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About Classical Swine Fever (CSF)

A summary of classical swine fever and the virus that causes the disease.

 

CSF is an economically important contagious disease of swine world-wide. It was first recognized in Ohio in 1833. The disease occurs in much of Asia, Central and South America, and parts of Europe and Africa. Many countries are free of the disease among which are Australia, Canada, Ireland, New Zealand, Scandinavian countries and the United States.

CSF is an OIE list A disease.

CSFV (previously called hog cholera virus) is a member of the family Flaviviridae, genus Pestivirus. CSFV is closely related to the ruminant pestiviruses which cause Bovine Viral Diarrhoea (BVDV) and Border Disease (BDV).

 

Micrograph image of CSF virus particles (courtesy ICTV)
CSF virus

The virions are spherical, 50 nm in diameter, and consist of a tightly adherent lipid envelope covered with indistinct peplomers surrounding a spherical nucleocapsid with probable icosahedral symmetry. The single-stranded RNA (ssRNA) of positive polarity of the virus is infective and is about 12.5 kb long. Although CSFV can replicate in non-porcine cells, porcine kidney cells (PK15) are used most frequently for virus growth. Virus replication is restricted to the cytoplasm of the cell and does not result in a cytopathic effect. The first progeny virus is released from the cells at 5-6 hours post-infection. Virion assembly occurs on membranes of the endoplasmic reticulum, but performed capsids and budding are not seen. Instead, fully formed virions appear within the cisternae of the endoplasmic reticulum and are released via exocytosis or cell lysis.

Pigs and wild boar are the only natural hosts of CSFV. Incubation period of CSFV is 2-14 days, but under field conditions clinical symptoms may become evident in a holding not until two to four weeks or even later after virus introduction. Field strains of CSFV vary widely in virulence and the clinical signs of the disease are extremely variable. Strains of high virulence induce acute disease and high mortality, whereas moderately virulent strains generally give rise to subacute or chronic infections. Postnatal infection with low-virulence CSFV results in mild disease or subclinical infection. However, such low-virulence strains can produce mortality in porcine fetuses and new-born piglets.

 

Farrowed sow showing severe depression, generalised erythema and conjunctivitis (courtesy of DEFRA)
CSF signs

Acute, chronic and prenatal forms of classical swine fever can be distinguished. Weaners and fattening pigs most often display the acute form of CSF. The initial signs are anorexia, lethargy, fever, conjunctivitis, swollen lymphnodes, respiratory signs and constipation followed by diarrhoea. The typical haemorrhages of the skin are usually observed on the ear, tail, abdomen and the inner side of the limbs during the second and third week after infection until death. Neurological signs are frequently seen, such as a staggering hindlimb gait, incoordination of movement, and convulsions. A constant finding is fever. This is usually higher than 40°C, but in CSF infected adult animals fever may not exceed 39.5°C. CSFV causes severe leukopenia and immunnosuppression, which often leads to enteric or respiratory secondary infections. The signs of these secondary infections can mask or overlap the most typical signs of CSF and may mislead the farmer or veterinarian. Death occurs usually within 1 month. Recovery with production of antibodies does occur, most often in adult breeding animals which do not display severe clinical signs. Antibodies against CSFV are detectable from 2-3 weeks post infection onwards.

Pathological changes visible on post mortem examination are most frequently observed in lymph nodes, tonsils, spleen and kidneys. The lymph nodes become swollen, oedematous and haemorrhagic.Haemorrhages of the kidney may vary in size from hardly visible petechiae to ecchymotic haemorrhages. Similar haemorrhages can also be observed in the urinary bladder, larynx, epiglottis and heart and sometimes widespread over the serosae of the abdomen and chest. A non-purulent encephalitis is often present. Lesions due to secondary infections may also be seen which may mislead the veterinarian.

The chronic course of infection occurs when pigs are not able to develop an effective immune response against CSF virus. Initial signs of a chronic infection are similar to the acute infection. Later, predominately non-specific signs are present, intermittent fever, chronic enteritis and wasting. The typical haemorrhages of the skin are usually missing. Animals can survive 2-3 months before their eventual death. CSFV is shed from the onset of clinical signs constantly until death. Antibodies may be temporarily detected in serum samples. Pathological changes are less typical, especially concerning the lack of haemorrhages on organs and serosae. In animals showing chronic diarrhoea, necrotic lesion in the ileum, the ileocaecal valve and the rectum are common. As clinical signs of chronic CSF are rather non-specific many other diseases must be considered for differential diagnosis. In an infected pig holding fever can be detected at least in some animals.

CSFV is able to pass across the placenta of pregnant animals, and infect fetuses, whereas in the sows the disease is often subclinical. The outcome of transplacental infection of fetuses largely depends on the time of gestation and virus virulence. Infection during early pregnancy may result in abortions and stillbirths, mummification and malformations. All this leads to a reduction of the fertility index in the holding.

Infection of sows at up to 90 days of pregnancy can lead to the birth of persistently viraemic piglets, which may be clinically normal at birth and survive for several months. After birth they may show poor growth, wasting or occasionally congenital tremor. This course of infection is referred to as "late onset CSF". These piglets may play a crucial role in spreading the disease and in the maintenance of virus persistence within a population as they constantly shed virus until death. Detection of CSF may be particularly difficult in breeding pig holdings, as the course of the infection may be very mild and confused with many other pathological conditions.

During the 1990s severe outbreaks of CSF occurred within the domestic pig population of several EU Member States (e.g. Belgium, Germany, The Netherlands, Italy, Spain, United Kingdom). The largest outbreak occurred in the Netherlands in 1997. Total costs for the eradication of the disease from the EU were several billions USD. Several countries, including those of the EC, have eradication programs in force, based on rapid diagnosis, stamping out of infected herds and preventive culling, supplemented by other control measures. Emergency vaccination of the pig population in case of an outbreak is an additional option.

Despite these efforts, CSFV has still not been eliminated in many non-EU countries. This may be accounted for by the high density of pigs in certain areas, the movement over long distances of pig and pork products, and a frequent inability to trace the source of outbreaks. Furthermore, in several countries (including EU Member States) endemic CSF in wild boar and feral pigs poses a permanent threat of (re-)introduction into the domestic pig population.

For more information:

  • Veterinary Virology, 3rd Edition (Academic Press, 1999)
  • Diseases of Swine, 8th Edition (Iowa State University Press, 1999)

 

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