Gut colonization by extended-spectrum ß-lactamase-producing Escherichia coli in dairy herd in Brazil: successful dissemination of a One Health clone.

The overuse of antimicrobials in livestock has contributed to the emergence and selection of clinically relevant multidrug-resistant bacteria. In Brazil, there is no conclusive information on the occurrence of Escherichia coli producing extended-spectrum ß-lactamase (ESßL) in cattle breeding, which is an important sector of agribusiness in this country. Herein, we investigated the presence of ESßL-positive E. coli strains in dairy cattle from a commercial farm with routine practice of therapeutic cephalosporins. Ninety-five rectal swab samples were collected from healthy dairy calves and cows under treatment with ceftiofur. Samples were screened for the presence of ESßL producers, and positive isolates were identified by MALDI-TOF, with subsequent screening for genes encoding ESßL variants by PCR and sequencing. The presence of ESßL (CTX-M-15)-producing E. coli was confirmed in calves, and lactating and dry cows. Most ESßL strains with genetic homologies ≥ 90% were grouped into two major PFGE clusters, confirming the suscessful expansion of clonally related lineages in animals from different lactating cycles, on the same property. Four representatives CTX-M-15-positive E. coli strains had their genomes sequenced, belonging to the clonal complex (CC) 23 and sequence type (ST) 90. A phylogeographical landscape of ST90 was performed revealing a global One Health linkage. Our results highlight the intestinal microbiota of dairy cattle as a hotspot for the spread of critical priority ESßL-producing E. coli and demonstrate that ST90 is an international clone genomically adapted to human and animal hosts, which deserve additional investigation to determine its zoonotic potential and impact in food chain.

The role of bacterial metabolism in human gut colonization.

Can we anticipate the emergence of the next pandemic antibiotic-resistant bacterial clone? Addressing such an ambitious question relies on our ability to comprehensively understand the ecological and epidemiological factors fostering the evolution of high-risk clones. Among these factors, the ability to persistently colonize and thrive in the human gut is crucial for most high-risk clones. Nonetheless, the causes and mechanisms facilitating successful gut colonization remain obscure. Here, we review recent evidence that suggests that bacterial metabolism plays a pivotal role in determining the ability of high-risk clones to colonize the human gut. Subsequently, we outline novel approaches that enable the exploration of microbial metabolism at an unprecedented scale and level of detail. A thorough understanding of the constraints and opportunities of bacterial metabolism in gut colonization will foster our ability to predict the emergence of high-risk clones and take appropriate containment strategies.

The CpxRA two-component system of adherent and invasive Escherichia coli contributes to epithelial cell invasion and early-stage intestinal fitness in a dysbiotic mouse model mediated by type 1 fimbriae expression.

Adherent and invasive Escherichia coli (AIEC) is a pathobiont that is involved in the onset and exacerbation of Crohn's disease. Although the inducible expression of virulence traits is a critical step for AIEC colonization in the host, the mechanism underlying AIEC colonization remains largely unclear. We here showed that the two-component signal transduction system CpxRA contributes to AIEC gut competitive colonization by activating type 1 fimbriae expression. CpxRA from AIEC strain LF82 functioned as a transcriptional regulator, as evidenced by our finding that an isogenic cpxRA mutant exhibits reduced expression of cpxP, a known regulon gene. Transcription levels of cpxP in LF82 increased in response to envelope stress, such as exposure to antimicrobials compromising the bacterial membrane, whereas the cpxRA mutant did not exhibit this response. Furthermore, we found that the cpxRA mutant exhibits less invasiveness into host cells than LF82, primarily due to reduced expression of the type 1 fimbriae. Finally, we found that the cpxRA mutant is impaired in gut competitive colonization in a mouse model. The colonization defects were reversed by the introduction of a plasmid encoding the cpxRA gene or expressing the type 1 fimbriae. Our findings indicate that modulating CpxRA activity could be a promising approach to regulating AIEC-involved Crohn's disease.

Possible link between colonization of the gastrointestinal tract by Citrobacter rodentium in C57BL/6 mice and microbiota composition.

Colonization resistance, conferred by the host's microbiota through both direct and indirect protective actions, serves to protect the host from enteric infections. Here, we identified the specific members of the gut microbiota that impact gastrointestinal colonization by Citrobacter rodentium, a murine pathogen causing colonic crypt hyperplasia. The gut colonization levels of C. rodentium in C57BL/6 mice varied among breeding facilities, probably due to differences in microbiota composition. A comprehensive analysis of the microbiota revealed that specific members of the microbiota may influence gut colonization by C. rodentium, thus providing a potential link between the two.

Maternal Diet Determines Milk Microbiome Composition and Offspring Gut Colonization in Wistar Rats.

Mother's milk contains a unique microbiome that plays a relevant role in offspring health. We hypothesize that maternal malnutrition during lactation might impact the microbial composition of milk and affect adequate offspring gut colonization, increasing the risk for later onset diseases. Then, Wistar rats were fed ad libitum (Control, C) food restriction (Undernourished, U) during gestation and lactation. After birth, offspring feces and milk stomach content were collected at lactating day (L)4, L14 and L18. The V3-V4 region of the bacterial 16S rRNA gene was sequenced to characterize bacterial communities. An analysis of beta diversity revealed significant disparities in microbial composition between groups of diet at L4 and L18 in both milk, and fecal samples. In total, 24 phyla were identified in milk and 18 were identified in feces, with Firmicutes, Proteobacteria, Actinobacteroidota and Bacteroidota collectively representing 96.1% and 97.4% of those identified, respectively. A higher abundance of Pasteurellaceae and Porphyromonas at L4, and of Gemella and Enterococcus at L18 were registered in milk samples from the U group. Lactobacillus was also significantly more abundant in fecal samples of the U group at L4. These microbial changes compromised the number and variety of milk-feces or feces-feces bacterial correlations. Moreover, increased offspring gut permeability and an altered expression of goblet cell markers TFF3 and KLF3 were observed in U pups. Our results suggest that altered microbial communication between mother and offspring through breastfeeding may explain, in part, the detrimental consequences of maternal malnutrition on offspring programming.

Factors Influencing Neonatal Gut Microbiome and Health with a Focus on Necrotizing Enterocolitis.

Maturational changes in the gut start in utero and rapidly progress after birth, with some functions becoming fully developed several months or years post birth including the acquisition of a full gut microbiome, which is made up of trillions of bacteria of thousands of species. Many factors influence the normal development of the neonatal and infantile microbiome, resulting in dysbiosis, which is associated with various interventions used for neonatal morbidities and survival. Extremely low gestational age neonates (<28 weeks' gestation) frequently experience recurring arterial oxygen desaturations, or apneas, during the first few weeks of life. Apnea, or the cessation of breathing lasting 15-20 s or more, occurs due to immature respiratory control and is commonly associated with intermittent hypoxia (IH). Chronic IH induces oxygen radical diseases of the neonate, including necrotizing enterocolitis (NEC), the most common and devastating gastrointestinal disease in preterm infants. NEC is associated with an immature intestinal structure and function and involves dysbiosis of the gut microbiome, inflammation, and necrosis of the intestinal mucosal layer. This review describes the factors that influence the neonatal gut microbiome and dysbiosis, which predispose preterm infants to NEC. Current and future management and therapies, including the avoidance of dysbiosis, the use of a human milk diet, probiotics, prebiotics, synbiotics, restricted antibiotics, and fecal transplantation, for the prevention of NEC and the promotion of a healthy gut microbiome are also reviewed. Interventions directed at boosting endogenous and/or exogenous antioxidant supplementation may not only help with prevention, but may also lessen the severity or shorten the course of the disease.

Quorum sensing-activated phenylalanine metabolism drives OMV biogenesis to enhance mosquito commensal colonization resistance to Plasmodium.

Gut microbiota and its symbiotic relationship with the host are crucial for preventing pathogen infection. However, little is known about the mechanisms that drive commensal colonization. Serratia bacteria, commonly found in Anopheles mosquitoes, potentially mediate mosquito resistance to Plasmodium. Using S. ureilytica Su_YN1 as a model, we show that a quorum sensing (QS) circuit is crucial for stable colonization. After blood ingestion, the QS synthase SueI generates the signaling molecule N-hexanoyl-L-homoserine lactone (C6-HSL). Once C6-HSL binds to the QS receptor SueR, repression of the phenylalanine-to-acetyl-coenzyme A (CoA) conversion pathway is lifted. This pathway regulates outer membrane vesicle (OMV) biogenesis and promotes Serratia biofilm-like aggregate formation, facilitating gut adaptation and colonization. Notably, exposing Serratia Su_YN1-carrying Anopheles mosquitoes to C6-HSL increases Serratia gut colonization and enhances Plasmodium transmission-blocking efficacy. These findings provide insights into OMV biogenesis and commensal gut colonization and identify a powerful strategy for enhancing commensal resistance to pathogens.

Dynamic genetic adaptation of Bacteroides thetaiotaomicron during murine gut colonization.

To understand how a bacterium ultimately succeeds or fails in adapting to a new host, it is essential to assess the temporal dynamics of its fitness over the course of colonization. Here, we introduce a human-derived commensal organism, Bacteroides thetaiotaomicron (Bt), into the guts of germ-free mice to determine whether and how the genetic requirements for colonization shift over time. Combining a high-throughput functional genetics assay and transcriptomics, we find that gene usage changes drastically during the first days of colonization, shifting from high expression of amino acid biosynthesis genes to broad upregulation of diverse polysaccharide utilization loci. Within the first week, metabolism becomes centered around utilization of a predominant dietary oligosaccharide, and these changes are largely sustained through 6 weeks of colonization. Spontaneous mutations in wild-type Bt also evolve around this locus. These findings highlight the importance of considering temporal colonization dynamics in developing more effective microbiome-based therapies.

Differences in carbon metabolic capacity fuel co-existence and plasmid transfer between Salmonella strains in the mouse gut.

Antibiotic resistance plasmids can be disseminated between different Enterobacteriaceae in the gut. Here, we investigate how closely related Enterobacteriaceae populations with similar nutrient needs can co-bloom in the same gut and thereby facilitate plasmid transfer. Using different strains of Salmonella Typhimurium (S.Tm SL1344 and ATCC14028) and mouse models of Salmonellosis, we show that the bloom of one strain (i.e., recipient) from very low numbers in a gut pre-occupied by the other strain (i.e., donor) depends on strain-specific utilization of a distinct carbon source, galactitol or arabinose. Galactitol-dependent growth of the recipient S.Tm strain promotes plasmid transfer between non-isogenic strains and between E. coli and S.Tm. In mice stably colonized by a defined microbiota (OligoMM12), galactitol supplementation similarly facilitates co-existence of two S.Tm strains and promotes plasmid transfer. Our work reveals a metabolic strategy used by Enterobacteriaceae to expand in a pre-occupied gut and provides promising therapeutic targets for resistance plasmids spread.

Integration host factor regulates colonization factors in the bee gut symbiont Frischella perrara.

Bacteria colonize specific niches in the animal gut. However, the genetic basis of these associations is often unclear. The proteobacterium Frischella perrara is a widely distributed gut symbiont of honey bees. It colonizes a specific niche in the hindgut and causes a characteristic melanization response. Genetic determinants required for the establishment of this association, or its relevance for the host, are unknown. Here, we independently isolated three point mutations in genes encoding the DNA-binding protein integration host factor (IHF) in F. perrara. These mutants abolished the production of an aryl polyene metabolite causing the yellow colony morphotype of F. perrara. Inoculation of microbiota-free bees with one of the mutants drastically decreased gut colonization of F. perrara. Using RNAseq, we found that IHF affects the expression of potential colonization factors, including genes for adhesion (type 4 pili), interbacterial competition (type 6 secretion systems), and secondary metabolite production (colibactin and aryl polyene biosynthesis). Gene deletions of these components revealed different colonization defects depending on the presence of other bee gut bacteria. Interestingly, one of the T6SS mutants did not induce the scab phenotype anymore despite colonizing at high levels, suggesting an unexpected role in bacteria-host interaction. IHF is conserved across many bacteria and may also regulate host colonization in other animal symbionts.

Prolonged Streptococcus gallolyticus subsp. pasteurianus gut colonization in healthcare workers and potential transmission role in neonatal sepsis.

BACKGROUND: Streptococcus gallolyticus subsp. pasteurianus (SGSP) is a commensal in the intestinal tract and a potential pathogen of neonatal sepsis. During an 11-month period, four consecutive cases of SGSP sepsis were identified in one postnatal care unit (unit A) without evidence of vertical transmission. Therefore, we initiated this study to investigate the reservoir and mode of transmission of SGSP. METHOD: We performed cultures of stool samples from healthcare workers in unit A and unit B (another unit without SGSP sepsis). If SGSP was positive in feces, we performed isolate pulsotyping and genotyping by using pulsed-field gel electrophoresis (PFGE) and analyzing random amplified polymorphic DNA (RAPD) patterns, respectively. RESULTS: Five staff members in unit A showed positivity for SGSP. All samples from unit B were negative. We identified two major pulsogroups (groups C and D) by PFGE. In group D, the strains isolated from 3 consecutive sepsis patients (P1, P2 and P3) were closely related and clustered together as those from 2 staff members (C1/C2, C6). One staff (staff 4) had a direct contact history with patient (P1) confirmed to have the same clone. The last isolate of the patient in our study (P4) belonged to a distinct clone. CONCLUSION: We found prolonged gut colonization of SGSP in healthcare workers and its epidemiological relatedness to neonatal sepsis. Fecal-oral or contact transmission is a possible route of SGSP infection. Fecal shedding among staff may be associated with neonatal sepsis in healthcare facilities.

The defective gut colonization of Candida albicans hog1 MAPK mutants is restored by overexpressing the transcriptional regulator of the white opaque transition WOR1.

The transcriptional master regulator of the white opaque transition of Candida albicans WOR1 is important for the adaptation to the commensal lifestyle in the mammalian gut, a major source of invasive candidiasis. We have generated cells that overproduce Wor1 in mutants defective in the Hog1 MAP kinase, defective in several stress responses and unable to colonize the mice gut. WOR1 overexpression allows hog1 to be established as a commensal in the murine gut in a commensalism model and even compete with wild-type C. albicans cells for establishment. This increased fitness correlates with an enhanced ability to adhere to biotic surfaces as well as increased proteinase and phospholipase production and a decrease in filamentation in vitro. We also show that hog1 WOR1OE are avirulent in a systemic candidiasis model in mice.

Modelling the Gastrointestinal Carriage of Klebsiella pneumoniae Infections.

Klebsiella pneumoniae is a leading cause of nosocomial and community acquired infections, making K. pneumoniae the pathogen that is associated with the second largest number of deaths attributed to any antibiotic resistant infection. K. pneumoniae colonizes the nasopharynx and the gastrointestinal tract in an asymptomatic manner without dissemination to other tissues. Importantly, gastrointestinal colonization is a requisite for infection. Our understanding of K. pneumoniae colonization is still based on interrogating mouse models in which animals are pretreated with antibiotics to disturb the colonization resistance imposed by the gut microbiome. In these models, infections disseminate to other tissues. Here, we report a murine model to allow for the study of the gastrointestinal colonization of K. pneumoniae without tissue dissemination. Hypervirulent and antibiotic resistant strains stably colonize the gastrointestinal tract of in an inbred mouse population without antibiotic treatment. The small intestine is the primary site of colonization and is followed by a transition to the colon over time, without dissemination to other tissues. Our model recapitulates the disease dynamics of the metastatic K. pneumoniae strains that are able to disseminate from the gastrointestinal tract to other sterile sites. Colonization is associated with mild to moderate histopathology, no significant inflammation, and no effect on the richness of the microbiome. Our model sums up the clinical scenario in which antibiotic treatment disturbs the colonization of K. pneumoniae and results in dissemination to other tissues. Finally, we establish that the capsule polysaccharide is necessary for the colonization of the large intestine, whereas the type VI secretion system contributes to colonization across the gastrointestinal tract. IMPORTANCE Klebsiella pneumoniae is one of the pathogens that is sweeping the world in the antibiotic resistance pandemic. Klebsiella colonizes the nasopharynx and the gut of healthy subjects in an asymptomatic manner, making gut colonization a requisite for infection. This makes it essential to understand the gastrointestinal carriage in preventing Klebsiella infections. Current research models rely on the perturbation of the gut microbiome by antibiotics, resulting in an invasive infection. Here, we report a new model of K. pneumoniae gut colonization that recapitulates key features of the asymptomatic human gastrointestinal tract colonization. In our model, there is no need to disturb the microbiota to achieve stable colonization, and there is no dissemination to other tissues. Our model sums up the clinical scenario in which antibiotic treatment triggers invasive infection. We envision that our model will be an excellent platform upon which to investigate factors enhancing colonization and invasive infections and to test therapeutics to eliminate Klebsiella asymptomatic colonization.

Differentiation of Escherichia fergusonii and Escherichia coli Isolated from Patients with Inflammatory Bowel Disease/Ischemic Colitis and Their Antimicrobial Susceptibility Patterns.

Genotypically, 16S rRNA gene sequence analysis clearly differentiates between species. However, species delineation between Escherichia fergusonii and Escherichia coli is much more difficult and cannot be distinguished by 16S rRNA gene sequences alone. Hence, in this study, we attempted to differentiate E. fergusonii and E. coli isolated from faecal samples of disease-associated Korean individuals with inflammatory bowel disease (IBD)/ischemic colitis (IC) and test the antimicrobial susceptibility patterns of isolated strains. Phylogenetic analysis was performed using the adenylate kinase (adk) housekeeping gene from the E. coli multi locus sequence typing (MLST) scheme. Antimicrobial susceptibility and minimum inhibitory concentration (MIC) of all disease-associated strains in addition to healthy control isolates to 14 antibiotics were determined by broth microdilution-based technique. Next, 83 isolates from 11 disease-associated faecal samples were identified as E. fergusonii using 16S rRNA gene sequence analysis. Phylogenetic analysis using the adk gene from E. coli MLST scheme revealed that most of the strains (94%) were E. coli. A total of 58 resistance patterns were obtained from 83 strains of disease-associated (IBD/IC) isolates. All isolates were resistant to at least one tested antimicrobial agent, with the highest resistance against erythromycin (88.0%), ampicillin (86.7%), ciprofloxacin (73.5%), cephalothin (72.3%), gentamicin (59%), trimethoprim-sulfamethoxazole (53%), cefotaxime (49.4%), and ceftriaxone (48.2%). A total of 90.7% of isolates were extended-spectrum beta-lactamase (ESBL)-producers among the resistant strains to third-generation cephalosporins (cefotaxime or ceftriaxone). ESBL-producing E. coli isolates from patients with Crohn's disease (CD), ulcerative colitis (UC), and ischemic colitis (IC) were 92.3%, 82.4%, and 100%, respectively. In conclusion, adk-based phylogenetic analysis may be the most accurate method for distinguishing E. coli and E. fergusonii from Escherichia genus. We identified four loci in adk gene sequences which makes it easier to discriminate between E. coli and E. fergusonii. Additionally, we believe that gut colonization by multidrug-resistant ESBL-producing E. coli may play a significant role in IBD/IC pathogenesis.

Gut colonization and subsequent infection of neonates caused by extended-spectrum beta-lactamase-producing Escherichia coli and Klebsiella pneumoniae.

The gut microbiota harbors diverse bacteria considered reservoirs for antimicrobial resistance genes. The global emergence of extended-spectrum beta-lactamase (ESBL)-producing Enterobacterales (ESBL-PE) significantly contributes to healthcare-associated infections (HAIs). We investigated the presence of ESBL-producing Escherichia coli (ESBL-PEco) and ESBL-producing Klebsiella pneumoniae (ESBL-PKpn) in neonatal patients' guts. Furthermore, we identified the factors contributing to the transition towards ESBL-PEco and ESBL-PKpn-associated healthcare-associated infections (HAIs). The study was conducted from August 2019 to February 2020, in a Neonatal Intensive Care Unit of the Hospital Infantil de México Federico Gómez. Rectal samples were obtained upon admission, on a weekly basis for a month, and then biweekly until discharge from the neonatology ward. Clinical data, culture results, and infection information were gathered. We conducted antimicrobial tests, multiplex PCR assay, and pulsed-field gel electrophoresis (PFGE) to determine the antimicrobial resistance profile and genetic relationships. A comparison between the group's controls and cases was performed using the Wilcoxon and Student t-tests. Of the 61 patients enrolled, 47 were included, and 203 rectal samples were collected, identifying 242 isolates. In 41/47 (87%) patients, colonization was due to ESBL-PEco or ESBL-PKpn. And nine of them developed HAIs (22%, 9/41). ESBL-PEco resistance to cephalosporins ranged from 25.4% to 100%, while ESBL-PKpn resistance varied from 3% to 99%, and both bacteria were susceptible to carbapenems, tigecillin, and colistin. The prevalent bla CTX-M-group-1 gene accounted for 77.2% in ESBL-PEco and 82.2% in ESBL-PKpn, followed by bla TEM 50% and bla OXA-1 43.8% in ESBL-PEco and bla TEM 80.2% and bla SHV 76.2% in ESBL-PKpn. Analysis of clonality revealed identical colonizing and infection isolates in only seven patients. Significant risk factors included hospital stay duration, duration of antibiotic treatment, and invasive device usage. Our findings suggest high ESBL-PEco and ESBL-PKpn rates of colonization often lead to infection in neonates. Attention should be paid to patients with ESBL-PE.

From intestinal colonization to systemic infections: Candida albicans translocation and dissemination.

Candida species are the most prevalent cause of invasive fungal infections, of which Candida albicans is the most common. Translocation across the epithelial barrier into the bloodstream by intestinal-colonizing C. albicans cells serves as the main source for systemic infections. Understanding the fungal mechanisms behind this process will give valuable insights on how to prevent such infections and keep C. albicans in the commensal state in patients with predisposing conditions. This review will focus on recent developments in characterizing fungal translocation mechanisms, compare what we know about enteric bacterial pathogens with C. albicans, and discuss the different proposed hypotheses for how C. albicans enters and disseminates through the bloodstream immediately following translocation.

Insight into the Relationship between Oral Microbiota and the Inflammatory Bowel Disease.

Inflammatory bowel disease has been a growing concern of lots of people globally, including both adults and children. As a chronic inflammatory disease of the intestine, even though the etiology of inflammatory bowel disease is still unclear, the available evidence from clinic observations has suggested a close association with microorganisms. The oral microbiota possesses the characteristics of a large number and abundant species, second only to the intestinal microbiota in the human body; as a result, it successfully attracts the attention of researchers. The highly diverse commensal oral microbiota is not only a normal part of the oral cavity but also has a pronounced impact on the pathophysiology of general health. Numerous studies have shown the potential associations between the oral microbiota and inflammatory bowel disease. Inflammatory bowel disease can affect the composition of the oral microbiota and lead to a range of oral pathologies. In turn, there are a variety of oral microorganisms involved in the development and progression of inflammatory bowel disease, including Streptococcus spp., Fusobacterium nucleatum, Porphyromonas gingivalis, Campylobacter concisus, Klebsiella pneumoniae, Saccharibacteria (TM7), and Candida albicans. Based on the above analysis, the purpose of this review is to summarize this relationship of mutual influence and give further insight into the detection of flora as a target for the diagnosis and treatment of inflammatory bowel disease to open up a novel approach in future clinical practice.

B4galnt2-mediated host glycosylation influences the susceptibility to Citrobacter rodentium infection.

Histo-blood group antigens in the intestinal mucosa play important roles in host-microbe interactions and modulate the susceptibility to enteric pathogens. The B4galnt2 gene, expressed in the GI tract of most mammals, including humans, encodes a beta-1,4-N-acetylgalactosaminyltransferase enzyme which catalyzes the last step in the biosynthesis of the Sd(a) and Cad blood group antigens by adding an N-acetylgalactosamine (GalNAc) residue to the precursor molecules. In our study, we found that loss of B4galnt2 expression is associated with increased susceptibility to Citrobacter rodentium infection, a murine model pathogen for human enteropathogenic Escherichia coli. We observed increased histopathological changes upon C. rodentium infection in mice lacking B4galnt2 compared to B4galnt2-expressing wild-type mice. In addition, wild-type mice cleared the C. rodentium infection faster than B4galnt2-/- knockout mice. It is known that C. rodentium uses its type 1 fimbriae adhesive subunit to bind specifically to D-mannose residues on mucosal cells. Flow cytometry analysis of intestinal epithelial cells showed the absence of GalNAc-modified glycans but an increase in mannosylated glycans in B4galnt2-deficient mice compared to B4galnt2-sufficient mice. Adhesion assays using intestinal epithelial organoid-derived monolayers revealed higher C. rodentium adherence to cells lacking B4galnt2 expression compared to wild-type cells which in turn was reduced in the absence of type I fimbriae. In summary, we show that B4galnt2 expression modulates the susceptibility to C. rodentium infection, which is partly mediated by fimbriae-mannose interaction.

Comparison between Perianal Swab and Stool Specimens for Detecting Colonization with Extended-Spectrum Beta-Lactamase-Producing and Fluoroquinolone-Resistant Enterobacterales.

Stool specimens are frequently used to detect gastrointestinal tract colonization with antimicrobial-resistant enteric bacteria, but they cannot be rapidly collected. Perianal swab specimens can be collected more quickly and efficiently, but data evaluating their suitability as a specimen type for this purpose are sparse. We performed selective culture for extended-spectrum ß-lactamase-producing Enterobacterales (ESBL-E) and fluoroquinolone-resistant Enterobacterales (FQRE) using paired perianal swab and stool specimens that were collected within 1 day of each other from hematopoietic cell transplant recipients and patients with acute leukemia. Nineteen (7.6%) of 251 stool specimens yielded ESBL-E and 64 (26%) of 246 stool specimens yielded FQRE. The positive percent agreement of perianal swab specimens compared to stool specimens was 95% (18/19; 95% confidence interval [CI], 74% to 100%) for detecting ESBL-E and 95% (61/64; 95% CI, 87% to 99%) for detecting FQRE. The concordance between specimen types was 98% (95% CI, 97% to 100%). Perianal swabs are a reliable specimen type for surveillance of the gastrointestinal tract for ESBL-E and FQRE.