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. 2026 Jan 29;18:100852. doi: 10.1016/j.ijregi.2026.100852

Global threats in local wards: Dissemination of high-risk clones resistant to last-generation cephalosporins and carbapenems in Iraqi hospitals

Ehsan Adnan Hashim 1,§, Meriem Souguir 1,§, Véronique Métayer 2, Antoine Drapeau 2, Sana Azaiez 1, Hayder Ali Muhammed 3, Jean-Yves Madec 2, Marisa Haenni 2,⁎, Wejdene Mansour 1
PMCID: PMC12934271  PMID: 41756521

Highlights

  • •

    Overall, 40.4% (42/104) of the studied isolates were expanded-spectrum cephalosporins-resistant or carbapenems-resistant.

  • •

    High genetic diversity of sequence types (STs), except for Acinetobacter baumannii.

  • •

    Detection of international high-risk clones (Escherichia coli ST131, Pseudomonas aeruginosa ST773).

  • •

    Dissemination of multidrug-resistant in young people in hospitals in Iraq.

Keywords: P. aeruginosa, A. baumannii, ST773, NDM-1, Iraq, Enterobacterales

Abstract

Objectives

To conduct the first comprehensive molecular characterization of multidrug-resistant Gram-negative pathogens isolated from patients in six Iraqi hospitals.

Methods

Samples (n = 104) were collected from outpatients across six hospitals in Iraq between March and September 2022. Bacterial isolates were identified using standard microbiological techniques. Antimicrobial susceptibility testing was performed according to EUCAST guidelines. Genomic DNA was extracted and subjected to whole-genome sequencing (WGS).

Results

Over 104 samples, 42 resistant isolates were identified: Escherichia coli (n = 15), Klebsiella pneumoniae (n = 7), Pseudomonas aeruginosa (n = 15), and Acinetobacter baumannii (n = 5). WGS revealed genetic diversity, with the dominance of high-risk clones such as E. coli sequence type (ST131) (n = 6), K. pneumoniae ST14, ST15 or ST394 and P. aeruginosa ST308 or ST773. The extended-spectrum beta-lactamase phenotype in E. coli and K. pneumoniae was mainly conferred by the blaCTX-M-15 gene. Carbapenem-resistance was predominantly mediated by the blaNDM-1 gene, which was identified in K. pneumoniae ST15 and ST2943 isolates, and in P. aeruginosa ST308 and ST773. In A. baumannii ST2 isolates, carbapenem-resistance was due to the presence of the blaOXA-23 gene.

Conclusions

These findings highlight the dissemination of high-risk clones resistant to expanded-spectrum cephalosporins and carbapenems in geographically diverse Iraqi hospitals, underscoring the urgent necessity to establish comprehensive national antimicrobial resistance surveillance and infection control strategies.

Introduction

Antimicrobial resistance (AMR) represents a real threat to public health worldwide, leading to considerable morbidity and mortality rates with nearly 1.27 million deaths caused directly by AMR in 2019 [1]. In 2024, the World Health Organization (WHO) revised its list of bacterial priority pathogens and classified Enterobacterales resistant to expanded-spectrum cephalosporins (ESC) and carbapenems (CP) and CP-resistant (CP-R) Acinetobacter baumannii as part of the “critical” group [2]. The reason for this classification is the severity of the infections caused by these pathogens, their capacity to disseminate resistance by horizontal gene transfer and their overall burden, especially in low and middle-income countries [3,4]. CP-R Pseudomonas aeruginosa were removed from the critical group but still appear in the “high” group because of their importance in hospital settings [2].

In Enterobacterales, ESC-resistant (ESC-R) is globally mediated by extended-spectrum beta-lactamases (ESBLs) belonging to the CTX-M family [5], which are mostly plasmid-borne and can thus disseminate inside and across different sectors of the One Health scheme. Carbapenemase genes are also often carried by plasmids and transposons; the most frequently identified genes are blaOXA-48, blaNDM, blaVIM, blaKPC and blaIMP, with proportions varying depending on the country, the host, or the bacterial species studied [6]. In P. aeruginosa, CP-R can also be mediated by mutations in the OprD porin [7]. Both ESC-R and CP-R bacteria adapt very rapidly and are often multidrug-resistant (MDR), leading to longer hospital stays and higher in-patient mortality [8].

Iraq, an upper-middle-income country with a population of nearly 46.1 million inhabitants, lacks systematic surveillance of AMR within its healthcare system, both in hospitals and the community, except for a sporadic scientific publications [9,10]. Iraq previously implemented a National Action Plan on AMR for the period 2018–2022, which included the establishment of an integrated national AMR surveillance system. Unfortunately, persistent violence and the added pressure of the COVID-19 pandemic have obstructed the full implementation of this plan [11,12]. Building on this framework, Iraq has finalized an updated National Action Plan for 2026–2030, designed to strengthen the fight against AMR through multisectoral coordination and a One Health approach, incorporating concrete measures for surveillance, prevention and action across the human, animal, and environmental health sectors [13]. According to the study by Murray et al. [1], Iraq ranks 80th out of 204 countries for the age-standardized mortality rate per 100,000 population associated with AMR. In the North Africa and Middle East region, Iraq holds the 9th highest age-standardized mortality rate among 21 countries. Five pathogens are of particular concern in Iraq: Escherichia coli, Klebsiella pneumoniae, P. aeruginosa and A. baumannii, which are responsible for the highest number of AMR-related deaths [1].

Given the numerous challenges and the lack of essential data needed to understand the emergence and spread of resistance genes, plasmids or clones, there is an urgent need of active surveillance in Iraq to implement appropriate interventions [14,15]. In line with this knowledge gap, our goal was to collect and characterize at a molecular level ESC-R and CP-R Gram-negative bacteria circulating within the Iraqi community between March and September 2022, focusing on outpatient services in various hospitals across Iraq. By addressing these objectives, we aimed at laying the first stone toward a national surveillance of AMR and supporting the development of effective strategies to combat this growing threat.

Materials and methods

Samples collection and bacterial isolation

Clinical samples (n = 104) were collected between March and September 2022 from six different hospitals in Iraq (Najaf Al-Ashraf Teaching Hospital, Hospital Alhala Education, Al Marjan Teaching Hospital, AL-Diwaniya Teaching Hospital, Middle Euphrates Burn Center and Al Hussein Teaching Hospital) (Figure S1). Samples came from urinary tract infections (n = 50), burned patients (n = 36), acute otitis media (n = 2), respiratory tract infections (n = 13), and orchitis (n = 3). The patients' demographic data (age, gender) were recorded, along with the origin of the sample and the isolation date (Table S1).

The detection of ESC-R and CP-R Enterobacterales, and CP-R P. aeruginosa and A. baumannii, was performed on non-selective media according to the standard routine procedures of the central microbiology laboratory of the Alameen Center for Advanced Research and Biotechnology in Najaf. Bacterial identification was carried out using conventional culture methods followed by biochemical identification using Api20E and Api20NE galleries (bioMérieux).

Antimicrobial susceptibility testing

Susceptibility testing was performed using the disk diffusion method on Mueller-Hinton agar, according to the guidelines and clinical breakpoints of the Antibiogram Committee of the French Society for Microbiology (CA-SFM, https://www.sfm-microbiologie.org/wp-content/uploads/2024/06/CASFM2024_V1.0.pdf). Antibiotics used and corresponding breakpoints are indicated in Table S2. The following quality control strains were used: E. coli ATCC 25922 for Enterobacterales isolates and P. aeruginosa ATCC 27853 for P. aeruginosa and A. baumannii isolates. ESBL-producing Enterobacterales were detected using the double disk synergy test between amoxicillin + clavulanic acid, ceftiofur, cefquinome and ceftazidime. The minimum inhibitory concentrations (MICs) for colistin were determined using broth microdilution, following EUCAST recommendations [16].

Illumina short-read sequencing and data analyses

DNA was extracted using the NucleoSpin Microbial DNA extraction kit (Macherey-Nagel, Hoerdt, France) and sequencing was performed using a NovaSeq 6000 instrument (Illumina, San Diego, CA, USA; outsourced to Eurfins Genomics, Ebersberg, Germany). Quality control of the reads was performed using FastQC and low-quality sequences were trimmed using Trimmomatic v0.39. De novo assembly was performed using Shovill v1.0.4 and the quality of assemblies was assessed using QUAST v5.0.2 (Table S3). Identification was performed using Kraken (https://github.com/DerrickWood/kraken). Sequence types (STs), resistance genes and virulence factors were determined using the CGE online tools (http://www.genomicepidemiology.org/) MLST 2.0, ResFinder 4.7.2 and VirulenceFinder 2.0.3, while replicon content and plasmid formula were identified using PlasmidFinder 2.1 and pMLST 2.0.

Phylogenetic analysis

The cgMLST phylogeny was determined through the pyMLST pipeline v2.0.1 (https://github.com/bvalot/pyMLST) using the scheme available on the www.cgmlst.org/ncs, which comprised 2513 alleles for E. coli, 2358 for K. pneumonia, 3867 for P. aeruginosa and 2390 for A. baumannii. The cut-off for highly related strains was <10 allelic differences. The resulting trees were visualized using iTol v7 (https://itol.embl.de/). Distance matrix between isolates was performed using snp-dists v0.8.2 (Table S4).

Long-read sequencing

To get better insight into a subset of plasmids, MinION long-read sequencing libraries were prepared according to the Oxford Nanopore Technologies (ONT, UK) using the ligation sequencing kit (SQK-LSK114). Sequencing was performed on an Mk1B MinION sequencer using a R10.4.1 version flow cell (FLO-MIN114) and the basecalling was performed with Dorado v0.4.2. Hybrid assembly of both Illumina short reads and Nanopore long reads was performed using Unicycler v0.4.8. Annotation was performed using Bakta 1.9.1 and the genetic environments of blaESBL and carbapenemase genes were explored using BLASTn.

Data availability

The project was deposited in GenBank under the BioProject accession number PRJNA1294745.

Results

Between March and September 2022, 104 samples were obtained from outpatients visiting six Iraqi hospitals, with 79.8% of the samples originating from the Najaf Al-Ashraf Teaching Hospital (n = 49) and from the Middle Euphrates Burn Center (n=36) (Table S1, Figure S1). Over the 104 samples, 65 were collected from female (62.5%) and 39 from male (37.5%), aged between 17 to 50 years (median age: 28 years) and mainly suffering from urinary tract infections (UTI, n = 50) or burns (n = 36). From these samples, 42 (40.4%, 42/104) resistant isolates were collected and identified as 15 P. aeruginosa (15/35, 42.9%), 15 E. coli (15/28, 53.6%), seven K. pneumoniae (7/21, 33.4%) and five A. baumannii (5/19, 26.3%) (Table S2). One isolate per sample and per patient was collected, except for one patient suffering from UTI that presented both an E. coli and a P. aeruginosa isolate. Resistant isolates were collected from 28 female (28/65, 43.1%) and 13 male patients (13/39, 33.4%). The proportion of resistant bacteria identified was 42.0% (21/50) in UTIs and 30.5% (11/36) in burned patients, with a majority of E. coli and K. pneumoniae in UTIs (12/21, 57.1%) and of A. baumannii and P. aeruginosa in burned patients (9/11, 81.8%).

Genetic diversity of resistant isolates

Genomic analyzes revealed that the 15 collected E. coli belonged to eight different STs, most of which were high-risk pandemic clones (Figure 1a). The most frequently identified clones were ST131 (n = 6), ST405 (n = 2) and ST69 (n = 2), the other ones being singletons. The two ST69, identified in May and June 2022, were clonally related (<10 allelic differences) and came from two different patients suffering from UTIs and visiting the same ward. Clonal relationship (0-3 allelic differences) was also observed for five ST131 isolates collected from patients suffering from UTIs (n = 4) and otitis (n = 1) and treated in three different hospitals. There were no known genetic links between the different patients and hospitals displaying clonal isolates. The last ST131 slightly diverged genetically (53-55 allelic differences). The seven K. pneumoniae isolates belonged to five different STs, with ST394 and ST14 each identified from two different patients (Figure 1b). In each of these two STs, isolates were clonally related (0-1 allelic difference) and were sampled over a period of 2 to 3 days from patients suffering from respiratory tract infections (RTI, for ST14) or UTIs (for ST394).

Figure 1.

Figure 1 dummy alt text

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cgMLST-based phylogeny of E.coli (a) and K. pneumoniae (b) isolates. The ST of the isolate appears beside the identifier. Associated metadata (hospital of origin and pathology) are indicated in the middle of the figure. On the right panel, resistance genes identified in at least one isolate are listed. Filled squares indicate the presence of the gene, empty squares indicate the absence of the gene.

RTI, respiratory tract infection; ST, sequence type; UTI, urinary tract infection.

The 15 P. aeruginosa isolates originated from three hospitals and belonged to nine different STs. The most frequently identified STs were ST308 (n = 4), ST773 (n = 3, excluding isolate #63054, which is a single-locus variant (SLV) of ST773) and ST664 (n = 2), while the other clones were singletons (Figure 2). The four ST308 isolates were highly similar (0-6 allelic differences); they came from three patients suffering from UTI and visiting the same ward, and from a fourth patient presenting RTI and who was treated in another hospital. The three ST773 isolates were also clonally related (0-7 allelic differences) even though they came from two hospitals and three patients visiting different wards because of UTI, RTI, or burns. On the contrary, the SLV of ST773 (isolate #63054) differed from the ST773 isolates by 151-152 SNPs, excluding clonality. Finally, the five A. baumannii isolates all belonged to ST2 but clustered in two different groups differing by 14 alleles. Four isolates came from burn patients attending the same hospital, but also from one patient suffering from UTI and visiting another hospital.

Figure 2.

Figure 2 dummy alt text

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cgMLST-based phylogeny of P. aeruginosa isolates. The ST of the isolate appears beside the identifier. Associated metadata (hospital of origin and pathology) are indicated in the middle of the figure. On the right panel, resistance genes identified in at least one isolate are listed. Filled squares indicate the presence of the gene, empty squares indicate the absence of the gene.

RTI, respiratory tract infection; ST, sequence type UTI, urinary tract infection.

Phenotypic and genotypic characterization of expanded-spectrum cephalosporins- and carbapenems-resistant Enterobacterales

Thirteen out of the 15 E. coli isolates presented an ESBL phenotype, one presented an AmpC phenotype, and one presented both an ESBL and AmpC phenotype. No CP-R isolate was identified. In 13 isolates, the ESBL phenotype was due to the blaCTX-M-15 gene, mostly carried on the chromosome, while the blaCTX-M-55 gene, carried on an IncF plasmid, was detected in the last ESBL-positive isolates (Figure 1a, Table S2). The AmpC phenotype was conferred by the blaDHA-1 gene located on IncF plasmids. All but one isolate (ST409-blaCTX-M-55) were MDR, displaying resistances to at least two additional antibiotic families. The most frequently identified genes were sul1 (n = 11), tet(A) (n = 9), catB3 (n = 9), dfrA17 (n = 8) and aadA5 (n = 8).

All seven K. pneumoniae carried the blaCTX-M-15 (usually carried on an IncF plasmid), and additional resistances to sulfonamides, trimethoprim and aminoglycosides (streptomycin and/or kanamycin) were identified, conferred by the dfr14 (n = 6), sul2 (n = 5) and aph(6)-Id (n = 5) genes. Additionally, one ST15 and one ST2943 isolate carried the blaNDM-1 gene that conferred carbapenem-resistance (MIC to imipenem/meropenem >32 mg/l) (Figure 1b, Table S2). In the ST15 isolate, which co-harbored the blaCMY-6 and the rmtC genes, the blaNDM-1 gene was located on the chromosome. In the ST2943 isolate, the blaNDM-1 gene was harbored on an IncFIIk plasmid also carrying the sul1 gene. On this plasmid, the blaNDM-1 gene was directly preceded by the rmtC gene and bracketed between an IS5 and an IS91-like transposase.

Phenotypic and genotypic characterization of P. aeruginosa and A. baumannii isolates

Over the 15 P. aeruginosa isolates, seven presented the presence of a metallo-beta-lactamase gene (Figure 2, Table S2) which conferred high-level resistance to imipenem and meropenem (MIC>32 mg/l). The blaNDM-1 gene was identified in all three ST773 and in three out of the four ST308, while the blaVIM-11 gene was carried by ST1047. In all cases, the carbapenemase was carried on the chromosome. In ST773 isolates, the blaNDM-1 gene was located (together with the sul1, floR2, tet(G) and rmtB4 genes) on an ICE-like element of 74°888 bp. In ST308 isolates, the blaNDM-1 gene was embedded in a 76.1 kb ICE-like element identical to the ICETn43716385 described by Ding et al. [17]. The blaNDM-1, msr(E) and floR genes were located together, each separated by a transposase element. Additionally, all ST308 isolates carried the aadA11 and rmtF genes, outside the ICE-like element. The blaVIM-11 gene in the ST1047 isolate was located on a class 1 integron with no other co-harbored resistance gene and the isolate was susceptible to amikacin. The eight isolates that did not present any metallo-beta-lactamase gene presented MICs to imipenem and meropenem of ≥12 mg/L. Mutations (stop codons) in the oprD coding region were observed in 5/8 isolates (Table S2). In the last three isolates, carbapenem-resistance might be due to the over-expression of efflux pumps. Finally, one isolate (ST41) presented the ESBL-conferring gene blaPER-1.

Five CP-R A. baumannii isolates were collected from four burned patients and from a UTI. All carried the blaOXA-23 and the armA genes conferring respectively high-level resistances to carbapenems (MIC to imipenem and meropenem >32 mg/l) and amikacin (MIC>256 mg/l).

Discussion

The dissemination of AMR, in particular in Gram-negative bacteria, lowers the chances to successfully treat infectious diseases and constitutes a real public health risk worldwide [18]. The situation is particularly critical in low- and middle-income countries, where the general population has over-the-counter access to a broad range of antibiotics, while hospitalized patients do not have access to the latest molecules on the market. The goal of this study was to characterize the occurrence of critically important pathogens (i.e., Enterobacterales, P. aeruginosa and A. baumannii) in patients consulting six different hospitals in Iraq. This study provides important molecular data for understanding the dynamics of AMR transmission, and is intended to enrich the scientific database on AMR in Iraq, providing molecular data that were previously scarce. These data could potentially serve as a basis for public health authorities in Iraq to support the design and implementation of future AMR monitoring and intervention strategies. Results showed a high prevalence of resistant bacteria (40.4%, 42/104), with the identification of 15 ESBL-producing E. coli (15/42, 35.7%), seven ESC-R and CP-R K. pneumoniae (16.7%), 15 CP-R P. aeruginosa (35.7%) and five CP-R A. baumannii (11.9%) over the 104 samples analyzed. Patients carrying these resistant bacteria were young (median age of 28 years) which is of high concern since young people are at high risk of disseminating these bacteria through social contacts, whether professional or family-based. Also, even if this has to be confirmed by larger-scale studies, being a woman might be a risk factor of carrying a resistant bacteria (43.1% vs 33.4%).

While no genomic data were available yet from clinical samples in Iraq, a few phenotypic studies suggested important rates of resistance. Among 130 K. pneumoniae isolates collected from wounds in 2019-2021 in Baghdad, 74.6% were resistant to ceftazidime, 30.7% to ertapenem and 35.3% to amikacin [19]. In 2020, 25.2% (41/163) of the K. pneumoniae isolates from pneumonia were considered as ESBL-producers [20], while in 2021-2022, 40.6% of the K. pneumoniae and 61.6% of the E. coli isolates collected from UTIs were ESC-R [21]. In our study, 33.4% of the K. pneumoniae (including one carbapenemase producer) and 53.6% of the E. coli isolates were ESC-R, which is in line with published data. The first report of NDM-producing K. pneumoniae in Iraq was documented in 2010 from an Iraqi patient referred to France for treatment, after which NDM-1 became widespread in Baghdad, Iraq [22,23]. Also in Baghdad, a study performed on 55 P. aeruginosa isolates from diverse clinical sources showed that 35% and 40% of the isolates were respectively resistant to meropenem or imipenem [24].

Genomic analysis carried out as part of this study revealed considerable genetic diversity among E. coli, K. pneumoniae and P. aeruginosa isolates. Several high-risk pandemic clones were identified, such as E. coli ST131 (known as a major cause of UTIs combining resistance (CTX-M-15, resistance to fluoroquinolones) and virulence) or K. pneumoniae ST14 and ST15 [25]. Five ST131 were clonally related even though they came from three geographically distant hospitals, suggesting the frequent occurrence of this clone in Iraq. Two K. pneumoniae ST394 were collected one day apart in the same ward; this suggests the transmission (either by direct contacts or indirectly through the hospital’s personnel or medical devices) of this clone that has already been reported as the cause of a large outbreak (29 cases) in a French hospital [26]. The two main P. aeruginosa lineages identified in this study were ST308 and ST773. ST308 has been recurrently described as a metallo-beta-lactamase carrier over all continents except Africa [27,28]. More recently, a large-scale genomic study showed that this clone, together with ST773 and to a lesser extent ST357, is frequently carrying the blaNDM-1 gene [27]. And ST773 has also been recently found in Iraq as an important pathogen in diabetic foot infections (personal communication). In this study, the six NDM-1-carrying isolates indeed belonged to ST773 (n=3) and ST308 (n=3), while the only VIM-11-producing isolate belonged to an unrelated ST1047 clone. The blaNDM-1 gene was found on two types of large ICE-like genetic elements that might be horizontally transferred, one identified in ST308 and the other one in ST773 isolates, [17,29]. This latest element shared 99.9% identity and 100% coverage with the ICE described in ST773 isolates from Spain (accession number CP142443 and CP142449) and more recently from Iraq in a patient suffering from diabetic foot infection (personal communication) [29]. Reports of similar isolates are popping up all over the word, including in Iraq’s neighboring countries such as Saudi Arabia, warranting monitoring efforts to avoid their large-scale dissemination [30,31].

On the contrary, the five A. baumannii reported here all belonged to the ST2 clone, which is the most frequent international clone disseminating worldwide [32], and carried the blaOXA-23 and armA genes. Even though other CP-R STs have been reported in Iraq [32], a few studies have also confirmed the emergence of OXA-23-positive A. baumannii ST2, notably in four hospitals in the Kurdistan region [33]. In the Middle East, the occurrence of MDR A. baumannii has often been associated with war-related wounds, notably after the US military interventions in Afghanistan and Iraq [34]. This pathogen has gained international attention, having emerged as a highly resistant nosocomial pathogen in Iraq and subsequently spread via injured soldiers to hospitals in the US and UK [11]. This illustrates the global impact of conflict-associated infections, as recently reported for the above-described ST773 P. aeruginosa that was imported in Spain and the Netherland through Ukrainian patients [29].

This study has several limitations. First, the number of samples collected is small, especially for three hospital in which <10 isolates were obtained. Further larger-scale studies are now needed to understand the issue of AMR in each hospital to take measures to limit its spread. The implementation of a monitoring program and the nomination of a national reference laboratory that could centralize all pathogens of interest would be the ideal situation. A second limitation is that the origin of the isolates characterized here was not fully clear. Isolates were reported as coming from outpatients, so originating from the community. However, it is doubtful that burned or dialyzed people are really outpatients. Consequently, we considered in this study that collected isolates might have been acquired in the hospital. In future studies, it will be of utmost importance to characterize isolates that are circulating in the community on the one hand, and those that are associated to healthcare settings on the other hand.

Conclusion

This study provided molecular insights into the resistant Gram-negative pathogens that are circulating in Iraq. Results showed the occurrence of a diversity of high-risk clones spreading both ESC- and CP-resistance in young patients. This highlights the urgent need to implement a national surveillance system in Iraq, both in hospital settings and in the community. Further studies are now needed to have a broader picture of the AMR burden in this country and to identify potential sources of dissemination, so that effective actions can be taken in a near future to limit the spread of AMR.

Declaration of competing interest

The authors have no competing interests to declare.

Acknowledgments

Funding

This work was funded by internal funding from the Faculty of Medicine of Sousse and from internal funding of the ANSES (France).

Ethical approval statement

Not applicable.

Author contributions

EAH: Data collection, data analysis and writing; MS: Data analysis and writing; VM and AD: Lab work and data analysis; SA: Lab work; HAM: Supervision and revision of the manuscript; JYM: Revision of the manuscript; MH: Data analysis, writing, and validation; WM: Study design, data analysis, writing and supervision.

Footnotes

Supplementary material associated with this article can be found, in the online version, at doi:10.1016/j.ijregi.2026.100852.

Appendix. Supplementary materials

Figure S1. Map showing the locations of the six hospitals included in the study.

mmc1.pptx (235.6KB, pptx)
mmc2.xlsx (17.6KB, xlsx)
mmc3.xlsx (37KB, xlsx)
mmc4.xlsx (33.1KB, xlsx)
mmc5.xlsx (18.7KB, xlsx)

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Figure S1. Map showing the locations of the six hospitals included in the study.

mmc1.pptx (235.6KB, pptx)
mmc2.xlsx (17.6KB, xlsx)
mmc3.xlsx (37KB, xlsx)
mmc4.xlsx (33.1KB, xlsx)
mmc5.xlsx (18.7KB, xlsx)

Data Availability Statement

The project was deposited in GenBank under the BioProject accession number PRJNA1294745.

Articles from IJID Regions are provided here courtesy of Elsevier

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