4.1 Article

Clinical and pathological findings of a newly recognized disease of elephants caused by endotheliotropic herpesviruses

Journal

JOURNAL OF WILDLIFE DISEASES
Volume 36, Issue 1, Pages 1-12

Publisher

WILDLIFE DISEASE ASSN, INC
DOI: 10.7589/0090-3558-36.1.1

Keywords

elephant; Elephas maximus; endotheliotropic viruses; famciclovir; herpesvirus; Loxodonta africana; new disease; penciclovir

Funding

  1. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [K08AI001526] Funding Source: NIH RePORTER
  2. NIAID NIH HHS [1 K08 AI01526-01] Funding Source: Medline

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The unique clinical and pathological findings in nine Asian (Elephas maximus) and two African (Loxodonta africana) elephants from North American Zoos with a highly fatal disease caused by novel endotheliotropic herpesviruses are described. Identification of the viruses by molecular techniques and some epidemiological aspects of the disease were previously reported. Consensus primer polymerase chain reaction (PCR) combined with sequencing yielded molecular evidence that confirmed the presence of two novel but related herpesviruses associated with the disease, one in Asian elephants and the second in African elephants. Disease onset was acute, with lethargy, edema of the head and thoracic limbs, oral ulceration and cyanosis of the tongue followed by death of most animals in 1 to 7 days. Pertinent laboratory findings in two of three clinically evaluated animals included lymphocytopenia and thrombocytopenia. Two affected young Asian elephants recovered after a 3 to 4 wk course of therapy with the anti-herpesvirus drug famciclovir. Necropsy findings in the fatal cases included pericardial effusion and extensive petechial hemorrhages in the heart and throughout the peritoneal cavity, hepatomegaly, cyanosis of orrhages and edema throughout the myocardium and mild there were extensive microhemorrages hemorrhagic lesions with inflammation were evident in the tongue, liver, and large intestine. Lesions in these target organs were accompanied by amphophilic to basophilic intranuclear viral inclusion bodies in capillary endothelial cells. Transmission electron microscopy of the endothelial inclusion bodies revealed 80 to 92 nm diameter viral capsids consistent with herpesvirus morphology. The short course of the herpesvirus infections, with sudden deaths in all but the two surviving elephants, was ascribed to acute cardiac failure attributed to herpesvirus-induced capillary injury with extensive myocardial hemorrhage and edema.

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