Investigation the effects of antibiotics on staphylococcus hominis clinical isolates

Staphylococcus hominis is a Gram-positive, cocci-shaped, opportunistic pathogen that forms grape-like clusters. This bacterial species is present in the human microbiota along with other staphylococci and is commonly found on the head, arms, armpits and legs. However, as an opportunistic pathogen in immunocompromised individuals or in hospital settings, it causes bacteremia, endocarditis, skin and soft tissue infections and the incidence of these symptoms is increasing. The bacterium is also known to rapidly develop resistance to antibiotics, making infections difficult to treat. Empirical use of antibiotics, especially the administration of broad-spectrum antibacterial agents without a clear identification of the causative agent of the disease, is an important risk factor for the development of resistance to coagulase-negative staphylococci such as S. hominis, which are among the opportunistic pathogens. Especially in catheter-associated infections or implant surface colonization, members of the normal skin microbiota such as S. hominis may turn into resistant infectious pathogens due to their ability to form biofilms as a result of the off-target effects of empirical treatments. Therefore, antibiotic resistance profiles and biofilm formation capacities should be taken into consideration in the treatment of these bacteria and targeted therapy should be applied. In this thesis, hemolytic activities of 41 clinical S. hominis isolates were determined by blood agar method and antibiotic susceptibility profiles were determined by disk diffusion and minimum inhibitory concentrations with a total of 11 antibiotics belonging to different antibiotic groups. After these profiles were determined, biofilm production and siderophore activities of the isolates were investigated and S. aureus ATCC 29213 strain was used as a positive control. Of the 41 isolates, 46.3% showed beta, 53.7% gamma hemolytic activity. All isolates were resistant to clindamycin, one of the antistaphylococcal antibiotics. This was followed by erythromycin resistance in 37 isolates (90.2%), methicillin resistance in 34 isolates (82.9%) and trimethoprim- sulfamethoxazole resistance in 26 isolates (63.4%). All were sensitive to chloramphenicol antibiotic. Out of 41 isolates, 40 (97.6%) were multidrug resistant, while the remaining 1 isolate showed resistance only to clindamycin. Biofilm production and siderophore activity of the isolates were also investigated. Biofilm production was quantitatively determined by crystal violet binding assay and 31 out of 41 isolates (75.6%) showed significantly higher biofilm production than the control strain. Only 1 isolate (2.4%) showed lower biofilm production; the remaining 9 isolates (22%) showed similar biofilm production. In addition, biofilm production was investigated at lower values of the minimum inhibitory concentration (sub-MIC) of erythromycin, tetracycline, trimethoprim- sulfamethoxazole and vancomycin antibiotics used in the treatment of staphylococcal infection diseases. Biofilm production decreased in 4 of 5 isolates studied at 1⁄2 MIC of erythromycin antibiotic (p<0.05). At 1⁄2 MIC of tetracycline antibiotic, biofilm production increased in ATF-2 and ATF-29 and decreased in ATF-33 (p<0.05). At 1⁄2 MIC of vancomycin antibiotic, 15 of 31 isolates (48.4%) showed an increase in biofilm production, while 6 isolates (19.4%) showed a decrease (p<0.05). At 1⁄2 MIC of trimethoprim-sulfamethoxazole antibiotic, biofilm production increased in ATF-1, ATF- 2, ATF-6 and ATF-39, while it decreased in ATF-31 and ATF-33 (p<0.05). When siderophore activities were analyzed, none of the 41 isolates showed siderophore production equal to or higher than that of the control strain. In conclusion, although they are often overlooked, opportunistic pathogens play an important role in infectious diseases because they can be a gene source for the spread of antimicrobial resistance, have multiple antibiotic resistance, produce biofilms and cause hemolysis, which indicate the virulence characteristics of bacteria. This study underlines that clinical S. hominis isolates, especially in nosocomial infections, are a pathogen that should not be ignored for the above-mentioned reasons and has been understudied in the literature. The fact that almost all isolates have multidrug resistance and all of them can produce biofilms clearly shows the risk of failure of empirical approaches in the treatment of these bacteria.