Elephant herpes virus
EEHV - Elephant endotheliotropic herpes virus
Cutaneous papillomatosis
Three novel herpesviruses EEHV1A, EEHV1B and EEHV2 were identified originally as the causes of fatal haemorrhagic disease in 1999. However since 2007 many more types have been detected with a total number of 12 species and two subspecies. The eight known EEHV types are all members of the Proboscivirus genus and are the only ones associated with acute haemorrhagic disease. (Garner et al, 2009; Latimer et al, 2010).
African elephants:
These viruses can cause either benign localized skin nodules with pinkish color on the trunk and head or vulval lymphoid patches around genital openings, and have also been found in pulmonary nodules in otherwise healthy african elephants. The visible growths or lesions usually regress after several weeks and thought to represent occasional reactivation from hidden "latent" infections.
Asian elephants:
EEHV causes fatal haemorrhagic disease, attacking endothelial cells (blood vessels, heart and similar organs) among asian elephants and has become a very serious problem. This disease has a sudden acute onset and preferentially targets calves between the ages of one and eight years (with more than half of those between one and three years of age). The first case was identified in 1995 at the Washington Zoo and reported in Science in 1999 (the earliest confirmed case is from 1983).
Nearly 60 cases of EEHV hemorrhagic disease have now been confirmed worldwide, with at least 15 also suspected in Asia. Over 85% of known cases have been fatal. (Latimer et al., 2010). There have been 35 cases in North America and 21 in Europe, including nine animals that survived after treatment with an anti-herpesvirus drug (designed for use in humans) administered very quickly after diagnosis. Although most cases have involved juvenile captive-born Asian elephants only one was less than one year of age (not counting stillbirths), but several cases have involved older wild-born Asian adults and three were in African elephants.
Of 78 Asian elephants born in the United States and Canada between 1978 and 2007 that lived up to two months of age, 19 died of this disease, and six more might have if not treated successfully. Officially saved elephant babies include Doc, Chandra, Obert, Jade, Maliha and Barack.
EEHV1 has been proposed to spread from immune, otherwise healthy african elephants to asian elephant calves who may not have developed anti-bodies (Richman et al, 1999). However, there is increasing evidence that many healthy wild-born asian elephants in captivity periodically shed low levels of “reactivated” EEHV1 virus in trunk washes (Stanton et al, 2010) or have anti-bodies, implying that they not only carry “latent” infections, but therefore presumably survived mild infections when young.
Initial clinical signs (symptoms) include lethargy, facial and neck swelling (oedema) and purple tongue (cyanosis). DNA PCR tests can be carried out on the blood and serum within 12 to 24 hours. This “viremia” test has been used to confirm acute EEHV disease cases and to trigger successful famciclovir treatment of symptomatic animals. Without treatment, afflicted young elephants that have reached this stage of disease usually die very fast, in several cases within 24 hours, but there are nine confirmed examples of cures in which EEHV1 infected calves with positive PCR DNA blood tests survived after quick early treatment with famciclovir (500 mg/70 kg body-weight, 3-4 weeks). These animals became DNA negative after several days or weeks. Some surviving calves had a transient peak of up to 100,000 EEHV1 viruses/ml blood with mild symptoms, whereas those that died with or without treatment reached levels as high as 50 million viruses/ml blood (and had easily detectable virus in the serum as well). The blood test has never been positive in healthy animals, but unfortunately even this expensive drug treatment was not effective in many other cases.
Among the eight different types of Probosciviruses in elephants, five EEHV1A, EEHV1B, EEHV2, EEHV3 and EEHV4 have caused fatal disease. However, by far the major culprits have been an assortment of different strains of the two chimeric versions of EEHV1 (referred to as 1A and 1B). Several facilities have had deaths or cases from both EEHV1 subtype and several surviving calves have been known to be infected with first one and later the other subtype.
Recent genetic “fingerprint” analysis of the virus strains found in 24 cases of viremic EEHV1 infections (20 by EEHV1A and 4 by EEHV1B) in North America and Europe has revealed that the disease is sporadic. With only a few exceptions none of the EEHV1 strains found are sufficiently closely related to any of the others to have been directly epidemiologically connected. Therefore, there is no linear chain of transmission and each must instead have been acquired from one of numerous different unknown source animals (herdmates) and not from any of the other known cases. The exceptions are four instances in which two calves at the same facility became infected within just a few days of one another and both proved to have genetically identical EEHV1 viruses.
Current evidence has confirmed that EEHV2, EEHV3 and EEHV6 are native to African elephants where they hide in the pulmonary nodules. EEHV5 has only been found once in an elderly wild-born Asian elephant and may be native to and benign in Asian elephants. The presence or otherwise of anti-bodies to one Proboscivirus species might potentially provide protection against some of the others. EEHV1A was also found in an outbreak of skin nodules in a herd of African elephant calves just after importation from Zimbabwe to Florida in the 1980s, but it is not yet clear whether the natural hosts of EEHV1 in the wild are African or Asian elephants. The Proboscivirus group evidently initially evolved separately from all other herpesvirus groups together with its hosts when the ancestors of modern elephants separated from all other mammalian groups over 100 million years ago. They then branched into multiple EEHV species during the past 10 to 40 million years, which is from even before the Asian and African elephants and woolly mammoths diverged from a common ancestor about 7 million years ago. As in most mammals, several distinct species (five) of yet another very highly diverged type of herpesvirus called gamma herpesviruses or EGHVs are also often found in secretions from captive Asian and African elephants, but these do not cause any serious disease.
It is now also very clear that this is not just a disease of zoos or of captivity. There are pathologically consistent reports of at least 15 lethal haemorrhagic disease cases recently attributed to EEHV also in wild orphans and range calves within several Asian countries. Several of these have been confirmed by DNA PCR tests to be EEHV1 strains and a laboratory for collecting and testing suspected samples has been set up in India. Much additional research is urgently required to evaluate this situation within wild- range countries.
Note that latent herpesvirus infections are very common in nature, but they only rarely cross host species barriers or cause serious disease. In fact, most human adults unknowingly harbor latent infections by between four and seven of the eight different species of human herpesviruses, although (except in immunosuppressed AIDS and organ transplant patients) these only rarely cause more serious disease than chicken pox, roseolla, mononucleosis, cold sores and shingles. They are most commonly transmitted in saliva with only one HSV2 being sexually transmitted.
Herpes virus and captive breeding of elephants
Lately (2007) there has been criticism from animal welfare groups regarding captive breeding of elephants, accusing Zoos or other elephant breeding facilities of spreading the deadly Elephant Endotheliotropic Herpesvirus (EEHV).
I don't believe that running away from a problem by
stopping the captive breeding program is the way to solve
elephant herpesvirus....it is going to become a huge issue in
the wild too in the future as the fragmented populations and
controlled /captive breeding conditions in range countries
in Asia become to resemble more and more the conditions
in captivity here. It is better to figure out what is going on
here now and learn how to control it and to continue to
strengthen/enrich the gene pool in captivity as much as
possible.Gary S. Hayward, 2007
Herpes virus and artificial insemination
There is presently no evidence that it is transmitted by
artificial insemination. In fact the several progeny of Onyx
that have had it include at least three very different species
of elephant herpesviruses. Furthermore, the virus that
killed Haji the first born by AI is a novel EEHV1A/EEHV1B
chimera that again is a very different virus from all other
cases we have seen.Gary S. Hayward, 2007
Herpes virus research
There are Research Groups in both the USA and Europe that offer DNA and serology tests for the viruses (eg The Elephant Herpesvirus Laboratory run by Dr Laura Richman and Erin Latimer at the National Zoological Park in Washington DC). Funding for the laboratory and for the EEHV Molecular Virologyresearch at Johns Hopkins University are both partially supported by donations to and grants from the International Elephant Foundation). Information about the tests, samples and documentation is given on the website at Consent Form for Elephant Endothelial Herpes Virus (EEHV) Testing, Request Form for EEHV Testing, Elephant History Form for EEHV Testing and Endotheliotropic Herpesvirus (EEHV) Elephant Care International Fact Sheet by Susan Mikota DVM
Sources, among others; Gary S. Hayward, Ph D. Johns Hopkins School of Medicine
Dr Gary Hayward and elephants in Vandalur Zoo in Chennai, India.
