HIV-positive gay men have an increased risk of MRSA, even when they are doing well on HIV treatment, US investigators report in the July 1st edition of the Journal of Infectious Diseases.
“Our study highlights community-acquired MRSA colonization and infection as important problems among asymptomatic HIV-infected men who have sex with men without evidence of immune suppression”, write the study’s authors.
Skin colonisation by methicillin-resistant Staphylococcus aureus (MRSA) can lead to the development of MRSA infection. MRSA is now a leading cause of skin and soft tissue infections amongst HIV-positive individuals in the US.
However, there is currently little information on MRSA colonisation and infection in asymptomatic HIV-positive individuals with strong immune systems.
Investigators therefore designed a year long study comparing rates of MRSA carriage and infections in 107 HIV-positive gay men and 52 HIV-negative gay men. The study participants were screened for MRSA colonization and infection at three points during the study.
All the HIV-positive men were in good health and had a mean CD4 cell count of 599 cells/mm3. An undetectable viral load was present in 60% of individuals, with 69% taking antiretroviral therapy.
There were no significant differences between HIV-positive and HIV-negative individuals as regards age, race, education, use of healthcare, or recreational drug use.
HIV-positive patients had higher rates of MRSA colonisation at each point of the study than the HIV-negative controls (baseline, 5% vs 2%; final visit, 8% vs. 2%). Over the course of the study, the cumulative carriage of MRSA was 17% for the HIV-positive patients against 6% for the HIV-negative controls, a significant difference (p = 0.04).
Of the 21 MRSA isolates recovered, 15 were identified as strain USA300, the predominant community-acquired strain of MRSA in the US.
During the year long follow-up ten skin infections were diagnosed, all of which were in HIV-positive patients. Furthermore, all the individuals developing skin infections had MRSA colonisation.
Antibiotic use in the previous six months was associated with MRSA colonisation amongst the HIV-positive patients (p = 0.04). No other factors were associated with an increased risk of MRSA for the HIV-positive patients. The mean CD4 cell count of HIV-positive infections with MRSA was 612 cells/mm3. HIV treatment was being taken by 13 of the 18 individuals with the infection, most of whom had an undetectable viral load. The five patients not taking antiretroviral therapy all had a viral load below 15,000 copies/ml.
“Our observations indicate that HIV-1 infection is associated with a higher rate of…MRSA colonization, and MRSA skin and soft tissue infection”, comment the investigators.
They note that the MRSA strains isolated from the patients showed reduced susceptibility to commonly-used antibiotics including clindamycin, erythromycin, and ciprofloxacin.
“A significant observation in this study is the association between MRSA carriage and HIV-1 infection, because 18 of the 21 MRSA isolated cultures were recovered from HIV-1 infected individuals without evidence of immune suppression”, note the authors.
They suggest that either “underlying host-pathogen factors” or “sociodemographic factors and social and behavioural factors may have contributed to MRSA colonization and infection in this population.”
The investigators conclude by advocating “judicious use of antibiotics” in HIV-positive patients, and recommend that doctors maintain “a high level of suspicion regarding MRSA, independent of patients CD4 T lymphocyte count and treatment status.”
Shet A et al. Colonization and subsequent skin and soft tissue infection due to methicillin-resistant Staphylococcus aureus in a cohort of otherwise healthy adults infected with HIV type 1. J Infect Dis 200: 88-93, 2009.