Encephalomyocarditis virus (EMCV) is a rodent-borne picornavirus that is a global pathogen, causing fatal disease in mammalian species, most notably zoo animals and domestic swine. EMCV affects primarily the cardiopulmonary system, with the heart as a primary target; CNS involvement can also occur. Definitive diagnosis is based on virus isolation, RT-PCR assay, and genetic sequencing. Disease can be mitigated by autogenous vaccination and robust rodent control and abatement procedures.
Encephalomyocarditis virus (EMCV) is a rodent-borne pathogen, primarily of zoological animals and domestic swine, that has a worldwide distribution. It is a member of the family Picornaviridae, genus Cardiovirus, and is thus a single-stranded, positive-sense, nonenveloped RNA virus (1).
EMCV has been commonly recovered from numerous mammalian hosts, including rodents, carnivores, primates, ungulates, marsupials, and elephants (2). It has also been detected in birds and in arthropod vectors such as mosquitoes and ticks; however, no evidence suggests that it is normally associated with birds or is arthropod borne, and these infections are considered incidental (3, 4).
Rats and mice are believed to be the normal reservoir hosts of EMCV (5, 6). Although the virus is zoonotic, human EMCV infections are generally subclinical or are associated with mild to moderate symptoms (7). No human deaths resulting from EMCV infection have been reported.
The disease caused by EMCV (encephalomyocarditis) is named for its predilection for infecting the CNS and the cardiovascular system in experimental studies in mice, and both neurotropic and cardiotropic strains have been defined (8). In domestic swine and zoo animals, however, acute and subacute deaths are usually attributed to the effects of the virus on the myocardium—ie, cardiac insufficiency and pulmonary edema resulting in frothy fluid in the respiratory tract (9, 10).
Strains of EMCV that target the pancreas and cause diabetes in mouse studies have also been recognized (5); however, the importance of these findings for other mammals has not been established.
Epidemiology of Encephalomyocarditis Virus Infection
Although encephalomyocarditis virus isolates from various geographical regions might differ in pathogenicity, previously all EMCVs were considered to exist as a single serotype (EMCV-1). However, an EMCV variant first isolated from a wood mouse (Apodemus Leviticus) in Germany in 2005 was distinguished from EMCV-1 by serological testing and has been designated as EMCV-2 (11).
EMCV-1 infects a wide variety of animal hosts; the host range and pathogenicity of EMCV-2 remain to be determined. Putative additional types (EMCV-3 through EMCV-5) have been reported in the literature; however, these have been based on genetic/phylogenetic divergence rather than on antigenic testing, so only two serotypes (EMCV-1 and EMCV-2) are recognized currently (11, 12).
EMCV infection in nonrodent mammalian species has often been attributed to spillover from populations of wild mice and rats (13). In experimental infections of rodents, the virus is shed primarily in feces and urine, and such shedding is presumed to occur under natural conditions as well (14, 15).
Shedding of EMCV by rodents can contaminate food, water, and bedding material of larger mammals (13). Ingestion of infected rodents might be another means of infection.
Domestic swine shed EMCV in nasal secretions and feces during the first 3 days of experimental infection, and the virus can be transmitted to other pigs by direct contact during this time (16).
EMCV is resistant to adverse environmental conditions and can remain infectious for weeks to months (2).
Clinical Findings of Encephalomyocarditis Virus Infection
Swine infected with encephalomyocarditis virus might die acutely at any age as a result of myocardial failure or might have abortions in late pregnancy, fetal mummification, and apparent reproductive failure. A mortality rate approaching 100% has been described in suckling swine; the mortality rate becomes progressively lower in older animals (10).
With the recognition of porcine reproductive and respiratory syndrome virus (PRRSV) in North America in 1987, the overall importance of EMCV as a cause of reproductive disease in swine has been questioned. The high mutation rate of PRRSV complicates the maintenance of a reliable diagnostic RT-PCR assay, and virus isolation is time-consuming and challenging (17). Similar tests for EMCV are more straightforward for a diagnosis.
Most outbreaks of EMCV infection have been associated with captive animals in zoos, swine production units, and primate research centers. Sudden death is often the first indication of infection (13).
Pearls & Pitfalls
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Clinical signs of EMCV infection can include fever, anorexia, listlessness, trembling, staggering, dyspnea, and paralysis. EMCV is known to cross the placenta in swine and has been recovered from fetuses in cases of reproductive failure due to abortions in later stages of pregnancy; stillbirths and mummification can also occur (18, 19).
Reproductive problems due to EMCV infection have been reported to involve sows of all parities, often persisting in affected herds for months (20).
A variety of exotic mammals have been fatally infected with EMCV in zoological parks primarily in North America, Europe, Australia, and Asia. Affected animals prominently include, but are not limited to, elephants, rhinoceroses, hippopotamuses, and various ungulates and nonhuman primates (eg, chimpanzees, orangutans, baboons, lemurs, monkeys) (2, 12, 21, 22).
An incident of lion deaths at a zoo in the US was apparently associated with feeding of an African elephant carcass that had died as a result of EMCV infection (23).
Although the vast majority of reported wildlife deaths attributed to EMCV infection have been associated with animals in zoological facilities, an encephalomyocarditis outbreak in Kruger National Park in South Africa in 1993–1994 resulted in the deaths of 65 free-ranging elephants (24).
Reports of disease outbreaks due to EMCV are solicited and recorded at the Pirbright Institute in the UK.
Pathological Findings of Encephalomyocarditis Virus Infection
In typical cases of encephalomyocarditis virus infection, gross examination often reveals circular to linear pale or hemorrhagic foci in the myocardium (9, 20, 25). Some lesions can be necrotic, particularly in cases of acute death. However, changes can be subtle and obscured by postmortem autolysis.
Pulmonary edema with excessive fluid in the pleural, pericardial, and/or peritoneal cavities is often noted in EMCV cases (see ) (12, 20, 25). During histological examination, these lesions might be evident as necrosis and lysis of the sarcoplasm with variable mineralization and lymphocytic infiltration (20).
Necropsy photographs showing encephalomyocarditis virus infection in a mandrill (A) and a babirusa (B). A. Heart from a mandrill (Mandrillus sphinx), showing myocardial pallor without epicardial or myocardial hemorrhages. Clinical signs were intractable, progressive lethargy and dyspnea, decreased ventricular contractility, and signs consistent with congestive heart failure. B. Heart from a North Sulawesi babirusa (Babyrousa celebensis), showing broad, confluent areas of acute hemorrhage throughout the epicardium. Hemorrhages extended into the myocardium, interspersed with areas of myocardial pallor. Clinical presentation was sudden death with limited premonitory signs.
From Adhikari A, Feng KH, Shrestha A, et al. Zoological transmission of encephalomyocarditis virus in the United States: virus evolution, host ecology, and capsid antigenicity derived from an outbreak. PLoS Pathog. 2026;22(2):e1013861. doi:10.1371/journal.ppat.1013861
Microscopic EMCV lesions of the CNS can include meningeal inflammation, perivascular cuffing of the cerebral cortices and hippocampi, and neuronal degeneration with gliosis (26).
Diagnosis of Encephalomyocarditis Virus Infection
Virus isolation
RT-PCR assay
Genetic sequencing
Serological testing
Because the pale necrotic heart muscle lesions that can occur in fatal encephalomyocarditis virus infections are also evident in septic infarction or vitamin E/selenium deficiency, a definitive diagnosis via genetic sequencing is required. Genetic sequencing can be performed by RNA extraction from infected tissues (eg, heart) or, alternatively, from virus isolated in cell culture from tissue homogenates, followed by RT-PCR assay and Sanger sequencing.
Fresh or frozen tissues may be used for EMCV isolation, and tissue selection may be guided by histopathological lesions. Heart, lung, liver, kidney, spleen, and/or brain samples are often collected from acutely dead animals or aborted fetuses.
Baby hamster kidney (BHK) and African green monkey kidney (Vero E6) cells—both interferon-deficient cell lines—are routinely used for EMCV isolation (12). Ancillary methods, such as immunohistochemistry or in situ hybridization, can be useful in localizing viral antigen or RNA, respectively, to observed microscopic lesions.
Serological diagnosis via virus neutralization, hemagglutination inhibition, or ELISA is possible if acute and convalescent sera are collected; however, the frequency of subclinical EMCV infections limits the diagnostic value of testing single serum samples. Plaque reduction neutralization testing is the gold standard for determining neutralizing antibody titers. Blood for testing African elephants, believed to be highly susceptible to fatal EMCV infection, can be sampled from ear veins (see ).
African elephants are believed to be highly susceptible to fatal encephalomyocarditis virus infection, and many deaths are peracute without premonitory signs. Blood samples can be collected from ear veins for serological testing, as pictured here.
Courtesy of Dr. Jack Gaskin.
Treatment, Control, and Prevention of Encephalomyocarditis Virus Infection
Minimizing exposure to infected wild rats and mice
Implementing additional rodent mitigation strategies during outbreaks
Inactivating virus through disinfection
Protecting animals via autogenous vaccines
There is no specific treatment for encephalomyocarditis virus infection; however, the morbidity and mortality rates can be minimized by protecting at-risk animals from stress and excitement. EMCV appears to cyclically infect rodents and is most likely to affect swine and zoo animals when rodent populations are observed to increase above base levels. Rodent control is thus critical to minimize the exposure of susceptible species.
Instituting rodent mitigation strategies such as decreasing harborage and potential food sources, as well as increasing pest management efforts when necessary, is recommended, as is prompt and proper disposal of infected animals that have died (12).
EMCV is inactivated by the judicious use of many disinfectants labeled for use on production animals. The virus is destroyed by heat treatment at 60°C (140°F) for 30 minutes or by the use of disinfectants containing chlorine, iodine, or mercuric chloride (27).
Killed vaccines for the prevention of myocarditis in weaned swine have been patented but are no longer commercially available in the US, except as autogenous products. The current impetus for vaccine development has come largely from zoological facilities, where EMCV infection has remained a substantial problem.
Success with use of a genetically engineered, live attenuated virus vaccine against EMCV has been reported in primates, domestic swine, and various zoological species (28, 29).
Commercial EMCV vaccine production has been limited by the apparent lack of need in most domestic animal production situations.
Zoonotic Risk of Encephalomyocarditis Virus Infection
EMCV has rarely been recognized as a cause of human disease, and the severe myocarditis and acute fatal infections observed in many animal species have not been observed in human cases. Nevertheless, serological survey data indicate that EMCV infections in humans are common in many parts of the world (30); most are likely asymptomatic and/or undiagnosed.
Symptoms of EMCV infection in humans can include fever, chills, malaise, headache, photophobia, nausea, and vomiting (7).
Key Points
Encephalomyocarditis virus can cause sudden death from myocardial destruction in swine of any age; however, death is most common in young animals.
EMCV can also cause abortion in late stages of pregnancy, fetal mummification, and apparent reproductive failure in swine.
Spillover of EMCV into many zoo animals because of contamination of food and water supplies by infected rodent feces and urine has caused considerable mortality.
EMCV infections have been reported in humans but generally do not cause overt disease.
For More Information
Carocci M, Bakkali-Kassimi L. The encephalomyocarditis virus. Virulence. 2012;3(4):351-367.
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