Understanding the drivers of mortality in African savannah elephants.

Populations of African savannah elephants (Loxodonta africana) have been declining due to poaching, human-elephant conflict, and habitat loss. Understanding the causes of these declines could aid in stabilizing elephant populations. We used data from the Great Elephant Census, a 19-country aerial survey of savannah elephants conducted in 2014 and 2015, to examine effects of a suite of variables on elephant mortality. Independent variables included spatially explicit measures of natural processes and human presence as well as country-level socioeconomic measures. Our dependent variable was the carcass ratio, the ratio of dead elephants to live plus dead elephants, which is an index of recent elephant mortality. Carcass ratios are inversely proportional to population growth rates of elephants over the 4 yr prior to a survey. At the scale of survey strata (n = 275, median area = 1,222 km2 ), we found strong negative associations for carcass ratios with vegetation greenness at the time of the survey, overseas development aid to the country, and distance to the nearest international border. At the scale of ecosystems (n = 42, median area = 12,085 km2 ), carcass ratios increased with drought frequency and decreased with human density and overseas development aid to the country. Both stratum- and ecosystem-scale models explained well under one-half of the variance in carcass ratios. The differences in results between scales suggest that the drivers of mortality may be scale-specific and that the corresponding solutions may vary by scale as well.

Using species traits to predict detectability of animals on aerial surveys.

In animal surveys, detectability can vary widely across species. We hypothesized that detectability of animals should be a function of species traits such as mass, color, and mean herd size. We also hypothesized that models of detectability based on species traits can be used to predict detectability for new species not in the original data set, leading to substantial benefits for ecology and conservation. We tested these hypotheses with double-observer aerial surveys of 10 mammal species in northern Botswana. We combined all 10 species and modeled their detectability with species traits (mass, mean herd size, color) as predictors while controlling for observer effects, vegetation, and herd size. We found support for effects of mass and an interaction between herd size and mean herd size on detectability. This model accurately predicted the ratio of herds detected by two observers vs. one observer for 8 of 10 species. To test whether a model based on species traits could be applied to a new species, we serially deleted each species from the data set, fit a trait-based model to the remaining nine species, and used this model to predict detectability for the deleted species. The model was able to reproduce the species-trait model for seven species and accurately predicted the ratio of detections by one or two observers for a different set of seven species; the model was successful by both measures for five species. To our knowledge, this represents the first time that a mechanistic model for detectability of animals has been used to predict detectability for new species. Prediction failed for species with extreme values of traits, suggesting that predicting detectability is not possible near or beyond the boundaries of one's data set. The approach taken in this paper can potentially be used with a variety of taxa and may provide new opportunities to apply detectability corrections where they have not been possible before.

Viricidal effect of stimulated human mononuclear phagocytes on human immunodeficiency virus type 1.

Human monocytes stimulated with phorbol 12-myristate 13-acetate or opsonized zymosan in vitro were viricidal to human immunodeficiency virus type 1 (HIV-1) as measured by the inability of the virus to replicate in CEM cells. Monocytes, when stimulated, release myeloperoxidase (MPO) and produce H2O2; MPO reacts with H2O2 and chloride to form hypochlorous acid, a known microbicidal agent. The viricidal activity of stimulated monocytes was inhibited by the peroxidase inhibitor azide, implicating MPO, and by catalase but not heated catalase or superoxide dismutase, implicating H2O2. Stimulated monocytes from patients with chronic granulomatous disease (CGD) or hereditary MPO deficiency were not viricidal to HIV-1 unless they were supplemented with the H2O2-generating enzyme glucose oxidase or MPO, respectively. The viricidal activity of stimulated, glucose oxidase-supplemented CGD monocytes and MPO-supplemented MPO-deficient monocytes, like that of normal stimulated monocytes, was inhibited by azide and catalase. Monocytesmaintained in culture differentiate into macrophages with loss of MPO and decreased H2O2 production. The viricidal activity of 3- to 9-day monocyte-derived macrophages was decreased unless MPO was added, whereas the loss of viricidal activity by 12-day-old monocyte-derived macrophages was not reversed by MPO unless the cells were pretreated with gamma-interferon. These findings suggest that stimulated monocytes can be viricidal to HIV-1 through the release of the MPO/H2O2/chloride system and that the decreased viricidal activity on differentiation to macrophages results initially from the loss of MPO and, with more prolonged culture, also from a decreased respiratory burst that can be overcome by gamma-interferon.