Abstract:
Exposure and immunity to generalist pathogens differ among host species and vary
across spatial scales. Anthrax, caused by a multi-host bacterial pathogen, Bacillus
anthracis, is enzootic in Kruger National Park (KNP), South Africa and Etosha National
Park (ENP), Namibia. These parks share many of the same potential host species, yet the
main anthrax host in one (greater kudu (Tragelaphus strepsiceros) in KNP and plains zebra
(Equus quagga) in ENP) is only a minor host in the other. We investigated species and
spatial patterns in anthrax mortalities, B. anthracis exposure, and the ability to neutralize
the anthrax lethal toxin to determine if observed host mortality differences between
locations could be attributed to population-level variation in pathogen exposure and/or
immune response. Using serum collected from zebra and kudu in high and low incidence
areas of each park (18- 20 samples/species/area), we estimated pathogen exposure from
anti-protective antigen (PA) antibody response using enzyme-linked immunosorbent
assay (ELISA) and lethal toxin neutralization with a toxin neutralization assay (TNA).
Serological evidence of pathogen exposure followed mortality patterns within each
system (kudus: 95% positive in KNP versus 40% in ENP; zebras: 83% positive in ENP
versus 63% in KNP). Animals in the high-incidence area of KNP had higher anti-PA
responses than those in the low-incidence area, but there were no significant differences
in exposure by area within ENP. Toxin neutralizing ability was higher for host populations
with lower exposure prevalence, i.e., higher in ENP kudus and KNP zebras than their
conspecifics in the other park. These results indicate that host species differ in their
exposure to and adaptive immunity against B. anthracis in the two parks. These patterns
may be due to environmental differences such as vegetation, rainfall patterns, landscape
or forage availability between these systems and their interplay with host behavior (foraging or other risky behaviors), resulting in differences in exposure frequency and dose,
and hence immune response.
