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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.

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.

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.

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.

Considering the ecological diversity of E. coli, the main aim of this study was to determine the prevalence, phylogroup diversity, and antimicrobial susceptibility of E. coli isolated from 383 different clinical and environmental sources. In total, varied prevalence was observed of the 197 confirmed E. coli that were isolated (human–100%, animal–67.5%, prawn–49.23%, soil–30.58%, and water–27.88%). Of these isolates, 70 (36%) were multidrug-resistant (MDR). MDR E. coli was significantly associated with their sources (χ2 = 29.853, p = 0.001). Humans (51.67%) and animals (51.85%) carried more MDR E. coli than other environments. The eae gene indicative of recent fecal contamination was not detected in any isolate, indicating that these E. coli isolates could be present in these environments for a long time and became naturalized. Phylogroup B1 (48.22%) was the predominant group, being present in all hosts analyzed and with the commensal E. coli group A (26.9%) representing the second predominant group. According to chi-square analysis, phylogroup B1 was significantly associated with E. coli from humans (p = 0.024), soil (p < 0.001) and prawn samples (p < 0.001). Human samples were significantly associated with phylogroup B1 (p = 0.024), D (p < 0.001), and F (p = 0.016) of E. coli strains, whereas phylogroup A (p < 0.001), C (p < 0.001), and E (p = 0.015) were associated with animal samples. Correspondence analysis results also indicated the association of these phylogroups with their hosts/sources. The findings of this study exhibited a non-random distribution of phylogenetic groups, though the diversity index was highest for human E. coli phylogroups.

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.

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.

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).

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.

The genus Macavirus, subfamily Gammaherpesvirinae, comprises ungulate viruses that infect domestic and wild ruminants and swine. They cause asymptomatic latent infections in reservoir hosts and malignant catarrhal fever in susceptible species. Lung, spleen, bronchial lymph node, and tongue were collected from 448 cattle (348 necropsied, 100 slaughtered) in Switzerland, United Kingdom, Finland, Belgium, and Germany to determine their infection with bovine herpesvirus-6 (BoHV-6) and gammaherpesviruses of other ruminants, i.e., ovine herpesvirus-1 and -2, caprine herpesvirus-2, and bison lymphotropic herpesvirus, using quantitative PCR. Only BoHV-6 was detected, with an overall frequency of 32%, ranging between 22% and 42% in the different countries. Infection was detected across all ages, from one day after birth, and was positively correlated with age. There was no evidence of an association with specific disease processes. In positive animals, BoHV-6 was detected in all organs with high frequency, consistently in the lungs or spleen. Viral loads varied substantially. In BoHV-6-positive gravid cows, organs of fetuses tested negative for infection, indicating that the virus is not vertically transmitted. Our results confirm previous data indicating that BoHV-6 is a commensal of domestic cattle not associated with disease processes and confirm that infections with other macaviruses are rare and sporadic.

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.

The treatment of diarrhea in the postweaning period is a common reason for the use of antimicrobials in pig production, and Escherichia coli is the single most important causative agent for this condition. Colistin has recently been classified as a critically important antimicrobial for human health, as it is a last-resort drug against certain multi-drug-resistant Gram-negative bacteria. Therefore, the use of colistin has been significantly reduced in some countries, including Denmark. Despite this, the drug is still commonly used to treat diarrhea in pigs in many countries, and there is a need to understand the risks associated with this practice. We performed a prospective cohort study to investigate the effect of colistin treatment on the changes in the average minimum inhibitory concentration (MIC) in commensal E. coli in a pig herd where no colistin-resistant bacteria were detectable before treatment. One group of pigs was batch treated with colistin after the clinical observation of diarrhea, one group was batch treated with colistin approximately 10 days before the expected onset of diarrhea, and a control group was not treated with colistin but provided with nonantimicrobial antidiarrheal feed supplement. Treatment with colistin in the dose and time combinations used did not result in a significant increase in the average colistin MIC values in E. coli. Moreover, no E. coli strains showed a MIC above the breakpoint of >2 mg/L against colistin. Co-selection of resistance to other antimicrobials was not observed.

To increase our understanding of bacterial intestinal colonization in animal populations lacking substantial anthropogenic influence we studied the diversity of E. coli in cormorants from the pristine West-Mongolian steppe. E. coli were isolated from individual birds of two cormorant colonies located on small islands in lakes at least 100 km away from human settlements. Diversity of the isolates was studied using pulsed-field gel electrophoresis (PFGE). 137 isolates of cormorant colony-1 and 75 isolates of cormorant colony-2 resulted in 60 and 33 PFGE types, respectively. Representative strains of each PFGE type were analyzed via PCR in terms of phylogroups and extraintestinal virulence-associated genes (exVAGs). Bacterial adhesion to the chicken intestinal cell line CHIC-8E11 and antimicrobial resistance was also determined. Most isolates belonged to phylogroup B1 (68.3%) followed by B2 and E with B2 harboring the highest total number of exVAGs per isolate. Unexpectedly, a PFGE type with relatively few exVAGs displayed the highest isolation frequency, also showing a high adhesion rate. Comparative analysis of exVAGs to other E. coli populations of wildlife origin revealed that the secreted autotransporter toxin encoding sat gene was only present in cormorants. Overall, E. coli in cormorants maintained a high diversity under minimal anthropogenic influences, which likely enables intestinal colonization.

The human microbiota is an array of microorganisms known to interact with the host and other microbes. These interactions can be competitive, as microbes must adapt to host- and microorganism-related stressors, thus producing toxic molecules, or cooperative, whereby microbes survive by maintaining homeostasis with the host and host-associated microbial communities. As a result, these microbial interactions shape host health and can potentially result in disease. In this review, we discuss these varying interactions across microbial species, their positive and negative effects, the therapeutic potential of these interactions, and their implications on our knowledge of human well-being.

Human gingival epithelial cells (HGEps) and fibroblasts (HGFs) are the main cell types in peri-implant soft tissue. HGEps are constantly exposed to bacteria, but HGFs are protected by connective tissue as long as the mucosa–implant seal is intact. Streptococcus oralis is one of the commensal bacteria, is highly abundant at healthy implant sites, and might modulate soft tissue cells—as has been described for other streptococci. We have therefore investigated the effects of the S. oralis biofilm on HGEps and HGFs. HGEps or HGFs were grown separately on titanium disks and responded to challenge with S. oralis biofilm. HGFs were severely damaged after 4 h, exhibiting transcriptional inflammatory and stress responses. In contrast, challenge with S. oralis only induced a mild transcriptional inflammatory response in HGEps, without cellular damage. HGFs were more susceptible to the S. oralis biofilm than HGEps. The pro-inflammatory interleukin 6 (IL-6) was attenuated in HGFs, as was interleukin 8 (CXCL8) in HGEps. This indicates that S. oralis can actively protect tissue. In conclusion, commensal biofilms can promote homeostatic tissue protection, but only if the implant–mucosa interface is intact and HGFs are not directly exposed.

The objective of this study was to determine if the interaction between common oral commensal bacteria and oral epithelial cells would provide protective effects against the invasion of periodontopathogen Porphyromonas gingivalis. Oral epithelial OKF6/Tert cells were used in co-cultures with Streptococcus gordonii, Streptococcus oralis, Streptococcus mitis, and Streptococcus intermedius. The viability of OKF6/Tert cells following a bacterial challenge was evaluated by trypan blue exclusion. The adherence of commensal species was determined by CFU counts. P. gingivalis invasion in OKF6/Tert cells was assessed before and after exposure to commensal species according to CFU counts. Viability assays show that only S. gordonii and S. intermedius display low toxicity toward OKF6/Tert cells. Both commensals adhere to OKF6/Tert cells at an average ratio of 1 CFU to 10 cells. P. gingivalis invasion into host cells is significantly reduced by 25% or 60% after exposure to S. gordonii or S. intermedius, respectively. The results suggest that these commensal species bind to host cells and diminish P. gingivalis invasion. This is important in the context of periodontal disease since P. gingivalis primarily acts on the host by invading it. Therefore, efforts to decrease invasion will eventually lead to future therapies harnessing the mechanisms employed by oral commensal bacteria.

Antimicrobial resistance in pathogenic Neisseria parallels reduced antimicrobial susceptibility in commensal Neisseria in certain populations, like men who have sex with men (MSM). Although this reduced susceptibility can be a consequence of frequent antimicrobial exposure at the individual level, we hypothesized that commensal Neisseria are transmitted between sexual partners. We used data from a 2014 microbiome study in which saliva and tongue swabs were taken from 21 couples (42 individuals). Samples were analyzed using 16S rRNA gene sequencing. We compared intimate partners with unrelated individuals and found that the oral Neisseria communities of intimate partners were more similar than those of unrelated individuals (average Morisita−Horn dissimilarity index for saliva samples: 0.54 versus 0.71, respectively (p = 0.005); and for tongue swabs: 0.42 versus 0.63, respectively (p = 0.006)). This similarity presumably results from transmission of oral Neisseria through intimate kissing. This finding suggests that intensive gonorrhea screening in MSM may, via increased antimicrobial exposure, promote, rather than prevent, the emergence and spread of antimicrobial resistance in Neisseria. Non-antibiotic strategies such as vaccines and oral antiseptics could prove more sustainable options to reduce gonococcal prevalence.

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.

Chicken gastrointestinal tract is an important site of immune cell development that not only regulates gut microbiota but also maintains extra-intestinal immunity. Recent studies have emphasized the important roles of gut microbiota in shaping immunity against viral diseases in chicken. Microbial diversity and its integrity are the key elements for deriving immunity against invading viral pathogens. Commensal bacteria provide protection against pathogens through direct competition and by the production of antibodies and activation of different cytokines to modulate innate and adaptive immune responses. There are few economically important viral diseases of chicken that perturb the intestinal microbiota diversity. Disruption of microbial homeostasis (dysbiosis) associates with a variety of pathological states, which facilitate the establishment of acute viral infections in chickens. In this review, we summarize the calibrated interactions among the microbiota mediated immune modulation through the production of different interferons (IFNs) ILs, and virus-specific IgA and IgG, and their impact on the severity of viral infections in chickens. Here, it also shows that acute viral infection diminishes commensal bacteria such as Lactobacillus, Bifidobacterium, Firmicutes, and Blautia spp. populations and enhances the colonization of pathobionts, including E. coli, Shigella, and Clostridial spp., in infected chickens.

Flexible adaptation to the host environment is a critical trait that underpins the success of numerous microbes. The polymorphic fungus Candida albicans has evolved to persist in the numerous challenging niches of the human body. The interaction of C. albicans with a mucosal surface is an essential prerequisite for fungal colonisation and epitomises the complex interface between microbe and host. C. albicans exhibits numerous adaptations to a healthy host that permit commensal colonisation of mucosal surfaces without provoking an overt immune response that may lead to clearance. Conversely, fungal adaptation to impaired immune fitness at mucosal surfaces enables pathogenic infiltration into underlying tissues, often with devastating consequences. This review will summarise our current understanding of the complex interactions that occur between C. albicans and the mucosal surfaces of the human body.

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.

The human intestine is populated with an extremely dense and diverse bacterial community. Commensal bacteria act as an important antigenic stimulus producing the maturation of gut-associated lymphoid tissue (GALT). The production of immunoglobulin (Ig) A by B-cells in the GALT is one of the immune responses following intestinal colonization of bacteria. The switch of B-cells from IgM to IgA-producing cells in the Peyer’s patches and neighboring lamina propria proceeds by T-cell-dependent and T-cell-independent mechanisms. Several grams of secretory IgA (SIgA) are released into the intestine each day. SIgA serves as a first-line of defense in protecting the intestinal epithelium from enteric toxins and pathogenic microorganisms. SIgA has a capacity to directly quench bacterial virulence factors, influence the composition of the intestinal microbiota, and promote the transportation of antigens across the intestinal epithelium to GALT and down-regulate proinflammatory responses associated with the uptake of highly pathogenic bacteria and potentially allergenic antigens. This review summarizes the reciprocal interactions between intestinal B cells and bacteria, specifically, the formation of IgA in the gut, the role of intestinal IgA in the regulation of bacterial communities and the maintenance of intestinal homeostasis, and the effects of probiotics on IgA levels in the gastrointestinal tract.

Considering the ecological diversity of E. coli , the main aim of this study was to determine the prevalence, phylogroup diversity, and antimicrobial susceptibility of E. coli isolated from 383 different clinical and environmental sources. In total, varied prevalence was observed of the 197 confirmed E. coli that were isolated (human-100%, animal-67.5%, prawn-49.23%, soil-30.58%, and water-27.88%). Of these isolates, 70 (36%) were multidrug-resistant (MDR). MDR E. coli was significantly associated with their sources (χ 2 = 29.853, p = 0.001). Humans (51.67%) and animals (51.85%) carried more MDR E. coli than other environments. The eae gene indicative of recent fecal contamination was not detected in any isolate, indicating that these E. coli isolates could be present in these environments for a long time and became naturalized. Phylogroup B1 (48.22%) was the predominant group, being present in all hosts analyzed and with the commensal E. coli group A (26.9%) representing the second predominant group. According to chi-square analysis, phylogroup B1 was significantly associated with E. coli from humans ( p = 0.024), soil ( p < 0.001) and prawn samples ( p < 0.001). Human samples were significantly associated with phylogroup B1 ( p = 0.024), D ( p < 0.001), and F ( p = 0.016) of E. coli strains, whereas phylogroup A ( p < 0.001), C ( p < 0.001), and E ( p = 0.015) were associated with animal samples. Correspondence analysis results also indicated the association of these phylogroups with their hosts/sources. The findings of this study exhibited a non-random distribution of phylogenetic groups, though the diversity index was highest for human E. coli phylogroups.

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.

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.

The treatment of diarrhea in the postweaning period is a common reason for the use of antimicrobials in pig production, and Escherichia coli is the single most important causative agent for this condition. Colistin has recently been classified as a critically important antimicrobial for human health, as it is a last-resort drug against certain multi-drug-resistant Gram-negative bacteria. Therefore, the use of colistin has been significantly reduced in some countries, including Denmark. Despite this, the drug is still commonly used to treat diarrhea in pigs in many countries, and there is a need to understand the risks associated with this practice. We performed a prospective cohort study to investigate the effect of colistin treatment on the changes in the average minimum inhibitory concentration (MIC) in commensal E. coli in a pig herd where no colistin-resistant bacteria were detectable before treatment. One group of pigs was batch treated with colistin after the clinical observation of diarrhea, one group was batch treated with colistin approximately 10 days before the expected onset of diarrhea, and a control group was not treated with colistin but provided with nonantimicrobial antidiarrheal feed supplement. Treatment with colistin in the dose and time combinations used did not result in a significant increase in the average colistin MIC values in E. coli. Moreover, no E. coli strains showed a MIC above the breakpoint of >2 mg/L against colistin. Co-selection of resistance to other antimicrobials was not observed.

To increase our understanding of bacterial intestinal colonization in animal populations lacking substantial anthropogenic influence we studied the diversity of E. coli in cormorants from the pristine West-Mongolian steppe. E. coli were isolated from individual birds of two cormorant colonies located on small islands in lakes at least 100 km away from human settlements. Diversity of the isolates was studied using pulsed-field gel electrophoresis (PFGE). 137 isolates of cormorant colony-1 and 75 isolates of cormorant colony-2 resulted in 60 and 33 PFGE types, respectively. Representative strains of each PFGE type were analyzed via PCR in terms of phylogroups and extraintestinal virulence-associated genes (exVAGs). Bacterial adhesion to the chicken intestinal cell line CHIC-8E11 and antimicrobial resistance was also determined. Most isolates belonged to phylogroup B1 (68.3%) followed by B2 and E with B2 harboring the highest total number of exVAGs per isolate. Unexpectedly, a PFGE type with relatively few exVAGs displayed the highest isolation frequency, also showing a high adhesion rate. Comparative analysis of exVAGs to other E. coli populations of wildlife origin revealed that the secreted autotransporter toxin encoding sat gene was only present in cormorants. Overall, E. coli in cormorants maintained a high diversity under minimal anthropogenic influences, which likely enables intestinal colonization.

The human microbiota is an array of microorganisms known to interact with the host and other microbes. These interactions can be competitive, as microbes must adapt to host- and microorganism-related stressors, thus producing toxic molecules, or cooperative, whereby microbes survive by maintaining homeostasis with the host and host-associated microbial communities. As a result, these microbial interactions shape host health and can potentially result in disease. In this review, we discuss these varying interactions across microbial species, their positive and negative effects, the therapeutic potential of these interactions, and their implications on our knowledge of human well-being.

The objective of this study was to determine if the interaction between common oral commensal bacteria and oral epithelial cells would provide protective effects against the invasion of periodontopathogen Porphyromonas gingivalis . Oral epithelial OKF6/Tert cells were used in co-cultures with Streptococcus gordonii , Streptococcus oralis , Streptococcus mitis , and Streptococcus intermedius . The viability of OKF6/Tert cells following a bacterial challenge was evaluated by trypan blue exclusion. The adherence of commensal species was determined by CFU counts. P. gingivalis invasion in OKF6/Tert cells was assessed before and after exposure to commensal species according to CFU counts. Viability assays show that only S. gordonii and S. intermedius display low toxicity toward OKF6/Tert cells. Both commensals adhere to OKF6/Tert cells at an average ratio of 1 CFU to 10 cells. P. gingivalis invasion into host cells is significantly reduced by 25% or 60% after exposure to S. gordonii or S. intermedius , respectively. The results suggest that these commensal species bind to host cells and diminish P. gingivalis invasion. This is important in the context of periodontal disease since P. gingivalis primarily acts on the host by invading it. Therefore, efforts to decrease invasion will eventually lead to future therapies harnessing the mechanisms employed by oral commensal bacteria.

Antimicrobial resistance in pathogenic Neisseria parallels reduced antimicrobial susceptibility in commensal Neisseria in certain populations, like men who have sex with men (MSM). Although this reduced susceptibility can be a consequence of frequent antimicrobial exposure at the individual level, we hypothesized that commensal Neisseria are transmitted between sexual partners. We used data from a 2014 microbiome study in which saliva and tongue swabs were taken from 21 couples (42 individuals). Samples were analyzed using 16S rRNA gene sequencing. We compared intimate partners with unrelated individuals and found that the oral Neisseria communities of intimate partners were more similar than those of unrelated individuals (average Morisita-Horn dissimilarity index for saliva samples: 0.54 versus 0.71, respectively ( p = 0.005); and for tongue swabs: 0.42 versus 0.63, respectively ( p = 0.006)). This similarity presumably results from transmission of oral Neisseria through intimate kissing. This finding suggests that intensive gonorrhea screening in MSM may, via increased antimicrobial exposure, promote, rather than prevent, the emergence and spread of antimicrobial resistance in Neisseria . Non-antibiotic strategies such as vaccines and oral antiseptics could prove more sustainable options to reduce gonococcal prevalence.

Neisseria species are extremely well-adapted to their mammalian hosts and they display unique phenotypes that account for their ability to thrive within niche-specific conditions. The closely related species N. gonorrhoeae and N. meningitidis are the only two species of the genus recognized as strict human pathogens, causing the sexually transmitted disease gonorrhea and meningitis and sepsis, respectively. Gonococci colonize the mucosal epithelium of the male urethra and female endo/ectocervix, whereas meningococci colonize the mucosal epithelium of the human nasopharynx. The pathophysiological host responses to gonococcal and meningococcal infection are distinct. However, medical evidence dating back to the early 1900s demonstrates that these two species can cross-colonize anatomical niches, with patients often presenting with clinically-indistinguishable infections. The remaining Neisseria species are not commonly associated with disease and are considered as commensals within the normal microbiota of the human and animal nasopharynx. Nonetheless, clinical case reports suggest that they can behave as opportunistic pathogens. In this review, we describe the diversity of the genus Neisseria in the clinical context and raise the attention of microbiologists and clinicians for more cautious approaches in the diagnosis and treatment of the many pathologies these species may cause.

Flexible adaptation to the host environment is a critical trait that underpins the success of numerous microbes. The polymorphic fungus Candida albicans has evolved to persist in the numerous challenging niches of the human body. The interaction of C. albicans with a mucosal surface is an essential prerequisite for fungal colonisation and epitomises the complex interface between microbe and host. C. albicans exhibits numerous adaptations to a healthy host that permit commensal colonisation of mucosal surfaces without provoking an overt immune response that may lead to clearance. Conversely, fungal adaptation to impaired immune fitness at mucosal surfaces enables pathogenic infiltration into underlying tissues, often with devastating consequences. This review will summarise our current understanding of the complex interactions that occur between C. albicans and the mucosal surfaces of the human body., Competing Interests: The authors declare no conflicts of interest.