Cutaneous leishmaniasis in children-a case series1

Leishmaniasis currently threatens 350 million people in 88 countries around the world.90% of cutaneous leishmaniasis cases occur in Afghanistan, Brazil, Iran, Peru, Saudi Arabia and Syria. An epidemic of cutaneous leishmaniasis is ongoing in Kabul, Afghanistan with an estimated 200,000 cases. Lesions can be very disfiguring and particularly on the face, this may have long term psychological and social consequences.Over the last 10 years endemic regions have been spreading further afield and there has been a large increase in the number of recorded cases.Over the last 5 years, at the Hospital of Tropical diseases in London, we have been involved in the diagnosis and treatment of six children with cutaneous leishmanaisis due to L.tropica and three children with cutaneous leishmaniasis due to L.major. In our patients, species identification was made by Polymerase Chain Reaction (PCR).L.tropica cutaneous leishmaniasis usually manifests as dry, small, self-healing lesions mainly located on the face which heal with permanent scarring. L. major usually presents as multiple “wet” lesions. In leishmaniasis recidivans, also called lupoid leishmaniasis, brown-red or brown-yellow papules appear in or close to an old lesion of cutaneous leishmaniasis. These lesions usually occur in association with previous L. tropica infection and are thought to represent a delayed hypersensitivity reaction in the host.Two children in our series with L.tropica infection presented with features of lupoid leishmaniasis.Three children with L.tropica were treated as in patients with systemic sodium stibogluconate 20 mg/kg for 3–4 weeks.The remaining five children received intralesional sodium stibogluconate. In addition one of the children with lupoid leishmaniasis required surgical excision of 2 nodules. All patients responded well to treatment with minimal side effects. One child developed a rise in her ALT but this settled with a reduction in treatment dose.The diagnosis of cutaneous leishmaniasis infection has to be suspected in children presenting with chronic, nodular, or ulcerated facial lesions. Diagnosis should be confirmed with, Giemsa-stained smears looking for amastigotes, histology looking for favor of a genetic cause. The response to discontinuation of supplementation will clarify whether or not he has true AE or a simple zinc deficiency.1Odom R.B. James W.D. Berger T.G. Andrews’ Diseases of the Skin: Clinical Dermatology. Ninth edition. W.B. Saunders Company, 2000: 611-612Google Scholar, 2Kury S. Dreno B. Bezieau S. Giraudet S. Kharfi M. Kamoun R. Moisan J.P. Identification of SLC39A4, a gene involved in acrodermatitis enteropathica.Nature genetics. 2002; 31 (June 17’02): 239-240Crossref PubMed Scopus (407) Google Scholar, 3Grider A. Mouat M.F. The acrodermatitis enteropathica mutation affects protein expression in human fibroblasts: analysis by two-dimensional gel electrophoresis.J Nutr. 1998; 128 (1998 Aug): 1311-1314PubMed Google Scholar, 4Connors T.J. Czarnecki D.B. Haskett M.I. Acquired zinc deficiency in a breast-fed premature infant.Arch Dermatol. 1983; 119 (1983 Apr): 319-321Crossref PubMed Scopus (31) Google Scholar Leishmaniasis currently threatens 350 million people in 88 countries around the world. 90% of cutaneous leishmaniasis cases occur in Afghanistan, Brazil, Iran, Peru, Saudi Arabia and Syria. An epidemic of cutaneous leishmaniasis is ongoing in Kabul, Afghanistan with an estimated 200,000 cases. Lesions can be very disfiguring and particularly on the face, this may have long term psychological and social consequences. Over the last 10 years endemic regions have been spreading further afield and there has been a large increase in the number of recorded cases. Over the last 5 years, at the Hospital of Tropical diseases in London, we have been involved in the diagnosis and treatment of six children with cutaneous leishmanaisis due to L.tropica and three children with cutaneous leishmaniasis due to L.major. In our patients, species identification was made by Polymerase Chain Reaction (PCR). L.tropica cutaneous leishmaniasis usually manifests as dry, small, self-healing lesions mainly located on the face which heal with permanent scarring. L. major usually presents as multiple “wet” lesions. In leishmaniasis recidivans, also called lupoid leishmaniasis, brown-red or brown-yellow papules appear in or close to an old lesion of cutaneous leishmaniasis. These lesions usually occur in association with previous L. tropica infection and are thought to represent a delayed hypersensitivity reaction in the host. Two children in our series with L.tropica infection presented with features of lupoid leishmaniasis. Three children with L.tropica were treated as in patients with systemic sodium stibogluconate 20 mg/kg for 3–4 weeks. The remaining five children received intralesional sodium stibogluconate. In addition one of the children with lupoid leishmaniasis required surgical excision of 2 nodules. All patients responded well to treatment with minimal side effects. One child developed a rise in her ALT but this settled with a reduction in treatment dose. The diagnosis of cutaneous leishmaniasis infection has to be suspected in children presenting with chronic, nodular, or ulcerated facial lesions. Diagnosis should be confirmed with, Giemsa-stained smears looking for amastigotes, histology looking for favor of a genetic cause. The response to discontinuation of supplementation will clarify whether or not he has true AE or a simple zinc deficiency.1Odom R.B. James W.D. Berger T.G. Andrews’ Diseases of the Skin: Clinical Dermatology. Ninth edition. W.B. Saunders Company, 2000: 611-612Google Scholar, 2Kury S. Dreno B. Bezieau S. Giraudet S. Kharfi M. Kamoun R. Moisan J.P. Identification of SLC39A4, a gene involved in acrodermatitis enteropathica.Nature genetics. 2002; 31 (June 17’02): 239-240Crossref PubMed Scopus (407) Google Scholar, 3Grider A. Mouat M.F. The acrodermatitis enteropathica mutation affects protein expression in human fibroblasts: analysis by two-dimensional gel electrophoresis.J Nutr. 1998; 128 (1998 Aug): 1311-1314PubMed Google Scholar, 4Connors T.J. Czarnecki D.B. Haskett M.I. Acquired zinc deficiency in a breast-fed premature infant.Arch Dermatol. 1983; 119 (1983 Apr): 319-321Crossref PubMed Scopus (31) Google Scholar