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Dermonecrotic toxin (DNT) is an important bacterial virulence factor produced by the zoonotic pathogens Bordetella bronchiseptica and Pasteurella multocida. This study aims to explore the possibility of expressing different fragments of P. multocida toxin (PMT) in the chromosome of attenuated B. bronchiseptica to generate single-component mucosal vaccine candidates. To achieve this, a 954-bp fragment (basepairs 301 ∼ 1254) of the B. bronchiseptica aroA gene was replaced with an N-terminal, 930-bp fragment (basepairs 1-930; PMTN) or a C-terminal, 900-bp fragment (base pairs 2959 ∼ 3858; PMTC) of the PMT encoding gene toxA. The resulting strains, denoted as Bb-PMTN or Bb-PMTC, expressed PMTN and PMTC, as evidenced by ELISA using polyclonal against full-length of PMT. Phenotypical analyses revealed that Bb-PMTN and Bb-PMTC grew much slower than wild type strains in tryptic soy broth. These strains also displayed significantly decreased 161-fold-virulence compared to the wildtype strains in mouse models. Intranasal immunization of Bb-PMTN and Bb-PMTC in mice induced high levels of antibodies against B. bronchiseptica and PMT, as well as IFN-γ and IL-10 in mouse sera, and most importantly, high titers of sIgA in mouse lungs. Vaccination with these two engineering strains provided 100% protection of mice against lethal challenge with B. bronchiseptica and 80%∼100% protection against lethal challenge with PMT, with Bb-PMTN exhibiting 1.25-fold greater immunogenic efficacy over Bb-PMTC. This study highlights the use of B. bronchiseptica attenuated strains as live mucosal vectors to deliver heterologous antigens.

The mammalian respiratory epithelium forms the first line of defense against infections with P. multocida , an important zoonotic respiratory pathogen. In this study, we found that P. multocida infection increased respiratory epithelial permeability and promoted the induction of the HIF-1α–VEGFA axis in both mouse and murine cell models.

With the rising demand for short-term experiences in global health (STEGH) is an ever-increasing volume of literature that focuses attention on ethics and ethical concerns, such as the effects of STEGH on host populations. Such concerns have driven the development of ethical principles and guidelines, with discussions and debates largely centred around normative questions of positive/negative and benefit/harm for us/them. Using a critical medical humanities lens, this paper blurs these dichotomous framings and offers a more complex understanding of the effects and effectiveness of STEGH on hosts. I explore STEGH that send volunteers from North American universities to the Dominican Republic to participate in service-learning activities aimed at improving the lives of impoverished Haitian migrants living inbateyes. I address the following questions: What perspectives about the impacts of interventions on host communities manifest through STEGH? What tensions emerge through interactions among diverse stakeholders related to those perspectives, and with what effects? Drawing together critical theory and ethnography, I examined the perspectives of three stakeholder groups: student and faculty volunteers, host organisation staff, and hosts inbateycommunities. Data collected from observations and interviews were counterposed; I analysed interactions and interplay between stakeholders. My findings revealed conflicts around an emergent theme: counting efforts, or volunteers’ proclivity for numerical evidence of impactful STEGH for hosts. With attention on power relations, I argue that a preoccupation with quantifiable evidence eclipsed and erased the lived realities of hosts, thereby blocking a fully ethical engagement. These sociopolitical effects, often overlooked in conventional ethics assessments, are no less harmful and may reinforce rather than reduce inequalities that the global health movement seeks to eliminate. My study offers a compelling case for how the critical medical humanities lend critical insights in the name of improving global health.

Infections withPasteurella multocidacan cause significant zoonotic respiratory problems in both humans and animals.In vivotests in mouse infection models were used to investigate the mechanisms of respiratory epithelial barrier dysfunction during respiratory bacterial infection with these pathogens. Results revealed thatP. multocidainfection significantly increased epithelial permeability and increased expression of vascular endothelial growth factor A (VEGFA) and endothelial nitric oxide synthase (eNOS) in murine tracheae and lungs. In murine lung epithelial cell (MLE-12) models,P. multocidainfection decreased the expression of tight junctions (ZO-1) and adherens junctions (β-catenin, E-cadherin), but induced the activation of the hypoxia-inducible factor-1α (HIF-1α) and VEGFA signaling. When expression of HIF-1α is suppressed, the induction of VEGFA and ZO-1expression byP. multocidainfection is decreased. We also found that intervention of HIF-1α and VEGFA signaling affected infection outcomes caused by respiratory bacteria in mouse models. Most importantly, we demonstrated thatP. multocidainfection increased permeability of human respiratory epithelial cells and this process was associated with the activation of the HIF-1α and VEGFA signaling and likely contributes to the pathogenesis ofP. multocidain humans.ImportanceMammalian respiratory epithelium forms the first line of defense against infections withPasteurella multocida, an important zoonotic respiratory pathogen. In this study, we foundP. multocidainfection increased respiratory epithelial permeability and promoted the induction of the hypoxia-HIF-1α-VEGFA axis in both mouse and murine cell models. Similar findings were also demonstrated in human respiratory epithelial cells. The results from this study gain important knowledge about the pathogenesis ofP. multocidacausing infections in both animals and humans.

POINTS CLES Messages cles pour le public Au Canada, la chlamydia et la gonorrhee (causees respectivement par les bacteries Chlamydia trachomatis et Neisseria gonorrhoeae ) sont les infections bacteriennes transmissibles sexuellement (ITS) les plus communes[1][1],[2][2], et le nombre de cas

IntroductionChildren with inherited metabolic diseases (IMDs) often have complex and intensive healthcare needs and their families face challenges in receiving high-quality, family centred health services. Improvement in care requires complex interventions involving multiple components and stakeholders, customised to specific care contexts. This study aims to comprehensively understand the healthcare experiences of children with IMDs and their families across Canada.Methods and analysisA two-stage explanatory sequential mixed methods design will be used. Stage 1: quantitative data on healthcare networks and encounter experiences will be collected from 100 parent/guardians through a care map, 2 baseline questionnaires and 17 weekly diaries over 5–7 months. Care networks will be analysed using social network analysis. Relationships between demographic or clinical variables and ratings of healthcare experiences across a range of family centred care dimensions will be analysed using generalised linear regression. Other quantitative data related to family experiences and healthcare experiences will be summarised descriptively. Ongoing analysis of quantitative data and purposive, maximum variation sampling will inform sample selection for stage 2: a subset of stage 1 participants will participate in one-on-one videoconference interviews to elaborate on the quantitative data regarding care networks and healthcare experiences. Interview data will be analysed thematically. Qualitative and quantitative data will be merged during analysis to arrive at an enhanced understanding of care experiences. Quantitative and qualitative data will be combined and presented narratively using a weaving approach (jointly on a theme-by-theme basis) and visually in a side-by-side joint display.Ethics and disseminationThe study protocol and procedures were approved by the Children’s Hospital of Eastern Ontario’s Research Ethics Board, the University of Ottawa Research Ethics Board and the research ethics boards of each participating study centre. Findings will be published in peer-reviewed journals and presented at scientific conferences.

Graphical abstract, Highlights • Sample-dependent inconsistencies in PCR-based and metagenomic sequencing analyses. • Caveats associated with contig-based assembly programs for microbiome studies. • More sample diversity/complexity yields more chimeric reads from PCR amplification. • BlastBin includes consideration of chimeric reads for assigning and counting taxa. • BlastBin enables recovery of information lost due to chimera formation. • BlastBin 16S rRNA profiles more closely resemble metagenomic read-based profiles., The next frontier in the field of microbiome studies is identification of all microbes present in the microbiome and accurate determination of their abundance such that microbiome profiles can serve as reliable assessments of health or disease status. PCR-based 16S rRNA gene sequencing and metagenome shotgun sequencing technologies are the prevailing approaches used in microbiome analyses. Each poses a number of technical challenges associated with PCR amplification, sample availability, and cost of processing and analysis. In general, results from these two approaches rarely agree completely with each other. Here, we compare these methods utilizing a set of vaginal swab and lavage specimens from a cohort of 42 pregnant women collected for a pilot study exploring the effect of the vaginal microbiome on preterm birth. We generated the microbial community profiles from the sequencing reads of the V3V4 and V4V5 regions of the 16S rRNA gene in the vaginal swab and lavage samples. For a subset of the vaginal samples from 12 subjects, we also performed metagenomic shotgun sequencing analysis and compared the results obtained from the PCR-based sequencing methods. Our findings suggest that sample composition and complexity, particularly at the species level, are major factors that must be considered when analyzing and interpreting microbiome data. Our approach to sequence analysis includes consideration of chimeric reads, by using our chimera-counting BlastBin program, and enables recovery of microbial content information generated during PCR-based sequencing methods, such that the microbial profiles more closely resemble those obtained from metagenomic read-based approaches.

The cellular specificity, potency, and modular nature of bacterial protein toxins enable their application for targeted cytosolic delivery of therapeutic cargo. Efficient endosomal escape is a critical step in the design of bacterial toxin-inspired drug delivery (BTIDD) vehicles to avoid lysosomal degradation and promote optimal cargo delivery. The cytotoxic necrotizing factor (CNF) family of modular toxins represents a useful model for investigating cargo-delivery mechanisms due to the availability of many homologs with high sequence identity, their flexibility in swapping domains, and their differential activity profiles. Previously, we found that CNFy is more sensitive to endosomal acidification inhibitors than CNF1 and CNF2. Here, we report that CNF3 is even less sensitive than CNF1/2. We identified two amino acid residues within the putative translocation domain (E374 and E412 in CNFy, Q373 and S411 in CNF3) that differentiate between these two toxins. Swapping these corresponding residues in each toxin changed the sensitivity to endosomal acidification and efficiency of cargo-delivery to be more similar to the other toxin. Results suggested that trafficking to the more acidic late endosome is required for cargo delivery by CNFy but not CNF3. This model was supported by results from toxin treatment of cells in the presence of NH4Cl, which blocks endosomal acidification, and of small-molecule inhibitors EGA, which blocks trafficking to late endosomes, and ABMA, which blocks endosomal escape and trafficking to the lysosomal degradative pathway. These findings suggest that it is possible to fine-tune endosomal escape and cytosolic cargo delivery efficiency in designing BTIDD platforms.

Background Intracapsular tonsillectomy has emerged as a novel alternative to traditional tonsillectomy where the tonsillar capsule is left intact with a small amount of overlying tonsillar tissue. There is growing evidence to suggest that intracapsular tonsillectomy is associated with reduced post-operative pain, haemorrhage and readmission rates. The aim of this study was to assess the reported benefits of intracapsular tonsillectomy within the ENT department at a tertiary paediatric hospital. Method Retrospective analysis comparing two cohorts of 72 consecutive paediatric patients undergoing coblation intracapsular and extracapsular tonsillectomy between March-2019 and November-2020. Patient age at procedure, removal of adenoids, indication, surgeon grade, and discharge time were recorded. Post-tonsillectomy bleeding and 30-day readmission rates were used as the main outcome measures. Results The median age in both groups was 5 years. The intracapsular cohort demonstrated a lower 30-day readmission rate (8.3% vs. 15.3%), lower primary (24hours) post-op bleed rate (4.2% vs. 12.5%) when compared to the extracapsular cohort. Eight cases were conducted as day cases in total, all Intracapsular, with none of these patients requiring readmission within 30 days. Discussion Coblation Intracapsular tonsillectomy is an effective and low-risk alternative to extracapsular techniques. It is hoped with the reduced associated risks and morbidity associated with the procedure, the department can move towards day case tonsillectomy procedures resulting in a reduction in overall healthcare costs and improved patient experience.

The results of this study indicate a discordance between gut microbiome composition and evolutionary history in primates, calling into question previous notions about host genetic control of the primate gut microbiome. Microbiome similarities between humans consuming nonindustrialized diets and monkeys characterized by subsisting on eclectic, omnivorous diets also raise questions about the ecological and nutritional drivers shaping the human gut microbiome. Moreover, a more detailed understanding of the factors associated with gut microbiome plasticity in primates offers a framework to understand why humans following industrialized lifestyles have deviated from states thought to reflect human evolutionary history. The results also provide perspectives for developing therapeutic dietary manipulations that can reset configurations of the gut microbiome to potentially improve human health., The gut microbiome of primates, including humans, is reported to closely follow host evolutionary history, with gut microbiome composition being specific to the genetic background of its primate host. However, the comparative models used to date have mainly included a limited set of closely related primates. To further understand the forces that shape the primate gut microbiome, with reference to human populations, we expanded the comparative analysis of variation among gut microbiome compositions and their primate hosts, including 9 different primate species and 4 human groups characterized by a diverse set of subsistence patterns (n = 448 samples). The results show that the taxonomic composition of the human gut microbiome, at the genus level, exhibits increased compositional plasticity. Specifically, we show unexpected similarities between African Old World monkeys that rely on eclectic foraging and human populations engaging in nonindustrial subsistence patterns; these similarities transcend host phylogenetic constraints. Thus, instead of following evolutionary trends that would make their microbiomes more similar to that of conspecifics or more phylogenetically similar apes, gut microbiome composition in humans from nonindustrial populations resembles that of generalist cercopithecine monkeys. We also document that wild cercopithecine monkeys with eclectic diets and humans following nonindustrial subsistence patterns harbor high gut microbiome diversity that is not only higher than that seen in humans engaging in industrialized lifestyles but also higher compared to wild primates that typically consume fiber-rich diets. IMPORTANCE The results of this study indicate a discordance between gut microbiome composition and evolutionary history in primates, calling into question previous notions about host genetic control of the primate gut microbiome. Microbiome similarities between humans consuming nonindustrialized diets and monkeys characterized by subsisting on eclectic, omnivorous diets also raise questions about the ecological and nutritional drivers shaping the human gut microbiome. Moreover, a more detailed understanding of the factors associated with gut microbiome plasticity in primates offers a framework to understand why humans following industrialized lifestyles have deviated from states thought to reflect human evolutionary history. The results also provide perspectives for developing therapeutic dietary manipulations that can reset configurations of the gut microbiome to potentially improve human health.

The results of this study highlight parallel gut microbiome traits in human and nonhuman primates, depending on subsistence strategy. Although these similarities have been reported before, the functional and ecological bases of this convergence are not fully understood., Compared with urban-industrial populations, small-scale human communities worldwide share a significant number of gut microbiome traits with nonhuman primates. This overlap is thought to be driven by analogous dietary triggers; however, the ecological and functional bases of this similarity are not fully understood. To start addressing this issue, fecal metagenomes of BaAka hunter-gatherers and traditional Bantu agriculturalists from the Central African Republic were profiled and compared with those of a sympatric western lowland gorilla group (Gorilla gorilla gorilla) across two seasons of variable dietary intake. Results show that gorilla gut microbiomes shared similar functional traits with each human group, depending on seasonal dietary behavior. Specifically, parallel microbiome traits were observed between hunter-gatherers and gorillas when the latter consumed more structural polysaccharides during dry seasons, while small-scale agriculturalist and gorilla microbiomes showed significant functional overlap when gorillas consumed more seasonal ripe fruit during wet seasons. Notably, dominance of microbial transporters, transduction systems, and gut xenobiotic metabolism was observed in association with traditional agriculture and energy-dense diets in gorillas at the expense of a functional microbiome repertoire capable of metabolizing more complex polysaccharides. Differential abundance of bacterial taxa that typically distinguish traditional from industrialized human populations (e.g., Prevotella spp.) was also recapitulated in the human and gorilla groups studied, possibly reflecting the degree of polysaccharide complexity included in each group’s dietary niche. These results show conserved functional gut microbiome adaptations to analogous diets in small-scale human populations and nonhuman primates, highlighting the role of plant dietary polysaccharides and diverse environmental exposures in this convergence. IMPORTANCE The results of this study highlight parallel gut microbiome traits in human and nonhuman primates, depending on subsistence strategy. Although these similarities have been reported before, the functional and ecological bases of this convergence are not fully understood. Here, we show that this parallelism is, in part, likely modulated by the complexity of plant carbohydrates consumed and by exposures to diverse xenobiotics of natural and artificial origin. Furthermore, we discuss how divergence from these parallel microbiome traits is typically associated with adverse health outcomes in human populations living under culturally westernized subsistence patterns. This is important information as we trace the specific dietary and environmental triggers associated with the loss and gain of microbial functions as humans adapt to various dietary niches.

POINTS CLES En 2019, on a estime a 6 par 100 000 le nombre de nouveaux cas de cancer de l’œsophage diagnostiques chez les Canadiens[1][1]. Evalue a 15 %, le taux de survie net a 5 ans est parmi les plus faibles de tous les pronostics de cancer[1][1]. Les hommes presentent une incidence

Background: Different typing systems including capsular genotyping, lipopolysaccharide (LPS) genotyping, multilocus sequence typing (MLST), and virulence genotyping based on the detection of different virulence factor-encoding gene (VFG) profiles have been applied to characterize Pasteurella multocida strains from different host species. However, these methods require much time and effort in laboratories. Particularly, relying on one of these methods is difficult to address the biology of P. multocida from host species. Recently, we found that assigning P. multocida strains according to the combination of their capsular, LPS, and MLST genotypes (marked as capsular genotype: LPS genotype: MLST genotype) could help address the biological characteristics of P. multocida circulation in multiple hosts. However, it is still lack of a rapid, efficient, intelligent and cost-saving tool to diagnose P. multocida according to this system. Results: We have developed an intelligent genotyping and host tropism prediction tool PmGT for P. multocida strains according to their whole genome sequences by using machine learning and web 2.0 technologies. By using this tool, the capsular genotypes, LPS genotypes, and MLST genotypes as well as the main VFGs of P. multocida isolates in different host species were determined based on whole genome sequences. The results revealed a closer association between the genotypes and pasteurellosis rather than between genotypes and host species. Finally, we also used PmGT to predict the host species of P. multocida strains with the same capsular: lipopolysaccharide: MLST genotypes. Conclusions: With the advent of high-quality, inexpensive DNA sequencing, this platform represents a more efficient and cost-saving tool for P. multocida diagnosis in both epidemiological studies and clinical settings.

[See related article at [www.cmaj.ca/lookup/doi/10.1503/cmaj.200697][2]][2] KEY POINTS In 2019, an estimated 6 new cases of esophageal cancer were diagnosed per 100 000 Canadians.[1][2] The 5-year net survival rate, estimated at 15%, is among the poorest of all cancer prognoses. [1][2] Men have a

Membrane localization domain (MLD) was first proposed for a 4-helix-bundle motif in the crystal structure of the C1 domain of Pasteurella multocida toxin (PMT). This structure motif is also found in the crystal structures of several clostridial glycosylating toxins (TcdA, TcdB, TcsL, and TcnA). The Ras/Rap1-specific endopeptidase (RRSP) module of the multifunctional autoprocessing repeats-in-toxins (MARTX) toxin produced by Vibrio vulnificus has sequence homology to the C1-C2 domains of PMT, including a putative MLD. We have determined the solution structure for the MLDs in PMT and in RRSP using solution state NMR. We conclude that the MLDs in these two toxins assume a 4-helix-bundle structure in solution.

SUMMARY Pasteurella multocida is a highly versatile pathogen capable of causing infections in a wide range of domestic and wild animals as well as in humans and nonhuman primates. Despite over 135 years of research, the molecular basis for the myriad manifestations of P. multocida pathogenesis and the determinants of P. multocida phylogeny remain poorly defined. The current availability of multiple P. multocida genome sequences now makes it possible to delve into the underlying genetic mechanisms of P. multocida fitness and virulence. Using whole-genome sequences, the genotypes, including the capsular genotypes, lipopolysaccharide (LPS) genotypes, and multilocus sequence types, as well as virulence factor-encoding genes of P. multocida isolates from different clinical presentations can be characterized rapidly and accurately. Putative genetic factors that contribute to virulence, fitness, host specificity, and disease predilection can also be identified through comparative genome analysis of different P. multocida isolates. However, although some knowledge about genotypes, fitness, and pathogenesis has been gained from the recent whole-genome sequencing and comparative analysis studies of P. multocida, there is still a long way to go before we fully understand the pathogenic mechanisms of this important zoonotic pathogen. The quality of several available genome sequences is low, as they are assemblies with relatively low coverage, and genomes of P. multocida isolates from some uncommon host species are still limited or lacking. Here, we review recent advances, as well as continuing knowledge gaps, in our understanding of determinants contributing to virulence, fitness, host specificity, disease predilection, and phylogeny of P. multocida.

Instructors – Get your examination copy now! Visit http://asmscience.org/instructors for more information. Help your students save on textbooks! Email us and receive a coupon to share with your students for 20% off of the purchase of a print copy. This highly anticipated update of the acclaimed textbook draws on the latest research to give students the knowledge and tools to explore the mechanisms by which bacterial pathogens cause infections in humans and animals. Written in an approachable and engaging style, the book uses illustrative examples and thought-provoking exercises to inspire students with the potential excitement and fun of scientific discovery. Completely revised and updated, and for the first time in stunning full-color, Bacterial Pathogenesis: A Molecular Approach, Fourth Edition, builds on the core principles and foundations of its predecessors while expanding into new concepts, key findings, and cutting-edge research, including new developments in the areas of the microbiome and CRISPR as well as the growing challenges of antimicrobial resistance. All-new detailed illustrations help students clearly understand important concepts and mechanisms of the complex interplay between bacterial pathogens and their hosts. Study questions at the end of each chapter challenge students to delve more deeply into the topics covered, and hone their skills in reading, interpreting, and analyzing data, as well as devising their own experiments. A detailed glossary defines and expands on key terms highlighted throughout the book. Written for advanced undergraduate, graduate, and professional students in microbiology, bacteriology, and pathogenesis, this text is a must-have for anyone looking for a greater understanding of virulence mechanisms across the breadth of bacterial pathogens. Interested in purchasing this title as an electronic publication? Click here for the electronic version on Vital Source! Click here for the electronic version on RedShelf! Paperback, 683 pages, full-color illustrations, index.

E. coli strain Sanji is the first sequenced and analyzed genome of the recently emerged pathogenic XDR strains with sequence type ST167 and novel in silico serotype O89b:H9. Comparison of the genomes of Sanji with other ST167 strains revealed distinct sets of different plasmids, mobile IS elements, and antibiotic resistance genes in each genome, indicating that there exist multiple paths toward achieving XDR. The emergence of these pathogenic ST167 E. coli strains with diverse XDR capabilities highlights the difficulty of preventing or mitigating the development of XDR properties in bacteria and points to the importance of better understanding of the shared underlying virulence mechanisms and physiology of pathogenic bacteria., Extensive drug resistance (XDR) is an escalating global problem. Escherichia coli strain Sanji was isolated from an outbreak of pheasant colibacillosis in Fujian province, China, in 2011. This strain has XDR properties, exhibiting sensitivity to carbapenems but no other classes of known antibiotics. Whole-genome sequencing revealed a total of 32 known antibiotic resistance genes, many associated with insertion sequence 26 (IS26) elements. These were found on the Sanji chromosome and 2 of its 6 plasmids, pSJ_255 and pSJ_82. The Sanji chromosome also harbors a type 2 secretion system (T2SS), a type 3 secretion system (T3SS), a type 6 secretion system (T6SS), and several putative prophages. Sanji and other ST167 strains have a previously uncharacterized O-antigen (O89b) that is most closely related to serotype O89 as determined on the basis of analysis of the wzm-wzt genes and in silico serotyping. This O89b-antigen gene cluster was also found in the genomes of a few other pathogenic sequence type 617 (ST617) and ST10 complex strains. A time-scaled phylogeny inferred from comparative single nucleotide variant analysis indicated that development of these O89b-containing lineages emerged about 30 years ago. Comparative sequence analysis revealed that the core genome of Sanji is nearly identical to that of several recently sequenced strains of pathogenic XDR E. coli belonging to the ST167 group. Comparison of the mobile elements among the different ST167 genomes revealed that each genome carries a distinct set of multidrug resistance genes on different types of plasmids, indicating that there are multiple paths toward the emergence of XDR in E. coli. IMPORTANCE E. coli strain Sanji is the first sequenced and analyzed genome of the recently emerged pathogenic XDR strains with sequence type ST167 and novel in silico serotype O89b:H9. Comparison of the genomes of Sanji with other ST167 strains revealed distinct sets of different plasmids, mobile IS elements, and antibiotic resistance genes in each genome, indicating that there exist multiple paths toward achieving XDR. The emergence of these pathogenic ST167 E. coli strains with diverse XDR capabilities highlights the difficulty of preventing or mitigating the development of XDR properties in bacteria and points to the importance of better understanding of the shared underlying virulence mechanisms and physiology of pathogenic bacteria.

UIUC Keck Center, J. Craig Ventner Institute, the University of Illinois, the J.S. Guggenheim Foundation, the C.R Woese Institute for Genomic Biology, the University of Colorado, NSF BCS 0935374, NSF BCS 0820709, and NSF BCS 1441409

The mammalian gastrointestinal (GI) microbiome, which plays indispensable roles in host nutrition and health, is affected by numerous intrinsic and extrinsic factors. Among them, antibiotic (ATB) treatment is reported to have a significant effect on GI microbiome composition in humans and other animals. However, the impact of ATBs on the GI microbiome of free-ranging or even captive great apes remains poorly characterized. Here, we investigated the effect of cephalosporin treatment (delivered by intramuscular dart injection during a serious respiratory outbreak) on the GI microbiome of a wild habituated group of western lowland gorillas (Gorilla gorilla gorilla) in the Dzanga Sangha Protected Areas, Central African Republic. We examined 36 fecal samples from eight individuals, including samples before and after ATB treatment, and characterized the GI microbiome composition using Illumina-MiSeq sequencing of the bacterial 16S rRNA gene. The GI microbial profiles of samples from the same individuals before and after ATB administration indicate that the ATB treatment impacts GI microbiome stability and the relative abundance of particular bacterial taxa within the colonic ecosystem of wild gorillas. We observed a statistically significant increase in Firmicutes and a decrease in Bacteroidetes levels after ATB treatment. We found disruption of the fibrolytic community linked with a decrease of Ruminoccocus levels as a result of ATB treatment. Nevertheless, the nature of the changes observed after ATB treatment differs among gorillas and thus is dependent on the individual host. This study has important implications for ecology, management, and conservation of wild primates.

SummaryTo understand how the gut microbiome is impacted by human adaptation to varying environments, we explored gut bacterial communities in the BaAka rainforest hunter-gatherers and their agriculturalist Bantu neighbors in the Central African Republic. Although the microbiome of both groups is compositionally similar, hunter-gatherers harbor increased abundance of Prevotellaceae, Treponema, and Clostridiaceae, while the Bantu gut microbiome is dominated by Firmicutes. Comparisons with US Americans reveal microbiome differences between Africans and westerners but show western-like features in the Bantu, including an increased abundance of predictive carbohydrate and xenobiotic metabolic pathways. In contrast, the hunter-gatherer gut shows increased abundance of predicted virulence, amino acid, and vitamin metabolism functions, as well as dominance of lipid and amino-acid-derived metabolites, as determined through metabolomics. Our results demonstrate gradients of traditional subsistence patterns in two neighboring African groups and highlight the adaptability of the microbiome in response to host ecology.