A case report of double etiology of ecthyma gangrenosum

Abstract

Rationale: Ecthyma gangrenosum is a cutaneous infection, most commonly occurring during sepsis evolution with Pseudomonas aeruginosa on an immunocompromised background. There have been rare case reports in previously healthy children and rarer are the cases with double etiology. Patient concerns: We present the case of a female Caucasian patient, aged 1 year and 8 months, who developed severe sepsis during flu evolution with predominant respiratory and cerebral manifestations. On admission, at skin level, there was noticed a necrotic coccygeal ulceration (with rapid increasing dimensions 0.5/0.5 cm in 24 hours), and with the transformation from a dry necrosis in a sphacelus at the periphery and progression of necrosis in depth. Diagnoses: The patient was diagnosed with ecthyma gangrenosum from which Pseudomonsa aeruginosa and Enterococcus faecalis were isolated from the samples that were harvested intraoperatively, decision that was taken considering the appearance of CT scan and the extremely rapid expansion of necrosis. Excisional debridement with necrectomy, lavage, and dressing being performed. The invasion of the fascia was excluded intraoperatively. Interventions: Treatment with Meropenem for 14 days was initiated, as well as amikacin and linezolid, the latter being replaced with teicoplanin for 14 days. Red blood cells transfusion, intravenous immunoglobulins, anticonvulsants were also administered. Outcomes: Under treatment the evolution was favorable. Lessons: This case brings into discussion a double etiology of ecthyma gangrenosum, in a previously healthy child that occurred in the evolution of influenza. The evolution was favorable under broad-spectrum antibiotic treatment and surgical excision.

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

“…Pseudomonas aeruginosa was responsible for slightly more than half of the episodes of EG, and it was combined with E. faecalis in one episode, an association previously described by Birlutiu et al. in 2019 5 . Other microorganisms ( S. aureus , F. solani , E. faecalis , A. hydrophila , and S. malthophila ) found in this study have also been previously reported as causal agents of EG 1 .…”

“…Pseudomonas aeruginosa was responsible for slightly more than half of the episodes of EG, and it was combined with E. faecalis in one episode, an association previously described by Birlutiu et al in 2019. 5 Other microorganisms (S. aureus, F. solani, E. faecalis, A. hydrophila, and S. malthophila) found in this study have also been previously reported as causal agents of EG. 1 There was one episode caused by three different agents: S. maltophila, E. faecium, and S. haemolyticus; interestingly, neither E. faecium nor S. haemolyticus have been previously reported in EG.…”

“…2,18 The most frequent combination of symptoms at the onset of the disease was fever and pain in almost two-thirds of the patients. Fever has been described in many patients with EG, 2,5,11,15 but the association of fever and pain has not been previously emphasized. We suggest that the presence of fever and/or pain in the setting of rapidly evolving cutaneous bullous or necrotic lesions should prompt the clinical suspicion of EG and the installment of empiric treatment pending culture results.…”

“…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 …”

“…[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.…”