Wound Management Strategy for Treatment of Localized Cutaneous Leishmaniasis Using the TIME Framework

Michela Iannone, MD; Teresa Oranges, MD, PhD; Valentina Dini, MD, PhD; Marco Romanelli, MD, PhD; Agata Janowska, MD

Disclosures

Wounds. 2021;33(1):E6-E9. 

In This Article

Abstract and Introduction

Abstract

Introduction: The current drugs available for the treatment of cutaneous leishmaniasis (CL) often cause several adverse events, and the risk–benefit ratio is low due to the risk of severe complications. Current treatment recommendations are based on data from areas endemic for leishmaniasis and are not always perfectly applicable, especially in cases of imported CL. Thus, it is crucial to assess the level of severity in each case to provide the most appropriate treatment modality. The World Health Organization recommends simple wound care (with unspecified strategies) or local therapy as first-line treatment. Systemic treatments should be reserved for selected patients. Additionally, there is little evidence in the literature regarding local treatments, such as paromomycin ointments, imiquimod, local infiltration with antimonials, and physical treatments such as cryotherapy or thermotherapy.

Objective: The authors report the use of the tissue debridement, infection/inflammation management, moisture balance, and edge assessment (TIME) model of wound bed preparation in a case of localized ulcerated CL.

Case Report: A 32-year-old female developed ulcerated nodules at the sites of insect bites that occurred during a trip to Columbia and was diagnosed with localized CL. Wound management included daily wound bed cleansing, surgical debridement, and antimicrobial and secondary polyurethane foam dressings. The lesions completely healed in 30 days.

Conclusions: In the present case, the TIME approach simplified the local management of ulcerated CL, thereby improving both the healing process and cosmetic outcome. Further studies with a placebo-controlled group will be necessary to confirm the data.

Introduction

Leishmaniasis is a disease caused by intracellular protozoan parasites belonging to the Leishmania genus. The disease is the result of the bite of a female sand fly (phlebotomine), which transmits the Leishmania parasites to the vertebrate host. Clinical manifestations vary, from simple self-healing skin ulcers to severe chronic mucocutaneous infections and life-threatening visceral diseases.[1] The severity of symptoms depends on both the parasitic species and the immune system of the infected host.[2]

The most common forms of leishmaniasis in people are cutaneous leishmaniasis (CL) and visceral leishmaniasis. Cutaneous leishmaniasis is the most prevalent clinical type of the disease and affects between 1 million and 1.5 million people globally.[1] Cutaneous leishmaniasis is characterized by an effective Th1 response activated by dendritic cells that uptake and process antigens (pattern recognition receptors–pathogen-associated molecular patterns interaction), migrate to the lymphoid organs, and activate the maturation of naive T cells.[1] The pivotal cytokines involved in this immune response are IL-12, IFN-g, and IL-17, which trigger a strong inflammatory response of macrophages against parasites. The progression of the disease may be related to the activation of a Th2 response that leads to the production of IL-4 and IL-10.[1] In addition, the Th1/Th2 interaction is not completely understood. Reports have suggested the involvement of CD8+ T cells, natural killer cells, and T regulatory cells with complex interactions modulated by the parasite.[1,3] Histopathological examination, immunohistochemistry, immunofluorescence, and electron microscopy have revealed the immunology of CL in vivo.[4] A correct diagnosis is usually obtained with medical and travel history, clinical findings (papules, plaques, ulcers, and/or nodules), and histological features.[5] In particular, histological examinations of amastigotes and Leishman-Donovan bodies have a sensitivity of 50% to 70%.[5] Cultural examination is difficult to perform, has a low sensitivity (30%), and is considered a second-level diagnostic test.[5] Additional diagnostic tests include isoenzyme analysis, monoclonal antibody analysis, and polymerase chain reaction studies. While the polymerase chain reaction study has a high sensitivity (97%), it is expensive and does not have a well-defined specificity.[5]

There are currently few drugs to treat CL, and several adverse events as well as poor evidence of efficacy have limited their use in treatment.[6] First-line treatments include simple wound care (with unspecified strategies) or topical treatments (paromomycin-containing ointments, imiquimod, local infiltration with antimonials, and physical treatment such as cryotherapy or local heat therapy).[6] Systemic treatments include pentavalent antimonials as first-line treatment and amphotericin B, allopurinol, ketoconazole, and miltefosine as second-line treatments.[5,6]

The authors report a clinical case of ulcerated CL to propose a specific wound care approach based on wound bed preparation (WBP) strategy realized through the tissue debridement, infection/inflammation management, moisture balance, and edge assessment (TIME) model. This systematic approach may simplify the local management of ulcerated CL, thereby potentially improving both the healing process and cosmetic outcome as well as limiting the risk of complications and need for systemic therapy.

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