[Study of antibiotic influence on adherence capacity of gram positive and gram negative bacteria to the cellular substrate].

Bacterial adherence to the cellular substrate (skin and mucosa) represents a precondition of infectious pathology. It was demonstrated that bacteria which adhere and form biofilms on catheters and other inert materials used in medicine are resistant to the therapeutic antibiotic concentrations being protected by the biofilm mathrix and generating severe and hard to treat infections. There are only few studies on the influence of antibiotics on the bacterial adhesins synthesis and bacterial adherence to the cellular substrate. The purpose of this study was to investigate the influence of subinhibitory concentrations of antibiotics on adherence capacity of Listeria monocytogenes, Vibrio cholerae and Aeromonas hydrophyla to the cellular substrate represented by HEp-2 cells. Suspensions (approximately 10(10) cells/ml) of bacterial cultures developed on solid media were incubated for 30 minutes in the presence of subinhibitory concentrations of penicillin, ampicillin, amoxicilin with clavulanic acid, ceftazidim, norfloxacin, kanamycin, chloramphenicole and vancomycin. Study of bacterial adherence to the cellular substrate was done by Cravioto's modified method. The quantitative evaluation of adherence/invasion capacity of bacterial suspensions pretreated with antibiotics was done by comparing the adherence/invasion index with controls without antibiotics. Penicillin, amoxicillin with clavulanic acid and vancomycin have significantly stimulated the adherence of Listeria monocytogenes strain and inhibited the adherence of Vibrio cholerae and Aeromonas hydrophyla strains. Ampicillin and chloramphenicole exhibited no significant effect on bacterial adherence capacity. The influence of kanamycin, ceftazidim and norfloxacin could not be interpreted due to the occurrence of a severe cytotoxic effect manifested by cell monolayer detaching, probably due to the action of antibiotic suspensions or to the increase of bacterial virulence under the selective pressure of the antibiotic.