Over the three-year period from 2009 to 2011, we found that the incidence of clinically-diagnosed SSTIs in this population was nearly 500 episodes per 10,000 person-years. By contrast, this rate is more than double the incidence of clinically-diagnosed pneumonia (approximately 190 per 10,000) in this population (unpublished data), although pneumonia is more likely to result in hospitalization.
In one of the few U.S. population-based studies of the incidence of community-onset SSTIs published in the last decade, Simonsen et al., using 1997 to 2002 data from a Western U.S. medical insurance claims database, reported the incidence rate of cellulitis and abscess in persons less than 65 years of age to be 241 per 10,000 person years [31
]. The corresponding rate in our population for 2009–2011 (when restricting the analysis to cellulitis and abscess in persons under 65 years of age) was essentially the same (about 244 per 10,000 person-years).
In the multivariate model adjusting for gender, age group, race/ethnicity, and diabetes status, being under 5 years of age, and having diabetes were the two largest risk factors for being diagnosed with an SSTI. The increased risk of SSTIs among diabetics may, in part, be related to increased opportunities to get diagnosed, variations in care-seeking behavior, and other comorbidities, rather than directly related to diabetes [44
]. However, one study that adjusted for some of these factors also found that diabetics were at increased risk of skin infections [35
]. White race was also a risk factor for being diagnosed with SSTI. In a post-hoc analysis, we found that the relationship of age to the rate of clinically-diagnosed SSTI was different depending on race/ethnicity. Notably, unlike whites, the highest rate of SSTI in Asians, Hispanics, and Native Americans was in the youngest age group, rather than the elderly. Among African-Americans, although the youngest age group also had a higher rate of SSTI than the elderly, persons 18-
50 years of age had the highest rate of SSTI. That the effect of age group was significantly different by race/ethnicity, reminds us that models that include only main effects may mask important differences.
Because of inability to determine microbiologic etiology of many SSTIs, and potential bias with respect to which SSTIs get cultured, it is difficult to infer the true underlying proportion of SSTIs due to given pathogens. The sample of SSTIs that get cultured are not representative of all SSTIs, especially given that many SSTIs are typically not culturable (e.g., cellulitis without abscess). In our setting, 23% of SSTI episodes were cultured, and a potentially clinically-relevant pathogen was isolated in 54% of those episodes. Over 80% of pathogen-positive specimens were S
while only 10% were BHS. However, studies indicate that non-culturable cellulitis may be more likely to be caused by BHS than S
], so BHS may represent a more important cause of SSTIs than the results of cultures indicate.
isolates, we found that 46% were MRSA. Prior studies have shown that S
is the leading cause of cultured SSTIs [7
], and that the percent of these that were MRSA increased during the early 2000’s [7
]. However, most of these studies only included hospitalized cases [7
] or were for special populations (i.e., children [51
] and the uninsured [49
]). In a 2004 study of specimens (n
422) taken from ambulatory patients with SSTIs (n
422), Moran et al. reported that S
was isolated in 76% of the specimens, and 78% of these were MRSA [47
]. MRSA may have been more prevalent in the Moran et al. population compared to KPNC in part because of the larger percent of African-Americans and Hispanics in that population, which, in the KPNC population, were more likely to have S
SSTIs that were MRSA than Whites or Asians. In a study of San Francisco Bay Area outpatients (n
529) presenting with purulent or fluid-producing SSTIs during 2006–2007, Weiss et al. found that, among those with microbiologic testing, 22% of specimens were positive for MRSA and 30% for methicillin-sensitive S
]. These compare to 20% (MRSA) and 24% (MSSA) in our study, when the denominator was all SSTIs with microbiologic testing.
While diabetes was associated with higher risk of SSTIs (and higher absolute rates of MRSA), it was not associated with an increased risk of MRSA infection compared to MSSA – in fact, it was associated with a decreased risk. This finding is consistent with a recent study of hospitalized patients with complicated SSTIs and a positive blood or skin culture, which found that not having evidence of diabetes corresponded to an increased likelihood of the culture being MRSA [53
]. In part, these findings in our population may be related to a higher propensity of providers to order cultures for diabetics. We found that 31% of SSTI episodes for diabetics were cultured, while only 22% of SSTI episodes for non-diabetics were cultured, and that the cultures obtained from diabetics were more likely to be blood than were the cultures from non-diabetics (24% vs. 11%). Thus, for diabetics, providers may have disproportionately ordered cultures for types of SSTIs that were less likely to MRSA. These findings related to diabetics should be further explored.
Consistent with a number of prior studies [12
], we found that, among persons with S
infections, African-Americans and persons living in lower-income census blocks were at substantially increased risk of their S
being methicillin-resistant. We also found that Asians were at substantially lower risk of being diagnosed with an SSTI, and that their SSTI-related S
isolates were substantially less likely to be methicillin-resistant than those of other racial/ethnic groups. No US population-based study has, to our knowledge, previously reported on rates of SSTI and likelihood of S
being methicillin-resistant in persons of Asian race vis-à-vis persons of other racial/ethnic groups. However, Liu et al. reported that, among San Francisco residents, Asian/Pacific Islanders had the lowest rates of community-onset and hospital-onset MRSA disease, much of which was likely related to SSTI [54
]. Our findings with respect to Asians are novel and should be confirmed in other populations.
Our selection criteria explicitly excluded SSTIs diagnoses that we thought likely be represent nosocomial or chronic infections, and thus our incidence rates and microbiology results do not reflect inclusion of those types of infections. In addition, our findings reflect the routine practice of providers in this health plan with respect to diagnosing and microbiologic testing, and these practices may differ from those of other settings. The differences we found in risk of SSTIs among the different gender, race/ethnicity, and age groups, may to some extent reflect differences in the propensity of persons in these groups to seek treatment. As an observational study, our analysis of risk factors could be affected by unmeasured confounders. We did not include, for example, nursing home status, family size, injection drug use, or medical conditions other than diabetes. We included diabetes as a risk factor due to the high prevalence of the condition, and because prior literature suggests its relationship to increased risk of SSTI [35
]. However, other conditions – in particular, immuno-compromising conditions such as HIV – might also be associated with increased risk of SSTIs. In this study we did not assess severity or health services utilization. Therefore, higher risk of clinically-diagnosed SSTIs does not necessarily imply more severity or greater overall cost of care. Cultures were included based on their temporal proximity to a patient’s SSTI diagnosis. It is possible that some patients may have multiple infections, and that the pathogen we associated with the SSTI infection may not have been the cause of that infection.