African Swine Fever - Highly virulent - 10-100 % mortality by 7-10

days after exposure;

African Swine Fever is a tick-borne, contagious, febrile,
systemic viral disease of swine
- Moderately virulent - Acute illness, a high %
• Highly contagious viral disease of domestic pigs of
with up to 100% mortality pigs survive;

• Pigs die as a result of a hemorrhagic fever - Low virulence - Seroconversion only.

• Some pigs may develop subacute or chronic Environmental Persistence
forms of the disease
• Stable at pH 4-13
• Control depends on the slaughter and
destruction of all infected and in-contact pigs • Survives at least:
- 11 days in feces (room temp)
• There is no vaccine for African Swine Fever - 1 month in soiled pig pens
• Is a serious transboundary animal disease - 70 days in blood on wooden boards
- 15 weeks in putrefied blood
with the potential for rapid international spread - 18 months in blood at 4oC
Etiology • Survival in pork products:
• The ASF virus is the 15 weeks in chilled meats
only member of the genus asfivirus in the
family Asfarviridae*. 300 days in cured hams (“Parma hams”)

• Large (~ 200 nm) 15 years in frozen carcasses

lipoprotein-enveloped, Host Range
icosahedral,
double- stranded DNA virus Ornithodoros ticks are believed to be the original host

• ASFV is the only DNA virus that can qualify as Soft ticks
an arbovirus. - Ornithodorus erraticus from ASF-infected farms.
- Ornithodorus porcinus porcinus (moubata) from
• * “ASFAR” warthog burrows.
• African - Ornithodorus ticks in Haiti, Dominican Republic
and California.
• Swine
• ASFV is believed to be a tick virus with
• Fever domestic pigs and wild pigs as accidental hosts.
• And • African Domestic pigs
• Related viruses In Africa:
ASFV is a large, dsDNA, enveloped virus • Warthogs
recently classified in the new family
Asfarviridae • Bush pigs

Rare example of a DNA arthropod-borne virus • Giant forest hogs

The stability of the virus is a notable feature: In Europe:

Infectivity is retained after 15 weeks in chilled meat, • Wild pigs

and for 5-6 months in processed hams • European wild boar
Strain Virulence • African wild swine
• Marked variations in virulence of isolates: - Wart hog

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 - Giant forest hog
- Bush pig - Fetuses may be anasarcous.

• NOTE –
- May find petechiae in placenta, skin, and
Collared peccary
myocardium, and a mottled liver.
not susceptible
Clinical Signs
Incubation Period
• Coagulopathy, abnormal clotting
• Following intranasal-oral exposure, pigs
develop fever and leukopenia in 48 to 72 • Thrombocytopenia
hours
• Hemorrhages
• 5 days or less after
• Sudden death in peracute
infection by tick bite.
• High fever, low appetite, huddling, shallow
• 5-15 days after contact with ASFV-infected
breathing, reluctant to move
pigs.
• These signs are influenced by the virulence and
. Morbidity:
the physiological state (age, pregnancy status)
High morbidity — usually 100% in pigs that have
• There are three categories:
contact with one another; 100% in naïve pigs
• Highly Virulent Isolate
Mortality:
• Moderately Virulent Isolate
Highly virulent isolates have about 100% mortality
• Low-Virulent Isolate
Moderately virulent isolates range from low
Clinical Signs:
percentage to 60-70%.
High and Moderate
Age
• Similar for first 4-6 DPI (days post infection)
Pregnancy status
• After about 2 DPI, pigs develop:
Other diseases have effect
1. Fever of 105-107°F
General Clinical Signs
2. Moderate anorexia
• In contrast to pigs with hog cholera:
3. Leukopenia
– African Swine Fever pigs do not
• After 4-6 DPI, differences related to different
develop conjunctivitis or encephalitis
isolates will be apparent
– Despite high fever, ASF infected pigs
White skinned pigs will have erythematous skin.
stay in good condition, whereas hog
cholera infected pigs drastically lose If left alone, pigs will lie down
weight
Clinical Signs:
• Some groups of pigs may develop diarrhea, but Highly Virulent
it is not a direct effect of the virus.
• Pigs eat and move less
• Pigs may also develop dark red to purple
• Most die between 7 and 10 DPI.
discoloration of skin on ears, tail, extremities,
or skin on hams. (This is a nonspecific sign also • It is not unusual to see
seen in other diseases)
a pig walking and find
Abortion
it dead a short time later
• Occurs whether isolates are high, moderate or
low in virulence.

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 • Peracute
- Sudden death
• Acute
- Fever (105-107oF) –
-Discolored skin
- Huddling
- Diarrhea / melena
- Abortions
- Death
Clinical Signs:
Moderately Virulent
• Infected pigs usually have high fever for 10 to
12 DPI. Some mortality occurs at this time.
• After 12 to 14 DPI, temperatures and leukocyte
count begins to return to normal levels.
• Very young pigs may have high mortality rate
and lesions similar to those caused by highly
virulent isolates
• Some pigs will die at 7 to 8 DPI, frequently
caused by hemorrhage into the stomach
• Underlying causes: ASF infection causes
prolonged bleeding time
Clinical Signs:
Low-Virulence
• Other low-virulent isolates will cause pigs to
have low fever for 2 to 3 weeks, then develop
reddened areas of skin that become raised and
necrotic.
• Painless enlargements of joints may also
appear
• This form is chronic, and may reoccur. The
animal will eventually die during an acute
episode of the disease.
• Many nonpregnant animals infected with low-
virulence isolates may seroconvert but not
show other signs of infection
• Pregnant animals will abort
Clinical Signs:
Chronic
• Transient / recurrent fever
• Stunting / emaciation
• Pneumonia
• Skin ulcers
• mvvlose coordination, stunted, heart and lung
lesions
• Chronic cough
• Fluid in pericardial sac: fibrinous endocarditis
• Joint inflammation
• Decubitous lesions on boney prominenses
Gross Lesions
Highly Virulent Virus
• Peracute deaths
- Lesions may be poorly developed
• Animals that die 7 or more DPI
- Classic lesions likely.
• Three lesions most consistent with ASF
infection:
1. Greatly enlarged dark red to black friable spleen
2. Enlarged hemorrhagic gastrohepatic lymph nodes
3. Enlarged hemorrhagic renal lymph nodes
• Other lesions are more variable:
• Dark red to purple areas of
skin on ears, feet, and tail.
• Petechial hemorrhages on
serosal surfaces
• Renal cortical petechial /
ecchymotic hemorrhages
• Perirenal edema
• Edema of the gall bladder
• Swollen liver
• Pulmonary edema
Gross Lesions
Moderately Virulent Virus
• From 8-12 DPI
- Gross lesions are similar whether pigs are
infected with a moderately virulent or highly
virulent ASFV.
• The main difference between these two types
of isolates:
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 - Splenomegaly is still present,
- More normal color and is not friable.
Gross Lesions
Low Virulent Virus
• The most common lesions in chronic ASF:
-Necrotic skin lesions
-Consolidated lung lobules
-Generalized lymphadenopathy
-Swollen joints
-Pericarditis
Epidemiology:
Sylvatic cycle in Africa
• Infected Argasid ticks in warthog burrows
transmit virus to young warthogs.
- Pigs remain infected for life.
- Transtadial, transovarial, sexual transmission.
• Pigs can be raised successfully in confinement
with double fencing, proper isolation, and
sanitary procedures.
Epidemiology:
Epidemic cycle
• Introduction into domestic swine by feeding
garbage / swill contaminated with pork scraps.
• Blood contaminated sources
• Direct contact and fomites
- People
- Vehicles
- Equipment
- Feed
Transmission
• Transmission by contact and ticks
• The soft tick has been proven a vector
• Primary Method:
• Feeding of uncooked garbage
containing African Swine Fever
infected pork scraps to pigs.
• Wild suids in Africa are carriers of the virus
• Acquire the virus from Ornithodoros moubata
that invade warthog burrows
• Young warthogs become infected as neonates
and retain high viral titres for up to about 3
weeks
• Where ASF becomes endemic in domestic pigs,
the virus is maintained by carrier pigs
• Ingestion  Tonsil  Local LNs  Viremia
• Virus in excretions and secretions, blood.
• Carrier pigs incriminated in maintaining
infection in herds.
• Pigs with mild forms of ASF may shed virus for
~ 30 days.
• Bites of infected ticks.
Once a pig is infected, the disease spreads by:
– Direct contact
– Contaminated people, vehicles, feed
– Carrier pigs
– Equipment
Diagnosis
• African Swine Fever should always be
suspected where there are febrile pigs
• Necropsy findings include:
– Greatly enlarged spleen, dark red to
black in color, friable spleen
– Very enlarged, hemorrhagic
gastrohepatic lymph nodes
– Very enlarged, hemorrhagic renal
lymph nodes
• Hog Cholera vs. African Swine Fever
– Hog cholera infected pigs become
depressed and lose weight, whereas
ASF infected pigs have neither
symptoms
– Hog cholera is also characterized by a
foul-smelling diarrhea
Diagnosis
Laboratory Specimens
• Serum / clotted blood
• EDTA, heparin blood
• Lymph nodes
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 • Spleen • Erysipelas

• Tonsil • Eperythrozoonosis

• Lung • Septicemias

• Liver • Porcine Reproductive and Respiratory

Syndrome (PRRS)
• Kidney
• Porcine Dermatitis and Nephropathy Syndrome
• Virus isolation
(PDNS)
- Haemadsorption test (HAD) of
leukocyte cultures.
- Haemadsorption autorosette
test of PBLs of suspect pigs.

• Pig inoculation

- Requires inoculation of naïve

and CSF-vaccinated pigs.
- Not recommended with newer
tests available.

Diagnosis
Laboratory Diagnosis

• Virus antigen detection

- Direct fluorescent antibody Classical Swine Fever
test (DFAT) Classical Swine Fever is also called
• Virus genome detection Hog Cholera
- Polymerase Chain Reaction
(PCR) “The most typical feature of CSF:
- PCR-based sequencing method which it is so atypical.”
permits detection and characterization of
ASFV variants. • Specific viral disease of Pigs.
- Useful for molecular epidemiological
• Notifiable disease in the most of the countries.
clarification of ASFV
• Most Economically damaging Pandemic
Genotyping field strains of African swine fever virus
Disease
by partial p72 gene characterization
• Compulsory Vaccination,Slaughter and
Diagnosis
Eradication policies –Adopted by Many
Field Diagnosis
Countries.
• Peracute and Acute Infection
• Unvaccinated ,Susceptible herds-100%
• 3 Classic Lesions: Morbidity
1. Large dark friable spleen
• Fortunately-Only One serotype
2. Large hemorrhagic gastrohepatic LNs
3. Large hemorrhagic renal LNs • Characterized by High Fever

• Renal petechiae, serosal hemorrhages • Malaise

Differential Diagnosis • Inappetance

• Classical Swine Fever • Diarrhoea

• Salmonellosis • Paralysis

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 • Abortions,Mummification • Inactivated at pH < 3.0 or > 11.0

• Birth of SHAKING PIGLETS • Susceptible to organic solvents (ether,

chloroform)
• CSF is a highly contagious viral disease of
swine. • Inactivated by most disinfectants: 1-2% NaOH
suitable
• Mortality varies from almost zero to 100%.
Route of Infection of CSF
• Only the domestic pig and wild boar are
susceptible naturally. • Ingestion: e.g. contaminated swill

• “Hog cholera, also known as swine fever,is a
disease native to America. It is highly
contagious and its prevalence led to the first
notice of an animal disease by the federal
government in 1860.”
• 1976 Last US outbreak
• 1978 US declared “Hog Cholera” free
• CSF was first described in 1810 in Tennessee,
where it spread to other states in the US. In
1822 described in France, in 1833 describe in
Germany, in 1899 described in south America,
1900 described in South Africa.
• …can survive for months in refrigerated meat
and for years in frozen meat
Etiology
• Only one serotype
• Lipid enveloped virus
• Virus family Flaviviridae,
Virus genus Pestivirus
• Contact with the conjunctiva
• Mucous membranes
• Skin abrasions
• Insemination
Oral nasal route
Environmental Persistence:
Moderately Fragile
• Survival in Pork Products
– Up to 85 days in chilled pork.
– >4 years in frozen pork.
– Readily killed by cooking e.g. 30 min
65oC.
• Survival in environment
– Months in contaminated pig pens in
temperate climates.
– 15 days in liquid phase of manure
slurry.

• Related Pestiviruses: Geographic Distribution

– Bovine Viral Diarrhea (BVD) • Distributed nearly worldwide

– Border Disease Virus of Sheep, • Higher prevalence

Reindeer and Giraffe – East & Southeast Asia, India, China,
Stability of CSF Virus : moderately fragile South and Central America

• Survives well in cool, moist & protein rich • Africa???

environments • Eradicated in:
– E.g. Stored Meat – U.S.
• Can survive some forms of meat processing – Australia
– Survives curing and smoking – New Zealand
• Partially resistant to heat – Canada
– Readily killed by cooking – Parts of Europe

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Host Range • 2-14 days (O.I.E.)

Domestic swine and European wild boar • Severe Acute form:

are the only natural reservoir of 2-6

classical swine fever virus • The days incubation; death at 10-20 days post
infection
Collared Peccary is only mildly susceptible.
Syndromes
Transmission
Virulence, immune status, age, breed, and pregnancy
• VERY CONTAGIOUS
figure in the clinical picture.
• Causes devastating epidemics
• Highly virulent strains: prevalent
• Direct Transmission decades ago - causes Peracute and Classic
Acute disease
• Contact between sick and healthy
animals: all tissues, excretions, • Moderately virulent strains:
secretions, semen and blood prevalent today - causes Subacute
(oronasal). Disease

• Transplacental infection: Carrier Sow • Low virulent strains: prevalent today

Syndrome. - causes Chronic Disease and Carrier
Sow Syndrome/Persistent Infection
• Airborne spread to neighbors possible
if high density pig farms.

• Indirect Transmission • Seroconversion only after 2-3 weeks

• Feeding uncooked garbage with – CSF virus is immunosuppressive like

infected meat. BVD in cattle

• Fomites: vehicles, equipment, boots, – Cellular tropism of virus

clothes.
– Endothelial, lymphoreticular,
• How is CSFV often introduced into a new macrophages, some epithelial
country?

• Garbage!
Acute Disease
• How does CSFV travel once established? (Classic Disease)

• Movement/Fomites Mortality: approaches 100%.

• The main source of infection is the PIG, either

live animal contact or uncooked pig products
Viral shedding: 10-20 days until antibodies
• Mechanical transmission
Clinical Signs
• Fomites very important
High Fever: 106-108oF (>41oC)
• Veterinarians and farm
Depression
workers
Conjunctivitis
• Discarded infected pig meat
Constipation, then Diarrhea
Incubation
Skin hemorrhages/Cyanosis
• 3-4 days average, 3-15 days range depending
Pile up for warmth
on strain, route and dose

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Anorexic and gaunt • Initial: resembles Subacute

Staggering gait – Fever

Convulsions – Anorexia

Abortion – Depression

Death 10-20 days post infection – Leukopenia

• Pathology • Second: improve, look

~normal
– Severe tonsilitis
• Final: ‘runts’ with ‘Initial’
– Severe leukopenia
Phase signs.
– Hemorrhagic swollen lymph nodes
Lesions
– Hemorrhages renal cortex
Button ulcers in cecum and colon (caused by bacteria)
– Petechiation of the bladder, larynx,
Calcification rib cartilage
epiglottis, heart, intestinal mucosa,
skin Glomerulonephritis

– Spleenic infarcts ‘Carrier Sow Syndrome’

– Necrotic gastroenteritis Mortality: In pregnant sow disease goes unnoticed.

Sow may shed virus for months especially at
– Encephalitis
farrowing
Subacute Disease
High Mortality: In piglets infected congenitally or
Mortality: reduced post-natally. Piglets look healthy at birth, shed virus
for 6-12 month before dying
Viral shedding: until death.
‘Carrier Sow Syndrome’ Clinical Signs
Clinical signs with subacute disease
• Clinical Signs in Sows
are similar to acute disease,
– Usually mild (fever)
but considerably less severe.
– or subclinical.
*As with Acute CSF, the disease is clinically and
pathologically consistent with a generalized septicemia • Clinical Signs in Piglets

Fever for 2-3 weeks – Stillbirths, deformities, mummies,

105-106oF – born dead, or congenital tremors.

(>41oC) – Some are born healthy:

Death within 30 days post infection – become persistent shedders to

maintain CSF in breeding herd;
Chronic Disease
– are immuno-tolerant but will
Mortality: High; Invariably die in 1-3 months eventually die of ‘late onset’ disease at
Viral Shedding: May shed virus for months 6-12 months of age.

Long term carriers of virus in tissues: lymph nodes, Congenital Form of CSF
lung, spleen. • Weak "Shaker" piglets
Low virulent strain or infection of vaccinated herd. • Persistently infected
Three clinical phases: – Viraemic – sero-negative piglets

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 • Life-long viraemia • Pasteurella-Weaners&Growers

• Will in time lead to complications and death • Haemophilus

Constipation followed by diarrhea • Salmonellosis (septicemic)

Reproductive disorders • Erysipelas-

Diagnosis • Eperythrozoonosis-Mycoplasma suis

• History Differential diagnosis should include anthrax,

trypanosomiasis, piroplasmosis, purpura
• Clinical signs
hemorrhagica, equine infectious anemia, and equine
• Post Mortem findings viral arteritis. However, supraorbital edema is not
often seen in other diseases on the differential list. The
– Hemorrhage in lymph nodes, kidneys, most prevalent form of the virus may dictate if the
tonsils, etc. supraorbital edema is present.
– Splenic infarcts: nearly PromedDifferential diagnosis
pathognomonic
• Purpura hemorrhagica
• Histopathology
• Botulism
– Degeneration and necrosis of
endothelial cells • High doses of pyrrolizidine alkaloids

– LN: lymphocytic depletion & reticular • Equine infectious anemia

hyperplasia
HS-Pigs
• Laboratory testing: required for confirmation
• Acute disease is characterised by: Severe
Laboratory Testing for CSF sudden pneumonia affecting all the lung tissue.

• Virus isolation • High temperatures.

– In Swine Cell Cultures; Inoculation in • Discharges from the nose.

Live Pigs to confirm.
• High mortality.
• Antigen Detection
• Pigs show rapid breathing.
– Direct Fluorescent Antibody Test
• Blue discoloured skin particularly on the
(DFAT)
extremities of the ears (caused by toxins or
– Monoclonal antibody-Avidin Biotin heart sac infections).
Complex (ABC)
Control
• Nucleic Acid Detection
• Isolation.
– Polymerase Chain Reaction (PCR) –
• Vaccination.
Conventional & Real-time
• Culling.
• Antibody Detection
• Do not feed uncooked Garbage/Meat
– ELISA
products.
– Immunoperoxidase Test (IPT)
• Bio security measures.
– Virus Neutralization Test
• Vaccine –Freez dried- 1st-2wks age
Differential Diagnosis
• Others-2m
• African Swine Fever
• Dose-1ml-I/M

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