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Folia Medica 2011; 46 No 1:35-403. Community-associated Methicillin-ResistantStaphylococcus aureus (CA-MRSA) http://www.cdc.gov/ncidod/dhqp/ar_mrsa ca.html.2005.4. Naomi TS, LeDell KH, Como-Sabetti K. Comparisonof community- and health care-associatedmethicillin-resistant Staphylococcus aureus infection.Jama 2003;290(22):2976-84.5. Petrović Jeremić LJ. Učestalost meticilin-rezistentnihStaphylococcus aureus (MRSA) sojevakod zdravih kliconoša u Pomoravskom okrugu.Acta Medica Medianae 2010;49(1):33-36.6. Šiširak M, Zvizdić A, Hukić M. Methicillin-resistantStaphylococcus aureus (MRSA) as a cause ofnosocomial wound infections. Bosnia Journal ofBasic Medical Sciences 2010;10(1):34-37.7. Nurkić M. Causes of infection surgical wound.The fourth Symposium of Hospital Infection Controlof Bosnia and Herzegovina, Tuzla, Bosniaand Herzegovina, Juny 14 th -16 th , 2006. Proceedings:9-19.8. Bischoff WE, Wallis ML, Tucker KB, ReboussinBA, Shertz RJ. Staphylococcus aureus nasal carriagein a student community: prevalence clonalrelationships and risk factors. Infect Control HospEpidemiol 2004; 25(6):485-91.9. Wertheim HF, Melles DC, Vos MC, van LeeuwenW, van Belkum A, Verbrugh HA et al. The roleof nasal carriage in Staphylococcus aureus infections.Lancet Infect Dis 2005; 5(12):751-62.10. Eveillard M, Martin Y, Hidri N, Boussougant Y,Joly-Guillou ML. Carriage of methicillin-resistantStaphylococcus aureus among hospital employees:prevalence, duration, and transmission tohouseholds. Infect Control Hosp Epidemiol 2004;25:114-20.11. Cesur S, Cokca F. Nasal carriage of methicillinresistantStaphylococcus aureus among hospitalstaff and outpatients. Infect Control Hosp Epidemiol2004; 25:169-71.12. Hacek DM, Suriano T, Noskin GA, Kruszynski J,Reisberg B, Peterson LR. Medical and economicbenefit of a comprehensive infection control programthat includes routine determination of microbialclonality. Am J Clin Pathol. 1999; 111:647-654.40
Original PapersDetection of Cytokines IFN γ, TNF α and IL 10 in Acute andChronic Human ToxoplasmosisSabaheta Bektaš 1 , Snježana Balta 1 , Mufida Aljičević 2 , Edina Bešlagić 21Department of Microbiology,Institute for Public Health of Canton Sarajevo2Department of Microbiology,Faculty of Medicine, University of SarajevoCorresponding Author:Edina BešlagićDepartment of Microbiology,Faculty of Medicine, University of SarajevoObjective: Cytokines are low-level molecular proteins secretedby wide spectrum of cells and included in the mediationand the regulation of non-specific and specific acquired immuneresponse. T. gondii infection is strong trigger of naturaland acquired immunity regulated by vast range of protectiveand regulatory cytokines. The aim of this research is to analyzeand verify the level of production of cytokines (IFN-γ,TNF-α and IL 10). Materials and methods: This research wasclinical-experimental study which involved experimental andcontrol group. First group of subjects was represented by 40patients seropositive to T. gondii, out of which 26 patients hadacute toxoplasma infection and 14 ones had chronic toxoplasmainfection. Second group consisted of 30 subjects seronegativeto T. gondii. Their serums were tested for the presenceand concentration of specific cytokines (IFN-γ, TNF-αand IL10). The levels of mentioned cytokines were verifiedby the Elisa test (enzyme-linked immunosorbent assay) usingcommercial kits: IFN-γ-EASIA (Biosource Europe S.A,Nivelles, Belgium), Human TNF-α/TNFSF1A (R&D SystemsInc, Minneapolis, USA) and Human IL-10 (R&D SystemsInc, Minneapolis, USA). Results: Acute phase of infectionis expressed by significant increase of IFN-γ level related toothers cytokines (p
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