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MELLING. 1992. Gram-positive bacilli isolated during epidemiological investigations which, on the basis of conventional tests, resemble Bacillus anthracis but which fail to produce the capsule or to induce anthrax in test animals have long been dismissed in clinical and veterinary laboratories as B . cereus or simply as unidentified Bacillus spp. and thereupon discarded as inconsequential. In this study, the application of newly available DNA probe, polymerase chain reaction and specific toxin antigen detection technology has revealed that a proportion of such strains are B . anthracis which lack the plasmid carrying the capsule gene (pX02). While these techniques cannot, of course, be used to confirm the identities of strains resembling B . anthracis but which also lack the plasmid carrying the toxin genes (pXOl), the likelihood that these also are bonaJde B . anthracis becomes more acceptable. (As yet no naturally occurring pXOl-/2+ strains have been found.) At this point, the significance of the presence of such avirulent forms of B. anthracis in specimens can only be a subject for speculation, but the possibility that they may be indicators of virulent parents somewhere in the system being examined must be considered.

The word ‘problem’ is seen with some frequency in relation to clear differentiation between Bacillus anthracis and B. cereus. In fact, although the close relationship of these two species is undisputed, it is only in the case of a few borderline isolates, rarely encountered in practice, that any sort of identification problem exists. Until recently this was only important to the taxonomist who found it unsatisfactory not to be able to identify definitively such isolates. To most others, if the isolate was unable to produce anthrax in a laboratory animal, it was discarded as irrelevant without being named, or it was called B. cereus or given a name such as B. anthracis similis, or even a totally unrelated name. More recently, in view of the new light in which B. anthracis is increasingly seen, resulting from its putative association with bioaggression, clear identification has become a more critical issue. This paper reviews the current state of the art and suggests the way forward for the future.

A massive outbreak of anthrax in the wildlife of the Malilangwe Wildlife Reserve in Zimbabwe between August and November 2004 resulted in the death of almost all the reserve's estimated 500 kudu (Tragelaphus strepsiceros). Other species badly affected were nyala (Tragelaphus angasi), bushbuck (Tragelaphus scriptus), waterbuck (Kobus ellipsiprymnus) and roan antelope (Hippotragus equinus), which suffered losses of approximately 68 per cent, 48 per cent, 44 per cent and 42 per cent of their populations, respectively. Buffalo (Syncerus caffer) were also badly affected and although their population suffered only a 6 per cent loss, the numbers of deaths ranked second highest after kudu. To the authors' knowledge, this is the first record of anthrax in wildlife in Zimbabwe.

To mitigate the effects of zoonotic diseases on human and animal populations, it is critical to understand what factors alter transmission dynamics. Here we assess the risk of exposure to lethal concentrations of the anthrax bacterium, Bacillus anthracis, for grazing animals in a natural system over time through different transmission mechanisms. We follow pathogen concentrations at anthrax carcass sites and waterholes for five years and estimate infection risk as a function of grass, soil or water intake, age of carcass sites, and the exposure required for a lethal infection. Grazing, not drinking, seems the dominant transmission route, and transmission is more probable from grazing at carcass sites 1-2 years of age. Unlike most studies of virulent pathogens that are conducted under controlled conditions for extrapolation to real situations, we evaluate exposure risk under field conditions to estimate the probability of a lethal dose, showing that not all reservoirs with detectable pathogens are significant transmission pathways.Understanding the ecological processes that drive zoonotic disease outbreaks is important in mitigating their effects on human and animal populations. One critical factor affecting infectious disease dynamics is spatio-temporal heterogeneity in transmission 1,2 . For directly transmitted pathogens, this heterogeneity can be described through peer to peer contact rates and the structure of social networks in host populations [3][4][5] . When pathogens are acquired from environmental reservoirs, the pathogen's distribution in the environment and the interaction between host behavior and reservoir becomes the crucial link in transmission. Despite the global burden of diseases with environmental reservoirs (like cholera, tularemia, polio, botulism, anthrax, bubonic plague, leptospirosis, enteropathogenic E. coli and others 6 ), microbial ecology in the field is currently understudied due to the difficulties of monitoring microbes in their natural environment. Though progress is being made in risk assessment studies, more data are needed on diseases currently posing threats to public health, livestock health, and wildlife health. Moreover, to calibrate the risk and thus an appropriate response to emerging diseases following environmental change or the release of bioweapons, we need to know their long-term behavior in natural systems.The distribution of infectious agents in the environment is typically aggregated due to pulsed releases from infected hosts, creating heterogeneity in the risk of exposure for future hosts. Public health scientists assess risk of infection by identifying disease agents, quantifying exposure, and characterizing dose-response relationships 7,8 .