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. 1996 Nov;35(11):791-3.
doi: 10.1111/j.1365-4362.1996.tb02975.x.

Microbiology of infected atopic dermatitis

Affiliations

Microbiology of infected atopic dermatitis

I Brook et al. Int J Dermatol. 1996 Nov.

Abstract

Background: Bacterial infections occur frequently in lesions of atopic dermatitis (AD). The objectives of the study were to establish the aerobic and anaerobic microbiology of secondarily infected AD.

Methods: A retrospective review was carried out of clinical and microbiology laboratory records and of data obtained from patients with secondarily infected AD lesions, whose specimens of infected sites were processed for the presence of aerobic and anaerobic bacteria.

Results: Bacterial growth was noted in 41 specimens. Aerobic or facultative anaerobic bacteria only were present in 15 patients (36%), anaerobic bacteria only in eight (20%), and mixed anaerobic-aerobic flora was present in 18 (44%). Seventy-two isolates were recovered (1.8 per specimen), 34 aerobic or facultative bacteria, 35 strict anaerobes, and three Candida sp. The predominant aerobic and facultative bacteria were Staphylococcus aureus (12 isolates), Group A beta hemolytic streptococcus in five isolates, and Escherichia coli in four. The predominant anaerobes were Peptostreptococcus spp. (13 isolates), pigmented Prevotella and Porphyromonas spp. in eight, and Fusobacterium spp. in four isolates. Single bacterial isolates were recovered in 14 patients (34%), seven of which were S. aureus. Twenty-one of the organisms isolated from 16 patients (39%) produced the enzyme beta-lactamase. Organisms that resided in the mucous membranes close to the lesions predominated in these infections. Enteric gram-negative rods and Bacteroides fragilis group predominated in lesions on legs and buttocks. Group A beta-hemolytic streptococci, pigmented Prevotella, and Porphyromonas and Fusobacterium spp. were most frequently recovered in lesions of the finger, scalp, face, and neck.

Conclusions: The polymicrobial etiology of secondarily infected AD lesions and the association of bacterial flora with the anatomic site of the lesions are demonstrated.

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