Pedro Martinez1, Denisse Garzón, Salim Mattar. 1. Universidad de Córdoba, Institute for Tropical Biological Research, Monteria, Colombia. pjmartinezr@hotmail.com
Abstract
OBJECTIVE: Describe the presence of CTX-M-1 phylogenetic subgroup extended-spectrum β-lactamases (ESBL), associated with TEM and SHV genes, and the gene encoding cephalosporinase, CMY-2 in Escherichia coli and Klebsiella pneumoniae isolates from community-acquired urinary tract infections. METHODS: 102 E. coli and 21K. pneumoniae were collected from patients with culture-proven urinary tract infection (UTI), during February and March, 2011. Antimicrobial susceptibility test was performed by disk diffusion according to the standards of the Clinical Laboratory Standard Institute. Screening for cephalosporins-resistant E. coli and K. pneumoniae was performed by PCR assay for bla(TEM), bla(SHV), bla(CTX-M-1),(-2),(-8),(-9), bla(PER-2) and bla(CMY-2) genes. Statistical analysis was performed by chi-squared test and multivariate logistic regression analysis. RESULTS: ESBL production was detected in 12 (11.7%) E. coli and four (19%) K. pneumoniae isolates. TEM ESBLs were detected in seven E. coli and three K. pneumoniae isolates. SHV ESBLs were found in four K. pneumoniae isolates. CTX-M-1 phylogenetic subgroup was positive in seven E. coli and three K. pneumoniae isolates. CMY-2 β-lactamase gene was detected in nine E. coli and one K. pneumoniae isolates. A significant association of ESBL expression in E. coli was observed with resistance to tobramycin (p≤0.001), tetracycline (p=0.043), and ciprofloxacin (p≤0.001). In K. pneumoniae isolates, significant association was found with resistance to tobramycin and ciprofloxacin (p=0.006), and trimethoprim-sulfamethoxazole (p=0.043). Multivariate analyses did not show association between ESBL production in E. coli and K. pneumoniae, and resistance to non-β-lactams drugs. CONCLUSIONS: CTX-M ESBL in uropathogens isolated from the community is cause for concern due to the enormous potential for multidrug resistance from strains that produce these enzymes, which could lead to failure of empirically-administered therapies and development of complicated UTIs.
OBJECTIVE: Describe the presence of CTX-M-1 phylogenetic subgroup extended-spectrum β-lactamases (ESBL), associated with TEM and SHV genes, and the gene encoding cephalosporinase, CMY-2 in Escherichia coli and Klebsiella pneumoniae isolates from community-acquired urinary tract infections. METHODS: 102 E. coli and 21K. pneumoniae were collected from patients with culture-proven urinary tract infection (UTI), during February and March, 2011. Antimicrobial susceptibility test was performed by disk diffusion according to the standards of the Clinical Laboratory Standard Institute. Screening for cephalosporins-resistant E. coli and K. pneumoniae was performed by PCR assay for bla(TEM), bla(SHV), bla(CTX-M-1),(-2),(-8),(-9), bla(PER-2) and bla(CMY-2) genes. Statistical analysis was performed by chi-squared test and multivariate logistic regression analysis. RESULTS:ESBL production was detected in 12 (11.7%) E. coli and four (19%) K. pneumoniae isolates. TEM ESBLs were detected in seven E. coli and three K. pneumoniae isolates. SHV ESBLs were found in four K. pneumoniae isolates. CTX-M-1 phylogenetic subgroup was positive in seven E. coli and three K. pneumoniae isolates. CMY-2 β-lactamase gene was detected in nine E. coli and one K. pneumoniae isolates. A significant association of ESBL expression in E. coli was observed with resistance to tobramycin (p≤0.001), tetracycline (p=0.043), and ciprofloxacin (p≤0.001). In K. pneumoniae isolates, significant association was found with resistance to tobramycin and ciprofloxacin (p=0.006), and trimethoprim-sulfamethoxazole (p=0.043). Multivariate analyses did not show association between ESBL production in E. coli and K. pneumoniae, and resistance to non-β-lactams drugs. CONCLUSIONS: CTX-M ESBL in uropathogens isolated from the community is cause for concern due to the enormous potential for multidrug resistance from strains that produce these enzymes, which could lead to failure of empirically-administered therapies and development of complicated UTIs.
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