Leishmaniasis Recidivans in a Palestinian Bedouin Child

Abstract

In February 2005, a 12-year-old Palestinian Bedouin child with a small lesion on his upper cheek just below the right eye was referred to Leishmania Research Unit medical laboratory in Jericho for diagnosis of suspected cutaneous leishmaniasis. He lived in a rocky desert area by Wadi-Qelt, approximately 4 km from Jericho City center and attended the school in the adjacent Aqabat Jabr refugee camp, which borders Jericho City. He remained confined to this area for the few months before the lesion's appearance. The lesion was less than 1 cm in diameter, was bacterially clean, and had a small encrusted crater in its center. The lesion was 2 months old when first examined. There were no indications of previous cutaneous leishmaniasis, but other family members described having been exposed to cutaneous leishmaniasis. The family's residential area was rocky and cavernous with a continuously flowing stream that provided Jericho with drinking and irrigation water. There were irrigated banana plantations nearby. Extracellular amastigotes were seen in tissue smears stained with Giemsa stain (Figure 1). These parasites were identified as Leishmania tropica by DNA analysis. This was done by amplifying the internal transcribed spacer-1 of the ribosomal RNA genes, using a Gene Amp PCR-system 9700 (Applied Biosystems, Foster City, CA) followed by restriction fragment length polymorphism.1,2 The DNAs of leishmanial species reference strains were included for comparison (Figure 2). The patient was treated with sodium stibogluconate injected intralesionally at 10 mg/kg/d every other day for 3 weeks, then twice a week for 2 months, and once a week thereafter for 3 months. The lesion seemed to re-epithelialize during the 3 months from February to early May. The patient was lost to follow-up until November 2005, when he returned with a small, red, smooth macule. This enlarged, and papules typical of Leishmaniasis recidivans appeared at its margins. Microscopic examination and DNA analysis were repeated and again showed the presence of L tropica. The patient was treated with intralesional sodium stibogluconate for another 5 months. The patient returned a third time in April 2006, 14 months after initial presentation, with a more severe and destructive nodular condition (Figure 3). Microscopic examination and DNA analysis were repeated, during which 2 tubes of rabbit blood-agar semisolid medium were inoculated with tissue aspirate to isolate the parasite. This time, no amastigotes were seen in the stained smears, and the internal transcribed spacer-1-PCR results were negative, but culture medium in 1 tube grew promastigotes. The lesion remained active throughout further treatment. The Bedouin family said they would apply a traditional therapy. Figure 1. Giemsa-stained smear showing extracellular amastigotes (original magnification ×1000). Download figure to PowerPoint Figure 2. Restriction fragment length polymorphism analysis of the amplified internal transcribed spacer-1-Gene Amp PCR products (Applied Biosystems, Foster City, CA) following digestion with HaeIII: left to right, the World Health Organization reference strains of Leishmania infantum (MHOM/TN/1980/IPT1), Leishmania tropica (MHOM/AZ/1974/SAF-K27), and Leishmania major (MHOM/TM/1973/5ASKH); leishmanial DNA from the patient's samples taken in February 2005; and leishmanial DNA following the relapse in November 2005. Download figure to PowerPoint Figure 3. The 12-year-old Palestinian boy with Leishmaniasis recidivans, showing small papules at the edge of the central lesion after several months of almost complete cure. After 5 months of antimony treatment following relapse, promastigotes were isolated, while the microscopic examination and internal transcribed spacer-1-Gene Amp PCR (Applied Biosystems, Foster City, CA) results were negative. Download figure to PowerPoint