Elephant Disease Fact sheets       

Encephalomyocarditis (EMC, EMCV)
Elephant Care International Fact Sheet

Susan Mikota DVM


Etiology

  • genus Cardiovirus, Family Picornoviridae

  • worldwide distribution

  • isolated from many mammals, including humans

Epizootiology

  • rodents reservoir host

  • pigs primary domestic animal host

  • occurs in many captive  non-domestic species, especially primates

  • African and Asian elephants susceptible

  • sporadic occurrences in South Africa, Australia, U.S.

    • first cases in Florida 1974-1977 (5 confirmed ; 7 suspect) / 20 lions died

    • primarily Southeast U.S.

    • elephant cases in at least 8 zoos in 6 states

    • South Africa 1993-1994 – 60 cases in free-ranging bulls

    • fall and winter outbreaks in U.S.


Transmission and Pathogenesis

  • incubation 9-10 days

  • oral; fecal and/or  urine contamination of food

  • no evidence of eleph to eleph transmission

  • subclinical infections possible

  • replicates in myocardial cells and kills them

Clinical Signs in Elephants

  • sudden death 

  • anorexia, lethargy

  • +/- respiratory signs

  • subclinical infection possible

  • recovered animals +/-  weak hearts / future anesthesia risk

Diagnosis

  • antemortem dx rare due to rapid clinical course

·        gross lesions:  pale streaks in the myocardium, hydrothorax; hydropericardium ; pulmonary edema; froth in tracheobronchial tree

  • histopath: myocardial degeneration and necrosis with lymphocytic infiltrates

  • virus particles may be visible on electron microscopy

  • definitive diagnosis: virus isolation, PCR, mouse inoculation

  • serological test for antibodies available – Texas A&M


Differential diagnosis

  • herpes virus

  • hypovitaminosis E

  • cardioactive glycoside plant poisoning (oleander)

 Management

  • no specific treatment

  • prevention by rodent control is crucial

  • vaccine available in South Africa

  • commercial pig vaccine in U.S.

  • experimental elephant vaccines in U.S. (Dr. Kay Backues, Tulsa Zoo)

  • zoos in endemic areas may vaccinate; further studies needed

 Zoonotic potential

·        humans susceptible; sporadic cases (rare)

·        laboratory workers; adolescents

·        aseptic meningitis; polio-like syndrome

 Links for general information

1. Merck Manual On-Line

·  http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/53400.htm

2. AAZV vaccination info

·  http://www.aazv.org/eleph_emcv2003.htm

 

EMCV References June 2005

 Elephant Care International Bibliographic Database (www.elephantcare.org)

   1.   McLelland,D., Kirkpatrick,J.F., Rose,K., and Dixon,R. 2001. Studies on encephalomycarditis
         virus (EMCV) in a zoologic context. AAZV,AAWV,ARAV,NAZWV Joint Conf, pp. 337.

   2.   Backues,K.A., Hil,M., Palmenberg,C., Miller,C., Soike,K.F., and Aguilar,R. 1999. Genetically engineered Mengo virus vaccination of multiple captive wildlife species. Journal of Wildlife Diiseases 35(2):384-387.

   3.   Mikota,S.K. 1999. Diseases of the Elephant: A Review. Verh.ber.Erkrg.Zootiere 39:1-15.

   4.   Hunter,P., Swanepoel,S.P., Esterhuysen,J.J., Raath,J.P., Bengis,R.G., and Van der Lugt,J.J. 1998. The efficacy of an experimental oil-adjuvanted encephalomyocarditis vaccine in elephants, mice and pigs. Vaccine 16(1):55-61.
Abstract: An oil-adjuvanted inactivated encephalomyocarditis (EMC) vaccine was developed to protect a wild population of elephants against a natural outbreak of disease. The experimental vaccine was initially tested for efficacy by challenging mice and pigs. Mice showed protection against challenge and pigs developed high antibody levels. Since both vaccinated and control pigs failed to develop clinical disease, apparently due to the low virulence of the strain in this species, protection in pigs could not be evaluated. Three wild elephants and 12 captive elephant calves given the vaccine developed high antibody titres. All of the captive elephants were protected from a challenge 2 months after vaccination, whereas 6 controls (not vaccinated but challenged) developed fatal or sub-clinical myocarditis. This is apparently the first report of an inactivated EMC vaccine inducing high antibody titres in domestic and wild animals. Due to the potency of this vaccine and the acceptability of the oil adjuvant used, it has potential for use in animals in zoological collections as well as in the pig industry.

   5.   Backues,K.A., Aguilar,R.A., Hill,M., and Palemberg,A.C. 1997. A new modified live virus vaccine for encephalomyocarditis (EMC) virus protection, preliminary trials at the Audubon Zoo. Proc. Amer.Assoc. of Zoo Vet, pp. 166-167.

   6.   Barnard,B.J.H. 1997. Antibodies against some viruses of domestic animals in southern African wild animals. Onderstepoort Journal of Veterinary Research 64(2):95-110.
Abstract: Twenty-four species of South African wild animals were tested for the presence of antibodies to the viruses of 16 common diseases of domestic animals around 1993-5. Positive results were obtained for African horse sickness, equine encephalomyelitis virus, equine herpesvirus-1, bovine herpesvirus-1, Allerton disease (Herpes mammillitis; bovine herpesvirus 2), lumpy skin disease, parainfluenza, encephalomyocarditis, bluetongue, Wesselsbron disease, bovine ephemeral fever, and Akabane disease complex. No antibodies could be demonstrated against the viruses of equine influenza, equine infectious anaemia, equine viral arteritis or Rift Valley fever. The negative results support observations that the latter diseases, with the exception of equine viral arteritis, are absent in South Africa. The number of animal species found positive for a specific virus, ranged from 0-16. No antibodies were found in crocodiles or warthogs, whereas antibodies against Wesselsbron and bovine herpesvirus-1 were present in 16 species. Antibodies against viruses of horses were found almost exclusively in zebras and, although elephants reacted to African horse sickness, no neutralizing antibodies against it could be demonstrated in their sera. Zebras were also found to be positive for Wesselsbron and Akabane, which are usually regarded as viruses of ruminants. Antibodies against most viruses were encountered in all vegetation zones in South Africa, but most viruses were more prevalent in the high-rainfall zone in KwaZulu-Natal.

   7.   Emerson,C.L. and Wagner,J.L. 1996. Antibody responses to two encephalomyocarditis virus vaccines in rhesus macaques (Macaca mulatta). J Med Primatol 25(1):42-45.
Abstract: Two groups of rhesus macaques (Macaca mulatta) housed in rodent-controlled outdoor corrals were inoculated with two different encephalomyocarditis virus (EMCV) vaccines. One group (n = 45) received a vaccine made from an inactivated field isolate of virus cultured during an outbreak at a zoo in Florida. This vaccine produced fourfold increases in the titers of 28 animals (62%); the increases persisted for at least 18 months (last test) after a single injection of the vaccine. The other group (n = 51) received a vaccine made from an inactivated porcine field strain of the virus. This vaccine did not produce titers in any of the vaccinees.

   8.   Osorio,J.E., Hubbard,G.B., Soike,K.F., Girards,S., van der Werf,S., Moulin,J., and Palmenberg,A.C. 1996. Protection of non-murine mammals against encephalomyocarditis virus using a genetically engineered Mengo virus. Vaccine 14(2):155-161.

   9.   Grobler,D.G., Raath,J.P., Braack,L.E.O., Keet,D.F., Gerdes,G.H., Barnard,B.J.H., Krick,N.P.J., Jardine,J., and Swanepoet,R. 1995. An outbreak of encephalomyocarditis-virus infection in free ranging African elephants in the Kruger National Park. Onderstepoort Journal of Veterinary Research 62:97-108.
Abstract: An increase in unexplained elephant mortality was seen in the Kruger National Park (KNP) from December 1993 to November 1994, concurrent with a wide-spread increase in the KNP rodent population.  The majority of animals were found dead.  Examination of carcasses ruled out common causes of death, including poaching, anthrax, intraspecific fighting, and intoxication.  Sixty-four animals died from unexplained causes during the perceived outbreak, 83% of which were adult bulls.  Eight carcasses were in sufficiently good condition for tissues to be collected for diagnostic testing.  Cardiac failure appeared to be the most likely cause of death in seven of the animals, with gross findings of pulmonary edema, hepatic congestion, ascities, and hydrothorax.  Myocarditis and necrosis of myocytes were the most striking findings on histopathological examination.  Heart tissue from three animals was submitted for virus isolation; all three yielded encephalomyocarditis (EMC) virus.  Serologic testing for EMC virus antibody was performed on the KNP between 1984 and 1994.  Results demonstrated that the virus has  been present in the KNP from 1987 on.  EMC virus antibody was not detected in preserved rodent tissues until 1993, prior to the rodent population explosion and the outbreak of disease in elephants.  It is unclear whether rodents play a role in transmitting the virus to other animals or if they reflect a general circulation of the virus in multiple species in a given environment.  One lion cub which was found dead with bacterial pneumonia had a serum neutralizing antibody titer to EMC virus of 128.  It is hypothesized that this animal may have been predisposed to pneumonia through the formation of lung edema as a result of EMC virus infection.  Three lions that were seen feeding on the carcass of an elephant with lesions compatible with EMC virus infection were monitored for seroconversion, which did not occur.  EMC virus disappears rapidly from most tissues after death and probably was not present in the tissues consumed by the lions.  The predilection for male elephants could not be explained, although increased mortality among males has also been demonstrated with EMC virus in mice.

10.   Raath,J.P. and Bengis,R.G. 1995. The evaluation of a vaccine against encephalomyocarditis infection in elephants (Loxodonta africana) under controlled conditions. Proceedings, American Association of Zoo Veterinarians, Wildlife Disease Association, American Association of Wildlife Veterinarians. Joint Conference, East Lansing, Michigan, August 12-17, 1995., pp. 304-308.
Abstract: Encephalomyocarditis killed 64 elephants in the Kruger National Park between October 1993 and November 1994. An inactivated vaccine was inoculated into 14 elephants aged 6-8 years, 6 of which were challenged later with virulent virus. 3 of 4 infected, unvaccinated elephants developed the clinical disease and 2 died. Vaccinated elephants developed antibodies at 1-4 weeks after vaccination, and the 6 challenged animals remained healthy.

11.   Wells,S.K., Gutter,A.E., Soike,K.F., and Baskin,G.B. 1989. Encephalomyocarditis virus: Epizootic in a zoological collection. Journal of Zoo and Wildlife Medicine 20(3):291-296.
Abstract: Encephalomyocarditis virus (EMCV) was isolated from eight nonhuman primates, one Thomson's gazelle (Gazella thomsoni), and one dromedary camel (Camelus dromedarius) that died peracutely between January 1985 and October 1987 at Audubon Park Zoo, New Orleans, Louisiana.  Gross pathology consisted of excessive pericardial fluid, epicardial hemorrhages, and pale foci within the myocardium.  Microscopic changes included myofiber necrosis, edema, and mononuclear cell infiltration within the myocardium.      Anti-EMCV antibody was found in a variety of species including a capybara (Hydrochoerus hydrochaeris), which subsequently died of a necrotizing myocarditis but from which virus was not isolated.  Although one hospital staff member had a high anti-EMCV antibody titer, all primate keepers were seronegative.      Encephalomyocarditis virus was recovered from 38 wild rodents, one opposum (Didelphis virginiana), and one rabbit (Sylvilagus sp.) collected on the zoo grounds.  Fifty-five percent of the positive samples were found in areas where confirmed deaths had occurred or antibody-positive animals were housed.  A killed vaccine was developed and administered to six domestic cats, 12 primates, and one camel.  Antibody response to vaccination was variable.

12.   Gaskin,J.M. 1988. Encephalomyocarditis: A potentially fatal virus infection of elephants. Proc.Ann.Elephant Workshop 9, pp. 133-136.

13.   Gaskin,J.M., Andresen,T.L., Olsen,J.H., Schobert,E.E., Buesse,D., Lynch,J.D., Walsh,M., Citino,S., and Murphy,D. 1987. Encephalomyocarditis in zoo animals: Recent experiences with the disease and vaccination. Proceedings of the 1st International Conference on Zoological and Avian Medicine:491.
Abstract: Encephalomyocarditis (EMC), a specific viral infection caused by a group of antigenically related viruses in the family Picornaviridae, a genus of Cardiovirus, continues to be a source of sporadic mortality loss in zoo animals in Florida.  Deaths in a young Nyala antelope, 2 chimpanzees, 3 llamas, a two-toed sloth, 3 ringtail lemurs, a ruffed lemur, and an orangutan have recently been confirmed by virus recovery.  Experimental vaccine trials were initiated in pygmy goats, Barbados sheep, and white mice using B-propiolactone inactivated virus preparations.  Various adjuvants, including aluminum hydroxide, mineral oil, and dimethyl dioctadecyl ammonium bromide (DDAB) were used to enhance the immune responses to inactivated virus.  The vaccine preparations produced varying levels of hemagglutinations-inhibition (HI) antibodies in the immunized animals.  Experimental challenge of unvaccinated weaned pigs, pygmy goats, and Barbados sheep demonstrated that, although they seroconverted, they did not become ill when exposed to the virulent EMC virus strains used in this study. Laboratory mice, however, proved to be very susceptible when exposed to these same strains, and either died acutely or developed posterior paresis and paralysis subsequent to challenge.  All experimental vaccine preparations protected mice against challenge.  In vaccinated goats and sheep, the oil-emulsion-adjuvanted and DDAB-adjuvanted vaccines produced the highest and most persistent HI antibody titers.  Sera obtained from African elephants were screened for HI antibodies to EMC virus.  Ninety-three African elephant sera from the Kruger National Park in the Republic of South Africa had titers of less than 10 hemagglutination-inhibition units (HIU) while 4 of 76 imported juvenile African elephants had titers from 10-40 HIU and the rest had no titer.  EMC virus infections are apparently acquired in Florida from reservoir hosts and HI titers of 40 HIU or higher indicate subclinical infection with the virus.  Experimental vaccines may help prevent EMC in susceptible species; HI responses to vaccination in various exotic species are being evaluated.

14.   Seaman,J.T. and Finnie,E.P. 1987. Acute myocarditis in a captive African elephant (Loxodonta africana). Journal of Wildlife Diseases 23(1):170-171.

15.   Murname,T.G., 1981. Encephalomyocarditis. In Steele,J.H. (Editor). CRC Handbook Series in Zoonoses, Section B: Viral Zoonoses.Ames, Iowa The Iowa State University Press, pp. 137-147.

16.   Gaskin,J.M., Jorge,M.A., Simpson,C.F., Lewis,A.L., Olson,J.H., Schobert,E.E., Wollenman,E.P., Marlowe,C., and Curtis,M.M. 1980. The tragedy of encephalomyocarditis virus infection in zoological parks of Florida. Proceedings American Association of Zoo Veterinarians:1-7.

17.   Tesh,R.B. and Wallace,G.D. 1978. Observations on the natural history of encephalomyocarditis virus. American Journal of Tropical Medicine and Hygiene 27:133-143.

18.   Simpson,C.F., Lewis,A.L., and Gaskin,J.M. 1977. Encephalomyocarditis virus infection of captive elephants. Journal of the American Veterinary Medical Association 171(9):902-905.
Abstract: Four Asian elephants at each of 2 widely separated zoologic gardens in Florida died following a fulminating illness.  Tissue suspensions obtained from an elephant from each of the zoologic gardens were inoculated into newborn mice, 3- to 4-week-old mice, buffalo green monkey and baby hamster kidney cell cultures.  Encephalitis and myocarditis developed in the mice.  The cell cultures were destroyed within 24 to 72 hours, and intracytoplasmic viral inclusions were observed in infected cells by electron microscopy.  The viral agent was neutralized by known antiserum to encephalomyocarditis virus.

19.   Gainer,J.H. 1969. Encephalomyocarditis virus infections in Florida, 1960-1966. Journal of the American Veterinary Medical Association 151:421-425.

20.   Gainer,J.H., Sandifur,J.R., and Bigler,W.J. 1968. High mortality in a Florida swine  herd infected with encephalomyocarditis virus.  An accompaning epizootiologic survey. The Cornell Veterinarian 58:31-47.

21.   Gainer,J.H. and Murchison,T.E. 1961. Encephalomyocarditis virus infection of swine. Vet.Med. 56:173-175.

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