Classical Swine Fever (CSF)
peste clasica, swine fever, varkenspest, peste porcine, Schweinepest, hog cholera
- *Cause
- *Clinical signs
- *Reproductive effects
- *Autopsy findings
- *Diagnosis
- *Differential diagnosis
- *Literature
- *Occurrence and spread
Cause
CSF is caused by infection with CSF (hog cholera) virus, which is a member of the Pestivirus genus of the Flaviviridae family of RNA viruses.
Formerly it was classified in the Togaviridae along with flaviviruses.
Clinical signs
Clinical signs usually appear 5-10 days after infection (occasionally longer). An individual pig may show one of four types of clinical effect:
a) Peracute (sudden death)
Especially at the beginning of a farm outbreak, young pigs may be found dead without any prior sign of illness;
b) Acute CSF (most common form)
Fever (40.5-41.5 °C,105-107°F) is often the first sign, then depression, weakness, anorexia, conjunctivitis. Constipation may be followed by diarrhoea or vomiting. There may be purple discoloration of abdominal skin, or necrosis of the tips of extremities (ears, tail, vulva). Neurological signs may occur: incoordination, tremors, convulsions, circling.
There is a high mortality (close to 100%) of acutely affected pigs, usually within a week of initial signs.
Other infections may occur concomitantly with CSF, the classic example being Salmonella choleraesuis
c) Chronic CSF
This form of disease occurs particularly with some low virulence strains of virus or when CSF strikes in vaccinated herds.
Weight loss, hair loss, dermatitis, discoloration of abdomen or ears. Affected pigs may recover or relapse.
d) Subclinical CSF
Occurs particularly in pigs infected before birth, or in pigs which have been vaccinated.
No signs are seen, but they may be infectious to other pigs.
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Reproductive effects
There may be abortions, stillbirths, mummifications and also congenital tremor of piglets.
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Autopsy findings
Peracute cases may show no gross lesions. In acute cases there are haemorrhagic lesions at autopsy. The haemorrhages are most marked under the kidney capsule, lymph nodes, ileocaecal valve, bladder and larynx.
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Occurrence and spread
Outbreaks have occurred widely in the world. The disease is enzootic in some European countries, South America and the Far East.
In the European Union (EU) CSF is enzootic in the wild boar populations of Germany & Italy (Sardinia). The island of Sardinia had 17 outbreaks of classical swine fever in 1998 and 6 in 1999. African swine fever is also enzootic (endemic) in Sardinia. In March 1999 four CSF outbreaks occurred in the regions of Piedmont and Emilia-Romagna in Italy.
CSF was eradicated from Britain in 1966, although there have subsequently been limited outbreaks in 1971, 1986 and 1987 as a result of infected meat being fed in swill.
Eradicated from the USA in 1978, after a 16 year programme.
Pig is the only species clinically affected. The virus can replicate transiently in sheep and cattle. Wild boars can be a reservoir.
Pigs can become infected by ingestion, inhalation, genital (semen) infection or by contamination of abrasions. Most spread of CSF is by contact with infected pigs or feeding of inadequately cooked garbage (swill). Spread by fomites (e.g. clothing or needles) or by biting insects is also possible.
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Diagnosis
In herds with suspicious clinical symptoms, diagnosis can be confirmed by:
serology (blood antibody tests): 24hr for ELISA, 5 days for serum neutralisation test (SNT)
fluorescent antibody test on cryostat sections of autopsy tissues from pigs with clinical symptoms of CSF (24hr for result)
virus isolation from affected pigs: 3-5 days for result.
The tissues of choice for virus detection are the tonsils, but mandibular, maxillary and mesenteric lymph nodes and any other organs showing lesions can be useful.
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Differential diagnosis
In 1996, eight suspected cases of CSF were reported to the U.K. Veterinary Laboratories Agency. Five of these followed autopsies undertaken at regional Veterinary Investigation Laboratories. Two cases were subsequently diagnosed as thrombocytopenic purpura, the most common differential diagnosis for swine fever. Amongst the others were individual cases of erysipelas, Pasteurella infection and colisepticaemia.
The other three reported suspect cases were all negative for swine fever.
In 1995, 10 suspected cases of CSF were reported to the U.K. Veterinary Laboratories Agency. All were negative. In young pigs the commonest differential disease is Purpura haemorrhagica. Similar autopsy findings in older pigs are usually due to blocking of capillaries by immune complexes, mostly involving Erysipelothrix. The classic sources of mistaken CSF diagnoses in the 1950s and 1960s were Streptococcal septicaemia and Salmonella choleraesuis infection. These are only occasionally seen nowadays in the U.K.
Reference: Lund, L.J., (1996), The Pig Journal, Vol. 37, p.55.
A new swine disease which closely resembles CSF is porcine dermatitis and nephropathy syndrome (PDNS). Many cases of PDNS are being reported as suspected swine fever outbreaks.
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Literature
books on swine fever & other pig diseases
diskette guide to classical & African swine fever resources on the Internet
"Immunohistochemical detection of hog cholera viral glycoprotein 55 in paraffin embedded tissues.", Mulas, J.M.D.L. et al (1997), J. Veterinary Diagnostic Investigation, 9, 10-16.
"Swine fever warning!", Meredith, M.J. (1997), UK Vet, May 1997.
"Epidemiological characteristics of an outbreak of classical swine fever in an area of high pig density.", Koenen, F. et al (1996), Veterinary Record, 139, 367-371.
"Simulation studies on the epidemiological impact of national identification and recording systems on the control of classical swine fever in belgium.", Saatkamp, H.W. et al (1996), Prev. Vet. Med., 26, 119-132.
"Classical swine fever 1993-1994 Belgium", Vanthemsche, P (1996), The Pig Journal, 37, 43-53.
"Notifiable diseases of pigs", Robertson, I. and Owen, J. (1994), In Practice, May 1994, 110-128.
"Hog cholera: An update of present knowledge", Terpstra, C (1991), Brit. Vet. J. 147, 397-406.
"Epizootiology of swine fever", Terpstra, C. (1987), Vo.9, Suppl.1, 50S-60S.
"Pathogenesis and epidemiology of hog cholera", Liess, B. (1986), Ann. Rech. Vet. 18, 139-145.