Diarrhoeagenic Escherichia coli in mother-child Pairs in Ile-Ife, South Western Nigeria.

BACKGROUND: Diarrhoeagenic Escherichia coli (DEC) pathotypes are among the most common bacterial causes of morbidity and mortality in young children. These pathogens are not sought routinely and capacity for their detection is limited in Africa. We investigated the distribution and dissemination of DEC in 126 children paired with their mothers in a Nigerian community. METHODS: A total of 861 E. coli were isolated from 126 children with diarrhoea and their mothers. Antimicrobial susceptibility of each isolate was determined by Kirby-Bauer disc diffusion technique. All the isolates were screened for DEC markers by multiplex PCR. Genetic relatedness of DEC strains was determined by flagellin typing and Insertion element 3 (IS3)-based PCR. RESULTS: DEC were identified from 35.7% of individuals with the most common pathotype being shiga toxin-producing E. coli (42, 16.7%). Identical pathotypes were found in 13 (10.3%) of the mother-child pairs and in three of these strains from mothers and their children showed identical genetic signatures. Over 90% of DEC isolates were resistant to ampicillin, sulphonamide, tetracycline, streptomycin or trimethoprim, but only 9 (7.2%) were ciprofloxacin resistant CONCLUSION: The data suggest that healthy mothers are asymptomatic reservoirs of multiply-resistant strains that are pathogenic in their children and there are instances in which identical strains are found in mother-child pairs.

Rectal carriage of extended-spectrum ß-lactamase-producing Enterobacteriales among neonates admitted into a special care baby unit, southwest Nigeria.

BACKGROUND: The intestinal microbiota of neonates can be colonised by extended-spectrum ß-lactamase-producing Enterobacteriales (ESBL-PE) with the risks of subsequent infections. The antimicrobial resistance profile of the gut flora of neonates is not well defined in Nigeria. This study determined the burden of rectal carriage of ESBL-PE among neonates. METHODS: We conducted a prospective longitudinal study among neonates admitted into a tertiary hospital from September 2019 to November 2019. Stools were sampled at admission and weekly until exit and processed by standard laboratory methods including polymerase chain reaction to identify ESBL genes. The ESBL-PE colonisation period prevalence at admission and acquisition rate were determined. RESULTS: The period prevalence of the ESBL-PE colonisation and acquisition rate were 46.5% (59/127) and 34.6% (36/104), respectively. Prolonged rupture of the amniotic membrane (PROM; >24 h; p=0.004, odds ratio [OR] 0.297), number of neonates on admission in the same room (p<0.001, OR 0.053) and presence of an ESBL-PE colonisers (p=0.004, OR 0.272) were independent risk factors for ESBL-PE rectal colonisation. ESBL-PE colonisation did not correlate with mortality (Fisher's exact test 1.342, p=0.196). CONCLUSIONS: The rate of ESBL-PE neonatal rectal colonisation is high in our settings and this underscores the need for a review of neonatal admission protocols, embracing of antibiotic stewardship in the management of PROM, resistance surveillance and implementation of infection prevention and control in the neonatal unit.

Rapid evolution of fluoroquinolone-resistant Escherichia coli in Nigeria is temporally associated with fluoroquinolone use.

BACKGROUND: Antibiotic resistance has necessitated fluoroquinolone use but little is known about the selective forces and resistance trajectory in malaria-endemic settings, where selection from the antimalarial chloroquine for fluoroquinolone-resistant bacteria has been proposed. METHODS: Antimicrobial resistance was studied in fecal Escherichia coli isolates in a Nigerian community. Quinolone-resistance determining regions of gyrA and parC were sequenced in nalidixic acid resistant strains and horizontally-transmitted quinolone-resistance genes were sought by PCR. Antimicrobial prescription practices were compared with antimicrobial resistance rates over a period spanning three decades. RESULTS: Before 2005, quinolone resistance was limited to low-level nalixidic acid resistance in fewer than 4% of E. coli isolates. In 2005, the proportion of isolates demonstrating low-level quinolone resistance due to elevated efflux increased and high-level quinolone resistance and resistance to the fluoroquinolones appeared. Fluoroquinolone resistance was attributable to single nucleotide polymorphisms in quinolone target genes gyrA and/or parC. By 2009, 35 (34.5%) of isolates were quinolone non-susceptible with nine carrying gyrA and parC SNPs and six bearing identical qnrS1 alleles. The antimalarial chloroquine was heavily used throughout the entire period but E. coli with quinolone-specific resistance mechanisms were only detected in the final half decade, immediately following the introduction of the fluoroquinolone antibacterial ciprofloxacin. CONCLUSIONS: Fluoroquinolones, and not chloroquine, appear to be the selective force for fluoroquinolone-resistant fecal E. coli in this setting. Rapid evolution to resistance following fluoroquinolone introduction points the need to implement resistant containment strategies when new antibacterials are introduced into resource-poor settings with high infectious disease burdens.

Antimicrobial resistance in Escherichia coli strains from urinary tract infections.

BACKGROUND: An increase in resistance against many different drugs among urinary tract infection (UTI) E coli isolates has been observed in the last 2 decades. This study determined the trends of antimicrobial resistance in E coli to commonly used antibiotics. METHODS: The study was conducted in Ile-Ife, southwest Nigeria. Patients with features suggestive of UTI were investigated for presence of significant bacteriuria. Urine isolates were identified. Antimicrobial susceptibility was evaluated in accordance with standard bacteriological methods. RESULTS: Of 442 urine specimens, 158 (35.8%) yielded significant growth, including 41 (25.6%) with E coli. Among the E coil isolates, antimicrobial susceptibility varied in prevalence by agent in descending order as follows: nitrofurantoin (80%), ofloxacin (24%), ciprofloxacin (15%), nalidixic acid (10%), cotrimoxazole (5%), and amoxicillin/clavulanic acid (2%). No isolate was susceptible to amoxicillin, gentamicin, or tetracycline. All were also found to be resistant to at least 3 commonly used drugs. All 25 isolates tested for extended-spectrum beta-lactamase (ESBC) production were found to be presumptive ESBCs producers. CONCLUSION: The results demonstrate the continued susceptibility of E coil to nitrofurantoin and their widespread and increasing resistance to amoxicillin, gentamicin, cotrimoxazole, ciprofloxacin, ofloxacin, and tetracycline. Nitrofurantoin is a--and, in this locale, perhaps the only--rational drug for empiric treatment of uncomplicated UTI. There is a need for a comprehensive study of the involvement of ESBC-producing E coli in UTI in this environment.

A large self-transmissible resistance plasmid from Nigeria contains genes that ameliorate a carrying cost.

Antimicrobial resistance is rapidly expanding, in a large part due to mobile genetic elements. We screened 94 fecal fluoroquinolone-resistant Escherichia coli isolates from Nigeria for six plasmid-mediated quinolone resistance (PMQR) genes. Sixteen isolates harbored at least one of the PMQR genes and four were positive for aac-6-Ib-cr. In one strain, aac-6-Ib-cr was mapped to a 125 Kb self-transmissible IncFII plasmid, pMB2, which also bears blaCTX-M-15, seven other functional resistance genes and multiple resistance pseudogenes. Laboratory strains carrying pMB2 grew faster than isogenic strains lacking the plasmid in both rich and minimal media. We excised a 32 Kb fragment containing transporter genes and several open-reading frames of unknown function. The resulting 93 Kb mini-plasmid conferred slower growth rates and lower fitness than wildtype pMB2. Trans-complementing the deletion with the cloned sitABCD genes confirmed that they accounted for the growth advantage conferred by pMB2 in iron-depleted media. pMB2 is a large plasmid with a flexible resistance region that contains loci that can account for evolutionary success in the absence of antimicrobials. Ancillary functions conferred by resistance plasmids can mediate their retention and transmissibility, worsening the trajectory for antimicrobial resistance and potentially circumventing efforts to contain resistance through restricted use.

Correction: Classes 1 and 2 integrons in faecal Escherichia coli strains isolated from mother-child pairs in Nigeria.

[This corrects the article DOI: 10.1371/journal.pone.0183383.].

Classes 1 and 2 integrons in faecal Escherichia coli strains isolated from mother-child pairs in Nigeria.

BACKGROUND: Antimicrobial resistance among enteric bacteria in Africa is increasingly mediated by integrons on horizontally acquired genetic elements. There have been recent reports of such elements in invasive pathogens across Africa, but very little is known about the faecal reservoir of integron-borne genes. METHODS AND FINDINGS: We screened 1098 faecal Escherichia coli isolates from 134 mother-child pairs for integron cassettes by PCR using primers that anneal to the 5' and 3' conserved ends of the cassette regions and for plasmid replicons. Genetic relatedness of isolates was determined by flagellin and multi-locus sequence typing. Integron cassettes were amplified in 410 (37.5%) isolates and were significantly associated with resistance to trimethoprim and multiple resistance. Ten cassette combinations were found in class 1 and two in class 2 integrons. The most common class 1 cassette configurations were single aadA1 (23.4%), dfrA7 (18.3%) and dfrA5 (14.4%). Class 2 cassette configurations were all either dfrA1-satI-aadA1 (n = 31, 7.6%) or dfrA1-satI (n = 13, 3.2%). A dfr cassette was detected in 294 (31.1%) of trimethoprim resistant strains and an aadA cassette in 242 (23%) of streptomycin resistant strains. Strains bearing integrons carried a wide range of plasmid replicons of which FIB/Y (n = 169; 41.2%) was the most frequently detected. Nine isolates from five different individuals carried the dfrA17-aadA5-bearing ST69 clonal group A (CGA). The same integron cassette combination was identified from multiple distinct isolates within the same host and between four mother-child pairs. CONCLUSIONS: Integrons are important determinants of resistance in faecal E. coli. Plasmids in integron-containing strains may contribute to dispersing resistance genes. There is a need for improved surveillance for resistance and its mechanisms of dissemination and persistence and mobility of resistance genes in the community and clinical settings.

Prolonged febrile illness due to CTX-M-15 extended-spectrum ß-lactamase-producing Klebsiella pneumoniae infection in Nigeria.

We report on an 8-year-old patient with septicaemia unresponsive to therapy for five weeks. Undetected, extended-spectrum ß-lactamase (ESBL) production by the infecting Klebsiella strain was regarded as responsible for treatment failure. Intravenously administered imipenem during the sixth week led to sustained resolution of fever. Resource-limited hospitals can incur prohibitive costs from ESBL-producer infections because of diagnostic limitations and consequent treatment failure involving prolonged supportive therapy.