Table 1.
Antibiotic susceptibility and pathotypes of three E. coli isolates used in the infectivity study.
Table 2.
Antibiotic sensitivity of confirmed E. coli isolates from hospital wastewater.
Table 3.
Antibiotic resistance patterns of E. coli isolates from hospital wastewater.
Table 4.
Antibiotic resistance patterns of pathogenic E. coli pathotypes.
Fig 1.
Distribution of E. coli pathotypes isolated from hospital wastewater over one month.
Enteroinvasive E. coli and Enteropathogenic E. coli were not detected during the study. Key: ETEC–Enterotoxigenic E. coli; EAEC–Enteroaggregative E. coli; EHEC–Enterohaemorrhagic E. coli; DEC- diarrhoeagenic E. coli.
Fig 2.
Weekly distribution of E. coli pathotypes obtained from hospital effluent.
Key: ETEC–Enterotoxigenic E. coli; EAEC–Enteroaggregative E. coli; EHEC–Enterohaemorrhagic E. coli; DEC- diarrhoeagenic E. coli.
Fig 3.
(a-c) Infectivity of Hela cells by clinical (positive control) and environmental strains of pathogenic E. coli. a. Adherence of clinical and environmental EAEC and EHEC to Hela cells. ETEC was negative for adhesion. b. Invasion of Hela cells by clinical and environmental ETEC, EAEC, and EHEC. c. Intracellular survival of clinical and environmental ETEC and EHEC in Hela cells. EAEC was negative for intracellular survival. Clinical strains refer to positive controls, and the environmental isolates to representative isolates (BHE16, ETEC; BHE59, EAEC; BHE94, EHEC) obtained in this study. At each time point, bars with similar lowercase letters indicate that adherence, invasion, or intracellular activity are not significantly different (p > 0.05) between the two strains. For each strain, bars with different upper case letters indicate that adherence, invasion, or intracellular activity are significantly different (p < 0.05) between the two time points.