaired nutrition. There are few or
no signs with light infections. Occasionally, a parasitized pig dies
as a consequence of intestinal perforation followed by peritonitis.
DISEASES CAUSED BY PARASITES
Diagnosis and control
Diagnosis is usually made based on gross observations of worms
and sites of attachment at necropsy. Ova are quite characteristic
and are easily detected through laboratory fecal examinations
Control is through avoidance of exposure to contaminated lots
or pastures and to beetles, the usual intermediate hosts. Beetles
should be eradicated around feed storage areas and other sites
accessible to swine. There is little data on treatment, but levami-
sole has been recommended.
Threadworm
Definition, occurrence, and historical information
Parasitism by the nematode Strongyloides ransomi occurs only in
pigs. The organism is widespread and has importance in warmer
climates. It can affect any age, including fetuses, but is more
common in nursing piglets. Losses in modern, indoor production
settings are relatively minor.
Etiology, pathogenesis, and epidemiology
Only asexual females of S ransomi are important in parasitism of
swine. Free-living generations can produce progeny that are either
free-living (heterogonic cycle) or parasitic (homogonic cycle).
PARASITES
Free-living generations can alternate with parasitic generations.
The asexual females are almost microscopic, about 3.3 to 4.5
mm long, and live in the mucosa of the anterior small intestine,
usually the duodenum. The ova are thin shelled, larvated, and
are passed in the host’s feces. Infective larvae hatch in 1 to 2 days.
They require warmth and moisture for survival and are usually
eliminated by desiccation, sunshine, and good sanitary practices.
Survival is enhanced by 3 key mechanisms: the ability of S
ransomi to survive for some time in a nonparasitic form, the
availability of 4 possible routes of transmission, and the ability to
achieve patency in piglets in only a few days.
Parasitic larvae may infest pigs by penetration of the skin (per-
cutaneous), ingestion in feed (oral), ingestion in colostrum
(transcolostral), or through direct invasion of developing fetuses
(transplacental or perinatal). In all cases, the asexual female
reaches the mucosa of the small intestine, where many ova are
produced and passed in the feces of the host.
Larvae sequestered in muscle or in the mammary fat of sows are
mobilized during the periparturient period and are transmitted
to piglets in the colostrum. This is the most common route of
transmission to neonatal piglets. Larvae in colostrum arrive at the
intestinal mucosa without migration.
Larvae that penetrate the skin of young pigs enter the blood
stream and are carried to the lungs. After breaking out into alveoli
followed by tracheal migration to the pharynx, the larvae are
swallowed and reach the small intestine. Larvae taken into the
mouth penetrate the mucous membranes of the oral cavity and
after a similar migration, reach the small intestine.
MINOR INTESTINAL NEMATODES 135
 SWINE DISEASE MANUAL

Adults that develop in the small intestine irritate the intestine,
with the severity depending upon the number of parasites. The
parasites cause a blunting and atrophy of intestinal villi, resulting
in leakage of proteins into the gut and failure of the intestine
to absorb nutrients and fluids effectively. These alterations lead
to anemia, diarrhea, dehydration, and emaciation. Migration
of larvae through the lungs causes small hemorrhages as well as
thickening and inflammation of alveolar septa that impair respira-
tion. In mild infections there are few or no signs. Most mortality
occurs in piglets less than 2 weeks old. Diarrhea, dehydration and
unthriftiness can occur in pigs up to 3 months old.
Diagnosis and control
Diarrhea in nursing pigs may suggest the possibility of infection
with S ransomi. However, all other common causes of diarrhea
must be excluded first, especially infections with rotaviruses,
coronaviruses, Escherichia coli, Clostridium perfringens, C difficile,
and coccidiosis. Strongyloides ransomi, if present, can be identi-
fied in mucosal scrapings or histologic sections. The thin-shelled,
PARASITES
larvated ova can be identified by laboratory fecal examination
but must be differentiated from larvated ova of lungworms.
Lesions may not be readily apparent on gross examination. On
microscopic examination of the small intestine, there is villus
atrophy and blunting. Adult parasites can be seen in tunnels in
the epithelium of glandular crypts of the mucosa. In the lung,
there is inflammation and thickening of alveolar walls, scattered
hemorrhages, and perhaps migrating larvae. Neither hemorrhages
nor larvae are likely to be numerous.
Avoidance of pastures with an environment favorable to the para-
site will reduce exposure of sows and piglets. Indoor housing and
confinement rearing, combined with good sanitation, will reduce
the likelihood of threadworm infection. Avermectins given to the
sow a week or two prior to farrowing will control transmission of
larvae to fetuses.

136 MINOR INTESTINAL NEMATODES


Roundworm
Alternate names and abbreviations
Ascaris, worms, roundworms, large roundworms, ascarids, ascariasis
Definition
Ascariasis is the infestation of swine by the roundworm, Ascaris
suum, which can cause pneumonia, hepatitis, and ill-thrift.
Occurrence
Ascariasis occurs worldwide. All ages are affected but ascariasis is
more severe in young, growing pigs. It is the most prevalent and
economically important internal parasite of swine. Infection and
migration of ascarid larvae can occur in other animals, including
humans, but larvae usually do not develop to the adult stage in
the intestine of these other species. Migrating larvae occasionally
infect cattle, calves, and lambs and can cause severe eosinophilic
pneumonia.
Historical information
The ascarid of humans, A lumbricoides was once believed to be the
same as A suum; there is some truth to this notion as hybrids have
been identified that can infect both humans and pigs. Knowledge
of the life cycle is particularly important for this parasite, as effec-
tive economical control strategies must be tailored to each farm
site based on that knowledge.
Etiology
Mature ascarids are 15- to 40-cm-long, thick-bodied, round
worms. After a 7- to 8-week prepatent period, the prolific mature
ascarids can lay almost 2 million eggs per day. Adults generally
survive in a pig for around 6 months before the gradual sponta-
neous expulsion of adults occurs over the next 6 months. Heavy
infections can result in hundreds of ascarids in the intestine of a
single pig.
Ascarid ova are thick-shelled, yellowish brown, almost spher-
ical, 50 to 80 µm by 40 to 60 µm, and are coated with a sticky
proteinaceous cover. Ascarid ova are ingested and hatch in the
intestine. The larvae penetrate the mucosa and pass through the
bloodstream to the liver, lungs, and other sites. They reach the
liver 2 to 4 days after ingestion and are present in lungs within 10
days. Once arriving in the lung, they break into alveoli and bron-
chioles, move up the mucociliary escalator, are coughed up to the
pharynx, and are re-swallowed. These larvae reach the intestine
14 to 20 days after initial ingestion. There they become adults
over the next 6 weeks. There is a total prepatent period of approx-
imately 8 weeks after ova are ingested before eggs are passed in
feces. Ova passed in feces require 2 to 4 weeks to mature in the
environment before they become infective.
DISEASES CAUSED BY PARASITES
Epidemiology
Each adult ascarid can lay millions of eggs per day. The eggs are
extremely hardy and quite resistant to environmental degradation
and disinfectants. Ova may be inactivated by intensive steam
cleaning or prolonged exposure to full sunlight. Ova can survive
for years in the environment and can remain viable in swine efflu-
ent water for at least 14 months. Eggs are transported by infested
pigs, insects, fomites, blowing dust, pig manure, and effluent.
Eggs are often disseminated through the feces of purchased swine,
including breeding stock. Once a location is infested, ascariasis
often persists in the pig population despite intensive measures
to eliminate it. The extremely high number of eggs that are pro-
duced, the resistance of eggs to environmental degradation, and
the multiple means in which they can be disseminated contribute
to their persistence on infected farms.
Pathogenesis
Ascarids cause local inflammation in the intestine and compete
with the host for nutrients. This adversely affects growth of pigs,
especially those on marginal or poorly balanced diets. With heavy
infections, the most significant effect of the disease is a result of
PARASITES
the migrating larvae causing lesions in the liver and lungs, includ-
ing scarring of liver and interstitial pneumonia. Rarely, larvae are
carried to ectopic sites (eg, the retina or brain), which may cause
signs of impaired vision or central nervous system lesions. Ascarid
impact also includes immunosuppression that affects the duration
and severity of other swine respiratory and systemic diseases and
can influence the response of swine to some vaccines.
Clinical signs
Signs in young, growing pigs include unthriftiness, failure to gain
weight, rough hair coat, pendulous abdomen, chronic paroxysmal
coughing, and, occasionally, abdominal expiratory dyspnea. Low
levels of ascarid exposure will stimulate development of active
immunity. The most severe consequences of ascarid infection
occur when immunologically naïve pigs are placed into contam-
inated sites. Farrowing and nursery facilities often have a low
prevalence of ascarid egg contamination such that young pigs
will have had little or no exposure to the parasite. Hence, these
animals are at risk of severe disease when subsequently placed in
contaminated finishing barns. Severe, sometimes fatal, respira-
tory disease may result in 7 to 14 days after naïve pigs of any age
are placed in facilities heavily contaminated with ascarid eggs.
Affected pigs are afebrile, “thump,” are gaunt, and are often mis-
diagnosed as having bacterial or viral pneumonia. Other effects in
heavily exposed gilts include delayed estrus, poor conception rate,
pneumonia, or death. Severe liver insult can lead to stunting.
ROUNDWORM 137
 SWINE DISEASE MANUAL
Lesions
Scarring in the liver first appears by 7 to 14 days after exposure as
scattered, gray to white “milk spots” (0.2 to 1 cm in diameter) vis-
ible under the liver capsule. These lesions will eventually resolve
over 2 to 4 months; therefore, slaughter checks for liver lesions
may not always be a reliable method to monitor for the presence
or severity of ascarids in a herd if the infestation is occurring at a
young age. In heavy infections, diffuse interlobular fibrosis may
affect the entire liver and lead to its condemnation.
After their passage and molting in liver, larvae reach the lungs 7
to 14 days after ova ingestion. There they break out of capillaries
into alveoli and cause small focal hemorrhages and an inflam-
matory reaction that interferes with the clearance mechanism of
airways. Obstruction of smaller airways with atelectasis and/or
emphysema (verminous pneumonia) can lead to secondary bacte-
rial infections that present as a suppurative bronchopneumonia.
From the lungs, the larvae are transported or coughed into the
pharynx, swallowed, then reside in the small intestine without
attachment or demonstrable lesions. Since ascarids have some
mobility, they can sometimes be found in the stomach or in the
major bile and pancreatic ducts at necropsy, and occasionally may
obstruct the bile duct, leading to bile stasis and icterus.
PARASITES
Diagnosis
Diagnosis of acute ascarid infestations requires postmortem
examination of several typically affected pigs that have been sacri-
ficed. Fecal flotations are not reliable during the first 6 to 8 weeks
following infestation as the ova that were consumed by the pig
have not yet become patent adults. This is an important concept
because most of the pathologic changes and clinical impact of
ascarid infestation in swine occur well before ova are passed or
worms are grossly visible. Diagnosis of early infestations is made
by observation of typical liver and lung lesions with confirmation
by histopathology of the liver and lung. Postmortem examination
also permits the evaluation of concurrent diseases, including
other agents of pneumonia, hepatitis and icterus, enteritis, and
other parasitisms.
Diagnosis of more chronic infestations (infected greater than
2 months) and/or monitoring for parasitism is done by identifying
eggs using fecal flotation examinations or by finding grossly visible
ascarids in the small intestine. Ascarids or their ova may not be
present in animals that have been recently dewormed, but scarring
in the liver or hemorrhages in the lung may still be apparent.
138 ROUNDWORM
Control
A complete knowledge of the life cycle of ascarids and the infes-
tation status of a herd or group of pigs is required to make timely
and economical deworming decisions. All deworming programs
need to be designed to fit the specific situation, parasite load,
and management practices present on each production site. One
program does not fit all situations.
Prevention of ascariasis is far better than treatment but may be
difficult to achieve on many production sites. Swine raised in
confinement with a good ascariasis control program usually have
few ascarids. Some of the measures that confinement operators
implement may include: deworming the sows during gestation
(usually about a week before farrowing), washing the sows to
remove parasite eggs prior to putting them in sanitized farrowing
crates, early weaning of 2- to 4-week-old pigs (before ascarid eggs
have become infective in the farrowing environment), installing
slatted flooring which minimizes contact between pigs and feces,
and using all-in, all-out production systems with thorough clean-
ing between groups.
In modern swine production systems, many pigs are produced
in sanitary confinement systems that may be free of ascarid
infection. When these pigs are placed in sanitized modern con-
finement finishers, deworming may not be warranted. However,
when naïve pigs are placed in contaminated grow-finish facilities,
they may develop mild to severe pneumonia as they ingest numer-
ous eggs from the environment. Feeding a continuous dewormer
(pyrantel) for the first 30 days is a control option in this situation.
Pigs in such conditions should be dewormed early after infesta-
tion and then at 8- to 10-week intervals to prevent additional
egg contamination of the site. Modern confinement facilities
that recycle effluent water may increase the risk of ascarid ova
exposure. In these instances, routine deworming at 8- to 10-week
intervals may also be warranted.
In operations that utilize pasture or open-lot housing, deworming
the sows before moving them to clean pasture is a good practice.
Pasture rotation will greatly reduce the exposure of swine to
worm eggs, especially if the land is tilled when not pastured.
Anthelmintics should be selected on the basis of the entire spec-
trum of nematode species present on the farm, including ascarids.
A monitoring system should be established and followed. Some-
times parasite problems change as a consequence of introduction
of other kinds of parasites, facility changes, or climatic changes
that influence the number and variety of parasites.

Trichinellosis
Alternate names and abbreviations
Trichinella, trichina, trichinosis, pork worm
Definition
Trichinella spiralis is a parasite that infects swine, other carniv-
orous animals, and people. The parasites are usually ingested
through consumption of infected meat.
Occurrence
Most carnivorous, warm-blooded animals can become infected
with this parasite. Animal sources of human trichinellosis include
consumption of meat that is eaten raw or has been incompletely
cooked. In particular, meat from feral and domestic pigs, bears,
some sea mammals, and horses has been associated with significant
localized outbreaks in humans. Species implicated as sources of
infection for swine include previously infected pigs, rodents, and
scavenged wildlife carcasses. Meat scraps from infected, slaughtered
animals that are included in uncooked swill are a significant source
of infection for commercial swine in some countries.
The incidence of infection in swine is low in countries that
routinely inspect meat for T spiralis. In the US, food safety and
eradication efforts have resulted in a nondetectable prevalence in
commercial swine.
Historical information
Trichinellosis once caused outbreaks of severe illness in people, but
control measures were developed and adopted by many pork-pro-
ducing countries in response to the problem. In many countries
including the US, T spiralis infection of swine is essentially erad-
icated from commercial swine production. In recent years, most
of the US human cases of trichinellosis are a result of eating game
meat (especially bear meat) and not from exposure to pork.
Etiology
Trichinella spiralis has 4 separately named strains, each with
minor anatomical differences; they may simply represent different
ecotypes of the same species.
Mature T spiralis females are 3 to 4 mm long and are found in the
duodenal and jejunal mucosa. A fertilized female produces 500 to
1000 larvae over a period of 2 to 6 weeks.
The parasite’s life cycle begins with ingestion of infected muscle
that contains encysted T spiralis larvae. Trichinae within muscle
fibers are liberated when cyst walls are exposed to gastric secre-
tions after consumption. The larvae reach maturity in the small
intestine in about 4 days. They mate, and mature females pene-
trate into the mucosa and liberate larvae in lymphatics. Some lar-
vae escape into the lumen of the gut and are eliminated in feces.
Recently voided feces may be infectious, but this is considered a
minor mode of transmission.
DISEASES CAUSED BY PARASITES
Larvae in the lymphatics soon gain access to the systemic circula-
tion. Many are destroyed by body defenses. Those that gain access
to muscle fibers penetrate them, usually 1 per fiber. A larva within
a fiber often induces a change in the fiber that causes it to enlarge
and act as a nurse cell. In 2 to 3 months, the larva reaches a length
of over 100 µm and is enclosed in a cyst-like structure in the mod-
ified muscle cell. Here it can survive for up to 11 years.
Larvae have a predilection for certain striated muscles, generally
those that are normally quite active (eg, diaphragm, intercostal,
lingual, laryngeal, masseter, and ocular muscles). The larvae occa-
sionally localize in cardiac muscle fibers. Once encysted, larvae
must be ingested by another mammal for the cycle to be repeated.
Epidemiology
Survival of T spiralis is promoted by the wide range of animals
that serve as intermediate hosts, by the long survival of larvae in
muscle fibers, and by the scavenging, cannibalistic nature of pigs.
In swine, transmission often occurs when pigs scavenge Trichinel-
la-infected carcasses of swine, rats, or other animals. Transmission
also occurs when uncooked garbage containing pork or other
meat scraps that harbor T spiralis are fed to pigs. Tail-biting of
PARASITES
infected pigs and ingestion of larvae in feces are other possible
sources of exposure.
Pathogenesis
Trichinella spiralis has a relatively low pathogenicity for swine but
can cause severe clinical signs in humans.
Clinical signs
Clinical signs are seldom observed in swine naturally infected
with T spiralis. Experimentally infected swine show signs of
intense muscle pain and have decreased weight gain, but most
recover and weight gain improves. In infected miniature swine,
hypergammaglobulinemia and eosinophilia have been reported.
Lesions
In swine, gross lesions are not usually visible unless there is white
streaking from calcification of affected muscle fibers. On micro-
scopic exam, the encysted parasites are easily observed. If there
are degenerated or necrotic muscle fibers, an inflammatory reac-
tion with many eosinophils may be present around them.
Diagnosis
The prevalence of trichinae in the US swine population is so low
as to be reliably undetectable. In many countries, techniques used
for surveillance include trichinoscopic examination of muscle
(often diaphragm muscle) which appears to be one of the most
likely sites to contain T spiralis larvae. In this test, the muscle
TRICHINELLOSIS 139
 SWINE DISEASE MANUAL
is homogenized and enzymatically digested in order to release
the larvae from their cysts for efficient visualization by the tech-
nician. An enzyme-linked immunosorbent assay (ELISA) and
polymerase chain reaction assay are also available. Trichinella-free
production certification in the US currently relies on an ELISA.
Control
In the US, an educational program was developed with the
objective of emphasizing the need to thoroughly cook pork for
control of human trichinellosis. Concurrent with this program,
commercial pork production practices in the US changed, signifi-
cantly reducing the opportunity for pigs to become infected with
the parasite. As a result, the incidence of human trichinellosis
decreased dramatically. In 2011, the United States Department
of Agriculture Food Safety and Inspection Service recognized
trichinae to be of minimal risk in commercial US pork, and the
PARASITES
140 TRICHINELLOSIS
recommendation for cooking temperature for pork was decreased
from 160°F (71°C) to 145°F (63°C).
In addition to changes in the behavior of consumers and the
pork industry, regulations have also been developed that govern
how ready-to-eat pork products must be processed to ensure the
destruction of T spiralis. Today, the Pork Quality Assurance pro-
gram promoted by the National Pork Board continues to encour-
age good production practices that make T spiralis infection in
swine unlikely. The program has been implemented by many
producers; virtually all US pork processors require their suppliers
to be enrolled.
No effort should be made to treat animals suspected of having
trichinellosis, although they should be reported to state public
health and animal health authorities.

Whipworm
Alternate names and abbreviations
Trichuris, trichuriasis
Definition
Infestation of swine with the swine whipworm, Trichuris suis.
Occurrence
Trichuris suis infections occur in domestic and feral swine; infec-
tion has also been reported in some primates, including humans.
Although very uncommon in confinement-reared pigs, infection
remains relatively common in swine raised on pasture or on dirt
lots. All age groups are susceptible, but most infestations occur
in swine less than 12 months old. In adults, clinical signs can be
induced when infection occurs in the face of severe stress. How-
ever, whipworms commonly infest adult pigs at a subclinical level
and serve as a major source of infection for other swine. All major
swine-producing countries have whipworm.
Historical information
Whipworm infections were common in the past when more
swine were raised outdoors on pasture; the infection remains
reasonably common today in swine reared in the same settings.
Rearing of swine in confinement housing has led to the elimina-
tion of whipworms as a significant problem for most producers.
In outdoor operations, newer anthelmintics have allowed for
improved control over this once troublesome parasite.
Etiology
Trichuris suis is the name of the whipworm in swine. Mature
female whipworms are 6 to 8 mm long and males are about half
that length. The life span of adults is 4 to 5 months. The ante-
rior two-thirds of the parasite is quite thin and, when seen at
necropsy, is buried in the mucosa of the intestine. The posterior
one-third is visibly thicker and usually seen protruding into
the intestinal lumen. However, worms are generally too small
to be seen until at least 3 weeks postinfection. Microscopically,
ova are approximately 65 by 25 µm, yellow to brown in color,
double-operculated, and easily recognized. Ova passed in feces
become infective in 3 to 4 weeks. The prepatent period is 7 to 8
weeks but clinical signs can be observed within 1 to 2 weeks of
severe infestation. Ova production tends to be sporadic and there
are times when there are few ova in the feces.
Epidemiology
Although adult worms have a relatively short life span and lay ova
only sporadically, ova remain infective in most environments for
up to 6 years. This long period of survival tends to perpetuate the
species, even if pasture rotation is practiced. Adult swine tend to
harbor low levels of infection resulting in a continual source of
ova contamination in the environment.
DISEASES CAUSED BY PARASITES
Pathogenesis
After ingestion of larvated eggs, L3 larvae hatch and enter the
mucosa of the anterior small intestine. The larvae reside there
temporarily, return to the intestinal lumen for a period of time,
and then deeply reinvade the mucosa or submucosa of the cecum
and colon. This penetration results in diffuse mucofibrinous to
mucohemorrhagic typhlocolitis. Focal ulcerations may be com-
plicated by microorganisms that include Salmonella, Lawsonia,
Brachyspira, and Balantidium.
The inflammatory reaction around the parasites results in edem-
atous thickening of the wall of the gut and the formation of
inflammatory nodules around some parasites. In heavy infections,
a fibrinous pseudomembrane may form on the mucosa. Regional
lymph nodes may be swollen.
Clinical signs
Clinical effects are directly related to severity of infestation and
presence of concurrent diseases. Mild infestations are subclinical.
Signs include anorexia, mucoid or mucohemorrhagic diarrhea, dehy-
dration, and rarely death if severely affected. Signs are most apparent
2 to 4 weeks following exposure to contaminated facilities.
PARASITES
Lesions
During early stages (1 to 3 weeks postinfestation), whipworms
are not visible as they migrate within the large intestinal mucosa.
There is a mucoid to mucohemorrhagic typhlocolitis with
excessive mucus, fibrin, and blood on the mucosa. Lesions vary
in extent from focal to diffuse and in acute stages often resemble
those of swine dysentery. The affected gut wall is thickened and
edematous.
Histopathology is required for diagnosis and will reveal the
migrating larvae. Later, mature whipworms become visible with
careful gross examination. Worms often protrude from inflamma-
tory nodules in the gut wall, and purulent exudate may be visible
around them. Gentle traction on parasites will free them from
the gut wall, revealing the thin anterior end buried in the mucosa.
Dilated lymphoglandular complexes should not be mistaken as
lesions of either whipworms or nodular worms. Inflammation of
the cecal and colonic walls can be quite extensive and severe even
when only few adult worms are observed.
Diagnosis
Diagnosis is accomplished by necropsy of a typically affected
pig. Mature parasites are easily found in the cecum or colon and
can be identified by their size and whip-like form. Immature
worms are much smaller than adults but can cause severe lesions
if numerous. For identification, they require careful observation,
perhaps with the aid of flotation over a dark background or use
of a magnifying lens or by histopathology. The severe lesions of
the immature worms closely resemble, and must be differentiated
WHIPWORM 141
 SWINE DISEASE MANUAL
from, those of swine dysentery, salmonellosis, and proliferative
enteritis, any of which may be concurrently present.
The presence of ova can be determined by laboratory fecal exam-
inations by 7 weeks after infestation, but clinical signs and lesions
will often be quite severe before ova are present. The double-oper-
culated eggs are distinctive, but ova production is often sporadic
and there may be few or no ova in a single fecal sample. The
number of ova found on fecal examinations may not be a reliable
indicator of the number of worms present.
PARASITES
142 WHIPWORM
Control
Control depends on avoidance of exposure to contaminated pas-
tures or lots. Tillage of pastures or lots not being used can reduce
the number of eggs that survive. In outdoor operations, it is help-
ful to treat the pregnant sows with an appropriate anthelmintic
a week or two prior to farrowing and/or before moving them to
clean pasture. This reduces exposure of the piglets to eggs. Raising
swine in confinement, without access to soil, usually results in
good control.
Not all anthelmintics have good efficacy against T suis, so a
careful evaluation of a product’s spectrum of activity is warranted
before incorporating it into a control program.
 Section V

Miscellaneous

Atresia ani, Aural hematoma, Congenital tremors, Cystitis and pyelonephritis, Dermatosis vegetans......................145
Ectopic ossification, Epitheliogenesis imperfecta, Gastric ulcer ........................................................................................146
Hemorrhagic bowel syndrome, Hernias, Hydronephrosis, Hypogalactia and MMA...................................................148
Hypoglycemia, Megacolon, Mulberry heart disease and related conditions...................................................................149
Osteochondrosis, Pityriasis rosea, Porcine stress syndrome................................................................................................151
Prolapses, Pustular dermatitis, Rabies, Ringworm.................................................................................................................152
Shoulder ulcers in sows, Skin necrosis of piglets, Splayleg (spraddleleg), Sunburn and photosensitization.............153
Torsion and volvulus, Vestibular syndrome, Vices (tail biting, ear biting, flank biting, navel sucking).....................154

OTHER

143
 144
OTHER

Atresia ani
The congenital absence of a patent anus at birth is rather
uncommon in swine. The cause is not known, but it may either
have a genetic component or result from an insult to the fetus in
Aural (ear) hematoma
Aural hematomas are common lesions in pigs with large, depen-
dent ears. They are generally a result of some type of trauma to
the ear followed by hemorrhage between the skin and cartilage
(or within the cartilage). The subcutaneous clot of blood resolves
over several weeks to months, in most cases leaving the pinna
thickened and misshapen. The inciting trauma often results from
bites inflicted by penmates or from violent head shaking. Head
Congenital tremors
In this disease, some or all of a newborn litter of pigs have
mild-to-violent tremors of part or all of their bodies. The trem-
ors are worse when piglets are active or stimulated and are often
absent while they sleep. If severe, the tremors will prevent nurs-
ing and affected piglets will starve. However, if piglets can nurse,
the condition can gradually resolve even though a mild tremor
may persist well into finishing phase.
This disease, recognized for over 100 years, usually occurs in gilt
litters, especially after introduction of a new boar. Subsequent
mating of the same boar and dam will result in normal, unaf-
fected piglets, suggesting that natural immunity occurs. A spe-
cific cause of congenital tremors remains elusive, but occurrence
of these “shaker pigs” has been associated with in utero viral
Cystitis and pyelonephritis
These conditions are usually the result of ascending bacterial
infections. Various bacteria, including Actinobaculum (formerly
Eubacterium or Corynebacterium) suis and coliforms, have been
isolated from the lesions. The infections usually occur in older
sows and are a cause of sporadic deaths. Death often occurs
during or shortly after advanced pregnancy, a time of maximum
stress on kidney function. Anything that interferes with adequate
water intake or the complete emptying of the bladder via urina-
tion may predispose the pig to urogenital infection.
Dermatosis vegetans
This hereditary defect originated in the Landrace breed. The
defect can be expressed as foot deformities present at birth, or
later as widely distributed expanding cutaneous lesions that
involve small to large areas of skin. Skin lesions are usually appar-
ent by the third week of life although some develop later. Skin
ATRESIA ANI, AURAL HEMATOMA, CONGENITAL TREMORS, CYSTITIS, DERMATOSIS VEGETANS 145
MISCELLANEOUS
critical developmental stages in utero. The resultant megacolon
may not be clinically apparent until several weeks of age.
shaking is associated with mange, infestation with lice, or feed
particles in the ears. Treatment or drainage of the acute (hema-
toma) stage of the fluctuant ear lesion is not usually attempted,
nor is it likely to be successful. Segregation rather than treatment
is the recommended intervention. Amputation of the ear is some-
times performed in severe cases.
infections (eg, classical swine fever and other viruses), genetic
predispositions, or in utero exposure to certain chemicals.
Recently, experimental in utero infection of fetuses with atypical
porcine pestivirus (a different pestivirus than classical swine fever
virus) reproduced typical clinical signs in newborn piglets. The
affected piglets were born viremic and remained viremic indefi-
nitely. It appears this virus is quite widespread globally and only
causes disease when it infects naïve or susceptible dams at breeding
or during gestation. Atypical porcine pestivirus can be detected
in boar semen, which is one likely mode of transmission. Once
infected, herds are generally immune and clinical cases disappear.
Frequency of splayleg often increases during congenital tremor
outbreaks.
OTHER
Actinobaculum suis is present in the preputial diverticulum of
most boars. The organisms may be transmitted to the sow during
copulation. Sows with cystitis or nephritis often have hematuria,
which is one of the earliest signs of infection, often within 3
weeks after breeding. This is followed by progressive loss of body
weight.
These conditions are uncommon in boars.
lesions begin as papules and expand to form roughened plaques
that soon become papillomatous. Most affected pigs die within
6 weeks. Many that survive have dyspnea related to interstitial
pneumonia of giant cell type.
 SWINE DISEASE MANUAL
Ectopic ossification of mesentery
Sows and boars over 3 years of age are occasionally found to
have ectopic ossification of the root of the intestinal mesentery.
The cause of these bony spicules radiating through the mes-
Epitheliogenesis imperfecta
This inherited condition is known to occur in at least 4 breeds
and is characterized by the absence of discrete areas of skin, usu-
ally over a part of the back or thigh. Lesions occasionally occur
on the anterior surface of the tongue. Hydroureter and hydro-
Gastric ulcer
Alternate names and abbreviations
Stomach ulcers, ulceration of the pars esophagea, ulcer
Definition
In swine, gastric ulceration refers to the destruction of the normal
epithelium of the pars esophagea (nonglandular region of the
stomach). This ulceration can involve part or all of the entire area
of the pars esophagea.
Occurrence
The lesions occur in pigs from weaning onwards. The prevalence
is variable but can be quite high (5% to 90%) in some farms or
production systems. Clinical signs are usually noticed only in pigs
8 weeks of age or older, including adults, with highest prevalence
in pigs 3 to 6 months of age. Ulcers occur in all breeds, both
sexes, and in most major swine-raising countries.
OTHER
Historical information
Ulceration of the pars esophagea was first reported in Illinois in
1897. Subsequently, the lesion was identified in at least 30 other
countries. Although the ulcers are most often subclinical, death
losses can be severe.
Etiology
The etiology is unknown but multiple risk factors have been iden-
tified, some of which are probably additive in their effect. Risk
factors commonly mentioned include:
• The feeding of finely ground feed (less than 400 µm particle
diameter)
• Pelleted rations (perhaps due to the finely ground feed used
when making pellets)
• Concentrated, nutrient dense diets that are low in fiber
• Stressors (eg, anxiety, fear, pain, fatigue, crowding, fasting,
prolonged transportation, social stress from mixing with
unfamiliar pigs, poor air quality, etc)
146 ECTOPIC OSSIFICATION, EPITHELIOGENESIS IMPERFECTA, GASTRIC ULCER
entery is not known. Little significance is ascribed to the pres-
ence of ectopic ossification, but it may be involved in mechani-
cal injuries such as intestinal volvulus or accidents.
nephrosis commonly accompany the condition. Fetuses with
extensive lesions may be aborted. Piglets born alive with extensive
lesions usually die from bacterial invasion and septicemia. Minor
defects may heal.
• Hot weather, potentially related to decreased feed intake,
heat stress, or stress associated with limited access to water
• Out-of-feed events due to plugged or empty feeding systems
• Chronic or acute disease (both of which may contribute to
anorexia)
• Greater occurrence reported in barrows (versus gilts) and in
high-lean genotypes
• Feeding rations with copper as a growth promoter, perhaps
without adequate zinc
• Ad libitum feeding of whey or skimmed milk.
• Diets high in wheat or cornstarch
• High levels of unsaturated fats in the diet, often accompa-
nied by inadequate levels of vitamin E
A primary infectious etiology has not been proven. Several agents
have been associated with increased prevalence and severity of
ulcers, including Helicobacter species and Gastrospirillum spe-
cies, but a causal role has never been established. In some severe
outbreaks of gastric ulcers in swine, porcine circovirus type 2 has
been demonstrated within lesions. Gastric ulceration is a com-
mon sequel to outbreaks of influenza A and porcine respiratory
disease complex, particularly during the summer months.
Infectious organisms (Helicobacter pylori) and the use of non-
steroidal anti-inflammatory agents are strongly associated with
human gastric ulcers, which occur in the glandular portions of
the fundus and pylorus. When pigs are used as research models
for human ulcers caused by those risk factors, ulcers are induced
in the glandular mucosa. However, gastric ulcers in pigs typically
occur in the nonglandular pars esophagea, and the risk factors
associated with gastric ulcers in humans are not associated with
typical gastric ulcers in swine.
Epidemiology
Both etiology and epidemiology are speculative. Epidemiology is
difficult to assess as it is likely to be multifactorial. Risk factors
that appear important in one herd or production system do not
remain consistently important across others.

Pathogenesis
Irrespective of the risk factor that triggers formation of a gastric
ulcer, the pathogenesis of the lesion has been well characterized.
Gastric ulcers result from a disruption to the pH gradient in the
fluid contents of the stomach that normally exists between the
proximal end of the stomach (pars esophagea; relatively higher
pH) and the distal end (pylorus; relatively lower pH). Although
causal factors are not clearly defined, when gastrin-stimulated
acid secretion becomes excessive, the overly fluid, very low-pH
stomach content moves to the region of the pars esophagea. The
stratified squamous epithelium in this region becomes hyper-
keratotic in response to the abnormally acidic environment and,
if the insult persists, ulcers form. Preulcerative hyperkeratosis is
extremely common in growing swine, probably because of low
fiber diets.
The pars esophagea undergoes hyperkeratosis and parakeratosis,
creating fissures that expose the underlying lamina propria. This
progression from hyperkeratosis to the ulcerative process can
occur very quickly, often within 24 hours of the insult, with
significant ulcers, erosions, and hemorrhagic lesions possible in
5 to 7 days. If the insulting acidity persists or animals become
anorexic, part or all of the stratified squamous epithelium may
slough off, leaving one or more deep ulcers. Blood vessel walls of
various sizes within the lamina propria and submucosa may also
become eroded and hemorrhage will then occur. If blood loss is
slow and/or intermittent, melena, generalized pallor, and anemia
may be observed. If a few large vessels are eroded, the animal may
die from an acute massive hemorrhage.
Ulcers can resolve if they are not severe, although resolution of
lesions occasionally results in stricture of the terminal esophagus
or pars esophagea.
Clinical signs
Preulcerative hyperkeratosis of the pars esophagea is a common
precursor to actual ulceration. However, hyperkeratosis does not
appear to influence feed consumption, nor is it noticeable clinically.
In fact, many swine are subclinically affected, evidenced by the high
prevalence of lesions in apparently normal pigs at slaughter. With-
holding feed can cause some preulcerative lesions to erode in a rela-
tively short time (as little as 2 to 3 days), which may initiate clinical
signs. The clinical effects of ulcers are usually related to blood loss.
Acutely affected pigs may be found dead with carcass pallor. Others
may have black tarry feces (melena), anemia, and generalized pallor.
Other signs that can sometimes be observed include anorexia,
grinding of the teeth, or unthriftiness.
Lesions
Typical gastric ulcers occur only in the nonglandular region
(pars esophagea) of the stomach at the junction of stomach and
esophagus. Pigs that are in the early stage of developing ulcers have
an altered pars esophagea, which instead of being snowy white, is
MISCELLANEOUS
raised, roughened, somewhat nodular, usually bile stained, and
sometimes fissured with hyperkeratosis. Ulcers vary greatly in
size, shape, number, and depth. Large ulcers are often deep and
have smooth, rolled, and raised borders. Sometimes the ulcerated
area involves the entire pars esophagea and may partially obstruct
the esophagus. The terminal part of the esophagus may also be
hypertrophied. In animals that have recovered from deep ulcers,
a puckered or stellate scar often remains.
Necropsy of pigs that die suddenly will have pallor of the skin
and internal organs and tissues. There may be large blood clots
in the stomach and/or dark, unclotted blood mixed with ingesta
and feces throughout the intestine. The intestinal and/or colonic
contents are often very dark, black, or tar colored. The entire
pars esophagea may completely ulcerate down to the level of the
muscular wall, giving the false impression of intact glandular
mucosa. Complete destruction of the pars esophagea is easy to
miss at necropsy; the color of that area may be a uniform gray and
without hemorrhage. The absence of clotted blood in the stomach
does not rule out gastric ulcer. Careful examination of the pars
esophagea is warranted since hemorrhage may be intermittent.
Death caused by gastric ulcer does require a large amount of clot-
ted blood to be found in the stomach or intestines at the time of
death.
Differential diagnoses include other causes of hemorrhagic
diarrhea such as porcine proliferative enteritis, swine dysentery,
salmonellosis, and whipworms.
Control
For pale or anemic pigs, treatment is of questionable efficacy but
may include Vitamin K, hematinics, segregation, and supportive
therapy including oral protein supplements. Access to fiber (hay
or pasture) or products that reduce gastric emptying will some-
OTHER
times aid in recovery.
Prevention is based on correcting those risk factors suspected
of contributing to ulcer formation. Minimizing stressors and
preventing out-of-feed events are always warranted. Altering the
ration to minimize the effects of some of the possible risk factors
is helpful. Changing to a more coarsely ground feed (less than
an average diameter of 700 µm) and changing from a pelleted
diet to a meal diet is often recommended. The quality of the
feed ingredients should be improved if some of the feedstuffs
were stored for long periods, are of poor quality, or contain
mycotoxins. Efforts to decrease heat stress in warm weather are
beneficial. The successful control of some of the severe swine
diseases, especially porcine circovirus type 2, influenza A, and
Actinobacillus pleuropneumoniae has decreased the losses attrib-
utable to gastric ulcers on some swine farms.
GASTRIC ULCER 147
 SWINE DISEASE MANUAL
Hemorrhagic bowel syndrome
Hemorrhagic bowel syndrome refers to a condition whereby
previously healthy growing or finishing pigs die acutely, with
bloating and pallor at time of death. The condition was originally
described in whey-fed pigs as “whey-bloat,” but now often refers
to sporadic deaths of individual pigs that meet the following
diagnostic criteria:
• There is carcass pallor and the abdomen is distended by
abdominal viscera.
• The small intestine is diffusely dilated, thin-walled, and
distended with unclotted brownish blood, watery fluid, and
gas; the large intestine may be similarly affected or relatively
normal.
• The stomach is normal in appearance and has normal
contents.
The diagnosis is by default and is made only after ruling out other
causes of sudden death and intestinal hemorrhage by postmortem
examination, appropriate laboratory testing, and histopathology.
Hernias (inguinal and umbilical)
Both inguinal and umbilical hernias occur sporadically in swine.
Inguinal hernias, where loops of intestine can pass through an
incompletely closed inguinal ring, are believed to be heritable
to some extent but heritability is unlikely to be associated with a
single gene. The overall incidence of inguinal hernias in a normal
swine population is low unless mating to a boar that is genetically
predisposed to pass the risk on to his offspring.
Inguinal hernias can be bilateral or unilateral, with most
OTHER
occurring on the left side. Protrusion of intestines through the
inguinal canal can follow castration of pigs when an inguinal
hernia is not detected prior to surgery. In pigs left uncastrated,
Hydronephrosis
It is common to find variably sized, sometimes large, fluid-filled
cysts in the kidneys of healthy swine. This incidental finding is
Hypogalactia and Mastitis, Metritis, Agalactia (MMA)
Hypogalactia and MMA usually occur within 3 days of farrowing
and are characterized by inadequate milk production. Although
hypogalactia is the most consistent sign, mastitis from bacterial
infection, fever, vaginal discharge, listlessness, weakness, anorexia,
sternal recumbency, and refusal of the dam to permit nursing by
the piglets may be present in affected sows.
148 HEMORRHAGIC BOWEL SYNDROME, HERNIAS, HYDRONEPHROSIS, HYPOGALACTIA AND MMA
Hemorrhagic bowel syndrome should be differentiated from
partial or complete intestinal torsion or intestinal volvulus, which
are common causes of sporadic death. An acute hemorrhagic gas-
tric ulcer usually has very dark or black blood in the intestine and
lacks intestinal dilation. The hemorrhagic form of ileitis may have
blood clots and/or segmental thickening of intestinal mucosa.
Acute enterotoxemia with intestinal congestion associated with
hemolytic Escherichia coli or Salmonella is often a differential in
nursery pigs.
The actual cause of hemorrhagic bowel syndrome is unknown
but anecdotal risk factors include out-of-feed events and other
circumstances that foster feed engorgement (eg, commingling,
weather events, etc), liquid feeding, and feeding of whey prod-
ucts. Diets higher in fiber may help ameliorate the occurrence of
hemorrhagic bowel syndrome and other intestinal accidents.
strangulation of the intestine within an inguinal hernia can occur,
but the most significant effect of the condition is the economic
discount applied to the pig at time of slaughter. Surgical repairs
have been described that are rapid and very successful.
Umbilical hernias occur in both sexes and tend to develop as a
result of poor umbilical cord management in neonates, chronic
navel infections, or navel sucking by penmates. The condition is
not thought to be inherited. Prevention is achieved by practicing
excellent hygiene in the farrowing house along with the appro-
priate use of antimicrobials. Surgical repair is possible but rarely
practical.
observed during postmortem examinations conducted for unre-
lated conditions or at slaughter.
Dams usually recover within a few days to several weeks if
the inciting cause is effectively and rapidly managed. Piglets
are at high risk of dying from starvation unless cross-fostered
or provided with supplemental milk replacer. Although the
cause(s) is unknown, many risk factors have been associated
with hypogalactia. These include lack of nursing stimulation

(too few pigs, or pigs are small and weak), bacterial metritis or
mastitis with endotoxemia, errors in ration formulation or poor
feeding management, confinement with little opportunity for
exercise, constipation, obesity, moldy feeds (ergotism), and poor
sanitation in the farrowing environment. The condition is difficult
to eliminate completely from farms; however, if it occurs any
more than sporadically, a comprehensive evaluation of all aspects
of gestation and farrowing management and nutrition should be
undertaken to help identify the root cause or main risk factors.
Mastitis, often clinically undetected, is likely responsible for many
cases of hypogalactia. Endotoxin from various Gram-negative
Hypoglycemia in neonatal piglets
Hypoglycemia is a common cause of death in neonatal piglets.
Glycogen reserves become depleted when piglets are starving,
chilled, competing for limited number of functional nipples,
or when inadequate milk is available. Chilling may occur if the
effective temperature in the piglet sleeping area is less than 95°F
(35°C) during the first week of life.
Signs of hypoglycemia include loss of condition, weak vocaliza-
tion, faltering gait, cold skin, and recumbency. These signs are
Megacolon
Enlargement and dilation of the colon with feces is usually the
result of rectal stricture, atresia ani, or, less frequently, colonic
atony. Atresia ani leads to megacolon in pigs up to 4 weeks of age.
Postnatal rectal strictures are a frequent sequel to rectal prolapse.
Damaged rectal tissues from prolapse - irrespective of whether
the prolapse has reduced on its own, been surgically repaired,
traumatized, or chewed off by penmates - can heal with fibrosis,
Mulberry heart disease and related conditions
Vitamin E and selenium responsive myocardial damage (uncom-
pensated oxidative metabolic stress) can present with variable
clinical signs, though 3 closely related, overlapping syndromes are
most commonly associated with the condition.
The most frequent presentation is mulberry heart disease,
which is clinically manifested as sudden death in fast growing,
previously healthy young pigs, usually a few weeks to 2 months
of age. However, in some cases, death due to mulberry heart
disease may be preceded by dyspnea, recumbency, pallor, and
leg paddling. At necropsy, it is common for these pigs to have
hydropericardium (often accompanied by soft fibrin clots),
MISCELLANEOUS
bacteria, especially Escherichia coli, may be the cause of many
cases of mastitis. Suppression of prolactin by endotoxin from any
source results in less than normal milk production.
The prevalence of MMA has decreased markedly in the past
several decades with the use of modern sanitary practices and
the routine use of perforated, dry flooring. Most problems with
hypogalactia can be solved through management with careful
attention to sanitation, nutritional formulation, and feeding
management.
followed by paddling, frothing at the mouth, coma, and death
if no intervention occurs. If chilling occurs, the piglets should
be put in a warm environment with a supplemental heat source
such as heat lamps. If the piglets are not receiving an adequate
amount of milk, cross-fostering or milk supplementation can
be beneficial. Porcine milk replacers, bovine colostrum, or
evaporated milk diluted equally with water can be used for
supplemental nutrition until piglets are able to consume nutri-
ent-dense solid food.
causing constriction of the rectum. The outcome is restricted
fecal flow with intermittent defecation or total obstruction,
causing the colon to dilate with accumulated feces while the pig
OTHER
slowly wastes away.
Colonic atony with patent rectum has been reported as a result of
feeding lupine-seed meal. The neural control of tone and peristal-
tic movement is lost, causing the colon to simply dilate with feces.
noncollapsing lungs, and visible hemorrhages on the surface
of the heart that tend to occur in alternating areas of necrosis
and hemorrhage, creating the lesion for which the condition is
named. Straw-colored fluid is often present in the pleural cavity,
and the lungs are edematous. Typically, there are hemorrhages
throughout the myocardium. Microscopically, the affected
areas of the heart will show capillary hemorrhage and swollen,
fragmented, and sometimes mineralized muscle cells. There
are degenerative changes in the arteriole walls at many sites.
Although the mechanism of pathology is not clear, most cases of
mulberry heart disease occur when vitamin E is low. However,
HYPOGLYCEMIA, MEGACOLON, MULBERRY HEART DISEASE 149
 SWINE DISEASE MANUAL
mulberry heart disease does occur in pigs with seemingly
adequate levels of vitamin E in tissue or serum, suggesting
that other oxidative stress or antioxidants may be involved.
Supplemental vitamin E can sometimes ameliorate death loss.
Hepatosis dietetica is a more rarely encountered presentation of
the disease, particularly since the allowable limit of selenium sup-
plementation in livestock feed was raised to 0.3 ppm. Although
sudden death is a common occurrence in hepatosis dietetica,
death may be preceded by weakness, pallor, dyspnea, and ill-thrift.
In this syndrome, irregular focal-to-large areas of necrosis and
hemorrhage are seen in the liver, giving its surface a mottled or
speckled appearance; the liver may appear swollen, and the gall
bladder often is edematous. Myocardial necrosis and pulmonary
edema may also be present. Microscopically, much of the liver
parenchyma will have characteristic massive coagulative necrosis.
Sinusoids in affected areas may be distended with blood but
occasionally the necrotic areas will be ischemic. Prudent supple-
mentation with selenium will usually limit further death loss due
to hepatosis dietetica. Hepatosis dietetica may be present along
with mulberry heart disease or white muscle disease but can also
occur in isolation.
The most infrequent manifestation of the condition in pigs is
called white muscle disease, which appears to be much more com-
mon in calves, lambs, and chickens than in swine. Skeletal muscle
pallor or streaks of white, gritty mineralization are observed,
particularly in the longissimus dorsi muscle or ham muscles. His-
tologically, there is loss of myocyte structure with vacuolation,
fragmentation, and mineral deposition in type I fibers. Affected
pigs present with ataxia, weakness progressing to paralysis and
recumbency, and often death. Hemorrhage does not feature sig-
nificantly in the skeletal muscle lesions nor is there evidence that
lesions of mulberry heart disease and white muscle disease tend to
OTHER
occur simultaneously in affected pigs.
The underlying pathophysiological mechanisms that result in
lesions of mulberry heart disease, white muscle disease, and
hepatosis dietetica are not well understood but it is thought they
are associated with the formation of free radicals in tissue and an
inability of the pig to scavenge them, resulting in “uncompen-
sated oxidative metabolic stress.” Free radicals are highly reactive
molecules generated during normal oxidative metabolism which
are typically neutralized by the cell using antioxidant scavengers
such as superoxide dismutase, and vitamins E and C. Selenium
has an essential involvement in glutathione peroxidase activity,
hence its perceived role in the disease process as well. Unscav-
enged free radicals induce damage to cellular proteins, membrane
lipids, and nucleic acids. If adequate free radical scavengers are
150 MULBERRY HEART DISEASE
not available, severe cellular injury and death can occur. This
explains the severe tissue damage that is associated with all 3 clin-
ical conditions.
Feeds high in the concentration of polyunsaturated fatty acids,
copper, vitamin A, or mycotoxins can either denature vitamin
E or make it less bioavailable. Grains from soils deficient in sele-
nium, or selenium antagonists in mixed feeds can result in feeds
low in selenium. Both vitamin E and selenium are important
metabolic antioxidants. Besides the syndromes described below,
pigs deficient in vitamin E and/or selenium may be more suscep-
tible to other diseases.
Diagnosis of these syndromes is made on the basis of clinical pre-
sentation, gross lesions, and microscopic lesions in heart, liver, or
muscles, and analysis for vitamin E and selenium levels in the liver
or serum.
For prevention or treatment of a deficiency, pigs can be injected
with vitamin E and/or selenium and tissue levels will rapidly
increase. Also, prevention is possible through appropriate supple-
mentation of feed or drinking water. Sows injected in late gesta-
tion give birth to pigs with increased levels of both compounds.
The acute manifestation of the 3 syndromes described above may
not always be completely responsive to supplemental vitamin E
and/or selenium administration. For example, mulberry heart
disease appears to be more responsive to vitamin E compared to
hepatosis dietetica, and white muscle disease seems to respond
better to supplemental selenium. However, even when mulberry
heart disease occurs in the face of normal vitamin E levels, deaths
can usually be prevented by providing additional vitamin E, often
at levels that far exceed those recommended by the National
Research Council. Supplementation with vitamin E using highly
bioavailable parenteral or oral forms is quite safe and effective.
Selenium levels should be verified as adequate but excessive sele-
nium supplementation should be avoided because of the poten-
tial for toxicity.
In outbreaks, feed content and quality as well as feed storage
conditions should be examined carefully to determine if feed
quality has been compromised. Improper feed storage, high
copper levels, high fat levels, and poor-quality feed constituents
can result in destruction of vitamin E in a feed that has otherwise
been adequately formulated. Pigs on pasture usually get enough
vitamin E and selenium unless the soil is deficient in selenium.
Small piglets deficient in vitamin E are quite susceptible to iron
toxicity when injected with iron dextran for anemia prevention.
Deaths occur with myocardial lesions that closely resemble those
of mulberry heart disease.

Osteochondrosis
Osteochondrosis, also referred to as dyschondroplasia, is a gener-
alized skeletal disease where the cartilage in physeal or epiphyseal
growth plates fails to properly ossify. The condition often occurs
in rapidly growing pigs approaching market weight or breeding
age. The disease is characterized clinically by abnormal gait or
lameness with characteristic pathologic lesions in cartilage and
bone. Lesions of the articular surfaces of joints include corru-
gations and ulcerations of cartilage, separation of cartilage from
underlying bone, and development of cartilaginous cysts. Physeal
cartilaginous lesions include fractures between the diaphysis and
epiphysis, or islands of cartilage within epiphyseal or diaphyseal
bone. Lesions are often bilateral and symmetrical. Common sites
of lesions in joint cartilage include the medial femoral condyle,
humeral condyle, humeral head, glenoid of the scapula, distal
ulna, and lumbar vertebrae. Common sites of physeal lesions
include distal ulna and femur, head of the femur or humerus, and
ischial tuberosity.
Pityriasis rosea
Pityriasis rosea is a dermatitis usually seen in 4- to 12-week-old
pigs and is characterized by 1- to 10-cm-diameter, raised, red-
dened, ring-shaped lesions on the skin. Lesions first develop on
the skin of the ventral abdomen but occasionally start in other
areas. The cause is unknown. Papules first develop on the ventral
abdomen and inner thighs. These early lesions expand to form
circular, coalescing lesions with an expanding rim. Older lesions
Porcine stress syndrome
Porcine stress syndrome, sometimes called malignant hyper-
thermia or transport myopathy, is a complex, genetically linked
myopathy usually triggered by stress or excitement. It can also be
triggered by exposure to several different anesthetics, including
halothane, and by depolarizing muscle relaxants. Signs that can
appear include tremors of the tail, back, or leg muscles, muscle
rigidity, inability to walk, respiratory distress, hyperthermia,
blotchy dermal hyperemia, acute right heart failure, and death.
Postmortem lesions include early, rapid, and complete rigor mor-
tis, pulmonary edema, and pale soft musculature that often con-
tains hemorrhages. When slaughtered, swine with porcine stress
syndrome produce carcasses that are blanched, wet, and may drip
OSTEOCHONDROSIS, PITYRIASIS ROSEA, PORCINE STRESS SYNDROME 151
MISCELLANEOUS
Despite much research, the basic cause(s) is unknown. However,
the clinical expression of lameness is related to the presence of
one or more risk factors. Dyschondroplasia has been attributed to
rapid growth and early excessive weight-bearing pressure on carti-
lage, but is usually accompanied by additional risk factors. Genetic
influences for rapid growth are believed to play some role. Other
possible risk factors for disease expression include nutritional
deficiencies, flooring and housing that induce trauma, concurrent
joint infections, and lack of exercise. The number of pigs with
lesions is often much higher than the incidence of lameness would
suggest. Although some clinically affected pigs recover, most
affected gilts and sows are culled because of the time required for
healing and the overall poor response to therapy.
often have healed centers. Lesions heal in about 4 weeks without
intervention. Pityriasis rosea is easily diagnosed by gross exam-
ination and does not require any treatment. The condition is not
pruritic and seems to have no apparent effect on the health or
growth rate of affected pigs. Nearly all affected pigs recover spon-
taneously and completely.
OTHER
excessive amounts of fluid. The meat from pigs with this condi-
tion is referred to as pale, soft, exudative pork. In the marketplace,
shoppers discriminate against pork with these characteristics.
The basic abnormality is an inherited defect in the mechanisms
for the uptake, storage, and release of calcium in muscle fibers.
Efforts to eliminate porcine stress syndrome through genetic
selection have led to success in identification and elimination of a
stress gene by virtually all large, commercial swine genetics compa-
nies. A polymerase chain reaction test is widely available for iden-
tifying hetero- and homozygous carriers of the halothane gene;
both types of carrier animals should be culled when identified.
 SWINE DISEASE MANUAL
Prolapses (rectal, vaginal, and uterine)
Prolapse of rectal or vaginal tissues (including prolapse of the
uterus) usually occurs sporadically in swine, but on rare occasions
these conditions can also appear as an outbreak or cluster of cases.
All age groups are susceptible to prolapses, but occurrence in
suckling piglets is quite uncommon.
Prolapse of the rectum is usually the result of increased abdominal
pressure from piling (for warmth in cold weather or due to stress
during transport), severe coughing, or straining and trauma at par-
turition. Rectal prolapse has also been associated with the straining
and anal irritation that accompany some severe enteric diseases,
especially salmonellosis. The feeding of whey, brewer’s grains, or
low-fiber diets has preceded some outbreaks. Another common
risk factor that has been suggested is the presence of mycotoxins
(especially zearalenone) in the feed or bedding. Estrogenic myco-
toxins and phytoestrogens can cause vulvovaginal edema and irrita-
tion in prepuberal gilts or sows. These compounds are considered
a risk factor for rectal strictures when more obvious risk factors
are not present. Rectal stricture is a common sequel to prolapse of
the rectum.
The condition can be repaired surgically by amputation or, if the
tissue is not overly traumatized, by replacement followed by use
of a purse-string suture. When prolapses occur in an outbreak
Pustular dermatitis
Pustular dermatitis is usually observed only in nursing piglets.
It is caused by a beta-hemolytic, Lancefield type C Streptococcus
infection. Pustules appear in the inguinal area and inner surface
OTHER
of the rear legs but occasionally occur at other locations. The
Rabies
Rabies is a highly fatal viral disease that occurs in swine bitten
by an infected carrier animal. The incubation period is quite
variable, reportedly 9 days to 4 months. Clinical signs are similar
to those described in other species and include sudden onset
of incoordination, prostration, chewing movements, excessive
salivation, inability to squeal, muscular spasms and tremors, and
perhaps twitching of the nose. Death usually occurs within 3 to
Ringworm
Ringworm (fungal infection) occurs occasionally in swine and
may affect any age group. Although cases are often sporadic,
occasional outbreaks affect many animals, especially sows. Most
ringworm is caused by the fungi Microsporum nanum or Tricho-
phyton verrucosum.
152 PROLAPSES, PUSTULAR DERMATITIS, RABIES, RINGWORM
situation, effort needs to be directed towards rapid identification
of the triggering factor(s). The response to individual treatment
of prolapses is markedly improved by timely intervention within
a few hours of their occurrence.
Prolapse of the vagina or rectum sometimes occurs as a conse-
quence of flaccidity and relaxation of the birth canal in sows close
to parturition, perhaps exacerbated by trauma. Prolapse of the
vagina usually occurs first and may then be followed by prolapse
of the rectum. Genetic factors have been shown to contribute
to prolapses of the vagina and uterus in some breeds, but more
likely risk factors include trauma (bite wounds), severe coughing,
or straining caused by constipation, cystitis, vaginitis, or urethral
obstruction.
Outbreaks of uterine prolapses in periparturient sows, which have
seemingly increased in recent years, are both a welfare concern
and a substantial contributor to sow mortality. Although many
risk factors and contributors have been proposed, none have been
proven as causal. Factors investigated include exposure to estro-
genic mycotoxins, improper calcium and phosphorus status, inad-
equate vitamin levels, specific pig genotypes, sow body condition,
and increased litter size. Since no specific cause has been reported
with convincing evidence or reproduced experimentally, efforts to
elucidate the cause and risk factors continue.
pustules soon rupture and are replaced by dark brown to black
crusts. The streptococci are easily isolated from pustules. The
piglets usually recover spontaneously. Recovery may be hastened
by treatment with an appropriate antibiotic.
4 days of the onset of clinical signs. Furious type rabies seldom
occurs in swine. There are no gross lesions. Microscopic lesions
are typical for viral encephalitis but can be quite variable. The
typical rabies viral inclusions are often not present. Diagnosis is
usually confirmed by fluorescent antibody testing on brainstem
and cerebellum sections.
Lesions can occur anywhere, but on older swine they are usually
seen on the neck or behind the ears. Ringworm lesions begin as
brown expanding areas a few centimeters in diameter but eventu-
ally may enlarge to 5 to 10 cm in diameter. Mature lesions have a
central, brown crust; hair loss is minimal or absent and lesions are
nonpruritic.

In adult swine, ringworm must be differentiated from sarcoptic
mange, especially if lesions are behind the ears. In young growing
pigs, ringworm must be differentiated from pityriasis rosea and
exudative epidermitis. The diagnosis of ringworm can usually
be confirmed by microscopic examination of skin scrapings or
Shoulder ulcers in sows
Thin sows lying on hard floors in farrowing or gestation crates
may develop ulcers over the spine of the scapula. Contributing
factors include poor body condition, lack of adequate bedding or
mats, prolonged recumbency while farrowing or nursing piglets,
high humidity or wetness (often from coolers used during hot
months), and reduced activity because of confinement. Lesions
Skin necrosis of piglets
Young pigs on concrete or other hard floors often develop pres-
sure-related lesions on knees, coronets, or other sites over bony
prominences. Although lesions may initially appear insignificant,
they can become infected and lead to bacteremia, most frequently
Splayleg (spraddleleg)
This abnormality of neonatal piglets is characterized by lateral
extension of the hind legs accompanied by an inability to adduct
the legs; the front legs may be variably affected. The principle
lesion in affected muscles is myofibrillar hypoplasia, related in
part to delayed development and in part to degenerative change.
Anecdotal or speculated causes or risk factors include: genetic
predisposition, slippery or sloped floors, porcine stress syndrome
in the parents, dietary deficiencies, low birth weight, and
Sunburn and photosensitization
Sunburn is injury to the skin caused by excessive exposure to the
ultraviolet rays of sunlight. Pigs that are unaccustomed to direct
sunlight may be sunburned if not exposed gradually to their
outdoor environment. The white or light-colored breeds are more
severely affected. Although suckling and weanling pigs are most
likely to be affected, all age groups are susceptible. The ears and
back receive more direct exposure to sunlight and are often more
severely sunburned. Sunburned skin is reddened, edematous, hot,
and painful. Later, the affected areas appear roughened and may
peel. A common clinical presentation of sunburned pigs is a brief
attack of pain manifested as squealing or dipping the back while
walking. In some cases, a pig may drop to its stomach, then get up
and walk. Presumably, this is a response to feeling pain over the
lumbar area. There have been reports of abortions associated with
sunburn.
SHOULDER ULCERS, SKIN NECROSIS, SPLAYLEG, SUNBURN/PHOTOSENSITIZATION 153
MISCELLANEOUS
lesions. Ringworm is usually self-limiting, but lesions may require
months for healing to occur. Lesions are most common during
the winter months. Ringworm can be treated but is typically left
to resolve on its own. Ringworm should be considered conta-
gious to people.
are more likely to develop and are more severe during the 3 weeks
after farrowing. The ulcers are the result of ischemia from pressure
on the skin leading to skin necrosis over the spine of the scapula.
Control measures including maintaining an appropriate level of
body condition (fat) in sows, use of bedding or mats, and assuring
crates are of adequate size to allow frequent repositioning.
with Streptococcus species, Staphylococcus species, or Trueperella
pyogenes, with metastasis to joints or other sites. Losses can be
substantial. Prevention is achieved through good sanitation, pro-
vision of good quality flooring materials, and use of floor mats.
congenital tremors. Recently, this condition has also been
associated with in utero infection with atypical porcine pestivirus,
one of the causes of congenital tremors (myoclonia congenita).
If affected piglets are helped to nurse and protected from acciden-
tal injury by the sow, many will recover in 1 to 2 weeks. Tying the
front legs or the back legs loosely together with sticky tape will
OTHER
increase the likelihood of survival.
Photosensitization should be differentiated from sunburn. Pho-
tosensitization occurs only in areas of white skin and is a result
of exposure to a photodynamic agent (via ingestion, injection,
or skin contact) followed by exposure to sunlight. Sunlight
includes wavelengths that activate the photosensitization process.
Photosensitizing agents are present in some pastures (alfalfa,
clover, oats, rape, buckwheat, and others). Also, several common
pharmaceuticals (phenothiazine, tetracyclines, sulfonamides, and
others) may act as photosensitizing agents. The mechanism of
tissue injury probably varies with the different agents.
Lesions tend to be more severe with photosensitization than
with sunburn, often resulting in exudation of serum onto the
skin’s surface. Exudation is followed by drying and fissuring. The
lesions tend to be mildly pruritic. Skin necrosis with sloughing of
 SWINE DISEASE MANUAL
severely affected areas (white skin areas) often follows the acute
reaction. Conjunctivitis, sometimes with corneal opacity and
temporary blindness, may accompany photosensitization. Pigs
Torsion and volvulus
Torsions of the stomach and/or the intestines around the dorso-
ventral axis of the mesentery occur sporadically in pigs. Affected
animals die quickly without any warning and will appear pale
and bloat very rapidly during and after death. There is no single,
proven cause. Factors believed to contribute to torsions include
rapid ingestion of a large amount of feed or water (as with once
per day feeding), overly crowded pens with associated piling and
Vestibular syndrome
A syndrome characterized by turning of the head to the affected
side and a tendency to circle in that direction. The condition usu-
ally occurs in young, growing pigs. The syndrome is a consequence
of either bacterial meningitis affecting the vestibular nerve or phar-
Vices (tail biting, ear biting, flank biting, navel sucking)
Tail-biting, ear-biting, flank-biting, and navel-sucking behaviors
can often be attributed to management factors (comingling pigs,
out-of-feed events, facility hazards, overcrowding, and innumer-
able sources of “stress”) in groups of growing pigs. Morbidity
and mortality can be high, particularly when confounded by
secondary bacterial infections. Through careful observation, one
can often identify the few individuals within an affected group
OTHER
that are responsible for the abnormal behavior and are inflicting
trauma on numerous penmates.
The cause of the offending behavior is often simply ascribed to
“stress.” A disciplined approach is required to identify the true
source(s) of the stress, which may include: facility limitations
(inadequate feed or water space, overstocking, etc), nutritional
compromise (mineral or salt imbalances in rations, maladjust-
ment to solid feed immediately postweaning, etc), environmental
inadequacies (drafts, full effluent pits, temperature variation, high
humidity, etc), hygiene deficiencies, and concurrent infectious
154 TORSION AND VOLVULUS,VESTIBULAR SYNDROME,VICES
with sunburn or photosensitization should be kept out of sun-
light. Photosensitizing agents, once identified, should be avoided.
competition for feeder space, use of highly fermentable ration
ingredients that produce excessive amounts of gas in the stomach
or colon, and advanced pregnancy. Torsion of the stomach seems
more prevalent in sows that become agitated during once daily or
intermittent feeding protocols. Torsion of the intestine and/or
colon must be differentiated from hemorrhagic bowel syndrome.
yngitis with extension of the infection up the Eustachian tube to
the middle and internal ear. At necropsy, exudate is often demon-
strable in the middle ear. A less likely cause is as a sequel to cerebral
edema resulting from sodium intoxication or edema disease.
diseases. Systemic bacterial infections and toxemia are suspected
to be contributory but sometimes hard to prove. Agents some-
times implicated include sepsis or toxemia with Actinobacillus,
Streptococcus, Erysipelothrix, Salmonella, Mycoplasma hyorhinis,
or Escherichia coli. Immune-mediated vascular damage from
infectious insult has also been speculated.
Control requires careful observation at s levels: first, to accurately
identify the offending pigs and second, to identify the risk factors
that may be contributing to the aggressive behavior. It is important
that the aggressive pigs inflicting trauma be separated from the
group to prevent more cases. In addition to being removed to
a hospital pen environment, pigs with severe lesions will likely
require systemic antibiotic therapy to prevent extension of bacterial
infections locally or systemically. The administration of anti-in-
flammatory medication may also be warranted. Concurrently, the
risk factors and potential infectious or nutritional contributors to
stress should be systematically analyzed and eliminated.
 Section VI

Nutritional diseases, toxicoses, and poisonings

Mycotoxicoses................................................................................................................................................................................157
Nutritional deficiencies and excesses........................................................................................................................................159
Toxins (plants, feed additives, chemicals, and gases).............................................................................................................162

TOXICOSES

155
 156
TOXICOSES

Mycotoxicoses
Mycotoxicosis is the consequence of ingestion of grains or forage
containing toxic metabolites produced by certain fungi. Fungi
that produce toxins often do so only under specific conditions
of warmth, moisture, and humidity. Growth and storage factors
that adversely affect plants or their seeds (grains) often influence
mycotoxin production. Mycotoxins can develop in field grains,
damaged grains, or improperly stored feeds. Importantly, myco-
toxins are heat resistant and can be concentrated in various distill-
ers byproducts, often at 3 times the level of the original source.
Of the over 200 mycotoxins identified to date, at least 7 have
been reported to cause disease in swine. Some fungi produce
more than one mycotoxin. Several different fungi can produce
different mycotoxins in a single mixed feed. The toxins may be
additive and may potentiate one another. When metabolized,
they may be converted into other toxic substances. While toxico-
logical effects are numerous and often confusing, one should be
careful not to implicate mycotoxins in disease processes without
credible evidence.
Mycotoxins produce their toxic effects in several ways, including
impairment of metabolic, nutritional, or endocrine functions.
Some mycotoxins damage the liver and reduce average daily feed
intake, growth, and feed efficiency. Some mycotoxins are terato-
genic or carcinogenic. Some are immunosuppressive and predis-
pose pigs to secondary diseases. Several mycotoxins decrease the
reproductive performance of sows. Metabolites are sometimes
passed in the milk of sows to piglets in their litters. The effect
of mycotoxins varies with the amount ingested (dose), the time
over which it is consumed (duration), and the age of exposed
swine. Young pigs are usually much more susceptible than adults.
Within a herd, there can be great variability in response to a
mycotoxin.
Mycotoxicoses can present with either chronic or acute onset.
Most exposures are probably chronic or subacute as a result of
consuming small amounts of toxin over a long period of time.
In these instances, there may be few signs of toxicosis other than
decreased appetite, slow growth, and increased susceptibility to
secondary diseases. Acute outbreaks may have more obvious signs
that will vary for each of the different mycotoxins. Diagnosis of
chronic mycotoxicosis is often difficult because clinical signs are
seldom overt, and lesions are not specific. By the time a mycotox-
icosis is considered, the suspected feed may already be consumed,
with none having been collected and stored properly for analysis.
Prevention of mycotoxicosis is largely through careful selection
and proper storage of high-quality grains and other feed ingredi-
ents and the careful maintenance and cleanliness of feed prepa-
ration equipment. It is often worthwhile to properly dry and
store samples of representative batches of grain that are used on
a farm in the event they are needed for analysis later. Producers
anticipating problems should locate a competent laboratory and
NUTRITIONAL DISEASES, TOXICOSES, AND POISONINGS
get information on appropriate sample collection and storage
techniques.
There are few, if any, highly effective treatments for most mycotox-
icoses. A ration or ingredient suspected of containing toxin should
be replaced with nontoxic components. If a large quantity of the
feed remains, it can sometimes be fed to less susceptible species or
diluted with good quality feed so that the mycotoxin is no longer
being fed at a toxic concentration. There are several mycotoxin
binders on the market that can be used to prevent the absorption
of some of the mycotoxins from the pig’s gut. Any investment in
binders should take into account both their efficacy in controlling
the particular mycotoxins that are suspected and their suitability
for use in the feed matrix to which they will be applied.
Mycotoxins have been suggested as a primary cause of abortion
in swine, but none have shown that effect in an experimental
setting. Astute veterinarians should be reluctant to implicate
mycotoxins as a cause of ill-defined maladies without appropriate
investigation and evidence.
Aflatoxicosis
This mycotoxicosis is caused by mycotoxins produced by Aspergil-
lus flavus, Aspergillus parasiticus or Penicillium puberulum. Four
major toxins (B1, B2, G1, G2) are produced, with B1 being of the
greatest significance as a potent hepatotoxin. Fungi growing on
peanuts, corn, wheat, and several other cereal grains commonly
produce the toxins. Maximum aflatoxin formation occurs under
conditions related to the specific grain, its moisture content, stor-
age temperature, and humidity.
There is a marked age-related difference in susceptibility to afla-
toxicosis. Young nursing or weaned growing pigs are much more
susceptible than adults. When aflatoxin is ingested by a lactating
dam, toxic metabolites are passed in her milk and serve as a
source of exposure to the nursing pigs. These toxins reduce feed
intake, average daily gain, and feed efficiency. Since aflatoxins are
immunosuppressive, signs of toxicosis often include an increase in
previously controlled secondary diseases.
TOXICOSES
Acute aflatoxicosis is uncommon in swine. Usually, it is a sub-
acute to chronic disease caused by daily ingestion of smaller
amounts of aflatoxin over several weeks. Lesions vary among
pigs in the same affected group but are predominantly those of
hepatopathy. In more severe cases there are sudden deaths, hem-
orrhages in multiple tissues, and icterus. The liver may be swollen,
fatty, and have areas of necrosis. There may be a prolonged
clotting time. With subacute to chronic hepatotoxicosis, the liver
may be reduced in size and fibrotic, and ascites may be present.
Diagnosis is usually based on some combination of a history
of slow growth (often accompanied by secondary diseases that
seem unresponsive to treatment), an elevation of serum enzymes
MYCOTOXICOSES 157
 SWINE DISEASE MANUAL
associated with hepatocellular damage, and lesions related to
liver pathology. Microscopic hepatic lesions include bile duct
hyperplasia and enlargement of hepatocytes. In swine, chronic
aflatoxin toxicity can occur with at levels as low as 300 ppb in the
feed; acute toxicity requires concentrations beyond 1000 ppb.
Aflatoxin is considered to be carcinogenic in humans.
Ergotism
Claviceps purpurea is a fungus of many grasses and several cereal
grains, especially rye, oats, and wheat. The sclerotium of the
fungus is a dark, elongated body and can be seen on cereal grain
heads and in processed grains. The fungus produces 3 major
alkaloids that cause ergotism. The primary lesions caused by the
alkaloids include arteriolar vasoconstriction and endothelial cell
injury that often leads to thrombosis. When present in low levels,
the alkaloids can result in reduced growth rates. Larger amounts
lead to ischemic necrosis followed by a dry, gangrenous sloughing
of parts of extremities, especially tails, ears, and hooves. Symp-
toms of ergotism are exacerbated by cold weather. In pregnant
sows, ergotism can inhibit mammary development, reduce litter
size, reduce birth weights, and cause a profound postfarrowing
agalactia. The agalactia is believed to be related to inhibition of
prolactin secretion.
Diagnosis of ergotism is based on lesions and the gross or micro-
scopic identification of significant numbers of ergot sclerotia in
grains or the feed. Laboratory quantitative analysis can be used to
confirm the presence of clinically significant amounts of alkaloids
in ingredients or feedstuffs.
Fumonisin toxicosis
The fumonisins include 2 principal toxins produced by Fusarium
moniliforme. Signs of acute toxicity in growing and adult pigs are
primarily related to the respiratory system and include dyspnea,
cyanosis, weakness, and death within 4 to 10 days. Pulmonary
lesions include marked pulmonary edema and hydrothorax.
Pregnant sows that survive acute toxicity frequently abort in the
days following their recovery. Growing pigs that survive the acute
syndrome suffer from clinical signs related to a hepatotoxicosis
manifested as icterus, hepatic necrosis, and megalocytosis. Differ-
ences in lesions and clinical presentation seem to be dose related.
TOXICOSES
Recent research has demonstrated that fumonisins decrease the
ability of intravascular macrophages to clear blood-borne bacteria
in swine, thereby potentially increasing susceptibility to respi-
ratory disease. Fumonisins are a well-known cause of leukoen-
cephalomalacia in horses and are carcinogenic in humans at high
concentrations.
158 MYCOTOXICOSES
Trichothecene toxicoses
There are numerous structurally related toxic compounds pro-
duced by certain Fusarium species that are classified as tricho-
thecene mycotoxins. At least 3 of these are of importance in pig
production. Trichothecenes are cytotoxic to many cell types and
are strongly immunosuppressive. Signs of trichothecene toxicity
usually include feed refusal, salivation, and sometimes vomiting.
With chronic exposure, there may be paresis, paralysis, or sei-
zures. Lesions often include gastroenteritis, hemorrhagic diathe-
sis, skin irritation, and necrosis.
Diagnosis of trichothecene-related toxicosis can be difficult. The
presence of moldy or caked feed or a reluctance to consume feed
may suggest the presence of a trichothecene toxicosis. Improve-
ment following a change in feed suggests the original feed was
contaminated.
Deoxynivalenol (DON, vomitoxin)
Deoxynivalenol is a commonly occurring mycotoxin in corn and
wheat. Despite its common name of “vomitoxin,” swine rarely
consume a large enough dose to produce vomiting. However,
reduced feed intake is quite prominent and often the only clinical
sign observed.
T-2 toxin
In swine, the experimental administration of T-2 toxin, alone and
with aflatoxin, has resulted in crusting and ulceration of the skin
of the snout, lips, buccal commissures, and prepuce.
Zearalenone (F-2)
This mycotoxin is produced by Fusarium graminearum and may be
present in moldy corn, standing corn, other grains, and in pelleted
cereal feeds. It has an estrogenic effect that results in vulvovagi-
nitis and precocious mammary development in prepuberal gilts.
Swelling and enlargement of the vulva sometimes lead to tenesmus
with prolapse of the rectum. Similar estrogenic effects in gilts have
occurred as a result of consuming estrogens from other sources,
including alfalfa or other naturally occurring phytoestrogens.
When consumed by nursing sows, some of the metabolites of
zearalenone are passed to the offspring through the milk and can
lead to estrogenic effects in the piglets, namely enlargement of the
external genitalia and uterus. When the toxin is consumed by sows
near the midpoint of their estrous cycles, it has a luteotropic effect
and can cause persistent anestrus or pseudopregnancy. Fewer pigs
per litter are born to sows given zearalenone in the preimplantation
period (7 to 10 days postmating). Zearalenone, when consumed in
very high doses, can cause reduced libido, decreased testicular size,
and preputial enlargement in young boars.

Nutritional deficiencies and excesses
General comments
Nutritional diseases are relatively uncommon in modern swine pro-
duction. When they do occur, they are usually the result of mixing
errors or poor quality-control practices rather than formulation
errors. Both short- and long-term effects of deficiencies or excesses
can be risk factors for expression of other diseases, so nutritional
contributors to infectious diseases should be considered whenever
investigating unusual disease outbreaks. Feed analysis for micro-
nutrients is an inexact science exacerbated by sampling variation,
which can contribute to misdiagnosis or confusion.
Vitamin and mineral deficiencies
Iodine deficiency (goiter)
Hyperplastic thyroid glands (goiter) occasionally occurs in swine,
usually due to iodine deficiency in the pregnant sow, a genetic
defect in the sow for the biosynthesis of thyroid hormones, inges-
tion of goitrogenic substances (certain plants, drugs, or chemi-
cals) by the gestating sow, or iodine toxicity from dams being fed
an excess of iodine.
In swine, goiter usually occurs in iodine-deficient regions where
iodized salt has not been included in the dam’s feed. Deficiency
of iodine leads to the birth of weak or dead pigs that are largely
devoid of hair and may have a mucinous edema over enlarged
foreparts of the body with the skin in these areas thick and
doughy. The tongue is often edematous and may protrude from
the oral cavity. Enlarged thyroid glands (goiter) in piglets may
not be visible externally but often can be palpated or observed at
necropsy. In mature swine, iodine deficiency is not usually a sig-
nificant disease, although gestation may be prolonged by as much
as 7 days. Iodine deficiency is easily avoided by using iodized salt
in the ration of gestating sows.
Iron and/or copper deficiency (anemia) and toxicity
Piglets are born with very little iron reserves. Colostrum and milk
from the sow provide relatively little iron, perhaps only 15% to
50% of the daily requirement. The suckling piglet’s rapid growth
and expansion of blood volume make it highly likely that iron
deficiency and anemia will develop unless an exogenous source of
iron is made available. This is especially true for rapidly growing
piglets raised in confinement and not having access to soil or feces
that contain iron. A small amount of copper is essential for the
utilization of iron. Copper deficiency can also lead to anemia that
has many of the same clinical signs and lesions as iron deficiency.
Signs and lesions of iron deficiency are primarily related to severe
anemia. Piglets not supplemented with iron will be quite pale and
lose body condition and thrift after about 1 week of age. At nec-
ropsy, these pigs will have pallor, watery thin blood, a thin-walled
heart, and edema of the lungs, muscles, and connective tissues.
Occasionally, pigs weaned at 3 to 4 weeks of age will develop
NUTRITIONAL DISEASES, TOXICOSES, AND POISONINGS
rapid breathing; sudden deaths can occur. Anemic piglets are
quite susceptible to bacterial infection and have little resistance to
environmental chilling.
Diagnosis is often by a history that documents a lack of iron
supplementation at birth concomitant with typical clinical signs
and postmortem lesions. Several laboratory procedures used to
confirm anemia include hematocrit, red cell count, and examina-
tion of stained blood smears revealing a microcytic, hypochromic
anemia. Hematology and serum chemistry will reveal reduced
serum iron and transferrin saturation and a low hematocrit.
Prevention is possible by administration of supplemental iron
(100 to 200 mg) to all pigs in the first few days of life, prefera-
bly by injection. Parenteral administration is most commonly
practiced and has the advantage of precise dosage. Iron dextran
should be injected only into the neck muscles in order to prevent
any possibility of staining valuable areas of the carcass. Oral iron
products are available and can be effective, but one cannot be sure
that all pigs receive an appropriate dose when using these prod-
ucts. When improperly used, both forms of administration can
lead to iron toxicity, which is manifested as acute death following
administration. Pigs deficient in vitamin E/selenium are highly
susceptible to iron toxicity. Copper toxicity can occur at high
doses due to mixing errors.
Pigs raised outdoors with access to soil do not usually have a
requirement for iron supplementation, but many producers still
find it a beneficial practice even in these situations.
Zinc deficiency (parakeratosis)
Parakeratosis is a zinc-responsive dermatosis usually observed in
swine 2 to 4 months of age. Pigs not allowed access to soil or not
supplemented with zinc are more likely to have parakeratosis. The
disease is caused by a relative deficiency of zinc. The deficiency is
usually caused by feeding an unbalanced diet that has one or more
of the following features: excessive calcium, excessive phytic acid
(sometimes present in soybean meal), or a low concentration of
essential fatty acids. These features all adversely affect the avail-
ability of dietary zinc. In addition, enteric pathogens or changes in
TOXICOSES
intestinal flora can adversely influence zinc absorption. Parakerato-
sis is most often caused by consumption of excessive calcium.
Affected pigs show few signs of illness other than skin lesions and
reduced growth rate. Initial lesions appear as reddened macules
and papules on the ventrolateral abdomen and medial surface
of the thighs; these lesions often go unobserved. The lesions
are slowly covered by thick, roughened scales and crusts. More
obvious lesions soon become apparent on the lower legs and on
the dorsum. Lesions can sometimes be seen around the eyes, ears,
snout, and tail and may eventually become generalized. Affected
areas of the skin are hyperkeratotic and there may be fissuring of
the epidermis with secondary infection of the fissures. A unique
NUTRITIONAL DEFICIENCIES AND EXCESSES 159
 SWINE DISEASE MANUAL

feature occasionally seen is a focal or diffuse hyperkeratosis on
the tongue. Parakeratosis is a microscopic feature of the affected
epidermis and gives this dermatosis its name.
Parakeratosis must be differentiated from sarcoptic mange and
exudative epidermitis. Parakeratosis is nonpruritic, whereas
sarcoptic mange is highly pruritic. Exudative epidermitis tends
to occur in younger, smaller pigs. Pigs with parakeratosis will
recover if excessive calcium is removed from the ration and it is
properly supplemented with zinc. Most good commercial or care-
fully compounded rations are now supplemented with adequate
levels of zinc salts. Although once common, parakeratosis seldom
occurs today unless a feed mixing error occurs.
Calcium, phosphorus, and vitamin D (rickets and
osteoporosis)
Rickets is a disease of growing bones; consequently, it is usually
seen in young, growing pigs in which there is a deficiency, an
imbalance, or a failure of utilization of calcium, phosphorous, or
vitamin D. Rickets is most often caused by a dietary deficiency
of vitamin D or phosphorus. The basic abnormality is a failure
of mineralization of osteoid and cartilaginous matrix, especially
in growth plates. This is most obvious as a thickening and irreg-
ularity of growth plates in long bones. In confined animals not
exposed to sunlight or properly supplemented, vitamin D may
be inadequate. In pastured swine fed little or no grain or protein
supplement, phosphorus may be inadequate.
Signs of rickets include poor growth, short stature, enlargement
of the ends of long bones, lameness, and deformation of the
weight-bearing long bones. Necropsy lesions include an unusual
number of recent or healing fractures, ribs that bend markedly
before breaking with a weak “snap,” and widened, thickened, and
irregular growth plates. Abnormal growth plates are best seen on
longitudinally sawed long bones.
Osteoporosis is a lesion of mature bones. It follows removal of
much of the mineral content of the bones. It results from an
imbalance between bone formation and resorption in favor of
resorption. In the process, there may be a softening of the bone
(osteomalacia). Osteoporosis often occurs in prolific sows that
mobilize minerals to meet the demands of high milk production.
TOXICOSES
Properly balanced rations that include adequate calcium, phos-
phorus present in the proper ratio, and vitamin D are essential for
the prevention of rickets and osteoporosis. Treatment tends to be
unrewarding for both rickets and osteoporosis.
Vitamin D toxicity can occur with excess supplementation,
usually manifested as ectopic tissue mineralization in kidney,
stomach, lung, and elsewhere.
Other vitamins
Deficiencies or excesses of other fat-soluble vitamins have been
reported and are usually due to ration mis-formulation, mixing
errors, or prolonged storage in poor conditions. There are reports
of vitamin A deficiencies causing fetal malformations and ill-thrift,
and excessive vitamin A resulting in bone malformations and
altered gait. Vitamin K deficiency is also rare but can occur under
similar circumstances. Exposure to coumarin-like compounds,
either naturally occurring or as warfarin, has also caused hemor-
rhagic episodes that will respond to vitamin K supplementation.
Common B vitamins include thiamine (B1), riboflavin (B2),
niacin (B3), pantothenic acid (B5), pyridoxine (B6), biotin (B7),
folic acid (B9), and cobalamin (B12). B-vitamin deficiencies are
quite rare, with similar risk factors as mentioned in the previous
paragraph. Deficiency conditions that have been reported include
polioencephalomalacia (B1), anemia (B12), and altered gait with
myelopathy (various). Reports of B-vitamin toxicities in swine are
extremely rare.
Element and mineral toxicities
Arsenic
Pigs are relatively resistant to inorganic arsenic toxicosis but can
develop severe hemorrhagic gastroenteritis when exposed to
older, arsenic-containing pesticides at levels greater than 100 mg/
kg (45.4 mg/lb) of arsenic per bodyweight.
Organic phenylarsonic forms of arsenic have toxicological prop-
erties very different from those of inorganic arsenicals. Roxarsone
and arsanilic acid were traditionally used to promote growth and
to treat swine dysentery and Mycoplasma suis, but they are rarely
used in modern agriculture and are banned in many countries.

Poisoning is dose related. Signs of chronic poisoning with arsan-

Gilts in their first lactation are also susceptible, since their skeletal
ilic acid or roxarsone include goose-stepping, hind limb ataxia,
development may have been incomplete prior to pregnancy,
limb paresis, and blindness. A presumptive diagnosis can often be
allowing insufficient time to build a mineral reserve. Osteoporo-
based on a history of misuse of the compounds and the presence
sis often results in fractures in the latter part of a nursing period,
of characteristic clinical signs in chronically affected swine. The
immediately after weaning, or during the mating period just after
diagnosis may be assisted by toxicological assays of kidney, liver,
weaning. Inappropriate ration formulation or mixing is the most
muscle, and feed. The neurotoxic effect of poisoning is sometimes
important etiological risk factor.
reversible if the compound is removed within 2 or 3 days of the
Signs of osteoporosis include lameness, recumbency, fractures, appearance of signs. Blindness and long-standing peripheral
and paraplegia. At necropsy, fractures can often be demonstrated nerve damage may be permanent.
in the femur, humerus, or lumbar vertebrae. There may be distor-
tions or deformities of the pelvis.

160 NUTRITIONAL DEFICIENCIES AND EXCESSES


Copper, iron, selenium, and zinc
Pigs tolerate fairly high doses of copper, which is sometimes
added to feed to improve health and growth. Copper toxicity in
pigs manifests as acute hemolytic anemia, hemoglobinuria, and
secondary nephropathy. Toxicity can occur when dietary copper
exceeds 4,000 ppm or when pigs are inadvertently exposed or
overdosed via water or by injection.
Iron toxicity can occur when pigs are inadvertently exposed to
concentrated supplements orally or when overdosed by injection.
Rapid respiration and cardiovascular collapse usually occur
within hours of exposure. Pigs deficient in vitamin E are reported
to be at greater risk for iron toxicity.
Acute selenium intoxication causes posterior paresis due to acute
poliomyelomalacia of the ventral horns of the spinal cord. Feed
formulation or mixing errors are the usual source of the toxicity for
weaned pigs. Overdoses of injectable selenium supplements can
cause sudden death with cardiovascular collapse. In chronic selenium
toxicosis, hair loss and separation of the hoof from the coronary band
occurs and may precede paresis due to spinal cord lesions. Diagnosis
is by recognition of clinical signs, histopathology of spinal cord, and
tissue analysis for selenium. There is no treatment.
Zinc in the oxide form is tolerated well by pigs and has been com-
monly supplemented in feed to improve health and performance.
Other salts of zinc may interfere with absorption of other cations
and, at high doses, can lead to arthritis or internal hemorrhage.
Lead and mercury
In contrast to most species, pigs are very resistant to lead poison-
ing. Pigs fed various salts of lead have achieved very high blood
levels with no clinical effect. However, suspicions of lead exposure
may warrant blood analysis to assure adulterated pork products
do not enter the food chain.
Swine exposure to mercury is usually limited; however, accidental
exposure to pesticides or seeds treated with mercurial fungicides
does occur. Gastroenteritis, nephropathy, ataxia, central nervous
disturbance, blindness, and death can result.
Selenium
Selenium toxicity can occur with injections, excess supplemen-
tation from mixing errors, or in geographical areas where soil
selenium levels are high. Clinical signs of chronic toxicity include
hair loss and separation of hoof from the coronary band. Acute
toxicity is manifested as paresis due to spinal cord malacia.
NUTRITIONAL DISEASES, TOXICOSES, AND POISONINGS
Sodium ion intoxication (salt poisoning or water
deprivation)
Salt poisoning can occur in pigs as a consequence of water
deprivation or from sudden ingestion of too much salt; the latter
tends to be a rare occurrence. Sodium intoxication in water-deprived
pigs can occur even if the feed contains an appropriate level of salt,
although the risk is increased when salt levels in the feed are excessive.
Clinical signs are precipitated or magnified by allowing the
water-deprived pigs sudden, unlimited access to water. Water
deprivation can occur for many reasons but commonly may be
the result of freezing of the water source, plugged water nipples,
or inadvertently leaving a water valve closed. Operators may
not always be forthright in admitting human errors related to
water deprivation. Salt poisoning has also been known to occur
following prolonged shipping without access to water, followed
by unlimited access to water. Salt poisoning is also reported in
swine after ingestion of salty brine from overflowing, loose-salt
boxes provided for other livestock, or following ingestion of large
amounts of whey. This type of poisoning is also more likely in
water-deprived pigs.
Clinical signs of sodium ion toxicosis are caused by the acute
cerebral edema associated with rapid rehydration. Because the
condition most often occurs secondary to water deprivation (rather
than a primary toxic intake of salt), salt poisoning frequently occurs
at a pen or herd level. Signs include aimless wandering, blindness,
deafness, and head pressing. Affected pigs sometimes dog-sit,
slowly raise their nose upward and backward, and then fall on their
side in spasms that may be followed by paddling of the legs. They
may then arise and continue their wandering.
Diagnosis associated with water deprivation may be suggested by
history, signs, and elevated sodium levels in serum or cerebrospinal
fluid. Gross lesions may be absent or limited to mild gastritis, and
perhaps the presence of dehydrated fecal pellets in the rectum.
Histopathologic confirmation of the condition is by observation
of rather unique meningeal and cerebral perivascular cuffing by
eosinophils in the brain. Later and less reliably, there may be lami-
nar subcortical polioencephalomalacia or necrosis. Salt poisoning
must be differentiated from all other encephalitic diseases. In an
affected pen, a clue to the occurrence of water deprivation will be
TOXICOSES
the absence of any urine or wet feces on the pen floor.
Water-deprived or affected pigs should be reintroduced to water
slowly, given only small amounts of water at frequent intervals.
This may reduce mortality. Pigs showing clinical signs usually die,
regardless of treatment.
NUTRITIONAL DEFICIENCIES AND EXCESSES 161
 SWINE DISEASE MANUAL
Toxins (plants, feed additives, chemicals, and gases)
General comments
Historically, rooting and the inquisitive behavior of pigs coupled
with outdoor rearing practices provided pigs with access to a
broad range of potential toxins and poisons. The list of potential
toxins to which pigs are susceptible is quite long; however, modern
production practices and improvements in pharmaceuticals and
parasiticides now limit exposure to many traditionally common
toxins and poisons.
Suspected cases of poisoning should be systematically investi-
gated as appropriate for suspected toxicants. In many cases of
vague signs or sudden deaths, there is a coincidental recollec-
tion of recent exposure to a “toxin.” This association can easily
be interpreted as causal for current illnesses or deaths of animals
and should be regarded with caution.
Several of the more common toxicants (plants, feed additives,
organic/inorganic toxicants, chemicals, gases) for swine are
listed below.
Plants
Cocklebur poisoning
Cockleburs (Xanthium species) are widely distributed in the mid-
western US as weeds in fencerows, ditches, and low or marshy
areas. The toxic principle, carboxyatractyloside, is present in the
seeds and young seedlings of the plant, especially during the
cotyledonary (2-leaf ) stage of growth. Seedlings may be ingested
by pigs on pasture, especially after spring rains when burs sprout
in low-lying areas, or pigs may ingest seeds present in mixed or
ground feeds. Pigs can be found dead after consuming only mod-
est numbers of seedlings. Because the clinical course of disease is
brief (several hours), signs may not be observed, and lesions may
be absent from dead pigs. Mortality is sporadic unless plants are
numerous. In experimentally poisoned pigs, signs include depres-
sion, hypoglycemia, occasional nausea, incoordination, convul-
sions, and death. Lesions include serofibrinous effusions in body
cavities and subcutaneous edema. There can sometimes be edema
of the gall bladder wall and mild gastroenteritis. Microscopic
lesions include centrilobular hepatotoxicosis with centrilobular
TOXICOSES
accentuation of the liver pattern.
Diagnosis is often difficult unless cocklebur seedlings can be
found in the pasture or seeds can be found in the feed. Cocklebur
poisoning must be differentiated from poisonings caused by
ingestion of coal tar (clay shooting pigeons), mycotoxins, gossy-
pol (cotton seed), and others.
Gossypol
Gossypol is a polyphenolic binaphthalene compound found
in varying amounts in cottonseed meal. Prolonged feeding of
162 TOXINS (PLANTS, FEED ADDITIVES, CHEMICALS, AND GASES)
cottonseed meal with high gossypol content can cause ill-thrift or
heart failure and death. Toxicity from gossypol is rare with prop-
erly formulated swine diets fed in most commercial production
systems.
Nightshade
Consumption of Solanum nigrum (black nightshade) occasion-
ally causes acute depression, incoordination, muscular tremors,
recumbency with kicking of feet, and death in some cases. The
leaves and green berries are the most toxic parts of the plant, but
they are quite bitter and rarely consumed unless no other forage
is available.
Pigweed poisoning
Pigs allowed access to pastures or lots containing pigweed
(Amaranthus retroflexus) may be poisoned, usually in the late
summer or fall. Signs appear within 5 to 10 days after exposure
and include trembling, weakness, incoordination, knuckling, and
almost complete rear leg paralysis. Morbidity is variable, although
mortality can be high (75% to 80%) in pigs that develop clinical
signs. Lesions are consistent with acute nephrosis and heart
failure; the hallmark gross lesion is severe perirenal edema. The
kidneys are normal in size but may appear blanched. Often,
there is ascites, hydrothorax, or edema of the ventral body wall.
Long-standing cases may have renal fibrosis. Microscopic lesions
in the kidneys of acutely affected pigs include necrosis of both
proximal and distal convoluted tubules with numerous casts
in tubules. Diagnosis is usually made from a history of sudden
death, typical clinical signs, severe perirenal edema at necropsy,
and plant identification. The toxic principle is not known. There
is no widely accepted treatment for affected pigs. Pigs should be
denied access to the plants. New cases may develop for as many as
10 additional days after exposure has been terminated.
Feed additives
Carbadox
In the US, carbadox may be used to control swine dysentery and
bacterial enteritis when included in the feed at 50 ppm and, less
commonly, as a growth promotant when fed at 10 to 25 ppm.
Levels greater than 100 ppm can cause decreased feed consump-
tion, growth retardation with degeneration of the adrenal cortex,
and, at higher doses, posterior paresis.
Ionophores
Ionophores (eg, narasin, lasalocid, monensin) are sometimes
used in animal feeds to improve rate of gain and feed efficiency.
Most cases of toxicity with ionophores are from mixing errors,
inadvertent inclusion of an ionophore in the swine feed, or most
importantly, simultaneous administration of the antibiotic tiamu-
lin in feed or water.

In the US, narasin is labeled for use in swine at 15 to 30 ppm
and is considered relatively safe when used per label instructions
and in the absence of the antibiotic tiamulin. Clinical signs of
anorexia, weakness, and ataxia can occur when narasin is fed at
levels greater than 90 ppm. The greatest risk for poisoning with
narasin (and all ionophores) is with the simultaneous adminis-
tration of tiamulin, which effectively blocks the metabolism and
excretion of narasin (and all ionophores) creating a buildup and
toxicity. Pigs poisoned with this combination will have acute
ataxia with pain, necrosis of skeletal muscles, and rapid death.
There is no specific treatment other than immediate removal of
feed and medicated water.
Poisoning with monensin or lasalocid is relative rare and is usu-
ally due to the inadvertent administration of very high doses in
feed, or lower doses in feed coupled with simultaneous tiamulin
administration.
Ractopamine
In the US, ractopamine is a beta-2 agonist used in the last 3 to 6
weeks of the finishing period to stimulate muscle growth. Poten-
tial adverse effects that are sometimes reported include muscle
tremors, tachycardia, hypotension, prostration, and hypokalemia.
Confirmed cases of ractopamine toxicity are rare.
Sulfonamides
Overdoses of sulfonamides in feed, particularly with restricted
water intake, can cause acute nephrosis. Toxicity can be exacer-
bated by preexisting kidney diseases or simultaneous presence of
mycotoxins (eg, citrinin, rubritoxin, ochratoxin) in feed.
Rodenticides
Swine are susceptible to inadvertent exposures to anticoagulant
rodenticides (eg, warfarin, diphacinone, chlorophacinone,
bromadiolone, brodifacoum, or pindone) that have been placed
around pig premises. Toxic doses increase clotting time, leading
to internal hemorrhages as well as epistaxis or melena. Vitamin
K can be a helpful treatment should accidental exposure occur,
although not all rodenticides are vitamin K responsive. Bro-
methalin causes depression, ataxia, and death. Cholecalciferol
(vitamin D3 and analogs) are effective rodenticides causing
hypercalcemia and tissue mineralization. Careful placement and
maintenance of baiting stations is critical in helping to avoid
inadvertent exposures. Baits should be fixed in place so that
rodents are not able to remove the bait and bring it into contact
with pigs. Internationally, there have been incidents of rodenti-
cide residues found in pork due exactly to this reason.
Chemical toxins
Toxicoses from chemicals, particularly insecticide and parasiticide
exposures, are less frequent now due to the availability of safer
products, eradication programs for lice and mange, and the exten-
sive use of confinement housing, which has minimized challenges
with many internal parasites.
TOXINS (PLANTS, FEED ADDITIVES, CHEMICALS, AND GASES) 163
NUTRITIONAL DISEASES, TOXICOSES, AND POISONINGS
Chemical products of historical and ongoing importance include
organophosphates, carbamates, and chlorinated hydrocarbon
compounds administered at excessive doses. More often than
not, toxicity is a result of their accidental addition to feed or
their presence as contaminants of feed ingredients, equipment, or
swine premises.
Clinical signs of organophosphate or carbamate toxicity result
from stimulation of the parasympathetic nervous system, leading
to salivation, urination, defecation, vomiting, and death. Muscu-
lar tremors may be present, but seizures are rare. Diagnosis is by
clinical signs, history of exposure, and finding depressed cholin-
esterase activity in brain or whole blood. Acute cases will respond
to atropine administration.
Chlorinated hydrocarbon insecticides are stimulatory, with clin-
ical signs that include hyperesthesia, muscle spasms, and muscle
fasciculation leading to seizures. Diagnosis is by clinical signs,
history, and confirming the offending compound in brain, liver,
or stomach contents. Treatment is symptomatic.
Pyrethroid compounds for fly control are relatively nontoxic
to swine. Many pyrethroid pesticides are marketed for various
purposes, but most are considered safe for swine unless there is
massive exposure.
Other chemicals of historical importance include organic mer-
cury (fungicide), pentachlorophenol (wood preservative), and
chromate-copper arsenate (wood preservative), but most of these
and related products are no longer available in the US.
Most modern herbicides used for weed control are rarely associ-
ated with toxicity in swine. There is very little risk from overspray,
with adverse reactions limited mostly to oral consumption of
concentrates, which can sometimes cause gastric irritation or
vague signs. Paraquat is an exception causing chronic pulmonary
interstitial fibrosis as a sequel to exposure.
Gases and ventilation failure
Five gases (ammonia, carbon dioxide, carbon monoxide, hydro-
gen sulfide, and methane) are associated with swine environ-
ments, especially confinement rearing. Ammonia (NH3) and
hydrogen sulfide (H2S) are normally generated from the decom-
TOXICOSES
position of swine excrement.
Carbon dioxide (CO2) can cause deaths but is perhaps a lesser
threat than carbon monoxide (CO), because it is heavier than air
and usually accumulates only in slurry pits below pig housing and
working areas.
Methane (CH4) is an explosion hazard. In recent years, the num-
ber of accidental methane explosions and fires has increased in
barns with deep underfloor manure storage. This is presumably
due to variation in fermentation characteristics of excrement and
its composition, likely from dietary inputs such as inclusion of
distillers waste products. All 5 gases represent potential threats
 SWINE DISEASE MANUAL

to both swine and people, but ammonia, carbon monoxide, and
hydrogen sulfide toxicities are the most common and are dis-
cussed in more detail below.
Ammonia toxicity
Ammonia gas (NH3) is formed by the decomposition of animal
waste and is present at some level in most animal facilities. The
odor can be detected by most people at concentrations of around
10 ppm, a level which appears to have little detrimental effect on
pig health. However, when the concentration reaches 50 ppm
or more, NH3 may act as an irritant of the mucous membranes
of the eyes, nasal passages, and lungs and cause ocular and nasal
discharge. Concentrations of NH3 that are high enough to be
irritating to mucous membranes of pig farm workers likely have a
similar effect on animals continuously exposed.
Research on swine suggests that toxic concentrations of NH3 (over
50 to 100 ppm) reduce growth rate, reduce bacterial clearance from
the lungs (interferes with mucociliary apparatus), exacerbate nasal
turbinate lesions in pigs infected with organisms of progressive
atrophic rhinitis (Bordetella bronchiseptica, Pasteurella multocida),
and may influence the course of other infectious diseases.
Carbon monoxide toxicity
Carbon monoxide (CO) has a much greater affinity for hemoglo-
bin than does oxygen and is therefore highly effective at displacing
oxygen from the blood. It combines with hemoglobin to form car-
boxyhemoglobin, reduces oxygen exchange, and causes mortality.
Carbon monoxide is produced by incomplete combustion of any
carbonaceous fuel, but most poisonings occur because of improp-
erly functioning (yellow versus blue flame) space heaters or fur-
naces. Carbon monoxide is a colorless, odorless, and tasteless gas.
Recognition of malfunctioning heaters should alert one to the
possibility of poisoning. In late-term pregnant sows, a high level
of stillbirths and neonatal mortality is associated with CO poi-
soning. The sows themselves may show no other signs. Affected
piglets usually show no lesions other than a pink to bright red
color imparted to their blood and tissues by carboxyhemoglobin.
Blood from affected piglets and fetuses with CO poisoning is
usually characterized as “cherry-red” in color. The concentration
TOXICOSES
A “sewer gas odor/rotten egg smell” detectable by humans from
0.1 to 5 ppm is sometimes offensive but is not toxic. Levels from
10 ppm to 100 ppm can cause eye and respiratory irritation.
Humans cannot detect the odor of H2S at levels greater than
150 to 250 ppm because of olfactory paralysis induced by the
gas. H2S levels greater than 300 ppm affect the nervous system.
Immediate collapse and respiratory paralysis occur at levels
greater than 1000 ppm.
Hydrogen sulfide is heavier than air and accumulates in liquid
manure-holding pits below confinement buildings. The gas usually
remains dissolved in the liquid component of swine effluent and
remains below the toxic level in air unless the effluent is agitated.
Effluent storage pits are often agitated just prior to and during
the emptying process at which time high levels of H2S can be
released. If inhaled in high concentration, H2S can cause instant
fatal systemic intoxication of exposed swine or people by directly
suppressing the respiratory center in the brain. High levels of the
gas paralyze a worker’s sense of smell and may give a false sense of
security. Workers trying to rescue affected swine or coworkers are at
a very high risk of asphyxiation from a single breath.
Exposure to toxic levels of H2S can be avoided by emptying and
cleaning the pit when the building is empty. Adequate ventilation
should be provided (fans on, curtains down) whenever pits are
agitated to keep H2S at a nontoxic level.
Ventilation failure
Mechanical ventilation of confinement swine facilities is com-
mon in temperate and cool climates. Death losses in confinement
buildings are usually due to mechanical failures or power loss
rather than simply an accumulation of toxic gases and poisoning.
Importantly, ventilation failure can rapidly lead to very high
temperatures and humidity causing hyperthermia and death. The
increased concentration of toxic gases can contribute or cause
death by intoxication (eg, hydrogen sulfide) or asphyxiation (car-
bon dioxide or carbon monoxide). Suffocation (the obstruction
of air passages) as a cause of death is usually the result of piling of
pigs in cold weather.
Any investigation of acute deaths suspected to be due to venti-
lation failure should be approached with caution, putting safety

of carboxyhemoglobin in fetal thoracic fluid or blood of an

first. Human deaths from hydrogen sulfide intoxication are too
affected pig can be used to confirm CO poisoning.
common, as this gas kills quickly.
Hydrogen sulfide toxicity
Hydrogen sulfide gas (H2S) inhaled at toxic levels is dangerous
and fatal to both pigs and people. The danger of high concen-
trations (greater than 100 ppm) of H2S should be recognized,
respected, and avoided, but the usual low level of the gas in closed
confinement facilities (less than 0.2 ppm) is not toxic and is of
little consequence.

164 TOXINS (PLANTS, FEED ADDITIVES, CHEMICALS, AND GASES)

 Section VII

Tables

Anthelmintics and parasiticides for swine...............................................................................................................................167

Arthritis in neonatal and growing swine..................................................................................................................................168
Central nervous system (CNS) diseases in swine: comparative approach to diagnosis.................................................169
Diarrheal diseases common at various ages.............................................................................................................................171
Diarrheal diseases in swine: comparative approach to diagnosis........................................................................................172
Internal parasites...........................................................................................................................................................................175
Intestinal hemorrhage: differential diagnosis..........................................................................................................................177
Mycoplasma-related diseases......................................................................................................................................................179
Reproduction: causes of low farrowing rate............................................................................................................................180
Reproductive failure: infectious causes ...................................................................................................................................181
Respiratory disease in swine: comparative approach to diagnosis......................................................................................183
Skin lesions: differential diagnosis............................................................................................................................................186
Vesiculating viral diseases............................................................................................................................................................189
Zoonotic agents found in swine and humans.........................................................................................................................190

TABLES

165
 166
TABLES
 DISEASES CAUSED BY VIRUSES

Anthelmintics and parasiticides for swine

Many effective anthelmintics are available for the treatment of internal and external parasites. Following are guidelines that show
the relative efficacy of the major categories of active ingredients against the major parasites of swine in the US. Manufacturers
generally have excellent resource materials that describe the effectiveness of their products against the various life cycle stages
of parasites, and the reader is encouraged to refer to them when making usage choices.

Agent Products
Common
Name name Piperazine Pyrantel Avermectins Levamisole Dichlorvos Fenbendazole
Ascaris suum Roundworm + + + + + +
Stomach
Ascarops strongylina - - - - + +
worm
Cystoisospora suis,
Coccidiosis - - - - - -
Eimeria species
Globocephalus
Hookworm - - + + + +
urosubulatus
Gongylonema Esophageal
- - + + - +
pulchrum worm
Haematopinus suis Lice - - + - - -
Red stomach
Hyostrongylus rubidus - - + - + +
worm
Macracanthorhynchus Thorny-
- - +/- +/- - -
hirudinaceus headed worm
Metastrongylus
Lungworm - - + + - +
species
Oesophagostomum Nodular
+/- + + + + +
species worm
Physocephalus Stomach
- - - - + +
sexalatus worm
Sarcoptes scabiei Mange mite - - + - - -
Stephanurus dentatus Kidneyworm - - + + - +
Strongyloides ransomi Threadworm - - + + +/- +/-
Trichuris suis Whipworm - - - +/- + +

TABLES

ANTHELMINTICS AND PARASITICIDES 167

 SWINE DISEASE MANUAL

Arthritis in neonatal and growing swine

In young pigs, arthritis is usually caused by infection, although trauma from handling, being laid on by the sow, and entrapment
in gating or equipment must also be ruled out. Arthritis in this age group is most commonly seen in the carpus (front knee),
rear hock, and claw. Though less frequently affected, the shoulder, stifle, and atlanto-occipital joints should also be examined.
Culture is often the only way to differentiate the various etiologic agents; sterile procedures should be used as some agents are
slow-growing or difficult to culture.

Diseases and agent
Erysipelas
(Erysipelothrix
rhusiopathiae)
GlÄsser’s disease
(Haemophilus
parasuis)
Mycoplasmal arthritis
(Mycoplasma
hyosynoviae)
Mycoplasmal
polyserositis/arthritis
(Mycoplasma hyorhinis)
Septic arthritis
(Pyogenic Streptococcus,
Staphylococcus,
Trueperella, and other
endemic bacteria)
Streptococcal arthritis
(Streptococcus suis type 2)
TABLES
Age group
affected Nature of lesions
Growers through Rear hock, carpus, and toes most
adult, rarely in often affected. Joints are swollen
nursery age pigs. and very painful in both acute and
chronic phases.
Nursery See “streptococcal arthritis” above,
(occasionally in although fibrinous response and
growers) periarticular inflammation may be
more dramatic.
Usually pigs from Excessive serosanguinous joint fluid
8 to 24 weeks in acute phase, with yellowing of
of age synovial membranes and pannus
developing over time.
Usually pigs from Swollen joints, serosanguinous
3 to 10 weeks or serofibrinous synovial fluid in
of age acute phase with pannus and joint
erosion developing in advanced
stages. Pleuritis, pericarditis, and
polyserositis frequently present.
All ages One or more hot, swollen joints
in acute phase, with increased
turbidity of synovial fluid.
Periarticular fibrosis and pyogenic
abscesses in advanced cases.
Nursery Acute suppurative polyarthritis;
(occasionally in concurrent meningitis and
growers) polyserositis is common. Sometimes
accompanied by valvular
endocarditis. See “GlÄsser’s disease”.
Signs, other lesions, comments
May occur during, or as a sequel
to, an acute occurrence of systemic
erysipelas (diamond skin disease).
May also present more insidiously
as increased prevalence of swollen
joints at the herd level, without any
acute outbreak or mortality.
Frequently accompanied by
serofibrinous or fibrinopurulent
pleuritis, pericarditis, and peritonitis
(or in combination), and meningitis.
Urgent treatment is required, or
death is likely. Important differential
for streptococcal arthritis.
Stiffness and shifting lameness in
hind legs are common. Recovery can
be protracted, though acute cases
should respond well to antibiotic
injections. Occasionally, young adults
(replacement gilts) are affected.
Abdominal tenderness with sternal
recumbency sometimes present,
related to pleuritis. Morbidity less
than 25%, mortality usually low.
Risk factors in neonates include poor
technique or dirty instruments used
during piglet processing (teeth, tails,
castration). Sometimes accompanied
by fever, depression, and other
evidence of septicemia.
Painful, swollen joints, and fever.
Central nervous system signs
common when meningitis is present.
Urgent treatment is required,
or death is likely. Can be major
contributor to chronic arthritis on
some farms. Important differential for

Glasser’s disease.

168 ARTHRITIS
 TABLES

Central nervous system (CNS) diseases in swine:

comparative approach to diagnosis
In addition to the diseases described in this table, other less frequent causes of CNS signs include a host of other viruses (eg,
classical swine fever (CSF), porcine reproductive and respiratory syndrome virus (PRRSV), porcine circovirus associated disease
(PCVAD), paramyxovirus, Japanese encephalitis, rabies, etc) and toxicities (organophosphate, carbamate, chlorinated hydrocar-
bons) that are not included below. Diseases that include CNS signs, particularly when they occur at a group or herd level rather
than in sporadic individuals, need to be aggressively investigated. It is important to sample multiple pigs in various stages of the
disease and to include a complete set of fresh and fixed tissues when making a laboratory submission.

Disease Agent/Cause Clinical signs Diagnostic features and methods

Bacterial Various Most often observed in postweaning Histopathology of brain will confirm
meningitis bacteria, to early growing pigs, although suppurative meningoencephalitis. Culture
including any age can be affected. Acutely of brain, meningeal swabs, or cerebrospinal
Streptococcus affected pigs show incoordination, fluid will often result in identification of the
suis, blindness, deafness, nystagmus, organism. Polyarthritis, myocarditis, and
Haemophilus tremors, opisthotonus, convulsions, pneumonia very typically accompany the
parasuis, and unconsciousness, paddling, and are central nervous signs of the disease. Most
other sporadic often simply found suddenly dead. herds are endemically infected with all of
bacteria these agents, although sporadic outbreaks
(Streptococcus, can contribute 2% to 5% to group mortality.
E coli, Stress and viral infections such as porcine
Trueperella, reproductive and respiratory syndrome can
Salmonella, etc). exacerbate the frequency and severity of the
condition.
Edema disease Shigatoxin-like Usual occurrence is within 2 weeks Edema present in the eyelids, forehead,
enterotoxin after weaning. Clinical signs include stomach wall, and mesocolon is highly
elaborated by acute onset of ataxia, incoordination, suggestive of the diagnosis. Diagnosis
E coli, usually recumbency, and occasionally sometimes difficult to confirm with certainty
of a hemolytic perhaps edema of eyelids, face, nose, though culture of hemolytic E coli (with
colony-type. or lips. Most affected pigs die within confirmed genotype for shiga-like toxin)
2 days and some die peracutely. from the ileum/colon is useful. However,
Survivors can develop head tilt, histopathology that shows angiopathy with
incoordination, and unthriftiness. polioencephalomalacia and malacia in brain
stem is pathognomonic when present.
Hemagglutinating Betacoronavirus Assumed to be endemic in the US, Viral encephalitis is observed histologically
encephalomyelitis with symptomatic infections rare. In and by PCR, ISH, or isolation.
(HEV) naïve piglets less than 4 weeks of age,
vomiting, dehydration, wasting, coma,
and eventual death occur. Tremors,
convulsions, and paddling may occur.
Case mortality can approach 100%.
FA = fluorescent antibody; IHC = immunohistochemistry; ISH = in situ hybridization; PCR = polymerase chain reaction

Table continued on next page

TABLES

CNS DISEASES: COMPARATIVE APPROACH 169

 SWINE DISEASE MANUAL

Table cont’d. Central nervous system (CNS) diseases in swine: comparative approach to diagnosis

Disease Agent/Cause Clinical signs Diagnostic features and methods

Pseudorabies Suid herpesvirus Piglets less than 3 weeks of age present In a naïve herd, one is likely to see signs
(PRV) 1, also known as with incoordination, ataxia, salivation, across all age groups; the disease is exotic
pseudorabies virus opisthotonus, seizures, recumbency with in US commercial industry. Diagnosis
(PRV) or Aujeszky’s paddling, or sudden death. Older pigs confirmed by detection of virus in tissues
disease virus can show similar, but less prevalent and (tonsil, brain, spleen, lung, lymph nodes)
severe, signs. Growing pigs and adults by FA, IHC, ISH, or PCR. Highly accurate
often present with acute respiratory serologic tests are available that can
signs; pregnant sows may abort. discriminate between vaccinated and
unvaccinated pigs.
Salt poisoning Sodium ion Acute onset, usually with numerous History of water restriction or deprivation
intoxication due to affected pigs due to a pen- or barn-level followed by unrestricted access to water.
water deprivation. out-of-water event; the condition can The condition can occur regardless of salt
occur after as little as 24 hours without level in the diet; the key feature of the
water. Affected pigs wander, appear disease is almost always water deprivation.
blind, head-press, dog-sit, experience The pathognomonic histologic lesion
periodic convulsions, become prostrate, is eosinophilic meningoencephalitis,
and eventually enter a coma with death sometimes with polioencephalomalacia.
almost inevitable. Brain tissue can be assessed for sodium
levels although this is not usually required
when adequate history is available.
Spinal Miscellaneous Primary signs from compromised Careful clinical examination, review of
myelitis, viral or bacterial spinal cord function may include herd history, and knowledge of recent
myelopathy, infections persistent or sporadic occurrence of management changes on the farm will aid
and/or (including tetanus ataxia, paralysis, or posterior paresis. in arriving at a diagnosis. Necropsy should
clinical signs or botulism), Morbidity can help in the diagnosis, as be guided by the observed clinical signs in
referable to toxins (selenium, infectious causes often affect multiple order to localize the site(s) of compromise.
spinal cord arsenicals, pigs simultaneously, while traumatic Histopathology on brain and spinal cord
organophosphates, causes usually involve only individual as well as liver, muscle, and other tissues
heavy metals), animals. Toxicities or deficiencies may should be undertaken. Appropriate
deficiencies have very high morbidity. Pigs with these antigen-based tests can be selected based
(B-vitamins, conditions often remain centrally aware on the situation and test availability.
minerals), of their environment and surroundings, Chemistry or toxin screens on liver and/or
trauma (injection while encephalitic diseases tend to be feed may be warranted.
sites, fractures, associated with compromised awareness.
electrocution), or
other insults.
Teschen or Teschoviruses Historically, Teschen disease outbreaks in Histopathology shows viral myelitis or
Talfan disease or similar Europe had high morbidity and mortality encephalomyelitis and presence of virus
picornaviruses in all age groups. The disease has changed demonstrated by isolation, PCR, or ISH.
(eg, Sapelovirus, over time and now usually presents with Picornaviruses are common and definitive
Enterovirus, low morbidity but high case mortality, the genotyping is required to confirm
Astrovirus, and result of polioencephalomalacia-related diagnosis. Teschen-like strains occur
others) ataxia and paralysis. The disease is exotic sporadically in the US while most herds are
to the US. endemically infected with low virulence
strains.
TABLES

FA = fluorescent antibody; IHC = immunohistochemistry; ISH = in situ hybridization; PCR = polymerase chain reaction

170 CNS DISEASES: COMPARATIVE APPROACH

 TABLES

Diarrheal diseases common at various ages

Age is an important criterion when establishing a list of differential diagnoses for diarrhea in pigs. The table below compares
the likelihood of diarrhea being produced as a primary outcome of infection by different agents. It is important to remember
that diarrhea may accompany nonenteric diseases as a result of disruptions to the pig’s appetite, systemic illness and fever, or
chronicity. Always examine the entire animal when trying to establish a diagnosis.

Unweaned Grow/finish
Disease piglets Nursery pigs pigs Adults
Enterotoxigenic E coli ++++ +++ + (early -
grower)
Porcine rotavirus ++++ +++ + (early -
grower)
Clostridium difficile ++++ - - -
Clostridium perfringens type A ++++ - - -
Clostridium perfringens type C ++++ + (rare) - -
Coccidiosis (Cystoisospora suis or Eimeria species) ++++ ++ + -
Enteric salmonellosis (Salmonella Typhimurium, + ++++ ++++ +
others)
Septicemic salmonellosis (Salmonella Choleraesuis) + +++ +++ +
Swine dysentery (Brachyspira hyodysenteriae) + (rare) ++ ++++ ++
Proliferative enteropathy (Lawsonia intracellularis) + (rare) ++ ++++ ++
Whipworm infection (Trichuris suis) - ++ ++++ +++
Swine enteric coronavirus diseases ++++ +++ ++ +++

- Agent rarely causes diarrhea in age group.

+ to ++++ Relative increases in likelihood, severity, or prevalence of diarrhea in age group.

TABLES

DIARRHEAL DISEASES AT VARIOUS AGES 171

 SWINE DISEASE MANUAL

Diarrheal diseases in swine: comparative approach to

diagnosis
Many disease processes in pigs can result in diarrhea. Fortunately, the age of the affected pigs, the appearance of the feces, and
the nature of the clinical signs, when combined with appropriate diagnostic tests, can usually help one determine the primary
cause of the diarrhea.

Disease and agent Ages affected Diagnostic features and methods

Rotaviral enteritis Neonates up to 6 weeks
(Rotavirus A, B, or C) of age. Group C more
common in neonates while
group A more common
in late lactation and
postweaning.
Swine enteric coronavirus All age groups susceptible
diseases if previously unexposed.
(Porcine epidemic Most severe in piglets less
diarrhea virus) than 4 weeks old.
Nonfatal diarrhea with occasional vomiting. Microscopic segmental
atrophic enteritis. Infection confirmed by detecting agent in feces of
acutely affected pigs (PCR, EM, or antigen-ELISA) or by positive stain (FA
or IHC) on small intestinal sections.
Acute epidemics produce severe diarrhea, rapid dehydration, and
vomiting with nearly 100% mortality in neonatal piglets. Postweaned
pigs have profuse diarrhea, sometimes with yellowish color due to
maldigestion and malabsorption. Sows have less severe diarrhea and may
vomit; systemic illness may lead to lethargy and inability to effectively
nurse litter. Endemic disease occurs when only partial immunity exists
in the herd and results in milder disease, but with similar clinical signs,
though with much lower mortality. Infection confirmed by histologic
lesions of severe atrophic enteritis and positive antigen staining (FA or
IHC), or by PCR on feces from acutely affected pigs.

Swine enteric coronavirus All age groups susceptible In the absence of partial cross-protective immunity from prior infection
diseases if previously unexposed. with porcine respiratory coronavirus, signs and diagnosis are as above
(Transmissible Most severe in piglets less for porcine epidemic diarrhea. Widespread endemic porcine respiratory
gastroenteritis virus) than 4 weeks old. coronavirus has mitigated the severity of transmissible gastroenteritis virus
over the last 30 years. Partial immunity results in milder clinical signs and
less severe lesions.
Swine enteric coronavirus All age groups susceptible Acute outbreaks present with diarrhea in all age pigs but with low
diseases if previously unexposed. mortality. Once herd immunity develops, clinical signs disappear.
(Porcine delta Infection confirmed by observation of segmental atrophic enteritis and
coronavirus) PCR on feces from acutely affected pigs.
Enteric colibacillosis Neonates through 2 to 4 Watery diarrhea and possibly vomiting; clinical signs most severe in
(Escherichia coli) weeks postweaning. neonates less than 1 week old and during the first 2 weeks postweaning.
Affected pigs have few gross lesions, although occasionally fibrinous
polyserositis can be seen in neonates. Microscopically, Gram-negative
rods will be seen attached to intestinal epithelium.Infection confirmed
by isolation of uniform population of E coli from small intestine; colony
type can be smooth, mucoid, or hemolytic. PCR can be used to confirm
presence of enterotoxins and pili.
Clostridial diarrhea Neonates from few hours Moderately severe diarrhea with variable morbidity and low mortality.
(Clostridium difficile) old to 10 days of age. Mesocolonic edema may be observed and colon often filled with
creamy feces. Histology reveals multifocal suppurative and erosive colitis.
Infection confirmed by identification of alpha or beta enterotoxins using
antigen-ELISA on fresh feces.
TABLES

PCR = polymerase chain reaction; EM = electron microscopy; antigen-ELISA = enzyme-linked immunosorbent assay;
FA = fluorescent antibody; IHC = immunohistochemistry

172 DIARRHEAL DISEASES: COMPARATIVE APPROACH


Table cont’d. Diarrheal diseases in swine: comparative approach to diagnosis
Disease and agent
Clostridial diarrhea
(Clostridium perfringens
type A)
Clostridial diarrhea
(Clostridium perfringens
type C)
Enteric salmonellosis
(Salmonella enterica
serotype Typhimurium)
Septicemic salmonellosis
(Salmonella enterica
serotype Choleraesuis )
Swine dysentery Postweaning to adult.
(Strongly beta-hemolytic
Brachyspira species
including B hyodysenteriae,
B hampsonii, and
B suanatina)
PCR = polymerase chain reaction; EM = electron microscopy; Ag-ELISA = enzyme-linked immunosorbent assay; FA = fluorescent antibody;
IHC = immunohistochemistry
Ages affected
Neonates 2 to 10 days
of age.
Neonates from 8 hours
old to 3 weeks of age.
All ages susceptible if
previously unexposed,
although most common in
nursery and growing pigs.
All ages susceptible if
previously unexposed,
although most common in
nursery and growing pigs.
TABLES
Diagnostic features and methods
Variably severe diarrhea with variable morbidity, low mortality,
and no obvious gross lesions. Histology may show mild multifocal
suppurative enteritis associated with abundant Gram-positive
rods.
Infection confirmed by ruling out other causes, in combination
with indicative histopathology, isolation, and genotyping of an
enterotoxigenic (beta-2 toxin) C perfringens type A.
Acute presentation may appear only as an unexplained death,
sometimes accompanied by acute diarrhea (sometimes with
hemorrhage). Small intestine will be segmentally hyperemic to
hemorrhagic grossly, with transmural intestinal necrosis with
hemorrhage and emphysema microscopically. Morbidity may
be sporadic but with high case fatality. Some piglets (perhaps
those recovering from the acute infection) develop a chronic
form of the disease characterized by diarrhea and ill-thrift.
Fibrinonecrotic enteritis and colitis are evident histologically.
Infection confirmed by appropriate histopathology and isolation
of C perfringens type C determined to be beta toxin positive by
PCR.
Acute diarrhea with bile-stained feces and loss of condition.
Lesions of necrotizing enteritis of large (and sometimes small)
intestine and enlarged mesenteric lymph nodes. Occasionally
observe congestion in lungs or other evidence of septicemia.
Chronic cases may have “button ulcers” in large intestine.
Infection confirmed by culture and identification of bacteria from
intestine or regional lymph nodes. Salmonella Typhimurium and
Salmonella Heidelberg most commonly associated with enteritis;
other salmonellae serotypes are commonly isolated but their role
in disease is often unclear.
Cases may occur as an outbreak or sporadically in individuals.
Clinical signs of sepsis with red or purple skin lesions on ears, tail,
snout, feet, and abdomen, and dyspnea; diarrhea may not appear
until several days after the acute stage of disease. At necropsy,
congested lungs, splenomegaly, and hepatomegaly are common,
with enteritis lesions variably present. Infection confirmed by
evidence of necrotizing enterocolitis and culture of the bacterium
from intestine, lymph nodes, and systemic sites such as liver
and lung. Paratyphoid nodules in the liver are an important
microscopic feature of the disease.
Acutely affected pigs have mucohemorrhagic diarrhea. Gross
lesions are limited to the large intestine, which presents with
mucohemorrhagic to fibrinonecrotic typhlocolitis. Microscopic
lesions are restricted to mucosal layer with organisms observed
in epithelium and crypts. Infection confirmed by isolation of a
strongly beta-hemolytic Brachyspira from mucosa or feces. PCR
can detect some isolates but not all.
TABLES
Table continued on next page
DIARRHEAL DISEASES: COMPARATIVE APPROACH 173
 SWINE DISEASE MANUAL
Table cont’d. Diarrheal diseases in swine: comparative approach to diagnosis
Disease and agent
Spirochetal colitis
(Weakly beta-hemolytic
Brachyspira species
including B pilosicoli,
B murdochii, B intermedia,
and B innocens)
Proliferative enteritis
(Lawsonia intracellularis)
Coccidiosis
(Cystoisospora suis)
Coccidiosis
(Eimeria species)
Whipworm infection
(Trichuris suis)
PCR = polymerase chain reaction; EM = electron microscopy; Ag-ELISA = enzyme-linked immunosorbent assay; FA = fluorescent antibody;
IHC = immunohistochemistry
TABLES
174 DIARRHEAL DISEASES: COMPARATIVE APPROACH
Ages affected Diagnostic features and methods
Growing and finishing pigs. Can present as a sporadic or persistent mild nonhemorrhagic
diarrhea, generally without other overt clinical signs; gross
lesions are unremarkable. Microscopically, will see attachment
of the organism to enterocytes in the colon, microerosions in
the epithelium, and nonsuppurative inflammation. Infection
is confirmed by rule-out of dysenteric Brachyspira species,
characteristic histopathology, and identification of the organism,
usually by PCR.
Postweaning to adult. In its subclinical form, disease may only be evident by poor
performance or weight loss. Acute forms of the disease are
accompanied by hemorrhagic diarrhea, hemorrhage in the
intestine (usually clotted), and thickened intestinal mucosa of the
distal small intestine and colon. Chronic infections are typified
by fibrinonecrotic enteritis and/or colitis with mucosal thickening
due to crypt enterocyte hyperplasia and inflammation. Infection
confirmed by observation of typical gross and microscopic lesions
and presence of L intracellularis demonstrated by IHC or PCR.
From 5 to 25 days of age. Sporadic diarrhea and wasting, pigs may be recruited in waves.
Microscopic lesions include atrophic enteritis, sometimes with
segmental fibrinonecrotic enteritis in caudal small intestinal
sections. Infection confirmed by observation of immature stages
of Cystoisospora suis within the epithelium. The severity of
coccidiosis is highly dose- and age-dependent.
Susceptible naïve pigs Enterocolitis with organisms visible in the intestinal or colonic
postweaning. epithelium by microscopy. Infection confirmed by observation
of immature stages of Eimeria within the gut epithelium. Fecal
flotations may demonstrate high numbers of oocysts, but this is
not sufficient for a diagnosis. PCR generally not available. The
severity of coccidiosis is highly dose- and age-dependent.
Postweaning to adult. Mucoid or mucohemorrhagic diarrhea with loss of condition
is suggestive of the disease. Inflammatory nodules, often with
protruding parasites, can be seen in mucosa of large intestine.
Large numbers of parasites are not necessary to create severe
disease. Clinical signs are very similar to those produced with
swine dysentery; the two diseases can occur together. Prepatent
period is around 8 weeks and eggs are shed intermittently.
Infection is confirmed by visualization of the parasite or ova and is
supported by histopathology and clinical signs.
 TABLES

Internal parasites
Although much of modern swine production now takes place in indoor facilities and over fully perforated flooring, parasites
seem to persist on many farms. Eradication is rarely an option, so long-term control strategies, usually based on periodic treat-
ment with anthelmintics, are required. An effort should be made to understand what parasites are present on a farm and when
(and from where) the infection is occurring, so that the best value can be derived from a control program.

Disease and agent Usual location and size of adult Life cycle Mode of infection Treatment
Ascariasis Small intestine, bile duct, and Direct Orally from AVE, DCV,
(Ascaris suum) stomach contaminated FBZ, LVM, PIP,
150 to 300 mm environment. PRT
Coccidiosis Caudal half of small intestine Direct Orally from Totrazuril
(Cystoisospora suis) 20 µm diameter contaminated or related
environment. compounds
Cysticercosis Cysticerci form in skeletal and cardiac Indirect; pig is the Orally from None
(Taenia solium) muscles. intermediate host environment
Cysts range from 10 to 20 mm for this human contaminated with
tapeworm. human sewage.
Esophageal worm Sub-epithelium of esophagus Indirect; requires Ingestion of beetle AVE, FBZ, LVM
(Gongylonema and in the tongue dung beetles. with encysted larvae.
pulchrum) 30 to 60 mm
Hookworm Small intestine of feral and pastured Direct Cutaneous contact AVE, DCV,
(Globocephalus swine in southern US. with larvae. FBZ, LVM
urosubulatus) 6 to 8 mm
Kidney worm Large adults in perirenal tissues, Indirect; requires Consume earthworms AVE, FBZ, LVM
(Stephanurus kidney, and ureters. Juveniles can be earthworms. Direct; carrying larvae; some
dentatus) found in ectopic sites. some evidence evidence larvae can
20 to 50 mm exists. penetrate skin of pigs.
Liver flukes Liver of pigs on pastures used by Indirect; requires Orally from None
(Fasciola hepatica) sheep. snails. contaminated
30 mm environment.
Lungworm Edge of diaphragmatic lobes of lung Indirect; requires Consume earthworms AVE, FBZ, LVM
(Metastrongylus 20 to 50 mm earthworms. Direct; carrying larvae.
species) some evidence
exists.
Mycoplasma suis On erythrocytes Unknown Uncertain; Tetracyclines
0.8 to 1.0 µm diameter transplacental, direct
contact, insect bites,
and contaminated
instruments have
been implicated.
Red stomach worm Stomach Direct Orally from AVE, DCV, FBZ
(Hyostrongylus Less than 10 mm contaminated
rubidus) environment.

AVE = avermectin; DCV = dichlorvos; FBZ = fenbendazole; LVM = levamisole; PIP = piperazine; PRT = pyrantel.
TABLES

Table continued on next page

INTERNAL PARASITES 175

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Table cont’d. Internal parasites

Disease and agent Usual location and size of adult Life cycle Mode of infection Treatment
Stomach worms Stomach Indirect; requires Ingestion of beetles DCV, FBZ
(Ascarops strongylina and 10 to 20 mm dung beetles. with encysted larvae.
Physocephalus sexalatus)
Thorny-headed worm Small intestine (usually ileum) Direct Prenatal, AVE, LVM
(Macracanthorhynchus Up to 30 cm transcolostral, oral,
hirudinaceus) or cutaneous contact
with larvae.
Threadworm Small intestine of suckling pigs Direct Prenatal, AVE, DCV, FBZ,
(Strongyloides ransomi) 30 to 45 mm transcolostral, oral, LVM
or cutaneous contact
with larvae.
Trichinosis Muscle of many mammals, Many carnivorous Ingest muscle Not practical
(Trichinella spiralis) especially swine and bears. or omnivorous containing encysted
Adults 2 to 4 mm, encysted mammals. larvae (raw garbage,
larvae animal carcasses,
0.8 to 1.3 mm rats, mice, cats, or
cannibalism)
Whipworm Cecum and large intestine Direct Orally from DCV, FBZ, LVM
(Trichuris suis) 50 to 80 mm contaminated
environment.
AVE = avermectin; DCV = dichlorvos; FBZ = fenbendazole; LVM = levamisole; PIP = piperazine; PRT = pyrantel.
TABLES

176 INTERNAL PARASITES

 TABLES

Intestinal hemorrhage: differential diagnosis

The listed diseases are usually seen in postweaning and growing pigs. Intestinal hemorrhage in neonatal pigs is very rare; in
the US it is usually associated only with Clostridium perfringens type C. The list of diseases and conditions that cause intestinal
hemorrhage is limited, so a logical approach to diagnosis that incorporates knowledge about the clinical signs, the location and
character of the hemorrhage, and the epidemiology and history of the outbreak, combined with the rational use of diagnostic
support, will usually identify the cause.

Enlargement
Disease Cecal and of ileocecal Diagnostic features
and agent Ileal lesions colonic lesions lymph nodes and methods
Enteric Usually mild to Severe, segmental or Mild to severe, Bile-stained feces with fibrin
salmonellosis moderate severity, with multifocal, fibrinous to often with common. Some serotypes may
(Salmonella segmental fibrinous or fibrinonecrotic colitis. edema and produce necrotic hepatic foci
enterica serotype necrotic exudates. congestion. or pneumonia.
Typhimurium)
Gastric ulcer Dark, tar-like blood Dark, tar-like blood None. Pig (or carcass) will usually
(Multiple risk (melena) in intestinal (melena) in lumen. No be pale. Ulcer may bleed
factors have been lumen. No pathology pathology present. intermittently over days to
described) present. weeks or the pig may bleed out
acutely if ulcer affects a major
vessel in the gastric wall. The
pars esophagea of the stomach
should always be examined for
the presence of an ulcer.
Hemorrhagic Transmural congestion Colon may have bloody Sometimes Cause unknown but must be
bowel syndrome of intestine contents from pathology mild edema differentiated from intestinal
(Exact cause and accompanied by that occurred in the and congestion volvulus through careful
pathogenesis unclotted blood or small intestine but no present. necropsy.
unknown) bloody fluid in the overt pathology present
lumen. in tissue.
Intestinal (or Entire intestine dilated No mucosal lesions. Sometimes Sporadic occurrence with rapid
stomach) volvulus with bloody fluid and Contents may be edema in death of healthy pigs. Typically,
or torsion gas, without mucosal normal, or bloody fluid lymph nodes. affected pigs will have feed in
lesions. With intestinal and gas may be present stomach (highly unusual for ill
volvulus, the proximal similar to small intestine. pigs). Twist may be observed
duodenum may be in the mesentery or mesenteric
normal with abrupt root, and abdominal organs
transition to congestion are often displaced. It can
at caudal flexure. be surprisingly difficult to
confirm what has occurred and
careful necropsy is required.
This condition is an important
differential for hemorrhagic
bowel syndrome.

Table continued on next page

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Table cont’d. Intestinal hemorrhage: differential diagnosis

Enlargement
Disease Cecal and of ileocecal Diagnostic features
and agent Ileal lesions colonic lesions lymph nodes and methods
Proliferative Mild to severe, gross and Variably present and Mild to severe Ileum may be rigid and hose-
enteritis microscopic proliferative much less common with segmental like. Clinical cases often occur
(Lawsonia changes in mucosa. than ileal lesions. When mesenteric sporadically in herd, although
intracellularis) Frank blood (often changes are present they edema small outbreaks do occur. The
clotted) can be variably can range from mild to sometimes condition frequently exists at a
present. Chronic cases severe and are restricted present. subclinical level.
often accompanied by to the proximal cecum/
fibrinonecrotic changes colon.
to mucosa.
Swine dysentery None. Severe, diffuse, Mild or absent. Mucohemorrhagic feces are
(Strongly mucohemorrhagic very common. Blood in feces is
beta-hemolytic colitis; fibrin visible in often fresh, red, and mixed with
Brachyspira chronic stages. mucus.
species including
B hyodysenteriae,
B hampsonii, and
B suanatina)
Vitamin K May contain unclotted No mucosal lesions in None. Petechial or ecchymotic
deficiency blood. No lesions cecum or colon. hemorrhage at other systemic
(warfarin toxicity) present in mucosa. locations.
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178 INTESTINAL HEMORRHAGE: DIFFERENTIAL DIAGNOSIS

 TABLES

Mycoplasma-related diseases
The following table consolidates the key differentiating features of each of the 4 mycoplasmal diseases that occur on US swine
farms, so the reader can clearly understand how each needs to be approached differently with regard to prevention, diagnosis,
and control.

Disease and agent Signs and lesions Diagnostic features and methods
Mycoplasmal arthritis Age: Usually 10- to 24-week-old pigs. History, signs, and lesions are suggestive.
(Mycoplasma May respond well to lincomycin, tylosin, or
Clinical: Lameness, difficulty in arising, reluctant
hyosynoviae) tetracycline injection. Histopathology and
to walk and kneeling in some. Often in straight-
detection of organism in joints by PCR or
legged, muscular pigs with hidden joint swellings.
isolation from acutely infected pigs. Needs
Serofibrinous, blood-tinged synovial fluid with
to be differentiated from Haemophilus
synovial membranes swollen.
parasuis, Streptococcus suis, erysipelas, and
Lesions: Arthritis with serofibrinous effusion and osteochondrosis dessicans.
grossly visible villous proliferation of synovium.
Mycoplasmal Age: Three weeks old to adults, especially Often diagnosed on the basis of clinical signs
pneumonia or enzootic 2 to 4 months. and lung lesions at necropsy or slaughter.
pneumonia Confirm disease by demonstrating organisms
Clinical: Persistent dry cough, dyspnea with
(Mycoplasma by IHC, ISH or FA in lesions. Confirm presence
flare-ups of pneumonia. Good appetite but
hyopneumoniae) by PCR on lung or airway swabs. Difficult to
unthrifty.
culture. Serology (ELISA, CF) can be used
Lesions: Clearly demarcated cranioventral for herd diagnosis. Improved environment,
lobules with grey consolidation and reduced stocking density and vaccination can
mucopurulent exudate in airways. Morbidity help in control.
variable/mortality low. Histologically have
marked lymphoid hyperplasia around airways,
often with mucopurulent exudate in airways and
adjacent alveoli.
Mycoplasmal Age: Usually in 3- to 10-week-old pigs, Isolation or PCR from acute septic lesions
polyserositis and sometimes older. at systemic sites. Morbidity 20% to 35%
arthritis but mortality low. Infection may persist in
Clinical: Acutely affected pigs visibly ill and with
(Mycoplasma hyorhinis) joints, but many lame pigs slowly recover but
fever. Abdominal tenderness with preference
fibrinous adhesions and poor gains persist.
for sternal recumbency. Lameness. Sometimes
Needs to be differentiated from Haemophilus
dyspnea.
parasuis, Streptococcus suis, and Actinobacillus
Lesions: Serofibrinous pericarditis, pleuritis, and suis. Mycoplasma hyorhinis does not cause
peritonitis. Later there may be fibrous adhesions. meningitis or central nervous system signs.
Arthritis often severe in one or more joints.
Later, villous hyperplasia, possibly pannus may
occur.
Mycoplasma suis Age: Any age; usually in suckling or nursery pigs, History and clinical signs are usually not specific
or in sows. enough to be helpful in establishing a diagnosis.
Anemia may be present and the organism may
Clinical: Range from vague signs to pallor,
be detected by PCR in blood or splenic tissue.
anemia, unthriftiness, dysgalactia, skin cyanosis,
Organisms can be visualized by microscopy in
fever, and icterus.
blood smears. Serology useful on herd basis
Lesions: Anemia, icterus, and splenic but is not widely available. The historic name of
enlargement. this disease is eperythrozoonosis.
TABLES

ELISA = enzyme-linked immunosorbent assay; IHC = immunohistochemistry; CF = complement fixation; FA = fluorescent antibody;
PCR = polymerase chain reaction.

MYCOPLASMA-RELATED DISEASES 179

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Reproduction: causes of low farrowing rate

Low farrowing rate can be a challenging problem to solve on farms. Its occurrence can be insidious rather than sudden and
the cause is often multifactorial in nature. The table below provides a framework to assist in ensuring one looks broadly at all
potential contributors to a farrowing rate problem rather than focusing only on infectious etiologies.

Conception failure
Regular returns to estrus (19 to 24 days)
Risk factor Cause Comments
Management Number of matings per service
Mating quality and technique
Estrus detection and timing of mating
Artificial insemination Semen viability, temperature, AI technique, dose
Natural service Boar semen quality, copulation, blood/trauma
Gilt/Sow factors Infectious diseases Urogenital (ascending) infections, systemic disease
Farrowing interval Lactation length, wean-to-service interval
Parity Age and weight at first mating
Body condition Critical factor to manage during lactation
Boar factors Age, genotype, season, temperature Genotype, libido, ambient temperature too high
Infectious diseases Reduced sperm count due to systemic disease,
Trauma, blood in semen remember delayed effect due to spermatogenic cycle

Pregnancy failure
Irregular returns to estrus (greater than 25 days)
Risk factor Cause Comments
Gilt/Sow factors Infectious diseases Ascending or systemic infections
Gilt acclimatization Inadequate acclimatization of gilts (vaccine and
exposure)
Endocrine dysfunction Primary dysfunction of endocrine organ
Parity Age and weight at first mating
Feed Mycotoxins Zearalenone, phytoestrogens, others
Feed additives Carbadox
Dietary micronutrients Vitamins, trace minerals
Nutrient balance and intake Amino acids, energy, body condition
Environment Season Seasonal infertility syndrome (summer and fall matings)
Temperature Excessively cold or hot
Housing Fighting and stress due to commingling groups, trauma
Movement or commingling Embryo loss surrounding implantation (10 to 25 days
postmating postmating)
TABLES

180 REPRODUCTION: CAUSES OF LOW FARROWING RATE

 TABLES

Reproductive failure: infectious causes

In addition to the most common infectious causes of reproductive failure described in the table below, many other diseases
can contribute directly to reproductive failure or indirectly through the effects of systemic disease processes. These diseases
include, but are not limited to, influenza A, classical swine fever, African swine fever, Japanese encephalitis, and virulent
enteroviral infections. Sporadic abortions may also occur from bacterial infections such as erysipelas, Streptococcus, Salmonella,
Trueperella, and others by either systemic or ascending urogenital routes (through both artificial insemination and natural
service). Any acute generalized illness that occurs during advanced pregnancy can lead to abortion.

Disease and agent
Brucellosis
(Brucella suis)
Leptospirosis
(Leptospira species)
Porcine circovirus
associated disease
(Porcine circovirus type
2 and type 3)
Porcine parvovirus
(Porcine parvovirus 1)
Signs and lesions
Very uncommon disease in most commercial
industries; it has been essentially eliminated
from the US indoor-housed commercial
industry. When exposure does occur, infertility
is the most common outcome, although any
manifestation of reproductive failure may occur.
Abortion can occur at any stage of pregnancy.
In boars, orchitis may develop as a result of the
infection.
During an acute outbreak in a naïve herd,
abortions and stillbirths can occur, particularly
during late pregnancy. Piglets from infected
dams are often weak and many will die within a
few days. Adult sows often show few other signs
of disease.
A common virus in swine around the world
that is associated with sporadic outbreaks
of increased fetal death, mummies, or dams
confirmed pregnant but failing to farrow.
Reproductive failure as a result of infection with
these viruses is relatively uncommon compared
to their impact on performance and disease of
postweaning pigs.
Vary with gestational stage at infection. Disease
is most common in gilts. Infection increases
number of mummies, returns to estrus, failure
to farrow, stillbirths, and pseudopregnancy.
Net result is fewer pigs born alive per litter.
Abortions or fetal anomalies are not a feature.
Affected dams remain asymptomatic.
Diagnostic features and methods
Disease is present in some feral swine in the
US; these serve as a reservoir for the infection.
Brucellosis is a serious zoonosis and cases of
the disease occur in feral pig hunters every
year. Diagnosis of the disease in pigs is typically
achieved through serology and sometimes by
bacterial culture.
After recovery from infection (usually as a
result of antibiotic therapy), subsequent
mating and reproduction return to normal.
Leptospirosis can also cause nephritis and
hepatitis in nonpregnant pigs. Diagnosis in
an infected sow or litter may require use of
several testing strategies, including paired
serology, culture, PCR, or tissue staining.
Serology not useful for diagnosing virus
involvement in reproductive disease. Virus
should be identified by PCR, ISH, or FA in
fetal tissues to confirm the role of the virus in
disease.
Parvovirus is a major cause of embryonic and
fetal death, particularly in gilts. Diagnosis can
be made by PCR or FA staining of fetal lungs or
hearts collected from mummified fetuses less
than 16 cm in length.

IHC = immunohistochemistry; FA = fluorescent antibody; PCR = polymerase chain reaction; ISH = in situ hybridization.

Table continued on next page

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Table cont’d. Reproductive failure: infectious causes

Disease and agent
Porcine reproductive and
respiratory syndrome
(Porcine reproductive and
respiratory syndrome virus
type 1 and type 2)
Pseudorabies
(Suid herpesvirus 1, also
known as pseudorabies
virus or Aujeszky’s disease
virus)
Signs and lesions
Acutely infected sows may abort, or abortion
may occur from fetal infection several weeks
after sows are infected. Decreased conception
and farrowing rates during and just after
an outbreak are common. At a herd level,
outbreaks significantly increase numbers of
stillbirths, weak pigs, mummies, premature
farrowings, third trimester abortions, and
preweaning deaths. In well-managed outbreaks,
herd immunity can occur, with improvements
expected in 3 to 5 months.
Clinical signs depend on the gestational stage
at time of infection. Dams infected in the first
trimester may absorb their fetuses and return
to estrus; those in second or third trimester may
abort or have increased mummified, stillborn,
or weak pigs. Dams infected near term may have
congenitally infected piglets that die within a few
days; central nervous signs or sudden deaths are
common in these pigs. Recovered (or vaccinated)
sows are protected from clinical signs.
Diagnostic features and methods
In addition to reproductive disease in the
breeding herd, respiratory signs and illness
may occur in any age group. PCR testing
of serum collected from acutely ill sows
(especially if sows are ill) and tissue from
aborted or weak-born piglets can confirm
diagnosis. Depending on stage of infection,
both sample types (dam serum and piglet
tissue) are often necessary to confirm
diagnosis. Serology on convalescent sows is
useful if previous infection status of the herd
and/or vaccination status are known.
If endemic, reproductive signs less common
than central nervous signs or respiratory signs
in growing pigs. Diagnosis can be achieved
through serology, virus isolation, IHC, PCR.
Pseudorabies has been eradicated from the US
commercial industry, although the disease still
occurs in feral pigs in parts of the country.

IHC = immunohistochemistry; FA = fluorescent antibody; PCR = polymerase chain reaction; ISH = in situ hybridization.
TABLES

182 REPRODUCTIVE FAILURE: INFECTIOUS CAUSES

 TABLES

Respiratory disease in swine: comparative approach

to diagnosis
Respiratory disease is perhaps the most common malady faced by swine producers and veterinarians. The term porcine respi-
ratory disease complex aptly describes the multifactorial nature of most respiratory disease problems that are encountered. In
addition to management factors that may contribute to the occurrence or severity of the problem, the table below provides a
convenient comparative description of the most common infectious agents that are likely to be encountered. Not included are
Ascaris suum and lungworms, both of which can cause acute respiratory clinical signs when acute heavy exposures occur.

Disease Agent/Cause Clinical signs Diagnostic features and methods

Atrophic rhinitis Bordetella Sneezing, snorting, nasal discharge,
bronchiseptica and epistaxis (severe cases). Tear
and/or toxigenic staining from the medial canthi of
Pasteurella the eyes is very characteristic of the
multocida disease. Coughing is not a feature of
the disease. In endemically infected
herds it is usual to see deviation of
the snout in at least some pigs. Most
modern production systems have
eliminated the disease.
Inclusion body Porcine Sneezing, nasal discharge or
rhinitis cytomegalovirus occlusion, and mouth-breathing
in young piglets 3 to 6 weeks of
age. Morbidity can be very high
but mortality due to the disease is
negligible. In most cases, the disease
has only a minor and very transient
effect on gain and does not appear to
predispose the pig to other diseases.
Influenza A Influenza A virus of In acute outbreaks, signs include
swine (IAV-S) sudden onset and rapid spread
of fever, serous nasal discharge,
and dyspnea with high morbidity.
Prostration and coughing, sometimes
severe, follow. Most pigs recover in
7 to 10 days. In large populations,
perhaps in combination with viral
evolution, endemic infections in some
herds are characterized by a more
insidious onset and clinical disease that
occurs only in some subpopulations
within the herd or barn at any given
time. Subtypes H1N1 and H3N2
are most common in the US though
ongoing evolution and interspecies
transmission is well recognized.
Variable degrees of turbinate atrophy and
snout deviation. Secondary pneumonia
often present but related to other agents.
History, signs, and typical lesions (often
noted during slaughter check) may be
sufficient for a diagnosis. When assessing
risk of atrophic rhinitis in purchased stock,
culture of nasal swabs or turbinates followed
by toxigenicity testing by PCR may be
necessary.
Grossly, may see only moderate clear to
mucopurulent nasal discharge. Microscopic
evidence of rhinitis with edema, petechial
hemorrhages, and mucopurulent nasal
exudate. Signs and lesions are nearly
pathognomonic, especially when
characteristic intranuclear inclusions in the
turbinates or Harderian glands are noted.
Multifocal to diffuse, red, firm areas of
pneumonia, although characteristically
there is a lobular cranioventral distribution
of gross lesions. Secondary bacterial
bronchopneumonia is common. History
and clinical signs are very suggestive of the
acute form though less helpful in chronic/
endemic situations. Morbidity is typically
very high and, unless complicated by
other diseases, mortality tends to be low.
Diagnostic tests are widely available, with
most cases confirmed by PCR on lung tissue
or nasal swabs. Antigen staining of lung
tissue using IHC or FA is a common and
reliable technique for diagnosis. Subtyping
(by PCR and/or sequencing) is an important
monitoring tool. Serology by ELISA is also
available.

ELISA = enzyme-linked immunosorbent assay; IHC = immunohistochemistry; FA = fluorescent antibody; PCR = polymerase chain reaction;
TABLES

ISH = in situ hybridization; VI = virus isolation.

Table continued on next page

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Table cont’d. Respiratory disease in swine: comparative approach to diagnosis
Disease Agent/Cause Clinical signs
Mycoplasmal Mycoplasma Persistent, dry cough and slow
pneumonia hyopneumoniae growth, typically at a high
prevalence but negligible mortality.
The disease is endemic in nearly
all herds unless specific steps have
been undertaken to eliminate the
infection.
Pneumonic Pasteurella Coughing, dyspnea, fever, and
pasteurellosis multocida prostration.
Pleuropneumonia Actinobacillus In acute outbreaks, pigs show high
pleuropneumoniae fever, prostration, dyspnea, and
mouth-breathing, usually with high
morbidity and mortality. Dead pigs
often present with blood-tinged
foam coming from nose. Many pigs
that recover from acute illness will
continue to present with a chronic
cough and appear unthrifty. In
endemically infected herds, the
disease may simply contribute to
poor grower-finisher performance
(with sporadic outbreaks of the
acute form) and complaints of
high levels of pleuritis by the
abattoir. Disease severity can vary
substantially based on the strain or
serotype of A pleuropneumoniae
that is present.
ELISA = enzyme-linked immunosorbent assay; IHC = immunohistochemistry; FA = fluorescent antibody; PCR = polymerase chain reaction;
ISH = in situ hybridization; VI = virus isolation.
TABLES
184 RESPIRATORY DISEASE: COMPARATIVE APPROACH
Diagnostic features and methods
Grey-to-purple pneumonia and atelectasis
in cranioventral lobules. Marked lymphoid
hyperplasia around airways. History,
signs, and lesions are very suggestive of
the disease. Antigen staining (FA, IHC) on
affected lung or PCR on lung or airway
swabs to confirm infection. Serology
has some value as an epidemiological or
monitoring tool on a herd basis.
Fibrinous bronchopneumonia seen
cranioventrally but often extending into
diaphragmatic lobes. Pleuritis, adhesions,
and abscesses are variably present.
Pasteurella multocida can be readily isolated
from lung lesions and is often a component
of porcine respiratory disease complex.
Necrohemorrhagic pneumonia with
fibrinous pleuritis. Chronic cases have
pleural adhesions, often accompanied by
necrotic foci in the lung. Lesions tend to be
most common in diaphragmatic lobes. Signs
and lesions are highly suggestive of the
diagnosis, although the agent can usually
be readily cultured or detected by PCR.
Serotyping of the organism is important in
developing appropriate control strategies
and for biosecurity monitoring. Serological
tests are available but can be quite
serotype specific – negative test results are
not definitive.

Table cont’d. Respiratory disease in swine: comparative approach to diagnosis
Disease Agent/Cause Clinical signs
Porcine Porcine Causes reproductive failure in
reproductive reproductive sows and respiratory disease in all
and respiratory and respiratory ages. High preweaning mortality
syndrome syndrome virus is common after outbreaks in
type 1 and type 2 a breeding herd. Respiratory
disease is accompanied by fever
and dyspnea, which can persist for
weeks. The disease is a frequent and
important contributor to porcine
respiratory disease complex.
Pseudorabies Suid herpesvirus 1 Central nervous system signs and
death predominate in neonates.
Respiratory disease tends to
predominate in swine greater
than 3 weeks old with sneezing,
coughing, nasal discharge, dyspnea,
and occasionally seizures or other
central nervous signs. The disease
in growing-finishing pigs can be
clinically indistinguishable from
influenza A.
ELISA = enzyme-linked immunosorbent assay; IHC = immunohistochemistry; FA = fluorescent antibody; PCR = polymerase chain reaction;
ISH = in situ hybridization; VI = virus isolation.
RESPIRATORY DISEASE: COMPARATIVE APPROACH 185
TABLES
Diagnostic features and methods
In younger pigs, focal or diffuse interstitial
pneumonia is common in any or all lobes,
often complicated by bronchopneumonia
due to secondary bacterial infection.
Thoracic lymph nodes (and others) are
often enlarged. Numerous diagnostic tests
are available, although PCR on tissues or
serum and histopathology with antigen
stains (IHC, FA, ISH) are in most common
use. The virus is generally easy to isolate.
Genotyping of the strain involved in an
outbreak or circulating endemically on a
farm is common and epidemiologically
useful.
Characteristic white, necrotic foci in liver
and spleen occur in suckling piglets. Rhinitis,
tracheitis, tonsillitis, and keratoconjunctivitis
can be seen in postweaning pigs. Often
there is nonsuppurative encephalitis,
tracheitis, bronchiolitis, and alveolitis
that accompany the respiratory disease,
sometimes with grossly visible necrotic
pharyngitis, laryngitis, and tracheitis.
Infection can be confirmed by FA, VI, or
PCR on tonsil, spleen or brain, and by
histopathology with antigen staining (IHC).
Serological tests that can differentiate
vaccine from wild-type virus are a critical
part of eradication programs. The US
commercial industry is free of the disease
but feral pigs in some areas are endemically
infected.
TABLES
 SWINE DISEASE MANUAL

Skin lesions: differential diagnosis

Skin lesions can be readily diagnosed in most instances if one takes into account the history, epidemiology, and clinical signs asso-
ciated with the presenting disease. In many cases, diagnostic testing may not be required. However, when a condition is occurring
at a high prevalence, diagnostic testing is warranted. Remember to examine the entire pig when faced with a disease process that
is presenting primarily as a skin problem. The skin lesion may simply be a symptom of a more significant systemic illness.

Disease and agent Signs and lesions
Actinobacillosis Sporadic cause of raised, red, rhomboid-shaped
(Actinobacillus suis)
lesions in growing and mature pigs.
Aural hematoma Hemorrhage and serous exudate between skin
(Trauma) and cartilage of ear pinna. Over days to weeks,
fluid accumulation tends to resolve, resulting in a
thickened and deformed ear. Lesions can be very
large and appear to be quite painful during the
acute stages.
Dermatosis vegetans Rare and semilethal hereditary defect. Coronary
(Congenital defect) band lesion and hoof deformities on one or
more feet of neonate initially appear as red
macules but expand and become papillomatous
over a few weeks.
Ear necrosis Areas of ulceration, infection, and necrosis on
(Multiple causes) tips or margins of ear(s). Pathogenesis poorly
understood, and it is unlikely there is a single
cause; risk factors are not well identified.
Microscopic vasculitis with bacterial infection is
observed.
Epitheliogenesis Missing areas of skin at birth, often over back,
imperfecta rump, or mouth.
(Congenital defect)
Erysipelas Acute outbreaks characterized by appearance
(Erysipelothrix of red, raised, rhomboid-shaped lesions on skin, animal is treated promptly for the systemic disease.
rhusiopathiae) often accompanied by high fever and joint pain.
As lesions resolve, necrotic plaques or scabs peel
off. Occasionally see necrosis of ear and tail tips.
Exudative Brownish exudative lesions on skin of axilla and
epidermitis groin but spreading to head, face, and other
(Staphylococcus areas. Severe cases can involve almost the entire
hyicus) body and develop over a few days to a week.
Pigs tend to be systemically ill with low fever,
lethargy, and poor growth.
Lice Intense rubbing and scratching behavior. Eggs
(Haematopinus suis) can be seen attached to hair on jowls, flanks,
inner surface of legs, and behind ears. Anemia
can develop with severe infestations.
TABLES
Diagnostic features and methods
Signs and internal and cutaneous lesions can
(rarely) resemble those of acute erysipelas.
Condition usually a result of some trauma to the
ear including bites, violent head shaking,
fighting from commingling, and mange (itching).
Defect originally detected in Landrace breed but
currently there is less breed predisposition due
to evolution of composite breeds/genetics. Most
affected piglets die within a few weeks
although pigs that do survive develop
interstitial pneumonia containing characteristic
multinucleate giant cells.
Infection occasionally results in septicemia and
death but more generally the condition appears
to have minimal effect on the pig.
Small lesions often heal by scarring, although most
affected pigs tend to succumb to
secondary effects of the condition.
Acute skin lesions usually resolve without issue if
Triggering factors are poorly understood for
this toxin-mediated disease. Risk factors include
irritation or wounds to the skin which precede the
lesion and likely provide a niche for the
bacterial infection to establish. Treatment is
seldom satisfactory.
Chronic infestations will lead to unthriftiness and
anemia. Lice are easy to see and are just a bit
smaller than a housefly.

186 SKIN LESIONS: DIFFERENTIAL DIAGNOSIS

 TABLES

Table cont’d. Skin lesions: differential diagnosis

Disease and agent Signs and lesions Diagnostic features and methods
Photosensitization White areas of skin inflamed and pruritic. Lesions Many plants and drugs are photodynamic.
(Photodynamic often become necrotic over a few days to weeks, Conjunctivitis may accompany the dermatitis.
agents) followed by peeling. Sunlight is required for the lesions to develop,
although pigs do not need to be housed
exclusively outdoors to receive adequate
exposure.
Pityriasis rosea Raised, expanding, nonexudative, circular lesions Lesions resolve within a few weeks to months
(Unknown) in 6- to 14-week-old pigs. Lesions usually on without treatment. Disease may go unnoticed
ventral abdomen and inguinal areas. Lesion unless ventrum is examined. Lesions are not
margins look quite inflamed but do not appear pruritic. Affected pigs do not seem to suffer from
to be painful. any ill effects due to pityriasis rosea.
Porcine dermatitis Red to purple, circular, 1-cm-diameter Diagnosis by recognition of typical skin lesions
and nephropathy lesions appear on perineal, rump, and ventral and histopathology on skin and kidney. Usually
syndrome regions. Lesions may enlarge and coalesce. The sporadic but morbidity can approach 10%. No
(immune-mediated) accompanying nephropathy may lead to death in treatment. Condition appears to be a sequel
days to weeks. to some systemic viral infections, notably
porcine circovirus type 2 and type 3, porcine
reproductive and respiratory syndrome virus, and
classical swine fever.
Pustular dermatitis Pustules on ventral abdomen, inguinal area, Most pigs recover in a few weeks. Risk factors
(Streptococcus inner thighs, eyes, lips, or ears. Pustules rupture for the condition are poorly understood but
species) and are then replaced by black scabs. Several the lesions are likely a result of both traumatic
bacteria have been implicated but Lancefield skin wounds and hematogenous spread from
group C Streptococcus species are most common. other bacteremias (eg, tail-docking wounds,
A specific condition called “facial pyoderma” can umbilical infections, etc). Providing clean bedding,
develop on the cheeks and jowls of neonates improving sanitation, and using good hygiene will
from wounds caused by fighting among limit occurrence. Recovery can be hastened by
littermates. antibiotic treatment.
Ringworm Approximately circular, expanding, hairless areas Condition is usually self-limiting and does not
(Microsporum nanum that develop crested scabs. Lesions typically have appear to have any significant effect on the pig.
or Trichophyton a clearly demarcated margin that may be slightly The disease is zoonotic but direct contact with
verrucosum) raised. The lesion is nonpruritic. the lesion (and abrasion on the human skin) is
probably required for transmission. Other fungi
are occasionally identified. Usually a condition of
older swine and quite common in sows.
Skin necrosis of Abrasive lesions on knees, fetlocks, coronets, Lesions often are more serious than realized. The
piglets hocks, or elbows. The condition can lead to condition is prevented by use of less abrasive
(Bacterial dermatitis) septicemia and contribute to infectious arthritis, surfaces in the farrowing environment, maintaining
valvular endocarditis, and other diseases. Left good hygiene, and providing adequate clean
unmanaged, high case mortality can result. bedding when used.
Sunburn Pigs may drop to their belly from pain associated If shade is provided, pigs will not lay in the sun.
with sunburn on their back. Reddening, Providing access to wallows will help prevent the
thickening, then peeling of affected skin is condition. Unpigmented skin more susceptible.
typical. Condition usually found on the back
and ears.
TABLES

Table continued on next page

SKIN LESIONS: DIFFERENTIAL DIAGNOSIS 187

 SWINE DISEASE MANUAL

Table cont’d. Skin lesions: differential diagnosis

Disease and agent Signs and lesions Diagnostic features and methods
Swinepox Initially appear as 5 to 10 mm round to oval All age groups are susceptible but is most often
(Swinepox virus) lesions on ventrum but can extend over the seen in young, growing pigs. Infection assumed to
body. Lesions progress from papules through the be endemic in the US and the clinical condition is
vesicle, pustule, and scab stages, similar to other rarely encountered; no surveillance has occurred
pox viruses. recently to determine the true prevalence.
Congenital pox is sporadic but quite striking in
affected newborn piglets.
Vesicular diseases Round to oval vesicles on feet and coronary Lesions are similar for all of the listed vesiculating
(foot-and-mouth bands, in and around the mouth or tongue, on viral diseases. All suspicious vesicular diseases
disease, vesicular snout, in nostrils, and occasionally elsewhere. should be investigated and reported promptly, as
stomatitis, vesicular all of the agents except Senecavirus A are exotic
exanthema, swine to the US.
vesicular disease,
Senecavirus A)
Vices and Tail, ear, or flank bite wounds. Moribund swine Numerous risk factors have been studied and
cannibalism often have red, linear bite marks. Sows may show confirmed to contribute to these conditions. In
vulvar bite wounds when housed in groups. particular, overcrowding, insufficient feed or
While all tend to occur sporadically on farms, waterer space, and lack of enrichment are thought
tail-biting can occasionally appear as an outbreak to be key risk factors to manage in preventing the
within a pen or barn. conditions.
TABLES

188 SKIN LESIONS: DIFFERENTIAL DIAGNOSIS

 TABLES

Vesiculating viral diseases

Foot-and-mouth disease, of primary concern, is exotic to the US. If it should be introduced to the US (or other areas currently
free of the disease), there would be significant immediate effects on trade, pig movements, and business continuity. Unfortu-
nately, vesicles produced by all of the diseases listed below, including Senecavirus A, are indistinguishable; therefore, any vesicle
occurrence should prompt urgent investigation. While most of the swine-oriented veterinary diagnostic laboratories in the US
are able to provisionally differentiate the diseases below, the obligation of producers and veterinarians is to report suspicious
vesicular lesions to the appropriate regulatory officials in their state.

Disease Family and genus of virus Other animals affected Comments

Foot-and-mouth disease Picornaviridae Most ruminants, wild US free of the disease.
Aphthovirus and domestic.
Senecavirus A Picornaviridae Swine only. Sporadic cause of vesicles that
Senecavirus A must be differentiated from
other vesiculating diseases. The
US and many other parts of the
world experienced a significant
reemergence of this disease since
about 2013.
Swine vesicular disease Picornaviridae Swine, occasionally humans. Never reported in the US, although
Enterovirus infrequent and sporadic cases occur
in Italy.
Vesicular exanthema and Caliciviridae Swine, sea lions, opal-eye Disease has not been seen since 1956,
San Miguel sea lion virus Calicivirus fish, several kinds of seals, although San Miguel sea lion virus is
and other marine animals. known to occur in marine animals off
the western US coast suggesting that a
threat of the disease remains.
Vesicular stomatitis Rhabdoviridae Cattle, horses, some wildlife, Endemic in parts of the southeastern
Vesiculovirus and humans. and southwestern US; disease
common in parts of Central and South
America. Periodic small outbreaks
occur annually in the US. Insect vector
is likely but poorly understood.

TABLES

VESICULATING VIRAL DISEASES 189

 SWINE DISEASE MANUAL

Zoonotic agents found in swine and humans

Producers and veterinarians have an important role in public health. A number of agents (many of which do not cause disease in
pigs) are carried by pigs and can be transmitted to people, be they farm staff, family members, veterinarians, abattoir workers, or
the general public. The table below provides an overview of the agents known to be zoonotic that are most common on farms.

Modes of transmission to humansd,e

OIE listed disease

Included in SDMb

Exotic to the US

Direct contact

Vector-borne

Food borne
Fomites
Aerosol
(2019)c

Oral
Agenta
Bacillus anthracis X X X X X X
Balantidium coli X
Brucella suis X X X
Burkholderia pseudomallei X X X X
Campylobacter species X X
Cryptosporidium suis X
Erysipelothrix rhusiopathiae X X1
Escherichia coli X X X X X
Francisella tularensis X X X X X
Giardia species X X
Hepatitis E virus X S S S S
Influenza A virus X X2
Japanese encephalitis virus X X X X
Leptospira interrogans X X X
Listeria monocytogenes X X
Menangle virus X X X
Methicillin-resistant Staphylococcus aureus (MRSA) S S
Microsporum species X X S
Mycobacterium species X X S S
Nipah virus X X X S X
Norwalk virus X X
Pasteurella multocida X S2 S1,2 S
Salmonella species X X X X
Sarcoystis suihominis X X
Streptococcus suis X X S
TABLES

190 ZOONOTIC AGENTS

 TABLES

Table cont’d. Zoonotic agents found in swine and humans

Modes of transmission to humansd,e

OIE listed disease

Included in SDMb

Exotic to the US

Direct contact

Vector-borne

Food borne
Fomites
Aerosol
(2019)c

Oral
Agenta
Taenia solium X X X
Toxoplasma gondii S S S X
Trichinella spiralis X X X
Trichophyton species X X S
Vesicular stomatitis virus X X
Yersinia enterocolitica X X X X X X

a All listed agents have the potential to infect and cause clinical disease in humans but not all are associated with clinical disease in swine.
b Agent has been described in this text, Swine Disease Manual, and is likely to be associated with clinical disease in swine.
c http://www.oie.int/animal-health-in-the-world/oie-listed-diseases-2019/. Published 2019. Accessed July 17, 2019.
d Adapted from Khan SU, Atanasova KR, Krueger WS, Ramirez A, Gray GC. Epidemiology, geographical distribution, and economic
consequences of swine zoonoses: a narrative review. Emerging Microbes & Infections, 2013 Dec; 2(12):e92.
e “X” indicates an established or primary route of transmission. “S” indicates a suspected route of transmission.
1 Requires damaged skin or mucosa
2 Droplets via close contact

TABLES

ZOONOTIC AGENTS 191

 192
TABLES
 INDEX

Index
A Aspergillus. See aflatoxicosis
acariasis. See mange astrovirus. See porcine astrovirus
Actinobacillus pleuropneumoniae (APP), 9-11, 12, 41, 44-45, atresia ani, 145, 149
147, 184t
atrophic rhinitis, 16-17, 44, 164, 183t
Actinobacillus suis, 9, 12-13, 26, 30, 40, 179t, 186t
Aujeszky’s disease. See pseudorabies
adenovirus. See porcine adenovirus
aural hematoma, 145, 186t
aflatoxicosis, 157
African swine fever (ASF), 63-64, 68, 107, 129, 181t B
Bacillus anthracis, 14-15, 190t
agalactia, 50, 148, 158
blue eye disease, 65-66
ammonia, 16-17, 45, 51, 163-164
bocavirus. See porcine bocavirus
anemia, 159
Bordetella bronchiseptica, 51. See also atrophic rhinitis
in association with
Brachyspira, 55-57, 141, 171t, 173-174t, 178t. See also swine
bovine viral diarrhea and border disease virus, 69
dysentery
copper toxicity, 161
Brucella suis, 53-54, 181t, 190t
gastric ulcer, 147
brucellosis. See Brucella suis
inclusion body rhinitis, 76
Bungowannah virus, 118
leptospirosis, 35-36
lice, 129, 186t C
calcium, 151, 152, 159, 160
Mycoplasma pneumonia, 41
carbadox, 162, 180t
Mycoplasma suis, 37-38, 179t,
carbon dioxide, 163, 164
porcine hemorrhagic enteropathy (PHE), 33
carbon monoxide, 163, 164
threadworm, 136
central nervous system (CNS) diseases, 169-170t
vitamin B12 deficiency, 160
chemical toxins, 163
anthelmintics, 167t, 175-176t. See also parasiticides circovirus. See porcine circovirus
anthrax, 14-15. See also Bacillus anthracis classical swine fever, 46, 67-69, 145, 169t, 181t, 187t
arsenic, 160 as a differential diagnosis, 10, 15, 26, 48, 63-64, 107
arsenicals, organic, 23, 55, 160, 170t Claviceps purpurea. See ergotism
arthritis Clostridium difficile. See diarrhea, clostridial
in neonatal and growing swine, 168t Clostridium perfringens, 107, 126, 136, 177t. See also diarrhea,
mycoplasmal, 39-40. See also Mycoplasma hyorhinis; clostridial
Mycoplasma hyosynoviae coccidiosis, 18, 125-126, 167t, 171t, 174t, 175t
ascariasis. See Ascaris suum as a differential diagnosis, 20, 23, 102, 107
Ascaris suum (roundworm), 137-138, 167t, 175t, 183t cocklebur poisoning, 162

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colibacillosis, 19-20, 21-24, 101-102, 107, 126, 172t. encephalitis

See also Escherichia coli
in association with
colitis, spirochetal, 55-57, 174t
African swine fever, 64
congenital tremors, 69, 119, 145, 153
bacterial meningitis, 169t
copper, 146, 150, 159-160
blue eye disease, 65-66
cysticercosis, 127-128, 175t. See also Taenia solium
classical swine fever, 68
cystitis, 145, 152
encephalomyocarditis virus, 70
Cystoisospora. See coccidiosis
Haemophilus parasuis, 29
D hemagglutinating encephalomyelitis (HEV), 75, 169t
Demodex. See mange, demodectic pneumonic pasteurellosis, 44
deoxynivalenol, 158 porcine adenovirus, 119
dermatosis vegetans, 110, 145, 186t porcine bocavirus, 120
diamond skin disease, See erysipelas porcine picornavirus, 90
diarrhea, 171t, 172-174t porcine reproductive and respiratory syndrome (PRRS), 94
clostridial, 18-20, 171t, 172-173t pseudorabies, 99, 185t
porcine epidemic, 96, 105-107. See also swine enteric rabies, 152
coronavirus diseases
salt poisoning, 170t
post-weaning, See colibacillosis
Streptococcus suis, 50-52
rotavirus, 101-102
Japanese, 81-82, 121, 169t, 181t, 190t
transmissible gastroenteritis, 23, 96-97, 105-107, 119.
See also swine enteric coronavirus diseases encephalomyocarditis virus, 70-71, 88, 89t
differential diagnosis endometritis. See metritis
central nervous system, 169t enterotoxemia, 18, 21, 148
diarrheal diseases, 171t, 172-174t enterovirus(es), 70, 88-91, 89t, 108, 170t, 189t
intestinal hemorrhage, 177-178t Enterovirus, 88, 89t, 108
reproductive failure, 180-182t Eperythrozoon suis (eperythrozoonosis) - archaic,
See Mycoplasma suis
respiratory disease, 183-185t
epitheliogenesis imperfecta, 146
skin lesions, 186-188t
ergotism, 148, 158
dysentery. See swine dysentery
erysipelas, 25-26, 168t, 181t
E as a differential diagnosis, 12, 15, 48, 68, 179t, 186t
ear biting, 154
Erysipelothix rhusiopathiae, 25-26, 40, 190t. See also erysipelas
Ebola virus, 117
Escherichia coli (E coli), 21-24, 47-48, 136, 148, 149, 154,
ectopic ossification, 146 169t, 171t, 172t, 190t, See also colibacillosis
edema disease, 154, 169t, See also colibacillosis exudative epidermitis, 27-28, 110, 132, 153, 160, 186t
Eimeria. See coccidiosis

Locators in boldface indicate main discussions. Those followed by t indicate tables.

194 INDEX
 INDEX

F I
F-2 toxin. See zearalenone ileitis, 32-34, 48, 56, 107, 148. See also Lawsonia
intracellularis
farrowing rate, low, 180t
inclusion body rhinitis, 17, 51, 76-77, 183t
feed additives, 162-163, 180t
influenza (IAV-S), 78-80, 87, 118, 130, 181t, 183t, 185t, 190t
filoviruses, 117
as a concurrent infection, 10, 29-30, 41-43, 44-45, 51
flank biting, 154
in association with gastric ulcers, 146-147
foot-and-mouth disease, 72-73, 88, 89t, 188t, 189t
insecticides, 110, 129, 163
as a differential diagnosis, 88, 103, 108, 111, 112-113,
internal parasites, 175-176t
fumonisin toxicosis, 158
intestinal hemorrhage, 177-178t
Fusarium, 158
intestinal nematodes, 134-136
G iodine, 28, 46, 50, 65, 70, 98
gastric ulcer, 33-34, 56, 79, 146-147, 148, 177t
iodine deficiency, 159
Glaesserella parasuis. See Haemophilus parasuis
ionophores, 162-163
Glasser’s disease, 29-31, 68, 168t. See also Haemophilus
iron
parasuis (HPS)
deficiency, 38, 159
goiter. See iodine deficiency
toxicity, 150, 159, 161
gossypol, 162
Isospora. See coccidiosis
greasy pig disease, 27-28. See also exudative epidermitis
J
H Japanese encephalitis, 81-82, 121, 169t, 181t, 190t
Haematopinus suis. See lice
Haemophilus parasuis (HPS), 23, 29-31, 40, 168t, 169t, 179t. K
See also Glässer’s disease kidney worm, 134, 175t
Haemophilus pleuropneumoniae. See Actinobacillus Kunjin virus (West Nile virus), 121
pleuropneumoniae
L
hemagglutinating encephalomyelitis, 74-75, 105, 107, 169t La Piedad Michoacan virus. See blue eye disease
hematoma, aural (ear), 145, 186t Lawsonia intracellularis, 32-34, 171t, 174t, 178t.
hemorrhage, intestinal, 177-178t See also ileitis
hemorrhagic bowel syndrome, 33, 146, 154, 177t lead, 161
hepatitis E virus, 117, 190t Leptospira (leptospirosis), 35-36, 181t, 190t
hernias, 148 lice, 27, 37, 110, 129, 145, 163, 167t, 186t
herpesvirus. See pseudorabies; inclusion body rhinitis lungworm, 130-131, 136, 167t, 175t, 183t
hog cholera. See classical swine fever
M
hydrogen sulfide, 163-164 Macracanthorynchus hirudinaceus. See thorny-headed worm
hydronephrosis, 148 mange, 132-133, 153, 163, 167t, 186t
hypogalactia, 148-149 as a differential diagnosis, 129, 145, 160
hypoglycemia, 149, 162 demodectic, 132
Locators in boldface indicate main discussions. Those followed by t indicate tables.
SWINE DISEASE MANUAL 195
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Marburg virus, 117 osteochondrosis, 40, 151, 179t

mastitis, 21, 148-149 osteoporosis, 160
megacolon, 145, 149
P
Menangle virus, 65, 118, 190t parainfluenza virus. See porcine parainfluenza virus
mercury toxicity, 161, 163 parakeratosis, 132, 147, 159-160. See also zinc
Metastrongylus. See lungworm paramyxovirus, 65, 118, 120, 169t
methane, 163 parasites, internal, 175-176t
metritis (endometritis), 53, 94, 99, 148-149 parasiticides, 129, 130, 133, 134, 162, 167t. See also
Microsporum nanum. See ringworm anthelminitics

minerals, 159-161, 170t, 180t pars esophagea, 86, 146-147, 177t

MMA (mastitis, metritis, agalactia), 148-149 parvovirus, 26, 27, 83-84, 86, 88, 90, 119, 181t

mulberry heart disease, 71, 149-150. See also selenium; Pasteurella multocida, 41-42, 44-45, 51, 164, 183t, 184t, 190t.
vitamin E See also atrophic rhinitis; pasteurellosis

Mycobacterium, 58-59, 190t pasteurellosis, 10, 44-45, 184t. See also atrophic rhinitis;
Pasteurella multocida
Mycoplasma hyopneumoniae, 10, 39, 41-43, 44-45, 51, 87,
179t, 184t pediculosis. See lice
Penicillium. See aflatoxicosis
Mycoplasma hyorhinis (MHR), 30, 39-40, 41, 154, 168t, 179t
pestivirus, 67, 69, 118, 145, 153
Mycoplasma hyosynoviae (MHS), 39-40, 41, 168t, 179t
phosphorus, 152, 160
Mycoplasma-related diseases, 179t
photosensitization, 132, 153-154, 187t
Mycoplasma suis, 37-38, 41, 129, 160, 175t, 179t
picornavirus, 70, 108, 170t. See also porcine picornavirus
mycotoxicosis, 157-158
pigweed poisoning, 162
mystery pig disease. See porcine reproductive and respiratory
syndrome (PRRS) pityriasis rosea, 27, 110, 129, 132, 151, 153, 187t
pneumonia
N
navel sucking, 148, 154 mycoplasmal (enzootic), 10, 41-43, 44, 179t, 184t.
See also Mycoplasma hyopneumoniae
nematode, 130, 138
pneumonic pasteurellosis. See pasteurellosis
nematodes, minor intestinal, 134-136
porcine adenovirus, 119
nightshade, 162
porcine astrovirus, 84, 119, 170t
Nipah virus, 65, 118, 190t
porcine bocavirus, 83, 119-120
nodular worm, 134-135, 141, 167t
porcine circovirus (PCV), 34, 85-87, 146, 147
nutritional deficiencies, excesses, 27, 90, 151, 154, 159-161
associated disease (PCVAD), 34, 38, 85-87, 120, 169t, 181t
O type 2 (PCV2), 30, 34, 40, 41, 84, 85-87, 119, 146, 147,
Oesophagostomum. See nodular worm 181t, 187t
organophosphate(s), 163, 169t, 170t type 3 (PCV3), 84, 85-87, 181t, 187t
Ornithodorus porcinus porcinus, 63 porcine cytomegalovirus. See inclusion body rhinitis

Locators in boldface indicate main discussions. Those followed by t indicate tables.

196 INDEX
 INDEX

porcine deltacoronavirus. See swine enteric coronavirus ringworm, 27-28, 152-153, 187t, 190-191t
diseases
rodenticides, 163
porcine dermatitis and nephropathy syndrome (PDNS), 187t.
rotavirus, 22, 48, 101-102, 119, 126, 171t, 172t
See also porcine circovirus associated disease
as a differential diagnosis, 23, 107, 136
porcine epidemic diarrhea (PED), 96, 105-107. See also
swine enteric coronavirus diseases roundworm, 137-138, 167t. See also Ascaris suum
porcine parainfluenza virus, 120
S
porcine paramyxovirus. See blue eye disease; paramyxovirus Salmonella, 12, 46-49, 141, 148, 154, 169t, 171t, 173t, 177t,
181t, 191t. See also salmonellosis
porcine parvovirus. See parvovirus
salmonellosis, 46-49, 56, 101, 102, 142, 152, 171t, 177t. See
porcine picornavirus, 88-91, 89t
also Salmonella
porcine pleuropneumonia, See Actinobacillus
as a differential diagnosis, 10, 26, 33-34, 38, 56, 68, 107, 147
pleuropneumoniae
salt poisoning. See sodium ion intoxication
porcine reproductive and respiratory syndrome (PRRS), 70,
83, 92-95, 117, 169t, 182t, 185t, 187t San Miguel sea lion disease, 111, 189t. See also vesicular
exanthema
as a concurrent infection, 10, 30, 40, 41, 44, 51
Sapelovirus, 84, 88-91, 89t, 170t
as a differential diagnosis, 17, 87
sapovirus. See porcine sapovirus
porcine respiratory coronavirus, 96-97, 105, 172t
Sarcoptes. See mange
porcine rubulavirus. See blue eye disease
scabies. See mange
porcine sapovirus, 120
selenium, 149-150, 159, 161, 170t
porcine stress syndrome, 151, 153
Seneca Valley virus. See Senecavirus A
pork measles. See cysticercosis; Taenia solium
Senecavirus A, 88, 89t, 103-104, 188t, 189t
pork worm. See Trichinella spiralis
shoulder ulcers, 153
postweaning multisystemic wasting syndrome (PMWS).
See porcine circovirus associated disease skin lesions, 186-188t
prolapse, 149, 152, 158 skin necrosis, 153, 187t
PRRS. See porcine reproductive and respiratory syndrome SMEDI, 83-84, 88-90. See also parvovirus
pseudorabies, 17, 23, 51, 66, 98-100, 170t, 182t, 185t sodium ion intoxication, 161, 170t
pustular dermatitis, 28, 152, 187t. See also Streptococcus spirochetal colitis, See swine dysentery
pyelonephritis, 145 splayleg, 145, 153
spraddleleg. See splayleg
R
rabies, 152, 169t Staphylococcus hyicus, See exudative epidermitis; greasy pig
disease
ractopamine, 163
Stephanurus dentatus. See kidney worm
reproductive failure, 181-182t
Streptococcus, 152, 153, 168t, 169t, 187t. See also pustular
rhinitis, 29, 30, 51, 94, 99, 185. See also atrophic rhinitis;
dermatitis
inclusion body rhinitis
Streptococcus suis, 23, 26, 30, 40, 50-52, 93, 168t, 169t,
rickets, 160
179t, 191t

Locators in boldface indicate main discussions. Those followed by t indicate tables.

SWINE DISEASE MANUAL 197
SWINE DISEASE MANUAL

Strongyloides, 23, 126. See also threadworm U

suid herpesvirus 1. See pseudorabies ulcers

sulfonamides, 25, 153, 163 button, 48, 68, 173t

sunburn, 132, 153-154, 187t gastric, 33-34, 56, 79, 146-147, 148, 177t

swine dysentery, 34, 55-57, 160, 162, 171t, 173-174t, 178t shoulder, 153

as a differential diagnosis, 33-34, 48, 107, 141-142, 147 V

swine enteric coronavirus diseases, 101, 105-107, 126, 171t, ventilation failure, 163-164
172t. See also transmissible gastroenteritis (TGE); porcine vesicular exanthema, 88, 103, 111, 188t, 189t
epidemic diarrhea (PED); porcine deltacoronavirus
(PDCoV) vesicular stomatitis, 103, 112-113, 188t, 189t, 191t

swine vesicular disease, 88, 89t, 103, 108-109, 188t, 189t vesiculating viral diseases, 189

swinepox, 110, 129, 188t vestibular syndrome, 51, 154

vices, 154, 188t
T
T-2 toxin, 158 vitamin deficiencies, 160

Taenia solium, 127-128, 175t, 191t vitamin D, 160, 163

tail biting, 139, 154, 188t vitamin E, 146, 149-150, 159, 161

Talfan disease, 88-91, 170t vitamin K, 147, 160, 163, 178t

Teschen disease, 88-91, 170t vitamins, 27, 150, 160, 170t, 180t

thorny-headed worm, 135, 167t, 176t volvulus, 146, 148, 154, 177t

threadworm, 135-136, 167t, 176t. See also Strongyloides vomiting and wasting disease. See hemagglutinating
encephalomyelitis
Torque teno virus, 121
vomitoxin, 158
torsion, 148, 154, 177t
transmissible gastroenteritis (TGE), 23, 96-97, 105-107, 119. W
See also swine enteric coronavirus water deprivation. See sodium ion intoxication

tremors, congenital, 69, 119, 145, 153 West Nile virus, 81, 121

Trichinella spiralis, 139-140, 176t, 191t whipworm, 33, 48, 56, 141-142, 147, 167t, 171t, 174t, 176t

trichinellosis, 139-140. See also Trichinella spiralis Z

trichinosis. See Trichinella spiralis zearalenone, 152, 158, 180t

Trichophyton verrucosum. See ringworm zinc, 24, 27, 146, 159-161. See also parakeratosis

trichothecene, 158 zoonotic agents, 190-191t

Trichuris suis. See whipworm

Trueperella, 153, 168t, 169t, 181t,
tuberculosis, 58-59. See also Mycobacterium

Locators in boldface indicate main discussions. Those followed by t indicate tables.

198 INDEX