Encephalomyocarditis Virus

Also known as: EMC — Encephalomyocarditis virus disease of pigs — encephalomyocarditis virus— EMCV .

Introduction

Encephalomyocarditis is caused by a single stranded RNA (ssRNA) virus called encephalomyocarditis virus (EMCV). It is a cardiovirus from the family Picornaviridae, and like other picornaviruses it stable over a wide range of pH. The virus is ether-resistant and can be inactivated at 60°C for 30 minutes, but some strains have shown a marked thermal stability. EMCV causes high mortality in young pigs and reproductive failures in breeding females. Piglets suffer from myocarditis and encephalitis and sudden deaths due to myocardial failure are common. The disease affects the nervous, reproductive, respiratory and circulatory system of pigs. Antibodies for EMCV have been demonstrated in human populations but there are no reports that the virus causes human heart disease.

Signalment

Host include chimpanzees, monkeys, elephants, lions, squirrels, mongooses, racoons and pigs, which are the main domestic animal host for the virus and most susceptible to EMCV infection. The major reservoir of the disease is rodents. Rats and other rodents infect swine feeds or water supplies directly or through diseased carcasses. Clinical problems in swine are mostly limited to tropical areas where the infection can cause significant economic losses. The disease has also been observed in different zoo animals.

Clinical Signs

Clinical signs include vomiting and regurgitation, anorexia, pyrexia, fasciculations, tachypnea, dyspnea, open mouth breathing and sudden death. Neurological signs include ataxia, generalised weakness, tetraparesis, inability to stand, tremor, dysmetria, lethargy and depression. Pregnant sows that become infected can suffer from infertility, mummified fetus, abortions, still births, small litter and weak new born.

Epidemiology

The mode of virus transmission is not clear but rodent-to-pig transmission is probably common. Infected pigs can shed the virus in faeces but pip to pig transmission has not yet been proved experimentally. The route of infection in swine is likely to be oral and experiments have shown this to be the case. Virus can be shed from infected pigs for up to 9 days in their faeces. Animals that survived from the acute disease produced EMCV antibodies and the course of infection depends upon the virus strain, dose, history and the individual’s immune system. Further experiments have shown that intramuscular infection can cause transplacental infection and foetal deaths in pregnant sows (Love and Grewal, 1986). Love RJ, Grewal AS, 1986. Reproductive failure in pigs caused by encephalomyocarditis virus. Australian Veterinary Journal, 63(4):128-129; 3 ref.

Distribution

Worldwide distribution but cases first reported in Central America, Florida and Australia.

Diagnosis

A presumptive diagnosis can be made on the above clinical signs especially high neonatal mortality, history of reproductive failure or dyspnea in young infected pigs. A definitive diagnosis can be confirmed by virus isolation from infected heart tissue from the acute phase of the disease. Baby hamster kidney (BHK-21), HeLa or Vero cell lines are commonly used for virus isolation.

Cardiomegaly and myocardial lesions with yellow or white necrotic foci (2-15mm diameter) are common and usually present on the epicardium of the right ventricle. These lesions can also be characteristic of Vitamin E and selenium deficiency. Acutely affected pigs may not show any gross lesions on post mortem. Infected foetuses can grossly vary depending on the stage of pregnancy and infection and myocardial lesions may be indistinguishable from other viral infections. Foetuses can be haemorrhagic, oedematous or apparently normal.

Histopathological findings include myocarditis with focal or diffuse accumulation of mononuclear cells, vascular congestion, oedema, degeneration of the myocardial fibres with necrosis and occasional mineralization of necrotic heart muscle is common. Brain tissue can be congestion with evidence of meningitis, perivascular infiltration (mononuclear cells) and neuronal degeneration. Nonsuppurative encephalitis and myocarditis has also been seen in naturally infected swine foetuses.

Detection of antibody specific to EMCV from still born piglets has been used to confirm foetal infection Joo et al., 1988; Joo HS, Kim HS, Leman AD, 1988. Detection of antibody to encephalomyocarditis virus in mummified or stillborn pigs. Archives of Virology, 100(1-2):131-134; 9 ref.

Kim et al., 1991). Kim HS, Joo HS, Christianson WT, Morrison RB, 1991. Evaluation of serologic methods for detection of antibodies to encephalomyocarditis virus in swine fetal thoracic fluids. Journal of Veterinary Diagnostic Investigation, 3(4):283-286; 20 ref.

Treatment

There is no specific treatment. Mortality levels in at risk pigs can be reduced by avoiding stress or excitation. .

Control

An inactivated vaccine for EMCV (for intramuscular injection) is commercially available in the USA. It is important to control rodent populations on farm to prevent the spread of disease and contamination of feeds or water supply. Good husbandry and hygiene protocols should be followed with the regular use of disinfectants.

References

Encephalomyocarditis Virus Learning Resources
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