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 all EMC viruses exist as a single serotype, isolates from various regions and countries can differ in pathogenicity and virulence.
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. Most outbreaks of EMC virus 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.
EMC viruses have rarely been recognized as the cause of human illness, and the severe myocarditis and acute fatal infections observed in many other species have not been reported in humans. Nevertheless, serologic surveys have revealed human EMC virus infections are common in many parts of the world; most are asymptomatic or not recognized.
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 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 often persist in affected herds for 2–3 mo and may affect sows of all parities.
Because the pale necrotic heart muscle lesions that may be observed 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 and Control
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 for minimizing 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 EMC virus vaccine production has been limited by the apparent lack of need in most domestic livestock situations.
Last full review/revision March 2012 by Jack M. Gaskin, DVM, PhD, DACVM