Mercy Akinyi

Molecular surveillance of Plasmodium falciparum parasites is important to track emerging and new mutations and trends in established mutations and should serve as an early warning system for antimalarial resistance. Dried blood spots were obtained from a Plasmodium falciparum malaria survey in school children conducted across eight counties in western Kenya in 2019. Real-time PCR identified 500 P. falciparum-positive samples that were amplified at five drug resistance loci for targeted amplicon deep sequencing (TADS). The absence of important kelch 13 mutations was similar to previous findings in Kenya pre-2019, and low-frequency mutations were observed in codons 569 and 578. The chloroquine resistance transporter gene codons 76 and 145 were wild type, indicating that the parasites were chloroquine and piperaquine sensitive, respectively. The multidrug resistance gene 1 haplotypes based on codons 86, 184, and 199 were predominantly present in mixed infections with haplotypes NYT and NFT, driven by the absence of chloroquine pressure and the use of lumefantrine, respectively. The sulfadoxine-pyrimethamine resistance profile was a "superresistant" combination of triple mutations in both Pfdhfr (51I 59R 108N) and Pfdhps (436H 437G 540E), rendering sulfadoxine-pyrimethamine ineffective. TADS highlighted the low-frequency variants, allowing the early identification of new mutations, Pfmdr1 codon 199S and Pfdhfr codon 85I and emerging 164L mutations. The added value of TADS is its accuracy in identifying mixed-genotype infections and for high-throughput monitoring of antimalarial resistance markers.

The social environment is a major determinant of morbidity, mortality and Darwinian fitness in social animals. Recent studies have begun to uncover the molecular processes associated with these relationships, but the degree to which they vary across different dimensions of the social environment remains unclear. Here, we draw on a long-term field study of wild baboons to compare the signatures of affiliative and competitive aspects of the social environment in white blood cell gene regulation, under both immune-stimulated and non-stimulated conditions. We find that the effects of dominance rank on gene expression are directionally opposite in males versus females, such that high-ranking males resemble low-ranking females, and vice versa. Among females, rank and social bond strength are both reflected in the activity of cellular metabolism and proliferation genes. However, while we observe pronounced rank-related differences in baseline immune gene activity, only bond strength predicts the fold-change response to immune (lipopolysaccharide) stimulation. Together, our results indicate that the directionality and magnitude of social effects on gene regulation depend on the aspect of the social environment under study. This heterogeneity may help explain why social environmental effects on health and longevity can also vary between measures. This article is part of the theme issue ‘The centennial of the pecking order: current state and future prospects for the study of dominance hierarchies’.

Background. Naturally acquired immunity to malaria develops over several years and can be compromised by concomitant infections. This study explored the influence of chronic schistosomiasis on clinical outcome and immunity to repeated malaria infection. Methods. Two groups of baboons (n=8 each), were infected with Schistosoma mansoni cercariae to establish chronic infections. One of the two groups was treated with Praziquantel to eliminate schistosome infection. The two groups plus a new malaria control group (n=8), were inoculated three times with Plasmodium knowlesi parasites at one-month intervals. Clinical data, IgG, IgG1, memory T-cells and monocyte levels were recorded. Results. We observed after three P. knowlesi infections; i) reduced clinical symptoms in all groups with each subsequent infection, ii) increase IgG and IgG1in the malaria control (Pk-only) group iii) increased IgG and IgG1, CD14 ⁺ and CD14 ⁻ CD16 ⁺ in the Schistosoma treated (Schisto/PZQ+Pk) group and iv) significantly lower IgG and IgG1 levels compared to Pk-only, reduced CD4 ⁺ CD45RO ⁺ and increased CD14 ⁻ CD16 ⁺ cells in the co-infected (Schisto+Pk) group. Conclusion. Chronic S. mansoni does not compromise establishment of clinical immunity after multiple malaria infections with non-classical monocytes seeming to play a role. Failure to develop robust antibody and memory T-cells may have a long-term impact on acquired immunity to malaria infection.

Emerging infectious diseases (EIDs) originating from wildlife present a significant threat to global health, security, and economic growth, thus combatting their emergence is a public health priority. Humans and non-human primates (NHPs) exhibit a high degree of overlap in their genetic and physiological similarities, hence making them susceptible to majority of pathogens that can cross the primate species boundaries. However, efforts to understand the potential infectious disease-causing pathogens harbored by wild primate populations has lagged and is yet to be fully explored. Disease surveillance in wildlife to identify probable infectious disease outbreaks has remained a challenge especially in developing countries due to logistical and financial constrains associated with both periodic and longitudinal sample collection. Such loopholes have hampered the preparedness to handle the emerging infectious diseases whenever they arise. In this review we focus on successes, challenges, and proposed solutions for EID surveillance in non-human primate populations in Kenya. We discuss,1) mechanisms of cross species transmission of EIDs, 2) the role of NHPS in EID transmission, 3) results from past NHP pathogen surveillance projects in Kenya and 4) challenges and proposed solutions for NHP-EID surveillance. Finally, we propose that more studies need to include investigations into understanding how cross species transmission occurs in diverse NHP populations and how this impacts one health.

Artemisinin resistance (AR) emerged in South East Asia 13 years ago and the identification of the resistance conferring molecular marker, Plasmodium falciparum Kelch 13 (Pfk13), 7 years ago has provided an invaluable tool for monitoring AR in malaria endemic countries. Molecular Pfk13 surveillance revealed the resistance foci in the Greater Mekong Subregion, an independent emergence in Guyana, South America, and a low frequency of mutations in Africa. The recent identification of the R561H Pfk13 AR associated mutation in Tanzania, Uganda and in Rwanda, where it has been associated with delayed parasite clearance, should be a concern for the continent. In this review, we provide a summary of Pfk13 resistance associated propeller domain mutation frequencies across Africa from 2012 to 2020, to examine how many other countries have identified these mutations. Only four African countries reported a recent identification of the M476I, P553L, R561H, P574L, C580Y and A675V Pfk13 mutations at low frequencies and with no reports of clinical treatment failure, except for Rwanda. These mutations present a threat to malaria control across the continent, since the greatest burden of malaria remains in Africa. A rise in the frequency of these mutations and their spread would reverse the gains made in the reduction of malaria over the last 20 years, given the lack of new antimalarial treatments in the event artemisinin-based combination therapies fail. The review highlights the frequency of Pfk13 propeller domain mutations across Africa, providing an up-to-date perspective of Pfk13 mutations, and appeals for an urgent and concerted effort to monitoring antimalarial resistance markers in Africa and the efficacy of antimalarials by re-establishing sentinel surveillance systems.

The social environment is a major determinant of morbidity, mortality, and Darwinian fitness in social animals. Recent studies have begun to uncover the molecular processes associated with these relationships, but the degree to which they vary across different dimensions of the social environment remains unclear. Here, we draw on a long-term field study of wild baboons to compare the signatures of affiliative and competitive aspects of the social environment in white blood cell gene regulation, under both immune stimulated and non-stimulated conditions. We find that the effects of dominance rank on gene expression are directionally opposite in males versus females, such that high-ranking males resemble low-ranking females, and vice-versa. Among females, rank and social bond strength are both reflected in the activity of cellular metabolism and proliferation genes. However, pronounced rank-related differences in baseline immune gene activity are near-absent for social bond strength, while only bond strength predicts the fold-change response to immune (lipopolysaccharide) stimulation. Together, our results indicate that the directionality and magnitude of social effects on gene regulation depend on the aspect of the social environment under study. This heterogeneity may help explain why social environmental effects on health and longevity can also vary between measures.

Zoonotic pathogens are among the most important causes of ill health all over the world. The presence of these pathogens in free ranging baboons may have significant implications for humans. In Kenya, the encroachment of wildlife habitats has led to increased interaction between humans and wildlife especially non‐human primates. The current study therefore aimed at investigating any possible zoonotic gastrointestinal helminths of olive baboons (Papio anubis) at the human–wildlife interface in two park borders and a ranch in Kenya, namely, Tsavo West National Park, Tana River Primate Reserve and Mutara Ranch, Laikipia, Kenya. One hundred and forty‐seven baboons were used in the study. They were trapped in the wild, sampled for stool marked and then released back to the wild. Gastrointestinal (GIT) helminths identified were Strongyloides, Oesophagostomum, Enterobius spp and Trichuris Trichiura from all the three sites while Schistosoma mansoni was only detected from Tsavo baboons and with very low incidence (2.1%). The prevalence of these parasites varied among the sites but significant difference in prevalence was only noted in Strongyloides and Oesophagostomum (p < 0.05) among the three sites. This therefore implies that even with control measures instituted on the human population, baboons will always be a source of zoonotic GIT helminths especially S. mansoni even if the incidence are low. There is need to put in place measures aiming to reduce their interactions with humans and also try to control these infections in the baboons. Baboons harbor Schistosoma mansoni which is infectious to humans. Humans can be infected through sharing of water resources, eating left overs since their fecal waste contaminate water and food. Control of the schistosomiasis in human population alone will still be a challenge if possible zoonotic sources are not looked at.

Aging, for virtually all life, is inescapable. However, within populations, biological aging rates vary. Understanding sources of variation in this process is central to understanding the biodemography of natural populations. We constructed a DNA methylation-based age predictor for an intensively studied wild baboon population in Kenya. Consistent with findings in humans, the resulting 'epigenetic clock' closely tracks chronological age, but individuals are predicted to be somewhat older or younger than their known ages. Surprisingly, these deviations are not explained by the strongest predictors of lifespan in this population, early adversity and social integration. Instead, they are best predicted by male dominance rank: high-ranking males are predicted to be older than their true ages, and epigenetic age tracks changes in rank over time. Our results argue that achieving high rank for male baboons—the best predictor of reproductive success—imposes costs consistent with a 'live fast, die young' life history strategy.

Background Natural infections with soil‐transmitted nematodes occur in non‐human primates (NHPs) and have the potential to cross primate‐species boundaries and cause diseases of significant public health concern. Despite the presence of NHPs in most urban centres in Kenya, comprehensive studies on their gastrointestinal parasites are scant. Objective Conduct a cross‐sectional survey to identify zoonotic nematodes in free‐ranging NHPs found within four selected urban and peri‐urban centres in Kenya. Methods A total of 86 NHPs: 41 African green monkeys [AGMs] (Chlorocebus aethiops), 30 olive baboons (Papio anubis), 5 blue monkeys (Cercopithecus mitis stuhlmanni) and 10 red‐tailed monkeys (Cercopithecus ascanius) were sampled once in situ and released back to their habitat. Microscopy was used to identify nematodes egg and larvae stages in the samples. Subsequently, PCR coupled with high‐resolution melting (PCR‐HRM) analysis and sequencing were used to identify nodule worms. Results NHPs inhabiting densely populated urban environs in Kenya were found infected with a rich diversity of nematodes including three potentially zoonotic nematodes including Oesophagostomum stephanostomum, Oesophagostomum bifurcum and Trichostrongylus colubriformis and co‐infections were common. Conclusion Phylogenetic analysis showed that O. stephanostomum from red‐tailed and blue monkeys have a close evolutionary relatedness to human isolates suggesting the zoonotic potential of this parasite. Moreover, we also report the first natural co‐infection of O. bifurcum and O. stephanostomum in free‐ranging AGMs.

Background: Natural infections with soil transmitted nematodes occur in non-human primates (NHPs) and have the potential to cross primate-species boundaries and cause diseases of significant public health concern. Despite their presence in most urban centres in Kenya, comprehensive studies on their gastrointestinal parasites are scant. Objective: Conduct a cross-sectional survey to identify zoonotic nematodes in free-ranging NHPs found within four selected urban and peri-urban centres in Kenya. Methods: A total of 86 NHPs: 41 African green monkeys [AGM] (Chlorocebus aethiops), 30 olive baboons (Papio anubis), 5 blue monkeys (Cercopithecus mitis stuhlmanni) and 10 red tailed monkeys (Cercopithecus ascanius) were sampled once in situ and released back to their habitat. Microscopy was used to identify nematodes egg and larvae stages in the samples. Subsequently, PCR coupled with high-resolution melting (PCR-HRM) analysis and sequencing were used to identify nodule worms. Results: NHPs inhabiting densely populated urban environs in Kenya were found infected with a rich diversity of nematodes including three potentially zoonotic nematodes including Oesophagostomum stephanostomum, Oesophagostomum bifurcum and Trichostrongylus colubriformis and co-infections were common. Conclusion: Phylogenetic analysis showed that O. stephanostomum from red tailed and blue monkeys have a close evolutionary relatedness to human isolates suggesting the zoonotic potential of this parasite. Moreover, we also report the first natural co-infection of O. bifurcum and O. stephanostomum in free-ranging AGMs. KEYWORDS: Non-human primates, Oesophagostomum, PCR-HRM, urban, zoonoses.

Several factors are thought to shape male parasite risk in polygynous and polygynandrous mammals, including male-male competition, investment in potentially immunosuppressive hormones, and dispersal. Parasitism is also driven by processes occurring at larger scales, including host social groups and populations. To date, studies that test parasite-related costs of male behavior at all three scales—individual hosts, social groups, and the host population—remain rare. To fill this gap, we investigated multi-scale predictors of helminth parasitism in 97 male savanna baboons (Papio cynocephalus) living in the Amboseli ecosystem in Kenya over a 5-year span. Controlling for multi-scale processes, we found that many of the classic indicators of male mating effort—high dominance rank, testosterone, and glucocorticoids—did not predict helminth infection risk. However, we identified two parasite-related costs associated with male behavior: (i) socially connected males exhibited higher Trichuris trichiura egg counts and greater parasite species richness than socially isolated males and (ii) males with stable group residency exhibited higher parasite species richness than males who frequently dispersed to new social groups. At the population level, males harbored more parasites following periods of drought than rainfall. Lastly, parasites exhibited positive covariance suggesting that infection risk increases if a host already harbors one or more parasite taxa. These results indicate that multi-scale processes are important in driving male parasite risk and that some aspects of male behavior are costly. Together, our results provide an unusually holistic perspective on the drivers of parasite risk in the context of male behaviors and life histories. Significance statement Infection by gastrointestinal helminths can have major consequences for host fitness, especially in the context of male mating effort. Multi-scale processes—from the host to its social group and population—are important for understanding key drivers of parasitism. We leveraged long-term data from one of the longest running behavioral ecology studies of a wild primate population in the world, the well-studied Amboseli baboon population in Kenya. We found that traditional indicators of male mating effort (attaining high dominance rank, high testosterone and glucocorticoids) did not predict parasitism. However, male social connectedness to females, competitive group demography, and harsh weather were all associated with higher parasitism. Because socially connected males faced the highest parasite risk, males may face a tradeoff between male-female relationships and parasitism. Our results show how processes at multiple scales contribute to variation in male parasite risk.

Helminth parasites can have wide‐ranging, detrimental effects on host reproduction and survival. These effects are best documented in humans and domestic animals, while only a few studies in wild mammals have identified both the forces that drive helminth infection risk and their costs to individual fitness. Working in a well‐studied population of wild baboons ( Papio cynocephalus ) in the Amboseli ecosystem in Kenya, we pursued two goals, to (a) examine the costs of helminth infections in terms of female fertility and glucocorticoid hormone levels and (b) test how processes operating at multiple scales—from individual hosts to social groups and the population at large—work together to predict variation in female infection risk. To accomplish these goals, we measured helminth parasite burdens in 745 faecal samples collected over 5 years from 122 female baboons. We combine these data with detailed observations of host environments, social behaviours, hormone levels and interbirth intervals (IBIs). We found that helminths are costly to female fertility: females infected with more diverse parasite communities (i.e., higher parasite richness) exhibited longer IBIs than females infected by fewer parasite taxa. We also found that females exhibiting high Trichuris trichiura egg counts also had high glucocorticoid levels. Female infection risk was best predicted by factors at the host, social group and population level: females facing the highest risk were old, socially isolated, living in dry conditions and infected with other helminths. Our results provide an unusually holistic understanding of the factors that contribute to inter‐individual differences in parasite infection, and they contribute to just a handful of studies linking helminths to host fitness in wild mammals.

In humans and other hierarchical species, social status is tightly linked to variation in health and fitness-related traits. Experimental manipulations of social status in female rhesus macaques suggest that this relationship is partially explained by status effects on immune gene regulation. However, social hierarchies are established and maintained in different ways across species: While some are based on kin-directed nepotism, others emerge from direct physical competition. We investigated how this variation influences the relationship between social status and immune gene regulation in wild baboons, where hierarchies in males are based on fighting ability but female hierarchies are nepotistic. We measured rank-related variation in gene expression levels in adult baboons of both sexes at baseline and in response to ex vivo stimulation with the bacterial endotoxin lipopolysaccharide (LPS). We identified >2,000 rank-associated genes in males, an order of magnitude more than in females. In males, high status predicted increased expression of genes involved in innate immunity and preferential activation of the NF-κB–mediated proinflammatory pathway, a pattern previously associated with low status in female rhesus macaques. Using Mendelian randomization, we reconcile these observations by demonstrating that high status-associated gene expression patterns are precursors, not consequences, of high social status in males, in support of the idea that physiological condition determines who attains high rank. Together, our work provides a test of the relationship between social status and immune gene regulation in wild primates. It also emphasizes the importance of social context in shaping the relationship between social status and immune function.

In humans and other hierarchical species, social status is tightly linked to variation in health and fitness-related traits. Experimental manipulations of social status in female rhesus macaques suggest that this relationship is partially explained by status effects on immune gene regulation. However, social hierarchies are established and maintained in different ways across species: while some are based on kin-directed nepotism, others emerge from direct physical competition. We investigated how this variation influences the relationship between social status and immune gene regulation in wild baboons, where hierarchies in males are based on fighting ability but female hierarchies are nepotistic. We measured rank-related variation in gene expression levels in adult baboons of both sexes at baseline and in response to ex vivo stimulation with the bacterial endotoxin lipopolysaccharide (LPS). We identified >2000 rank- associated genes in males, an order of magnitude more than in females. In males, high status predicted increased expression of genes involved in innate immunity and preferential activation of the NFkB-mediated pro-inflammatory pathway, a pattern previously associated with low status in female rhesus macaques. Using Mendelian randomization, we reconcile these observations by demonstrating that high status-associated gene expression patterns are precursors, not consequences, of high social status in males, in support of the idea that physiological condition determines who attains high rank. Together, our work provides the first test of the relationship between social status and immune gene regulation in wild primates. It also emphasizes the importance of social context in shaping the relationship between social status and immune function. SIGNIFICANCE Social status predicts fitness outcomes in social animals, motivating efforts to understand its physiological causes and consequences. We investigated the relationship between social status and immune gene expression in wild baboons, where female status is determined by kinship but male status is determined by fighting ability. We uncover pervasive status-gene expression associations in males, but not females. High status males exhibit high levels of pro-inflammatory gene expression, in contrast to previous findings in hierarchies that are not competitively determined. Using Mendelian randomization, we show that this status-associated variation precedes dominance rank attainment: males who compete successfully for high status are already immunologically distinct. The nature of social hierarchies thus fundamentally shapes the relationship between social status and immune function.

In many mammals, maturational milestones such as dispersal and the attainment of adult dominance rank mark stages in the onset of reproductive activity and depend on a coordinated set of hormonal and socio-behavioral changes. Studies that focus on the link between hormones and maturational milestones are uncommon in wild mammals because of the challenges of obtaining adequate sample sizes of maturing animals and of tracking the movements of dispersing animals. We examined two maturational milestones in wild male baboons-adult dominance rank attainment and natal dispersal-and measured their association with variation in glucocorticoids (fGC) and fecal testosterone (fT). We found that rank attainment is associated with an increase in fGC levels but not fT levels: males that have achieved any adult rank have higher fGC than males that have not yet attained an adult rank. This indicates that once males have attained an adult rank they experience greater energetic and/or psychosocial demands than they did prior to attaining this milestone, most likely because of the resulting participation in both agonistic and sexual behaviors that accompany rank attainment. In contrast, natal dispersal does not produce sustained increases in either fGC or fT levels, suggesting that individuals are either well adapted to face the challenges associated with dispersal or that the effects of dispersal on hormone levels are ephemeral for male baboons.

The human population in Kenya has doubled over the last 25 years and is expected to rise twofold by 2050. Thus, pressure for human space has led to encroachment into wildlife habitats, increasing human-wildlife interactions. Such interactions pose serious health risks to both humans and wildlife, yet studies to understand these risks are limited in Kenya. To understand the possible predisposing factors for zoonoses at the human-wildlife interface, a survey was carried out in Nthongoni, an area bordering Tsavo and Chyulu Hills national parks in Kenya. Questionnaires were administered to 11 key informants and 200 residents from 35 villages. Our results indicate that the majority (75%) of the respondents suffered from crop raids and livestock depredation by wildlife. On their part, residents killed wildlife for: subsistence (41%), revenge (35%), bush-meat trade (22%), and other undisclosed reasons. Nineteen per cent of the respondents were knowledgeable about disease transmission through bush-meat. Qualitative data revealed helplessness, bitterness and revenge tendencies by farmers due to wildlife losses, which contributed to their poverty. This study enhances our understanding of human-wildlife interactions and the associated socioeconomic, health and conservation implications. It demonstrates the predicaments communities living adjacent to wildlife areas face and the need to involve them in sustainable management of the areas. We recommend identification of appropriate alternative livelihoods, to mitigate illegal bush-meat and agricultural practices that attract wildlife, leading to conflicts. In addition, responsive health and conservation education, and participatory research aimed at advising policy, are necessary to cushion the communities from wildlife damages.

Malaria and schistosomiasis co-infections are common and chronic schistosomiasis has been implicated in affecting the severity of acute malaria. But whether it enhances or attenuates malaria has been controversal due lack of appropriately controlled human studies and relevant animals models. To examine this interaction, we conducted a randomized controlled study using the baboon (Papio anubis) to analyse the effect of chronic schistosomiasis on severe malaria. Two groups of baboons (n=8 each) and a schistosomiasis control group (n=3) were infected with 500 S. mansoni cercariae. At 14 and 15 weeks post infection, one group was given praziquantel to treat their schistosomiasis infection. Four weeks later, the two groups plus a new malaria control group (n=8), were intravenously innoculated with 105 P. knowlesi parasites (Pk) and monitored daily for development of severe malaria. Eighty-one percent of baboons exposed to chronic S. mansoni infection with or without praziquantel treatment, survived malaria compared to only 25% of animals infected with Pk only (p=0.01). Schistosome infected animals also had significantly lower parasite burden (p=0.004) than the baboons in the Pk only group and were protected from severe anemia. Co-infection was associated with increased spontaneous production of IL-6 suggesting an enhanced innate immune responses while Pk only infected animals failed to develop mitogen-driven TNF-α and IL-10 indicating the inability to generate adequate protective and balancing immunoregulatory responses. These results indicate that chronic S. mansoni attenuates the severity of P. knowlesi co-infection in baboons by mechanisms that may enhance innate immunity to malaria.

Nonhuman primates in research environments provide special challenges for discussions of animal welfare. Captive nonhuman primates are extremely intelligent and capable animals, and few, if any, research environments can duplicate their natural conditions. However, there are numerous ways to functionally simulate critical aspects of the natural environment in captivity, thereby stimulating species-typical behavior patterns in captive primates. Evidence suggests that primate subjects that display many species-typical behavior patterns have enhanced welfare. Behavioral management techniques, including socialization strategies, environmental enrichment, and positive reinforcement training are used to provide primates in research environments with opportunities to control aspects of their environments and to make meaningful choices, in some cases, even facilitating participation in their own care. Such techniques typically not only enhance the primates' welfare, but also improve the quality and utility of the animals as research models by minimizing confounding influences.

Nonhuman primate species spend a conspicuous amount of time grooming during social interactions, a behaviour that probably serves both social and health-related functions. While the social implications of grooming have been relatively well studied, less attention has been paid to the health benefits, especially the removal of ectoparasites, which may act as vectors in disease transmission. In this study, we examined whether grooming behaviour reduced tick load (number of ticks) and haemoprotozoan infection status in a population of wild adult baboons (Papio cynocephalus). We found that younger and higher-ranking adults were groomed more often than older, low-ranking adults, and females were groomed more often than males. Animals that received more grooming, in turn, had lower tick loads. Baboons with lower tick loads had higher packed red cell volume (PCV or haematocrit), one general measure of health status. We detected a tick-borne haemoprotozoan, Babesia microti, but its low prevalence in the population precluded identifying sources of variance in infection.

Natural populations hold enormous potential for evolutionary genetic studies, especially when phenotypic, genetic and environmental data are all available on the same individuals. However, untangling the genotype-phenotype relationship in natural populations remains a major challenge. Here, we describe results of an investigation of one class of phenotype, allele-specific gene expression (ASGE), in the well-studied natural population of baboons of the Amboseli basin, Kenya. ASGE measurements identify cases in which one allele of a gene is overexpressed relative to the alternative allele of the same gene, within individuals, thus providing a control for background genetic and environmental effects. Here, we characterize the incidence of ASGE in the Amboseli baboon population, focusing on the genetic and environmental contributions to ASGE in a set of eleven genes involved in immunity and defence. Within this set, we identify evidence for common ASGE in four genes. We also present examples of two relationships between cis-regulatory genetic variants and the ASGE phenotype. Finally, we identify one case in which this relationship is influenced by a novel gene-environment interaction. Specifically, the dominance rank of an individual's mother during its early life (an aspect of that individual's social environment) influences the expression of the gene CCL5 via an interaction with cis-regulatory genetic variation. These results illustrate how environmental and ecological data can be integrated into evolutionary genetic studies of functional variation in natural populations. They also highlight the potential importance of early life environmental variation in shaping the genetic architecture of complex traits in wild mammals.

Babesia microti-like parasites have been reported to infect captive non-human primates (NHPs). However, studies on the prevalence of Babesia spp. in free-ranging NHPs are lacking. This investigation aimed at determining the prevalence of B. microti in wild-caught Kenyan NHPs. In total, 125 animals were studied, including 65 olive baboons (Papio cynocephalus anubis) and 60 African green monkeys ([AGMs] Chlorocebus aethiops). Nested polymerase chain reaction targeting Babesia β-tubulin genes was used to diagnose infection prevalence. Results indicated a prevalence of 22% (27/125) B. microti infection in free-ranging NHPs in Kenya. There was no statistically significant difference in B. microti infection prevalence between baboons and AGMs or male and female animals. This is the first report of the presence and prevalence of B. microti in free-ranging Kenyan NHPs.

Laboratory animal models are critical for pre-clinical studies in development and evaluation of diagnostic and treatment tools in sleeping sickness research. A monkey model provides a distinct advantage over lower laboratory animals due to access of the central nervous system through serial sampling of cerebrospinal fluid (CSF). A robust vervet monkey model developed using recent field isolate of Trypanosoma brucei rhodesiense (IPR 001), which attains induced late stage in 50 days, has been developed at Institute of Primate Research (IPR). Following experimental infection with 104 trypanosomes, the prepatent period was of 3-4 days, with CSF parasitosis observed 14-21 days. Treatment with diminazene aceturate 28 days after infection resulted in induced meningoencephalitis 20-26 days later. Monkeys in late stage trypanosomiasis had indicative clinical signs such as aggression and hind limb paresis. This provides a less expensive animal model for studies in sleeping sickness.