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Kamau, J.

Publications and source records attributed to Kamau, J..

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Eukaryotic composition across seasons and social groups in the gut microbiota of wild baboons

BackgroundAnimals coexist with complex microbiota, including bacteria, viruses, and eukaryotes (e.g., fungi, protists, and helminths). While the composition of bacterial and viral components of animal microbiota are increasingly well understood, eukaryotic composition remains neglected. Here we characterized eukaryotic diversity in the microbiomes in wild baboons and tested the degree to which eukaryotic community composition was predicted by host social group membership, sex, age, and season of sample collection. ResultsWe analyzed a total of 75 fecal samples collected between 2012 and 2014 from 73 wild baboons in the Amboseli ecosystem in Kenya. DNA from these samples was subjected to shotgun metagenomic sequencing, revealing members of the kingdoms Protista, Chromista, and Fungi in 90.7%, 46.7%, and 20.3% of samples, respectively. Social group membership explained 11.2% of the global diversity in gut eukaryotic species composition, but we did not detect statistically significant effect of season, host age, and host sex. Across samples, the most prevalent protists were Entamoeba coli (74.66% of samples), Enteromonas hominis (53.33% of samples), and Blastocystis subtype 3 (38.66% of samples), while the most prevalent fungi included Pichia manshurica (14.66% of samples), and Ogataea naganishii (6.66% of samples). ConclusionsProtista, Chromista, and Fungi are common members of the gut microbiome of wild baboons. More work on eukaryotic members of primate gut microbiota is essential for primate health monitoring and management strategies.

microbiology↗

Sex differences in immune function and disease risk are not easily explained by an evolutionary mismatch

The "Pregnancy Compensation Hypothesis" (PCH) posits that sex differences in the mammalian immune system reflect the effects of selection on female immunity during pregnancy, during which increased immunomodulation is required to reduce immune responses to the fetus, while maintaining the ability to respond to pathogens. In humans, fewer pathogens and lower parity in urban, industrialized environments has been suggested to leave female immune systems under-stimulated, creating an "evolutionary mismatch" which exacerbates sex differences in immunity and increases female autoimmune disease risk. Yet, robust tests of this mismatch hypothesis have not been conducted. Here, we first confirmed a sex-bias in autoimmune disease prevalence in a large dataset of individuals from the United Kingdom (UK Biobank). Second, we asked whether sex differences in immune function are affected by shifts toward urban, lower-parity lifestyles in a single population--the Turkana people of northwest Kenya. We found that lifestyle alters sex differences in immune cell type proportions, but not in gene expression levels. Contrary to expectations from the PCH, parity did not predict immune physiology. We then tested for generalizable trends across natural fertility mammalian populations versus urban humans (data from Turkana, NHANES, GTEx, Batwa and Bakiga, yellow baboons, and macaques). We did not find consistent relationships between lifestyle and sex-biases in immune biomarkers or between parity and the same immune outcomes. Indeed, we found that parity predicts autoimmune disease risk in the opposite direction than expected from the PCH, with higher parity associated with higher autoimmune disease risk while adjusting for relevant socioeconomic variables in the UK Biobank. Taken together, our work suggests that while sex clearly influences immune physiology and disease risk in urban settings, these effects are not easily explained by an evolutionary mismatch. Future work addressing how sex interacts with lifestyle change to generate disease is needed.

evolutionary biology↗

Adaptations to water stress and pastoralism in the Turkana of northwest Kenya

The Turkana people inhabit arid regions of east Africa--where temperatures are high and water is scarce--and they practice subsistence pastoralism, such that their diet is primarily composed of animal products. Working with Turkana communities, we sequenced 367 genomes and identified 8 regions putatively involved in adaptation to water stress and pastoralism. One of these regions includes a putative enhancer for STC1--a kidney-expressed gene involved in the response to dehydration and the metabolism of purine-rich foods such as red meat. We show that STC1 is induced by antidiuretic hormone in humans, is associated with urea levels in the Turkana themselves, and is under strong selection in this population (s[~]0.041). This work highlights that partnerships with subsistence-level groups can lead to new models of human physiology with biomedical relevance.

evolutionary biology↗

Evaluation of staA, viaB and sopE genes in Salmonella detection using conventional polymerase chain reaction (PCR)

Typhoid fever is caused by the bacteria Salmonella enterica subspecies enterica serovar Typhi (S. Typhi) and remains a significant health problem in many developing countries. The lack of adequate diagnostic capabilities in these poor resource settings have contributed greatly in making typhoid fever endemic in these regions. Reliable and inexpensive diagnostic tests are needed to improve the management of this disease burden. This study evaluated the ability of staA, viaB and sopE genes to detect Salmonella spp. Conventional polymerase chain reaction (PCR) amplification of staA, viaB and sopE genes of Salmonella was used to detect and differentiate between the three most prevalent Salmonella spp. in Kenya (S. Typhi, S. Typhimurium and S. Enteritidis). The staA primers (StaA-Forward / StaA-Reverse) and viaB primers (vi-Forward / vi-Reverse) were found to be specific only for the different strains of S. Typhi, producing PCR products of 585 bp and 540 bp respectively. No amplification was observed with S. Typhimurium, S. Enteritidis, E. coli and S. boydii bacterial strains. The sopE primers (SopE-Forward / SopE-Reverse) was demonstrated to be specific for all Salmonella spp. producing a 465 bp PCR product with no amplification observed with the E. coli and S. boydii bacterial strains. Conventional PCR using these staA and viaB primers for detection of S. Typhi shows great potential for diagnosis of typhoid fever however, further studies need to be carried out with actual food samples and human samples (blood, stool or saliva) to determine the effectiveness of this method in the detection of common Salmonella spp. in Kenya. Author summaryTyphoid fever is a severe disease caused by the bacteria Salmonella Typhi (S. Typhi) and is a significant health problem in many developing countries. The lack of adequate diagnostic capabilities in poor resource settings common in most public health facilities in Kenya and Africa in general, hinder prompt diagnosis of typhoid fever. Currently, the available diagnostic tests are often expensive and more so not readily available in most resource poor endemic areas. This has often led to misdiagnosis of the disease, thereby delaying appropriate treatment and making typhoid fever widespread in most resource poor areas. This study examines the ability of three different genes to detect and differentiate between the three most prevalent Salmonella strains in Kenya using a readily available and widely used genetic test known as conventional polymerase chain reaction (PCR). This research found that staA and viaB genes were specific only for S. Typhi, while the sopE gene was specific for all Salmonella strains. Consequently, conventional PCR using these staA and viaB genes for detection of S. Typhi shows great potential to be used as a readily available diagnostic tool to detect the presence of the S. Typhi organism in individuals or foods sample in Kenya.

molecular biology↗

Urbanization and market-integration have strong, non-linear effects on metabolic health in the Turkana tribe

Cardio-metabolic disease is a leading cause of death worldwide, with high prevalence in western, industrialized societies relative to developing nations and subsistence-level populations. This stark difference has been attributed to the dietary and lifestyle changes associated with industrialization, but current work has relied on health comparisons between separate, genetically distinct populations to draw conclusions. To more robustly determine how lifestyle impacts health, we collected interview and health biomarker data from a single population undergoing a rapid lifestyle transition. Specifically, we sampled Turkana individuals who practice subsistence-level, nomadic pastoralism (the traditional, ancestral way of life for this group), as well as individuals who no longer practice pastoralism and engage either minimally or strongly with the market economy. Comparisons across this lifestyle gradient revealed clear, non-linear effects of industrialization: only individuals with highly urban, market-integrated lifestyles experience increases in BMI, body fat, blood pressure, and other biomarkers of cardio-metabolic health. These health differences are partially mediated by increased consumption of refined carbohydrates, and more strongly by fine-scale measures of urbanicity. Finally, because many Turkana are transitioning between rural and urban areas within their lifetime, we were able to show that being born in an urban area is associated with worse adult metabolic health, independent of adult lifestyle. Together, these analyses provide comprehensive insight into the timing, magnitude, and causes of health declines in urban, industrialized groups - an area of critical study given the massive public health burden of cardio-metabolic disease and the rate at which developing nations are experiencing lifestyle transitions.\n\nSIGNIFICANCEThe \"mismatch\" between evolved human physiology and western, industrialized lifestyles is thought to explain to the current epidemic of cardiovascular disease (CVD). However, this hypothesis has been difficult to test in real time. To do so, we studied a traditional pastoralist group--the Turkana--that is currently transitioning from their ancestral way of life to an urban, industrialized lifestyle. We found that Turkana who move to cities exhibit poor cardio-metabolic health, partially because of a shift toward \"western diets\" high in carbohydrates. We also show that early life urbanicity independently predicts adult health, such that life-long city dwellers will experience the greatest CVD risk. Our work thus uncovers the timing, magnitude, and evolutionary causes of a major health gradient.

evolutionary biology↗