Abstract Background Staphylococcus aureus asymptomatically colonizes the anterior nares of 20-30% of the population, and nasal carriage is a major risk factor for invasive S. aureus disease. Furthermore, rates of S. aureus nasal colonization are higher (40-50%) during the first eight weeks of life and colonizing strains can be transmitted among household contacts. Affecting the same niche, influenza A virus (IAV) is a common cause of viral upper respiratory infection (URI), and IAV predisposes the host to post-URI secondary S. aureus pneumonia. Despite the frequency of S. aureus and IAV in a shared anatomic site, the effects of IAV on S. aureus nasal colonization and transmission are understudied, and infant animal models that may better represent the younger high-colonization age group are not reported. Infant mouse model Two index pups from each litter were inoculated with S. aureus, and on day three the entire litter was either infected with IAV or mock (PBS) solution. S. aureus shedding is monitored daily and nasal lavage was performed. Methods We established nasal colonization in infant B6 mice by inoculating 106 colony forming units (CFU) of S. aureus MRSA strain JE2 and quantified nasal shedding for seven days on S. aureus chromogenic agar plates. For transmission experiments, we colonized two index pups per cage with S. aureus and infected the groups of pups with Influenza A virus (IAV) or mock (PBS) control on day three after S. aureus colonization. Nasal shedding of S. aureus was quantified daily and nasal lavage was performed at day seven. Results Infant mice maintain S. aureus nasal colonization at seven days post-inoculation and they can transmit the colonizing strain to naive co-housed pups. IAV infection increases the S. aureus colonization burden 1000-fold by day 5 and the transmission to co-housed naïve pups by 63%. Conclusion Influenza A virus infection increases nasal colonization burden of S. aureus and transmission to S. aureus-naive close contacts in an infant mouse model. We anticipate the model to be a starting point for the study of bacteria-virus interactions that contribute to S. aureus colonization in a high-risk population. Moreover, our work will allow for the study of both S. aureus and IAV mechanisms that contribute to S. aureus transmission amongst close contacts. Disclosures All Authors: No reported disclosures
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