Ecthyma gangrenosum caused by <i>Streptococcus pyogenes</i>: Report of a case and review of the literature

Tanaka, Arisa; Yanagi, Teruki; Seo, Takashi; Mai, Shoko; Miyazawa, Hajime; Ujiie, Hideyuki

doi:10.1111/1346-8138.16396

Cited by 1 publication

(2 citation statements)

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“…Through the years, a different panorama has been established; it is well known that despite P. aeruginosa being responsible for up to 74% of the cases, other agents can also be involved, and immunocompetent patients can also be affected 1–3 . Other bacterial and fungal etiologies described for EG are Escherichia coli , Staphylococcus aureus , Citrobacter freundii , Klebsiella pneumoniae , Streptococcus pyogenes , Morganella morganii , Stenotrophomonas maltophila , Aeromonas hydrophila , Staphylococcus epidermidis , Streptococcus vestibularis , Enterococcus faecalis , Fusarium sp, and Candida albicans 1,4–9 …”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3] Other bacterial and fungal etiologies described for EG are Escherichia coli, Staphylococcus aureus, Citrobacter freundii, Klebsiella pneumoniae, Streptococcus pyogenes, Morganella morganii, Stenotrophomonas maltophila, Aeromonas hydrophila, Staphylococcus epidermidis, Streptococcus vestibularis, Enterococcus faecalis, Fusarium sp, and Candida albicans. 1,[4][5][6][7][8][9] EG usually starts as asymptomatic erythematous or violaceous macules, papules, or plaques with surrounding erythema which progress in 12-24 hours to hemorrhagic bullae and necrotic ulcerative eschars (Figures 1 and 2). 10 EG can present as single or multiple lesions affecting most often the perineum, lumbar and gluteal regions (57%), extremities (30%), face (6%), neck and torso (6%), but it can affect any body segment.…”

Section: Introductionmentioning

confidence: 99%

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Ecthyma gangrenosum in pediatric patients: 10‐year experience at the National Institute of Pediatrics

García‐López,

Medina‐Vera,

Orozco‐Covarrubias

et al. 2023

Int J Dermatology

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BackgroundEcthyma gangrenosum (EG) usually results from the hematogenous seeding of the skin in the setting of bacteremia, mostly by Pseudomonas aeruginosa, especially in immunocompromised patients. It presents as erythematous‐violaceous macules, or plaques with surrounding erythema before rapidly progressing to bullae and necrotic‐ulcerative eschars.MethodsWe performed a retrospective chart review of EG patients diagnosed at the National Institute of Pediatrics. Data included demographics, underlying disease, cutaneous lesions, location, evolution, microbiologic, histopathologic findings, and treatment. Data were analyzed by descriptive statistics; Mann–Whitney U test and Fisher's exact test were used to evaluate differences between groups.ResultsSeventeen patients with a mean age of 12.5 (6–16) years were included. The most common underlying disease was acute lymphoblastic leukemia (59%), three patients were not immunocompromised (17%). A total of 18 episodes of EG were recorded, 10 (55%) were disseminated at presentation. Systemic manifestations included fever (100%), pain (88.9%), asthenia and adynamia (22.2%). P. aeruginosa was isolated in 10 (55%) cases, followed by Staphylococcus aureus in four. Three patients had sepsis at onset (17%). A comparison between localized versus disseminated, pseudomonal versus nonpseudomonal, and bacteremic versus nonbacteremic EG was performed with no statistical difference between any of the groups, except for longer treatment time for pseudomonal EG, and longer hospitalization days for both pseudomonal EG and bacteremia.ConclusionsFever and pain in the setting of rapidly evolving necrotic lesions should prompt the clinical suspicion of EG and the installment of empiric treatment pending culture results.

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Section: Introductionmentioning

confidence: 99%