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Actinomyces organisms reside on mucosal surfaces of the oropharynx and the genitourinary tract. Polymicrobial infections with Actinomyces organisms are increasingly being reported in the literature. Since these infections differ from classical actinomycosis, lacking of specific clinical and imaging findings, slow-growing Actinomyces organisms can be regarded as contaminants or insignificant findings. In addition, only limited knowledge is available about novel Actinomyces species and their clinical relevance. The recent reclassifications have resulted in the transfer of several Actinomyces species to novel genera Bowdeniella, Gleimia, Pauljensenia, Schaalia, or Winkia. The spectrum of diseases associated with specific members of Actinomyces and these related genera varies. In human infections, the most common species are Actinomyces israelii, Schaalia meyeri, and Schaalia odontolytica, which are typical inhabitants of the mouth, and Gleimia europaea, Schaalia turicensis, and Winkia neuii. In this narrative review, the purpose was to gather information on the emerging role of specific organisms within the Actinomyces and related genera in polymicrobial infections. These include Actinomyces graevenitzii in pulmonary infections, S. meyeri in brain abscesses and infections in the lower respiratory tract, S. turicensis in skin-related infections, G. europaea in necrotizing fasciitis and skin abscesses, and W. neuii in infected tissues around prostheses and devices. Increased understanding of the role of Actinomyces and related species in polymicrobial infections could provide improved outcomes for patient care. Key messages Due to the reclassification of the genus, many former Actinomyces species belong to novel genera Bowdeniella, Gleimia, Pauljensenia, Schaalia, or Winkia. Some of the species play emerging roles in specific infection types in humans. Increasing awareness of their clinical relevance as an established or a putative pathogen in polymicrobial infections brings about improved outcomes for patient care. [ABSTRACT FROM AUTHOR]

Simple Summary: Recent research has helped us understand more about the role of microbes in the health and disease of the lungs. The detection of microbes and microbial products in sputum may improve early lung cancer diagnosis. The monitoring of the microbiome of the lungs over time may help predict the response to and side effects of treatment. However, studies have not yet examined how diet and air pollution affect the lung microbiome and how it might be linked to the development and progression of lung cancer. By examining the lung microbiome, dietary patterns, and air pollutants, we hope to prevent and manage lung cancer in the future. The past several years have provided a more profound understanding of the role of microbial species in the lung. The respiratory tract is a delicate ecosystem of bacteria, fungi, parasites, and viruses. Detecting microbial DNA, pathogen-associated molecular patterns (PAMPs), and metabolites in sputum is poised to revolutionize the early diagnosis of lung cancer. The longitudinal monitoring of the lung microbiome holds the potential to predict treatment response and side effects, enabling more personalized and effective treatment options. However, most studies into the lung microbiota have been observational and have not adequately considered the impact of dietary intake and air pollutants. This gap makes it challenging to establish a direct causal relationship between environmental exposure, changes in the composition of the microbiota, lung carcinogenesis, and tumor progression. A holistic understanding of the lung microbiota that considers both diet and air pollutants may pave the way to improved prevention and management strategies for lung cancer. [ABSTRACT FROM AUTHOR]

Staphylococcus aureus possesses sar family genes, including sarA, S, R, T, U, V, X, Y, Z, and rot, which are transcription factors involved in biofilm formation and quorum sensing. In contrast, Staphylococcus epidermidis has sarA, R, V, X, Y, Z, and rot genes; specifically, SarA, Z, and X are involved in biofilm formation. The expression of the sar family members in S. epidermidis isolated from clinical and non-clinical environments is unknown. This study aimed to establish if clinical and non-clinical isolates of S. epidermidis express the sar family members. We genotyped isolates from clinical ocular infections (n = 52), or non-clinical healthy conjunctiva (n = 40), and healthy skin (n = 50), using multilocus sequence typing (MLST) and the staphylococcal chromosomal cassette mec (SCCmec). We selected strains with different genotypes and representatives of each source of isolation, and the presence of the sar family genes was detected using PCR and RT-qPCR to determine their expression. The sar family genes were present in all selected strains, with no observed differences. The relative expression of the sar family showed that all selected strains expressed each gene weakly, with no significant differences observed between them or between different sources of isolation. In conclusion, the presence and relative expression of the sar family genes are very similar among strains, with no differences based on their origin of isolation and genotype. [ABSTRACT FROM AUTHOR]

Candida species primarily exist as harmless commensals in the gastrointestinal tract of warm-blooded animals. However, they can also cause life-threatening infections, which are often associated with gut microbial dysbiosis. Identifying the microbial actors that restrict Candida to commensalism remains a significant challenge. In vitro models could enable a mechanistic study of the interactions between Candida and simulated colon microbiomes. Therefore, this study aimed to elucidate the spatial and temporal colonization kinetics of specific Candida , including C. albicans, C. tropicalis , and C. parapsilosis , and their relative Nakaseomyces glabratus , by using an adapted SHIME® model, simulating the ileum, and proximal and distal colons. We monitored fungal and bacterial colonization kinetics under conditions of eubiosis (commensal lifestyle) and antibiotic-induced dysbiosis (pathogenic lifestyle). Our findings highlighted the variability in the colonization potential of Candida species across different intestinal regions. The ileum compartment proved to be the most favourable environment for C. albicans and C. parapsilosis under conditions of eubiosis. Antibiotic-induced dysbiosis resulted in resurgence of opportunistic Candida species, especially C. tropicalis and C. albicans. Future research should focus on identifying specific bacterial species influencing Candida colonization resistance and explore the long-term effects of antibiotics on the mycobiome and bacteriome. [ABSTRACT FROM AUTHOR]

The study was conducted to identify cluster patterns of enteric microorganisms with potential etiological relevance for infectious gastroenteritis in stool samples of individuals from Ghana, which is a known high-endemicity setting for infectious gastroenteritis. These patterns were compared to previous observations with specimens from Colombian indigenous people in order to assess potentially stable clustering for temporally and spatially distinct populations from high-endemicity regions. By doing so, the study aimed to identify stable clusters as markers of microbial interaction with potential importance for etiological relevance assignment in cases of multiple enteric pathogen detections. Stool samples from 1569 Ghanaian individuals (875 from HIV patients, 30 from HIV-negative control adult patients, and 644 from children < 2 years of age) were assessed for enteric microorganisms by applying real-time PCR. As a result, nucleic acids of bacterial microorganisms were most frequently detected, followed by protozoa, microsporidia, and helminths. Interestingly, the cluster assessment confirmed interaction patterns known from the previous analysis with Colombian indigenous people, demonstrating a high likelihood of Blastocystis hominis for clustering with other microorganisms and a prominent, potentially mediating role of Dientamoeba fragilis for microbial interactions within the clusters. In conclusion, the assessment confirmed conserved clustering of enteric microorganisms with potential etiological relevance for human infectious gastroenteritis over geographically distinct high-endemicity settings. Furthermore, the composition of abundant microorganisms is more important than regional factors for the determination of the interplay of enteric microorganisms in the human gut. Thereby, some microbial pathogens and commensals seem more susceptible to a changing microbial composition in the human gut than others. [ABSTRACT FROM AUTHOR]

Background: Surgical site infections (SSIs) can be caused by various factors, including contamination of the surgical field. Perioperative cultures can be employed in clean orthopedic procedures to detect bacterial contamination that may occur during surgery. Aims and Objectives: The study aimed to evaluate the correlation between suction tip cultures and surgical wounds in clean orthopedic surgeries. Materials and Methods: A cross-sectional study was conducted at Yenepoya Medical College Hospital, Mangalore, Karnataka, with 250 patients in whom drain tips were sent for culture and followed up for 3 months to assess for SSI. Skin commensals from the nasal and groin samples were analyzed for the presence of bacteria. Results: A total of 250 patients meeting the inclusion and exclusion criteria were included. Thirty patients were positive for drain tip culture, and 12 (4.8%) patients had SSI during the 3rd month follow-up period, showing a statistically significant relationship between drain tip culture and SSIs (P=0.001). Skin commensals constituted 67% (nasal) and 100% in the groin of perioperative contaminants, accounting for 4.8% of SSIs. Conclusion: Suction drain tip culture and skin commensal analysis may be good predictors of SSIs. Intraoperative surgical site contaminants can be identified using perioperative cultures. Timely administration of suitable antibiotics and local wound care for perioperative contamination can help minimize the incidence of SSI. [ABSTRACT FROM AUTHOR]

The skin is the outermost organ of the human body and serves as a protective barrier against external pathogens and environmental factors. It is colonised by a diverse community of microorganisms, collectively known as the skin microbiome. From birth to death, the skin undergoes dynamic changes in microbial composition influenced by endogenous physiological host factors, environmental exposure and various diseases. These microorganisms play a crucial role in maintaining the health and functionality of the skin. They contribute to the education and moderation of the immune system, protect against pathogenic invaders and regulate various physiological processes, such as maintaining a healthy barrier. Dysbiosis, characterised by microbial imbalance, is associated with various skin disorders, among others atopic dermatitis and acne vulgaris. In recent years, interest has been growing in understanding the role of the skin microbiome in health and disease. Understanding these complex interactions has led to the development of novel therapeutic approaches that target the skin microbiome, including prebiotic and probiotic therapy. This article provides an overview of the current knowledge of the skin microbiome and its impact on human health and disease. [ABSTRACT FROM AUTHOR]

Gopher tortoises (Gopherus polyphemus), the only land tortoises native to the southeastern United States, are found throughout their range in a variety of upland habitat types, with their use of upland pine-dominated habitats receiving most attention. Fewer studies have examined their use of coastal beach dune habitats, but some of the highest gopher tortoise burrow densities have been observed in this vulnerable, yet critical, habitat. Gopher tortoises construct extensive burrows for their own use, and these burrows have also been shown to support numerous other animals (i.e., commensal species) that may depend on them for critical needs (e.g., shelter, food). Motion-activated wildlife cameras allow for nonintrusive and continuous observation of burrow activity with minimal disturbance to the animals and habitat. Here we examined 10 gopher tortoise burrows over a 12-mo period using motion-activated wildlife cameras in beach dune habitat in an undeveloped section of coastline in northeast Florida. Gopher tortoises were most frequently observed during the spring and summer months (April–August), and most often during daylight hours. Gopher tortoise behaviors such as burrow maintenance, mating, foraging, and resting were all observed more during April through August, which is a slightly earlier start than these activities have been observed in inland populations. We observed a commensal community of 51 animal taxa using tortoise burrows and their aprons, 29 of which we were able to identify to species. The commensal community was generally similar to those in inland habitats, but we did observe some taxa that were previously undocumented at gopher tortoise burrows including 2 bird species and 8 insect taxa. These commensals displayed varied diel and seasonal activity patterns, with many taxa observed at burrows concurrently occupied by gopher tortoises. Considered together, our observations of gopher tortoise behavior and their commensal community in coastal beach dunes provide valuable insights into the importance of this understudied habitat and highlight distinct differences from inland ecosystems. [ABSTRACT FROM AUTHOR]

At a rapid pace, biologists are learning the many ways in which resident microbes influence, and sometimes even control, their hosts to shape both health and disease. Understanding the biochemistry behind these interactions promises to reveal completely novel and targeted ways of counteracting disease processes. However, in our protocols and publications, we continue to describe these new results using a language that originated in a completely different context. This language developed when microbial interactions with hosts were perceived to be primarily pathogenic, as threats that had to be vanquished. Biomedicine had one dominating thought: winning this war against microorganisms. Today, we know that beyond their defensive roles, host tissues, especially epithelia, are vital to ensuring association with the normal microbiota, the communities of microbes that persistently live with the host. Thus, we need to adopt a language that better encompasses the newly appreciated importance of host-microbiota associations. We also need a language that frames the onset and progression of pathogenic conditions within the context of the normal microbiota. Such a reimagined lexicon should make it clear, from the very nature of its words, that microorganisms are primarily vital to our health, and only more rarely the cause of disease. This article is part of the theme issue 'Sculpting the microbiome: how host factors determine and respond to microbial colonization'. [ABSTRACT FROM AUTHOR]

Copyright of Crustaceana is the property of Brill Academic Publishers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Crustaceana is the property of Brill Academic Publishers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archaeology in Oceania is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The genus Xanthomonas has been primarily studied for pathogenic interactions with plants. However, besides host and tissue-specific pathogenic strains, this genus also comprises nonpathogenic strains isolated from a broad range of hosts, sometimes in association with pathogenic strains, and other environments, including rainwater. Based on their incapacity or limited capacity to cause symptoms on the host of isolation, nonpathogenic xanthomonads can be further characterized as commensal and weakly pathogenic. This study aimed to understand the diversity and evolution of nonpathogenic xanthomonads compared to their pathogenic counterparts based on their cooccurrence and phylogenetic relationship and to identify genomic traits that form the basis of a life history framework that groups xanthomonads by ecological strategies. We sequenced genomes of 83 strains spanning the genus phylogeny and identified eight novel species, indicating unexplored diversity. While some nonpathogenic species have experienced a recent loss of a type III secretion system, specifically the hrp2 cluster, we observed an apparent lack of association of the hrp2 cluster with lifestyles of diverse species. We performed association analysis on a large data set of 337 Xanthomonas strains to explain how xanthomonads may have established association with the plants across the continuum of lifestyles from commensals to weak pathogens to pathogens. Presence of distinct transcriptional regulators, distinct nutrient utilization and assimilation genes, transcriptional regulators, and chemotaxis genes may explain lifestyle-specific adaptations of xanthomonads. [ABSTRACT FROM AUTHOR]

Actinomycosis, an oral cavity commensal, causes cervicofacial infection in patients associated with an immunosuppression state and local mucosal injuries. Bone involvement by this commensal is rare. In the present case, we report a case of left peri mandibular soft tissue, soft to firm, tender swelling in a 39‐year‐old immunocompetent male diagnosed as Actinomycosis infection on fine needle aspiration cytology (FNAC) and cell block preparation. [ABSTRACT FROM AUTHOR]

Enterococcus faecalis is a bacterium which accompanies us from the first days of our life. As a commensal it produces vitamins, metabolizes nutrients, and maintains intestinal pH. All of that happens in exchange for a niche to inhabit. It is not surprising then, that the bacterium was and is used as an element of many probiotics and its positive impact on the human immune system and the body in general is hard to ignore. This bacterium has also a dark side though. The plasticity and relative ease with which one acquires virulence traits, and the ability to hide from or even deceive and use the immune system to spread throughout the body make E. faecalis a more and more dangerous opponent. The statistics clearly show its increasing role, especially in the case of nosocomial infections. Here we present the summarization of current knowledge about E. faecalis, especially in the context of its relations with the human immune system. [ABSTRACT FROM AUTHOR]

Mucochytrium quahogii, also known as QPX or Quahog Parasite Unknown, is the causative agent of QPX disease in the hard clam (Mercenaria mercenaria). Host–pathogen–environment interactions between M. quahogii, the hard clam, and temperature were explored in a microcosm experiment. Hard clams were housed in individual tanks with sterile seawater under two temperature regimes: low (13 °C) temperature, which is thought to be optimal for QPX disease development, and high (20 °C) temperature, which has been shown to promote "healing" of QPX-infected clams. Hard clam tissue, pallial fluid, seawater, and shell biofilms were collected and assayed for M. quahogii. The release of M. quahogii from naturally infected live hard clams into seawater was detected only in the low temperature treatment, suggesting that temperature influences the release of potentially infectious cells. M. quahogii was commonly found in hard clam pallial fluid, even after 9 weeks in the lab, suggesting pallial fluid is a stable reservoir of M. quahogii within its primary host and that M. quahogii is not a transient component of the hard clam microbiota. Overall, results support a host-specific relationship and that M. quahogii is a commensal member of the hard clam microbiota, supporting its classification as an opportunistic pathogen. [ABSTRACT FROM AUTHOR]

Antimicrobial resistance (AMR) in Escherichia coli of animal origin presents a threat to human health. Although animals are not the primary source of human infections, humans may be exposed to AMR E. coli of animal origin and their AMR genes through the food chain, direct contact with animals, and via the environment. For this reason, AMR in E. coli from food producing animals is included in most national and international AMR monitoring programmes and is the subject of a large body of research. As pig farming is one of the largest livestock sectors and the one with the highest antimicrobial use, there is considerable interest in the epidemiology of AMR in E. coli of porcine origin. This literature review presents an overview and appraisal of current knowledge of AMR in commensal E. coli of the porcine gastrointestinal tract with a focus on its evolution during the pig lifecycle and the relationship with antimicrobial use. It also presents an overview of the epidemiology of resistance to extended spectrum cephalosporins, fluoroquinolones, and colistin in pig production. The review highlights the widespread nature of AMR in the porcine commensal E. coli population, especially to the most-used classes in pig farming and discusses the complex interplay between age and antimicrobial use during the pig lifecycle. [ABSTRACT FROM AUTHOR]

Tritrichomonas muris is a common flagellated protist isolated from the cecum of wild rodents. This commensal protist has been shown previously to alter immune phenotypes in laboratory mice. Other trichomonads, referred to as Tritrichomonas musculis and Tritrichomonas rainier, also naturally colonize laboratory mice and cause immune alterations. This report formally describes two new trichomonads, Tritrichomonas musculus n. sp., and Tritrichomonas casperi n. sp., at the ultrastructural and molecular level. These two protists were isolated from laboratory mice and were differentiated by their size and the structure of their undulating membrane and posterior flagellum. Analysis at the 18S rRNA and trans‐ITS genetic loci supported their designation as distinct species, related to T. muris. To assess the true extent of parabasalid diversity infecting laboratory mice, 135 mice bred at the National Institutes of Health (NIH) were screened using pan‐parabasalid primers that amplify the trans‐ITS region. Forty‐four percent of mice were positive for parabasalids, encompassing a total of eight distinct sequence types. Tritrichomonas casperi and Trichomitus‐like protists were dominant. T. musculus and T. rainier were also detected, but T. muris was not. Our work establishes a previously underappreciated diversity of commensal trichomonad flagellates that naturally colonize the enteric cavity of laboratory mice. [ABSTRACT FROM AUTHOR]

The abundance of gut commensals has historically been associated with health-promoting effects despite the fact that the definition of good or bad microbiota remains condition-specific. The beneficial or pathogenic nature of microbiota is generally dictated by the dimensions of host-microbiota and microbe-microbe interactions. With the increasing popularity of gut microbiota in human health and disease, emerging evidence suggests opportunistic infections promoted by those gut bacteria that are generally considered beneficial. Therefore, the current review deals with the opportunistic nature of the gut commensals and aims to summarise the concepts behind the occasional commensal-to-pathogenic transformation of the gut microbes. Specifically, relevant clinical and experimental studies have been discussed on the overgrowth and bacteraemia caused by commensals. Three key processes and their underlying mechanisms have been summarised to be responsible for the opportunistic nature of commensals, viz. improved colonisation fitness that is dictated by commensal-pathogen interactions and availability of preferred nutrients; pathoadaptive mutations that can trigger the commensal-to-pathogen transformation; and evasion of host immune response as a survival and proliferation strategy of the microbes. Collectively, this review provides an updated concept summary on the underlying mechanisms of disease causative events driven by gut commensal bacteria. [ABSTRACT FROM AUTHOR]

Chronic inflammatory periodontal disease develops in part from the infiltration of a large number of classically activated inflammatory macrophages that release inflammatory cytokines important for disease progression, including inflammasome-dependent interleukin (IL)-1β. Streptococcus gordonii is a normally commensal oral microorganism; while not causative, recent evidence indicates that commensal oral microbes are required for the full development of periodontal disease. We have recently reported that inflammatory macrophages counterintuitively allow for the increased survival of phagocytosed S. gordonii over nonactivated or alternatively activated macrophages. This survival is dependent on increased reactive oxygen species production within the phagosome of the inflammatory macrophages, and resistance by the bacterium and can result in S. gordonii damaging the phagolysosomes. Here, we show that activated macrophages infected with live S. gordonii release more IL-1β than non-activated macrophages infected with either live or dead S. gordonii , and that the survival of oral Streptococci are more dependent on macrophage activation than other Gram positive microbes, both classical pathogens and commensals. We also find that S. gordonii –dependent inflammatory macrophage inflammasome activation requires the cytoplasmic NLRP6. Overall, our results suggest S. gordonii is capable of evading immune destruction, increasing inflammatory mediators, and increasing inflammatory macrophage response, and that this ability is increased under conditions of inflammation. This work reveals additional mechanisms by which normally commensal oral streptococci-macrophage interactions can change, resulting in increased release of mature IL-1β, potentially contributing to an environment that perpetuates inflammation. [ABSTRACT FROM AUTHOR]

It is widely accepted that favorable fitness in commensal colonization is one of the prime facilitators of clonal dissemination in bacteria. The question arises as to what kind of fitness advantage may be wielded by uropathogenic strains of the two predominant fluoroquinolone- and multidrug-resistant clonal groups of E. coli—ST131-H30 and ST1193, which has permitted their unprecedented pandemic-like global expansion in the last few decades. The colonization-associated genes' content, carriage of low-cost plasmids, and integrons with weak promoters could certainly contribute to the fitness of the pandemic groups, although those genetic factors are common among other clonal groups as well. Also, ST131-H30 and ST1193 strains harbor fluoroquinolone-resistance conferring mutations targeting serine residues in DNA gyrase (GyrA-S83) and topoisomerase IV (ParC-S80) that, in those clonal backgrounds, might result in a commensal fitness benefit, i.e., beyond the antibiotic resistance per se. This fitness gain might have contributed not only to the widespread dissemination of these major clones in the healthcare setting but also to their long-term colonization of healthy individuals and, thus, circulation in the community, even in a low or no fluoroquinolone use environment. This evolutionary shift affecting commensal E. coli, initiated by mutations co-favorable in both antibiotics-treated patients and healthy individuals warrants more in-depth studies to monitor further changes in the epidemiological situation and develop effective measures to reduce the antibiotic resistance spread. [ABSTRACT FROM AUTHOR]

In humans, many diseases are associated with alterations in gut microbiota, namely increases or decreases in the abundance of specific bacterial groups. One example is the genus Faecalibacterium. Numerous studies have underscored that low levels of Faecalibacterium are correlated with inflammatory conditions, with inflammatory bowel disease (IBD) in the forefront. Its representation is also diminished in the case of several diseases, including colorectal cancer (CRC), dermatitis, and depression. Additionally, the relative presence of this genus is considered to reflect, at least in part, intestinal health status because Faecalibacterium is frequently present at reduced levels in individuals with gastrointestinal diseases or disorders. In this review, we first thoroughly describe updates to the taxonomy of Faecalibacterium , which has transformed a single-species taxon to a multispecies taxon over the last decade. We then explore the links discovered between Faecalibacterium abundance and various diseases since the first IBD-focused studies were published. Next, we examine current available strategies for modulating Faecalibacterium levels in the gut. Finally, we summarize the mechanisms underlying the beneficial effects that have been attributed to this genus. Together, epidemiological and experimental data strongly support the use of Faecalibacterium as a next-generation probiotic (NGP) or live biotherapeutic product (LBP). [ABSTRACT FROM AUTHOR]

Concept of microorganisms has largely been perceived from their pathogenic view point. Nevertheless, it is being gradually revisited in terms of its significance to human health and now appears to be the most dominant force that shapes the immune system of the human body and also determines an individual’s predisposition to diseases. Human inhabits bacterial diversity (which is predominant among all microbial communities in human body) occupying 0.3% of body mass, known as microbiota. On birth, a part of microbiota that child obtains is essentially a mother’s legacy. So, the review was initiated with this critical topic of microbiotal inheritance. Since, each body site has distinct physiological specifications; therefore, they contain discrete microbiome composition that has been separately discussed along with dysbiosis-induced pathologies originating in different body organs. Factors affecting microbiome composition and may cause dysbiosis like antibiotics, delivery, feeding method etc. as well as the strategies that immune system adopts to prevent dysbiosis have been highlighted. We also tried to bring into attention the topic of dysbiosis induced biofilms, that enables cohort to survive stresses, evolve, disseminate and infection resurgence that is still in dormancy. Eventually, we put spotlight on microbiome significance in medical therapeutics. We didn’t merely confine article to gut microbiota, that is being studied more extensively. Numerous community forms at diverse body sites are inter-related, and being exposed to awfully variable perturbations appear to be challenging to evaluate perturbation risks holistically. All aspects have been elaborately discussed to achieve a global depiction of human microbiota in order to meet urgent necessity for protocol standardisation. [ABSTRACT FROM AUTHOR]

Pseudomonas aeruginosa dominates the complex polymicrobial cystic fibrosis (CF) airway and is a leading cause of death in persons with CF. Interestingly, oral streptococcal colonization has been associated with stable CF lung function. The most abundant streptococcal species found in stable patients, Streptococcus salivarius, has been shown to downregulate pro-inflammatory cytokines in multiple colonization models. However, no studies have demonstrated how S. salivarius potentially improves lung function. Our lab previously demonstrated that the P. aeruginosa exopolysaccharide Psl promotes S. salivarius biofilm formation in vitro, suggesting a possible mechanism by which S. salivarius is incorporated into the CF airway microbial community. In this study, we demonstrate that co-infection of rats leads to enhanced S. salivarius colonization and reduced P. aeruginosa colonization. Histological scores for tissue inflammation and damage are lower in dual-infected rats compared to P. aeruginosa infected rats. Additionally, pro-inflammatory cytokines IL-1β, IL-6, CXCL2, and TNF-α are downregulated during co-infection compared to P. aeruginosa single-infection. Lastly, RNA sequencing of cultures grown in synthetic CF sputum revealed that P. aeruginosa glucose metabolism genes are downregulated in the presence of S. salivarius, suggesting a potential alteration in P. aeruginosa fitness during co-culture. Overall, our data support a model in which S. salivarius colonization is promoted during co-infection with P. aeruginosa, whereas P. aeruginosa airway bacterial burden is reduced, leading to an attenuated host inflammatory response. [ABSTRACT FROM AUTHOR]

Interactions between plants and neighboring microbial species are fundamental elements that collectively determine the structure and function of the plant microbiota. However, the molecular basis of such interactions is poorly characterized. Here, we colonize Arabidopsis leaves with nine plant‐associated bacteria from all major phyla of the plant microbiota and profile cotranscriptomes of plants and bacteria six hours after inoculation. We detect both common and distinct cotranscriptome signatures among plant–commensal pairs. In planta responses of commensals are similar to those of a disarmed pathogen characterized by the suppression of genes involved in general metabolism in contrast to a virulent pathogen. We identify genes that are enriched in the genome of plant‐associated bacteria and induced in planta, which may be instrumental for bacterial adaptation to the host environment and niche separation. This study provides insights into how plants discriminate among bacterial strains and lays the foundation for in‐depth mechanistic dissection of plant–microbiota interactions. Synopsis: The molecular basis of interactions between plants and commensal microbial species is poorly characterized. This study reveals common and distinct cotranscriptome signatures among plant–commensal bacteria pairs. The transcriptomes of commensals are distinct from that of a virulent pathogen and similar to that of a disarmed pathogen.Plant immunity appears to inhibit the metabolic activity of commensal bacteria.Commensal genes associated with plant colonization tend to be induced during interactions with plants.Transcriptome responses of plants and interacting microbiota members are incongruent. [ABSTRACT FROM AUTHOR]

The order Amphipoda is one of the largest orders in the Crustacea, many species of which are involved in symbiotic relations with other animals. Despite the considerable diversity of the Amphipoda both in number of species and ecology, polychaete-commensalism has been poorly known and described from few species. In particular, there has been little discussion of the evolutionary origins of polychaete-commensalism relationships. Amphipods in the family Leucothoidae are known as commensal inhabitants of filter-feeding invertebrates, where they utilize the feeding current produced by their hosts. Leucothoids are typically found from three types of filter-feeding hosts: sponges, ascidians, and bivalve molluscs. Relatively little is known about leucothoids that associate with other types of hosts. An undescribed species of the genus Leucothoe associated with burrows of terebellid polychaetes from Japan has been found. We herein describe this species as Leucothoe vermicola sp. nov., providing COI mtDNA and 18S rDNA sequences for DNA barcoding. This is the first record of a symbiotic association between Leucothoidae and Terebellidae. We also provide a hypothesis of the phylogenetic position of L. vermicola sp. nov. and evolution of the polychaete-commensalism in this species. The polychaete-commensalism in the present new species may have resulted from the entry of generalist species into polychaete hosts, rather than from host-conversion from a specialist species. [ABSTRACT FROM AUTHOR]

Oral Prevotella are known as anaerobic commensals on oral mucosae and in dental plaques from early life onwards, including pigmented P. melaninogenica, P. nigrescens, and P. pallens and non-pigmented Prevotella species. Many Prevotella species contribute to oral inflammatory processes, being frequent findings in dysbiotic biofilms of periodontal diseases (P. intermedia, P. nigrescens), cariotic lesions (P. denticola, Alloprevotella (formerly Prevotella) tannerae), endodontic infections (P. baroniae, P. oris, P. multisaccharivorax), and other clinically relevant oral conditions. Over the years, several novel species have been recovered from the oral cavity without knowledge of their clinical relevance. Within this wide genus, virulence properties and other characteristics like biofilm formation seemingly vary in a species- and strain-dependent manner, as shown for the P. intermedia group organisms (P. aurantiaca, P. intermedia, P. nigrescens, and P. pallens). Oral Prevotella species are identified in various non-oral infections and chronic pathological conditions. Here, we have updated the knowledge of the genus Prevotella and the role of Prevotella species as residents and infectious agents of the oral cavity, as well as their detection in non-oral infections, but also gathered information on their potential link to cancers of the head and neck, and other systemic disorders. [ABSTRACT FROM AUTHOR]

Recent studies have shown that the gut microbiome changes brain function, behavior, and psychiatric and neurological disorders. The Gut–Brain Axis (GBA) provides a neuronal pathway to explain this. But exactly how do commensal bacteria signal through the epithelial layer of the large intestine to activate GBA nerve afferents? An in vitro model is described. We differentiated two human cell lines: Caco2Bbe1 into mature epithelium on 0.4-micron filters and then SH-SY5Y into mature neurons in 24-well plates. These were co-cultured by placing the epithelium-laden filters 1 mm above the neurons. Twenty-four hours later they were tri-cultured by apical addition of 107Lactobacillus rhamnosus or Lactobacillus fermentum which settled on the epithelium. Alone, the Caco2bbe1 cells stimulated neurite outgrowth in underlying SH-SY5Y. Beyond this, the lactobacilli were well tolerated and stimulated further neurite outgrowth by 24 h post-treatment, though not passing through the filters. The results provide face validity for a first-of-kind model of transepithelial intestinal lumen-to nerve signaling. The model displays the tight junctional barrier characteristics found in the large intestine while at the same time translating stimulatory signals from the bacteria through epithelial cells to attracted neurons. The model is easy to set-up with components widely available. [ABSTRACT FROM AUTHOR]

A small bivalve mollusk previously only known from the Pleistocene of Los Angeles County has recently been found living intertidally near Santa Barbara, California. The bivalve has been determined to be Cymatioa cooki (Willett, 1937), a member of the Galeommatoidea J.E. Gray, 1840. We document the habitat for the newly discovered C. cooki, and compare it to C. electilis (Berry, 1963), the other extant member of this genus recorded from the region. Cymatioa cooki is rare, and while many galeommatoid species have been shown to be commensal with other invertebrates, we have been unable to determine any specific commensal relationships for it. [ABSTRACT FROM AUTHOR]

Mucochytrium quahogii, commonly known as QPX (Quahog Parasite Unknown), is the causative agent of QPX disease in hard clams (Mercenaria mercenaria), but poor understanding of the relationship between host and pathogen has hindered effective management. To address this gap in knowledge, we conducted a two-year study quantifying the distribution and abundance of M. quahogii in hard clam tissue, pallial fluid, and the environment. M. quahogii was broadly distributed in clams and the environment, in areas with and without a known history of QPX disease. M. quahogii in clams was not strongly related to M. quahogii in the environment. M. quahogii was always present in either the tissue or pallial fluid of each clam, with an inverse relationship between the abundance in the two anatomical locations. This study suggests that the sediment–water interface and clam pallial fluid are environmental reservoirs of M. quahogii and that there is a host-specific relationship between M. quahogii and the hard clam, supporting its classification as a commensal, opportunistic pathogen. There appears to be minimal risk of spreading QPX disease to naïve clam populations because M. quahogii is already present and does not appear to be causing disease in hard clam populations in locations unfavorable for pathogenesis. [ABSTRACT FROM AUTHOR]

Streptococcus anginosus together with S. constellatus and S. intermedius constitute the Streptococcus anginosus group (SAG), until recently considered to be benign commensals of the human mucosa isolated predominantly from oral cavity, but also from upper respiratory, intestinal, and urogenital tracts. For years the virulence potential of SAG was underestimated, mainly due to complications in correct species identification and their assignment to the physiological microbiota. Still, SAG representatives have been associated with purulent infections at oral and non-oral sites resulting in abscesses formation and empyema. Also, life threatening blood infections caused by SAG have been reported. However, the understanding of SAG as potential pathogen is only fragmentary, albeit certain aspects of SAG infection seem sufficiently well described to deserve a systematic overview. In this review we summarize the current state of knowledge of the S. anginosus pathogenicity factors and their mechanisms of action. [ABSTRACT FROM AUTHOR]

We describe a new species of polyclad, Emprosthopharynx lysiosquillae sp. nov., based on specimens collected from the body surface of the mantis shrimp Lysiosquilla maculata (Fabricius, 1793) captured in Kujuzaki, Urasoe, Okinawa Island, Japan. This is the first report of symbiotic polyclads collected from stomatopods. The polyclads were collected from large-sized L. maculata individuals (more than ca. 300 mm in total length); 1–35 polyclads were observed per mantis shrimp. Emprosthopharynx lysiosquillae sp. nov. is distinguished from other congeners by possessing (i) submarginal eyespots that are not arranged on the median line, (ii) a bell-shaped pharynx, and (iii) a posterodorsally curved penis stylet, and by lacking (iv) a common sperm duct. We provide partial sequences of the mitochondrial cytochrome c oxidase subunit I (COI) gene as a DNA barcode for E. lysiosquillae sp. nov. From phylogenetic analyses based on concatenated sequences of 16S, 18S, and 28S ribosomal DNA and COI, we demonstrate that Emprosthopharynx represented by our new species forms a relatively robust clade with Hoploplana Laidlaw, 1902. We discuss (i) the superfamily- and family-level affiliations of Emprosthopharynx, (ii) the possibility of host preference in E. lysiosquillae sp. nov., and (iii) the functions of a putative adhesive organ and grooves on the pharynx found in the present polyclads. [ABSTRACT FROM AUTHOR]

Despite its commonly overlooked role as a commensal, Ralstonia mannitolilytica becomes an emerging global opportunistic human pathogen and a causative agent of various infections and diseases. In respiratory illnesses, including cystic fibrosis and chronic obstructive pulmonary disease (COPD), R. mannitolilytica is also identified presumably as colonizer. In this study, one distinctive clone of R. mannitolilytica was firstly identified as colonizer for the first 20 days during hospitalization of a patient. It was then identified as a causative agent for catheter-related bloodstream infection with negative identification after effective treatment, verifying its transition from commensal to pathogen. In conclusion, we provide convincing evidence that during hospitalization of a patient, R. mannitolilytica transitioned from commensal to pathogen in the respiratory tract leading to catheter-related bloodstream infection (CRBSI). [ABSTRACT FROM AUTHOR]

Identified in the late nineteenth century as a single species residing on human skin, Malassezia is now recognized as a diverse genus comprising 18 species inhabiting not only skin but human gut, hospital environments, and even deep-sea sponges. All cultivated Malassezia species are lipid dependent, having lost genes for lipid synthesis and carbohydrate metabolism. The surging interest in Malassezia results from development of tools to improve sampling, culture, identification, and genetic engineering, which has led to findings implicating it in numerous skin diseases, Crohn disease, and pancreatic cancer. However, it has become clear that Malassezia plays a multifaceted role in human health, with mutualistic activity in atopic dermatitis and a preventive effect against other skin infections due to its potential to compete with skin pathogens such as Candida auris. Improved understanding of complex microbe-microbe and host-microbe interactions will be required to define Malassezia's role in human and animal health and disease so as to design targeted interventions. [ABSTRACT FROM AUTHOR]

The physical barrier of the intestine and associated mucosal immunity maintains a delicate homeostatic balance between the host and the external environment by regulating immune responses to commensals, as well as functioning as the first line of defense against pathogenic microorganisms. Understanding the orchestration and characteristics of the intestinal mucosal immune response during commensal or pathological conditions may provide novel insights into the mechanisms underlying microbe-induced immunological tolerance, protection, and/or pathogenesis. Over the last decade, our knowledge about the interface between the host intestinal mucosa and the gut microbiome has been dominated by studies focused on bacterial communities, helminth parasites, and intestinal viruses. In contrast, specifically how commensal and pathogenic protozoa regulate intestinal immunity is less well studied. In this review, we provide an overview of mucosal immune responses induced by intestinal protozoa, with a major focus on the role of different cell types and immune mediators triggered by commensal (Blastocystis spp. and Tritrichomonas spp.) and pathogenic (Toxoplasma gondii, Giardia intestinalis, Cryptosporidium parvum) protozoa. We will discuss how these various protozoa modulate innate and adaptive immune responses induced in experimental models of infection that benefit or harm the host. [ABSTRACT FROM AUTHOR]

Identified in the late nineteenth century as a single species residing on human skin, Malassezia is now recognized as a diverse genus comprising 18 species inhabiting not only skin but human gut, hospital environments, and even deep-sea sponges. All cultivated Malassezia species are lipid dependent, having lost genes for lipid synthesis and carbohydrate metabolism. The surging interest in Malassezia results from development of tools to improve sampling, culture, identification, and genetic engineering, which has led to findings implicating it in numerous skin diseases, Crohn disease, and pancreatic cancer. However, it has become clear that Malassezia plays a multifaceted role in human health, with mutualistic activity in atopic dermatitis and a preventive effect against other skin infections due to its potential to compete with skin pathogens such as Candida auris. Improved understanding of complex microbe-microbe and host-microbe interactions will be required to define Malassezia's role in human and animal health and disease so as to design targeted interventions. [ABSTRACT FROM AUTHOR]

We assessed the potential for microbial interactions influencing a well-documented host–pathogen system. Mycoplasma agassizii is the known etiological agent of upper respiratory tract disease in Mojave desert tortoises (Gopherus agassizii), but disease in wild animals is extremely heterogeneous. For example, a much larger proportion of animals harbor M. agassizii than those that develop disease. With the availability of a new quantitative PCR assay for a microbe that had previously been implicated in disease, Pasteurella testudinis, we tested 389 previously collected samples of nasal microbes from tortoise populations across the Mojave desert. We showed that P. testudinis is a common commensal microbe. However, we did find that its presence was associated with higher levels of M. agassizii among the tortoises positive for this pathogen. The best predictor of P. testudinis prevalence in tortoise populations was average size of tortoises, suggesting that older populations have higher levels of P. testudinis. The prevalence of co-infection in populations was associated with the prevalence of URTD, providing additional evidence for an indirect interaction between the two microbes and inflammatory disease. We showed that URTD, like many chronic, polymicrobial diseases involving mucosal surfaces, shows patterns of a polymicrobial etiology. [ABSTRACT FROM AUTHOR]

Neisseria meningitidis and Neisseria gonorrhoeae are two obligate human pathogens that have evolved to be uniquely adapted to their host. The meningococcus is frequently carried asymptomatically in the nasopharynx, while gonococcal infection of the urogenital tract usually elicits a marked local inflammatory response. Other members of the Neisseria genus are abundant in the upper airway where they could engage in co-operative or competitive interactions with both these pathogens. Here, we briefly outline the potential sites of contact between Neisseria spp. in the body, with emphasis on the upper airway, and describe the growing yet circumstantial evidence for antagonism from carriage studies and human volunteer challenge models with Neisseria lactamica. Recent laboratory studies have characterized antagonistic mechanisms that enable competition between Neisseria species. Several of these mechanisms, including Multiple Adhesin family (Mafs), Two Partner Secretion Systems, and Type VI secretion system, involve direct contact between bacteria; the genetic organisation of these systems, and the domain structure of their effector molecules have striking similarities. Additionally, DNA from one species of Neisseria can be toxic to another species, following uptake. More research is needed to define the full repertoire of antagonistic mechanisms in Neisseria spp., their distribution in strains, their range of activity, and contribution to survival in vivo. Understanding the targets of effectors could reveal how antagonistic relationships between close relatives shape subsequent interactions between pathogens and their hosts. [ABSTRACT FROM AUTHOR]

Gut bacteria are often described by the neutral term commensals. However, the more we learn about their interactions with hosts, the more apparent it becomes that gut commensals often contribute positively to host physiology and fitness. Whether hosts can prefer beneficial bacteria, and how they do so, is not clear. This is of particular interest in the case of the bacterivore C. elegans , which depends on bacteria as food source, but also as gut colonizers that contribute to its physiology, from development to immunity. It is further unclear to what extent worms living in their microbially-diverse habitats can sense and distinguish between beneficial bacteria, food, and pathogens. Focusing on Enterobacteriaceae and members of closely related families, we isolated gut bacteria from worms raised in compost microcosms, as well as bacteria from the respective environments and evaluated their contributions to host development. Most isolates, from worms or from the surrounding environment, promoted faster development compared to the non-colonizing E. coli food strain. Pantoea strains further showed differential contributions of gut isolates versus an environmental isolate. Characterizing bacterial ability to hinder pathogenic colonization with Pseudomonas aeruginosa , supported the trend of Pantoea gut commensals being beneficial, in contrast to the environmental strain. Interestingly, worms were attracted to the beneficial Pantoea strains, preferring them over non-beneficial bacteria, including the environmental Pantoea strain. While our understanding of the mechanisms underlying these host-microbe interactions are still rudimentary, the results suggest that hosts can sense and prefer beneficial commensals. [ABSTRACT FROM AUTHOR]

Dogs, as reservoir hosts, have been implicated in the decline of carnivore populations across the globe. We conducted a serosurvey of free-ranging dog populations to assess the population level exposure rates to three viral pathogens, canine parvovirus (CPV), canine distemper virus (CDV) and canine adenovirus (CAV) in a Trans-Himalayan landscape in India that is home to the endangered Snow Leopard. A total of 97 dogs were sampled across six villages as a part of a surgical sterilization campaign during the study period. Samples were tested for IgG antibodies using a table top ELISA kit. Exposure rates to the three viral pathogens in the dog populations was high; 100% for CPV, 54% for CDV and 66% for CAV, with high positive immunoglobulin titer values for CAV and CPV, and low to moderate values for CDV. Overall conservation efforts for native carnivores need to address the role of free-ranging domestic dogs in disease transmission. [ABSTRACT FROM AUTHOR]

Neutrophils play a crucial role in eliminating bacteria that invade the human body; however, cathepsin G can induce biofilm formation in a non-biofilm-forming Staphylococcus epidermidis 1457 strain, suggesting that neutrophil proteases may be involved in biofilm formation. Cathepsin G, cathepsin B, proteinase-3, and metalloproteinase-9 (MMP-9) from neutrophils were tested on the biofilm induction in commensal (skin isolated) and clinical non-biofilm-forming S. epidermidis isolates. From 81 isolates, 53 (74%) were aap+, icaA−, icaD− genotype, and without the capacity of biofilm formation under conditions of 1% glucose, 4% ethanol or 4% NaCl, but these 53 non-biofilm-forming isolates induced biofilm by the use of different neutrophil proteases. Of these, 62.3% induced biofilm with proteinase-3, 15% with cathepsin G, 10% with cathepsin B and 5% with MMP -9, where most of the protease-induced biofilm isolates were commensal strains (skin). In the biofilm formation kinetics analysis, the addition of phenylmethylsulfonyl fluoride (PMSF; a proteinase-3 inhibitor) showed that proteinase-3 participates in the cell aggregation stage of biofilm formation. A biofilm induced with proteinase-3 and DNAse-treated significantly reduced biofilm formation at an early time (initial adhesion stage of biofilm formation) compared to untreated proteinase-3-induced biofilm (p < 0.05). A catheter inoculated with a commensal (skin) non-biofilm-forming S. epidermidis isolate treated with proteinase-3 and another one without the enzyme were inserted into the back of a mouse. After 7 days of incubation period, the catheters were recovered and the number of grown bacteria was quantified, finding a higher amount of adhered proteinase-3-treated bacteria in the catheter than non-proteinase-3-treated bacteria (p < 0.05). Commensal non-biofilm-forming S. epidermidis in the presence of neutrophil cells significantly induced the biofilm formation when multiplicity of infection (MOI) 1:0.01 (neutrophil:bacteria) was used, but the addition of a cocktail of protease inhibitors impeded biofilm formation. A neutrophil:bacteria assay did not induce neutrophil extracellular traps (NETs). Our results suggest that neutrophils, in the presence of commensal non-biofilm-forming S. epidermidis, do not generate NETs formation. The effect of neutrophils is the production of proteases, and proteinase-3 releases bacterial DNA at the initial adhesion, favoring cell aggregation and subsequently leading to biofilm formation. [ABSTRACT FROM AUTHOR]

The study of the recent colonization of a symbiont and its interaction with host communities in new locations is an opportunity to understand how they interact. The use of isotopic ratios in trophic ecology can provide measurements of a species' isotopic niche, as well as knowledge about how the isotopic niches between symbiont and host species overlap. Stable isotope measurements were used to assess the sources of carbon assimilated by the host species (the bivalves Mytilus galloprovincialis and Scrobicularia plana) and their associated symbiont pea crab Afropinnotheres monodi , which occurs within these bivalves' mantle cavities. The mixing model estimates suggest that all of them assimilate carbon from similar sources, particularly from pseudofaeces and particulate organic matter in this symbiotic system based on filter feeding. The symbiotic species occupy comparable trophic levels and its association seems to be commensal or parasitic depending on the duration of such association. The pea crab A. monodi reflects a sex-specific diet, where males are more generalist than the soft females because the latter's habitat is restricted to the host bivalve. The high isotopic overlap between soft females and M. galloprovincialis may reflect a good commensal relationship with the host. [ABSTRACT FROM AUTHOR]

Campylobacter jejuni represents an eminent zoonotic germ responsible for foodborne infections causing campylobacteriosis. In addition, infections with C. jejuni constitute a risk factor for the occurrence of inflammatory bowel disease (IBD). In the latter case, patients show inflammatory reactions not only against C. jejuni, but also against the non-infectious microbiota. However, the involved mechanisms and molecular basis are still largely unclear. We recently reported that C. jejuni breaches the intestinal epithelial barrier by secretion of serine protease HtrA (high temperature requirement A), which cleaves several major tight and adherens junction proteins. In the present study, we aimed to study if HtrA-expressing C. jejuni may also trigger the transepithelial migration of non-pathogenic gastrointestinal microbiota. Using confocal immunofluorescence and scanning electron microscopy, we demonstrate that C. jejuni wild-type (wt) as well as the isogenic ∆htrA mutant bind to the surface of polarized intestinal Caco-2 epithelial cells, but do not invade them at the apical side. Instead, C. jejuni wt, but not ∆htrA mutant, disrupt the cellular junctions and transmigrate using the paracellular route between neighboring cells. Using transwell filter systems, we then co-incubated the cells with C. jejuni and non-invasive microbiota strains, either Escherichia coli or Lactococcus lactis. Interestingly, C. jejuni wt, but not ∆htrA mutant, induced the efficient transmigration of these microbiota bacteria into the basal compartment. Thus, infection of the intestinal epithelium with C. jejuni causes local opening of cellular junctions and paracellular translocation in an HtrA-dependent manner, which paves the way for transmigration of microbiota that is otherwise non-invasive. Taken together, these findings may have impacts on various Campylobacter-associated diseases such as IBD, which are discussed here. [ABSTRACT FROM AUTHOR]

Trillions of microorganisms exist in the human intestine as commensals and contribute to homeostasis through their interactions with the immune system. In this review, we use previous evidence from published papers to elucidate the involvement of commensal-specific T cells (CSTCs) in regulating intestinal inflammatory responses. CSTCs are generated centrally in the thymus or peripherally at mucosal interfaces and present as CD4+ or CD8+ T cells. Bacteria, fungi, and even viruses act commensally with humans, warranting consideration of CSTCs in this critical relationship. Dysregulation of this immunological balance can result in both intestinal inflammation or damaging autoimmune responses elsewhere in the body. Given the relative novelty of CSTCs in the literature, we aim to introduce the importance of their role in maintaining immune homeostasis at barrier sites such as the intestine. [ABSTRACT FROM AUTHOR]

The genus Escherichia has been extensively studied and it is known to encompass a range of commensal and pathogenic bacteria that primarily inhabit the gastrointestinal tracts of warm-blooded vertebrates. However, the presence of E. coli as a model organism and potential pathogen has diverted attention away from commensal strains and other species in the genus. To investigate the diversity of Escherichia in healthy chickens, we collected fecal samples from antibiotic-free Lohmann Brown layer hens and determined the genome sequences of 100 isolates, 81 of which were indistinguishable at the HC0 level of the Hierarchical Clustering of Core Genome Multi-Locus Sequence Typing scheme. Despite initial selection on CHROMagar Orientation medium, which is considered selective for E. coli, in silico phylotyping and core genome single nucleotide polymorphism analysis revealed the presence of at least one representative of all major clades of Escherichia, except for E. albertii, Shigella, and E. coli phylogroup B2 and cryptic clade I. The most frequent phylogenomic groups were E. coli phylogroups A and B1 and E. ruysiae (clades III and IV). We compiled a collection of reference strains isolated from avian sources (predominantly chicken), representing every Escherichia phylogroup and species, and used it to confirm the phylogeny and diversity of our isolates. Overall, the isolates carried low numbers of the virulence and antibiotic resistance genes typically seen in avian pathogenic E. coli. Notably, the clades not recovered are ones that have been most strongly associated with virulence by other studies. [ABSTRACT FROM AUTHOR]

Microorganisms are an essential part of life on the earth and can exist in association with virtually any living thing. The environmental microbiome is much more diverse than the human microbiome. It is reported that most microbes existing in the environment are difficult to culture in the laboratory. Whereas both pathogenic and beneficial microbes may be prevailing in the environment, the human body can have three categories of microbes- beneficial, pathogenic, and opportunistic pathogenic. With at least 10-fold more cells than human cells, microbes as normal flora are critical for human survival. The microbes present in the human body play a crucial role in maintaining human health, and the environmental microbiome influences the human microbiome makeup. The interaction between the environmental and human microbiome highly influences human health, however it is poorly understood. In addition, as an established infection is associated with health-seeking behavior, a large number of studies have focused on the transmission and dynamics of infectious microorganisms than the noninfectious or beneficial ones. This review will summarize how the interaction between the environmental and human microbiome affects human health and identify approaches that might be beneficial for humans to improve health by being exposed to the natural environment. [ABSTRACT FROM AUTHOR]

Escherichia coli is a commensal bacterial gut inhabitant in vertebrates, while some strains are pathogens. Analysis of the genetic substructure within E. coli has identified nine phylogenetic groups within the species, as group A, B1, B2, C, D, E, F, G and cryptic clade I. These groups vary in attributes such as host characteristics, pathogenicity, antibiotic sensitivity patterns and virulence profiles. The current study was conducted to determine the distribution of phylogenetic groups, commonly encountered sequence types (ST), and group B2 subgroups (SG) of human faecal E. coli in a sample population in the Kandy District, Sri Lanka. A total of 158 faecal swabs, collected from healthy individuals, were cultured on MacConkey agar and presumptive E. coli isolates were confirmed by a negative reaction on Simmons citrate agar. E. coli isolates were characterized according to their phylogenetic group, SG, and ST distribution by a series of PCR protocols. Results revealed a predominance of group B2 (28 %), followed by B1 (23 %), A (17 %), D (14 %), C (5 %), F (4 %), and E (3 %). Within phylogroup B2, SG III was predominant while ST 73, 95, and 131 were detected at low frequencies. ST 69 accounted for 20 % of the group D isolates. Distribution of phylogroups was independent of host gender except group D, which was significantly over-represented by males. As B2 E. coli are strongly associated with extraintestinal infections and a high degree of virulence, characterization of these human faecal E. coli isolates for antibiotic susceptibility and virulence profiles would be of clinical importance. [ABSTRACT FROM AUTHOR]

Background : Antibiotic-resistant Escherichia coli can colonize the intestinal tract of healthy children, causing concern when antibiotic resistance is related to the presence of transferable mechanisms, such as extended-spectrum 13-lactamases (ESBLs). Materials and Methods: Fecal samples from 41 healthy children from two villages of rural Peru were cultured on ceftriaxone-disks. ESBL production was confirmed with double disk synergy. In all ESBL-produced isolates, antibiotic susceptibility to 12 antibacterial agents was established by disk diffusion, while clonal relationships were determined by repetitive extragenic palindromic-polymerase chain reaction (REP-PCR). Presence of ST131 was determined using PCR. Results:Ceftriaxone-resistant microorganisms were recovered from 39 samples belonging to 22 out of41 children (53.7°/o). Of these, 80 ceftriaxone-resistant and two ceftriaxoneintermediate E. coli from inside ceftriaxone-halos were confirmed as ESBL-producers. All isolates were multidrug-resistant. In 79/80 (98.8%) ceftriaxone-resistant isolates, the presence of blacrx-M was detected alone (58 isolates, or together with other D-lactamase (blarEM 17 isolates; blaoxA-1-like, 3 isolates; blarEM + blao>

The root microbiome refers to the community of microbes living in association with a plant's roots, and includes mutualists, pathogens, and commensals. Here we focus on recent advances in the study of root commensal community which is the major research object of microbiome‐related researches. With the rapid development of new technologies, plant–commensal interactions can be explored with unprecedented breadth and depth. Both the soil environment and the host plant drive commensal community assembly. The bulk soil is the seed bank of potential commensals, and plants use root exudates and immune responses to build healthy microbial communities from the available microbes. The plant microbiome extends the functional system of plants by participating in a variety of processes, including nutrient absorption, growth promotion, and resistance to biotic and abiotic stresses. Plants and their microbiomes have evolved adaptation strategies over time. However, there is still a huge gap in our understanding of the regulatory mechanisms of plant–commensal interactions. In this review, we summarize recent research on the assembly of root microbial communities and the effects of these communities on plant growth and development, and look at the prospects for promoting sustainable agricultural development through the study of the root microbiome. [ABSTRACT FROM AUTHOR]

Insects frequently confront different microbial assemblages. Bacteria inhabiting an insect gut are often commensal, but some can become pathogenic when the insect is compromised from different stressors. Herbivores are often confronted by various forms of plant resistance, but how defenses generate opportunistic microbial infections from residents in the gut are not well understood. In this study, we evaluated the pathogenic tendencies of Serratia isolated from the digestive system of healthy fall armyworm larvae (Spodopterafrugiperda) and how it interfaces with plant defenses. We initially selected Serratia strains that varied in their direct expression of virulence factors. Inoculation of the different isolates into the fall armyworm body cavity indicated differing levels of pathogenicity, with some strains exhibiting no effects while others causing mortality 24 h after injection. Oral inoculations of pathogens on larvae provided artificial diets caused marginal (< 7%) mortality. However, when insects were provided different maize genotypes, mortality from Serratia increased and was higher on plants exhibiting elevated levels of herbivore resistance (< 50% mortality). Maize defenses facilitated an initial invasion of pathogenic Serratia into the larval hemocoel¸ which was capable of overcoming insect antimicrobial defenses. Tomato and soybean further indicated elevated mortality due to Serratia compared to artificial diets and differences between plant genotypes. Our results indicate plants can facilitate the incipient emergence of pathobionts within gut of fall armyworm. The ability of resident gut bacteria to switch from a commensal to pathogenic lifestyle has significant ramifications for the host and is likely a broader phenomenon in multitrophic interactions facilitated by plant defenses. [ABSTRACT FROM AUTHOR]