Wedad S Hamdi, Afraa Fadul, Fabio Culurgioni, Amna Gameil, Manal Yaghmour, Peter V Coyle, Mohamed Ali Ben Hadj Kacem, Naema Al Molawi, Anitha Amudhavalli, Mohammad Bakr, Honar Cherif, Einas Al-Kuwari
Introduction. Allogeneic haematopoietic stem cell transplantation (allo-HSCT) is a treatment option for haematological malignancies. Allo-HSCT patients are more susceptible to viral infections due to immunosuppression.Gap Statement. The bone marrow transplant programme in Qatar, established within the past decade, remains in a developmental phase. A thorough evaluation of infection-related outcomes is essential to identify areas for improvement and to enhance infection control measures.Aim. This study aims to estimate the incidence, clinical impact and outcomes of viral respiratory tract infection (vRTI) in allo-HSCT recipients.Methodology. A total of 64 allo-HSCT patients were included in this study. Respiratory samples were collected from patients presenting with respiratory symptoms or during episodes of febrile neutropenia without an identified source. Nasopharyngeal swabs were the primary sampling method for upper respiratory tract infections (URTIs), while sputum, bronchoalveolar lavage or tracheal aspirates were obtained in patients with lower respiratory tract involvement or those requiring mechanical ventilation. During the high-risk COVID-19 pandemic period, pre-admission screening for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was routinely performed for all patients undergoing transplantation or chemotherapy. All samples were assessed using multiplex PCR assays. Viral agents, outcomes of vRTI occurring in the period of 1 year after allo-HSCT, clinical symptoms, infection-related complications and risk factors were reviewed.Result. A total of 64 allo-HSCT patients were reviewed; 41 of them (53%) had vRTI. SARS-CoV-2, respiratory syncytial virus (RSV), rhinovirus, influenza and parainfluenza were the most common viruses. Importantly, 19 patients (46.3%) had URTI, and 22 patients (53.7%) progressed to pneumonia. The risk of vRTI was significantly related to non-corticosteroid immune suppressants (P≤0.01) and to lymphopenia (P≤0.05). RSV (66.7%), coronaviruses (229E, NL63, OC43 and HKU1) (60%) and rhinovirus (58.3%) were the most dominant viruses associated with the development of pneumonia. Thirteen patients (20.3%) were admitted to the ICU; eight of them were associated with vRTI (61.5%). Ten deaths were reported (15.6%); vRTI was the primary cause of death in one of the deceased patients.Conclusion. Early detection and intervention strategies are crucial in mitigating the impact of these infections. The immune alteration effect of prophylaxis immune suppressants and antiviral therapy exacerbates the risk of infections among allo-HSCT patients. Novel antiviral approaches based on enhancing antiviral immune responses, vaccines and non-pharmaceutical preventive strategies are required to improve outcomes in allo-HSCT patients.
{"title":"Clinical characteristics and outcomes of viral respiratory infections in allogeneic haematopoietic stem cell transplantation recipients: a single-centre experience.","authors":"Wedad S Hamdi, Afraa Fadul, Fabio Culurgioni, Amna Gameil, Manal Yaghmour, Peter V Coyle, Mohamed Ali Ben Hadj Kacem, Naema Al Molawi, Anitha Amudhavalli, Mohammad Bakr, Honar Cherif, Einas Al-Kuwari","doi":"10.1099/jmm.0.002071","DOIUrl":"https://doi.org/10.1099/jmm.0.002071","url":null,"abstract":"<p><p><b>Introduction.</b> Allogeneic haematopoietic stem cell transplantation (allo-HSCT) is a treatment option for haematological malignancies. Allo-HSCT patients are more susceptible to viral infections due to immunosuppression.<b>Gap Statement.</b> The bone marrow transplant programme in Qatar, established within the past decade, remains in a developmental phase. A thorough evaluation of infection-related outcomes is essential to identify areas for improvement and to enhance infection control measures.<b>Aim.</b> This study aims to estimate the incidence, clinical impact and outcomes of viral respiratory tract infection (vRTI) in allo-HSCT recipients.<b>Methodology.</b> A total of 64 allo-HSCT patients were included in this study. Respiratory samples were collected from patients presenting with respiratory symptoms or during episodes of febrile neutropenia without an identified source. Nasopharyngeal swabs were the primary sampling method for upper respiratory tract infections (URTIs), while sputum, bronchoalveolar lavage or tracheal aspirates were obtained in patients with lower respiratory tract involvement or those requiring mechanical ventilation. During the high-risk COVID-19 pandemic period, pre-admission screening for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was routinely performed for all patients undergoing transplantation or chemotherapy. All samples were assessed using multiplex PCR assays. Viral agents, outcomes of vRTI occurring in the period of 1 year after allo-HSCT, clinical symptoms, infection-related complications and risk factors were reviewed.<b>Result.</b> A total of 64 allo-HSCT patients were reviewed; 41 of them (53%) had vRTI. SARS-CoV-2, respiratory syncytial virus (RSV), rhinovirus, influenza and parainfluenza were the most common viruses. Importantly, 19 patients (46.3%) had URTI, and 22 patients (53.7%) progressed to pneumonia. The risk of vRTI was significantly related to non-corticosteroid immune suppressants (<i>P</i>≤0.01) and to lymphopenia (<i>P</i>≤0.05). RSV (66.7%), coronaviruses (229E, NL63, OC43 and HKU1) (60%) and rhinovirus (58.3%) were the most dominant viruses associated with the development of pneumonia. Thirteen patients (20.3%) were admitted to the ICU; eight of them were associated with vRTI (61.5%). Ten deaths were reported (15.6%); vRTI was the primary cause of death in one of the deceased patients.<b>Conclusion.</b> Early detection and intervention strategies are crucial in mitigating the impact of these infections. The immune alteration effect of prophylaxis immune suppressants and antiviral therapy exacerbates the risk of infections among allo-HSCT patients. Novel antiviral approaches based on enhancing antiviral immune responses, vaccines and non-pharmaceutical preventive strategies are required to improve outcomes in allo-HSCT patients.</p>","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mary Jane Lynch, Jialun Wu, Olivia McAuliffe, Conor P O'Byrne, Cormac G M Gahan
Introduction. Molecular epidemiological and phenotypic analyses of Listeria monocytogenes strains can inform our understanding of factors that influence onward transmission, virulence potential and ability to control the pathogen in foods or in clinical settings. Bile acids represent a host-specific barrier to microbial colonization of the gastrointestinal tract and are, therefore, not encountered in the external environment. We tested the hypothesis that tolerance of bile acids may be an evolutionary adaptation across L. monocytogenes clonal complexes (CCs), which varies with genotype and/or is associated with clinical isolates.Hypothesis. We hypothesized that strains of L. monocytogenes may differ in bile tolerance (a potential virulence-associated trait) and herein examine this phenomenon according to CC, strain origin and genotype.Aim. To assess 205 genome-sequenced isolates of L. monocytogenes for tolerance of porcine bile acids and bile salt hydrolase (BSH) activity.Methodology. Survival of L. monocytogenes strains was determined following exposure to porcine bile acids under conditions that mimic the small intestinal environment. BSH activity was assayed against pure taurodeoxycholic acid and glycodeoxycholic acid using an agar plate deconjugation assay. Genomes were analysed for polymorphisms in known bile tolerance loci.Results. Isolates demonstrated distinct inter-individual variances in bile tolerance under anaerobic conditions that mimic the intestinal environment. Strains isolated from cases of human disease were significantly more bile-tolerant than those isolated from natural environments or foods. There was no correlation between levels of bile tolerance and the size of bile precipitation zones on the BSH agar plate assay. No significant patterns were seen upon analysis of known or putative bile tolerance loci; however, individual strains with naturally occurring sigB operon mutations demonstrated reduced bile tolerance.Conclusion.L. monocytogenes strains isolated from clinical cases of listeriosis demonstrated elevated bile resistance consistent with a likely enhanced capacity to cause gastrointestinal infection preceding invasive disease. The data suggest the potential importance of bile tolerance in L. monocytogenes infection and highlight underlying molecular mechanisms by which strains vary in their natural levels of bile tolerance.
{"title":"Phenotypic and phylogenetic analyses of <i>Listeria monocytogenes</i> strains reveal enhanced bile tolerance in clinical isolates.","authors":"Mary Jane Lynch, Jialun Wu, Olivia McAuliffe, Conor P O'Byrne, Cormac G M Gahan","doi":"10.1099/jmm.0.002063","DOIUrl":"10.1099/jmm.0.002063","url":null,"abstract":"<p><p><b>Introduction.</b> Molecular epidemiological and phenotypic analyses of <i>Listeria monocytogenes</i> strains can inform our understanding of factors that influence onward transmission, virulence potential and ability to control the pathogen in foods or in clinical settings. Bile acids represent a host-specific barrier to microbial colonization of the gastrointestinal tract and are, therefore, not encountered in the external environment. We tested the hypothesis that tolerance of bile acids may be an evolutionary adaptation across <i>L. monocytogenes</i> clonal complexes (CCs), which varies with genotype and/or is associated with clinical isolates.<b>Hypothesis.</b> We hypothesized that strains of <i>L. monocytogenes</i> may differ in bile tolerance (a potential virulence-associated trait) and herein examine this phenomenon according to CC, strain origin and genotype.<b>Aim.</b> To assess 205 genome-sequenced isolates of <i>L. monocytogenes</i> for tolerance of porcine bile acids and bile salt hydrolase (BSH) activity.<b>Methodology.</b> Survival of <i>L. monocytogenes</i> strains was determined following exposure to porcine bile acids under conditions that mimic the small intestinal environment. BSH activity was assayed against pure taurodeoxycholic acid and glycodeoxycholic acid using an agar plate deconjugation assay. Genomes were analysed for polymorphisms in known bile tolerance loci.<b>Results.</b> Isolates demonstrated distinct inter-individual variances in bile tolerance under anaerobic conditions that mimic the intestinal environment. Strains isolated from cases of human disease were significantly more bile-tolerant than those isolated from natural environments or foods. There was no correlation between levels of bile tolerance and the size of bile precipitation zones on the BSH agar plate assay. No significant patterns were seen upon analysis of known or putative bile tolerance loci; however, individual strains with naturally occurring <i>sigB</i> operon mutations demonstrated reduced bile tolerance.<b>Conclusion.</b> <i>L. monocytogenes</i> strains isolated from clinical cases of listeriosis demonstrated elevated bile resistance consistent with a likely enhanced capacity to cause gastrointestinal infection preceding invasive disease. The data suggest the potential importance of bile tolerance in <i>L. monocytogenes</i> infection and highlight underlying molecular mechanisms by which strains vary in their natural levels of bile tolerance.</p>","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476152/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145126243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
For thousands of years, parasitic infections have represented a constant challenge to human health. Despite constant progress in science and medicine, the challenge has remained mostly unchanged over the years, partly due to the vast complexity of the host-parasite-environment relationships. Over the last century, our approaches to these challenges have evolved through considerable advances in science and technology, offering new and better solutions. Unfortunately, in the twenty-first century, this diagnostic evolution was suddenly confronted with a dramatic change of biological relationships, never witnessed in history before the uncontrolled expansion of the human population, globalization and hyperconnectivity technology have exerted a massive socioeconomic impact on individuals, communities and the environment, sending a ripple effect throughout the world of parasites. Urbanization, pollution and the unsustainable exploitation of natural resources have caused shifts in biomass and the fragmentation of habitats, leading to the movement of parasites into new hosts and territories. At the same time, changes in human population structure and distributions due to armed conflict and poverty created massive migration of entire nations and communities, resulting in the redistribution of parasitic diseases. To make the situation worse, the population of many receiving countries of North America and Europe is ageing, leading to a critical shortage of a specialized workforce essential to deal with the new diagnostic challenges. Unfortunately, this vicious circle is not yet apparent to all. The highly specialized field of parasitology is at a particular risk for such major crises in the near future. Heightened awareness of such risks is an essential step to start discussions and planning to mitigate these very real health threats.
{"title":"Parasitology of the twenty-first century: are we moving in the right direction?","authors":"Kinga Kowalewska-Grochowska, Romina Reyes, Pauline Tomlin","doi":"10.1099/jmm.0.002064","DOIUrl":"10.1099/jmm.0.002064","url":null,"abstract":"<p><p>For thousands of years, parasitic infections have represented a constant challenge to human health. Despite constant progress in science and medicine, the challenge has remained mostly unchanged over the years, partly due to the vast complexity of the host-parasite-environment relationships. Over the last century, our approaches to these challenges have evolved through considerable advances in science and technology, offering new and better solutions. Unfortunately, in the twenty-first century, this diagnostic evolution was suddenly confronted with a dramatic change of biological relationships, never witnessed in history before the uncontrolled expansion of the human population, globalization and hyperconnectivity technology have exerted a massive socioeconomic impact on individuals, communities and the environment, sending a ripple effect throughout the world of parasites. Urbanization, pollution and the unsustainable exploitation of natural resources have caused shifts in biomass and the fragmentation of habitats, leading to the movement of parasites into new hosts and territories. At the same time, changes in human population structure and distributions due to armed conflict and poverty created massive migration of entire nations and communities, resulting in the redistribution of parasitic diseases. To make the situation worse, the population of many receiving countries of North America and Europe is ageing, leading to a critical shortage of a specialized workforce essential to deal with the new diagnostic challenges. Unfortunately, this vicious circle is not yet apparent to all. The highly specialized field of parasitology is at a particular risk for such major crises in the near future. Heightened awareness of such risks is an essential step to start discussions and planning to mitigate these very real health threats.</p>","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12451759/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Leptospirosis is a re-emerging zoonosis caused by a diverse range of pathogenic Leptospira, which are divided into species, serogroups and serovars. Although advances in genomics have recently refined species classification, serotyping, which is based on the antigenic variability of lipopolysaccharides O-antigens, still relies heavily on traditional and labour-intensive methods. In addition, the molecular basis of serovar diversity is not fully understood, which poses challenges for rapid and accurate serovar and/or serogroup identification. However, identification of serovars remains crucial for epidemiological studies, surveillance, diagnostics, understanding host-pathogen interactions and vaccine development. In this review, we assess current techniques for Leptospira serovar and serogroup identification and explore emerging DNA-based methodologies for serovar and serogroup prediction.
{"title":"Shaping the future of <i>Leptospira</i> serotyping.","authors":"Alexandre Giraud-Gatineau, Kouessi Dagbo, Helena Pětrošová, Catherine Werts, Fréderic J Veyrier, Mathieu Picardeau","doi":"10.1099/jmm.0.002059","DOIUrl":"10.1099/jmm.0.002059","url":null,"abstract":"<p><p>Leptospirosis is a re-emerging zoonosis caused by a diverse range of pathogenic <i>Leptospira</i>, which are divided into species, serogroups and serovars. Although advances in genomics have recently refined species classification, serotyping, which is based on the antigenic variability of lipopolysaccharides O-antigens, still relies heavily on traditional and labour-intensive methods. In addition, the molecular basis of serovar diversity is not fully understood, which poses challenges for rapid and accurate serovar and/or serogroup identification. However, identification of serovars remains crucial for epidemiological studies, surveillance, diagnostics, understanding host-pathogen interactions and vaccine development. In this review, we assess current techniques for <i>Leptospira</i> serovar and serogroup identification and explore emerging DNA-based methodologies for serovar and serogroup prediction.</p>","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12451757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><p><b>Introduction.</b> This study centres on how coronavirus disease 2019 (COVID-19) disrupts the intestinal microbiota and amplifies systemic inflammation and evaluates ozone water enemas as a strategy to restore gut microbial balance and activate the SIRT1 (silent information regulator of transcription 1)-Nrf2 (nuclear factor erythroid 2-related factor 2)/HO-1 (heme oxygenase-1) pathway for alleviating post-viral sequelae. Our findings demonstrate that ozone water intervention markedly improves the intestinal microenvironment in mice receiving COVID-19 patient-derived microbiota and attenuates systemic inflammation, offering a viable adjunctive approach for COVID-19 management.<b>Hypothesis.</b> Despite significant progress in reducing the incidence of COVID-19, its long-term consequences, including hepatic dysfunction, pulmonary injury and gut microbiota dysbiosis, remain challenging. While ozonated water enema therapy has shown efficacy in alleviating inflammation and neutralizing oxidative stress, the precise mechanisms by which ozonated water attenuates COVID-19 progression are not fully understood. We hypothesized that ozonated water enemas could enrich gut microbiota composition in COVID-19 patients, thereby optimizing the gut environment following faecal transplantation in a murine model.<b>Aim.</b> The overarching aim of this investigation was to ascertain whether ozonated water enemas could exert a salutogenic effect on the gut microbiota in a mouse model, as well as on the holistic gut and systemic health of critically ill COVID-19 patients subsequent to faecal transplantation.<b>Methodology.</b> The entire experiment was conducted over a 14-day period. WT mice were randomly allocated into three groups: Sham, FMT (faecal microbiota transplantation) and FMT+O<sub>3</sub> (FMT with ozonewater enema treatment). Mid-stage faecal specimens were collected from 21 severe COVID-19 patients and randomly divided into seven subgroups (three specimens per subgroup). These specimens were transplanted into the WT mice of the FMT and FMT+O<sub>3</sub> groups via faecal gavage on days 1 through 7. The healthy control group (Sham) received oral administration of ddH₂O instead. Starting on day 8 post-transplantation, the FMT+O<sub>3</sub> group underwent ozone water enema treatment for seven consecutive days. During this treatment period, assessments were performed to evaluate intestinal barrier function, inflammatory changes and alterations in gut microbiota. Additionally, improvements in intestinal, hepatic, pulmonary and systemic lesions were examined.<b>Results.</b> Our findings indicate that ozonated water enemas modulate the SIRT1-Nrf2/HO-1 pathway, significantly enhancing the intestinal environment in mice that received FMT from COVID-19 patients. This intervention increased microbiota populations, strengthened intestinal barrier integrity and reduced intestinal and systemic inflammatory responses.<b>Conclusion.</b> The results highlight the
{"title":"Ozone water enema activates SIRT1-Nrf2/HO-1 pathway to ameliorate gut dysbiosis in mice receiving COVID-19 patient-derived faecal microbiota.","authors":"Zehua Su, Jiaqi Lin, Xuejiao Zeng, Xin Li, Qianhao Hou, Qing Wang, Chunzheng Liu, Jiawen Qin, Yuling Li, Jinyuan Zhang, Xiangrui Wang, Shuwen Qian, Lijun Liao","doi":"10.1099/jmm.0.002038","DOIUrl":"10.1099/jmm.0.002038","url":null,"abstract":"<p><p><b>Introduction.</b> This study centres on how coronavirus disease 2019 (COVID-19) disrupts the intestinal microbiota and amplifies systemic inflammation and evaluates ozone water enemas as a strategy to restore gut microbial balance and activate the SIRT1 (silent information regulator of transcription 1)-Nrf2 (nuclear factor erythroid 2-related factor 2)/HO-1 (heme oxygenase-1) pathway for alleviating post-viral sequelae. Our findings demonstrate that ozone water intervention markedly improves the intestinal microenvironment in mice receiving COVID-19 patient-derived microbiota and attenuates systemic inflammation, offering a viable adjunctive approach for COVID-19 management.<b>Hypothesis.</b> Despite significant progress in reducing the incidence of COVID-19, its long-term consequences, including hepatic dysfunction, pulmonary injury and gut microbiota dysbiosis, remain challenging. While ozonated water enema therapy has shown efficacy in alleviating inflammation and neutralizing oxidative stress, the precise mechanisms by which ozonated water attenuates COVID-19 progression are not fully understood. We hypothesized that ozonated water enemas could enrich gut microbiota composition in COVID-19 patients, thereby optimizing the gut environment following faecal transplantation in a murine model.<b>Aim.</b> The overarching aim of this investigation was to ascertain whether ozonated water enemas could exert a salutogenic effect on the gut microbiota in a mouse model, as well as on the holistic gut and systemic health of critically ill COVID-19 patients subsequent to faecal transplantation.<b>Methodology.</b> The entire experiment was conducted over a 14-day period. WT mice were randomly allocated into three groups: Sham, FMT (faecal microbiota transplantation) and FMT+O<sub>3</sub> (FMT with ozonewater enema treatment). Mid-stage faecal specimens were collected from 21 severe COVID-19 patients and randomly divided into seven subgroups (three specimens per subgroup). These specimens were transplanted into the WT mice of the FMT and FMT+O<sub>3</sub> groups via faecal gavage on days 1 through 7. The healthy control group (Sham) received oral administration of ddH₂O instead. Starting on day 8 post-transplantation, the FMT+O<sub>3</sub> group underwent ozone water enema treatment for seven consecutive days. During this treatment period, assessments were performed to evaluate intestinal barrier function, inflammatory changes and alterations in gut microbiota. Additionally, improvements in intestinal, hepatic, pulmonary and systemic lesions were examined.<b>Results.</b> Our findings indicate that ozonated water enemas modulate the SIRT1-Nrf2/HO-1 pathway, significantly enhancing the intestinal environment in mice that received FMT from COVID-19 patients. This intervention increased microbiota populations, strengthened intestinal barrier integrity and reduced intestinal and systemic inflammatory responses.<b>Conclusion.</b> The results highlight the","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444790/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145076882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sedreh Nassirnia, Valentin Scherz, Gilbert Greub, Giorgia Caruana, Patrick Taffé, Katia Jaton, Sebastien Papis, Klara M Posfay-Barbe, Anne Mornand, Isabelle Rochat-Guignard, Claire Bertelli, Sandra A Asner
Introduction. Sputum is the most used sample type to monitor the lower respiratory tract microbiota in cystic fibrosis (CF), but young patients often cannot expectorate.Hypothesis. We hypothesized that throat swabs could reflect lower airway colonization and assessed the concordance of bacterial community composition between paired sputum and throat swab samples from children with CF.Aim. We aimed to compare bacterial community diversity and composition between sputum and throat swabs in the full cohort and in patients with paired samples from the same visit.Methodology. The prospective longitudinal multicentre MUCOVIB cohort included 379 samples from 61 CF children. Using V3-V4 16S rRNA amplicon metagenomics, we compared bacterial community diversity and composition between sputum and throat swabs in the full cohort and in 11 patients with paired samples from the same visit.Results. Sputum and throat swabs exhibited similar bacterial diversity, regardless of the exacerbation status, and presented a substantial agreement for detecting pathogens (Cohen's kappa: 0.6). Differences in bacterial abundance were observed (P=0.001), but not presence/absence (P=0.098). Community typing revealed three distinct community types, with 86% of paired samples falling into the same cluster, highlighting the homogeneity between sputum and throat swab microbiota. Network analysis demonstrated slight, non-random similarities in microbial interactions between sample types (adjusted Rand index=0.08 and 0.10). The average beta-diversity distances between samples collected from the same visit were shorter (0.505±0.056 95% confidence interval), compared with sputum (0.695±0.017) or throat swab (0.704±0.045) from the same patient collected during different visits.Conclusion. Throat swabs can provide representative information on lower respiratory microbiota. Clinicians should collect throat swabs rather than relying on sputum samples from previous visits to guide antibiotic prescriptions in CF children unable to expectorate.
{"title":"Concordance between upper and lower airway microbiota in children with cystic fibrosis.","authors":"Sedreh Nassirnia, Valentin Scherz, Gilbert Greub, Giorgia Caruana, Patrick Taffé, Katia Jaton, Sebastien Papis, Klara M Posfay-Barbe, Anne Mornand, Isabelle Rochat-Guignard, Claire Bertelli, Sandra A Asner","doi":"10.1099/jmm.0.002079","DOIUrl":"10.1099/jmm.0.002079","url":null,"abstract":"<p><p><b>Introduction.</b> Sputum is the most used sample type to monitor the lower respiratory tract microbiota in cystic fibrosis (CF), but young patients often cannot expectorate.<b>Hypothesis.</b> We hypothesized that throat swabs could reflect lower airway colonization and assessed the concordance of bacterial community composition between paired sputum and throat swab samples from children with CF.<b>Aim.</b> We aimed to compare bacterial community diversity and composition between sputum and throat swabs in the full cohort and in patients with paired samples from the same visit.<b>Methodology.</b> The prospective longitudinal multicentre MUCOVIB cohort included 379 samples from 61 CF children. Using V3-V4 16S rRNA amplicon metagenomics, we compared bacterial community diversity and composition between sputum and throat swabs in the full cohort and in 11 patients with paired samples from the same visit.<b>Results.</b> Sputum and throat swabs exhibited similar bacterial diversity, regardless of the exacerbation status, and presented a substantial agreement for detecting pathogens (Cohen's kappa: 0.6). Differences in bacterial abundance were observed (<i>P</i>=0.001), but not presence/absence (<i>P</i>=0.098). Community typing revealed three distinct community types, with 86% of paired samples falling into the same cluster, highlighting the homogeneity between sputum and throat swab microbiota. Network analysis demonstrated slight, non-random similarities in microbial interactions between sample types (adjusted Rand index=0.08 and 0.10). The average beta-diversity distances between samples collected from the same visit were shorter (0.505±0.056 95% confidence interval), compared with sputum (0.695±0.017) or throat swab (0.704±0.045) from the same patient collected during different visits.<b>Conclusion.</b> Throat swabs can provide representative information on lower respiratory microbiota. Clinicians should collect throat swabs rather than relying on sputum samples from previous visits to guide antibiotic prescriptions in CF children unable to expectorate.</p>","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 9","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145202476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kyra P Watral, David A Kaufman, Timothy J Boly, Jennifer R Bermick
Introduction. Infection is a leading cause of mortality during the first year of life, with the neonatal period being particularly high risk. It is critical to identify non-antibiotic approaches to improve neonatal infection outcomes due to the non-specific clinical signs of neonatal infection and negative consequences of early-life antibiotic exposure. Lactoferrin is a protein found in all mammalian milk that has a variety of antimicrobial properties. Clinical trials have shown that lactoferrin supplementation during the neonatal period decreases rates of sepsis.Knowledge Gap. It remains unclear if there is an optimal lactoferrin preparation for human neonates.Aim. Compare bacterial growth inhibition capabilities between different commercially available bovine-derived lactoferrin (bLF) preparations.Methodology. This study uses a broth microdilution in vitro assay to directly compare the antibacterial effects and shelf stability of different bLF preparations against three common neonatal pathogens: Escherichia coli, Klebsiella pneumoniae and Streptococcus pneumoniae.Results. Bacterial growth inhibition differed significantly between bLF manufacturers and between different bLF lots/batches from the same manufacturer. Approximately half of the bLF products demonstrated decreased bacterial growth inhibition capabilities within 7-14 days after solubilization.Conclusion. These findings may help select optimal bLF products for clinical use in the neonatal population, but additional in vivo studies are needed to confirm our in vitro findings.
{"title":"Growth inhibition of common neonatal pathogens differs between bovine lactoferrin products.","authors":"Kyra P Watral, David A Kaufman, Timothy J Boly, Jennifer R Bermick","doi":"10.1099/jmm.0.002056","DOIUrl":"https://doi.org/10.1099/jmm.0.002056","url":null,"abstract":"<p><p><b>Introduction.</b> Infection is a leading cause of mortality during the first year of life, with the neonatal period being particularly high risk. It is critical to identify non-antibiotic approaches to improve neonatal infection outcomes due to the non-specific clinical signs of neonatal infection and negative consequences of early-life antibiotic exposure. Lactoferrin is a protein found in all mammalian milk that has a variety of antimicrobial properties. Clinical trials have shown that lactoferrin supplementation during the neonatal period decreases rates of sepsis.<b>Knowledge Gap.</b> It remains unclear if there is an optimal lactoferrin preparation for human neonates.<b>Aim.</b> Compare bacterial growth inhibition capabilities between different commercially available bovine-derived lactoferrin (bLF) preparations.<b>Methodology.</b> This study uses a broth microdilution <i>in vitro</i> assay to directly compare the antibacterial effects and shelf stability of different bLF preparations against three common neonatal pathogens: <i>Escherichia coli</i>, <i>Klebsiella pneumoniae</i> and <i>Streptococcus pneumoniae</i>.<b>Results.</b> Bacterial growth inhibition differed significantly between bLF manufacturers and between different bLF lots/batches from the same manufacturer. Approximately half of the bLF products demonstrated decreased bacterial growth inhibition capabilities within 7-14 days after solubilization.<b>Conclusion.</b> These findings may help select optimal bLF products for clinical use in the neonatal population, but additional <i>in vivo</i> studies are needed to confirm our <i>in vitro</i> findings.</p>","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12396925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144984412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cecilia Sahl, Agnes Andersson, Natalie Larsson, Magnus Paulsson, Oonagh Shannon, Lisa I Påhlman
Background.Achromobacter xylosoxidans and Pseudomonas aeruginosa are two pathogens that cause persistent airway infections in individuals with cystic fibrosis (CF). The persistence of P. aeruginosa is partly due to a high capacity to form biofilms and the ability to exert antagonism against other bacteria. Loss of microbial diversity in conjunction with chronic P. aeruginosa colonization is strongly correlated with low lung function in CF. A. xylosoxidans and P. aeruginosa are frequently co-isolated in CF airway cultures. This study aims to investigate the reciprocal effects on growth inhibition and biofilm formation between P. aeruginosa and A. xylosoxidans in vitro.Method. Six isolates of A. xylosoxidans, isolated from three CF patients in early and late stages of a chronic infection, were cultured together with a CF isolate of P. aeruginosa. Biofilm formation was assessed using a microtiter assay and crystal violet staining. Quantitative PCR was used to quantify species proportions in biofilms. Growth curves were performed to compare planktonic growth rates.Results. Three A. xylosoxidans isolates, all of which were from early-stage infections, inhibited biofilm formation of P. aeruginosa. The inhibition was concentration-dependent and required the interaction of live bacteria during the early stages of biofilm development. The inhibitory effect was not caused by nutrient depletion of the planktonic cells. The selected A. xylosoxidans isolate had a stronger capacity to adhere to plastic surfaces compared to the P. aeruginosa isolate.Conclusions. A. xylosoxidans can inhibit P. aeruginosa biofilm formation in vitro. The observed effect requires active interactions between live cells during the attachment stage of biofilm formation, possibly due to differences in adhesion capacity.
{"title":"The cystic fibrosis pathogen <i>Achromobacter xylosoxidans</i> inhibits biofilm formation of <i>Pseudomonas aeruginosa</i>.","authors":"Cecilia Sahl, Agnes Andersson, Natalie Larsson, Magnus Paulsson, Oonagh Shannon, Lisa I Påhlman","doi":"10.1099/jmm.0.002051","DOIUrl":"10.1099/jmm.0.002051","url":null,"abstract":"<p><p><b>Background.</b> <i>Achromobacter xylosoxidans</i> and <i>Pseudomonas aeruginosa</i> are two pathogens that cause persistent airway infections in individuals with cystic fibrosis (CF). The persistence of <i>P. aeruginosa</i> is partly due to a high capacity to form biofilms and the ability to exert antagonism against other bacteria. Loss of microbial diversity in conjunction with chronic <i>P. aeruginosa</i> colonization is strongly correlated with low lung function in CF. <i>A. xylosoxidans</i> and <i>P. aeruginosa</i> are frequently co-isolated in CF airway cultures. This study aims to investigate the reciprocal effects on growth inhibition and biofilm formation between <i>P. aeruginosa</i> and <i>A. xylosoxidans in vitro</i>.<b>Method.</b> Six isolates of <i>A. xylosoxidans</i>, isolated from three CF patients in early and late stages of a chronic infection, were cultured together with a CF isolate of <i>P. aeruginosa</i>. Biofilm formation was assessed using a microtiter assay and crystal violet staining. Quantitative PCR was used to quantify species proportions in biofilms. Growth curves were performed to compare planktonic growth rates.<b>Results.</b> Three <i>A. xylosoxidans</i> isolates, all of which were from early-stage infections, inhibited biofilm formation of <i>P. aeruginosa</i>. The inhibition was concentration-dependent and required the interaction of live bacteria during the early stages of biofilm development. The inhibitory effect was not caused by nutrient depletion of the planktonic cells. The selected <i>A. xylosoxidans</i> isolate had a stronger capacity to adhere to plastic surfaces compared to the <i>P. aeruginosa</i> isolate.<b>Conclusions</b> <i>. A. xylosoxidans</i> can inhibit <i>P. aeruginosa</i> biofilm formation <i>in vitro</i>. The observed effect requires active interactions between live cells during the attachment stage of biofilm formation, possibly due to differences in adhesion capacity.</p>","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12316436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144765900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Erratum: The Ebola virus - going beyond the bleeding edge.","authors":"Saadiya K Umar, Mathew A Diggle","doi":"10.1099/jmm.0.002052","DOIUrl":"10.1099/jmm.0.002052","url":null,"abstract":"","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144877643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jennifer M Bosquez, Craig T Parker, Ben Pascoe, Kerry K Cooper
Introduction. Campylobacter jejuni is the leading cause of bacterial gastroenteritis worldwide. Infections with C. jejuni can result in two different diarrhoeal manifestations in humans: watery diarrhoea or bloody/inflammatory diarrhoea.Hypothesis/Gap Statement. Currently, little is known about C. jejuni and/or host factors associated with the elicitation of these two distinct diarrhoeal manifestations. We hypothesize that these factors may include growth and metabolic trait differences between C. jejuni strains associated with watery diarrhoea and bloody/inflammatory diarrhoea.Aim. Using C. jejuni strains with a defined diarrhoeal manifestation in the neonatal piglet model, we aimed to assess differences in temperature-dependent growth rates, motility, biofilm production and carbon utilization between diarrhoeal manifestation groups.Methodology. Strains were initially assessed for 192 different carbon sources using phenotypic microarrays followed by specific carbon utilization, growth, motility and biofilm assays at 37 and/or 42 °C.Results. We found that at 37 °C, watery diarrhoea-associated C. jejuni strains grew significantly faster compared with bloody/inflammatory diarrhoea-associated C. jejuni strains. However, there was no significant growth difference at 42 °C between the groups, due to bloody/inflammatory diarrhoea-associated strains growing faster at 42 °C compared with 37 °C. Additionally, at 37 °C, we found that l-fucose utilization was significantly higher among watery diarrhoea-associated strains, while l-glutamine utilization was significantly higher among bloody/inflammatory diarrhoea-associated strains.Conclusion. The results indicate there are distinct metabolic adaptations between watery and/or bloody/inflammatory diarrhoea-associated C. jejuni strains particularly at 37 °C, which may be one of the factors associated with differing diarrhoeal manifestations.
{"title":"Growth rates and metabolic traits differ by diarrhoeal manifestation in <i>Campylobacter jejuni</i> strains.","authors":"Jennifer M Bosquez, Craig T Parker, Ben Pascoe, Kerry K Cooper","doi":"10.1099/jmm.0.002053","DOIUrl":"10.1099/jmm.0.002053","url":null,"abstract":"<p><p><b>Introduction</b> <i>. Campylobacter jejuni</i> is the leading cause of bacterial gastroenteritis worldwide. Infections with <i>C. jejuni</i> can result in two different diarrhoeal manifestations in humans: watery diarrhoea or bloody/inflammatory diarrhoea.<b>Hypothesis/Gap Statement.</b> Currently, little is known about <i>C. jejuni</i> and/or host factors associated with the elicitation of these two distinct diarrhoeal manifestations. We hypothesize that these factors may include growth and metabolic trait differences between <i>C. jejuni</i> strains associated with watery diarrhoea and bloody/inflammatory diarrhoea.<b>Aim.</b> Using <i>C. jejuni</i> strains with a defined diarrhoeal manifestation in the neonatal piglet model, we aimed to assess differences in temperature-dependent growth rates, motility, biofilm production and carbon utilization between diarrhoeal manifestation groups.<b>Methodology</b>. Strains were initially assessed for 192 different carbon sources using phenotypic microarrays followed by specific carbon utilization, growth, motility and biofilm assays at 37 and/or 42 °C.<b>Results</b>. We found that at 37 °C, watery diarrhoea-associated <i>C. jejuni</i> strains grew significantly faster compared with bloody/inflammatory diarrhoea-associated <i>C. jejuni</i> strains. However, there was no significant growth difference at 42 °C between the groups, due to bloody/inflammatory diarrhoea-associated strains growing faster at 42 °C compared with 37 °C. Additionally, at 37 °C, we found that l-fucose utilization was significantly higher among watery diarrhoea-associated strains, while l-glutamine utilization was significantly higher among bloody/inflammatory diarrhoea-associated strains.<b>Conclusion</b>. The results indicate there are distinct metabolic adaptations between watery and/or bloody/inflammatory diarrhoea-associated <i>C. jejuni</i> strains particularly at 37 °C, which may be one of the factors associated with differing diarrhoeal manifestations.</p>","PeriodicalId":94093,"journal":{"name":"Journal of medical microbiology","volume":"74 8","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12396926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144984332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}