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The goal of the current study is to better understand how bacteria may adapt to survive under adverse environmental conditions by altering and improving their phenotypes. In this study, we report the consequences of phenotypic variation in Paenibacillus polymyxa E681 (E681), a plant growth-promoting rhizobacterium (PGPR), isolated from winter barley root that has a variety of advantageous effects on crop plants. In our previous study, two different types of bacterial cells in E681 were distinguished. We used the term F-type for the variant that doesn't produce endospores and B-type for the endospore-producing wild type. Under the circumstances of our experiment, the cucumber rhizosphere soil and the surface of the seeds produced phenotypic variance. On tryptic soy agar (TSA) plates, the B-type spontaneously converted into the F-type, but the reverse was not reversible. Intriguingly, the plant growth promotion test displayed that cucumber seedlings treated with F-type cells had characteristics resembling those of the untreated control. Whereas, growth promotion of cucumber seedlings treated with B-type depends on temperature conditions. In particular, an increased growth promotion was observed at a low temperature of 20°C. The phenotypic change from B-type to F-type did not occur at 20°C for 6 days in the growth curve analysis of E681, but it did occur on the fourth and second days at 30 and 37°C, respectively. Therefore, before using PGPR strains as a bacterial inoculant for sustainable agriculture, it is imperative to resolve phenotypic variance in these strains.
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Inflammatory bowel diseases (IBD) are often associated with dysregulated gut microbiota and excessive inflammatory microenvironment. Probiotic therapy combined with inflammation management is a promising approach to alleviate IBD, but the efficacy is hindered by the inferior colonization of probiotics in mucus-depleted inflammatory bowel segments. Here, we present modified montmorillonite armed probiotic Escherichia coli Nissle 1917 (MMT-Fe@EcN) with enhanced intestinal colonization and hydrogen sulfide (H2S) scavenging for synergistic alleviation of IBD. The montmorillonite layer that can protect EcN against environmental assaults in oral delivery and improve on-site colonization of EcN in the mucus-depleted intestinal segment due to its strong adhesive capability and electronegativity, with a 22.6-fold increase in colonization efficiency compared to EcN. Meanwhile, MMT-Fe@EcN can manage inflammation by scavenging H2S, which allows for enhancing probiotic viability and colonization for restoring the gut microbiota. As a result, MMT-Fe@EcN exhibits extraordinary therapeutic effects in the dextran sulfate sodium-induced mouse colitis models, including alleviating intestinal inflammation and restoring disrupted intestinal barrier function, and gut microbiota. These findings provide a promising strategy for clinical IBD treatment and potentially other mucus-depletion-related diseases.
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As there was no maximum permissible limit prescription for aflatoxin B1 (AFB1) in Ethiopia, this study has been conducted to generate data on AFB1 levels in Ethiopian groundnut accessions/landraces. Besides, an attempt was made to find out if there is any relationship between AFB1 and other parameters such as altitude of cultivation, individual seed weight, kernel colonization by Aspergillus flavus, total carbohydrates, protein and total free amino acids. Out of the 28 accessions studied, merely six accessions registered ≤2 ppb AFB1 and thus, they comply with maximum permissible limit set by European Union. Altitude of cultivation had no relationship with AFB1 levels. Interestingly, total carbohydrates in the seeds as well as kernel colonization by A. flavus showed statistically significant (p < 0.01) positive relationships with AFB1 levels. It is suggested to use kernel colonization measurement as an alternative to the expensive ELISA based AFB1 measurement. Besides, suitable pre- and post-harvest aflatoxin management strategies should be developed to alleviate the AFB1 levels in Ethiopian groundnut.
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The Advancing Climate Justice in Climate Adaptation Strategies for New York City (Equity) chapter of NPCC4 builds on the findings and recommendations from NPCC3 to identify additional metrics and adaptation efforts that can advance climate justice. First, the chapter assesses the efforts of the City to incorporate equity into climate adaptation efforts since NPCC3 and describes how the communities profiled in NPCC3 have implemented and evolved their approaches to addressing the intersecting climate, environmental, and social stressors that they continue to face. Second, it adds to the historical context of climate inequity by linking the bioregion's history of colonization, land dispossession, and slavery building on emerging evidence demonstrating how historical and contemporary land use patterns and decisions shape present and future climate risks and social vulnerability, including climate displacement. Third, it recommends a NYC-focused metric to identify areas of the city that are most vulnerable to the intersection of climate hazards, social vulnerability, and displacement. Finally, it highlights approaches to more equitable and just climate adaptation drawn from local, national, and international examples. As such, the chapter offers best practices that prioritize community-driven climate resilience approaches that are integrated, more equitable, and racially just.
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Helicobacter pylori (H. pylori) infection is the primary risk factor for the progress of gastric diseases. The persistent stomach colonization of H. pylori is closely associated with the development of gastritis and malignancies. Although the involvement of progranulin (PGRN) in various cancer types has been well-documented, its functional role and underlying mechanisms in gastric cancer (GC) associated with H. pylori infection remain largely unknown. This report demonstrated that PGRN was up-regulated in GC and associated with poor prognosis, as determined through local and public database analysis. Additionally, H. pylori induced the up-regulation of PGRN in gastric epithelial cells both in vitro and in vivo. Functional studies have shown that PGRN promoted the intracellular colonization of H. pylori. Mechanistically, H. pylori infection induced autophagy, while PGRN inhibited autophagy to promote the intracellular colonization of H. pylori. Furthermore, PGRN suppressed H. pylori-induced autophagy by down-regulating decorin (DCN) through the mTOR pathway. In general, PGRN inhibited autophagy to facilitate intracellular colonization of H. pylori via the PGRN/mTOR/DCN axis. This study provides new insights into the molecular mechanisms underlying the progression of gastric diseases, suggesting PGRN as a potential therapeutic target and prognostic predictor for these disorders.
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Autofagia , Células Epiteliais , Mucosa Gástrica , Infecções por Helicobacter , Helicobacter pylori , Progranulinas , Neoplasias Gástricas , Serina-Treonina Quinases TOR , Progranulinas/metabolismo , Serina-Treonina Quinases TOR/metabolismo , Humanos , Células Epiteliais/microbiologia , Células Epiteliais/metabolismo , Infecções por Helicobacter/microbiologia , Infecções por Helicobacter/metabolismo , Animais , Neoplasias Gástricas/microbiologia , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Mucosa Gástrica/microbiologia , Mucosa Gástrica/metabolismo , Camundongos , Transdução de SinaisRESUMO
OBJECTIVES: To investigate the clinical characteristics of Ureaplasma urealyticum (UU) infection and colonization in extremely preterm infants and its impact on the incidence of bronchopulmonary dysplasia (BPD). METHODS: A retrospective analysis was conducted on 258 extremely preterm infants who were admitted to the Department of Neonatology, Shenzhen Maternity and Child Healthcare Hospital, from September 2018 to September 2022. According to the results of UU nucleic acid testing and the evaluation criteria for UU infection and colonization, the subjects were divided into three groups: UU-negative group (155 infants), UU infection group (70 infants), and UU colonization group (33 infants). The three groups were compared in terms of general information and primary and secondary clinical outcomes. RESULTS: Compared with the UU-negative group, the UU infection group had significant increases in the incidence rate of BPD, total oxygen supply time, and the length of hospital stay (P<0.05), while there were no significant differences in the incidence rates of BPD and moderate/severe BPD between the UU colonization group and the UU-negative group (P>0.05). CONCLUSIONS: The impact of UU on the incidence of BPD in extremely preterm infants is associated with the pathogenic state of UU (i.e., infection or colonization), and there are significant increases in the incidence rate of BPD, total oxygen supply time, and the length of hospital stay in extremely preterm infants with UU infection. UU colonization is not associated with the incidence of BPD and moderate/severe BPD in extremely preterm infants.
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Displasia Broncopulmonar , Lactente Extremamente Prematuro , Infecções por Ureaplasma , Ureaplasma urealyticum , Humanos , Infecções por Ureaplasma/epidemiologia , Infecções por Ureaplasma/complicações , Ureaplasma urealyticum/isolamento & purificação , Recém-Nascido , Estudos Retrospectivos , Feminino , Masculino , Displasia Broncopulmonar/epidemiologia , Displasia Broncopulmonar/microbiologia , Displasia Broncopulmonar/etiologia , Tempo de InternaçãoRESUMO
BACKGROUND: Staphylococcus aureus (S. aureus) often colonizes the human skin, upper respiratory and genital tracts. In the female genital tract, it can be passed on to the newborn during vaginal delivery leading to either ordinary colonization, or neonatal infections notably umbilical stump sepsis, scalded skin syndrome, arthritis, or bacteraemia/sepsis. These infections are mediated by staphylococcal virulence factors such as (i) Staphylococcal Enterotoxins A, B, C, D, and E encoded by the sea, seb, sec, sed, see genes, (ii) Exfoliative Toxins A and B encoded by the eta and etb genes, (iii) Toxic Shock Syndrome Toxin 1 (TSST-1) encoded by the tst gene, (iv) Panton-Valentine Leukocidin (PVL) encoded by the pvl gene, and (v) Hemolysins alpha and delta encoded by the hla and hld genes, respectively. We determined the prevalence of S. aureus possessing one or more virulence factor genes and of methicillin resistant Staphylococcus aureus (MRSA) in this population. METHODS: This was a cross-sectional study, which used 85 S. aureus isolates from the Chlorohexidine (CHX) clinical trial study in Uganda. The isolates had been obtained by culturing vaginal swabs (VS) from 1472 women in labour, frozen at minus 80oC, then thawed, sub-cultured, and tested for the selected virulence genes sea, seb, sec, sed, see eta, etb, tst, pvl, hla and hld, and for the methicillin resistance determining gene (mecA). Data were analyzed using SPSS version 20. RESULTS: Of the 85 S. aureus isolates 13 (15.3%) were positive for one or more virulence factor genes, as follows: pvl 9/85 (10.6%), hld 5/85 (5.9%), sea 1/85 (1.2%) and seb genes 1/85 (1.2%). The other virulence genes (sec, sed, see, eta, etb, hla and tst) were not detected in any of the isolates. MRSA was detected in 55.3% (47/85) of the isolates, but only two of these carried the pvl virulence gene. CONCLUSION: This study demonstrated that 15% of the S. aureus colonizing the female lower genital tract of mothers in labour in central Uganda carried one or more virulence genes, mostly pvl, indicating potential for newborn infection with S. aureus acquired in the maternal birth canal. More than half of the isolates were MRSA.
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Staphylococcus aureus Resistente à Meticilina , Infecções Estafilocócicas , Vagina , Fatores de Virulência , Humanos , Feminino , Uganda/epidemiologia , Fatores de Virulência/genética , Infecções Estafilocócicas/microbiologia , Infecções Estafilocócicas/epidemiologia , Vagina/microbiologia , Gravidez , Staphylococcus aureus Resistente à Meticilina/genética , Staphylococcus aureus Resistente à Meticilina/patogenicidade , Staphylococcus aureus Resistente à Meticilina/isolamento & purificação , Estudos Transversais , Adulto , Staphylococcus aureus/genética , Staphylococcus aureus/patogenicidade , Staphylococcus aureus/isolamento & purificação , Staphylococcus aureus/efeitos dos fármacos , Prevalência , Adulto Jovem , Trabalho de Parto , Portador Sadio/microbiologia , Portador Sadio/epidemiologiaRESUMO
The gut microbiota is a complex and diverse community of microorganisms that colonizes the human gastrointestinal tract and influences various aspects of human health. These microbes are closely related to enteric infections. As a foreign entity for the host, commensal microbiota is restricted and regulated by the barrier and immune system in the gut and contributes to gut homeostasis. Commensals also effectively resist the colonization of pathogens and the overgrowth of indigenous pathobionts by utilizing a variety of mechanisms, while pathogens have developed strategies to subvert colonization resistance. Dysbiosis of the microbial community can lead to enteric infections. The microbiota acts as a pivotal mediator in establishing a harmonious mutualistic symbiosis with the host and shielding the host against pathogens. This review aims to provide a comprehensive overview of the mechanisms underlying host-microbiome and microbiome-pathogen interactions, highlighting the multi-faceted roles of the gut microbiota in preventing enteric infections. We also discuss the applications of manipulating the microbiota to treat infectious diseases in the gut.
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Biotic homogenization is a process whereby species assemblages become more similar through time. The standard way of identifying the process of biotic homogenization is to look for decreases in spatial beta-diversity. However, using a single assemblage-level metric to assess homogenization can mask important changes in the occupancy patterns of individual species. Here, we analysed changes in the spatial beta-diversity patterns (i.e. biotic heterogenization or homogenization) of British bird assemblages within 30 km × 30 km regions between two periods (1988-1991 and 2008-2011). We partitioned the change in spatial beta-diversity into extirpation and colonization-resultant change (i.e. change in spatial beta-diversity within each region resulting from both extirpation and colonization). We used measures of abiotic change in combination with Bayesian modelling to disentangle the drivers of biotic heterogenization and homogenization. We detected both heterogenization and homogenization across the two time periods and three measures of diversity (taxonomic, phylogenetic, and functional). In addition, both extirpation and colonization contributed to the observed changes, with heterogenization mainly driven by extirpation and homogenization by colonization. These assemblage-level changes were primarily due to shifting occupancy patterns of generalist species. Compared to habitat generalists, habitat specialists had significantly (i) higher average contributions to colonization-resultant change (indicating heterogenization within a region due to colonization) and (ii) lower average contributions to extirpation-resultant change (indicating homogenization from extirpation). Generalists showed the opposite pattern. Increased extirpation-resultant homogenization within regions was associated with increased urban land cover and decreased habitat diversity, precipitation, and temperature. Changes in extirpation-resultant heterogenization and colonization-resultant heterogenization were associated with differences in elevation between regions and changes in temperature and land cover. Many of the 'winners' (i.e. species that increased in occupancy) were species that had benefitted from conservation action (e.g. buzzard (Buteo buteo)). The 'losers' (i.e. those that decreased in occupancy) consisted primarily of previously common species, such as cuckoo (Cuculus canorus). Our results show that focusing purely on changes in spatial beta-diversity over time may obscure important information about how changes in the occupancy patterns of individual species contribute to homogenization and heterogenization.
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Candida auris is a pathogen of growing public health concern worldwide. However, risk factors contributing to C. auris infection in patients colonized with C. auris remain unclear. Understanding these risk factors is crucial to prevent colonization-to-infection transition and devise effective preventive strategies. This study aimed to investigate risk factors associated with C. auris infection compared to colonization. The study included 97 patients who acquired laboratory-confirmed C. auris in either matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry or VITEK 2 system from October 2019 to June 2023. Baseline demographics and known risk factors associated with C. auris infection were collected from electronic medical records. The infection group had C. auris from a sterile site, or non-sterile site with evidence of infection. The colonization group were followed up for a median of 30 days for any signs of infection. Associations between relevant variables and C. auris infection were assessed using multivariable logistic regression. The infection group (n=31) was more likely to be bedbound, with longer hospital stays and more arterial catheters. Chronic kidney disease (odds ratio [OR] 45.070), carriage of multidrug-resistant organisms (OR 64.612), and vasopressor use more than 20 days (OR 68.994) were associated with C. auris infection, after adjusting for sex, age, and prior colonization with C. auris. Chronic kidney disease, carriage of multidrug-resistant organisms, and prolonged vasopressor use emerged as significant risk factors for C. auris infection compared to colonization. They could be used to predict C. auris infection early in patients colonized with C. auris.
Identifying risk factors for Candida auris infection should be an essential component of care in patients colonized with C. auris. Chronic kidney disease, carriage of multidrug-resistant organisms, and prolonged vasopressor use emerged as significant risk factors for C. auris infection.
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Salmonella enterica serovar Typhimurium (S. Typhimurium) is a common foodborne enteric pathogen that infects humans or mammals and colonizes the intestinal tract primarily by invading the host following ingestion. Meanwhile, ClpV is a core secreted protein of the bacterial type VI secretion system (T6SS). Because elucidating ClpV's role in the pathogenesis of T6SS is pivotal for revealing the virulence mechanism of Salmonella, in our study, clpV gene deletion mutants were constructed using a λ-red-based recombination system, and the effect of clpV mutation on SL1344's pathogenicity was examined in terms of stress resistance, motility, cytokine secretion, gut microbiota, and a BALB/c mouse model. Among the results, ClpV affected SL1344's motility and was also involved in cell invasion, adhesion, and intracellular survival in the MDBK cell model but did not affect invasion or intracellular survival in the RAW264.7 cell model. Moreover, clpV gene deletion significantly reduced the transcription levels of GBP2b, IFNB1, IL-6, NLRP3, NOS2, and TNF-α proinflammatory factor levels but significantly increased transcription levels of IL-4 and IL-10 anti-inflammatory factors. Last, ClpV appeared to closely relate to the pathogenicity of S. Typhimurium in vivo, which can change the gut environment and cause dysbiosis of gut microbiota. Our findings elucidate the functions of ClpV in S. Typhimurium and illustrating interactions between T6SS and gut microbiota help to clarify the mechanisms of the pathogenesis of foodborne diseases.
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The intact immune system of mice exhibits resistance to colonization by exogenous microorganisms, but the gut microbiota profiles of the humanized mice and the patterns of human fecal microbiota colonization remain unexplored. Humanized NCG (huNCG) mice were constructed by injected CD34 +stem cells. 16S rRNA sequencing and fecal microbiota transplantation (FMT) technologies were used to detect the differences in microbiota and selective colonization ability for exogenous community colonization among three mice cohorts (C57BL/6J, NCG, and huNCG). Flow cytometry analysis showed that all huNCG mice had over 25% hCD45 +in peripheral blood. 16S rRNA gene sequence analysis showed that compared with NCG mice, the gut microbiota of huNCG mice were significantly altered. After FMT, the principal coordinates analysis (PCoA) showed that the gut microbial composition of huNCG mice (huNCG-D9) was similar to that of donors. The relative abundance of Firmicutes and Bacteroidetes were significantly increased in huNCG mice compared to NCG mice. Further comparison of ASV sequences revealed that Bacteroides plebeius, Bacteroides finegoldii, Escherichia fergusonii, Escherichia albertii, Klebsiella pneumoniae, and Klebsiella variicola exhibited higher abundance and stability in huNCG mice after FMT. Furthermore, PICRUSt2 analysis showed that huNCG mice had significantly enhanced metabolism and immunity. This study demonstrated that humanized mice are more conducive to colonization within the human gut microbiota, which provides a good method for studying the association between human diseases and microbiota.IMPORTANCEThe gut microbiota and biomarkers of humanized mice are systematically revealed for the first time. The finding that human fecal microbiota colonize humanized mice more stably provides new insights into the study of interactions between immune responses and gut microbiota.
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Group B Streptococcus (GBS) is a pathobiont responsible for invasive infections in neonates and the elderly. The transition from a commensal to an invasive pathogen relies on the timely regulation of virulence factors. In this study, we characterized the role of the SaeRS two-component system in GBS pathogenesis. Loss-of-function mutations in the SaeR response regulator decrease virulence in mouse models of invasive infection by hindering the ability of bacteria to persist at the inoculation site and to spread to distant organs. Transcriptome and in vivo analysis reveal a specialized regulatory system specifically activated during infection to control the expression of only two virulence factors: the PbsP adhesin and the BvaP secreted protein. The in vivo surge in SaeRS-regulated genes is complemented by fine-tuning mediated by the repressor of virulence CovRS system to establish a coordinated response. Constitutive activation of the SaeRS regulatory pathway increases PbsP-dependent adhesion and invasion of epithelial and endothelial barriers, though at the cost of reduced virulence. In conclusion, SaeRS is a dynamic, highly specialized regulatory system enabling GBS to express a restricted set of virulence factors that promote invasion of host barriers and allow these bacteria to persist inside the host during lethal infection. IMPORTANCE: Group B Streptococcus (or GBS) is a normal inhabitant of the human gastrointestinal and genital tracts that can also cause deadly infections in newborns and elderly people. The transition from a harmless commensal to a dangerous pathogen relies on the timely expression of bacterial molecules necessary for causing disease. In this study, we characterize the two-component system SaeRS as a key regulator of such virulence factors. Our analysis reveals a specialized regulatory system that is activated only during infection to dynamically adjust the production of two virulence factors involved in interactions with host cells. Overall, our findings highlight the critical role of SaeRS in GBS infections and suggest that targeting this system may be useful for developing new antibacterial drugs.
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The rhizosphere hosts complex and abundant microbiomes whose structure and composition are now well described by metagenomic studies. However, the dynamic mechanisms that enable micro-organisms to establish along a growing plant root are poorly characterized. Here, we studied how a motile bacterium utilizes the microhabitats created by soil pore space to establish in the proximity of plant roots. We have established a model system consisting of Bacillus subtilis and lettuce seedlings co-inoculated in transparent soil microcosms. We carried out live imaging experiments and developed image analysis pipelines to quantify the abundance of the bacterium as a function of time and position in the pore space. Results showed that the establishment of the bacterium in the rhizosphere follows a precise sequence of events where small islands of mobile bacteria were first seen forming near the root tip within the first 12-24 h of inoculation. Biofilm was then seen forming on the root epidermis at distances of about 700-1000 µm from the tip. Bacteria accumulated predominantly in confined pore spaces within 200 µm from the root or the surface of a particle. Using probabilistic models, we could map the complete sequence of events and propose a conceptual model of bacterial establishment in the pore space. This study therefore advances our understanding of the respective role of growth and mobility in the efficient colonization of bacteria in the rhizosphere.
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Bacillus subtilis , Lactuca , Raízes de Plantas , Rizosfera , Microbiologia do Solo , Bacillus subtilis/crescimento & desenvolvimento , Bacillus subtilis/metabolismo , Bacillus subtilis/fisiologia , Raízes de Plantas/microbiologia , Lactuca/microbiologia , Biofilmes/crescimento & desenvolvimento , Plântula/microbiologia , Plântula/crescimento & desenvolvimentoRESUMO
Older adults are more severely affected by infections caused by drug-resistant bacteria including Methicillin-Resistant Staphylococcus aureus (MRSA). We aimed to identify the MRSA colonization rates and associated factors among older adults aged more than 65-years-old. Among the 309 recruited, 152 (49.2â%) were males. Self-collected nasal swabs were used to isolate Staphylococcus aureus and MRSA with routine microbiological methods. Staphylococcus aureus was isolated from 36 (11.7â%) participants while 11 (3.6â%) were colonized with MRSA. We identified a significant association between the male sex and MRSA colonization (P=0.028, Chi-square test). However, this needs careful interpretation given the smaller number of outcome events. Other factors studied had no statistically significant association with MRSA colonization.
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Crown gall caused by Agrobacterium vitis (A. vitis) is one of the crucial issues restricting the to grape industry. In this study, Agrobacterium tumefaciens (Ag-8) was separated from the soil that could prevent the occurrence of grape crown gall. By the mutagenesis of Ag-8 transposon, the siaD gene deletion strain (ΔsiaD) showed significantly lower efficacy in grape and tomato plants for controlling grape crown gall, but the relevant mechanism was not clear. The biofilm formation and motility of ΔsiaD were significantly decreased, and the colonization ability of ΔsiaD in tomato roots was significantly reduced. RNA-seq analysis showed that the expression of nemR significantly reduced in the ΔsiaD and that the expression of nemR showed a high correlation with biofilm and motility. Further studies showed that the nemR gene deletion strain of Ag-8 (ΔnemR) showed significantly reduced motility, biofilm formation and control of grape crown gall compared to Ag-8, and the nemR gene complementary strain of Ag-8 (ΔnemR-comp) recovered to Ag-8 wild-type levels. The inoculation experiments of preventive, curative or simultaneous treatment further showed that the preferential inoculation with Ag-8 reduced the incidence of grape crown gall on tomato plants, and studies showed that the mutation of siaD affected the site competition between Ag-8 and A. vitis, and that the mutation of nemR was consistent with the previous results. This study provides a new strategy for the prevention and control of grape crown gall, which is of great significance to the grape industry to increase production and income.
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The intestinal retention and persistence of lactic acid bacteria (LAB) are strain-specific and affected by the bacterial surface components. However, the contribution of surface adhesins of LAB to intestinal adhesion and colonization remains unclear. In the present study, seven gene knockout mutants (genes related to surface adhesin synthesis) of Lacticaseibacillus paracasei S-NB were derived based on the Cre-lox-based recombination system. Results showed that the capsule layer appeared thinner in the cell wall of S-NBΔ7576, S-NBΔdlt, and S-NBΔsrtA mutants when compared with the wild-type (WT) S-NB. The effects of S-NB_7576 (wzd and wze genes, responsible for capsular polysaccharide synthesis) and S-NB_srtA (sortase A) mutation on the hydrophobicity, surface charge, and adhesion ability seem to vary strongly among seven mutant strains. In vivo colonization experiments showed a decrease in the colonization numbers of S-NBΔ7576 and S-NBΔsrtA in both the ileal and colon lumen from 2 to 8 days when compared with those of the WT S-NB. In conclusion, the synthesis of capsular polysaccharides and the transport of surface proteins are closely related to the adhesion ability and intestinal colonization of L. paracasei S-NB.
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Introduction: Although pets provide several social-emotional benefits for children, the risk of zoonosis must be considered among immunocompromised individuals. Methods: A prospective study was conducted in a tertiary hospital including immunocompromised patients younger than 20 years owning dogs and/or cats. Colonization and/or infection was evaluated by stool studies, bacterial swabs, blood polymerase chain reaction and serological studies in both patients and their pets, to evaluate potential zoonotic transmission occurrence. Results: We included 74 patients and their 92 pets (63 dogs, 29 cats). Up to 44.6% of the patients and 31.5% of the pets had at least 1 positive result. Up to 18.4% of pets' fecal samples were positive (bacteria, parasites or hepatitis E virus). No helminths were observed despite the high frequency of incorrect intestinal deworming practices. Among children, gastrointestinal microorganisms were found in 37.3% (primarily Clostridium difficile). Colonization by Staphylococcus pseudintermedius was common among pets (8.0%) but not among children (0.0%). No shared colonization between owners and pets was observed, except in one case (Blastocystis in both patient and pet feces). Among patients, serologies were positive for Strongyloides stercoralis (14.8%), Toxocara canis (3.2%), Bartonella henselae (19.1%) and hepatitis E (5.6%). Serology was positive for Rickettsia spp. (22.6%) and Babesia spp. (6.5%) in dogs and for Leishmania spp. (14.3%) and Toxoplasma spp. (14.3%) in cats. Conclusion: Exposure to zoonotic agents was detected in both patients and pets; however, shared colonization events were almost nonexistent. In our cohort, dogs and cats do not appear to entail high zoonosis transmission risk for immunocompromised patients.
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Background: The independent effects of extranasal-only carriage, carriage at multiple bodily sites, or the bacterial load of colonizing Staphylococcus aureus (SA) on the risk of developing SA surgical site infections and postoperative bloodstream infections (SA SSI/BSIs) are unclear. We aimed to quantify these effects in this large prospective cohort study. Methods: Surgical patients aged 18 years or older were screened for SA carriage in the nose, throat, or perineum within 30 days before surgery. SA carriers and noncarriers were enrolled in a prospective cohort study in a 2:1 ratio. Weighted multivariable Cox proportional hazard models were used to assess the independent associations between different measures of SA carriage and occurrence of SA SSI/BSI within 90 days after surgery. Results: We enrolled 5004 patients in the study cohort; 3369 (67.3%) were SA carriers. 100 SA SSI/BSI events occurred during follow-up, and 86 (86%) of these events occurred in SA carriers. The number of colonized bodily sites (adjusted hazard ratio [aHR], 3.5-8.5) and an increasing SA bacterial load in the nose (aHR, 1.8-3.4) were associated with increased SA SSI/BSI risk. However, extranasal-only carriage was not independently associated with SA SSI/BSI (aHR, 1.5; 95% CI, 0.9-2.5). Conclusions: Nasal SA carriage was associated with an increased risk of SA SSI/BSI and accounted for the majority of SA infections. Higher bacterial load, as well as SA colonization at multiple bodily sites, further increased this risk.
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The ability of bacteria to colonize diverse environmental niches is often linked to their competence in biofilm formation. It depends on the individual characteristics of a strain, the nature of the colonized surface (abiotic or biotic), or the availability of certain nutrients. Pseudomonas donghuensis P482 efficiently colonizes the rhizosphere of various plant hosts, but a connection between plant tissue colonization and the biofilm formation ability of this strain has not yet been established. We demonstrate here that the potential of P482 to form biofilms on abiotic surfaces and the structural characteristics of the biofilm are influenced by the carbon source available to the bacterium, with glycerol promoting the process. Also, the type of substratum, polystyrene or glass, impacts the ability of P482 to attach to the surface. Moreover, P482 mutants in genes associated with motility or chemotaxis, the synthesis of polysaccharides, and encoding proteases or regulatory factors, which affect biofilm formation on glass, were fully capable of colonizing the root tissue of both tomato and maize hosts. Investigating the role of cellular factors in biofilm formation using these plant-associated bacteria shows that the ability of bacteria to form biofilm on abiotic surfaces does not necessarily mirror its ability to colonize plant tissues. Our research provides a broader perspective on the adaptation of these bacteria to various environments.