Abstract
Background
Typhoid fever is a serious infection that primarily affects humans, with approximately 20 million cases reported each year, mostly in low- and middle-income countries (LMICs). Continuous monitoring of Salmonella enterica serovar Typhi (S. Typhi) in these endemic areas is crucial for tracking trends in antimicrobial resistance (AMR) and developing effective control measures. This study focused on S. Typhi isolates from children aged ≤ 16 years who showed symptoms of fever in Mukuru and Kibera informal settlements in Nairobi County, Kenya.
Methods
Blood samples for culture were collected from participants at four health facilities within Nairobi County. Antimicrobial susceptibility profiles were assessed using the Kirby–Bauer disc diffusion technique, and whole-genome sequencing (WGS) was performed on selected multidrug-resistant (MDR) isolates. The genomes were assembled and analysed using https://pathogen.watch/ to identify genotypes, resistance genes, and phylogenetic relationships.
Results
Out of 120 S. Typhi isolates tested, 50% were found to be MDR. Resistance to first-line antibiotics was common, with 65.6% resistant to ampicillin, 62.3% to sulfamethoxazole-trimethoprim, and 59% to chloramphenicol. Thirty-seven selected MDR isolates underwent WGS, all belonging to the genotype 4.3.1 (H58), which is the most prevalent MDR clade globally. These were further categorised into sublineage 4.3.1.1 EA (East Africa 1), accounting for 40.5% of the sequenced isolates. Genomic analysis identified several AMR genes, including blaTEM−1D, catA1, dfrA7, sul1, and sul2. Additionally, point mutations in the quinolone resistance-determining region (QRDR) of gyrA were found in 67.6% of the isolates, with the most common mutation being S83Y. These mutations are linked to decreased susceptibility to ciprofloxacin, a key treatment for typhoid in Kenya.
Conclusion
The high rate of MDR S. Typhi, especially in children who are most affected by the disease, raises significant public health concerns. The presence of QRDR mutations further complicates treatment options for typhoid fever, highlighting the urgent need for alternative approaches. These may include broader use of typhoid conjugate vaccines (TCVs), strengthening antimicrobial stewardship programs, and investing in improvements in water, sanitation, and hygiene (WASH) infrastructure in these endemic settings in Kenya.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12879-025-12317-z.
Keywords: Multi-drug resistance, Systemic, Children, S. Typhi, Mukuru, Kibera, Nairobi, Kenya
Background
Typhoid fever is a widespread infection in humans caused by the bacterium S. Typhi [1, 2]. In 2025, the Centre for Disease Control and Prevention (CDC) reported that approximately 9.2 million cases of typhoid fever occur worldwide each year, causing an estimated 133,000 deaths [3]. A separate report estimated a global incidence of 206 cases per 100,000 person-years in population-based studies occurring in sub-Saharan Africa (SSA) [4]. In 2021, 126,098 typhoid cases (251 cases per 100,000) were reported, resulting in 1,568 typhoid-related deaths in Kenya [5]. These reports underscore the ongoing public health challenge that typhoid fever presents in areas with limited resources, such as Kenya.
In regions where typhoid fever is endemic, the disease spreads due to inadequate water, sanitation and hygiene (WASH) infrastructure, overcrowding, and the consumption of unsafe street foods, particularly impacting children [6, 7]. If left untreated, it can lead to serious complications, such as intestinal perforation and neurological complications [8]. While blood culture is the most reliable diagnostic method for typhoid fever, many low-resource countries often rely on clinical symptoms for diagnosis, which can be inaccurate [9].
For many years, first-line antibiotics like ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole were effective in treating typhoid fever [6, 7, 10]. However, the rise of multidrug-resistant (MDR) S. Typhi has restricted their use, leading to a reliance on fluoroquinolones and third-generation cephalosporin’s as recommended by the World Health Organization (WHO) [1, 10]. Extensively drug-resistant (XDR) S. Typhi strains, which are resistant to both fluoroquinolones and third-generation cephalosporin’s, have emerged in South Asia and have been reported in cases associated with travellers’ worldwide [11]. Although azithromycin and carbapenems are still effective against XDR S. Typhi strains, their limited availability in LMICs creates significant treatment challenges [12].
Genomic research indicates that haplotype 58 (H58) is the predominant lineage of S. Typhi linked to MDR strains in Asia and SSA [13]. This lineage is marked by large conjugative plasmids like IncHI1 and mutations in the quinolone resistance-determining region (QRDR) of the gyrA gene, which decrease susceptibility to fluoroquinolones [14]. The growing presence of these resistant strains poses a risk to the effectiveness of existing treatment options of typhoid fever [13, 14].
Preventive measures, such as typhoid conjugate vaccines (TCVs), show great potential. Countries that have introduced TCVs report reductions in typhoid cases by 75–85% [6, 15–17]. These vaccines are given as a single intramuscular dose, are safe and generate an immune response in children under two years old, and are approved for use starting at six months of age, which is a significant improvement over older vaccines [15, 16, 18]. Despite the existence of preventive options, there is still a lack of local historical epidemiological data on MDR S. Typhi in many SSA regions. Such information is essential in providing baseline evidence for developing treatment guidelines, stewardship strategies, and the introduction of vaccines. This study focuses on multidrug-resistant S. Typhi isolates showing reduced susceptibility to ciprofloxacin and responsible for systemic infections in children living in the Mukuru and Kibera informal settlements in Nairobi County, Kenya.
Methods
Study design and setting
We carried out a cross-sectional study from November 2013 to November 2018 in two major informal settlements in Nairobi County, Kenya: Mukuru and Kibera. In Mukuru, participants were recruited from three outpatient health facilities: The Municipal County Council Clinic (MCC), Mukuru kwa Reuben Clinic (MR), and Medical Missionaries of Mary Clinic (MMM), all located about 20 km from Nairobi’s central business district. In Kibera, participants were recruited at Mbagathi County Referral Hospital (MB), the main referral facility for that area. A description of these two urban informal settlements has been included in previous published work by Kariuki et al., [14], and Mbae et al., [19]. These urban informal settlements are characterized by poor WASH infrastructure, abundance of street foods and crowded semi-structured housing. These living conditions predispose the residents of these settings to foodborne infections including typhoid fever [19].
Study population and eligibility criteria
The study included children aged 16 years and younger living in the Mukuru and Kibera settlements. Eligible participants were those who had (i) a fever lasting three days or more with an axillary temperature of 37.5 °C or higher, and (ii) with or without diarrhea. Children were excluded if they had received antibiotics before their visit or if they were unaccompanied by a parent or guardian. Written informed consent was obtained from parents or guardians for all study participants. Additionally, children aged 12 to 16 years provided verbal assent.
Blood sample collection and processing
Blood samples were collected in sterile conditions; 1 to 3 ml from children under 5 years and 8 to 10 ml from those aged 5 to 16 years. The samples were placed in BACTEC™ Peds Plus™ blood culture bottles (BD Diagnostics, Franklin Lakes, NJ, USA), and transported in cool boxes (without ice packs) to the Kenya Medical Research Institute (KEMRI) Microbiology Laboratory in Nairobi within six hours. Cultures were incubated at 37 °C using the BACTEC™ 9050 automated blood culture system. The positively flagged culture bottles were sub-cultured onto blood, chocolate, and MacConkey agar (Oxoid, Basingstoke, UK) to enhance the recovery of S. Typhi. Bottles that did not show a positive flag after seven days were sub-cultured before disposal to check for growth. Suspected colonies (pale colonies on MacConkey agar) were identified biochemically using API 20E strips (bioMérieux, France) and confirmed serologically with polyvalent O and monovalent antisera (9, d, Vi; Remel Europe Ltd).
Antimicrobial susceptibility testing (AST)
Antimicrobial susceptibility testing was conducted using the Kirby–Bauer disc diffusion method [20] on Mueller–Hinton agar (Oxoid, Basingstoke, UK). A bacterial suspension was made from isolated colonies and adjusted to a 0.5 McFarland turbidity. Plates (90 mm) were inoculated with a lawn culture, and antibiotic discs were applied using a dispenser. Eleven antibiotics from key therapeutic classes for Gram-negative bacteria were tested: amoxicillin-clavulanic acid (AMC, 20/10 µg), ampicillin (AMP, 10 µg), azithromycin (AZM, 15 µg), cefotaxime (CTX, 30 µg), cefpodoxime (CPD, 30 µg), ceftriaxone (CRO, 30 µg), chloramphenicol (CHL, 30 µg), ciprofloxacin (CIP, 5 µg), ceftazidime (CAZ, 30 µg), sulfamethoxazole-trimethoprim (SXT, 25 µg), and tetracycline (TET, 30 µg). Quality control was maintained using Staphylococcus aureus ATCC 25923 and Escherichia coli American type culture collection (ATCC) 25922. Results were interpreted following the Clinical and Laboratory Standards Institute (CLSI) guidelines (M100) [21]. MDR S. Typhi strain was defined as one resistant to all three first-line antibiotics: ampicillin, chloramphenicol, and sulfamethoxazole-trimethoprim.
Whole genome sequencing and assembly
Genomic DNA was extracted from a subset of the phenotypically confirmed MDR S. Typhi isolates using the Wizard® Genomic DNA Extraction Kit (Promega, Madison, WI, USA), following the manufacturer’s instructions. The purity and concentration of the DNA were evaluated using a NanoDrop™ One spectrophotometer (Thermo Fisher Scientific, Waltham, MA, USA). Library preparation was done using the Illumina DNA Prep tagmentation kit with unique dual indices. Sequencing was done on the Illumina NextSeq 2000 platform with 2 × 150 bp paired-end reads and an average coverage of 50×, with 2% PhiX control added to enhance base calling. The quality of raw sequencing reads was assessed using FastQC v0.11.9 [22]. Adapter sequences, low-quality bases (Q-score < 20), and ambiguous nucleotides were removed using Trimmomatic v0.39 [23]. High-quality reads were de novo assembled with Shovill v1.1.0, which utilizes SPAdes [24] as its core assembler and incorporates optimized pre- and post-assembly steps to improve efficiency and consistency. Assembly quality, including genome size, N50, and contig statistics, was assessed using QUAST v5.2 [25]. Genome assemblies were uploaded to https://pathogen.watch/ for in silico serotyping, genotyping, antimicrobial resistance gene detection, plasmid identification, and phylogenetic analysis.
Data analysis
Descriptive statistical methods, including frequency distributions and proportions, were utilised to summarise the socio-demographic characteristics of participants, as well as the prevalence and antimicrobial resistance profiles of S. Typhi, with a focus on multi-drug resistance and reduced susceptibility to fluoroquinolones. The Chi-square (χ²) test was applied to assess the relationships between categorical variables like age group, gender, and annual MDR prevalence to identify any significant associations. P > 0.05 was considered not statistically significant; a 95% confidence interval was used. The https://pathogen.watch/ platform was utilized to infer the distribution of S. Typhi genotypes circulating in the studied area, and the resulting phylogenetic trees were visualized and explored interactively using https://microreact.org/ to better understand the genetic connections and evolutionary traits among the strains in circulation.
Results
Participant demographics
From November 2013 to November 2018, 5559 patients were recruited and provided blood samples. Of these, 120 S. Typhi isolates were recovered (2.2%), Supplementary file 1. The age distribution indicated that most participants were ≤ 5 years, comprising 3855 (69.3%). The number of male participants 2,947 (53.1%) slightly exceeded that of females. Most study participants came from the Medical Missionary of Mary site, which targets Mukuru residents, totalling 1,964 (35.3%), Table 1. Age distribution was significantly associated with S. Typhi positivity, with children aged 6–10 years showing higher proportions 1260 (22.7%) (P = 0.0001). Male children were significantly more likely to be positive compared to females 2612 (53.1%) (P = 0.0018). Positivity varied significantly across study sites, with Medical Missionaries of Mary (MMM) and Mbagathi County Referral Hospital contributing the most positives (P = 0.0001), Table 1.
Table 1.
Participant demographics for children living in Mukuru and Kibera informal settlements, Nairobi, Kenya
| Variables | Participants N (%) |
S. Typhi positives N (%) |
|---|---|---|
| Age | ||
| ≤ 5 years | 3855 (69.3) | 54 (45) |
| 6–10 years | 1260 (22.7) | 49 (40.8) |
| 11–16 years | 444 (8.0) | 17 (14.2) |
| Gender | ||
| Male | 2947 (53.1) | 81 (67.5) |
| Female | 2612 (46.9) | 39 (32.5) |
| Study sites | ||
| Medical Missionaries of Mary | 1964 (35.3) | 44 (36.7) |
| Mukuru Kwa Reuben | 1404 (25.3) | 14 (11.7 |
| Municipal County Council | 1181 (21.3) | 18 (15) |
| Mbagathi County Referral Hospital | 1010 (18.1) | 44 (36.6) |
Antibiotic susceptibility profiles of S. Typhi
The 120 S. Typhi isolates exhibited varying AMR profiles, Supplementary file 1. Resistance of S. Typhi to first-line antibiotics was observed at; 78 (65.6%) for ampicillin, 74 (62.3%) for sulfamethoxazole-trimethoprim, and 70 (59%) for chloramphenicol, respectively. Generally, low resistance (≤ 5%), was observed against third-generation cephalosporins (ceftazidime 2 (1.6%), ceftriaxone 3 (2.5%), Cefpodoxime 2 (1.6%), and cefotaxime 6 (4.9%), Fig. 1.
Fig. 1.
Antibiotic susceptibility profiles of S. Typhi from children living in Mukuru and Kibera informal settlements, Nairobi, Kenya. AMC, amoxicillin-clavulanate; AMP, ampicillin; AZM, azithromycin; CAZ, ceftazidime; CHL, chloramphenicol; CIP, ciprofloxacin; CPD, cefpodoxime; CRO, ceftriaxone; CTX, cefotaxime; SXT, sulfamethoxazole-trimethoprim; TET, tetracycline
Prevalence of MDR S. Typhi
Of the 120 S. Typhi subjected to AST, 60 (50%) were reported as multidrug-resistant (isolates that exhibited combined resistance to ampicillin, chloramphenicol, and sulfamethoxazole-trimethoprim). Thus, the overall prevalence of MDR S. Typhi was 50% during the study period of 2013–2018. The annual prevalence of MDR S. Typhi was noted, with 2015, 2013, and 2018 showing the highest levels at 61%, 60%, and 58%, respectively. The lowest prevalence of MDR S. Typhi was recorded in 2016 at 36%.
MDR prevalence fluctuated year by year (36%–61%), but these differences were not statistically significant (P = 0.3920). The MDR levels remained persistently high rather than systematically increasing or decreasing, Table 2.
Table 2.
Annual prevalence of MDR S. Typhi among children residing in the Mukuru and Kibera informal settlements, Nairobi, Kenya
| Year | Annual S.Typhi isolations, N = 120 N (%) |
MDR S. Typhi N = 60 N (%) |
Prevalence of MDR S. Typhi (%) |
|---|---|---|---|
| 2013 | 5 (4.2) | 3 (5) | 60 |
| 2014 | 9 (7.5) | 4 (6.7) | 44 |
| 2015 | 36 (30) | 22 (36.7) | 61 |
| 2016 | 36 (30) | 13 (21.7) | 36 |
| 2017 | 22 (18.3) | 11 (18.3) | 50 |
| 2018 | 12 (10) | 7 (11.6) | 58 |
Genotypic characteristics of MDR S. Typhi
Of the 60 MDR S. Typhi, a subset (37;61.7%) was randomly selected for sequencing. All 37 sequenced MDR S. Typhi isolates were assigned to genotype 4.3.1 (H58). Within this lineage, the majority belonged to lineage 1 sub lineage 1 (4.3.1.1, n = 15; 40.5%), while the remaining isolates were evenly distributed between lineage 2 sub lineage 2 (4.3.1.2.2, n = 11; 29.7%) and lineage 2 sub lineage 3 (4.3.1.2.3, n = 11; 29.7%).
All sequenced isolates carried antimicrobial resistance (AMR) genes associated with resistance to first-line antibiotics. Specifically, blaTEM−1D conferred resistance to ampicillin, catA1 to chloramphenicol, and dfr7, sul1, and sul2 to trimethoprim-sulfamethoxazole. Plasmid analysis revealed that 17/37 (45.9%) isolates harboured plasmid replicons. Among these, 16 (94.1%) carried the large IncHI1A/IncHI1B (R27) plasmid, while one isolate (5.9%) carried a combination of four plasmid replicons: IncX4, IncFIA, IncFIB(AP001918), and IncFII(pRSB107), Supplementary file 1.
Reduced susceptibility to fluoroquinolones
Among the 120 S. Typhi isolates tested phenotypically, 90 (75%) exhibited intermediate susceptibility to ciprofloxacin. Whole genome sequencing of 37 MDR isolates demonstrated that 25 (67.6%) harboured point mutations in the gyrA and gyrB genes, which are known to confer reduced fluoroquinolone susceptibility.
The most common mutations were gyrA S83Y (12/25; 48%) and gyrB S464F (11/25; 44%), followed by gyrA D87G (2/25; 8%). Notably, more than half (13/25; 52%) of the isolates with these mutations also carried the IncHI1A/IncHI1B (R27) plasmid, suggesting co-selection of chromosomal and plasmid-mediated resistance determinants, Supplementary file 1.
Temporal and spatial distribution of MDR S. Typhi
The 37 sequenced MDR S. Typhi isolates belonging to the H58 lineage were distributed across all four study sites over the six-year study period (2013–2018). More than half were recovered from Mbagathi County Referral Hospital (n = 20; 55.6%), with the majority classified as sub lineage 4.3.1.1 (EA1).
The highest annual recovery was recorded in 2015, when 17 (42%) of the sequenced isolates were identified. Isolates were represented across the two major H58 lineages and three sub lineages, with no significant gender bias (male 19/37; 52.7% vs. female 17/37; 47.3%).
These findings highlight both the sustained circulation and the genetic diversity of H58 MDR S. Typhi in Nairobi’s informal settlements over time, Fig. 2.
Fig. 2.
Phylogenetic tree showing distribution of genotypes of MDR S. Typhi from children living in Mukuru and Kibera informal settlements, Nairobi, Kenya. A phylogenetic tree prepared on https://pathogen.watch/ and visualised on https://microreact.org/. The colour on the nodes represents the genotypes of the MDR S. Typhi from children living in Mukuru and Kibera informal settlements, Nairobi, Kenya. Key; MB-Mbagathi County Referal Hospital, MCC-Municipal County council, MMM-Medical Missionaries of Mary, MR-Mukuru kwa Reuben
Discussion
Typhoid fever continues to pose a significant public health issue in areas where it is endemic and resources are limited, particularly due to the ongoing presence of MDR strains of S. Typhi and the rise of XDR variants. This study reveals notable resistance to first-line antibiotics, with ampicillin exhibiting a resistance rate of 65%, sulfamethoxazole-trimethoprim at 62%, and chloramphenicol at 59%. These findings align with a previous study from Nairobi, which reported resistance rates of 72%, 72%, and 70%, respectively [26] as well as regional data that reflect similar trends in SSA [27–29]. The high levels of resistance are likely due to the widespread and often uncontrolled use of these antibiotics in affected populations. In addition, this could be attributed to the transmission of MDR S. Typhi lineages.
The reported prevalence of MDR S. Typhi was 50%, meaning that half of the isolates were resistant to all three first-line drugs. This figure is comparable to findings from South Africa (65%) [29] and Ghana (52%) [30] but higher than some other reports from Kenya (37%) [28]. Differences in MDR prevalence across various studies may be attributed to variations in study demographics, sampling methods, and geographic areas covered.
It was noted that 75% of the isolates showed reduced susceptibility to ciprofloxacin, which is concerning since it is recommended for treating typhoid fever in Kenya. This trend is consistent with earlier reports indicating that up to 69% of Kenyan isolates were not susceptible to ciprofloxacin [26]. Genomic analysis identified specific mutations in the gyrA and gyrB genes, such as S83Y and S464F, which are known to contribute to resistance against fluoroquinolones. Similar mutations have been frequently reported in SSA and Southeast Asia (SEA), particularly in codon 83 of gyrA [31–33].
The increase in these mutations is closely linked to the global spread of MDR H58 lineages, which are becoming increasingly resistant to fluoroquinolones [34]. Decreased susceptibility to ciprofloxacin whose preferred test of measure is minimum inhibitory concentration (MIC) has a significant clinical impact in management of typhoid fever. This drug may no longer be effective in treatment of infections caused by MDR S. Typhi.
All isolates sequenced in this study belonged to haplotype 58, the predominant lineage associated with MDR traits. This finding is consistent with previous studies from Kenya and other regions in SSA and Southeast Asia (SEA) [34–37]. Notably, nearly 46% of the isolates contained IncHI1A/B plasmids, which carry important AMR factors and are strongly associated with the persistence of MDR traits [35].The spread of H58 strains across SSA and SEA indicates both repeated introductions and ongoing local transmission, highlighting its role as a major contributor to AMR in typhoid fever [34–36].
Phylogenetic analysis showed a close relationship among isolates from two informal settlements in Nairobi, suggesting a shared ancestry and likely transmission within these interconnected communities [38, 39].This emphasizes the need for enhanced genomic surveillance in other Kenyan urban informal settlements to better understand the distribution and diversity of S. Typhi lineages.
Limitation of the study
We acknowledge that the dataset used (2013–2018) may not capture the most recent AMR trends of S. Typhi in Kenya. However, these data provide critical historical insight into the emergence and establishment of MDR H58 and early fluoroquinolone resistance during a pivotal period for typhoid epidemiology. These findings contribute essential baseline evidence that can inform current surveillance, contextualize recent reports, and support ongoing public health and policy efforts on AMR.
Conclusion
The high rates of MDR S. Typhi and reduced susceptibility to ciprofloxacin present a considerable challenge for treatment. Ciprofloxacin may no longer be a dependable option for treating typhoid fever in these regions. It is crucial to strengthen antimicrobial stewardship, promote responsible antibiotic use, and improve WASH infrastructure. Long-term control will rely on scaling up preventive measures, such as widespread administration of typhoid conjugate vaccines, and exploring alternative treatment options, including bacteriophage-based therapies.
Supplementary Information
Below is the link to the electronic supplementary material.
Acknowledgements
Authors of this manuscript appreciate all study participants, clinicians and the community health promoters in Mukuru and Kibera informal settlements. We also acknowledge Collins Kigen and the KEMRI fraternity for support in conducting of this research study.
Abbreviations
- AMR
Antimicrobial Resistance
- AST
Antimicrobial Susceptibility Testing
- ATCC
American Type Culture Collection
- CLSI
Clinical and Laboratory Standards Institute
- H58
Haplotype 58
- KEMRI
Kenya Medical Research Institute
- LMIC
Low- and Middle- Income Countries
- MDR
Multidrug Resistance
- MIC
Minimum Inhibitory Concentration
- QRDR
Quinolone Resistance Determining Region
- SEA
Southeast Asia
- SERU
Scientific Ethics and Review Unit
- SSA
sub Saharan Africa
- TCV
Typhoid Conjugate Vaccine
- WASH
Water, Sanitation and Hygiene
- WGS
Whole Genome Sequencing
- XDR
Extensively Drug Resistance
Author contributions
SK, CM, RO designed the study. CM coordinated the study. MM, PN, JC, NW, SA, EK, GO, SM, MK, BO conducted participant recruitment, consenting and sample collection. SMK, CW, AJ, EW, WB, DO, PM, CK, HM, NK, CK, MK, JK, DI, RN conducted sample processing. CM supervised sample collection and processing. RO, ZW, KK, CK conducted data analysis. SMK drafted the manuscript. All authors reviewed the draft manuscript. SK received the grant that funded the research.
Funding
The National Institute of Allergy and Infectious Diseases of the National Institutes of Health under Award Number R01AI099525 to Prof Sam Kariuki supported this study.
Data availability
All Data is provided within the manuscript or supplementary material. Fasta files appearing in this manuscript were deposited into Genbank and are publicly available on [SUB14367959 Genomes report | Submission Portal](https://submit.ncbi.nlm.nih.gov/wgs_common/report/SUB14367959).
Declarations
Ethics approval and consent to participate
Written informed consent was obtained from all parents or guardians of the participants. Children aged 12 to 16 years provided additional verbal assent. The study received ethical approval from the Kenya Medical Research Institute Scientific and Ethics Review Unit (SERU; reference SCC2076). Participant confidentiality and data anonymity throughout the study was ensured. The study was conducted in accordance with the ethical principles outlined in the Declaration of Helsinki for research involving human participants.
Consent for publication
Not applicable.
Disclaimer
The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health (NIH).
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
All Data is provided within the manuscript or supplementary material. Fasta files appearing in this manuscript were deposited into Genbank and are publicly available on [SUB14367959 Genomes report | Submission Portal](https://submit.ncbi.nlm.nih.gov/wgs_common/report/SUB14367959).