Abstract
Atopic dermatitis (AD) is an inflammatory skin condition strongly associated with Staphylococcus aureus colonization and infection. S.aureus strains shift in populations in ~10-year intervals depending on virulence factors. Shifts in S.aureus virulence factors may in part explain the racial differences observed in the levels of prevalence and severity of AD. AD S.aureus isolates collected from 2011 to 2014 (103 isolates) and in 2008 (100 isolates) were examined for the prevalence of genes encoding superantigens (SAgs). The strains from 2011 to 2014 were obtained from AD patients as a part of the National Institute of Allergy and Infectious Diseases (NIAID) Atopic Dermatitis Research Network (ADRN). The prevalence of SAg genes was investigated temporally and racially. The enterotoxin gene cluster (EGC) was more prevalent in the 2011-2014AD isolates than in the 2008AD isolates. The prevalences of virulence factor genes were similar in European American (EA) and Mexican American (MA) patients but differed in 6 of 22 SAg genes between EA and African American (AA) or MA and AA isolates; notably, AA isolates lacked tstH, the gene encoding toxic shock syndrome toxin 1 (TSST-1). The presence of tstH and sel-p (enterotoxin-like P) was associated with decreased clinical severity and increased blood eosinophils, respectively. The EGC is becoming more prevalent, consistent with the previously observed 10years of cycling of S.aureus strains. Race-specific S.aureus selection may account for differences in virulence factor profiles. The lack of TSST-1-positive (TSST-1+) AD S.aureus in AA is consistent with the lack of AAs acquiring TSST-1-associated menstrual toxic shock syndrome (TSS). IMPORTANCE Monitoring pathogen emergence provides insight into how pathogens adapt in the human population. Secreted virulence factors, important contributors to infections, may differ in a manner dependent on the strain and host. Temporal changes of Staphylococcus aureus toxigenic potential, for example, in encoding toxic shock syndrome toxin 1 (TSST-1), contributed to an epidemic of TSS with significant health impact. This study monitored changes in atopic dermatitis (AD) S.aureus isolates and demonstrated both temporal and host infection differences according to host race based on secreted superantigen potential. The current temporal increase in enterotoxin gene cluster superantigen prevalence and lack of the gene encoding TSST-1 in AAs predict differences in infection types and presentations.
Highlights
Atopic dermatitis (AD) is an inflammatory skin condition strongly associated with Staphylococcus aureus colonization and infection
Treatment of the chronic inflammatory skin disease AD is costly; upward of a billion dollars per year in health care costs goes into managing symptoms associated with the disease
These differences are not associated with previously identified host barrier defects such as stratum corneum ceramide composition, transepithelial water loss (TEWL), skin pH, or S. aureus nasal carriage [13, 20,21,22,23]
Summary
Atopic dermatitis (AD) is an inflammatory skin condition strongly associated with Staphylococcus aureus colonization and infection. The prevalences of virulence factor genes were similar in European American (EA) and Mexican American (MA) patients but differed in 6 of 22 SAg genes between EA and African American (AA) or MA and AA isolates; notably, AA isolates lacked tstH, the gene encoding toxic shock syndrome toxin 1 (TSST-1). The current temporal increase in enterotoxin gene cluster superantigen prevalence and lack of the gene encoding TSST-1 in AAs predict differences in infection types and presentations. AD is often a T helper 2 (Th2)-mediated disease, accompanied by increased serum total IgE production, circulating interleukin-4 (IL-4)/IL-13-expressing T cells, and eosinophilia [1,2,3] It is often associated with skin infections caused by herpes simplex virus and Staphylococcus aureus [4]. The enterotoxin gene cluster (EGC) is composed of 6 superantigen genes, seg, sel-i, sel-m, sel-n, sel-o, and sel-u, that are increasingly recognized as important to staphylococcal disease [3], despite previously being considered a cluster or “nursery” of SAg genes of unknown function or potentially giving rise to new toxins through recombination [7]
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