Difference between revisions of "Encephalomyocarditis Virus"
| Line 8: | Line 8: | ||
==Signalment== | ==Signalment== | ||
| − | Host include chimpanzees, monkeys, elephants, lions, squirrels, mongooses, racoons and pigs. '''Pigs''' are the '''domestic host''' for the virus and the '''most susceptible to EMCV''' infection. | + | Host include chimpanzees, monkeys, elephants, lions, squirrels, mongooses, racoons and pigs. '''Pigs''' are the '''domestic host''' for the virus and the '''most susceptible to EMCV''' infection. |
Clinical problems in pigs are mostly limited to tropical areas where the infection can cause significant economic losses. The disease has also been observed in different zoo animals. | Clinical problems in pigs are mostly limited to tropical areas where the infection can cause significant economic losses. The disease has also been observed in different zoo animals. | ||
| Line 18: | Line 18: | ||
==Epidemiology== | ==Epidemiology== | ||
| − | The mode of virus transmission is not clear but rodent-to-pig transmission is probably common. Infected pigs can shed the virus in faeces but pig to pig transmission has not yet been proved experimentally. | + | The mode of virus transmission is not clear but rodent-to-pig transmission is probably common and rodnets act as the '''major reservoir of the disease. Rats and other rodents probably infect pigs directly or through diseased carcasses and contaminated feeds or water supplies. |
| + | |||
| + | Infected pigs can shed the virus in faeces but pig to pig transmission has not yet been proved experimentally. | ||
The route of infection in swine is likely to be oral and experiments have shown this to be the case. Virus can be shed from infected pigs for up to 9 days in their faeces. Animals that survive acute disease produced EMCV antibodies and the course of infection depends upon the virus strain, dose, history and the individual’s immune system. Further experiments have shown that intramuscular infection can cause transplacental infection and foetal deaths in pregnant sows <ref name="Love and Grewal, 1986"> Love, R.J., Grewal, A.S., (1986). '''Reproductive failure in pigs caused by encephalomyocarditis virus'''. ''Australian Veterinary Journal'', 63(4):128-129; 3 ref.</ref> | The route of infection in swine is likely to be oral and experiments have shown this to be the case. Virus can be shed from infected pigs for up to 9 days in their faeces. Animals that survive acute disease produced EMCV antibodies and the course of infection depends upon the virus strain, dose, history and the individual’s immune system. Further experiments have shown that intramuscular infection can cause transplacental infection and foetal deaths in pregnant sows <ref name="Love and Grewal, 1986"> Love, R.J., Grewal, A.S., (1986). '''Reproductive failure in pigs caused by encephalomyocarditis virus'''. ''Australian Veterinary Journal'', 63(4):128-129; 3 ref.</ref> | ||
Revision as of 11:23, 30 June 2011
Also known as: EMC — Encephalomyocarditis virus disease of pigs — encephalomyocarditis virus— EMCV .
Introduction
Encephalomyocarditis virus (EMCV) is a single stranded RNA (ssRNA) virus that causes encephalomyocarditis in pigs. It is a cardiovirus from the family Picornaviridae, and like other picornaviruses it stable over a wide range of pH. The virus is ether-resistant and can be inactivated at 60°C for 30 minutes, although are more thermally stabile.
EMCV causes high mortality in young pigs and reproductive failures in breeding females. Piglets suffer from myocarditis and encephalitis and sudden death due to myocardial failure is common. The disease affects the nervous, reproductive, respiratory and circulatory system of pigs. Antibodies for EMCV have been demonstrated in human populations [1] but there are no reports that the virus causes human heart disease.
Signalment
Host include chimpanzees, monkeys, elephants, lions, squirrels, mongooses, racoons and pigs. Pigs are the domestic host for the virus and the most susceptible to EMCV infection.
Clinical problems in pigs are mostly limited to tropical areas where the infection can cause significant economic losses. The disease has also been observed in different zoo animals.
Clinical Signs
Clinical signs include vomiting and regurgitation, anorexia, pyrexia, fasciculations, tachypnea, dyspnea, open mouth breathing and sudden death. Neurological signs include ataxia, generalised weakness, tetraparesis, inability to stand, tremor, dysmetria, lethargy and depression. Pregnant sows that become infected can suffer from infertility, mummified fetus, abortions, still births, small litter and weak new born.
Epidemiology
The mode of virus transmission is not clear but rodent-to-pig transmission is probably common and rodnets act as the major reservoir of the disease. Rats and other rodents probably infect pigs directly or through diseased carcasses and contaminated feeds or water supplies.
Infected pigs can shed the virus in faeces but pig to pig transmission has not yet been proved experimentally. The route of infection in swine is likely to be oral and experiments have shown this to be the case. Virus can be shed from infected pigs for up to 9 days in their faeces. Animals that survive acute disease produced EMCV antibodies and the course of infection depends upon the virus strain, dose, history and the individual’s immune system. Further experiments have shown that intramuscular infection can cause transplacental infection and foetal deaths in pregnant sows [2]
Distribution
Worldwide distribution but cases first reported in Central America, Florida and Australia.
Diagnosis
A presumptive diagnosis can be made on the above clinical signs especially high neonatal mortality, history of reproductive failure or dyspnea in young infected pigs. A definitive diagnosis can be confirmed by virus isolation from infected heart tissue from the acute phase of the disease. Baby hamster kidney (BHK-21), HeLa or Vero cell lines are commonly used for virus isolation.
Cardiomegaly and myocardial lesions with yellow or white necrotic foci (2-15mm diameter) are common and usually present on the epicardium of the right ventricle. These lesions can also be characteristic of Vitamin E and selenium deficiency. Acutely affected pigs may not show any gross lesions on post mortem. Infected foetuses can grossly vary depending on the stage of pregnancy and infection and myocardial lesions may be indistinguishable from other viral infections. Foetuses can be haemorrhagic, oedematous or apparently normal.
Histopathological findings include myocarditis with focal or diffuse accumulation of mononuclear cells, vascular congestion, oedema, degeneration of the myocardial fibres with necrosis and occasional mineralization of necrotic heart muscle.Brain tissue can be congestion with evidence of meningitis, perivascular infiltration (mononuclear cells) and neuronal degeneration. Nonsuppurative encephalitis and myocarditis has also been seen in naturally infected swine foetuses.
Detection of antibody specific to EMCV from still born piglets has been used to confirm foetal infection [3], [4]
Treatment
There is no specific treatment. Mortality levels in at risk pigs can be reduced by avoiding stress or excitation.
Control
An inactivated vaccine for EMCV (for intramuscular injection) is commercially available in the USA. It is important to control rodent populations on farm to prevent the spread of disease and contamination of feeds or water supply. Good husbandry and hygiene protocols should be followed with the regular use of disinfectants.
References
- ↑ Tesh, R.B. (1978).The prevalence of encephalomyocarditis virus neutralizing antibodies among various human populations. American Journal of Tropical Medicine & Hygiene, 27:144-149.
- ↑ Love, R.J., Grewal, A.S., (1986). Reproductive failure in pigs caused by encephalomyocarditis virus. Australian Veterinary Journal, 63(4):128-129; 3 ref.
- ↑ Joo, H.S., Kim, H.S., Leman, A.D., (1988). Detection of antibody to encephalomyocarditis virus in mummified or stillborn pigs. Archives of Virology, 100(1-2):131-134; 9 ref.
- ↑ Kim, H.S., Joo, H.S., Christianson, W.T., Morrison, R.B., (1991). Evaluation of serologic methods for detection of antibodies to encephalomyocarditis virus in swine fetal thoracic fluids. Journal of Veterinary Diagnostic Investigation, 3(4):283-286; 20 ref.
| Encephalomyocarditis Virus Learning Resources | |
|---|---|
 Test your knowledge using flashcard type questions |
Encephalomyocarditis Virus Flashcards |