At about noon on March 26th, Steve Bellan was working in his office at Etosha Ecological Institute in northern Namibia when he got word of a fresh zebra carcass near the Gemsbokvlakte water hole, about 20 kilometers east on a dusty park road. Over the next hour, the bushy-haired Berkeley graduate student got his gear in order and hooked up a trailer to the back of his pick-up before rumbling out of the fortified rest camp with his metal carcass cage, a pipe and mesh box designed to keep scavenging jackals away. His mission: “A randomized control trial, but with carcasses as the participants,” he says, which will hopefully yield clues about how to combat a bacterium that kills hundreds of cattle and wildlife each year in the United States and thousands more in developing countries.

Etosha National Park is one of southern Africa’s great game parks—a 22,270–square kilometer protected area that encircles a shimmering white salt pan and is replete with elephants, rhinos, zebra, massive herds of impala, and, of course, all the predators that eat them: lions, hyenas, and the black-backed jackal. But where there is wildlife, there is anthrax (Bacillus anthracis). And Etosha is the only place in the world where wildlife seems to cope with yearly outbreaks.

By contrast, when outbreaks of anthrax occur at Kruger National Park in South Africa and Chobe National Park in Botswana every 5 or 10 years, they devastate sensitive mammal populations. During an outbreak that killed some 1500 animals in Malalangwe National Park in Zimbabwe in 2004, rangers were dispatched to burn their corpses and prevent scavengers from spreading the infection. It wasn’t easy—they spent 7 days stoking a fire to incinerate one hippo.

But no one really knows whether burning corpses or covering them up actually makes any sense. “Everyone has their own pet theory, but so little of it has actually been tested,” explains veterinarian Carrie Cizauskas, who works with Bellan on Etosha anthrax under a 5-year grant that their advisor, Wayne Getz, received last year from the NIH’s Ecology and Evolution of Infectious Diseases program.

During a visit to the park in April, the anthrax outbreak was in full flush and Bellan had tallied about 60 victims in the first few months of the season. The mischievous jackals were hard to miss: frolicking on road sides, lazing in the sun, weaving their way through camp sites, and even invading an elephant’s personal space at a nearby water hole.

Unlike “weaponized” anthrax, naturally occurring anthrax does not easily become airborne and requires a significant dose to trigger an infection. (No humans have caught anthrax in Etosha.) The bacterium is not passed from a living animal to another animal, but must take residence in the soil in the form of a spore that can last as long as a century. These spores are either inhaled or ingested by ungulates, killing them within days, or sometimes hours. When Bellan examines blood smears under a microscope, the dying red blood cells are outnumbered by thousands of Bacillus rods. During the four days after death, the bacterium has the ability to produce the deadly spores, which are clumped onto dirt and organic matter and can separate and lodge in the soil if the area is disturbed, say, by an animal rolling around in the dirt.

The efficacy of this process depends on some environmental signal, such as oxygen or nutrient levels. The purpose of Bellan’s carcass cage is to keep these scavengers away from the rotting corpse during the crucial 4-day period to understand whether they help or hurt sporulation (by consuming the latent anthrax), and to measure the persistence of anthrax in the soil over a period of months. If he finds that scavengers facilitate the spread of spores, that would suggest that burning corpses is a good idea. Or it may indicate that during an outbreak your only hope is to vaccinate the most threatened mammal populations.

All Bellan’s found so far, he says, are mountains of maggots. When he got back to that zebra carcass 4 days later, there was a foot-high pile of the squirming fly larvae, more than he’d ever seen. He removed the cage and sat back in his vehicle as 4 hyena and 16 jackal swooped in.

In response to the below comments:

The goal of this research is to understand the role scavenging plays in the ecology of B. anthracis in Etosha and elsewhere, not to create or evaluate carcass management techniques (despite what is said in the article above). Anthrax is considered a natural regulating factor in Etosha and is not managed nor is there interest in doing so. But good data on the role scavenging plays in transmission of anthrax is sparse. Scavengers do indeed pass spores in their feces, but at densities that are likely negligible in terms of transmission unless other processes act to amplify or concentrate spore density. Therefore, the primary role of scavengers in anthrax epidemiology would be the facilitation of sporulation at carcass sites. And the extent to which they do this may offer insight into patterns of anthrax incidence in wildlife.

While it is difficult to pre-empt scavengers at fresh carcasses, it is not impossible in a region where seasonally endemic anthrax allows one the infrequent experience of actually watching an animal fall over and die of the disease. The speed with which scavengers recruit to carcasses also varies across time and space. Scavengers are hungrier in the dry season when anthrax incidence is low, and carcasses get finished quickly. During the wet season when anthrax carcasses (and food in general) are common, carcasses do not get consumed as quickly. In some cases it appears as if the scavenger population is saturated and a tasty carcass remains almost completely unscavenged for several days in a region where scavengers are common. This experiment may offer insight into what this means for anthrax transmission.

As for the blow flies: The caged carcass with heaps of blow fly larvae depicted above was the only carcass that was already partly open when it was caged. Other caged carcasses attracted flies, but far fewer (see the bloated zebra carcass in the slideshow which is also four days old). As Braack & de Vos found in Kruger, it appears that these blowflies preferentially rest on browse at browsing height after feeding. As zebras are grazers, and Etosha?s anthrax occurs predominantly in grazers it seems that alternative explanations may be necessary to explain intraseasonal secondary transmission of the disease. However, we have not ruled out blowfly dispersal of spores and are looking into it.

The project is under researched. The blow flies will deposit millions of spores in a 3m-4m circle around the carcass on any surrounding browse. Plus scavengers are _very_ quickly onto any carcass after death -- usually within minutes -- and long before this grad student can get himself to the carcass site. Circumstances are thus already in place for spore production and site contamination.

What he needs to do is use an adaptation of the Argentine procedure: [1] When he gets there, spray the carcass with 5-10% formaldehyde to deter scavengers and do some site disinfection; [2] cover the carcass with a liberal thick amount of lime, preferably 'quick' lime; [3] cover all that with his cage; [4] when he comes back after 4-14 days (preferably the latter)to remove the cage, he should then cover the carcass with a heavy duty plastic tarp, weighted down with rocks. Check regularly for exploring foxes, etc.. After nine months remove tarp, bones, anything else remaining. Then check for site contamination levels. Good luck!

Have Steve and Carrie considered investigating bacilli in the maggots? I'm sure they're aware of Leo Braack's study - Braack, LEO; de Vos, V (1990): Feeding habits and flight range of blow-flies (_Chrysomyia_ spp.) in relation to anthrax transmission in the Kruger National Park, South Africa. Onderstepoort J. vet. Res. 57:141-142 - and the review by Hugh-Jones, ME & de Vos, V (2002): Anthrax and wildlife. Rev. Sci. Tec. OIE 21:359-383.

The Braack/de Vos study would suggest leaving the carcasses unopened in southern Africa could lead to greater dispersal of bacilli by blowflies while the Hugh-Jones/de Vos studies indicate that, under different circumstances, scavengers would facilitate spore-formation in the immediate vicinity of the carcass. It appears a trade-off between the two scenarios is likely. I would suggest that the relevant question in Etosha is whether jackals and other scavengers pass bacilli/spores in their faeces, as the blowflies evidently do. Perhaps a difference in scavenger abundance may explain the devastating effects of anthrax in the other southern African reserves.

Kind regards
Alan