Virus subtype suspected in Philippine swine.
When the Ebola Reston virus was discovered in pigs in the Philippines last year, it marked the virus's first known foray outside primates, and raised fears of a potential threat to human health.
Last week, a joint mission of 22 international health and veterinary experts returned from investigating the outbreak with more questions than answers about the virus's pathology and epidemiology.
The Ebola Reston virus was first discovered, in 1989, in crab-eating macaques imported to the United States from the Philippines. Since then, the virus has killed most infected monkeys, yet had no effect on the 25 people that it infected — unlike three of the four other strains of Ebola, which kill between 25% and 90% of the humans they infect.
Because few people come into close contact with primates in the Philippines, the risk of catching Ebola Reston in this way is relatively low. By contrast, the appearance of the virus in an important livestock species was unexpected and worrying, says Pierre Rollin, an Ebola expert at the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, who was part of the mission to the Philippines. "We never thought that pigs could be infected," he says.
Once inside the pig, it may be possible for the virus to mutate into a version that is deadly to humans, as the avian influenza virus is thought to have done. "And we still don't know what it might do to someone who is immunocompromised by HIV or by drugs," Rollin adds.
But there seems to be little threat to human health from the current form of the virus. It is destroyed by cooking, and there is no evidence of symptoms in pig handlers, who will soon be tested to find out if they have developed antibodies to the virus.
The investigation into the Ebola Reston infections began after farmers in the Philippines reported high mortality rates in their pigs in 2008. In September, samples from 28 dead pigs were sent to the Plum Island Animal Disease Center in New York, where researchers found evidence of the porcine reproductive and respiratory syndrome virus, also known as blue-ear pig disease, which has seen many outbreaks in Asia in recent years. But in six of the samples they also found Ebola Reston. This virulent, biosafety-level-4 pathogen requires special laboratory facilities, so the pig samples were rushed to the CDC labs in Atlanta for further analysis.
Despite the presence of other diseases in the samples — including swine fever, and the porcine circovirus type II — Rollin thinks that Ebola Reston is to blame for the pigs' deaths because histological samples showed that the virus had pervaded the spleen, similar to its mode of attack in monkeys. Further pathology tests are due to begin in spring at the Australian Animal Health Laboratory in Geelong, Victoria.
The infected pigs came from several farms on the island of Luzon, and on 13 January, health officials collected blood and tissue samples from hundreds of apparently healthy pigs there. Although Rollin does not expect to find the virus itself in these samples, the pigs may carry antibodies that should indicate an approximate mortality rate associated with exposure.
Rollin suspects that, as is the case with monkeys, the infections resulted from contact with a reservoir of the virus, rather than spreading from animal to animal. In 2005, outbreaks of human Ebola in Gabon and the Republic of the Congo were traced back to colonies of bats (E. M. Leroy et al. Nature 438, 575–576; 2005). "It's almost certainly the case [in the Philippines]," says Rollin.
The virus is likely to be spread by bat droppings falling into the pigs' feed, and the threat of infection could be reduced by moving fruit trees, where the bats roost, away from pig farms, or by putting roofs on pig enclosures. "We can't exterminate it, we just have to learn how to avoid it," says Rollin.
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