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Order Manual


Encephalomyocarditis (EMC) is a disease caused by a viral infection. Infection with EMC viruses is common in susceptible species, but clinical disease is unusual in domestic animals and humans.


Susceptible species include humans, primates, many species of rodents, marsupials, mongoose species, and several species of birds. In zoos, rapidly fatal infections have been reported in elephants, primates, and artiodactyls. Horses, cattle, swine, dogs, and cats are susceptible to infection, but except for swine, there is no clear evidence that EMC viruses are significant pathogens of domesticated species.

The encephalomyocarditis group of viruses (EMCV) is present throughout the world. Infection is common but clinical disease is rare in domestic animals and humans. A survey of 104 swine herds in Iowa found 13.8% of breeding stock and 8.5% of finishers had serum-neutralizing antibodies against EMCV. Approximately 90% of herds had one or more animals with antibody titers. Other serosurveys have reported similar, or higher, prevalence rates in swine.

Historical information

Columbia SK virus, the first strain of EMCV identified, was described in 1940. It was initially postulated to be a previously unrecognized strain of poliovirus, but this was later shown not to be the case. Infection in swine was not reported until outbreaks occurred in Panama (1958) and Florida (1960). Subsequently, clinical EMC was reported in Australia, Brazil, Cuba, Greece, New Zealand, and North America.

Considerable research on the EMC viruses in swine was conducted up to the mid 1990s. Much of the interest in EMC was generated because of an erroneous association with “mystery swine disease,” later proven to be caused by porcine reproductive and respiratory syndrome virus (PRRSV). Porcine reproductive and respiratory syndrome virus may have caused some outbreaks previously attributed to EMC. At present, the significance of EMC as a swine pathogen in the US is dubious.


The EMC group of viruses is classified in the genus Cardiovirus in the Picornaviridae family. They are nonenveloped, single-stranded RNA viruses and strains vary in virulence. These hemagglutinating viruses are stable and can be grown in cell cultures derived from several animal species. Areas contaminated with the EMC viruses can be disinfected with iodine-based disinfectants or 0.5 ppm residual chlorine.


Rats and mice are commonly considered to be the principal reservoirs of the virus, although the experimental evidence does not support this hypothesis. Transmission of EMC virus among rodent species is difficult to achieve and a chronic intestinal carrier state, a keystone epidemiologic feature in closely related picornaviruses (i.e. polioviruses or enteroviruses), does not occur. Infected rodents excrete virus and their diseased carcasses contain large amounts of virus. Presumably, swine are infected by ingesting feed or water contaminated by rats, mice, or the carcasses of animals that died from EMC. Infected swine excrete virus for about 9 days but it is not clear that they play an important role in transmission to other pigs. Virus has been isolated from certain tick and mosquito species, but vector competency studies have not shown transmission from infected arthropods.


Following experimental oral infection of piglets, viremia occurs. Lymphoid tissues contain virus and probably are the major sites of virus replication. The highest titers of virus occur in damaged heart muscle. Most deaths probably are related to right heart failure. Transplacental infections occur in fetuses near full term and many develop myocardial lesions. Pigs that survive develop antibodies that persist for long periods.

Clinical signs

Infection in swine is usually subclinical, but in rare cases it produces myocarditis and high mortality in nursing pigs and/or reproductive failure in dams. For unknown reasons, clinical outbreaks in swine generally occur in tropical or semi-tropical climates. Clinical disease in young piglets is often characterized by an acute course and sudden death. Less acute cases have respiratory signs with dyspnea, fever, anorexia, depression, trembling, staggering and paralysis. Mortality may approach 100% in neonatal and nursing pigs. Older pigs and adults usually have subclinical infection but some mortality may occur, even among adults. In pregnant sows and gilts, there are mid-to-near term abortions with an increase in stillbirths and mummified fetuses.


The characteristic gross lesions seen in acute disease are discrete, white, focal discolorations of the myocardium, at times accompanied by a nonsuppurative meningoencephalitis. The lesions in young piglets are those of right heart failure, including hepatomegaly, hydropericardium, hydrothorax, pulmonary edema and ascites. The heart may be enlarged, flabby, and pale red with subepicardial, petechial hemorrhages. Lesions are most marked in the right ventricle where there may be discrete yellow or white foci or diffuse, pale areas of myocardial necrosis. Similar myocardial lesions may be visible in the heart of late-aborted fetuses. Microscopic lesions include focal nonsuppurative interstitial myocarditis and myocardial necrosis; infiltration of small numbers of neutrophils may be evident.


Disease associated with EMC is rare but should be considered in cases where there is marked dyspnea and sudden deaths in preweaning age piglets, high preweaning mortality and an increase in late term abortions, or gross and/or microscopic myocardial lesions. Myocardial lesions must be differentiated from those of PRRSV, mulberry heart disease, toxoplasmosis, bacterial septicemia, and cardiac infarcts.

Definitive diagnosis requires isolation and identification of the virus, coupled with observation of typical lesions. The virus usually is isolated from the myocardium or spleen of acute cases in young piglets. A number of serologic assays (serum neutralization [SN], hemagglutination inhibition [HI], agar gel immunodiffusion [AGID], enzyme-linked immunosorbent assay [ELISA], latex agglutination) have been developed for the antibody detection. The SN assay is widely available and has been shown to be specific for antibodies against EMCV. No cross-neutralizing activity was found between EMCV and 62 human enterovirus serotypes or 11 porcine enterovirus serotypes. Serum neutralizing antibodies may persist for an extended period of time, so serologic evidence of recent infection requires demonstrating a 4-fold increase in neutralizing antibody titers in convalescent versus acute sera. Molecular diagnostic techniques (nucleic acid probe, polymerase chain reaction [PCR]) have been described, but are not widely available.


Until EMC is definitely demonstrated to be a significant cause of disease, it is better ignored. Elimination or reduction of feral rodent populations is recommended in order to minimize environmental contamination with virus. Feeds from all sources should be properly stored and kept free of contamination by rodents. Pigs from premises known to have EMC should not be added to known negative herds. Pigs, rodents, and other animals that have died should be removed promptly to avoid transmission through ingestion. Basic hygienic and sanitary practices should be followed. An inactivated vaccine is commercially available but its use should be clearly justified. There is no specific treatment.