Escherichia coli causing bloodstream infections in Mexican paediatric patients: molecular typing, antimicrobial resistance, virulence factors, and clinical features

Abstract

Background: Escherichia coli is one of the main pathogens causing bloodstream infections (BSIs) in paediatric patients. It is classified into pathogenic (B2, D and F) and commensal (A, B1 and C) phylogroups, with virulence mainly attributed to adhesins, toxins and iron acquisition systems. In recent years, the global spread of high-risk clones such as ST131 and ST405, often associated with extended-spectrum beta-lactamases (ESBLs), has contributed to increased resistance and limited treatment options. The BSI mortality rate in children varies from 14 to 21.6%. This study aimed to describe resistant mechanisms; virulence factors and clonal distribution of E. coli isolates that cause BSIs in children in Mexico and clinical features.

Methods: Thirty-eight ceftriaxone (CRO)-resistant E. coli isolates were included. Beta-lactamase and virulence genes were detected by PCR. Molecular typing included phylogroup determination, sequence types (ST), and pulsed-field gel electrophoresis (PFGE). Clinical information was acquired.

Results: CTX-M was the most frequently identified beta-lactamase (82%) and aac(6')-Ib-cr was present in 45%. Phylogroup distribution was A (21.1%), C (7.9%), D (28.9%), B2 (23.7%), and F (18.4%). The most common virulence factor was fimH (71%), while papC, sat and irp2 were significantly more frequently in the pathogenic phylogroups (P = 0.029, 0.011 and 0.006, respectively). PFGE identified 5 clusters, 20 non-related isolates and 4 non-typeable. Predominant clonal complexes (CC) were CC405 (23.7%) and CC131 (21.1%), with 82% of isolates belonging to high-risk clones. Survival rates differed significantly with moderate high-grade fever (P = 0.022). All patients who died had complications, compared to 34.8% of survivors (P < 0.0001). Mortality was higher in adolescents (53.3%), patients with leukaemia or lymphoma (40%), those with hospital-acquired infections (86.8%), those with an abdominal or pulmonary focus (33.3% each). No significant differences were found in of haematological parameters.

Conclusions: Both commensal and pathogenic E. coli strains cause BSIs in paediatric patients with underlying diseases. Resistance to 3GCs and 4GCs is mainly mediated by CTX-M, hence treatment with carbapenems was used. Infection-related deaths were more frequent in patients infected by pathogenic phylogroups, where papC, sat, and irp2 were more prevalent. High-risk clones were widely distributed among isolates.

Keywords: E. coli; BSI; ESBL; ExPEC; High-risk clone; Mexico; Paediatric patients; Phylogenetic groups; Virulence factors.

Fig. 1

Characteristics of the E. coli caused BSI in paediatric patients MLST: multilocus sequence typing, AMS: ampicillin-sulbactam, PTZ: piperacillin-tazobactam, AZT: aztreonam, CFZ: cefazolin, CXM: cefuroxime, FOX: cefoxitin, CAZ: ceftazidime, CRO: ceftriaxone, FEP: cefepime, MEM: meropenem, IPM: imipenem, CIP: ciprofloxacin, LEV: levofloxacin, AK: amikacin, GE: gentamicin, TOB: tobramycin, SXT: trimethoprim-sulfamethoxazole, CC: clonal complex, ST: sequence typing, CAI: community-acquired infection, HAI: hospital-acquired infection, SSTI: skin and soft tissue infections, ICU: intensive care unit, AMR: antimicrobial resistance. Data visualization was performed using R software (v4.5.0) with the ComplexHeatmap package (v2.24.0)

Fig. 2

Clonal relationship of the E. coli isolates associated with bacteraemia Dendrogram based on PFGE pattern analysis showing clonal relationships among isolates. Sequence types (ST), phylogroup and high-risk clones or clonal complex (HRC)/HRCC are indicated for each isolate. Four isolates were non-typeable (NT) by PFGE. MLST: multilocus sequence typing, CC: clonal complex, PFGE: pulsed-field gel electrophoresis and NR: non-related