Relative quantity of <i>Babesia</i> in lions sampled each year in the Serengeti (blue triangles) and Ngorongoro Crater (red circles) as determined by real-time PCR.

<p>Fatal outbreaks are highlighted in light red. Data are separated according to changes in sample preparation affecting levels of PCR product: (A) red blood cell pellets were extracted from all samples collected in 1984–1996, while (B) whole blood was collected for all subsequent samples. The relative quantity of hemoparasite DNA was calculated as average threshold PCR cycle divided by hemoglobin concentration and expressed as the fold difference greater than the sample with the smallest quantity of hemoparasite DNA. Levels of <i>Babesia</i> infection were significantly higher during the fatal outbreaks, in the Crater, and in assays performed on whole blood (all three factors significant at P<0.0001 in a multivariate analysis, <i>n</i> = 344).</p

<i>Babesia</i> infection in lions from the 2001 epidemic.

<p>A) Histopathology of <i>Babesia</i> hyperinfection in an adult lion that died during the epidemic. Small intestinal capillaries are occluded by parasitized red blood cells; B) Marked lymphocyte depletion in the lymph node of the same lion, indicating immunosuppression; C) Electron micrograph of intraerythrocytic piroplasms morphologically compatible with <i>Babesia</i> sp. in the deceased lion; D) Results of denaturant gradient gel electrophoresis for previously characterized carnivore hemoparasites and hemoparasites amplified by PCR from lion samples that demonstrated mixed infections. Lane 1, <i>Babesia canis</i>; lane 2, <i>Cytauxzoon felis</i>; lane 3, <i>B. gibsoni</i>; lane 4, mixture of <i>B. canis</i>, <i>C. felis</i>, and <i>B. gibsoni</i> isolates in lanes 1–3; lane 5, no DNA-negative control; lane 6, lion with <i>Babesia sp.</i> most similar genetically to <i>B. gibsoni</i>, <i>B. felis</i> and a previously uncharacterized <i>Babesia sp.</i>; lane 7, lion with <i>Babesia sp.</i> most similar genetically to <i>B. gibsoni</i> and <i>B. felis</i>; lane 8, lion with hemoparasites most similar genetically to <i>B. gibsoni</i> and <i>Hepatozoon felis</i>; lane 9, lion with a hemoparasite most similar genetically to <i>H. felis</i>.</p

Timing and impact of CDV outbreaks in (A) Serengeti and (B) Ngorongoro Crater.

<p>The heavy lines show the number of adults (≥4 yrs of age), and the narrow lines show the total populations. Blue bars indicate likely timing of “silent” outbreaks that were only detected retrospectively by serology; pink bars show fatal outbreaks. Note that serological data are unavailable for the Crater from 1991–2000. (C, D) Number of buffalo carcasses in the diet of the respective lion populations each year and bone marrow fat scores of Serengeti buffalo. Data are restricted to years with comparable levels of search effort. Red circles in the Serengeti (C) show the bone marrow fat scores (% of bone marrow that was fat) of buffalo carcasses. Note: Full-time lion staff was not stationed in the Crater during 1984–98.</p

Pride-level effects of hemoparasitemia on mortality rates during the fatal outbreaks in the Crater (red circle) and Serengeti (blue triangles).

<p>Prides with a greater proportion of individuals showing high hemoparasitemia also suffered higher mortality rates (P<0.01).</p

The effect of protected areas on pathogen exposure in endangered African wild dog (Lycaon pictus) populations.

Infectious diseases impact African wild dogs (Lycaon pictus), but the nature and magnitude of this threat likely varies among populations according to different factors, such as the presence and prevalence of pathogens and land-use characteristics. We systematically evaluated these factors to assist development of locally appropriate strategies to mitigate disease risk. Wild dogs from 16 sites representing five unconnected populations were examined for rabies virus, canine distemper virus (CDV), canine parvovirus, canine coronavirus, and Babesia spp. exposure. Analyses revealed widespread exposure to viral pathogens, but Babesia was never detected. Exposure to CDV was associated with unprotected and protected-unfenced areas where wild dogs likely have a high probability of domestic dog contact and, in the case of protected-unfenced areas, likely reside amongst high wildlife densities. Our findings also suggest that domestic dog contact may increase rabies and coronavirus exposure risk. Therefore, domestic dogs may be a source of CDV, rabies and coronavirus, while wildlife may also play an important role in CDV transmission dynamics. Relatively high parvovirus seroprevalence across land-use types suggests that it might persist in the absence of spillover from domestic dogs. Should intervention be needed to control pathogens in wild dogs, efforts to prevent rabies and coronavirus exposure might be directed at reducing infection in the presumed domestic dog reservoir through vaccination. If prevention of CDV and parvovirus infections were deemed a management necessity, control of disease in domestic dogs may be insufficient to reduce transmission risks, and vaccination of wild dogs themselves may be the optimal strategy