Evaluation of in vitro activity of manogepix against multidrug-resistant and pan-resistant Candida auris from the New York Outbreak

BackgroundCandida auris, an emerging multidrug-resistant yeast, causes deadly invasive infections with high mortality. C. auris strains often show high MICs to fluconazole and amphotericin B, and some are resistant to all 3 major antifungal classes, limiting treatment options. We tested 16 C. auris strains from a wide geographical area (Germany, Japan, S. Korea, and India) against 10 antifungals including APX001A (APXA), an antifungal with a novel mechanism of action (inhibition of the Gwt1 fungal enzyme). The prodrug APX001 (APX) is in clinical development and its efficacy was evaluated in an immunocompromised murine model of disseminated C. auris.MethodsMICs were determined by CLSI M27-A3 method. Mice were immunocompromised for the study. Treatment was initiated 2 hours post challenge. IP treatment groups included a vehicle control, APX 78mg/kg (mpk) BID, 78mpk TID, and 104mpk BID, and anidulafungin (AFG) 10mpk BID. Survival was monitored for 16d post inoculation.ResultsSusceptibility. APXA had significantly lower MIC50 and MIC90 values (concentration that inhibits 50 and 90% of the tested isolates, respectively) than the other tested antifungals with a MIC90 of 0.031 µg/mL (Table 1).Survival. 100% mortality in the vehicle-treated control group occurred by 6d. Significant efficacy was observed in all APX treatment groups with 90, 100, and 80% survival observed respectively for APX 78 mpk BID; 78 mpk TID and 104 mpk BID. AFG treatment resulted in 50% survival at 16d. Mice in all of the APX treated groups had a significantly higher % survival compared with the AFG and vehicle groups.ConclusionAPXA was the most active antifungal agent in vitro. The prodrug APX resulted in significantly better survival than AFG in a C. auris disseminated infection model. Thus APX may be a viable treatment for C. auris infections.Table 1: Susceptibility of 16 C. auris isolates against antifungalsDisclosuresK. J. Shaw, Amplyx Pharmaceuticals Inc.: Employee, Salary; M. Ghannoum, Amplyx Pharmaceuticals: Consultant, Research Contractor and Scientific Advisor, Consulting fee and Research grant; Cidara Therapeutics: Consultant and Research Contractor, Consulting fee and Research grant

Candida auris is an emerging fungal pathogen with high rates of multidrug resistance, posing a significant global health threat. Immunosuppressed patients are particularly vulnerable to multidrug-resistant (MDR) C. auris infections. This systematic review and meta-analysis (SR-MA) aimed to assess the global prevalence of MDR-C. auris isolates in humans and their resistance to antifungal drugs, primarily fluconazole (FLZ), voriconazole (VOR), and amphotericin B (AmB). A comprehensive search was conducted in PubMed, Scopus, and ScienceDirect databases on published studies regarding clinical C. auris isolates and the use of antifungal susceptibility testing assay from 17 March 2015 to 1 February 2024. Meta-analysis was conducted using random-effects models to determine the estimated pooled prevalence of MDR-C. auris isolates and their antifungal resistance profiles from immunosuppressed humans. A total of 81 research studies were included in the final analysis, with the overall pooled prevalence of the three most important antifungal drugs; FLZ (92.5% | 95% CI: 89.5-94.7), VOR (49.0% | 95% CI: 37.6-60.4), and AmB (51.0% | 95% CI: 42.3-59.7). According to the subgroup analyses, FLZ-resistant C. auris was the most prevalent isolate observed in the five continents reporting compared to the VOR- and AmB-resistant C. auris having lower pooled prevalence. Further, higher pooled prevalence of MDR-C. auris isolates were observed from males (68.2%, n=578) compared to females (37.1%, n=283). Finally, the global pooled prevalence for mortality in immunosuppressed patients with MDR-C. auris from 13 research studies was 41.5% (95% CI: 29.9-54.2). This SR-MA study establishes the variation of MDR-C. auris resistance patterns observed from different continents and the importance to conduct further research studies using potent antifungal drugs. Accordingly, it is imperative to establish stringent surveillance on the increasing prevalence of antifungal resistance particularly in low-income regions with limited research resources to prevent increasing prevalence of MDR-C. auris.

Candida auris causes prolonged colonization and bloodstream infections in hospitalized patients. Different C. auris clades vary in their geographic origin, disease spectrum, and antifungal resistance, but biological basis underlying such variations needs further examination. Therefore, we investigated susceptible and multidrug-resistant C. auris isolates, obtained early in the New York outbreak, to benchmark their pathogenic potential in caterpillar worms of greater wax moth Galleria mellonella. Healthy G. mellonella worms responded to C. auris in a strain-specific, dose-responsive pattern. Three drug-resistant, clade I C. auris 17-1, 18-1, and 18-2 isolates caused high mortality, while a control, drug-susceptible, clade II C. auris 16-1 caused lower mortality (P < 0.001) with graded inocula (1 × 104 to 1 × 107 CFU). Virulence correlated with fungal growth in hemolymph as C. auris 17-1, 18-1 and 18-2 reached high fungal cell load in the infected larvae, while C. auris 16-1 multiplied less proficiently. The degree of melanization was higher in worms infected with more pathogenic C. auris. Hemocoel histopathology showed more fungal elements and about 50 granulomas per profile for C. auris 17-1, 18-1 and 18-2 compared to 5 to 10 granulomas for C. auris 16-1. With more pathogenic C. auris isolates, the expression of gallerimycin, ceropin, and galiomycin increased significantly (P < 0.05). Thus, the induction of G. mellonella immune effector peptides, histopathological responses, and melanization are proportionate to C. auris pathogenic potential. However, G. mellonella from different vendors showed unpredictable quality upon delivery that impacted feasibility and reproducibility of planned studies. Our results indicate utility of G. mellonella experimental model for screening of C. auris pathogenesis depending upon quality of worms commercially available in the USA.IMPORTANCEThe New York metropolitan area continues to suffer from the largest, ongoing outbreak of drug-resistant Candida auris. It is necessary to gather more information to determine if C. auris isolates from this outbreak vary in their ability to cause more severe disease in affected patients. Therefore, we studied the experimental model of greater wax moth Galleria mellonella. We found that susceptible and drug-resistant NY C. auris isolates caused measurable disease in G. mellonella. There was a good correlation between pathogenic potential of C. auris and melanin in the infected worms, fungal elements in worm hemolymph, uptick in the genes involved in insect immunity, and histopathological changes. The worms sourced from various commercial vendors were of variable quality. We confirm that G. mellonella remains a facile model to study C. auris experimental disease.

The increasing prevalence of candidemia and invasive candidiasis infections caused by Candida auris represents a global health risk. Such infections are difficult to treat as they are often multidrug-resistant and are linked to high rates of mortality. Rezafungin is a second-generation echinocandin with antifungal activity against a range of Candida species, including wild type, and azole- and some echinocandin-resistant isolates. Its stability and prolonged half-life permit less frequent dosing compared with other echinocandins, leading to high front-loaded exposures and potential earlier mycological clearance from infection sites. These properties make rezafungin a candidate for the treatment of candidemia and invasive candidiasis infections due to C. auris. Accordingly, this narrative review article describes available evidence for the activity and effectiveness of rezafungin against C. auris isolates and infections. To date, the activity of rezafungin against C. auris isolates and infections has been demonstrated in in vitro and in vivo non-clinical experiments, and in pharmacokinetic/pharmacodynamic target attainment estimations utilizing clinical data. With similar potency to other echinocandins, rezafungin demonstrates in vitro and in vivo activity that is comparable to or better than that seen with other echinocandins, and similar to that for rezafungin in other Candida species. Like other echinocandins, its activity is reduced in fks-mutant isolates. Although there is currently a dearth of data on the therapeutic activity of rezafungin against C. auris, it is reasonable that rezafungin may be a viable choice for treating candidemia and invasive candidiasis caused by C. auris. Further clinical investigations are necessary.

Candida auris, initially identified in 2009, has rapidly become a critical concern due to its antifungal resistance and significant mortality rates in healthcare-associated outbreaks. To date, whole-genome sequencing (WGS) has identified five unique clades of C. auris, with some strains displaying resistance to all primary antifungal drug classes. In this study, we presented the first WGS analysis of C. auris from Bangladesh, describing its origins, transmission dynamics, and antifungal susceptibility testing (AFST) profile. Ten C. auris isolates collected from hospital settings in Bangladesh were initially identified by CHROMagar Candida Plus, followed by VITEK2 system, and later sequenced using Illumina NextSeq 550 system. Reference-based phylogenetic analysis and variant calling pipelines were used to classify the isolates in different clades. All isolates aligned ~90% with the Clade I C. auris B11205 reference genome. Of the 10 isolates, 8 were clustered with Clade I isolates, highlighting a South Asian lineage prevalent in Bangladesh. Remarkably, the remaining two isolates formed a distinct cluster, exhibiting >42,447 single-nucleotide polymorphism differences compared to their closest Clade IV counterparts. This significant variation corroborates the emergence of a sixth clade (Clade VI) of C. auris in Bangladesh, with potential for international transmission. AFST results showed that 80% of the C. auris isolates were resistant to fluconazole and voriconazole, whereas Clade VI isolates were susceptible to azoles, echinocandins, and pyrimidine analogue. Genomic sequencing revealed ERG11_Y132F mutation conferring azole resistance while FCY1_S70R mutation found inconsequential in describing 5-flucytosine resistance. Our study underscores the pressing need for comprehensive genomic surveillance in Bangladesh to better understand the emergence, transmission dynamics, and resistance profiles of C. auris infections. Unveiling the discovery of a sixth clade (Clade VI) accentuates the indispensable role of advanced sequencing methodologies.IMPORTANCECandida auris is a nosocomial fungal pathogen that is commonly misidentified as other Candida species. Since its emergence in 2009, this multidrug-resistant fungus has become one of the five urgent antimicrobial threats by 2019. Whole-genome sequencing (WGS) has proven to be the most accurate identification technique of C. auris which also played a crucial role in the initial discovery of this pathogen. WGS analysis of C. auris has revealed five distinct clades where isolates of each clade differ among themselves based on pathogenicity, colonization, infection mechanism, as well as other phenotypic characteristics. In Bangladesh, C. auris was first reported in 2019 from clinical samples of a large hospital in Dhaka city. To understand the origin, transmission dynamics, and antifungal-resistance profile of C. auris isolates circulating in Bangladesh, we conducted a WGS-based surveillance study on two of the largest hospital settings in Dhaka, Bangladesh.

The increasing incidence and dissemination of multidrug-resistant Candida auris represents a serious global threat. The emergence of pan-resistant C. auris exhibiting resistance to all three classes of antifungals magnifies the need for novel therapeutic interventions. We identified that two HIV protease inhibitors, atazanavir and saquinavir, in combination with posaconazole exhibited potent activity against C. auris in vitro and in vivo. Both atazanavir and saquinavir exhibited a remarkable synergistic activity with posaconazole against all tested C. auris isolates and other medically important Candida species. In a time-kill assay, both drugs restored the fungistatic activity of posaconazole, resulting in reduction of 5 and 5.6 log10, respectively. Furthermore, in contrast to the individual drugs, the two combinations effectively inhibited the biofilm formation of C. auris by 66.2 and 81.2%, respectively. Finally, the efficacy of the two combinations were tested in a mouse model of C. auris infection. The atazanavir/posaconazole and saquinavir/posaconazole combinations significantly reduced the C. auris burden in mice kidneys by 2.04- (99.1%) and 1.44-log10 (96.4%) colony forming unit, respectively. Altogether, these results suggest that the combination of posaconazole with the HIV protease inhibitors warrants further investigation as a new therapeutic regimen for the treatment of C. auris infections.

Candida auris (C. auris) belongs to the Candida genus and is a fungal yeast resistant to multiple drugs. It is highly virulent and evades current therapeutic remedies. It was first discovered in a Japanese hospital in 2009 from a patient’s external auditory canal1. C. auris infection has a high worldwide mortality, which ranges from 30% to 60%, and is frequently associated with bloodstream infections2. The rapid spread of C. auris infection occurred after 2009. The Centers for Disease Control and Prevention (CDC) has estimated the presence of C. auris isolates in 41 countries, typically in hospital settings, as of March 20203. CDC also reported outbreaks of infections with C. auris in 47 countries globally on February 15, 20214. The United States reported 2377 clinical cases and 5754 screening cases from January 2022 to December 20225. Twenty-six isolates of C. auris from India were different genetically and phenotypically from the ones found in Japan and Korea, which provided evidence for C. auris’s ability to mutate and its resistance to Azoles6. The mechanism of C. auris virulence factors is relatively unknown. According to genomic comparison, C. auris has the ability to adapt to different environments. Two mechanisms of its pathogenesis have been identified, which include hydrolytic enzyme production and attack host cells and tissues. It can also form biofilms that protect it from antifungal drugs and increase its ability in nosocomial transmission4. C. auris can be spread in health care facilities such as hospitals and nursing homes through direct patient-to-patient contact. Contaminated surfaces are a significant culprit in the spread when a person comes in contact with them. As C. auris colonizes the skin and can be transmitted into the environment, both properties make it easily transmissible. Population susceptible are immunocompromised people, recently hospitalized patients in areas where C. auris is endemic; catheter use, extended stay in ICU, previous history of antimicrobial exposure, and resistance to antifungal therapy7. Identifying this pathogen is tricky as the methods used to determine the yeast in laboratories often must be corrected for other fungi. Detection of C. auris requires reliable sampling procedures from the most common sites of colonization, including the axillae and groin. Nares, external auditory canals, urine, rectum, catheter sites, and vagina also serve as colonization sites8. Making use of water and soaps or using a hand sanitizer with a 60% alcohol content is effective in preventing infection. Health care workers should take proper precautions to use gowns and gloves in the hospital setting. Regular disinfection and cleaning of surfaces prevent the survival of C. auris. When referring a patient with C. auris, the health care facility on the receiving end should be informed of the patient’s infection or colonization status to take appropriate measures promptly9. The steadily rising incidence of C. auris outbreaks poses a significant public health threat. C. auris outbreaks are a challenge to control due to poor routine diagnostic detection, prompt transmission, and resistance to disinfection techniques. It is now a leading cause of fungal infections in many medical setups with high mortality rates. Rapid detection methods that provide reliable identification and diagnosis, as well as control measures and necessary precautions, will help contain the spread of C. auris in health care systems. Ethical approval None. Consent for publication None. Sources of funding None. Author contributions The conceptualization was done by H.F. and H.S.R. The literature and drafting of the manuscript were conducted by H.F., A.M.S., F.R., and B.S.R. The editing and supervision were performed by H.S.R. All authors have read and agreed to the final version of the manuscript. Conflict of interest disclosures The authors declare that they have no financial conflict of interest with regard to the content of this report. Research registration unique identifying number (UIN) Not applicable. Guarantor All authors take responsibility for the work, access to data and decision to publish. Provenancer and Peer review Not commissioned, externally peer reviewed.

Candida auris (C. auris) is an emerging fungal pathogen responsible for numerous nosocomial outbreaks worldwide over the past decade. Its resistance to multiple antifungal agents poses a significant challenge in clinical management. In addition, high rates of misdiagnosis and its ability to form biofilms further complicate treatment and control efforts. Immunocompromised patients, particularly those with chronic diseases or invasive medical devices, are at heightened risk. Despite its global prevalence, the true extent of C. auris infections remains uncertain due to several diagnostic challenges. Notably, limited availability of specialized molecular diagnostic tools in resource-limited settings exacerbates the underreporting of infections, leaving the full scope of its impact largely undetected. To investigate the prevalence and impact of C. auris on hemodialysis patients, as well as methods for prevention and management of C. auris infections in hemodialysis units. This review synthesizes data from peer-reviewed journals and clinical studies addressing C. auris epidemiology, diagnostic challenges, resistance patterns, and infection management, with a focus on patients with chronic kidney failure. Data on biofilm behavior, antifungal efficacy, and infection control practices in hemodialysis environments were analyzed to identify existing knowledge gaps. Candida auris infections occur more frequently in males (≈60%) and individuals over 65years of age. The pathogen colonizes various anatomical sites and thrives in hospital settings, withstanding temperatures up to 42°C and salinity levels up to 3%. Diagnostic errors are frequent: conventional biochemical methods misidentify up to 40% of cases, while molecular diagnostics offer ≥ 95% specificity. Existing antifungal lock solutions show limited effectiveness (50-60%), whereas hemodialysis patients are 3-4 times more likely to develop bloodstream infections due to the use of central venous catheters. Novel experimental antifungal combinations yield > 80% eradication rates in preclinical settings. Candida auris presents a significant threat to hemodialysis patients due to its resilience, misdiagnosis rates, and treatment resistance. Actionable recommendations include implementing molecular diagnostics in high-risk settings, developing targeted antifungal lock protocols, and enhancing surface decontamination practices in dialysis units to prevent biofilm formation and pathogen transmission.

Analyses of fluconazole uptake in clinical isolates of C. auris, with wide ranging drug resistance profiles, has revealed interesting differences within the species as well as major distinctions from other yeast species. We previously proposed that prevention of drug uptake is a potential mechanism of drug resistance and our C. auris data provide further support for this. We developed an assay using radio-labeled fluconazole to measure intracellular azole accumulation in fungal cells. The assay is performed under glucose-replete conditions to inhibit ATP-dependent efflux. A comparative study measuring fluconazole uptake in 63 C. auris isolates as well as a panel of other species such as C. albicans, S. cerevisiae, C. glabrata, C. krusie, C. lusitanea, C. tropicalis, and C. dublinienses revealed striking C. auris phenotypes that we have not seen in other fungal species. There is a strong correlation between fluconazole resistance and reduced drug uptake in C. auris. Fluconazole-resistant C. auris isolates had reduced levels of intracellular fluconazole accumulation compared to susceptible isolates. Drug-resistant C. auris isolates had the lowest drug accumulation of any of the yeast species tested. Fluconazole-susceptible C. auris isolates had dramatically increased fluconazole accumulation compared to the resistant isolates as well as when compared to other yeast species. Of the 63 C. auris isolates, 28 of 32 (∼88%) resistant isolates had extremely low fluconazole uptake, whereas 15 of 18 (∼83%) susceptible isolates had high fluconazole uptake. This association between reduced drug uptake and resistance could be a C. auris-distinctive mechanism of drug resistance.

Candida auris is an emerging, multidrug resistant pathogen, responsible for invasive hospital-acquired infections. Flucytosine is an effective anti-Candida drug, but which cannot be used as a monotherapy because of the risk of development of resistant mutants during treatment. It is therefore noteworthy to test possible combinations with flucytosine that may have a synergistic interaction. In this study, we determined the in vitro interaction between flucytosine and amphotericin B, micafungin, or voriconazole. These combinations have been tested against 15 C. auris isolates. The MIC range (Gmean) of flucytosine, amphotericin B, micafungin and voriconazole were 0.125 to 1 μg/mL (0.42 μg/ml), 0.25 to 1 μg/ml (0.66 μg/ml), 0.125 to 0.5 μg/ml (0.3 μg/ml) and 0.03 to 4 μg/ml (1.05 μg/ml), respectively. When tested in combination, indifferent interactions were mostly observed with fractional inhibitory concentration index values from 0.5 to 1, 0.31 to 1.01 and 0.5 to 1.06 for the combination of flucytosine with amphotericin B, micafungin and voriconazole, respectively. A synergy was observed for the strain CBS 10913 from Japan. No antagonism was observed for any combination. Combination of flucytosine with amphotericin B or micafungin may be relevant for the treatment of C. auris infections.

Candida auris is a novel and emerging pathogenic yeast which represents a serious global health threat. Since its first description in Japan 2009, it has been associated with large hospital outbreaks all over the world and is often resistant to more than one antifungal drug class. To date, five C. auris isolates have been detected in Austria. Morphological characterization and antifungal susceptibility profiles against echinocandins, azoles, polyenes and pyrimidines, as well as the new antifungals ibrexafungerp and manogepix, were determined. In order to assess pathogenicity of these isolates, an infection model in Galleria mellonella was performed and whole genome sequencing (WGS) analysis was conducted to determine the phylogeographic origin. We could characterize four isolates as South Asian clade I and one isolate as African clade III. All of them had elevated minimal inhibitory concentrations to at least two different antifungal classes. The new antifungal manogepix showed high in vitro efficacy against all five C. auris isolates. One isolate, belonging to the African clade III, showed an aggregating phenotype, while the other isolates belonging to South Asian clade I were non-aggregating. In the Galleria mellonella infection model, the isolate belonging to African clade III exhibited the lowest in vivo pathogenicity. As the occurrence of C. auris increases globally, it is important to raise awareness to prevent transmission and hospital outbreaks.

Since its first emergence in December 2019, due to its fast distribution throughout the world, SARS-COV-2 become a global concern. With the extremely increased number of hospitalized patients,this situation provided a potential basis for the transmission of nosocomial infections. Candida auris is a multidrug-resistant pathogen with improved transmission dynamicsand resistance traits. During the worldwide spread of COVID-19, cases or outbreaks of C. auris colonization or infection have been reported.Resistance to antifungal drugs has been observed in the causative agents of the majority of such cases. The focus in this review is on COVID-19-associated C. auris infections(case studies/outbreaks) and the pandemic's potential effect on antifungal drug resistance.

Candida auris is a multidrug-resistant yeast that rapidly spreads, making it the leading Candidate for the next pandemic. One main leading cause of emerging resistant C. auris isolates is nonsynonymous mutations. This study aimed to detect the Y132F mutation, one of the most important azole resistance-associated mutations in the ERG-11 gene of C. auris, by developing a reliable high-resolution melt (HRM)-based method. Five C. auris isolates from Iran, plus three control isolates from other Clades were used in the study. The antifungal susceptibility testing through micro broth dilution was performed to recheck their susceptibility to three azole antifungals, including fluconazole, itraconazole, and voriconazole. Moreover, the polymerase chain reaction (PCR) sequencing of the ERG-11 gene was performed. Following the bioinformatic analysis and HRM-specific primer design, an HRM-based assay was developed and evaluated to detect ERG-11 mutations. The minimum inhibitory concentrations of fluconazole among Iranian C. auris isolates ranged from 8 to 64 μg/mL. The PCR-sequencing of the ERG-11 gene and bioinformatic analyses revealed the mutation of Y132F, a substitution consequence of A to T on codon 395 in one fluconazole-resistant isolate (IFRC4050). The developed HRM assay successfully differentiated the targeted single nucleotide polymorphism between mutant and wild types (temperature [Tm]: 81.79 ℃ - cycle threshold [CT]: 20.06 for suspected isolate). For both mutant and non-mutant isolates, the mean Tm range was 81.79-82.39 °C and the mean CT value was 20.06-22.93. These results were completely in accordance with the findings of DNA sequencing. The fast-track HRM-based method successfully detected one of the most common mechanisms of resistance in the ERG-11 gene of C. auris within 3 h. Finally, the development of more panels of HRM assays for the detection of all azole resistance mutations in C. auris ERG-11 is recommended to expand the scope of the field and facilitate the elaboration of rapid and accurate methods of antifungal resistance assessment.

BackgroundThe globally emerging Candida auris pathogens poses heavy burden to the healthcare system. Their molecular analyses assist in understanding their epidemiology, dissemination, treatment, and control. This study was warranted to describe the genomic features and drug resistance profiles using whole genome sequencing (WGS) among C. auris isolates from Lebanon.MethodsA total of 28 C. auris clinical isolates, from different hospital units, were phenotypically identified by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) and tested for antifungal resistance using Vitek-2 system and E test. The complete genomes were determined by WGS using long reads sequencing (PacBio) to reveal the clade distribution and antifungal resistance genes.ResultsCandida auris revealed uniform resistance to fluconazole and amphotericin B, with full susceptibility to echinocandins. Among key resistance genes studied, only two mutations were detected: Y132F in ERG11 gene and a novel mutation, D709E, found in CDR1 gene encoding for an ABC efflux pump. Phylogenetically, C. auris genomes belonged to South Asian clade I and showed limited genetic diversity, suggesting person to person transmission.ConclusionThis characterization of C. auris isolates from Lebanon revealed the exclusivity of clade I lineage together with uniform resistance to fluconazole and amphotericin B. The control of such highly resistant pathogen necessitates an appropriate and rapid recovery and identification to contain spread and outbreaks.

Legionella is the causative agent of Legionnaires’ disease (LD). In Spain, Catalonia is the region with the highest incidence of LD cases. The characterisation of clinical and environmental isolates using molecular epidemiology techniques provides epidemiological data for a specific geographic region and makes it possible to carry out phylogenetic and population-based analyses. The aim of this study was to describe and compare environmental and clinical isolates of Legionella pneumophila in Catalonia using sequence-based typing and monoclonal antibody subgrouping. A total of 528 isolates were characterised. For data analysis, the isolates were filtered to reduce redundancies, and 266 isolates (109 clinical and 157 environmental) were finally included. Thirty-two per cent of the clinical isolates were ST23, ST37 and ST1 while 40% of the environmental isolates were ST284 and ST1. Although the index of diversity was higher in clinical than in environmental ST isolates, we observed that clinical STs were similar to those recorded in other regions but that environmental STs were more confined to particular study areas. This observation supports the idea that only certain STs trigger cases or outbreaks in humans. Therefore, comparison of the genomes of clinical and environmental isolates could provide important information about the traits that favour infection or environmental persistence.