1. The haemorrhagic diatheses (Classical swine fever and African swine fever)

2. The vesicular diseases (Foot and Mouth disease, Swine Vesicular disease, Vesicular

   Exanthema (eradicated). Vesicular Stomatitis affects ruminants and horses, not pigs)

3. The A’s (anthrax and Aujeszky’s disease)

4. The T’s (Teschen and Tuberculosis) 

There is one known serotype of the virus but strains differ in virulence. The virus is closely related to BVD, BD and may be confused with these infections clinically. It can survive for a long time in frozen or refrigerated meat, is resistant to heat and relatively stable. Spread is by pigs, human contacts, fomites, semen and wild boar and also by aerosol from large concentrations of pigs and via infected feed and lorries contaminated by organic matter. In the past waste feeding has been a major source of infection. Recent outbreaks have occurred in Germany from wild boar contact, Portugal, Sardinia, Eastern Europe, Rusia, China and the Phillipines. Also present in Central and South America.

Clinical signs are determined by virulence of the strain and the susceptibility of the host pig. Virulent strains cause the acute form of the disease.
Strains of low virulence cause a high proportion of chronic infections.

Large numbers of pigs become sick in a short period of time. They are drowsy, inactive, stand with arched backs. Others stand with drooping heads, straight tails. Some may vomit and some have diarrhoea. They are reluctant to rise and huddle together. Anorexia, and constipation are features. Temperature may be as high as 42oC. Conjunctivitis is frequent (see encrusted eyes). Sick pigs become gaunt with a weak and staggering gait. Some may become recumbent and have convulsions and other nervous signs. Purple skin

Outbreaks are prolonged and clinical signs include diarrhoea, lameness, poor growth performance and increased mortality. There are large numbers of runty pigs which eventually die. Infertility problems occur in the herd.

- In chronic cases lesions are often obscured by secondary infections. One of these features is “button ulcers” of the large intestine, particularly the ileocaecocolic junction. Joint are affected with chronic synovitis.

Outbreaks are prolonged and clinical signs include diarrhoea, lameness, poor growth performance and increased mortality. There are large numbers of runty pigs which eventually die. Infertility problems occur in the herd.

- In chronic cases lesions are often obscured by secondary infections. One of these features is “button ulcers” of the large intestine, particularly the ileocaecocolic junction. Joint are affected with chronic synovitis.

If a virulent strain is involved there is abortion. If the strain is of low virulence mummification, stillbirth, weak or shaker pigs are seen. Malformations of the visceral organs or brain occur regularly. Some pigs may be born viraemic after exposure in the first trimester of pregnancy. These do not mount an antibody response. In many herds where low virulence strains are endemic the only clinical sign may be poor reproductive performance.

- Abnormalities of the CNS particularly cerebellar hypoplasia are the most common feature.

Clinical signs, history and gross pathological lesions. If there is any suspicion of CSF on initial inspection it is important to notify the local AHVLA without delay. AHVLA will visit the unit and take responsibility for confirming the diagnosis or ruling it out. Confirmation requires laboratory diagnosis. Tonsils, spleen, lymph nodes, kidneys and distal ileum are taken for virus detection (fluorescent antibody, in-situ hybridisation, immunoperoxidase and virus isolation) and tissues taken in formalin for histopathology. Differential diagnoses are African swine fever, PDNS, acute septicaemias such as salmonellosis (especially S. cholerae suis) and BVD virus infection.

The disease spreads through tick bites and by direct contact with infected pigs (carrier pigs are found). No aerosols are produced. It is not as contagious as CSF. The pathogenesis in acute and chronic cases is similar to CSF. The incubation period is about one week. The only major difference from CSF is that it does not spread trans-placentally although acutely infected animals abort, probably due to fever. In highly virulent ASF infection there is little or no immune response. In infections with a less virulent virus there is a normal response. 

The virus is carried by wart hogs which are inapparent hosts, and it replicates in the soft tick Ornithodoros. Primary spread from country to country is through pork products carried by people, on planes, cruise liners etc. as well as through wild boar. It survives readily in salted and dried pork for about a year and in frozen pork for about 2 years. The disease is endemic in Sardinia (due to wild boar in central highlands acting as a persistent source of infection). A large, persistent outbreak which started in Georgia in 2008 has spread to many parts of Russia where it has become endemic and continues to spread. In July 2014 the first cases of ASV were detected in commercial pigs within the EU. Illegal movements of pigs and vehicles out of infected areas are thought to be the cause of the continued spread.

- probably already in the country  

The signs are similar to CSF. There is a reluctance to stand and pigs are depressed. There is high fever (42oC), reddened skin, moderate anorexia, but usually less than 25% mortality (which is less than in acute CSF). In pregnant animals there is abortion and high mortality. Affected animals become progressively more reddish/blue by 5-6 days and deaths occur from 7-10 days post infection. No meningitis/encephalitis is seen in young pigs.

Low virulence forms may cause a mild fever and joint lesions.

In chronic ASF there is consolidation of the lung, generalised lymphadenopathy, necrotic skin, swollen joints and pericarditis.

Clinical signs, history and gross pathology. Adopt the same approach as with CSF, ie notify the AHVLA in the event of any suspicion of ASF or CSF.

The diagnosis is confirmed by demonstration of the virus by immunoperoxidase testing of lymphoid tissues and virus isolation from the buffy coat. The virus remains present in the blood for 30-40 days after infection. Once infection is identified the lab can use direct immunofluorescent testing of tissues for viral antigen or detection of antibody by immunofluorescence. Each case is tested for antibody and antigen. Differential diagnoses are CSF, acute salmonellosis, acute erysipelas, PDNS and Aujeszky’s disease.

Isolation, eradication by slaughter out policy, disinfection, tracing. Deal with environmental factors (tick vectors and wild boar contacts).
No vaccine is available. 

Aetiology: A highly contagious vesicular disease which affects all cloven-footed animals caused by an aphtovirus (in the family picornaviridae).