Abstract

Encephalomyocarditis virus (EMCV) has caused the deaths of many species of animals in southern zoological parks and research institutions.^2,7 The Audubon Park Zoo was one of the first zoos to report an EMCV epizootic in its animal collection.⁷ Since this outbreak in the mid-1980s, EMCV had not struck animals at the Audubon Zoo until fall 1996. The recent outbreak has again subsided, but with current research being performed on Mengovirus, an antigenically identical close relative of EMCV, attempts were again made to vaccinate the Audubon Zoo’s collection against EMC virus. Primates and other species were vaccinated with a genetically engineered Mengovirus during their annual physical exams. Serum samples taken at the time of vaccination and 21 days later were submitted for serum neutralization titers to EMCV. Preliminary results on two species of primates, black howler monkey (Alouatta caraya), talapoin monkey (Cercopithecus talapoin), tapir (Tapirus terrestris), and babirusa (Babyrousa babyrussa), showed elevated titers 21 days postvaccination for talapoin monkeys and some elevation in titers for howler monkey and tapirs who had preexisting titers. No ill effects have been seen with vaccination.

Introduction

EMC virus is a member of the family Picornaviridae. The genus Cardiovirus contains EMCV, Mengovirus and MM, all of which are antigenically indistinct.⁸ Transmission and maintenance of the virus is thought to be through murine rodents. The past history at the Audubon Zoo has been consistent with this theory.^7,8 It is felt that the recent outbreak has again been associated with rodents, through disturbance of numerous rat nests due to construction on zoo grounds.

Disease caused by EMCV is peracute, with anorexia and depression seen for 12–24 h before death.¹ Often, death is the first visible sign.⁸ Gross lesions are limited to the cardiopulmonary system. Findings include hydropericardium, pale streaks throughout the myocardium, and pulmonary edema.¹ Histologically, lesions may show massive cardiac myocyte necrosis with edema and lymphocytic, plasmacytic and histocyte infiltrates. Pulmonary lesions of edema and congestion are secondary to acute cardiac failure.¹

The viruses of the genus Cardiovirus contain a unique sequence of homopolymeric polyribocytidylate segments that may contain from 60 to 420 pyrimidine nucleotide residues in a row.³ These poly(C) tracts and their length have been directly related to the virus’s pathogenicity.⁵ Genetically engineered mengoviruses with shortened poly(C) tracts were dramatically attenuated and steadfastly maintained their artificially truncated sequences during serial tissue culture passage.⁶ Laboratory mice receiving the short tract strains developed lifelong protective immunity against normally lethal challenge with wildtype cardioviruses.⁵ Vaccination with various length short poly(C) mengoviruses and subsequent virulent challenge with wildtype EMC virus has successfully protected mice, macaques, baboons and domestic swine.⁴

Methods and Results

Selected animals in the collection were injected during their annual physical exams with 5.0x10⁶ PFU (plaque forming units) of a genetically engineered Mengovirus (vMC0). Serum samples were collected at time of vaccination and 21 days later. Serum samples were tested by two separate laboratories by serum neutralization (Table 1).^2,4 Overall, results were positive with a rising titer 21 days after vaccination. No change was seen in some animals, it is not known whether the vaccine was ineffective or if more time was needed to see a measurable titer increase. An occasional animal appeared to have a preexisting titer to EMCV. A commercial version of this virus (vMC0), if available, may have efficacy for protection against EMCV-caused zoo animal mortality.

Table 1. Pre-existing and 21-day postvaccination titers and serum neutralization (SN) assays to (vMC0) vaccination in various species.

^a Delta Regional Primate Center, Three Rivers Road, Covington, LA.
^b Institute of Molecular Virology, University of Wisconsin, Madison, WI.

Acknowledgments

The authors would like to thank Jody Joyner, RVT, Sean MacConnell and the Audubon Park Zoo’s Mammal Department for their assistance.

Literature Cited

1.  Gutter, A.E. 1993. Encephalomyocarditis in zoo animals. In: Fowler ME, (ed.) Zoo & Wild Animal Medicine. Philadelphia: W.B. Saunders Co., Pp. 50–51.

2.  Hubbard, G.B., et al. 1992. An encephalomyocarditis virus epizootic in a baboon colony. Lab. Anim. Sci. 42(3):233–239.

3.  Martin, L.R., et al. 1996. Mutational analysis of the mengovirus Poly(C) Tract and surrounding heteropolymeric sequences. J. Virol. 70(3):2027–2030.

4.  Osorio, J.E., et al. 1996. Protection of non-murine mammals against encephalomyocarditis virus using a genetically engineered Mengo virus. Vaccine. 14(2):155–161.

5.  Osorio, J.E., L.R. Martin and A.C. Palmenberg 1996. The immunogenic and pathogenic potential of short Poly (C) tract mengo viruses. Virology. 223:344–350.

6.  Palmenberg, A.C. and J.E. Osorio 1994. Cardioviral Poly(C) tracts and viral pathogenesis. Arch. Virol. (Suppl) 9:67–77.

7.  Wells, S.K., A.E. Gutter, K.F. Soike and G.B. Baskin. 1989. Encephalomyocarditis virus: epizootic in a zoological collection. J. Zoo Wildl. Med. 20(3):291–296.

8.  Zimmerman, et al. 1994. Viral Encephalomyocarditis. In: CRC Handbook of Zoonoses. Pp. 423–436.