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SWINE FEVER 
Swine Fever, highly contagious, often fatal disease affecting pigs, also known as hog 
cholera. It is caused by two unrelated viruses: classical swine fever (CSF) and African swine 
fever (ASF). 
INTRODUCTION/THEORY/HISTORY 
The condition is treated with extreme caution by international health authorities because it 
causes severe economic damage in agricultural communities. Pigs contracting acute 
versions of CSF or ASF (which have many indistinguishable symptoms) can die within five 
days. Those with even mild cases of CSF typically die within a year, although in that time 
they may have a partial recovery. 
Swine fever spreads from pig to pig through oral and nasal secretions or through 
contaminated, recycled feed. The CSF virus, however, can also be transmitted between pigs 
through contaminated vehicles, contaminated syringes, contact with human beings, or 
through the air, and can be shed for a period of 10 to 20 days following infection. In each 
instance of the disease the chronic condition induces fever, weight loss, diarrhea, 
pneumonia, and ultimately death in 90 percent of cases. 
Protection against CSF is also made difficult by the tenacious, infectious quality of the virus, 
which can survive up to four years in frozen carcasses. As a result, many governments refuse 
to accept pig meat imports from countries with inadequate controls. These countries are 
unlikely to become approved exporters of live pigs or pig meat because of poor internal 
restraints on disease prevention and management. 
One of the international trading zones best regulated for swine fever is the European Union 
(EU). In 1980 the EU introduced a strict slaughter policy on both diseased and contact 
animals with the aim of eliminating both strains of this disease. Despite the effective 
administration of this policy, however, CSF still occurs naturally in parts of Italy and 
Germany. After ASF spread into Europe in 1957, it became established among wild pig 
populations in Sardinia and in isolated areas of northwestern Spain and Portugal. As a result, 
the EU’s domesticated pig herd still suffers from sporadic outbreaks of both CSF and ASF. 
Control was made more difficult by the discontinuation of internal border controls following 
the adoption of the single European market in 1993. 
The most recent outbreaks of ASF were recorded in Spain, Portugal, and Italy in 1993, while 
epidemics of CSF swept Germany, Italy, France, Belgium, and the Netherlands as recently 
as 1994. A typical protective strategy is to restrict the movement of breeding pigs, pig meat, 
and pig offal out of those areas which are known to harbor the disease. Some countries 
establish a surveillance area around infected premises, which are then cordoned off. All 
animals affected, or suspected of being affected, from these surveillance areas are then 
slaughtered. Compensation is often paid at half the market value for the disposal of pigs 
known to be infected, while the destruction of pigs only suspected of having been in contact 
with the disease is often compensated in full. 
During the 1994 CSF outbreak in Germany and the Netherlands, some 91,702 infected pigs 
were killed on 55 farms and the preventive slaughtering of 231,590 pigs was carried out on 
an additional 326 farms. The estimated administrative and slaughtering cost was £125 
million (about $188 million). No exact calculation of the total economic damage has been 
made.
2 
CLASSICAL SWINE FEVER (hog cholera) 
Aetiology 
Epidemiology 
Diagnosis 
Prevention 
Control 
References 
AETIOLOGY 
Classification of the causative agent 
Family Flaviviridae, genus Pestivirus , one serotype divided into three major genotypes 
and ten subtypes. Closely related to ruminant pestiviruses causing bovine virus diarrhea 
and border disease. 
EPIDEMIOLOGY 
Virulence of disease is related to strain of virus isolate, age of pig and immune status 
of herd. Virus is highly contagious. Acute disease is still the prevalent form in younger 
animals, with subacute and chronic forms often observed in older animals. 
Hosts 
Pigs and wild boar are the only natural reservoir of classical swine fever virus. All feral 
and wild pigs, including European wild boar, are susceptible. Collared peccaries were 
susceptible in one study, but recovered in 10 days. 
Transmission 
• Mainly by the oral and oronasal routes, via direct or indirect contact. 
• Direct contact between animals (secretions, excretions, semen, and blood) 
• Spread by farm visitors, veterinarians, pig traders 
• Indirect conta c t through premise s , implements , vehic le s , c lothe s , 
ins t ruments and needles 
• ‘Neighborhood effect’ during outbreaks in areas of high pig farm density: airborne 
transmission over short distances (up to 1 km in one study) 
• Insufficiently cooked waste food fed to pigs: most common means of entry into free 
countries 
• Transplacental infection: may create inapparent carrier piglets or congenita l 
abnormalities 
• Wild boar populations may harbour virus; domestic pigs in the affected area are at a high 
risk; and biosecurity is crucial
3 
Sources of virus 
• Blood, secretions and excretions (oronasal and lachrymal discharges, urine, faeces and 
semen) and tissues of sick or dead animals, including meat 
• Congenitally infected piglets are persistently viraemic and may shed the virus for 6– 
12 months before dying 
• Infection routes: ingestion (most common), contact with the conjunctiva or mucous 
membranes, skin abrasions, genital transmission, artificial insemination, percutaneous 
blood transfer 
Occurrence 
The disease occurs in much of Asia, Central and South America, and parts of Europe 
and Africa. Many countries are free of the disease. 
DIAGNOSIS 
Incubation period is 2–14 days. Clinical form varies with the strain of virus, the 
age/susceptibility of pigs and the occurrence of other pathogens in the herd (herd health 
status). 
Clinical diagnosis 
Acute form (more virulent virus strains and/or younger pigs) 
• Fever (41°C) 
• Anorexia, lethargy 
• Severe leucopenia 
• Multifocal hyperaemia and/or haemorrhagic lesions of the skin 
• Conjunctivitis 
• Enlarged, swollen lymph nodes 
• Cyanosis of the skin especially of extremities (ears, limbs, tail, snout) 
• Transient constipation followed by diarrhoea 
• Vomiting (occasional) 
• Dyspnoea, coughing 
• Ataxia, paresis and convulsion 
• Pigs huddle together 
• Death occurs 5–25 days after onset of illness 
• Mortality in young pigs can approach 100% 
Chronic form (less virulent virus strains or partially immune herds) 
• Dullness, capricious appetite, pyrexia, diarrhoea for up to 1 month 
• Ruffled appearance of pigs 
• Growth retardation 
• Apparent recovery with eventual relapse and death within about 3 months
4 
Congenital form (outcome depends on virulence of virus strain and stage of gestation) 
• Fetal death, resorption, mummification, stillbirth 
• Abortion 
• Congenital tremor, weakness 
• Runting and poor growth over a period of weeks or months leading to death
• Born clinically normal but persistently viraemic with no antibody response: 
important intermittent shedders of virus until dying in 6–12 months (late onset form). 
Mild form (usually older animals; outcome depends on virulence of virus strain): 
5 
• Transient pyrexia and inappetence 
• Recovery and (lifelong) immunity 
Lesions 
Acute form: Lesions are usually complicated by secondary infections 
• Leucopoenia and thrombocytopenia 
• Enlarged haemorrhagic lymph nodes are common 
• Widespread petechiae and ecchymoses, especially in the skin, lymph nodes, epiglott is, 
bladder, kidney and rectum 
• Severe tonsillitis with necrotic foci sometimes occurs 
• Multifocal infarction of the margin of the spleen is characteristic: nearly pathognomo nic 
but occurs infrequently with currently circulating strains 
• Lungs may be congested and haemorrhagic 
• Encephalomyelitis with perivascular cuffing is common 
Chronic form: Lesions are usually complicated by secondary infections 
• ‘Button’ ulcers in the caecum and large intestine mucosa 
• Generalised depletion of lymphoid tissue 
• Transverse striations of unmodelled growth cartilage at costochondral junct ions 
in growing pigs 
• Haemorrhagic and inflammatory lesions are often absent 
Congenital form 
Central dysmyelinogenesis, cerebellar hypoplasia, microcephaly, pulmonar y 
hypoplasia, hydrops and other malformations. 
Differential diagnosis 
Varies with form of the disease 
• African swine fever (indistinguishable clinico-pathologically. It is essentia l to 
send samples for laboratory confirmation.) 
• Septicaemias: erysipelas, eperythrozoonosis, salmonellosis, streptococcosis, 
pasteurellosis, actinobacillosis, and Haemophilus parasuis 
• Haemorrhage: porcine dermatitis and nephropathy syndrome, haemolytic disease of the 
newborn, coumarin poisoning, thrombocytopenic purpura 
• Runting: post weaning multisystemic wasting syndrome, enterotoxicosis, swine 
dysentery, campylobacteriosis 
• Abortions: Aujeszky’s disease (pseudorabies virus), encephalomyocarditis virus 
infection, porcine reproductive and respiratory syndrome, parvovirus 
• Nervous signs: viral encephalomyelitis, salt poisoning 
• Congenital infection with ruminant pestiviruses: Bovine virus diarrhea, Border disease
6 
Laboratory diagnosis 
Identification of the agent 
Method of choice for detecting herds early in infection is to collect whole blood and 
tissues from multiple febrile or recently dead animals. 
• Tonsil 
• Lymph nodes (pharyngeal, mesenteric) 
• Spleen 
• Kidney 
• Distal ileum 
• Blood in EDTA or Heparin (live cases) 
Identification of agents 
• Reverse transcription polymerase chain reaction (RT-PCR) or real time RT-PCR. 
• Virus isolation in cell culture, with virus detection by immunofluorescence 
or immunoperoxidase. Confirmatory identification with monoclonal antibodies. 
• Direct immunofluorescence test on cryostat sections of organs from affected pigs. 
PREVENTION AND CONTROL 
No treatment is possible. Affected pigs must be slaughtered and the carcasses buried 
or incinerated. 
Sanitary prophylaxis 
• Effective communication between veterinary authorities, veterinary practitioners and 
pig farmers 
• Effective disease reporting system 
• Strict import policy for live pigs, pig semen, and fresh and cured pig meat 
• Quarantine of pigs before admission into herd 
• Efficient sterilization (or prohibition) of waste food fed to pigs 
• Efficient control of rendering plants 
• Structured serological surveillance targeted to breeding sows and boars 
• Effective pig identification and recording system 
• Effective hygiene measures protecting domestic pigs from contact with wild boar 
Medical prophylaxis 
Vaccination with modified live virus strains is effective in preventing losses in countries 
where classical swine fever is enzootic, but is unlikely, on its own, to eliminate infect io n 
entirely. In countries which are free of disease, or where eradication is in progress, 
vaccination is normally prohibited.
Response to outbreaks 
• Slaughter of all pigs on affected farms 
• Safe disposal of carcasses, bedding, etc. 
• Thorough disinfection 
• Designation of infected zone, with control of pig movements 
• Detailed epidemiological investigation, with tracing of possible sources (up-stream) and 
possible spread (down-stream) of infection 
• Surveillance of infected zone, and surrounding area. 
AFRICAN SWINE FEVER 
 Aetiology 
 Distribution 
 Morbidity/mortality 
 Transmission 
 Clinical signs 
 Postmortem lesions 
 Diagnosis 
 Vaccination 
 Quarantine 
Aetiology 
African swine fever (ASF) is caused by a large, double stranded DNA virus, African swine fever 
virus (ASFV), which replicates predominantly in the cytoplasm and is the only member of the 
Asfarviridae family, genus Asfivirus. 
Geographic Distribution 
Endemic: southern Africa, island of Sardinia in Italy 
Recent outbreaks: the Caucasus, Georgia, Armenia, Russia, Ukraine 
Morbidity/mortality 
 Morbidity approaches up to 100% previously unexposed herds 
 Mortality varies with virulence of isolate, ranges from 0-100 % 
 May be asymptomatic in wild pigs 
 No treatment or vaccine 
 
Transmission 
 Direct contact: usually via the oral and nasal cavities. 
 Indirect contact: via uncooked garbage, insects, bite of infected ticks, mechanically by
bitting flies 
 Found in all tissues and body fluids 
Clinical signs 
Acute disease: they have an incubation period of 5 to 19 days 
The clinical signs include; 
 High fever 
 Moderate anorexia 
 Erythema,cyanosis 
 Recumbency 
 Bloody diarrhea 
 Abortion 
 Death 
Chronic disease: 
 Multifocal erythema on the ears, abdomen and raised or necrotic areas 
 Intermittent low fever 
 Coughing 
 Painless joint swelling 
 Emaciation and stunting 
 Death 
Postmortem lesions 
 Hemorrhagic 
 Spleen: enlarged, friable, dark red to blackish. 
 Lymph nodes 
 Kidneys 
 Heart 
 Focal skin necrosis 
 Fibrinous pericarditis 
 Generalized lymphadenopathy 
 Swollen joints 
 Consolidated lobules in lungs 
Diagnosis 
 Suspected African swine fever in pigs with: 
 Fever 
 Characteristic postmortem signs in spleen, lymph nodes 
 Laboratory tests 
 Virus isolation 
 Viral antibody detection 
 Polymerase chain reaction(PCR)
Differential diagnosis: 
 Classical swine fever 
 Acute PRRS 
 Porcine dermatitis and nephropathy syndrome 
 Erysipelas 
 Salmonellosis 
 Eperythrozoonosis 
 Heavy metal poisoning 
 Warfarin poisoning 
Vaccination 
No effective vaccine 
Just need to do our part: keep our pigs healthy, free from foreign animal diseases 
Quarantine 
Suspicion of African swine fever calls for quarantine of the entire herd, strict enforceme nts, 
authorities notified, diagnosis confirmed. The carcasses must be disposed by either burial or 
burning. 
REFERENCES 
• Brown C. & Torres A., Eds. (2008). - USAHA Foreign Animal Diseases, Seventh 
Edition. 
Committee of Foreign and Emerging Diseases of the US Animal Health Association. Boca 
Publications Group, Inc. 
• Coetzer J.A.W. & Tustin R.C., Eds. (2004). - Infectious Diseases of Livestock, 2nd Edition. 
Oxford 
University Press. 
• Fauquet C., Fauquet M., & Mayo M.A. (2005). - Virus Taxonomy: VIII Report of the 
International 
Committee on Taxonomy of Viruses. Academic Press. 
• Spickler A.R. & Roth J.A. Iowa State University, College of Veterinary 
Medicine - http://www.cfsph.iastate.edu/DiseaseInfo/factsheets.htm 
• World Organization for Animal Health (2009). - Terrestrial Animal Health Code. OIE, 
Paris. 
• World Organization for Animal Health (2008). - Manual of Diagnostic Tests and Vaccines 
for 
Terrestrial Animals. OIE, Paris. 
• Technical Part accompanying the “Diagnostic Manual” of Commission Decision 
2002/106/EC 
• Commission Decision 2002/106/EC approving of a “Diagnostic Manual”, Anonymous 
(2002)
Classical&african swine fever

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Classical&african swine fever

  • 1. 1 SWINE FEVER Swine Fever, highly contagious, often fatal disease affecting pigs, also known as hog cholera. It is caused by two unrelated viruses: classical swine fever (CSF) and African swine fever (ASF). INTRODUCTION/THEORY/HISTORY The condition is treated with extreme caution by international health authorities because it causes severe economic damage in agricultural communities. Pigs contracting acute versions of CSF or ASF (which have many indistinguishable symptoms) can die within five days. Those with even mild cases of CSF typically die within a year, although in that time they may have a partial recovery. Swine fever spreads from pig to pig through oral and nasal secretions or through contaminated, recycled feed. The CSF virus, however, can also be transmitted between pigs through contaminated vehicles, contaminated syringes, contact with human beings, or through the air, and can be shed for a period of 10 to 20 days following infection. In each instance of the disease the chronic condition induces fever, weight loss, diarrhea, pneumonia, and ultimately death in 90 percent of cases. Protection against CSF is also made difficult by the tenacious, infectious quality of the virus, which can survive up to four years in frozen carcasses. As a result, many governments refuse to accept pig meat imports from countries with inadequate controls. These countries are unlikely to become approved exporters of live pigs or pig meat because of poor internal restraints on disease prevention and management. One of the international trading zones best regulated for swine fever is the European Union (EU). In 1980 the EU introduced a strict slaughter policy on both diseased and contact animals with the aim of eliminating both strains of this disease. Despite the effective administration of this policy, however, CSF still occurs naturally in parts of Italy and Germany. After ASF spread into Europe in 1957, it became established among wild pig populations in Sardinia and in isolated areas of northwestern Spain and Portugal. As a result, the EU’s domesticated pig herd still suffers from sporadic outbreaks of both CSF and ASF. Control was made more difficult by the discontinuation of internal border controls following the adoption of the single European market in 1993. The most recent outbreaks of ASF were recorded in Spain, Portugal, and Italy in 1993, while epidemics of CSF swept Germany, Italy, France, Belgium, and the Netherlands as recently as 1994. A typical protective strategy is to restrict the movement of breeding pigs, pig meat, and pig offal out of those areas which are known to harbor the disease. Some countries establish a surveillance area around infected premises, which are then cordoned off. All animals affected, or suspected of being affected, from these surveillance areas are then slaughtered. Compensation is often paid at half the market value for the disposal of pigs known to be infected, while the destruction of pigs only suspected of having been in contact with the disease is often compensated in full. During the 1994 CSF outbreak in Germany and the Netherlands, some 91,702 infected pigs were killed on 55 farms and the preventive slaughtering of 231,590 pigs was carried out on an additional 326 farms. The estimated administrative and slaughtering cost was £125 million (about $188 million). No exact calculation of the total economic damage has been made.
  • 2. 2 CLASSICAL SWINE FEVER (hog cholera) Aetiology Epidemiology Diagnosis Prevention Control References AETIOLOGY Classification of the causative agent Family Flaviviridae, genus Pestivirus , one serotype divided into three major genotypes and ten subtypes. Closely related to ruminant pestiviruses causing bovine virus diarrhea and border disease. EPIDEMIOLOGY Virulence of disease is related to strain of virus isolate, age of pig and immune status of herd. Virus is highly contagious. Acute disease is still the prevalent form in younger animals, with subacute and chronic forms often observed in older animals. Hosts Pigs and wild boar are the only natural reservoir of classical swine fever virus. All feral and wild pigs, including European wild boar, are susceptible. Collared peccaries were susceptible in one study, but recovered in 10 days. Transmission • Mainly by the oral and oronasal routes, via direct or indirect contact. • Direct contact between animals (secretions, excretions, semen, and blood) • Spread by farm visitors, veterinarians, pig traders • Indirect conta c t through premise s , implements , vehic le s , c lothe s , ins t ruments and needles • ‘Neighborhood effect’ during outbreaks in areas of high pig farm density: airborne transmission over short distances (up to 1 km in one study) • Insufficiently cooked waste food fed to pigs: most common means of entry into free countries • Transplacental infection: may create inapparent carrier piglets or congenita l abnormalities • Wild boar populations may harbour virus; domestic pigs in the affected area are at a high risk; and biosecurity is crucial
  • 3. 3 Sources of virus • Blood, secretions and excretions (oronasal and lachrymal discharges, urine, faeces and semen) and tissues of sick or dead animals, including meat • Congenitally infected piglets are persistently viraemic and may shed the virus for 6– 12 months before dying • Infection routes: ingestion (most common), contact with the conjunctiva or mucous membranes, skin abrasions, genital transmission, artificial insemination, percutaneous blood transfer Occurrence The disease occurs in much of Asia, Central and South America, and parts of Europe and Africa. Many countries are free of the disease. DIAGNOSIS Incubation period is 2–14 days. Clinical form varies with the strain of virus, the age/susceptibility of pigs and the occurrence of other pathogens in the herd (herd health status). Clinical diagnosis Acute form (more virulent virus strains and/or younger pigs) • Fever (41°C) • Anorexia, lethargy • Severe leucopenia • Multifocal hyperaemia and/or haemorrhagic lesions of the skin • Conjunctivitis • Enlarged, swollen lymph nodes • Cyanosis of the skin especially of extremities (ears, limbs, tail, snout) • Transient constipation followed by diarrhoea • Vomiting (occasional) • Dyspnoea, coughing • Ataxia, paresis and convulsion • Pigs huddle together • Death occurs 5–25 days after onset of illness • Mortality in young pigs can approach 100% Chronic form (less virulent virus strains or partially immune herds) • Dullness, capricious appetite, pyrexia, diarrhoea for up to 1 month • Ruffled appearance of pigs • Growth retardation • Apparent recovery with eventual relapse and death within about 3 months
  • 4. 4 Congenital form (outcome depends on virulence of virus strain and stage of gestation) • Fetal death, resorption, mummification, stillbirth • Abortion • Congenital tremor, weakness • Runting and poor growth over a period of weeks or months leading to death
  • 5. • Born clinically normal but persistently viraemic with no antibody response: important intermittent shedders of virus until dying in 6–12 months (late onset form). Mild form (usually older animals; outcome depends on virulence of virus strain): 5 • Transient pyrexia and inappetence • Recovery and (lifelong) immunity Lesions Acute form: Lesions are usually complicated by secondary infections • Leucopoenia and thrombocytopenia • Enlarged haemorrhagic lymph nodes are common • Widespread petechiae and ecchymoses, especially in the skin, lymph nodes, epiglott is, bladder, kidney and rectum • Severe tonsillitis with necrotic foci sometimes occurs • Multifocal infarction of the margin of the spleen is characteristic: nearly pathognomo nic but occurs infrequently with currently circulating strains • Lungs may be congested and haemorrhagic • Encephalomyelitis with perivascular cuffing is common Chronic form: Lesions are usually complicated by secondary infections • ‘Button’ ulcers in the caecum and large intestine mucosa • Generalised depletion of lymphoid tissue • Transverse striations of unmodelled growth cartilage at costochondral junct ions in growing pigs • Haemorrhagic and inflammatory lesions are often absent Congenital form Central dysmyelinogenesis, cerebellar hypoplasia, microcephaly, pulmonar y hypoplasia, hydrops and other malformations. Differential diagnosis Varies with form of the disease • African swine fever (indistinguishable clinico-pathologically. It is essentia l to send samples for laboratory confirmation.) • Septicaemias: erysipelas, eperythrozoonosis, salmonellosis, streptococcosis, pasteurellosis, actinobacillosis, and Haemophilus parasuis • Haemorrhage: porcine dermatitis and nephropathy syndrome, haemolytic disease of the newborn, coumarin poisoning, thrombocytopenic purpura • Runting: post weaning multisystemic wasting syndrome, enterotoxicosis, swine dysentery, campylobacteriosis • Abortions: Aujeszky’s disease (pseudorabies virus), encephalomyocarditis virus infection, porcine reproductive and respiratory syndrome, parvovirus • Nervous signs: viral encephalomyelitis, salt poisoning • Congenital infection with ruminant pestiviruses: Bovine virus diarrhea, Border disease
  • 6. 6 Laboratory diagnosis Identification of the agent Method of choice for detecting herds early in infection is to collect whole blood and tissues from multiple febrile or recently dead animals. • Tonsil • Lymph nodes (pharyngeal, mesenteric) • Spleen • Kidney • Distal ileum • Blood in EDTA or Heparin (live cases) Identification of agents • Reverse transcription polymerase chain reaction (RT-PCR) or real time RT-PCR. • Virus isolation in cell culture, with virus detection by immunofluorescence or immunoperoxidase. Confirmatory identification with monoclonal antibodies. • Direct immunofluorescence test on cryostat sections of organs from affected pigs. PREVENTION AND CONTROL No treatment is possible. Affected pigs must be slaughtered and the carcasses buried or incinerated. Sanitary prophylaxis • Effective communication between veterinary authorities, veterinary practitioners and pig farmers • Effective disease reporting system • Strict import policy for live pigs, pig semen, and fresh and cured pig meat • Quarantine of pigs before admission into herd • Efficient sterilization (or prohibition) of waste food fed to pigs • Efficient control of rendering plants • Structured serological surveillance targeted to breeding sows and boars • Effective pig identification and recording system • Effective hygiene measures protecting domestic pigs from contact with wild boar Medical prophylaxis Vaccination with modified live virus strains is effective in preventing losses in countries where classical swine fever is enzootic, but is unlikely, on its own, to eliminate infect io n entirely. In countries which are free of disease, or where eradication is in progress, vaccination is normally prohibited.
  • 7. Response to outbreaks • Slaughter of all pigs on affected farms • Safe disposal of carcasses, bedding, etc. • Thorough disinfection • Designation of infected zone, with control of pig movements • Detailed epidemiological investigation, with tracing of possible sources (up-stream) and possible spread (down-stream) of infection • Surveillance of infected zone, and surrounding area. AFRICAN SWINE FEVER  Aetiology  Distribution  Morbidity/mortality  Transmission  Clinical signs  Postmortem lesions  Diagnosis  Vaccination  Quarantine Aetiology African swine fever (ASF) is caused by a large, double stranded DNA virus, African swine fever virus (ASFV), which replicates predominantly in the cytoplasm and is the only member of the Asfarviridae family, genus Asfivirus. Geographic Distribution Endemic: southern Africa, island of Sardinia in Italy Recent outbreaks: the Caucasus, Georgia, Armenia, Russia, Ukraine Morbidity/mortality  Morbidity approaches up to 100% previously unexposed herds  Mortality varies with virulence of isolate, ranges from 0-100 %  May be asymptomatic in wild pigs  No treatment or vaccine  Transmission  Direct contact: usually via the oral and nasal cavities.  Indirect contact: via uncooked garbage, insects, bite of infected ticks, mechanically by
  • 8. bitting flies  Found in all tissues and body fluids Clinical signs Acute disease: they have an incubation period of 5 to 19 days The clinical signs include;  High fever  Moderate anorexia  Erythema,cyanosis  Recumbency  Bloody diarrhea  Abortion  Death Chronic disease:  Multifocal erythema on the ears, abdomen and raised or necrotic areas  Intermittent low fever  Coughing  Painless joint swelling  Emaciation and stunting  Death Postmortem lesions  Hemorrhagic  Spleen: enlarged, friable, dark red to blackish.  Lymph nodes  Kidneys  Heart  Focal skin necrosis  Fibrinous pericarditis  Generalized lymphadenopathy  Swollen joints  Consolidated lobules in lungs Diagnosis  Suspected African swine fever in pigs with:  Fever  Characteristic postmortem signs in spleen, lymph nodes  Laboratory tests  Virus isolation  Viral antibody detection  Polymerase chain reaction(PCR)
  • 9. Differential diagnosis:  Classical swine fever  Acute PRRS  Porcine dermatitis and nephropathy syndrome  Erysipelas  Salmonellosis  Eperythrozoonosis  Heavy metal poisoning  Warfarin poisoning Vaccination No effective vaccine Just need to do our part: keep our pigs healthy, free from foreign animal diseases Quarantine Suspicion of African swine fever calls for quarantine of the entire herd, strict enforceme nts, authorities notified, diagnosis confirmed. The carcasses must be disposed by either burial or burning. REFERENCES • Brown C. & Torres A., Eds. (2008). - USAHA Foreign Animal Diseases, Seventh Edition. Committee of Foreign and Emerging Diseases of the US Animal Health Association. Boca Publications Group, Inc. • Coetzer J.A.W. & Tustin R.C., Eds. (2004). - Infectious Diseases of Livestock, 2nd Edition. Oxford University Press. • Fauquet C., Fauquet M., & Mayo M.A. (2005). - Virus Taxonomy: VIII Report of the International Committee on Taxonomy of Viruses. Academic Press. • Spickler A.R. & Roth J.A. Iowa State University, College of Veterinary Medicine - http://www.cfsph.iastate.edu/DiseaseInfo/factsheets.htm • World Organization for Animal Health (2009). - Terrestrial Animal Health Code. OIE, Paris. • World Organization for Animal Health (2008). - Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. OIE, Paris. • Technical Part accompanying the “Diagnostic Manual” of Commission Decision 2002/106/EC • Commission Decision 2002/106/EC approving of a “Diagnostic Manual”, Anonymous (2002)