Mem Inst Oswaldo Cruz, Rio de Janeiro, 112(9) September 2017
Original Article

Effect of secondary infection on epithelialisation and total healing of cutaneous leishmaniasis lesions

Liliane de Fátima Antonio1,+, Marcelo Rosandiski Lyra1, Maurício Naoto Saheki1, Armando de Oliveira Schubach1,3,4, Luciana de Freitas Campos Miranda1, Maria de Fátima Madeira1,3,4, Maria Cristina da Silva Lourenço2, Aline Fagundes1, Érica Aparecida dos Santos Ribeiro2, Leonardo Barreto2, Maria Inês Fernandes Pimentel1

1Fundação Oswaldo Cruz-Fiocruz, Instituto Nacional de Infectologia Evandro Chagas, Laboratório de Pesquisa Clínica e Vigilância em Leishmanioses, Rio de Janeiro, RJ, Brasil
2Fundação Oswaldo Cruz-Fiocruz, Instituto Nacional de Infectologia Evandro Chagas, Laboratório de Bacteriologia, Rio de Janeiro, RJ, Brasil
3Conselho Nacional de Desenvolvimento Científico e Tecnológico, Rio de Janeiro, RJ, Brasil
4Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brasil

Page: 640-646 DOI: 10.1590/0074-02760160557
381 views 227 downloads
ABSTRACT

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). u201cSecretionu201d and u201cburning sensationu201d influenced epithelialisation time but not total healing time. Positive detection of germs in the ulcer border and u201cpainu201d and u201cpruritusu201d 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.

Financial support: FIOCRUZ
+ Corresponding author: lilianedefatima@gmail.com
Received 28 December 2016
Accepted 6 April 2017

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