Nasal Colonization With Methicillin-Resistant Staphylococcus Aureus (Mrsa) Among Hiv-Infected Children

ABSTRACT Background: Methicillin-resistant Staphylococcus aureus (MRSA) poses a public health threat because it is extensively resistant to antimicrobials, is associated with persistent outbreaks in hospital and community settings, and is associated with markedly increased healthcare costs. Moreover, HIV-infected persons are at a higher risk for colonization with MRSA, and could potentially disseminate the pathogen to other individuals. In Ghana, little is known about MRSA in relation to at-risk populations, such as HIV-infected children. General aim: The aim of this study was to investigate nasal carriage of S. aureus and MRSA among HIV-infected and uninfected children in Accra, including the prevalence, risk factors and antibiogram. Methodology: This study was cross-sectional, and involved 107 HIV-infected children recruited at the Princess Marie Louis Children’s Hospital (PML) in Accra and an equal number of sex- and age group-matched apparently healthy children without HIV infection (control group) recruited from PML and its environs. Nasal swab specimens were collected from the study participants and cultured. S. aureus isolates were confirmed by the tube coagulase test, while MRSA was confirmed via PCR targeting the mecA gene. S. aureus susceptibility to standard antimicrobial agents was tested by the Kirby Bauer method. Antimicrobials tested included tetracycline (30 µg), erythromycin (15 µg), gentamicin (10 µg), rifampicin (5 µg), cotrimoxazole (1.25 + 23.75 µg), penicillin (10 µg), clindamycin (2 µg), fusidic acid (10 µg), cefoxitin (30 µg), linezolid (10 µg), and vancomycin (30 µg). A pretested structured questionnaire was also used to obtain data on demographic, household, and clinical features of the study participants. Binary logistic regression was performed to identify predisposing factors for S. aureus and MRSA carriage among both the HIV-infected and uninfected children. Results: The carriage prevalence of S. aureus and MRSA were 44.9% (n = 48) and 5.6% (n = 6) respectively among the HIV-infected individuals, and the corresponding values within the control group were 23.4% (n = 25) and 0.9% (n = 1). HIV infection was significantly associated with S. aureus colonization (p = 0.001; OR = 2.67), but not MRSA colonization (p = .055). The only significant predictor of S. aureus colonization in both study groups was absence of colonization with coagulase-negative Staphylococci (CONS): HIV-infected individuals (p < 0.001; OR = 0.078); HIV-uninfected individuals (p < 0.001; OR = 0.038). Also, the only significant predictor v of MRSA colonization among the HIV-infected participants was regular hand washing with soap (p = 0.043; OR = 6.462). None of the variables assessed showed significant associations with MRSA colonization among the HIV-uninfected participants. In both study groups, the S. aureus isolates showed no resistance to fusidic acid, linezolid and vancomycin. For the other antimicrobials, the resistance rates recorded in the HIV-infected and uninfected participants respectively were penicillin (98.1% vs. 96%), cotrimoxazole (62.3% vs. 72%), tetracycline (49.1% vs. 40%), rifampicin (30.2% vs. 36%), erythromycin (26.4% vs. 44%), clindamycin (18.9% vs. 52%), gentamicin (15.1 vs. 16%), and cefoxitin (11.3% vs. 4%). The proportion of S. aureus isolates that were multidrug resistant (MDR) was 62.3% (33/53) in the HIV-infected group and 80% (20/25) in the control group. Conclusions: Prevalence of MRSA appears to be generally low among both HIV-infected and HIV-uninfected children in Accra. HIV infection is a risk factor for nasal colonization with S. aureus among children in Accra, but may not be for MRSA. Probably due to the low MRSA carriage, determinants of MRSA nasal colonization among the study participants appear to be very limited, and this hardly involves demographic, household, and clinical features. Both HIV-infected and uninfected children are reservoirs of multidrug resistant S. aureus, which are entirely susceptible to fusidic acid, linezolid, and vancomycin.