Classical Swine Fever

Description

Classical swine fever is a highly contagious, haemorrhagic disease of swine which is caused by a Togavirus. Presentation may be actue, sub-acute, chronic or persistent, and the disease is indistinguishable in the field from African Swine Fever. Acutely, classical swine fever is characterised by severe depression, high fever and superficial and internal haemorrhages, with many cases resulting in death. Depression, anorexia and pyrexia are seen in chronic classical swine fever. Transplacental infection is also possible and results in persistently infected piglets.

Aetiology

The causative agent of classical swine fever is a small, enveloped virus of around 40nm diameter. The genome is comprised of single stranded RNA, which is positive sense and contains about 12,300 bases. The sequence of the genome is known, and codes four structural and seven non-structural proteins. The classical swine fever virus is relatively stable in excretions and in fresh meat products including ham, salami and other similar sausages. It is, however, easily inactivated by detergents, common disinfectants and heat.

Classical swine fever virus is a Togavirus within the Pestivirus genus of the Flaviviridae. As such, it is closely related to the bovine viral diarrhoea (BVD) virus of cattle, and the border disease virus of sheep.

Signalment

Domestic pigs and other swine of any age may become infected with classical swine fever.

Pathogenesis

After transmission by direct spread or by aerosol, classical swine fever virus gains entry to the host via mucous membranes or skin abrasions. An incubation period of around 7 days ensues, but this may vary from 4-10 days. Initially, virus infects the epithelial cells of the tonsillar crypts before spreading via the lymphatics to regional lymph nodes. From here, classical swine fever virus enters the blood stream and then replicates in the spleen, bone marrow and lymph nodes before spreading to further tissues. Replication in the endothelial cells of blood vessels leads to apoptosis, causing superficial and internal haemorrhages. CSFV also causes a thrombocytopenia which contributes to haemorrhage by impairing primary haemostasis. In acute CSF this angiopathy causes pig death in association with shock and the febrile response. Surviving swine go on to develop a chronic form of the disease where joint and enteric lesions are seen resulting from tissue infarction.

The outcome of transplacental infection of foetuses depends largely on the point of gestation and may result in abortions, stillbirths, mummifications, malformations or the birth of weak or persistently viraemic piglets. Although persistently infected piglets may be clinically normal at birth, they grow poorly, excrete virus over long periods and invariably die from CSF.

Diagnosis

Clinical Signs

T et al., 2000). The incubation period in individual animals is about one week to 10 days. Under field conditions, symptoms may only become evident in a holding 2–4 weeks after virus introduction, or even later (Laevens et al., 1999). The severity of clinical signs mainly depends on the age of the animal and the virulence of the virus, and in older breeding pigs the course of the infection is often mild or subclinical. The virulence of a CSF virus isolate is difficult to determine on a rational basis (Mittelholzer et al., 2000), as the same CSF virus isolate can cause different forms of CSF depending on age, breed and immune status of the host animal (Floegel-Niesmann et al., unpublished observation). Acute, chronic and prenatal forms of CSF can be distinguished, and there is no array of classical symptoms that is invariably associated with the disease. Piglets up to 12 weeks of age most often display the acute form. A constant finding is pyrexia, usually higher than 40 �C, but in adults the temperature may not exceed 39.5 �C. Initial signs are anorexia, lethargy, conjunctivitis, enlarged and discoloured lymph nodes, respiratory signs and constipation followed by diarrhoea. Neurological signs are frequently seen, such as a staggering gait with weakness of hind legs, incoordination of movement, and convulsions (Fig. 1). 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. The virus is shed from the infected animal by saliva, urine and faeces (Depner et al., 1994; Laevens et al., 1999). Pathological changes visible on post mortem examination are observed most often in lymph nodes, spleen and kidneys. The lymph nodes become swollen, oedematous and haemorrhagic (Fig. 2). Haemorrhages of the kidney may vary in size from petechiae to ecchymotic haemorrhages. Petechiae can also be observed in the urinary bladder, larynx, epiglottis and heart, and may be widespread over the serosae of the abdomen and chest. A non-purulent encephalitis is often present (Gruber et al., 1995). CSF virus causes severe leukopenia and immunosuppression, which often leads to secondary Fig. 1. Neurological signs of CSF. The back is hunched up and the hind legs are pushed under the abdomen. Wasting and haemorrhages on ears and hind legs are visible. Fig. 2. Swollen lymph nodes of the small intestine and necrosis of the ileocaecal valve (centre). 12 THE VETERINARY JOURNAL, 165, 1 enteric or respiratory infections. The signs of these secondary infections can mask or overlap the most typical signs of CSF and may mislead the veterinarian (Depner et al., 1999). In general, the acute form of African swine fever leads to a very similar clinical and pathological picture. CSF must also be considered in the differential diagnosis of erysipelas, porcine reproductive and respiratory syndrome (PRRS), cumarin poisoning, purpura haemorragica, post-weaning multisystemic wasting syndrome (PWMS), porcine dermatitis and nephropathy syndrome (PDNS), Salmonella or Pasteurella infections or any enteric or respiratory syndrome with fever not responding to antibiotic treatment. With increasing age of the infected pigs (fattening and breeding animals) the clinical signs are less specific and recovery with production of antibodies can occur. Antibodies against CSF virus become detectable 2–3 weeks postexposure to CSF virus (Laevens et al., 1998). CHRONIC COURSE OF CLASSICAL SWINE FEVER VIRUS INFECTION The chronic form of CSF is always fatal. It develops when pigs are not able to mount an effective immune response against the infection. Initial signs are similar to die acute infection. Later, predominantly non-specific signs are observed, e.g. intermittent fever, chronic enteritis and wasting. Animals may survive for 2–3 months before they die. CSF virus is shed from the onset of clinical signs constantly until death. Antibodies may be temporarily detected in serum samples, as the immune system starts to produce antibodies although they are not able to eliminate the virus from the host. Consequently the antibodies are neutralised by the virus and cease to be detectable (Depner et al., 1996). Pathological changes are less typical, especially the lack of haemorrhages on organs and serosae. In animals displaying chronic diarrhoea, necrotic and ulcerative lesions on the ileum, the ileocaecal valve and the rectum are common. Since clinical signs of chronic CSF are rather non-specific, a broad range of other diseases must be considered as part of any differential diagnosis. PRENATAL COURSE OF INFECTION AND LATE ONSET OF DISEASE Although the course of infection in the sow is often subclinical, CSF virus is able to cross the placenta of pregnant animals, thereby infecting fetuses during all stages of pregnancy. The outcome of transplacental infection of fetuses mainly depends on the time of gestation and viral virulence, respectively. Infection during early pregnancy may result in abortions and stillbirths, mummification and malformations. All of this will lead to a reduction in the fertility index in the holding. Infection of sows from about 50–70 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, theymay show poor growth, wasting or occasionally congenital tremor. This course of infection is referred to as �late onset CSF�. These piglets constantly shed large amounts of virus and are a dangerous virus reservoir, spreading the disease and maintaining the infection within the pig population (Van Oirschot and Terpstra, 1977). This situation is comparable to cattle persistendy infected with BVD virus. CSF must be considered in the differential diagnosis of reduced fertility due to parvovirus infection, PRRS, leptospirosis and Aujeszky�s disease.

Treatment

Control

• NOTIFIABLE disease
• Vaccination (live attenuated) in endemic countries:
  • Parts of EU are using vaccinated bait to control spread in wild boar population
  • Vaccination does not curtail spread: marker vaccine needed to distinguish virus exposure from vaccine-induced antibody