Swine Digestive Diseases Guide

VMED 5335- SWINE MEDICINE
Diseases of the Digestive System
MODULE 4
DISEASES OF THE DIGESTIVE SYSTEM
Overview
In this module, you will learn the etiology, clinical signs, diagnosis,
differential diagnosis, treatment, prevention and control of different
diseases of the digestive system of swine.
Objectives:
Upon completion of this module, you are expected to:
1. Differentiate swine diseases affecting the digestive system
2. Identify diagnostic methods and interpret results for accurate
disease diagnosis
3. Identify appropriate drugs or medications and therapy for
specific disease conditions
4. Discuss control and prevention of different swine diseases
Note: You may scan the QR codes and click the colored words for further information
TRANSMISSIBLE GASTROENTERITIS
“TGEV, Porcine Transmissible Gastroenteritis Virus, Transmissible Gastroenteritis Virus,
Porcine Transmissible Gastroenteritis Coronavirus”
One of the most significant diarrhea-producing diseases in young pigs that causes
vomiting and profuse diarrhea in pigs of all ages.
Etiology and Epidemiology

▪ The causative agent of the disease, TGE virus (TGEV) is a member of the genus
Coronavirus, family Coronaviridae. It infects and destroy the villous epithelial cells
of the jejenum and ileum, which results in severe villous atrophy, malabsorption,
osmotic diarrhea, and dehydration.
▪ TGEV is very stable when stored frozen, but labile at room temperature or above.
Furthermore, it is vulnerable to sunlight, drying and various disinfectants such
as sodium hypochrolite or iodines. The virus is resistant to acid allowing it
to pass through the stomach and infect the small intestine.
▪ Coronaviruses take their name from the halo-like array of envelope proteins that
surround the capsid. These are visible in a TEM negative stain as spiky processes
forming a ‘crown’ around the RNA core.
▪ TGE occurs in many major swine-raising countries, but in the Philippines, it is
considered as an Exotic disease. It can affect all ages of pigs but young pigs are
Lygene Harmony C. Culimay, DVM

Department of Veterinary Clinical Sciences
CVSM, Central Luzon State University
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the most susceptible. The incubation period is ~18 hours with a high morbidity at
pigs under 2-3 weeks of age that tend to show severe diarrhea and rapid
dehydration, and often result in death, and mortality rate is usually less than 10-
20%.
▪ Severe epidemics of the disease is more common during winter due to survival of
the virus in colder temperatures.
Clinical Signs and Lesions

▪ In acute outbreaks, the incubation period is very short, 18 hrs to three days. In
baby pigs the disease spreads rapidly to affect all susceptible pigs
▪ Vomiting is the initial sign seen followed by profuse watery diarrhea,
dehydration, and excessive thirst.
▪ In piglets, feces of nursing pigs often contain curds of undigested milk. Acute
watery diarrhea, wet and dirty hairy appearance of all the litter due to the profuse
diarrhea, and severe dehydration and thirst are also seen.
▪ Almost 100% mortality is seen within 2 to 3 days in piglets under 7 days of age
due to severe dehydration and electrolyte imbalance. There is no response to
antibiotic therapy.
▪ For weaners and growers, mortality is usually low and the disease disappears
spontaneously over a 3 to 5-week period. The clinical signs seen are vomiting and
a watery diarrhea, and dehydration which is resolved in about a week.
▪ When it comes to sow, there’s vomiting, diarrhea, inappetence and usually recover
over a 5 to 7-day period, and agalactia.
▪ Lesions seen in a dying piglet are severely dehydrated skin which is sometimes
soiled in liquid feces, distension of the small intestine with foamy, yellow,
odoriferous fluid and scattered milk curds, and intestinal wall is very thin and nearly
transparent. The stomach may be empty because of vomiting but sometimes is
filled with curdled milk. There often are yellow or gray urates on the renal papillae.
Watery colonic contents, often with undigested milk curd, usually have an acidic
pH.
▪ Older pigs have few remarkable lesions except that the colon contains liquid rather
than formed feces. Microscopically, there’s a marked villous atrophy, perhaps with
squamous metaplasia of epithelium, and elongation of crypts in scattered areas of
the jejunum and ileum.
Differential Diagnosis
• Colibacillosis
• Rotaviral enteritis
• Strongyloides infection
• Coccidiosis
• Porcine epidemic diarrhea
Diagnosis
▪ A presumptive diagnosis of TGE may be made on the basis of clinical signs but
laboratory diagnosis must be accomplished.

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▪ Virus Isolation, FAT, RT-PCR, ELISA, Immunofluorescence,

Immunohistochemistry, Electron Microscopy
Treatment, Control and Prevention

▪ The only available treatment for TGE is to alleviate starvation, dehydration, and
acidosis. Parenteral treatment with fluids, electrolytes, and nutrients are effective
in treating young pigs, but not practical under farm conditions.
▪ Administration of swine immunoglobulin has been also reported to be beneficial.
▪ After a TGE outbreak, at least 4weeks should elapse from the last sign of disease
before introducing such animals into a “clean” herd.
▪ Feedback methods for sows due to farrow in at least 2 weeks to orally expose
them to virulent autogenous virus, such as a slurry of minced intestines of acutely
infected pigs, so that they will be immune at farrowing. If the sows will farrow in
under 2 weeks, attempt to provide facilities and management procedures to avoid
exposure to TGEV until at least 3 weeks post farrowing.

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PORCINE EPIDEMIC DIARRHEA

A coronaviral disease affecting pigs of all ages which causes diarrhea
similar to Transmissible Gastroenteritis (TGE) except that it is much
less severe and with lesser mortality. PED is not a listed disease for
either the World Organization for Animal Health (OIE) or the USDA, so
no quarantines or movement restrictions are in place either
internationally or interstate.

▪ Porcine epidemic diarrhea virus is a coronavirus most closely related to TGE virus.
It is a single stranded, positive-sense RNA of the group 1 Coronavirus, family
Coronaviridae, with a diameter averaging 130 nm. It contains a centrally located
electron-opaque body and club-shaped projections of 18 to 23 nm, but the internal
structure is not yet known.
▪ PED is sensitive to ether and chloroform and loses its infectivity when heated
to or above 60˚C. It is reported to be susceptible to formalin (1%), anhydrous
sodium carbonate (4%), lipid solvents, iodophores in phosphoric acid (1%),
and sodium hydroxide (2%).
▪ The virus persists in consecutive litters of pigs after weaning and after they lose
their immunity from antibody in the milk.
▪ Porcine Epidemic Diarrhea has been found to only affect swine species of any
ages, causing diarrhea. It has been found in mice but mice are specifically
demonstrated to be non-competent vectors. The incubation period of the disease
is longer than TGE, 3-4 days, and if the affected swine recover, it is usually within
7 to 10 days.
▪ The disease is worldwide in distribution but most cases have been found in
European countries and in China. A large epidemic occurred in Europe in 1969. It
was first reported as a clinical entity in England in 1971 and was determined to be
a separate entity from porcine TGE in 1977. In the Philippines, the disease is
considered an emerging one.
▪ Spread of virus mainly occur through infected pigs and indirectly through virus-
contaminated fomites and via transport trucks. Feco-oral route is also an important
means of transmitting the disease within the herd since large amount of virus
particles are shed in the feces. Airborne transmission via fecal-nasal route has also
been noted.
▪ The morbidity may reach 100% but mortality is low. The disease may start in the
finishing pigs and spread rapidly to pregnant sows and their nursing piglets. It is
expected that the survivability and transmission of the virus will be enhanced in cold
weather.

▪ Diarrhea is the only direct virus-induced clinical sign observed. The diarrhea may
persist in the 6 to 10-week-old pigs and seronegative gilts introduced into the herd
may become infected and develop a profuse diarrhea which lasts a few days.
There are two considered forms of the disease. PED types I and II. Porcine

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Epidemic Diarrhea I causes diarrhea only in pigs 4-5 weeks of age, while
Porcine Epidemic Diarrhea II causes diarrhea in pigs of all ages.
▪ An acute outbreak on a susceptible breeding farm resembles TGE and is
characterized by watery diarrhea of pigs in all ages which may be flocculent
and fetid. Vomiting may occur. Dehydration and metabolic acidosis may be
secondary signs. Unlike TGE, the disease within the farm spreads more slowly.
Moreover, in all outbreaks, signs are most consistently seen in feeders, finishers,
and adult, which appear to be the most susceptible because outbreaks often
start in these age groups. Older pigs are more lethargic and depressed, and sick
pigs appear to have colic.
▪ Macroscopic and microscopic lesions of the disease are confined only in the small
intestine, particularly villous shortening or villous atrophy which is the main
characteristic of the disease.
▪ Acute back muscle necrosis may also occur but is not pathognomonic. At the
cellular level, PED protein E becomes localized in the endoplasmic reticulum with
small amounts being found in the nucleus of infected cells.
▪ Transmissible Gastroenteritis (TGE)
▪ TGE in its typical epidemic form causes a rapidly spreading diarrhea in animal of
all ages with high mortality in neonates, whereas PED spreads at slower rate, and
even if there’s diarrhea seen in the litters, other litter may survive and remain
healthy even in the absence of immunity.
▪ Colibacillosis
▪ Rotaviral enteritis
▪ Strongyloides infection
▪ Coccidiosis
Diagnosis
▪ direct immunofluorescence on cryostat sections of small intestine or colon,
▪ ELISA to detect viral antigens in feces or intestinal contents particularly in adult
pigs
▪ PCR
Treatment. Control and Prevention

▪ There’s no specific treatment for the disease and vaccines have not also been
documented. Crossprotection with between TGE and PEDV has not been found
even though both are Coronaviruses. Maternal protection through colostrum from
previously exposed sows can be quite effective but it is not long lasting and herds
can re-break.
▪ In order to control and prevent the disease, strict biosecurity should be
implemented in the farm, as well as quarantine. In case of an outbreak, pigs with
diarrhea should have free access to clean water and finishing pigs should have
withheld feed for 1-2 days.

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ROTAVIRAL DIARRHEA
Rotaviruses cause diarrhea in nursing and postweaned pigs, affecting
primarily the small intestine. If uncomplicated, diarrhea is accompanied
by high morbidity and low mortality.

There are at least 7 antigenically distinct serogroups of rotaviruses (A,
B, C, D, E, F, G) of which 4 (A, B, C, E) affect swine. Group A is by far
the most prevalent but type C has been associated with outbreaks. Immunity is not
cross-protective between serogroups and is incomplete between serovarieties.
Rotaviruses are very stable in the environment. They are resistant to temperature
changes, many chemicals, various pH levels, and many disinfectants. Rotavirus groups
A, B, and C are associated with diarrhea in piglets worldwide. They are easily
transmitted by direct contact. Healthy carrier sows may shed rotavirus in their feces during
the periparturient period, thereby exposing their litters to infection. Recently weaned pigs
are commonly exposed to rotaviruses that persist in nursery facilities and in other carrier
pigs during commingling.
Clinicals signs and Lesions
▪ The onset and severity of signs depends on dose ingested and amount of
protective antibody in the dam’s colostrum and milk. If neonatal pigs do not receive
protective levels of maternal antibody, they are likely to develop profuse watery
diarrhea in 12–48 hours. Diarrhea often begins in pigs 5 days to 3 weeks old
or immediately after weaning. The feces of nursing pigs are typically yellow or
gray and pasty in the early stages, and they progress to gray and pasty after ~2
days. Diarrhea commonly persists for 2–5 days. 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.
▪ There is moderate dehydration, affected pigs become gaunt and rough-
haired. Weaned pigs may have watery feces that contain poorly digested feed.
Vomiting occurs but is not a major clinical sign. Morbidity is variable but mortality
usually is low or none when good housing and husbandry is present. Signs,
morbidity and mortality are enhanced if there is concurrent disease, poor
husbandry or exposure to cold.
▪ The small intestine appears variably thin-walled, and the cecum and colon contain
watery feces. Microscopically, there is segmental villous atrophy.
Diagnosis
▪ Detection of rotavirus by PCR assay in feces sample
▪ Histopathologic evaluation- villous atrophy in the jejunum or ileum
▪ Electron Microscopy – direct examination of feces to identify rotaviral particles
▪ Fluorescent Antibody Technique
▪ Immunohistochemistry- demonstration of rotavirus in the epithelial cells
▪ ELISA- detection of rotaviral antigens in fresh fecal samples or intestinal fluid

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* Virus shedding is much greater during early stages of the disease so samples
should be obtained from acutely affected pigs.
▪ Coronaviral Enteritis
▪ Colibacillosis
▪ Cystoisospora suis enteritis

▪ Good husbandry and supportive therapy, electrolytes in water
▪ A dry, warm environment and good nutrition are important in reducing severity of
outbreaks
▪ Antibiotics may be indicated for secondary or concurrent bacterial diseases
such as enterotoxigenic E. coli
▪ Vaccination for group A rotavirus
▪ Feedback programs- intentional exposure of gilts and sows to feces from affected
piglets may be of benefit in increasing lactogenic immunity.
▪ all in/all out system with thorough cleaning and disinfection between farrowings
and a high standard of sanitation reduces exposure of piglets to rotavirus.
▪ all in/all out population of nurseries will decrease the dose and lessen the effects
of rotavirus infections postweaning
▪ Recommended disinfectants for cleaned surfaces include formaldehyde and
chlorine-based disinfectants including chlorox.

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COLIBACILLOSIS
“E. coli diarrhea, Baby pig scours, White scours, Enteric Colibacillosis,
Colibacteriosis, Colitoxemia, Gut Edema of Swine, Diarrhea neonatorum,
Diarrhea of baby pigs”
It is a common disease of nursing and weanling pigs caused by
colonization of the small intestine by enterotoxigenic strains of E. coli. It is
a term generally used to indicate an acute, often fatal enteritis and
gastroenteritis, usually of suckling pigs (new-born and recently weaned
piglets) and characterized by a yellowish white, watery diarrhea
accompanied by toxemia or septicemia.

▪ Escherichia coli are gram‐negative, peritrichously flagellated bacilli. The most
pathogenic strains form smooth to mucoid colonies, and some are beta-hemolytic.
Its virulence factors are fimbria, enterotoxins, endotoxin and capsule. The
common antigenic types of fimbriae associated with pathogenicity are F4 (K88),
F5 (K99), F6 (987P), F41 associated with neonatal colibacillosis, and F18 and F4
in postweaning colibacillosis. There is also a genetic susceptibility component,
because not all pigs express receptors for all fimbrial adhesins. The toxins
elaborated by pathogenic E. coli in swine (ETEC) are labile toxin (LT), stable
toxin A (StA), stable toxin B (StB), that act locally to induce fluid and electrolyte
secretion into the intestinal lumen, resulting in diarrhea, dehydration, and
metabolic acidosis, and Verotoxin (shiga-like toxin, SLT) which is responsible for
the systemic vascular effects of edema disease.
▪ Other strains of E. coli are Enterohemorrhagic E. coli (EHEC), Enteroinvasive E.
coli (EIEC), and Enteropathogenic E. coli (EPEC).
▪ The young pigs acquire the organisms by mouth or through the nasopharynx by
inhalation and swallowing it. Potentially pathogenic E. coli are present in the
intestinal tract and feces of many normal swine and dams often act as carrier. E.
coli organisms contaminate the skin and mammary glands of dams and are
ingested by nursing piglets. Pathogenic coliforms are magnified by fecal shedding
to further increase exposure of littermates. These pathogenic coliforms survive in
contaminated buildings and can infect successive litters of pigs. Once present, E.
coli tend to persist unless vigorous efforts are given to maintaining sanitation,
husbandry, and environment.
▪ Disease occurrence and severity is related to dose ingested and the level of
immunity derived from colostral immunity. Piglets with little colostral or inherent
immunity get sick first.

▪ Profuse watery diarrhea with rapid dehydration , acidosis, and death
▪ Affected piglets has a wet straight tail, stunted growth and subnormal temperature.
▪ The hair coat becomes rough, the pigs become dehydrated and have an
emaciated appearance before death
▪ Neonatal diarrhea may first be observed 2-3 hours after birth and may affect single
pigs or whole litters. Mortality may be very high in the first few days of life.
Diarrhea may be very mild with no evidence of dehydration or may be clear and
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watery. The feces vary in color from clear to yellowish-whitish or various

shades of brown. Sick pigs occasionally vomit.
▪ Diarrhea in pigs from the neonatal to the postweaning period is similar to that
observed in neonatal piglets but tends to be less severe and mortality is invariably
lower. The feces vary from grayish to whitish in unweaned piglets to brownish in
recently weaned piglet.
▪ Gross lesions: dehydration, dilation of the stomach which may contain undigested
milk curd or feed, venous infarcts on the greater curvature of the stomach, and
dilation of the small intestine with some congestion of the small intestinal wall. In
cases of ETEC infection complicated by shock, characteristic lesions include
marked congestion of the small-intestinal and stomach walls and blood-
tinged intestinal contents
▪ Histologic lesions: In ETEC infections, layers of E. coli are observed adhering to
the mucosal epithelial cells of most of the jejunum and ileum in the case of F4-
positive ETEC isolates, and of the posterior jejunum and/or the ileum in the case
of other ETEC isolates. Adhering bacteria may be found only in the crypts of
Lieberkühn, or more often covering the crypts and the tips of the villi. Vascular
congestion in the lamina propria with some hemorrhages into the intestinal lumen,
increased numbers of neutrophils and macrophages in the lamina propria and
migrating into the lumen, and some villous atrophy may be observed
Diagnosis
▪ Clinical signs are useful but not definitive
▪ Slide Agglutination Test
▪ Confirmation via culture with or without genotyping
▪ Histopathologic evaluation - observation of coliform colonization of small-intestinal
brush borders and isolation of the organism from the small intestine
▪ PCR
▪ Transmissible Gastroenteritis
▪ Rotaviral Infection
▪ Coccidiosis
▪ Strongyloides parasitism
▪ Antimicrobial treatment based on results of minimum inhibitory concentration

testing/ antibiotic sensitivity. Ciprofloxacin or Trimethoprim-sulfa has been
proven to be the most effective since it inhibits the secretory effect of enterotoxin.
Other drugs with the same action that are also proven effective are Ampicillin,
Amoxicillin, Streptomycin, Gentamycin.
▪ restoration of fluid and electrolyte balance is also necessary for a better recovery
▪ Control and prevention include reduction of predisposing factors, improving
sanitation, vaccination with Pilus-specific vaccine, and control of flies, etc.

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- breeding stock should be obtained from a single source with no problems

of colibacillosis.
- Dams should be acclimatized together for 3-6 weeks prior to breeding and
during gestation so they can develop immunity to endemically occurring
pathogens
- Pregnant dams often are vaccinated twice at 2–3-week intervals prior to
farrowing
- Use of the all in/all out system of raising piglets is recommended.
- Farrowing should occur in a facility thoroughly cleaned, disinfected, and
dried between farrowing
- Improve environment (ventilation, sanitation, control humidity).

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SWINE ILEITIS
Porcine Enteropathy, Porcine Proliferative Enteritis, Porcine Intestinal
Adenomatosis, Proliferative Hemorrhagic Enteropathy, Garden-hose
gut disease
It is a common diarrheal disease of growing-finishing and young

breeding pigs characterized by hyperplasia and inflammation of the
ileum and colon

▪ The causative agent is Lawsonia intracellularis which is an intracellular, bent, rod-
shaped, gram-negative bacteria that is related to certain anaerobic, sulfate-
reducing bacteria, Bilophila wadsworthia. This bacteria is known to cause intestinal
epithelial cell hyperplasia. The bacteria is also comma-shaped in appearance,
resembling Campylobacter.
▪ The disease occurs wordwide and is considered as one of the major causes of
mortality in swine. All ages of pigs are susceptible to the disease, but it is more
frequently seen in growers and finishers and young breeding pigs.
▪ Affected pigs are the source of infection since pigs can shed the organism for up
to 12 weeks after clinical signs have abated. In addition, boars and adult pigs act
as carriers which can transfer the infection to piglets, thus maintaining the cycle of
infection. The following are the means of transmission of ileitis:
1. Feco-oral route. Infected feces serve as the major vehicle for
movement of the organism around the farm and those herds that have
persistent problems are likely to have poor management of feces, dirty
pens and passages and heavily contaminated floor surfaces
2. Indirect transmission is also possible through contaminated fomites.
There are 4 recognized forms of the disease: Porcine Intestinal

Adenomatosis (PIA), Necrotic Enteritis (NE), Regional Ileitis (RI) and
Proliferative Hemorrhagic Enteropathy (PHE).
▪ Porcine intestinal Adenomatosis (PIA) is described as an abnormal

proliferation of the cells that line the intestines. It is more commonly seen in
weaned pigs (6-12 weeks old). Signs associated with this form are chronic
diarrhea, gradual wasting and loss of condition, followed in some cases by a
potbellied appearance. As a consequence, there can be marked variations in
sizes of pigs. There’s a characteristic thickening of the wall of the intestine due to
the proliferation of the cells. Moreover, the mesentery may be edematous and the
mesenteric lymph nodes are enlarged.
▪ Necrotic enteritis (NE) is where the proliferated cells of the small intestine die
and slough off (necrosis) with a gross thickening of the small intestine (hosepipe
gut). Signs are similar to PIA, however an acute form of NE manifested by bloody

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gut, quite similar to PHE, and the pig may die suddenly or appear very pale and
anemic and pass black bloody feces. The intestinal mucosa that appears
thickened became rugose which may be covered by a brownish or yellow
fibrinonecrotic membrane, and sometimes with petechial hemorrhages. The
yellow necrotic casts may be found in the ileum or passing through the colon.
▪ Regional Ileitis is the inflammation of the terminal part of small intestine. Signs
are also similar to PIA and it include anorexia and wasting. its main feature is the
rigidity of the affected bowel due to muscular hypertrophy and inflammatory
changes in the submucosa and lamina propria. In addition, the diffuse complete
mucosal necrosis after NE, going to a chronic case, also causes the intestine to
be rigid, resembling a garden hose
▪ Proliferative hemorrhagic enteropathy (PHE) is an illness of shorter duration
wherein there is massive bleeding into the small intestine, hence the common
name bloody gut. Signs include bloody scour, the pig may die suddenly, or it
appears very pale, anemic and passes black bloody feces. It commonly occurs in
pigs 16 weeks old upward. PHE is characterized by profusely hemorrhagic form,
with red or black, tarry feces. The main feature of PHE is the presence of clotted
blood in the intestinal lumen, often in the form of a cast with clotted fibrin and
necrotic tissue. The clots are commonly seen in the terminal ileum, mucosa of
which is thickened and adenomatous. PHE is the most acute of the four forms of
ileitis.
▪ Microscopically, the thickening of the ileal and/or large intestinal mucosa is
attributed to epithelial proliferation that resulted from the development of long
crypts lined with elongated epithelial cells.
Diagnosis
▪ Histopathology- strong association between thickening and disease

▪ Immunohistochemistry- tissues sample
o Positive: Bacteria is present at site of lesion
o Negative: Negative or infection is too early (slow growing bacteria) or too
late after infection
▪ ELISA : serum
o Positive: Past exposure (> 2-4 weeks) to vaccine or wildtype bacteria
o Negative:
o Negative to vaccine or wildtype bacteria
o Infection too early to detect (slow growing bacteria)
o Antibiotic use may suppress bacterial growth and lower immune response
▪ PCR: intestinal tissues, fecal swabs, feces
o Positive:
▪ Ct <20 strong link to intestinal lesions (IHC) and disease
▪ Ct>30 indicate organism present but not associated with intestinal
lesions (IHC negative) and thus not likely to have an economic
impact at that time.
o Negative: Negative or bacteria could have been missed if testing occurs too
early (slow growing bacteria) or too late after infection

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▪ IFA: serum sample

o Positive: Past exposure (> 2-4 weeks) to vaccine or wildtype bacteria
o Negative:
Negative to vaccine or wildtype bacteria
Infection too early to detect (slow growing bacteria)
Antibiotic use may suppress bacterial growth and lower immune response.
▪ Clostridial enteritis
▪ Colibacillosis
▪ Coccidiosis
▪ Gastric ulceration
▪ Spirochaetal Colitis
▪ Parasites
▪ Swine Dysentery
▪ TGE
▪ Salmonellosis
Treatment
▪ Antibiotic therapy administered parenterally or by feed or water is necessary to
reduce the severity of enteritis and prevent development of chronic, irreversible
necrotic enteritis. Tylosin, enrofloxacin and chlortetracycline are intracellular
antibiotics necessary to gain access to the organisms in the cells and can eliminate
them. Virginiamycin is used as a growth promoter which could be used to prevent
disease. While Tiamulin and tilmicosin also show effectivity.
Control and Prevention

▪ Avoid overstocking
▪ Reduction of stress
▪ All-in/All-out procedure
▪ Quarantine and isolation
▪ Strict biosecurity
▪ Vaccination
▪ Live Attenuated Vaccine

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SWINE DYSENTERY
Swine dysentery (SD) is a severe, infectious disease characterized by
mucohemorrhagic diarrhea and marked inflammation limited to
the large intestine (cecum and/or colon). All ages of swine may have
SD although it seldom is apparent in piglets less than three weeks old.
The disease occurs more frequently during the growing/finishing
periods.

▪ Brachyspira (previously, Serpulina or Treponema) hyodysenteriae, a
spirochete, gram-negative, anaerobic bacteria has the ability to survive under
a wide range of environmental conditions but is susceptible to heat, ultraviolet (UV)
light, and desiccation, as well as soaps and disinfectants. Two other species of
Brachyspira have been confirmed as etiologic agents of swine dysentery: B
hampsonii and B suanatina which produce strong beta hemolysis when
cultivated on blood agar under anaerobic incubation conditions.
▪ Transmission is fecal-oral. It can persist in lagoon water for at least two months,
moist feces for two months, and soil for 18 days. Other source of infection includes
contaminated transport vehicles. The organism can be transmitted by birds, flies,
and fomites. Carrier swine can transmit the agent for at least 90 days. Clinically
normal, purchased carriers, including breeding stock, often are the source of initial
exposure. Carrier sows often transmit to their piglets. Infected mice on premises
may also be a source of infection.
▪ Once ingested, Brachyspira proliferate in the large intestine and cause
degeneration and inflammation of the superficial mucosa, hypersecretion of mucus
by the mucosal epithelium, and multifocal hemorrhage from the mucosal surface.
Decreased ability of the mucosa to reabsorb endogenous secretions results in
diarrhea.

▪ Initial signs include anorexia and passage of soft feces usually gray to yellow and
continues and quickly becomes mucohemorrhagic (excess mucus and fresh blood
apparent)
▪ Fresh, red blood in mucus-containing feces often is profuse and the perineal area
may become blood stained.
▪ Prolonged diarrhea leads to dehydration, signs observed include sunken eyes,
marked weakness, hollow flanks and weight loss
▪ appetite is erratic but the animals continue to drink
▪ Occasionally, sudden death is observed. In untreated herds morbidity is high and
mortality can approach 50%.
▪ Lesions are confined to the cecum, spiral colon, and rectum. Moderate mesocolonic
edema may be observed, and mucosal lesions are often present at the apex of the
spiral colon. The affected mucosa is variably swollen and covered with a layer of
transparent to slightly opaque mucus, often with suspended flecks of blood. As

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disease progresses, a mixture of blood, fibrin, and necrotic debris accumulates in

the colonic lumen.
▪ Microscopically, there is moderate nonsuppurative colitis and typhlitis, mucosal
metaplasia, edema, and superficial epithelial necrosis. Spiral-shaped organisms
can be demonstrated within crypts, enterocytes, and debris by silver stain.
Diagnosis
▪ Clinical signs and postmortem examination findings are usually sufficient for a
presumptive diagnosis of swine dysentery. Disease restricted to large intestine
▪ Selective anaerobic bacterial culture - isolation of strongly beta-hemolytic
Brachyspira, confirmation of hemolytic phenotype because atypical weakly
hemolytic isolates of B hyodysenteriae have been reported
▪ Histopathologic evaluation- confirmation of diagnosis is based on
demonstration of typical histologic lesions in the large intestine
▪ PCR assays of feces
▪ Salmonellosis
▪ Spirochaetal colitis (B.pilosicoli)
▪ Proliferative enteropathy
▪ Whipworm infections
▪ Gastric Ulcers

▪ Administration of antimicrobials based on results of minimum
inhibitory concentration testing is an effective treatment for swine
dysentery if started early, and water medication may be preferred.
Pleuromutilins (e.g Tiamulin), carbadox, lincomycin, and tylosin are
commonly used, but the development of variable levels of antibiotic
resistance (e.g Tylosin) and withdrawal period of products (e.g Carbadox) limited the
range of treatments available for Swine Dysentery. When the first signs of the disease
are present, water must be medicated with lincomycin, tiamulin or tylosin for at least 7
days to prevent development of clinical disease. The most affected pigs must be injected
with lincomycin, tiamulin or tylosin
▪ All-in-all-out pig flow
▪ Biosecurity and rodent control
▪ Swine dysentery may be eradicated from infected premises without total
depopulation by implementing a persistent and carefully planned program that
includes treatment of carrier pigs with antimicrobials and thorough cleaning and
disinfection of vacated facilities
- Rodents and waterfowl are important reservoirs for Brachyspira spp, and
any eradication attempt must include elimination or reduction of exposure
to these reservoirs on the farm

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▪ Expression of swine dysentery is strongly influenced by diet and can be reduced

through alteration of dietary fiber where feeds containing more soluble fiber,
such as sugar beet pulp, are fed in place of feed components high in insoluble
fiber, such as distillers dried grains with soluble (DDGS).

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INTESTINAL SALMONELLOSIS
Salmonellosis is an important bacterial disease in swine for its capacity
to produce food intoxication in humans. Contaminated pork products
are not a primary source of food-borne salmonellosis outbreaks in
people but efforts to reduce salmonellae in the pork food chain are a
high priority for the swine industry. Only a few serotypes cause
disease, usually manifested as septicemia and/or enterocolitis,
sometimes by tissue localization of infection at various sites. Pigs of
all ages are susceptible; however, intestinal salmonellosis is most common in
weaned and growing-finishing pigs.

▪ From all the Salmonella serotypes (more than 2400), the more important ones
causing clinical disease in pigs are Salmonella Choleraesuis and Salmonella
Typhimurium. Salmonella enterica serotype Choleraesuis, variety
Kunzendorf (S Choleraesuis) sometimes produces necrotizing enterocolitis;
more commonly, it is associated with septicemic disease characterized by hepatitis
and pneumonia. Salmonella Typhimurium is usually associated with
enterocolitis and is a common source of food intoxication in humans. Recently,
however, S enterica serotype 4,[5],12:i:- has been detected with increasing
frequency in pigs with clinical signs of disease, and it has become one of the
predominant serotypes isolated from diseased swine. S Typhisuis infection is less
common and is associated with chronic ulcerative colitis. Pigs can be subclinical
carriers of S. Choleraesuis for long periods of time because the organism survives
in the mesenteric lymph nodes, located in the intestine.
▪ Salmonellae are small, hardy, ubiquitous, Gram-negative bacilli. All contain
endotoxin and are capable of elaborating a variety of other toxins. They can readily
survive in many swine environments but can be inactivated by chlorine, iodine and
phenol-based disinfectants.
▪ Transmission is thru feco-oral. The pigs start shedding the bacteria within minutes
from infection and can continue to shed up to 5 months after recovery from the
illness. Salmonella can be shed in oral fluids leading to nose-to-nose transmission.
It can also be carried in the intestinal tract of birds and rodents, leading to indirect
transmission of the pathogen.

▪ Affected pigs are commonly febrile
▪ reduced feed intake and dehydration
▪ Smelly diarrhea, liquid yellow feces that may contain shreds of necrotic debris.
Diarrhea in individual pigs usually lasts 3–7 days, and it may recur for multiple
bouts. Blood may appear sporadically in the feces but rarely with the profuseness
typical of swine dysentery or hemorrhagic porcine proliferative enteropathy

17
▪ Mortality usually is low and occurs only after several days of diarrhea. Most pigs
make complete clinical recovery, but a portion may remain as carriers and
intermittent shedders for at least 5 months.
▪ Pigs infected with enteropathogenic salmonellae (S Choleraesuis, S Typhimurium,
and S 4,[5],12:i:-) have an inflamed, segmentally thickened distal small intestine
and colon, usually with necrotic debris on the mucosal surface. The most indicative
lesion due to salmonellosis by Salmonella typhimurium is the presence of
pseudomembranes in the intestine, described as yellowish, fibrinonecrotic debris
giving the impression that the mucosa separated from the intestinal wall. Sharply
delineated deep button ulcers may be observed in more chronic lesion.
Infection with certain serotypes may be accompanied by generalized sepsis.
▪ The most consistent gross lesion in pigs suffering from S. typhimurium is
enterotyphlocolitis most often involving the ileum, cecum, and spiral colon and
occasionally extending to involve the descending colon and rectum.
▪ Microscopic lesions are also usually seen in the ileum, cecum and spiral colon,
often presenting as blood clots in nearby capillaries and damage in epithelial cells
with presence of neutrophils and macrophages. Lymph nodes will also have a high
number of neutrophils and necrosis may occur.
Diagnosis
▪ Isolation of the bacteria along with clinical signs and lesions is the only way to get
a definitive diagnosis
▪ Confirmation via culture and serotyping
-Culture of feces or intestinal mucosa using selective media, with or without
enrichment
- Culture of enlarged mesenteric lymph nodes is of higher diagnostic specificity for
enteropathogenic strains and should ideally be performed in tandem with mucosal
or fecal cultures
- Culture is typically followed by serotyping to confirm the serotype involved.
▪ Histologic examination- affected intestine and liver tissue to differentiate intestinal
salmonellosis from proliferative enteropathy and swine dysentery is of high
diagnostic value
▪ PCR assays are increasingly available, often with serotype-level specificity, that
can reduce the time to final etiologic diagnosis
▪ Rotavirus
▪ Coronavial Enteritis
▪ Coibacillosis
▪ Ileitis
▪ Swine Dysentery

18

▪ Antimicrobial treatment based on results of minimum inhibitory concentration
testing/ antibiotic susceptibility
- Parenteral administration of antimicrobials to acutely ill pigs and medication of
the affected group via water or feed may decrease the severity of an outbreak of
intestinal salmonellosis. Neomycin and lincomycin-spectinomycin are commonly
administered water medications.
▪ Vaccination- Live avirulent vaccines administered either intranasally or via drinking
water are effective for prevention of disease caused by S Choleraesuis and S
Typhimurium. Avirulent vaccines may also effectively reduce levels of salmonellae
in the tissues of swine at slaughter.
▪ Improve hygiene by ensuring proper cleaning and disinfection (disease is dose
dependent).
▪ All-in-all-out pig flow.
▪ Purchase animals (including breeding stock replacements) from known negative
sources
▪ Control rodents

19
CLOSTRIDIUM PERFRINGENS

Clostridium perfringens is a large, anaerobic, Gram-positive bacillus
with both vegetative and sporulated forms. Five toxigenic types (A,
B, C, D, E) are distinguished by major toxins they produce (alpha,
beta, epsilon, or iota); all types produce alpha toxins. Type C
organisms produce several toxins, especially a necrotizing beta toxin
which causes the severe necrotizing enteritis. Clostridium
perfringens type A produces alpha toxin and those pathogenic for swine also
produce beta2 toxin. CptA causes much milder enteric insult than CptC.
▪ Feces from carrier sows contain pathogenic clostridial organisms and, coupled
with 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
▪ Dose and immunity play a large role in disease occurrence. Immune dams (from
exposure and perhaps vaccination) likely provide colostral antitoxin immunity to
offspring

In swine, three common diseases associated with Clostridium perfringens (Cp) occur.
▪ Enterotoxemia associated with C. perfringens type C (CptC) is characterized by
variable morbidity and high mortality in neonates or suckling pigs (less than 1 week
old) with sudden deaths, bloody diarrhea, or necrotic enteritis. there may be
blackening of the abdominal skin. Infrequently, pigs develop a persistent, pasty-
gray diarrhea and become progressively emaciated. The peritoneal and pleural
cavities may contain excessive, blood-tinged fluid. Typical acute cases have a dark
red, necro-hemorrhagic small intestine. The lesions usually involve the entire small
intestine but, in some cases, may be segmental, usually in the jejunum or ileum
but sometimes cecum and colon are also affected.
▪ Clostridium perfringens type A is part of the normal flora of the swine intestine
but also cause diarrhea/ enteric disease in neonatal piglets and occasionally in
weaned pigs with moderate morbidity and lower mortality compared to CptC.
Affected piglets typically have a creamy to watery, yellowish diarrhea that is self-
limiting within ~5 days. Piglets' growth rates are suppressed. Lesions include
flaccid, thin-walled intetsines with gas distention.
▪ Clostridium difficile (Cd) infection of the cecum and colon produces diarrhea
with variable morbidity and mortality. nclude moderate to severe mesocolonic
edema, watery colonic contents, and occasionally respiratory symptoms or sudden
death
Diagnosis
▪ The acute, short course with high morbidity and mortality and typical gross lesions
in neonatal piglets are highly suggestive of type CptC enteritis.

20
▪ Direct smear staining of intestinal mucosa- Identification of a large population of

Gram-positive, rod-shaped bacteria in mucosal smears is strongly supportive of
the diagnosis
▪ Histologic Examination- demonstration of villous necrosis with mucosal
colonization by numerous large, gram-positive rods is adequate for confirmation
▪ Culture- identification of exceptionally large numbers of C. perfringens in
anaerobic cultures
▪ PCR genotyping
▪ E coli
▪ Rotavirus
▪ Coccidiosis
▪ Coronaviral enteritis
▪ Swine Dysentery
▪ Swine Ileitis
▪ Salmonella

▪ Clostridium is very sensitive to penicillin. In
▪ Vaccination- for sows, 6 and 3 weeks before farrowing, Naive gilts may benefit
from three vaccinations before their first farrowing to ensure sufficient colostral
antibodies
▪ In an acute outbreak, prophylactic administration of type C antitoxin or
antimicrobial (or both) parenterally or orally is protective if given to piglets within
2 hours of birth
▪ Sow’s feed can be medicated during 14 days before farrowing to minimize
contamination of environment at farrowing.
▪ Washing sows before placing in clean farrowing room.
▪ Proper cleaning and disinfection of farrowing room.

21
COCCIDIOSIS
A disease characterized by diarrhea in suckling and recently weaned
pigs.

The causative agent of coccidiosis in piglets is usually Isospora suis and
occasionally by other Eimeria spp. Most Eimeria spp have low
pathogenicity (causing approx 5% of infections) or do not occur in this
age group but occurs in older pigs, including gilts. It also infects wild boars.
Oocysts become infective in about 12 hours at temperatures of 68-97˚F. This is within the
range maintained in many confinement farrowing facilities. After ingestion of sporulated
oocysts, patency in neonatal pigs can occur in as little as five days.
Isospora suis goes through the usual stages of sporogeny, excystation, and endogenous
development with multiplication in intestinal epithelium, usually in jejunum and ileum, in
the cells on distal portions of intestinal villi, and in cryptal epithelium in severe infections.
Isospora suis infection occurs in piglets in all systems from indoor intensive to outside
extensive production. Piglets are mainly exposed to oocysts from others in contaminated
farrowing and rearing accommodation. Once infected, piglets magnify the numbers of
oocysts and heavily contaminate the environment. As a result of this buildup of oocysts,
piglets are able to ingest high numbers of oocysts, a requisite for producing clinical
disease. Sows rarely shed I suis species, although infection may be introduced to a new
herd by carrier sows. Inadequate sanitary practices between farrowing groups
undoubtedly facilitate this buildup.

▪ In piglets, infection most commonly occurs from 5–15 days of age. Affected piglets
develop diarrhea varying from creamy, pasty consistency or whitish feces to
profuse watery yellowish to grayish diarrhea. Piglets become covered with the
liquid feces, causing them to stay damp and have a rancid odor of sour milk.
▪ The piglets usually continue to nurse, develop a rough hair coat, become
dehydrated, and have depressed weight gains. Secondary infection by bacteria
and viruses can also result in high mortality, although mortality due to coccidiosis
on its own is relatively low.
▪ In older pigs, infection is usually mild. Those ill develop diarrhea, which may be
frothy, mucoid, or watery, with wasting. Clinical signs often start 9–12 days after
infection. Some pigs continue to grow poorly.
▪ 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.
▪ Microscopically, there is necrosis and, later, atrophy and fusion of some mucosal
villi, hyperplasia of cryptal epithelium and elongation of mucosal crypts. Shortened
villi may be covered by cuboidal or flattened epithelial cells. Various stages
of Isospora suis are apparent in parasitized cells.

22
Diagnosis
▪ Coccidiosis should be suspected if there is a diarrhea problem in sucking pigs from
7-21 days of age that does not respond particularly well to antibiotics.
▪ Fecal examinations- less sensitive, clinical signs develop before oocysts are
present in the feces. The oocysts do not pass out into the feces until approximately
3-4 days after diarrhea is seen, by which time the pig may have recovered. Feces
samples for laboratory examination should be taken from semi-recovered pigs
rather than pigs with scour.
▪ Histologic Examination- presence of large numbers of merozoites and male and
female gametocytes in the intestinal wall. There is villous atrophy, blunting of villi,
focal ulceration, increased mitotic activity in the crypt epithelium.
▪ PCR, Fluorescent Antibody Testing
▪ In older pigs, fecal sampling is the main diagnostic tool
▪ Postmortem findings assist in diagnosis. Impression smears of affected areas
show coccidial development stages
In piglets
▪ Rotaviral infection
▪ Colibacillosis
▪ transmissible gastroenteritis
▪ Clostridium perfringens type A or C infection
In older pigs
▪ Salmonellosis and Swine Dysentery
▪ Strongyloides ransomi
Treatment, Prevention and Control

▪ Sulfonamides can be used. Sulfamethazine (sulfadimidine) in drinking water may
be used but usually needs to be administered individually. Sulfaquinoxaline can be
effective. Trimethoprim sulfonamide by injection or orally can be useful.
▪ Treatment of individual clinically affected pigs with amprolium is administered at
10–25 mg/kg, PO, for 4–5 days, and to the rest of the group at 10 kg 25% premixed
per ton of feed to decrease oocyst shedding.
▪ Monensin at 100 g/ton feed can be used with variable results
▪ On farms known to be affected by coccidiosis, routine treatment of all piglets with
toltrazuril early-on will minimize the incidence and severity of coccidiosis.
Toltrazuril (20 mg/kg, PO, once) is licensed in some countries for coccidiosis
prevention in 3–5-day old piglets and is shown to decrease oocyst excretion,
incidence of diarrhea, and weight gain impairment in piglets with experimentally
induced coccidiosis.
▪ A vigorous, effective sanitation program, along with careful cleaning and
disinfection of farrowing crates between farrowing
- Strong bleach or ammonium compounds can be used for disinfection after
thorough cleaning of the crates
- steam cleaning of the entire farrowing facility may be necessary

23
- Sealing all surfaces with paint or a water seal may be preferable to break
the cycle of infection
- Installation of perforated metal or plastic flooring in the crates will be
beneficial in the control of coccidiosis and other neonatal enteric diseases.

24
GASTROINTESTINAL PARASITISM
In pigs, gastrointestinal helminths are almost always present; their main

effects are loss of appetite, reduction in daily gain, poor feed efficiency,
and potentiation of other pathogens. Only rarely do they cause death.
Adequate nutrition helps decrease the adverse effects of parasitism on
feed efficiency and average daily gain.
Ascaris suum is the most common intestinal nematode of pigs. Adult nematodes in
the intestine reduce feed efficiency and impair vitamin A absorption; heavy infections
cause emaciation. Larval migration incites inflammation in the liver and lungs.
Strongyloides ransomi (intestinal threadworm) larvae can be transmitted via

colostrum or acquired from contaminated skin of the dam. Parasitic larvae invade the host
either by penetration of the skin (percutaneous), ingestion in feed (oral), ingestion in
colostrum (transcolostral), or through direct invasion of developing fetuses
(transplacental/perinatal). In all cases, the asexual female reaches the mucosa of the
small intestine where many ova are produced and passed in feces of the host. Heavily
infected piglets develop severe diarrhea when 10–14 days old, with high mortality.
Diagnosis is based on direct microscopic examination of mucosal scrapings or histologic
sections.
Trichuris suis (whipworms) penetrate the mucosa of the cecum and colon and
cause multifocal inflammation. Heavy infections cause diarrhea and emaciation. The feces
are hemorrhagic; therefore, heavy whipworm infections may be confused clinically with
swine dysentery or proliferative enteropathy. Diagnosis is based on direct observation of
whipworms in the large intestine or on fecal flotation .
Hyostrongylus rubidus is the common stomach worm found in pasture-raised

pigs. It usually causes little harm
Cryptosporidium sp is an apicomplexan parasite that attaches to the mucosal

epithelium of the intestine of pigs ≥10 days old. It may cause villous atrophy in the lower
small intestine; however, inapparent infection is common. Malabsorption and diarrhea
may result

▪ Maintaining pigs on concrete or entirely on slatted floors
▪ Good sanitation is critical because fecal-oral transmission, via the contamination
of food, soil, or bedding, is the primary route by which pigs become infected
▪ Thermophilic composting of feces or bedding before use as fertilizer inactivates
Ascaris suum and Trichuris suis eggs. Both can survive for a few hours at 50°C
but only a few minutes at 55°C.

25
▪ Moving uninfected animals to safe pastures helps decrease parasite buildup;

however, eggs of A suum and T suis are capable of surviving 6–9 and 5–11 years,
respectively, in the environment, and reinfection will occur even with 2–3 years of
pasture rest
▪ Controlled application of Anthelmintics
- Benzimidazoles, including fenbendazole and flubendazole, are available
for in-feed administration. Flubendazole is available for in-water and top-
dressing use, and fenbendazole has an oral formulation.
- Two avermectin compounds, ivermectin and doramectin, are available as
injectables, although only ivermectin can be used in-feed
- Pyrantel tartrate is available as an in-feed formulation
- Dichlorvos, an organophosphate compound, was the first broad-spectrum
dewormer available for pigs and is still in use as an in-feed formulation
- Piperazine salts as an in-feed or in-water formulation
ASSESSMENT
1. Which internal Parasite of Swine is most likely to cause hematochezia?

a. Ascaris suum
b. Hyostrongylus rubidus
c. Trichuris suis
d. Eimeria sp.
2. When enterotoxemic E. coli interferes with normal intestinal function, the nutrient loss in
largest proportion is:
a. Calcium
b. Water
c. Lactose
d. Glucose
3. What is the most characteristic lesion associated with salmonellosis?

a. Pseudomembrane in the small intestine
b. Thickening of the ileum
c. Mucus and fresh blood in the spiral colon
d. Thinning of small intestines
4. Which of the following is not a bacterial cause of enteric diseases in swine?

a. Swine Ileitis
b. Swine Dysentery
c. Colibacillosis
d. Coccidiosis
5. What is the gold standard for the diagnosis of Porcine Proliferative Enteritis?
a. Virus Isolation
b. Immunohistochemistry
c. PCR
d. Histopathology
26
References
• Straw, BE, D’Allaire, S, Zimmerman, JJ, and Taylor, D. 2006. Diseases of Swine 9th ed.
Blackwell, Ames, Iowa.
• Zimmerman JJ., Karriker LA., Ramirez A., Schwartz KJ., Stevenson GW., Zhang J. 2019.
Diseases of Swine 11th Edition. Wiley-Blackwell.
• Iowa State University. Center for Food Security and Public Health. Retrieved from
http://www.cfsph.iastate.edu/?lang=en
• The Pig Site. Retrieved from http://www.thepigsite.com/diseaseinfo/
• The Merck Veterinary Manual
• Professional Pig Community. Pig Health. Retrieved from https://www.pig333.com/health/
• OIE (World Organization for Animal Health). Retrieved from http://www.oie.int/
• Swine Manual. 2022.Iowa State University of Science and Technology. Retrieved from
https://vetmed.iastate.edu/
• KAHN, C.M. et al. (eds.) (2010) The Merck Veterinary Manual. 10th Edition. Whitehouse
Station, New Jersey, U.S.A: Merck and Co., Inc.
• RADOSTITS, O.M. et al. (2006) Veterinary Medicine: A textbook of diseases of cattle,
sheep, goats, pigs, and horses. 10th Edition. New York: W.B. Saunders.
• UNITED STATES DEPARTMENT OF AGRICULTURE. (2014). Porcine Epidemic Diarrhea
(PED) – Technical Note. USDA APHIS Veterinary Services Center for Epidemiology and
Animal Health, CO
• PENNY, R. H. C., D. J. TAYLOR and W. J. SMITH. (1990) A Color Atlas of Diseases and
Disorders of Pigs. 2nd Edition. Mosby Elsevier Health Science
• Luppi, A. Swine enteric colibacillosis: diagnosis, therapy and antimicrobial resistance. Porc
Health Manag 3, 16 (2017). Retrieved from https://doi.org/10.1186/s40813-017-0063-4
• White M. 2012 Neonatal Colibacillosis. 2012 National Animal Disease Information Service.
Retrieved from https://www.nadis.org.uk/disease-a-z/pigs/neonatal-colibacillosis/
• Prodanov-Radulovic, Jasna & Petrovic, Tamas & Lupulovic, Diana & Marčić, Doroteja &
Petrović, Jelena & Grgić, Živoslav & Lazic, Sava. (2017). First Detection and Clinical
Presentation of Porcine Epidemic Diarrhea Virus (Pedv) in Serbia. Acta Veterinaria. 67.
10.1515/acve-2017-0031.
• Corwin RM. 1997. Pig Parasite Diagnosis. Retrieved from
https://www.aasv.org/shap/issues/v5n2/v5n2p67.pdf
• NSW Government. 2017. Internal parasites of pigs. Retrieved from
https://www.dpi.nsw.gov.au/__data/assets/pdf_file/0019/433018/Internal-parasites-of-
pigs.pdf
• Pork information Gateway. Salmonellosis and Salmonella Infection. Retrieved from
https://porkgateway.org/resource/salmonellosis-and-salmonella-infections/
• Rodriguez HA, Carvajal A., Nistal PR. 2012. Importance of the abattoir on the control of
salmonellosis. Pig health Article. Retrieved from
https://www.pig333.com/articles/importance-of-the-abattoir-on-the-control-of-
salmonellosis-1-2_5834/
• Zhitnitskiy P. Salmonella Typhimurium. Swine Diseases. Retrieved from
https://open.lib.umn.edu/swinedisease/chapter/salmonella-typhimurium/
• NADIS. Swine Dysentery. Retrieved from https://www.nadis.org.uk/disease-a-
z/pigs/swine-dysentery/
• E. R. Burrough. 2016. Swine Dysentery: Etiopathogenesis and Diagnosis of a Reemerging
Disease Volume 54, Issue 1. Retrieved from https://doi.org/10.1177/0300985816653795
27
• H.I. Field, D. Buntain, A.R. Jennings. 1953,.Terminal or regional ileitis in pigs. Journal of
Comparative Pathology and Therapeutics Volume 63 Pages 153-IN12, ISSN 0368-
1742.Retrieved from https://doi.org/10.1016/S0368-1742(53)80018-4
• Ramirez A.2021. Laboratory diagnostics: Ileitis (Lawsonia intracellularis). Pig Health.
Retrieved from https://www.pig333.com/articles/laboratory-diagnostics-for-ileitis-
lawsonia-intracellularis-in-pigs_17368/
• Burrough ER. 2021. Porcine Proliferative Enteropathy. Retrieved from
https://www.msdvetmanual.com/digestive-system/intestinal-diseases-in-pigs/porcine-
proliferative-enteropathy

28

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VMED 5335- SWINE MEDICINE

Diseases of the Digestive System

Etiology and Epidemiology

Lygene Harmony C. Culimay, DVM

Clinical Signs and Lesions

Lygene Harmony C. Culimay, DVM

▪ Virus Isolation, FAT, RT-PCR, ELISA, Immunofluorescence,

Treatment, Control and Prevention

Lygene Harmony C. Culimay, DVM

PORCINE EPIDEMIC DIARRHEA

Etiology and Epidemiology

Clinical Signs and Lesions

Lygene Harmony C. Culimay, DVM

Treatment. Control and Prevention

Lygene Harmony C. Culimay, DVM

Etiology and Epidemiology

Clinicals signs and Lesions

Lygene Harmony C. Culimay, DVM

Treatment, Control and Prevention

Lygene Harmony C. Culimay, DVM

Etiology and Epidemiology

Clinical Signs and Lesions

watery. The feces vary in color from clear to yellowish-whitish or various

Treatment, Control and Prevention

▪ Antimicrobial treatment based on results of minimum inhibitory concentration

Lygene Harmony C. Culimay, DVM

- breeding stock should be obtained from a single source with no problems

Lygene Harmony C. Culimay, DVM

It is a common diarrheal disease of growing-finishing and young

Etiology and Epidemiology

Clinical Signs and Lesions

There are 4 recognized forms of the disease: Porcine Intestinal

▪ Porcine intestinal Adenomatosis (PIA) is described as an abnormal

Lygene Harmony C. Culimay, DVM

▪ Histopathology- strong association between thickening and disease

Lygene Harmony C. Culimay, DVM

▪ IFA: serum sample

Control and Prevention

Lygene Harmony C. Culimay, DVM

Etiology and Epidemiology

Clinical Signs and Lesions

Lygene Harmony C. Culimay, DVM

disease progresses, a mixture of blood, fibrin, and necrotic debris accumulates in

Treatment, Control and Prevention

Lygene Harmony C. Culimay, DVM

▪ Expression of swine dysentery is strongly influenced by diet and can be reduced

Lygene Harmony C. Culimay, DVM

Etiology and Epidemiology

Clinical Signs and Lesions

Lygene Harmony C. Culimay, DVM

Lygene Harmony C. Culimay, DVM

Treatment, Control and Prevention

Lygene Harmony C. Culimay, DVM

Etiology and Epidemiology

Clinical Signs and Lesions

Lygene Harmony C. Culimay, DVM

▪ Direct smear staining of intestinal mucosa- Identification of a large population of

Treatment, Control and Prevention

Lygene Harmony C. Culimay, DVM

Etiology and Epidemiology

Clinical Signs and Lesions

Lygene Harmony C. Culimay, DVM