Lk. Richman et al., Clinical and pathological findings of a newly recognized disease of elephants caused by endotheliotropic herpesviruses, J WILDL DIS, 36(1), 2000, pp. 1-12
The unique clinical and pathological findings in nine Asian (Elephas maximu
s) 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 so
me epidemiological aspects of the disease were previously reported. Consens
us primer polymerase chain reaction (PCR) combined with sequencing yielded
molecular evidence that confirmed the presence of two novel but related her
pesviruses associated with the disease, one in Asian elephants and the seco
nd in African elephants. Disease onset was acute, with lethargy, edema of t
he head and thoracic limbs, oral ulceration and cyanosis of the tongue foll
owed 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. Necrops
y findings in the fatal cases included pericardial effusion and extensive p
etechial hemorrhages in the heart and throughout the peritoneal cavity, hep
atomegaly, cyanosis of orrhages and edema throughout the myocardium and mil
d there were extensive microhemorrages hemorrhagic lesions with inflammatio
n were evident in the tongue, liver, and large intestine. Lesions in these
target organs were accompanied by amphophilic to basophilic intranuclear vi
ral inclusion bodies in capillary endothelial cells. Transmission electron
microscopy of the endothelial inclusion bodies revealed 80 to 92 nm diamete
r viral capsids consistent with herpesvirus morphology. The short course of
the herpesvirus infections, with sudden deaths in all but the two survivin
g elephants, was ascribed to acute cardiac failure attributed to herpesviru
s-induced capillary injury with extensive myocardial hemorrhage and edema.