Memorias do Instituto Oswaldo Cruz · 2017
Effect of secondary infection on epithelialisation and total healing of cutaneous leishmaniasis lesions.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Antonio Liliane de Fátima, Lyra Marcelo Rosandiski, Saheki Maurício Naoto, Schubach Armando de Oliveira, Miranda Luciana de Freitas Campos, Madeira Maria de Fátima, Lourenço Maria Cristina da Silva, Fagundes Aline, Ribeiro Érica Aparecida Dos Santos, Barreto Leonardo, Pimentel Maria Inês Fernandes
Аннотация
BACKGROUND: Cutaneous leishmaniasis (CL) generally presents with a single or several localised cutaneous ulcers without involvement of mucous membranes. Ulcerated lesions are susceptible to secondary contamination that may slow the healing process.
OBJECTIVE: This study verified the influence of non-parasitic wound infection on wound closure (epithelialisation) and total healing.
METHODS: Twenty-five patients with a confirmed diagnosis of CL and ulcerated lesions underwent biopsy of ulcer borders. One direct microbial parameter (germ identification in cultures) and four indirect clinical parameters (secretion, pain, burning sensation, pruritus) were analysed. FINDINGS Biopsies of ten lesions showed secondary infection by one or two microorganisms (Staphylococcus aureus, Pseudomonas aeruginosa, Enterococcus faecalis, Streptococcus pyogenes and Candida parapsilosis). "Secretion" and "burning sensation" influenced epithelialisation time but not total healing time. Positive detection of germs in the ulcer border and "pain" and "pruritus" revealed no influence on wound closure.
CONCLUSIONS: Our borderline proof of clinical CL ulcer infection inhibiting CL wound healing supports the need to follow antimicrobial stewardship in CL ulcer management, which was recently proposed for all chronic wounds.
OBJECTIVE: This study verified the influence of non-parasitic wound infection on wound closure (epithelialisation) and total healing.
METHODS: Twenty-five patients with a confirmed diagnosis of CL and ulcerated lesions underwent biopsy of ulcer borders. One direct microbial parameter (germ identification in cultures) and four indirect clinical parameters (secretion, pain, burning sensation, pruritus) were analysed. FINDINGS Biopsies of ten lesions showed secondary infection by one or two microorganisms (Staphylococcus aureus, Pseudomonas aeruginosa, Enterococcus faecalis, Streptococcus pyogenes and Candida parapsilosis). "Secretion" and "burning sensation" influenced epithelialisation time but not total healing time. Positive detection of germs in the ulcer border and "pain" and "pruritus" revealed no influence on wound closure.
CONCLUSIONS: Our borderline proof of clinical CL ulcer infection inhibiting CL wound healing supports the need to follow antimicrobial stewardship in CL ulcer management, which was recently proposed for all chronic wounds.