Classical swine fever

viral infection of pigs
also called hog cholera
mnemonics are mentioned

1. CLASSICAL SWINE FEVER ABHIJITH SP CVAS POOKODE

2. INTRODUCTION A highly contagious infectious viral disease of pigs. Very important viral disease of pigs all over the world. Clinically, it is indistinguishable from African swine fever and can cause very serious losses. Synonyms: swine fever, European swine fever, Hog Cholera, Swine plague.

3. EPIDEMIOLOGY CSF is present in Europe, east and central Africa, Mexico, other central American countries, most of South America. It is also very present in the Indian sub-continent, China, east and south east Asia, (Korea, Indonesia, Philippines, Thailand, Vietnam). In the region, the disease has been recorded in Australia (eliminated since 1962), French Polynesia (eliminated since 1972), New Zealand (eliminated since 1953) Northern Mariana (eliminated since 1968). These outbreaks resulted from imported pig meat or food refuse from ships being swill fed to pigs. Hog cholera has been eradicated in the United States [1978].

4. AETIOLOGY Flaviviridae—Pestivirus-CSFV. Virions do not form inclusion bodies. Spherical, enveloped virions, with icosahedral capsid. Genome is a linear [+] sense ss RNA. The Virus does not hemagglutinate or hemadsorb. The virus is moderately fragile and does not persist in the environment or spread long distances by the airborne route.

5. SUSCEPTIBLE HOST Mainly pigs and warthogs. Pigs, both domestic ( Sus scrofa domesticus ) and wild ( Sus scrofa scrofa ), are the only natural hosts. There is no evidence that CSFV infects humans. Per-acute case mortality=100%

6. TRANSMISSION The most common method of transmission is through direct contact between healthy swine and those infected with CSF virus. The virus is shed in saliva, nasal secretions, urine, and feces. Contact with contaminated vehicles, pens, feed, or clothing may spread the disease. Animals that are chronic carriers of the disease (persistently infected) may show no clinical signs of illness but may shed the virus in their feces. Offspring of infected sows can become infected in the uterus, and can shed the virus for months. CSF virus can survive in pork and processed pork products for months when meat is refrigerated and for years when it is frozen. Pigs can become infected by eating CSF-infected pork meat or products. It has been proven that in parts of Europe, the wild boar population may play a role in the epidemiology of the disease. The disease has been spread through legal and illegal transport of animals, and by feeding swill containing infective tissues to pigs.

7. INCUBATION PERIOD 3–7 days, with death occurring within 10 days after infection.

8. PATHOGENESIS Entry of organism to the body through oral/nasal route. Initial virus replication occurs in the tonsils with invasion of the regional lymph nodes. Primary viremia results in Secondary replication in endothelial cells , bone marrow , and lymphoid organs —hemorrhages, edema, leukopenia, and thrombocytopenia. Transplacental transmission occurs.

9. CLINICAL SIGNS 1. Acute form (more virulent virus strains and/or younger pigs) Fever (41°C) • Anorexia, lethargy 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)

10. CLINICAL SIGNS Transient constipation followed by diarrhea Vomiting (occasional) Dyspnea, coughing Ataxia, paresis and convulsion Pigs huddle together Death occurs 5–25 days after onset of illness Mortality in young pigs can approach 100%

11. CLINICAL SIGNS 2. Chronic form (less virulent virus strains or partially immune herds) Dullness, capricious appetite, pyrexia, diarrhea for up to 1 month Ruffled appearance of pigs Growth retardation Poor reproductive performance may be the only sign in some breeding herds infected with less virulent strains Apparent recovery with eventual relapse and death within about 3 months

12. CLINICAL SIGNS 3 . 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 viremic with no antibody response: important intermittent shedders of virus until dying in 6–12 months (late onset form).

13. CLINICAL SIGNS 4. Mild form (usually older animals; outcome depends on virulence of virus strain) Transient pyrexia and inappetence . Recovery and (lifelong) immunity.

14. MACROSCOPIC LESIONS CHRONIC FORM ‘Button’ ulcers in the cecum and large intestine mucosa. Strawberry appearance lymph node. Turkey egg like kidney. Generalised depletion of lymphoid tissue Transverse striations of unmodelled growth cartilage at costochondral junctions in growing pigs. Anasarca, Cerebellar Hyperplasia ACUTE FORM Leucopoenia and thrombocytopenia. Enlarged haemorrhagic lymph nodes are common. Widespread petechiae and ecchymoses, especially in the skin, lymph nodes, epiglottis, bladder, kidney and rectum Severe tonsillitis with necrotic foci sometimes occur. Multifocal infarction of the margin of the spleen is characteristic: nearly pathognomonic but occurs infrequently with currently circulating strains. Lungs may be congested and hemorrhagic.

15. Button shaped Ulcers

16. Splenic infarction in the spleen in pigs with hog cholera. Infarcts are also seen with porcine circovirus, septicemic salmonellosis, and Mycoplasma hemosuis

17. Multifocal Fibro necrotic Colitis: Button Ulcers

18. Petechia and Cyanosis of ears

19. Turkey Egg Like Kidney

20. MICROSCOPIC LESION DIC with microthrombi, fibrinoid necrosis of vessel. Hydropic degeneration . Proliferation of endothelium.

21. DIAGNOSIS Virus isolation: tonsil,pharynx , blood, spleen, lymph nodes, etc. Antigen detection: FA or immunoperoxidase staining; ELISA. Serology: Virus neutralization assay, ELISA, etc.

22. PREVENTION AND CONTROL When an outbreak occurs, many actions must be set in place urgently:   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 Surveillance of infected zone, and surrounding area

23. FACTS. The virus is susceptible to ether, chloroform, ß-propiolactone (0.4%). CSF is one of the diseases for which the OIE has a procedure for the official recognition of disease status. There is no known risk that the CSF virus may cause any disease in humans.

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