PURPOSE OF THE STUDY:
Eczema and eczema severity are risk factors for food sensitization and allergy. S. aureus colonization is associated with more severe eczema. Is S. aureus colonization a risk factor for food allergy in patients with eczema, and if so, is this due to eczema severity or the colonization itself?
640 children in the Learning Early About Peanut Allergy (LEAP) study, which enrolled infants aged 4 to 11 months of age with severe eczema, egg allergy, or both.
Subjects were randomized to early peanut introduction (“consumers”) or avoidance (“avoiders”) and then evaluated for peanut allergy at age 60 months, after which consumers stopped eating peanut. All children were reevaluated at 72 months of age. Eczema was evaluated at baseline and at 12, 30, 60, and 72 months of age and graded with the SCORAD index. Skin and nasal swabs for S aureus assessment were obtained at baseline and at 12, 30, and 60 months of age.
48.8% of the participants had some form of S. aureus colonization (32.2% skin and 32.3% nasal) on at least one study visit, with no differences between consumers and avoiders. Colonization was associated with eczema severity, which generally decreased over time. However, eczema worsened in those with immediately preceding skin S. aureus colonization. Egg and peanut specific IgE were associated with skin S. aureus positivity at any time point, even corrected for eczema severity. Those with skin and/or nasal colonization were 1.57 (95% CI, 1.02–2.42; P = .042) times as likely to have persistent egg allergy at 60 months of age. Within the peanut consumption group, skin-colonized subjects were 7.13 (95% CI, 1.14–44.47; P = .035) times as likely to have developed peanut allergy by 60 months. Within the avoidance group, there was no greater risk for peanut allergy at 60 months in the subjects with colonization. All odds ratios were corrected for eczema severity.
Even after correcting for eczema severity, S. aureus colonization increases the likelihood of food sensitization as well as the development and persistence of food allergy.
As the authors point out, the fact that S. aureus was associated with a greater risk of peanut allergy among peanut consumers but not peanut avoiders suggests that peanut consumption was less effective in the prevention of peanut allergy among those with S. aureus. One possible mechanism is that staphylococcal enterotoxin B (SEB) leads to TH2–polarized immune responses. Future studies that attempt to decrease S. aureus in at-risk infants would seem appropriate to determine if this can lessen the development of eczema and or food allergy.