Encephalomyocarditis (EMC) is a significant viral infection of swine and zoologic mammals. It is caused by members of the genus Cardiovirus in the family Picornaviridae and recognized in many parts of the world. Although EMC virus (EMCV) isolates from various regions and countries have differed in pathogenicity and virulence, until recently all EMC viruses were considered to exist as a single serotype (EMCV-1). A cardiovirus isolated from a wood mouse in Germany in 2012 was distinguished from EMCV-1 by serologic and molecular means and has been designated EMCV-2. Although EMCV-1 infects a wide variety of hosts, the host range and pathogenicity of EMCV-2 remains to be determined.
Swine may die acutely at any age due to associated myocardial failure or may be affected with near-term abortions, fetal mummification, and apparent reproductive failure. Type A strains cause porcine reproductive problems, whereas type B strains cause heart failure. With the recognition of porcine reproductive and respiratory syndrome (PRRS) in 1987, however, the overall significance of EMCV-1 as a cause of reproductive disease in swine has been questioned. The high mutation rate of the PRRS arterivirus complicates the maintenance of reliable diagnostic PCR assays for that virus, while a concurrent EMCV infection may be easily detected by virus isolation. Most outbreaks of EMCV infection have been associated with captive animals in swine production units, primate research centers, and zoos. Sudden death is often the first indication of infection. A variety of exotic mammals have been fatally afflicted with EMC in zoologic parks in the USA, Australia, and other parts of the world and have included African elephants, rhinoceroses, hippopotamuses, sloths, llamas, various antelope species, and many types of nonhuman primates (chimpanzees, orangutans, baboons, monkeys, lemurs, etc). An episode of lion deaths at a zoo in the USA was associated with the feeding of the carcass of an African elephant that had died of EMC, and a spontaneous outbreak of fatal EMC was reported in free-ranging African elephants at Kruger National Park in South Africa in 1995. Reports of outbreaks of EMCV-associated disease are solicited and recorded at the Pirbright Institute in the UK.
Cardioviruses are small, nonenveloped viruses that are almost always associated with rodents, and the disease in other mammalian species has often been attributed to spillover from populations of wild mice and rats. These, and presumably other rodent species, shed the viruses in feces and urine, which may contaminate food and water supplies of large mammals. Ingestion of rodents dead or dying of EMC may be another means of infection. Pigs shed virus in nasal secretions and feces during the first 3 days of experimental infection. During this short period, the virus may be transmitted to other pigs by contact. Cardioviruses are resistant to adverse environmental influences and may remain infective for weeks to months under favorable conditions.
Clinical Findings and Lesions
The disease is named for its predilection for the CNS and cardiovascular systems of experimental mice, and both encephalotropic and cardiotropic strains have been defined. In swine and zoologic species, however, acute and subacute deaths are almost always attributed to the destructive effects of the virus on the myocardium, with resultant cardiac insufficiency, pulmonary edema, and frothy transudation into the respiratory tract. Affected animals often appear to have asphyxiated in their own respiratory fluids. Other clinical signs may include fever, anorexia, listlessness, trembling, staggering, dyspnea, and paralysis. Mortality approaching 100% has been described in suckling swine but becomes successively lower in older age groups. Strains of EMC viruses that target the pancreas and are diabetogenic in experimental mice have been recognized, but the significance of this finding for other mammals has not been established.
EMC viruses are known to cross the placenta in swine and have been recovered from conceptuses in cases of reproductive failure due to near-term abortions (107–111 days of gestation), stillbirths, and mummifications. Reproductive problems have been reported to involve sows of all parities, often persisting in affected herds for 2–3 mo, but the possibly more significant contribution of PRRS should be investigated.
Because the pale necrotic heart muscle lesions that may be seen in fatal EMC infections are also seen in septic infarction or vitamin E/selenium deficiency, a definitive diagnosis requires virus recovery and identification. Heart, liver, kidney, and spleen collected from acutely dead animals or abortuses are the specimens of choice for virus isolation. Because EMC viruses are very stable, they may be recovered from frozen tissues.
Serologic diagnosis via virus neutralization, hemagglutination-inhibition, or ELISA is possible if acute and convalescent sera are collected, but the frequency of subclinical EMC infections makes single serum determinations of little value in aborting sows. Detection of antibody against EMC viruses in stillborn or large mummified fetuses is significant for fetal infection, however, because maternal immunoglobulins are not passed across the placenta in swine.
Treatment, Control, and Prevention
There is no specific treatment for EMC, but mortality may be minimized by avoiding stress or excitement in animals at risk. EMC viruses appear to cycle in rodents and are most likely to affect swine and zoo animals when rodent populations are high. Rodent control is thus critical to minimize exposure of susceptible species. Prompt and proper disposal of animals that have died of the disease is also recommended. EMC viruses are inactivated by the judicious use of many disinfectants labeled for livestock use.
Killed vaccines for the prevention of myocarditis in weaned swine have been patented but are no longer commercially available in the USA except as autogenous products. The current impetus for vaccine development has come largely from zoos and amusement parks where EMC has been problematic. Success with a genetically engineered attenuated virus vaccine has been reported in primates, pigs, and various zoologic hoofstock species. Commercial EMCV vaccine production has been limited by the apparent lack of need in most domestic livestock situations.
EMC viruses have rarely been recognized as the cause of human illness, and the severe myocarditis and acute fatal infections seen in many other species have not been reported in people. Nevertheless, serologic surveys have revealed human EMCV infections are common in many parts of the world; most are asymptomatic or not recognized. Human disease has been characterized by fever, chills, nausea, headache, nuchal rigidity, delirium, delusions, vomiting, photophobia, and pleocytosis.
Last full review/revision September 2013 by Jack M. Gaskin, DVM, PhD, DACVM