Abstract and Introduction
Abstract
Objective To understand the genotypic spectrum of environmental contamination of Staphylococcus aureus in households and its persistence.
Design Prospective longitudinal cohort investigation.
Setting Index participants identified at 2 academic medical centers.
Participants Adults and children with S. aureus skin infections and their household contacts in Los Angeles and Chicago.
Methods Household fomites were surveyed for contamination at baseline and 3 months. All isolates underwent genetic typing.
Results We enrolled 346 households, 88% of which completed the 3-month follow-up visit. S. aureus environmental contamination was 49% at baseline and 51% at 3 months. Among households with a USA300 methicillin-resistant S. aureus (MRSA) body infection isolate, environmental contamination with an indistinguishable MRSA strain was 58% at baseline and 63% at 3 months. Baseline factors associated with environmental contamination by the index subject's infection isolate were body colonization by any household member with the index subject's infection isolate at baseline (odds ratio [OR], 10.93 [95% confidence interval (CI), 5.75–20.79]), higher housing density (OR, 1.47 [95% CI, 1.10–1.96]), and more frequent household fomite cleaning (OR, 1.62 [95% CI, 1.16–2.27]). Household environmental contamination with the index subject's infection strain at 3 months was associated with USA300 MRSA and a synergistic interaction between baseline environmental contamination and body colonization by any household member with the index subject's infection strain.
Conclusions We found that infecting S. aureus isolates frequently persisted environmentally in households 3 months after skin infection. Presence of pathogenic S. aureus strain type in the environment in a household may represent a persistent reservoir that places household members at risk of future infection.
Introduction
Staphylococcus aureus is a common cause of skin infections in the community, many of which are methicillin resistant and infect previously healthy persons in many communities worldwide.[1–3] In the United States, the predominant community-associated methicillin-resistant S. aureus(CA-MRSA) genetic background, USA300 MRSA, has become the most common cause of community-associated skin infection[4] and an endemic pathogen in many hospitals.[5–7] Recurrent skin infections and multiple infections among household members of a patient with an S. aureus skin infection have been commonly reported.[8–11] While S. aureus transmission via the environment has been extensively studied within the healthcare setting,[12] little is known about the role of the environment in the transmission dynamics and reservoirs of highly pathogenic S. aureus genetic backgrounds, such as USA300 MRSA, in the community.[3,13]
Investigations of S. aureus transmission in the community setting have implicated skin-to-skin contact and contaminated fomites in the spread of infection.[14–17]S. aureus has been found to colonize the household environment[18–20] and, in experimental situations, can persist on household fomites for more than 2 months.[21] MRSA environmental contamination has been reported as 5%–8% among households without CA-MRSA disease[18,19] but 26%–32% in households with a CA-MRSA-infected person or where a member is a healthcare worker.[18,20] Investigations of household S. aureus environmental contamination are limited. None have examined genotyping data on both infection and colonizing S. aureusisolates of patients with S. aureus skin infections or employed more than 1 geographic locale.[18–20,22] Furthermore, persistence of pathogenic S. aureus persists in the household environment, and factors that predict persistence among household members are poorly understood.
To better understand the genotypic spectrum of environmental contamination of S. aureus in households and how these potential reservoirs persist, we examined longitudinal S. aureus environmental contamination of fomites in households of patients with skin infections.
Infect Control Hosp Epidemiol. 2014;35(11):1373-138. © 2014 The Society for Healthcare Epidemiology of America
