The most widely used definition of persistent carriage is a positive cultures from $80% of 10 weekly cultures. Persistent carriers typically carry a single bacterial strain at high levels of colonization over time, shed high levels of S. aureus into the environment and are at higher risk of infection than intermittent or non carriers. In contrast, intermittent carriers carry different strains, one strain at a time, at lower levels of colonization over time. Host genetic characteristics may contribute to nasal carriage. Biological evidence supports the hypothesis that host factors could influence persistent colonization by determining the immune response to S. aureus or adherence of S. aureus to the nasal epithelium. Persistent S. aureus carriers are more likely to reacquire colonization with their original S. aureus strain after decolonization and subsequent artificial inoculation of a mixture of S. aureus strains including their own, while non-carriers subjected to artificial inoculation return to non-colonization. A familial predisposition to nasal carriage was reported from a large community-based prevalence study in the 1960’s,ME0328 ; however, two twin studies were inconclusive. There have been a number of genetic association studies for persistent S. aureus colonization using a candidate gene approach. Investigators from the Netherlands phenotyped almost 4000 adults for persistent S. aureus colonization status and tested for associations with polymorphisms in specific genes associated with the host inflammatory response. Their findings were mixed with Loxapine Succinate some modestly positive and other negative associations. None of the significant associations have been replicated, perhaps, due to the paucity of studies on the subject. Thus, although the evidence is suggestive, there remains insufficient evidence either to confirm or refute a host genetic contribution to persistent S. aureus colonization. The objective of this study was to determine whether the phenotype or trait of persistent S. aureus colonization aggregates in family members in different households. Specifically, we compared the prevalence of persistent S. aureus colonization of the anterior nares between siblings of adults who were colonized with persistent S. aureus colonization and siblings of adults who were not colonized. The sensitivity and specificity of the first two anterior nares cultures to correctly categorize persistent S. aureus colonization status were calculated. The association between persistent S. aureus colonization and potential predictors was measured using the chi square test or Fisher’s exact test for categorical variables and the Student t test for normally distributed continuous variables. The strength of the association between the semi-quantitative culture results and the qualitative culture results was measured using the Spearman rank correlation coefficient for nonparametric data. We estimated the degree of familial aggregation by comparing the prevalence of persistent colonization in siblings of index cases who were persistent colonizers to the prevalence of persistent colonization in siblings of index cases who were not persistent colonizers. We summarized this comparison as a prevalence rate ratio. In addition, we computed the sibling relative risk as the prevalence of persistent colonization in siblings of index cases who were persistent colonizers divided by the prevalence of persistent colonization in the total population. Finally, we used a pedigree-based maximum likelihood procedure to estimate the heritability of persistent colonization by defining heritability as the proportion of the total trait variance attributable to the additive effects of genes.