Encephalomyocarditis Virus in Pigs

Encephalomyocarditis virus (EMCV) has been recognized as a swine pathogen responsible for sporadic outbreaks for the last thirty years. It is classified in the genus Cardiovirus in the family Picornaviridae. The EMCV group is generally regarded as a rodent virus with the principle vectors being rats and mice. The group can naturally infect a wide range of vertebrate species, including swine, which is the most susceptible of the domesticated animals. To date there is no clear evidence to support the role of EMCV as a pathogen in livestock other than swine.

The traditional manifestation of the disease in swine is characterized by acute onset of disease with sudden deaths due to myocardial failure in pre-weaning pigs. Anorexia, listlessness, trembling, staggering, paralysis, or dyspnea may also be observed. Younger pigs are usually more susceptible with mortality reaching up to 100% in the unweaned animals. Post-weaning pigs generally develop subclinical infections. EMCV has been recovered from stillborn and mummified fetuses demonstrating that transplacental infection may occur. Infected pregnant sows may have near-term abortions and low farrowing rates. Infertility problems seen in these animals are attributed to fetal mummifications after intrauterine deaths.

Oral transmission through either rodent feces or carcasses appears to be the most likely route of transmission. Virus strain, viral dose, history and susceptibility of the individual animal all appear to affect the course of infection.

It is important when making a diagnosis to differentiate EMCV from the other reproductive diseases. History can be an important component to the diagnosis of EMCV especially when it is one of reproductive failure with high preweaning mortality. This can be seen in sows of any parity, which can be used to distinguish from porcine parvovirus, which is primarily manifested in gilt litters. Dyspnea, due to heart failure, seen grossly as white necrotic lesions in the heart, is characteristic of EMCV but should be differentiated from Selenium/Vit. E deficiency. * Virus isolation and identification is considered necessary for a definitive diagnosis. Since there is no transmission of maternal immunoglobulins across the placenta in pigs, detection of antibody specific to EMCV from stillborn or large mummified fetuses is significant for fetal infection.

EMCV has no treatment, however, there is an apparently effective inactivated vaccine available in the United States. Energy should, therefore, be utilized to control the rodent population on the farms as well as minimize stress among the affected pigs. Disinfection can be accomplished using mercuric chloride or iodine-based solutions when necessary.

The virus seems to replicate in the intestine and cause a viremia within 2 days of infection. The highest titers are obtained from the head, but spleen, mesenteric lymph nodes, liver, pancreas and kidney also contain virus.

*Other gross lesions may include hydropericardium, hydrothorax, pulmonary edema and ascitis. The most common microscopic lesions are necroses of myocardial fibers with mononuclear cell infiltration. Perivascular accumulation of mononuclear cells can also be observed in the meninges and brain.