Encephalomyocarditis virus infection

T J L ALEXANDER

GENERAL INTRODUCTION: PICORNAVIRIDAE

Introduction and aetiology

Encephalomyocarditis virus (EMCV) infection affects a wide range of domestic and wild animal species as well as humans. Most infections are subclinical but, depending on the strain of virus and the host species involved, myocarditis and/or encephalitis accompanied by evidence of heart failure and nervous signs may occur. A stillbirth, foetal mummification, embryonic death and infertility (SMEDI) syndrome have also been associated with EMCV infection in pigs. The faeces and urine of rats would seem to be an important source of virus.

Encephalomyocarditis virus (EMCV) belongs to the genus Cardiovirus of the family Picornaviridae.^{1, 7, 10} There are several strains but only one serotype of EMCV. It has a similar structure to enteroviruses but is slightly larger and can be grown in a variety of cell cultures. Unlike enteroviruses, it haemagglutinates red blood cells from different animal species.^{1, 3, 7, 8} Similar to enteroviruses, it is also relatively resistant to heat, environmental factors, a wide range of pH, and commonly used disinfectants.^{1, 7, 8, 10}

Epidemiology

It is widely thought that rats and mice are the natural hosts and reservoirs of strains of the EMCV because antibodies are commonly detected in them and outbreaks of encephalomyocarditis (EMC) in other species frequently coincide with and increase in the rodent population.⁹ This concept has been questioned because workers in Hawaii reported that experimentally infected rats and mice infrequently produced a carrier state and that contact transmission among rodents is rare.¹¹ Many other vertebrate species, including pigs, cattle, horses, non-human primates and humans, animals in zoological gardens and game parks, and wild animals such as mongooses, opossums, raccoons, squirrels and birds, become infected from oral ingestion of infected faeces and urine.^{1, 4, 5, 8, 11, 12} Most infections are subclinical but, depending on the host and viral strain, they may result in acute and fatal illness.

Encephalomyocarditis virus has also been isolated from mosquitoes and ticks but there is no evidence that they play a role in the transmission of the disease.^{4, 11}

The virulence and host preference of different virus strains and the disease syndromes they produce vary from country to country and region to region. In pigs, the strains in North America cause a SMEDI syndrome^{2, 8, 10} which is also caused by other agents such as certain serotypes of porcine enterovirus and by porcine parvovirus (see Teschen, Talfan and reproductive diseases caused by porcine enteroviruses, and Porcine parvovirus infections), whereas strains in countries such as those in the Caribbean and Central America, and in Australia and South Africa more often cause acute encephalomyocarditis and death.^{4, 5, 10, 11, 12} Most of the strains in western Europe only produce subclinical infections.¹⁰

The epidemiology of encephalomyocarditis in pigs and other domestic and wild animal species is generally thought to depend on the behaviour and population density of rats ⁹ but some workers consider that it may depend more on transmission between other animal species.^{8, 9} Field observations, however, show that clinical disease in pigs tends to occur when rat numbers in pig buildings increase,^{2, 4} for example when sugar cane or sugar beet has been harvested and they are forced to find new habitats. Their faeces and urine frequently contain EMCV and in this way the environment, including water supplies and pig feed, become contaminated and thus a source of infection.^{8, 10} An explosive rise in the rat population in the northern part of the Kruger National Park in South Africa in 1993/4 coincided with an outbreak of EMC in elephants, resulting in acute mortality from heart failure.^{5, 12}

Pathogenesis and clinical signs

Natural infection is by the oral-faecal route and is followed by viraemia. The virus is thought to multiply in lymphoid tissues and is also found in the liver, pancreas and kidneys but the highest concentration is usually in the myocardium in which, depending on the viral strain, it may cause myocardial lesions leading to sudden death.^{3, 5, 8}In many affected mammals the main clinical sign is rapid collapse and death from cardiac failure or the animals are found dead.⁵ Following viraemia, some strains cause acute encephalitis and some cause reproductive failure in pigs. Sows which develop reproductive failure (the SMEDI syndrome) usually show no other clinical signs.^{2, 8, 10} The virus crosses the placenta in early pregnancy and infects the foetuses, causing patchy myocarditis and death. Dead foetuses may be oedematous and haemorrhagic or appear normal. Those which are not soon expelled become mummified.^{2, 7, 8, 10}

In pigs, acute EMC with sudden death occurs mainly in young pigs. Clinical signs may include fever, anorexia, depression dyspnoea, and, in some, nervous signs, such as trembling, abnormal gait and paresis or paralysis. The younger the pigs are when infected the higher the mortality which may be nearly 100 per cent in those which are infected before weaning.^{7, 8, 9, 10}

Pathology

Animals that die from acute cardiac failure in the acute stage of infection may have no gross lesions or only manifest epicardial haemorrhages. In those which have suffered from a more prolonged clinical disease, the heart is enlarged and pale, and scattered white to yellow foci of necrosis and/or fibrosis varying in diameter up to about 15 mm are present in the myocardium mainly of the right ventricle. Many of these lesions can be discernible beneath the epicardial surface below which they extend to varying depths into the myocardium. Hydropericardium, hydrothorax, pulmonary oedema, ascites and hepatic congestion may also be present.^{3, 5, 8, 10} Animals with nervous signs may reveal evidence of mild inflammation of the meninges or no gross lesions in the central nervous system (CNS) at all.^{8, 10} Histopathologically, animals that have died from cardiac failure manifest myocardial congestion, oedema, focal or diffuse accumulations of mononuclear cells, and degeneration and necrosis of myocardial fibres, sometimes with mineralization, and fibrosis.⁵ In the liver varying degrees of centrilobular degeneration and necrosis, and congestion are present.⁵ Cases which had shown CNS signs reveal a non-specific, non-suppurative meningoencephalitis with perivascular and diffuse infiltration of mononuclear cells as well as glial cell proliferation and some neuronal degeneration.^{8, 10, 11}

Mummification may occur in foetuses whose size depends on the stage of gestation at which they became infected. Some aborted foetuses may appear normal, but others may be oedematous or haemorrhagic. Some may reveal the presence of necrotic myocardial lesions that are visible grossly and/or histopathologically. In addition, microscopic lesions of non-suppurative encephalomyelitis lesions may be present in some foetuses.^{2, 8, 10}

Diagnosis and differential diagnosis

A provisional diagnosis can be made based on the myocardial and CNS lesions. A specific diagnosis should be based on isolation of the virus in tissue cultures from specimens collected from the heart and CNS and its subsequent identification using, for example, fluorescent antibody or neutralization tests. The classical method is the inoculation of emulsions of porcine tissues suspected to be infected into mice and chicken embryos. These will die in three to six days.^{1, 7, 8, 11}

The foetal heart lesions, if present, distinguish encephalomyocarditis infection from the SMEDI syndrome caused by other viral infections. The SMEDI syndrome caused by EMCV can be diagnosed specifically by demonstrating rising antibody levels in paired serum samples of the dam or by isolating the virus in tissue culture from aborted foetal tissues.^{2, 8, 10}

The heart lesions in EMC in pigs and other animal species must be distinguished from those caused by vitamin E or selenium deficiency and salinomycin poisoning or cardiotoxic plants (e.g. cardiac glycoside-containing plants). The histopathological CNS lesions in EMC are similar to those in many other viral encephalitides, such as Teschen/Talfan disease and Aujeszky’s disease.

Control

As infection occurs primarily via the oral–faecal route measures consistent with those that are employed to control diseases transmitted in this manner should be instituted, such as regular cleaning of pens and water sources and protection of feed against contamination with rat faeces and urine. In addition, as mice and rats are generally thought to be the commonest source of the virus, these should be eradicated from animal premises by standard methods. An effective experimental vaccine has been reported for use in outbreaks in zoological collections or in pig farms.⁶

References

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3. craighead, j.e., 1966. Pathogenicity ofMand E variants of the encephalomyocarditis (EMC) virus. 1. Myocardiotropic and neurotropic properties. American Journal of Pathology, 48, 333–343.
4. gainer, j.h., 1967. Encephalomyocarditis virus infections in Florida, 1960–1966. Journal of the American Veterinary Medical Association, 151, 421–424.
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6. hunter, p., swanepoel, s.p., esterhuysen, j.j., raath, j.p., bengis, r.g. & van der lugt, j.j., 1998. The efficacy of an experimental oil-adjuvanted encephalomyocarditis vaccine in elephants, mice and pigs. Vaccine, 16, 55–61.
7. joo, h.s., 1999. Encephalomyocarditis virus. In: straw, b.e., d’allaire, s., mengeling, w.l. & taylor, d.j., (eds). Diseases of Swine. 8th edn. Iowa: Iowa State University Press. pp. 139–135.
8. ramos, j.r., gomez, l., mayo, m. & sanchez, g., 1983. Infection due to encephalomyocarditis virus in swine and other species over 1975–1981. Revista Cubana de Ciencias Veterinarias, 14, 71–77.
9. seamna, j.t., boulton, j.g. & carrigan, m.j., 1986. Encephalomyocarditis disease of pigs associated with a plague of rodents. Australian Veterinary Journal, 63, 292–294.
10. taylor, d.j., 1995. Pig Diseases. 6th edn. Glasgow: Published by the author.
11. tesh, r.b. & wallace, g.d., 1978. Observations on the natural history of encephalomyocarditis virus. American Journal of Tropical Medicine and Hygiene, 27, 133–143.
12. williams, m.c., 1981. Encephalomyocarditis virus infection. Journal of the South African Veterinary Association, 52, 76.