Staphylococcal Skin Colonization in Children with Atopic Dermatitis: Prevalence, Persistence, and Transmission of Toxigenic and Nontoxigenic Strains

Hoeger, Peter H.; Lenz, W.; Boutonnier, A; Fournier, Jean‐Michel

doi:10.1093/infdis/165.6.1064

Cited by 127 publications

(126 citation statements)

References 26 publications

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“…Consistent with previous studies (12,16), S. aureus colonization was found in 75.7% of pediatric AD lesions, with MRSA accounting for 18.4% of S. aureus isolates in skin lesions of pediatric AD patients. This is the first report on the carriage rates of MRSA in skin lesions of pediatric AD patients.…”

Section: Discussionsupporting

confidence: 91%

Epidemiological Characteristics of Methicillin-Resistant Staphylococcus aureus Isolates from Children with Eczematous Atopic Dermatitis Lesions

Chung¹,

Jeon²,

Sung³

et al. 2008

J Clin Microbiol

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In this study, we investigated the rate of colonization of skin of children with atopic dermatitis (AD) by methicillin-resistant Staphylococcus aureus (MRSA) and characterized the isolates. Active skin lesions in pediatric AD patients were cultured with Rodac Staph (Komed, Korea). S. aureus isolates were examined for drug susceptibilities, analyzed for the eta, etb, tst, and pvl genes, and typed using agr polymorphism, pulsed-field gel electrophoresis of SmaI-restricted chromosomal DNA, and staphylococcal cassette chromosome mec (SCCmec) typing. Eighty-seven (75.4%) of 115 patients had cultivable S. aureus isolates, 16 of which (18.3%) were MRSA. All MRSA isolates were susceptible to chloramphenicol, rifampin, cotrimoxazole, and ciprofloxacin. While methicillin-susceptible S. aureus (MSSA) isolates were composed of 23 isolates of singular types and nine clusters comprising 48 isolates, MRSA isolates were typed into three clones: eight isolates of pulsotype A-agr-1-SCCmec IV, five isolates of pulsotype B-agr-3-SCCmec IIb-etb positive, and three isolates of pulsotype C-agr-3-SCCmec IV. Three SCCmec IVA MRSA isolates were tst positive, but none were positive for the pvl or eta gene. Among 71 MSSA isolates, 7 isolates were tst positive, 6 of which were pulsotype F-agr-3, and 9 of 10 agr-4 isolates were eta positive. The average ages of patients carrying MSSA, SCCmec IVA MRSA, and SCCmec IIb MRSA were 7.7 ؎ 4.6, 3.1 ؎ 1.5, and 8.2 ؎ 3.1 years, respectively. Among the patients carrying MRSA, two patients had been treated with oral antimicrobials, and one had been admitted to the hospital 18 months previously. In conclusion, community-acquired MRSA isolates of a few clones colonized the skin of patients with AD without risk factors for the acquisition of hospital-acquired MRSA, which suggested that the skin of children with AD may represent a significant reservoir of MRSA colonization in the community.

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Section: Discussionsupporting

confidence: 91%

Epidemiological Characteristics of Methicillin-Resistant Staphylococcus aureus Isolates from Children with Eczematous Atopic Dermatitis Lesions

Chung¹,

Jeon²,

Sung³

et al. 2008

J Clin Microbiol

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“…However, the mechanism of the cytokine imbalance in atopic dermatitis patients remains to be elucidated. Dermatitis lesions of AD patients are frequently infected with staphylococcal enterotoxin B (SEB)-producing Staphylococcus aureus (8,9), thus implying that either bacteria or bacterial factors might be involved in the pathogenesis of AD. NC/ Nga (NC) mice were established as an inbred strain from Japanese fancy mice in 1957 by Kondo (10 -12).…”

Section: A Topic Dermatitis (Ad)mentioning

confidence: 99%

The Mechanism of a Defective IFN-γ Response to Bacterial Toxins in an Atopic Dermatitis Model, NC/Nga Mice, and the Therapeutic Effect of IFN-γ, IL-12, or IL-18 on Dermatitis

Habu

Seki²,

Takayama³

et al. 2001

The Journal of Immunology

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NC/Nga (NC) mice raised under conventional conditions (Conv. NC mice) spontaneously develop dermatitis similar to human atopic dermatitis, whereas NC mice raised under the specific pathogen-free conditions do not develop dermatitis. In the present study, we show that the representative Th1 cytokine, IFN-γ levels in the sera of NC mice, injected with either staphylococcal enterotoxin B or endotoxin (LPS), to be severalfold lower than those of normal mice. The low IFN-γ response to staphylococcal enterotoxin B was correlated to the lack of regular Vβ8+ T cells and Vβ8+ NK T cells, and the low IFN-γ response to LPS was correlated to an impaired IL-18 production of macrophages. The CD3-stimulated IL-4 production from liver and spleen T cells from Conv. NC mice in vitro was greatly augmented. The serum IL-4 levels of untreated Conv. NC mice also were higher than those of normal mice and specific pathogen-free NC mice. Treatment of Conv. NC mice either with IFN-γ, IL-12, or IL-18 twice a week from 4 wk of age substantially inhibited the elevation of the serum IgE levels, serum IL-4 levels, and dermatitis, and IL-12 or IL-18 treatment also reduced the in vitro IL-4 production from CD3-stimulated liver T cells. The systemic deficiency in the Th1 response to bacterial stimulation thus leads to a Th2-dominant state and may induce an abnormal cellular immune response in the skin accompanied with an overproduction of IgE and a susceptibility to dermatitis in NC mice.

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“…The activating antigens involved are not known, but may include Staphylococcus aurem. Skin colonization and infection with this organism is an important factor in exacerbations of AD [39], and recent studies have demonstrated that bacterial anti gen-specific T cell clones (TCC) are of the Thl type producing IFN-7 [40,41], and that several staphylococcus-dcrived antigens and superantigens are potent inducers of IFN-7 production by T cells [42][43][44][45]. Interestingly, constitutive expression of [F*N-7 mRNA has also been documented in rheumatoid arthritis (RA), a condition in which T cell aciivation hits been postulated to contribute to the pathogenesis of disease.…”

Section: Discussionmentioning

confidence: 99%

Reduced interferon-gamma (IFN-γ) secretion with increased IFN-γ mRNA expression in atopic dermatitis: evidence for a post-transcriptional defect

Tang

Varigos

Kemp

1994

Clinical and Experimental Immunology

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SUMMARYReduced secretioti of IFN-7 in atopic itidividuals has been implicated iti the pathogenesis of disease, though the mechanisms leading to this reduced secretion have nol been elucidated. As production of IFN-'y has been shown to be predominantly regulated by its rate of transcription, expression of IFN-7 mRNA was examined in atopic children and in age-matched, non-atopic controls by polymerase chain reaction (PCR)-assisted mRNA amplification. Children with atopic dermatitis were found to have constitutive expression of IFN-7 mRNA in freshly isolated peripheral blood mononuclear cells (PBMC) and in unstimulated PBMC cultures which increased further following stimulation with phorbol myristate acetate (PMA)/Ca in vitro. In contrast, expression of IFN-7 mRNA in controls was only detected in stimulated cultures, as has been demonstrated previously for normal adults. These findings demonstrate ihat circulating T cells from atopic children have been activated in vivo, and suggest that T cell activation is a significant component of Ihe inflammatory process in dVopic dermatitis. Although expression of IFN-7 mRNA was increased in the atopic children, secretion was confirmed to be significantly lower than in controls, indicating that the defect(.'i) underlying reduced IFN-7 secretion in these individuals lie post-transcriptionally.

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Staphylococcal Skin Colonization in Children with Atopic Dermatitis: Prevalence, Persistence, and Transmission of Toxigenic and Nontoxigenic Strains

Cited by 127 publications

References 26 publications

Epidemiological Characteristics of Methicillin-Resistant Staphylococcus aureus Isolates from Children with Eczematous Atopic Dermatitis Lesions

Epidemiological Characteristics of Methicillin-Resistant Staphylococcus aureus Isolates from Children with Eczematous Atopic Dermatitis Lesions

The Mechanism of a Defective IFN-γ Response to Bacterial Toxins in an Atopic Dermatitis Model, NC/Nga Mice, and the Therapeutic Effect of IFN-γ, IL-12, or IL-18 on Dermatitis

Reduced interferon-gamma (IFN-γ) secretion with increased IFN-γ mRNA expression in atopic dermatitis: evidence for a post-transcriptional defect

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