Anthrax in Etosha A persistent plague

By Holly Ganz and Wendy Turner

Blood drips from the nostrils, mouth and rear end of a dead Burchell’s zebra lying on the ground near the edge of the Etosha Pan. The carcass exhibits the classic signs of anthrax, a deadly disease that has infected wildlife, livestock and humans since ancient times

Even though Louis Pasteur developed the first vaccine for anthrax in 1881, there are still many unanswered questions on why this disease continues to plague animal populations. Several times each week we get up early to drive transects, looking for animal carcasses in the Etosha National Park. Carcass sites are great places to see and photograph wildlife. In addition to observing scavengers, we are also interested in why the animals died. Was their death the result of predation or was an infectious disease, such as anthrax, involved?

After locating a carcass, we may have to wait until there aren’t any large predators around to collect samples to determine the cause of death. Without treatment, most animals die a few days after becoming infected with anthrax. We are following a long-standing tradition in Etosha, where monitoring animal mortalities was started more than forty years ago. As a result, we know that at least 3 800 animals have died from anthrax since 1966. And this number probably represents only a fraction of the actual number of anthrax deaths in Etosha.

Understanding the disease

Long-term monitoring of animal mortalities and prior research conducted in Etosha provide an extraordinary opportunity for understanding the disease. Professor Wayne Getz and associated researchers from the University of California at Berkeley initiated recent efforts to study anthrax in Etosha. We are working in collaboration with the Etosha Ecological Institute in Okaukuejo. Two research projects are currently underway, one examining the possibility that infection with gut parasites increases susceptibility to anthrax infection, and another examining whether there are different types of anthrax that infect different types of animals. Additional proposals were submitted to the Ministry of Environment and Tourism early in 2007 to explore the effects of scavengers and host genetics, physiology and immunology on disease outbreaks.

Many ungulates host worms and other parasites in their intestines, unless they are given deworming medicine. Parasitic worms attach to the gut using spines, hooks, or suckers that may cause small cuts in the gut lining. It is commonly believed that animals acquire an anthrax infection by consuming infectious spores while they are grazing. Cuts in the gut lining may provide a route for anthrax to invade the circulatory system from the digestive tract. We are investigating whether infections of worms and other parasites in the gut make an individual animal more likely to become infected with anthrax.

Seasonal outbreaks

To address this question, we are examining correlations between the timing of anthrax and parasite infections and making comparisons between the abundance of parasites found in anthrax carcasses and live animals. This investigation requires the collection of many faecal samples from living and dead hosts. It is especially hard to find carcasses with their guts intact because scavengers tend to get there first, so there is much joy when we do find one. What we have determined thus far is that both the number of animals dying from anthrax infection and the abundance of worms and other parasites in the gut reach a peak in the late wet season. In the process, we have uncovered a number of undescribed species and plan to identify and describe these parasites with the assistance of taxonomic experts.

We are also using samples collected from carcasses to determine whether there are different types of anthrax in Etosha and whether the types differ in their ability to infect certain host species. An unusual characteristic of anthrax is its ability to infect a wide variety of hosts. In Etosha, many different kinds of animals have died from anthrax infections, including Burchell’s zebra, elephant, blue wildebeest, springbok, black rhinoceros, giraffe, eland, greater kudu, gemsbok, Hartmann’s zebra, lion, cheetah, spotted hyaena, brown hyaena, black-backed jackal and ostrich.

While many different animal species are susceptible to anthrax, there seem to be differences in the seasonal timing as to when they develop infections. Pauline Lindeque showed in her dissertation research that the timing of disease outbreaks in Etosha differs between plains ungulates such as Burchell’s zebra and elephant. For zebra, peak anthrax mortalities occur in March/April, while for elephant, mortalities peak in November/December. Differences in the timing of anthrax infection between these animals may be due to adaptation by different anthrax types to particular host species. Surprisingly, it is unknown whether different host species are susceptible to different anthrax types. We hope to address this question in our research using recently developed genetic techniques.

When we come upon a carcass site, there are often scavengers around, busily defending and consuming the carcass. Everything happens fast; twenty-four hours later only bones and a few scraps of skin will remain. In the spread of anthrax the role of scavengers such as hyaena and vultures is controversial. By opening and moving carcasses, they may increase the area of soil saturated by contaminated blood and disperse infectious material. And when they leave the carcass site to return to their dens or roost, they may carry infectious material in their faeces. Alternatively, scavengers may destroy infectious material in the process of digestion, thereby cleaning up the site.

Stress possibly a factor

Stress may contribute to the timing of anthrax mortalities in zebra. Even with plentiful food available during the wet season, individual animals may become stressed by the demands of reproduction and lactation, along with the stress caused by increasing numbers of gut parasites. Genetic factors and host conditions influence the ability of a host to fight off a potential infection and probably play a role in the timing of anthrax outbreaks. Using Burchell’s zebra as the focal host for studies in genetics, physiology, and immunology, our proposed research expands the scope of efforts to understand the effects of gut parasites on the timing of anthrax outbreaks. Here, our goal is to identify genetic risk factors for susceptibility to anthrax infection. Additionally, we will characterise seasonal changes in host condition by assessing levels of stress and reproductive hormones, nutrition and immunity, as well as infection by gut parasites. We will test the hypothesis that seasonal changes in host condition explain the wet-season infection patterns observed in the Etosha zebra population.

The results of our field and laboratory studies will be used to develop a predictive model of host susceptibility and anthrax occurrence. We will model factors that contribute to the timing of anthrax outbreaks and examine the theoretical effectiveness of commonly enacted control measures, such as burning or burial of carcasses, exclusion of scavengers and vaccination of susceptible host populations.

This article appeared in the 2007/8 edition of Conservation and the Environment in Namibia.