Zoos bring together different animal species that would never encounter each other in the wild. This can have unforeseen consequences. When in 2010 one polar bear died and another fell severely ill in a German zoo, veterinarians were at a loss as to the cause of the symptoms. It has now been shown that the bears were infected with a recombinant zebra-derived virus, as reported by a team of researchers including Dr Simon Ho from the School of Biological Sciences, University of Sydney.
Keeping animals from around the world is an important component of the mission of zoos to educate the public and preserve endangered species. It has rarely been considered that such a species mix can have unpredictable consequences in terms of transferring pathogens among zoo animals. Pathogens usually adapt to a specific host, but some are opportunistic and can spread to new hosts when encountered.
The study by researchers from Germany and from the University of Sydney reports such a case of a virus jumping from one species to another. In 2010 a female polar bear, Jerka, died of encephalitis at the Wuppertal Zoo in Germany despite the best efforts to save her. Her male companion Lars exhibited similar symptoms but survived as a result of intervention and long-term care.
Encephalitis can be caused by a large number of viruses and bacteria, and identifying novel pathogens in wild animals is a huge challenge. However, the intensive investigation of Jerka, Lars, and nine other polar bears pointed to a zebra-derived herpes virus as the culprit. Surprisingly, the virus was also found in the polar bear Struppo, who died years earlier from renal failure in a different zoo without any contact with Jerka or Lars. This indicates that this virus has jumped independently before and might continue to do so.
The virus turned out to be a recombinant – a combination of the genetic material of two different viruses both found in zebras. It originated when the Equine herpesvirus EHV9 transferred a portion of its DNA to the related EHV1. This portion is notable for its role in causing neurological diseases even in horses. It remains unclear whether this novel virus emerged recently in the zoo zebra population or a long time ago in Africa, and whether the recombination event is responsible for the ability of the virus to jump to new hosts and cause deadly disease.
“When we started, there was an overwhelming number of potential pathogens that might have caused Jerka’s death”, said Prof. Alex Greenwood of the Leibniz-Institute for Zoo and Wildlife Research, lead author of the study. “At first it seemed easy, because we quickly got a signal for EHV. But when we looked at the viral DNA sequence, it could have been either EHV1 or EHV9. With more sequence data it became clear that there was one gene that was partly like one virus and partly like the other.”
Another open question is how the bears were infected. Polar bears in Wuppertal are not cared for by the same zookeepers as zebras. Direct contact is unlikely to be the route of transmission because the zebras are housed 68 metres away. However, bears and zebras are not the only hosts, with the parent viruses being associated with fatal encephalitis in other zoo species such as gazelles and guinea pigs. The authors of the study are now exploring the possibility that transmission could even occur through wild mice or rats.
Dr Simon Ho from the School of Biological Sciences, who analysed the viral genomes, pointed out that there have been similar outbreaks of encephalitis in Australian zoos. Earlier this year, four white rhinos mysteriously died in the Taronga Western Plains Zoo in New South Wales.
Being alert to the potentially fatal consequences of pathogens jumping between species, zoos can serve as sentinels for disease outbreaks and protect their animals. This important task will be complex, because same pathogens can produce no symptoms in some species while causing unexplained deaths in other species.
Read the scientific publication here:
A potentially fatal mix of herpes in zoos
Greenwood, Tsangaras, Ho, Szentiks, Nikolin, et al. (2012) Current Biology, 22: 1727–1731