Encephalomyocarditis (EMC)

Occurrence: Worldwide.
Age affected: All ages, human risk.
Causes: Encephalomyocarditis virus (EMCv); rodent infestations.
Effects: Sudden death, inappetence, vomiting, staggering, breathing difficulty, stillbirths, mummies.

Causes

The condition is caused by the encephalomyocarditis (EMC) virus, a picornavirus of rodents assigned to the cardiovirus group. There are four major viral proteins. It can be cultured readily, is resistant to a wide range of pH but most isolates are inactivated at 60°C for 30 minutes. There appear to be differences between isolates and more than one strain may exist. Infection is oral and the virus multiplies in the pig intestine, becomes systemic and then multiplies in heart muscle. Transplacental infection also occurs within 2 weeks of infection. Foetuses of all ages can be affected. Antibody develops in recovered pigs.

Mode of transmission

The virus is commonly present in rats and mice and these species are common sources of the virus for pigs. Infection is oral, by eating feed or drinking infected water and by eating the bodies of infected rodents. Pig to pig transmission has been recorded, but does not appear to be important or sustained in the field.

Clinical signs

Sudden death is common, particularly in piglets. Pigs with sub-lethal infections may show signs of fever to 41°C (105°F), cyanosis (blue colour) of the extremities, depression, staggering or difficulty in breathing. The blood levels of two enzymes found in heart muscle, serum creatine kinas-MB and lactate dehydrogenase I isoenzyme, may be raised. Sows and gilts may be fevered and abort at 107-111 days gestation. Failure to farrow and the birth of litters containing stillborn piglets and mummies of different sizes may occur over a period of 2-3 months. Animals with heart failure rarely recover completely.

The clinical picture of abortions and sudden deaths suggests encephalomyocarditis. Encephalomyocarditis reproductive disease must be distinguished from parvovirus and other infectious forms of reproductive failure. Blood biochemistry may demonstrate the presence of raised levels of serum creatine kinase-MB and lactate dehydrogenase I isoenzyme. Antibody to the virus may be demonstrated, but antibody-positive pigs may be clinically normal, and the finding merely indicates exposure of the herd.

Postmortem lesions

Carcasses of pigs which have died from encephalomyocarditis may be congested. Excess clear fluid is present in the chest, heart and abdominal cavities and oedema of the lungs and enlargement of the liver are common. The heart is soft and pale with white areas 2-15 mm in diameter, suggestive of dead tissue (necrosis), commonly on the outside of the right ventricle and extending for varying distances into the heart muscle (myocardium). Necrosis and inflammation of the myocardium is seen in acute cases. These lesions have healed by fibrosis in recovered animals. Mild meningo-encephalitis may be present. Affected foetuses may be mummified or have non-suppurative encephalitis, focal myocarditis, myocardial haemorrhage and excess fluid around the heart. Diagnosis is confirmed by isolating the virus, by nucleic acid methods (Polymerase Chain Reaction) and/or detection of specific antibodies. Antibody found in foetal chest fluid confirms past uterine infection.

Treatment and prevention

There is no treatment. Affected pigs should be assessed, and should killed if unlikely to recover. Separation of pigs from rodents or pigs from infected farms is the best method of prevention. Disinfection with chlorine (0.5 ppm) disinfectants can eliminate the virus and reduce spread. An inactivated oil adjuvanted vaccine has been shown to prevent reproductive failures and may be useful in countries where available.

Special note

Antibodies to the virus have been found in man, but there is currently no association with heart disease.