Swine fever

From Pig
Classical swine fever in affected pigs
Button ulcers - internal surface of colon (photo courtesy of L.D.Sims)
Haemorrhagic swollen lymph node - medial retropharyngeal (courtesy of Dr. Stan Done, Veterinary Laboratories Agency UK)
Widespread haemorrhages on visceral surfaces associated with swine fever

Classical swine fever is a contagious viral disease of pigs.

It was first described in the early 19th century in the USA. Later, a condition in Europe termed swine fever was recognized to be the same disease. Both names continue in use, although in Europe it is now called classical swine fever to distinguish it from African swine fever, which is clinically indistinguishable but caused by an unrelated virus[1].

Classical swine fever has the potential to cause devastating epidemics, particularly in countries that are free of the disease and do not practice vaccination, so that their total pig population is susceptible. For example, an outbreak in the Netherlands in 1997-98 involved 429 herds; >12 million pigs were killed either to control the spread of disease or for associated welfare reasons. Awareness and vigilance are essential so that outbreaks are detected early and control measures are instituted rapidly to prevent further spread.


Classical swine fever is caused by a small, enveloped RNA virus in the pestivirus group of the family Flaviviridae.

Classical swine fever virus infects only pigs and wild boar, although experimental infections can be induced in other species. It will grow in porcine cell cultures, notably the PK15 cell line, but does not generally cause a visible cytopathic effect in culture so that immunolabeling methods are essential to detect viral growth. The virus has only one serotype, although some minor antigenic variability between strains can be shown. Strain typing for epidemiologic mapping purposes can be done by genetic sequencing of the virus combined with phylogenetic analysis.

The virus is moderately fragile and does not persist in the environment or spread long distances by the airborne route. It can survive for prolonged periods in a moist, protein-rich medium such as meat, other tissues, and body fluids, particularly if kept cold or frozen. Virus survival times of several years in frozen pig meat, or months in chilled or cured meat, have been reported.

Classical swine fever is distributed worldwide. It is endemic in much of Latin America, some Caribbean islands, and pig-producing countries of Asia. It has not been reported in mainland Africa. Australia, New Zealand, Canada, and the USA are free of classical swine fever, as is most of western and central Europe, although sporadic outbreaks have occurred in a number of European countries during the past decade.

The main source of infection is the pig—either live animals or uncooked pig products. In endemic areas, the major concern is spread of disease by movement of infected pigs, which can be a cause of remote outbreaks where there is large-scale transport of pigs for finishing. In parts of Europe, the wild boar population may harbor the virus, although the significance of wild boar as a reservoir for domestic pigs remains controversial.

Another major risk is accidental introduction of the virus through imported pig meat and meat products that readily find their way into the porcine food chain through the feeding of waste food. The virus is readily inactivated by cooking, which emphasizes the importance of enforcing regulations on heat treatment of swill. Many countries have completely banned swill feeding.

Mechanical transmission on vehicles and equipment, as well as by personnel (notably veterinarians) travelling between pig farms, are also significant means of spread within an infected area.

If sows are infected with low to moderately virulent strains of virus during pregnancy and then recover, there is a high risk that their offspring may be carriers. Not all such carriers will show clinical signs of disease. Therefore, it is particularly important to investigate herds that have a high level of unexplained reproductive failure, congenital tremor, or other congenital abnormalities.

Clinical signs

The disease has acute and chronic forms, and virulence varies from severe, with high mortality, to mild or even subclinical. Low virulence strains are a special diagnostic problem; the only expression may be poor reproductive performance and the birth of piglets with neurologic defects (eg, congenital tremor).

The severe acute form is characterized by fever, inappetence, and depression. The incubation period is typically 2-6 days, with death at 10-20 days after infection. Fever (>41°C) persists until the terminal stage of disease, when body temperature may become subnormal. Constipation is common, followed by diarrhea. The principal lesion is a generalized vasculitis, seen in live pigs as hemorrhages and cyanosis in the skin, notably of the extremities. There may also be a generalized erythema. Vasculitis in the CNS may produce incoordination or even convulsions. At necropsy, the principal findings are widespread petechial and ecchymotic hemorrhages, especially in lymph nodes, kidneys, spleen, bladder, and larynx. Infarction may be seen, notably in the spleen. Most pigs show a nonsuppurative encephalitis with vascular cuffing.

In chronic disease, pigs often survive >30 days. After an initial acute febrile phase, pigs may show apparent recovery but then relapse, with anorexia, depression, fever, and progressive loss of condition. Histologically, there is atrophy of the thymus and lymphoid depletion. Button ulcers may develop in the intestine, particularly near the ileocecal junction.


Differential diagnoses include other febrile hemorrhagic diseases of pigs such as African swine fever, bacterial septicemias (eg, salmonellosis, erysipelas, etc), anticoagulant poisoning (coumarin derivatives), and hemolytic disease of the newborn. Hemorrhagic lesions must be distinguished from those that are seen in porcine dermatitis and nephropathy syndrome ( Porcine Dermatitis and Nephropathy Syndrome : Introduction) and postweaning multisystemic wasting syndrome ( Postweaning Multisystemic Wasting Syndrome: Introduction), which have become widespread in many pig-producing countries. With low virulence strains of classical swine fever virus, a variety of other cases of low reproductive performance and congenital tremors should be considered, including pseudorabies, parvovirus, BVD, border disease, and noninfectious causes.

Virologic tests are essential to confirm a diagnosis. Advice on sample submission should be sought from the laboratory. Suitable tissues are tonsil, maxillary or submandibular lymph nodes, mesenteric lymph nodes, spleen, ileum, and kidney. Whole blood with EDTA as anticoagulant can be used for virus isolation from a live acute case, or for antigen or nucleic acid detection. Clotted blood samples are taken when serologic tests for antibody are required. Serology is unlikely to be of use for acute disease but may be the method of choice for testing sows that have given birth to congenitally affected litters.

Antigen detection can be performed using direct immunofluorescence on frozen tissue sections, particularly of tonsil. Reading the sections requires highly skilled and experienced personnel. Its main advantage is a rapid result. Antigen detection can also be done using ELISA, which can be useful for large-scale screening of pigs for viremia in infected areas, eg, as a premovement check.

For virus isolation, cell cultures are inoculated with tissue suspensions and tested daily by immunofluorescence for the presence of virus. Final results may not be available for 4-7 days.

Virus characterization using virus-specific monoclonal antibodies is performed as a differential diagnostic test for BVD and border disease. Positive results of antigen detection or virus isolation tests should not be confirmed until virus characterization is done.

Nucleic acid detection is performed via reverse transcriptase-PCR to detect classical swine fever virus in clinical samples. With the use of suitable primers, it can differentiate the virus from BVD and border disease. Standardized methods have been described that permit scale-up to screen large numbers of blood samples, giving rapid results while retaining high sensitivity. This is particularly useful for screening herds during an outbreak. The most widely used serologic tests are virus neutralization and ELISA. Because the virus is noncytopathogenic in culture, the neutralization test requires an additional immunolabeling stage (using fluorescent or enzyme labels). The ELISA is more suited to large-scale serology, ie, for surveillance. Blocking ELISA can distinguish classical swine fever from BVD antibodies by use of appropriate monoclonal antibody reagents, although confirmatory testing is advised in cases of doubt. ELISA methods have been developed that can detect antibodies to a specific viral protein that is absent from so-called “marker vaccines.” Although potentially useful for identifying pigs infected with wild-type virus among a population vaccinated with the gene-deleted vaccine, the technique has not as yet found much acceptance for field use, and the ELISA for the deleted protein has rather low sensitivity.


No treatment should be attempted. Classical swine fever is on the OIE List A. Reporting the disease to authorities is compulsory in many countries. Confirmed cases and in-contact animals should be slaughtered, and measures taken to protect other pigs. This may involve herd slaughter combined with area restrictions on pig movements, or vaccination, depending on local disease control regulations.

Live attenuated vaccines are widely used in endemically infected areas; these are either derivatives of the lapinized “C” strain or strains adapted from cell cultures. They are effective at controlling clinical disease but allow the virus to continue circulating subclinically; therefore, vaccination is inappropriate in countries or regions with an eradication policy. Recently, genetic manipulation has resulted in the production of marker vaccines that do not express one of the viral glycoproteins. Because naturally infected pigs develop antibodies to this protein, the combination of marker vaccine and specific diagnostic test (see above) enables the theoretical differentiation of vaccinated from infected pigs. Although the vaccines have been granted marketing authorizations in Europe, their use in the field has not yet been permitted by disease control authorities. Such an approach may be adopted in the event of a major outbreak.