Molecular Characteristic, Antibiotic Resistance, and Detection of Highly Immunoreactive Proteins of Group B Streptococcus Strains Isolated From Urinary Tract Infections in Polish Adults

Abstract

Group B streptococcus (GBS) is one of the uropathogens that causes urinary tract infections (UTIs). The aims of this article were molecular characterization, an analysis of antimicrobial susceptibility profiles, adherence to bladder endothelial cells, and the detection of immunoreactive proteins of 94 clinical strains of GBS isolated from adult Polish patients with UTI. Antibiotic susceptibilities were determined by disk diffusion. Serotyping and Alp family genes detection were studied using multiplex PCR. Genetic profiles were determined by pulsed-field gel electrophoresis. The adherence ability of the studied strains was estimated by incubation on human bladder microvascular endothelial cell line. Immunoreactive proteins were studied by immunoblotting. Antibiotic susceptibility investigation revealed that 22% of GBS strains were resistant to erythromycin, whereas 18% demonstrated resistance to clindamycin. cMLSB was present in 76% of the resistant strains, M phenotype was detected in 14%, whereas iMLSB was present for 10%. The most common serotype was serotype III (31%), followed by serotype V (27%), and serotype Ia (17%). The genes that dominated among other Alp genes were: epsilon (29%), alp2 (27%), and rib (23%). The most common co-occurring serotypes and Alp genes were: Ia and epsilon, III and rib, III and alp2, V and alp2, and V and alp3 (p < 0.001). The PFGE method showed high clonality for serotype V and cMLSB (p < 001). The PFGE method showed high clonality for serotype V. Furthermore, this serotype was significantly associated with the cMLSB phenotype (p < 0.001). The most common immunoreactive proteins demonstrated masses of 50 kDa and 45–47 kDa. Although examined GBS isolates showed high genetic diversity, immunoreactive proteins were common for most of the studied GBS isolates, which may indicate their conservation, and allows to consider them as potential immunodiagnostic markers. Although the examined GBS isolates showed high genetic diversity, immunoreactive proteins were shared by most of the studied GBS isolates. It may indicate their conservation, thus allowing to consider them as potential immunodiagnostic markers.

Microbiological monitoring of antibiotic resistance of strains of Streptococcus agalactiae among pregnant women

“…It was established that 30% of the strains of GBS isolated from the urine of pregnant women of the Ukraine were resistant to erythromycin. Polish researchers established that 22% of GBS strains were resistant to this antibacterial drug (Dobrut et al, 2022). In China, 63% of GBS strains were resistant to erythromycin, in the USA -39.5% of such strains (Mohanty et al, 2021).…”

“…Researchers from United Arab Emirates found that 42% of GBS strains were resistant to clindamycin (Balachandran et al, 2022), and in Poland 18% of GBS strains were resistant to this antibacterial drug (Dobrut et al, 2022). In China, 44.4% of GBS strains isolated from the urine of pregnant women were resistant to clindamycin, in the USA -26.4% of such strains (Mohanty et al, 2021).…”

“…The expression of these genes is defined as the MLSB phenotype, which is associated with cross-resistance to macrolides, lincosamides, and streptogramin B. The MLSB phenotype can be both constitutive macrolide-lincosamide-streptogramin B (cMLSB) resistance and inducible resistance to macrolide-lincosamide-streptogramin B (iMLSB) (Guo et al, 2018;Dobrut et al, 2022). Streptococci can be resistant to macrolides through the production of ribosomal erm methylases, causing the MLSB phenotype, or through the expression of efflux pumps encoded by genes of the mef(A) class.…”

“…High levels of GBS resistance to streptomycin are determined by the production of ANT ( 6) or other enzymes or by ribosomal mutations. In enterococci with a high level of resistance to streptomycin, the synergistic effect between streptomycin and β-lactams is absent (Guo et al, 2018;Dobrut et al, 2022). GBS resistance to kanamycin is associated with the production of APH(3')-1-3 or bifunctional APH (2')-ACC(6) enzymes, which determine the reduction of synergism between kanamycin and amikacin and β-lactams and glycopeptides regardless of MIC levels.…”

“…GBS resistance to kanamycin is associated with the production of APH(3')-1-3 or bifunctional APH (2')-ACC(6) enzymes, which determine the reduction of synergism between kanamycin and amikacin and β-lactams and glycopeptides regardless of MIC levels. The high level of resistance to gentamicin is due to the production of bifunctional APH (2')-ACC(6) enzymes, which determine the reduction of synergism between all aminoglycosides (except streptomycin and arbekacin) and beta-lactams and glycopeptides, regardless of MIC levels (Guo et al, 2018;Dobrut et al, 2022). GBS resistance to tetracycline is most often caused by two mediated genes, tet(M) and tet(O), which are transmitted mainly by transposons (Ali et al, 2020;Khan et al, 2023).…”