Disease relevance of Impetigo

• Exfoliative toxin A, produced by Staphylococcus aureus, causes blisters in bullous impetigo and its more generalized form, staphylococcal scalded-skin syndrome [1].
• Toxin in bullous impetigo and staphylococcal scalded-skin syndrome targets desmoglein 1 [1].
• Here we report that Group A Streptococcus (GAS), a Gram-positive human-specific pathogen that causes pharyngitis, impetigo, invasive disease, necrotizing fasciitis, and autoimmune sequelae has long, surface-exposed, pilus-like structures composed of members of a family of extracellular matrix-binding proteins [2].
• A total of 88 patients were enrolled in a double-blind comparison of cefaclor and amoxicillin-clavulanic acid for the outpatient treatment of soft tissue infections (abscesses, cellulitis, and impetigo) [3].
• Sixty-two children aged 5 months to 13 years with impetigo were assigned to be treated with either mupirocin in three daily applications or erythromycin ethylsuccinate (40 mg/kg of body weight per day divided into four doses) according to a randomized treatment schedule [4].

High impact information on Impetigo

• These MRSA strains appear to be emerging clonal groups that have not been considered in previous epidemiological studies of ET-producing S. aureus in Japan and thus pose a significant threat for future treatment of patients with bullous impetigo and/or staphylococcal scalded-skin syndrome [5].
• A relationship between genetic background, agr group, and disease type was observed for several toxin-mediated diseases: for instance, agr group IV strains were associated with generalized exfoliative syndromes, and phylogenetic group AF1 strains with bullous impetigo [6].
• Clonal association of Staphylococcus aureus causing bullous impetigo and the emergence of new methicillin-resistant clonal groups in Kansai district in Japan [5].
• Selective distribution of a high-affinity plasminogen-binding site among group A streptococci associated with impetigo [7].
• We conclude that erythromycin-resistant S. aureus strains are commonly isolated from impetigo in our region.(ABSTRACT TRUNCATED AT 250 WORDS)[8]

Chemical compound and disease context of Impetigo

• Thus, mupirocin appears to be safe and effective in treating impetigo in children [4].
• Extended phenotypic and genotypic characterization of a limited number (n=31) of isolates from 2002 showed that fusidic acid-resistant strains of S. aureus were typically from patients with impetigo and isolates fell into a single clonal group [9].
• Comparison of oral cephalexin, topical mupirocin and topical bacitracin for treatment of impetigo [10].
• In general, patients with staphylococcal bullous impetigo responded promptly, with clearing of lesions evident within the first week, but delayed healing with persistence of staphylococci in lesions was more common in the group receiving dicloxacillin [11].
• After adjustment for household clustering and covariates, the incidence of impetigo among children living in households receiving triclocarban-containing soap (1.10 episodes per 100 person-weeks) was 23% lower than in households receiving placebo soap (P = 0.28) and 43% lower than the standard habit and practice controls (P = 0.02) [12].

Biological context of Impetigo

• Severity of nonbullous Staphylococcus aureus impetigo in children is associated with strains harboring genetic markers for exfoliative toxin B, Panton-Valentine leukocidin, and the multidrug resistance plasmid pSK41 [13].
• The place of fusidic acid in dermatology is in the treatment of mild to moderately severe skin and soft-tissue infections, e.g. impetigo, folicullitis, erythrasma, furunculosis, abscesses and infected traumatic wounds, whereas it is of less use in conditions such as hidradenitis suppurativa, chronic leg ulcers, burns and pressure sores [14].

Gene context of Impetigo

• Thus, ETA is associated with bullous impetigo and ETB is associated with generalized SSSS, possibly owing to a lower titer of anti-ETB neutralizing antibodies in the general population [15].
• Impetigo herpetiformis and hypoparathyroidism [16].
• Extremely low levels of epidermal skin-derived antileucoproteinase/elafin in a patient with impetigo herpetiformis [17].
• In our epidemiological investigation of human sera, the percentage of antibody to ETA in sera obtained from patients with impetigo (8%) was lower than those in sera of healthy males (23%) and females (29%) [18].
• Fibronectin-bound gold particles were bound more extensively to S. aureus strains isolated from furunculosis or furuncle than to those from bullous impetigo [19].

Analytical, diagnostic and therapeutic context of Impetigo

• Double-blind study comparing erythromycin and mupirocin for treatment of impetigo in children: implications of a high prevalence of erythromycin-resistant Staphylococcus aureus strains [8].
• Cephalosporins or azithromycin are preferred following penicillin treatment failures in selected patients as first-line therapy, based on a history of penicillin failures or lack of compliance and for impetigo [20].
• Several controlled clinical trials documented that mupirocin was significantly better than the polyethylene glycol vehicle alone or ampicillin and as effective as cloxacillin, dicloxacillin, or erythromycin in producing clinical and bacteriological cures in patients with impetigo and wound infections caused by gram-positive pathogens [21].
• However a significant difference was noted in the anti alpha-toxin levels in sera from both group of patients; that of SSSS patients was much lower than that of impetigo patients and of children in a control group [22].
• Screening S. aureus-isolates for the production of exfoliative toxin (ET) and discrimination between its two known variants (ETA, ETB) by immunodiffusion (ID), isoelectric focusing (IEF) and animal experiment were assessed methodologically using isolates from a patient with bullous impetigo and a patient with Ritter von Rittershain's disease [23].

References