Digestive leishmaniasis in acquired immunodeficiency syndrome: A light and electron microscopic study of two cases
ABSTRACT An increased incidence of visceral leishmaniasis in patients infected with the human immunodeficiency virus (HIV) is observed in areas in which both infectious diseases are endemic. Intensive worldwide traveling has also resulted recently in an increasing number of leishmanial and HIV coinfections in nonendemic areas. We describe the clinical, light microscopic, and ultrastructural features of two cases of imported, HIV-related, visceral leishmaniasis involving the alimentary tract, including the esophagus, the stomach, the duodenum, the ileum, the colon, and the rectum. We also discuss the differentiation of leishmanial infections from other HIV-related gastrointestinal opportunistic infections.
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ABSTRACT: Visceral leishmaniasis (VL) due to Leishmania infantum is endemic in Southern France and can be considered as an opportunistic infection in patients with acquired immunodeficiency syndrome (AIDS). Co-infection with Leishmania sp. and human immunodeficiency virus (HIV) is emerging, but pathological findings of leishmaniasis in AIDS have been poorly documented, and scattered case reports have include morphological descriptions. The clinicopathologic analysis of 16 patients with HIV and VL were evaluated. The clinical presentation was characteristic of VL, with fever, hepatosplenomegaly, and pancytopenia in 6 patients, and the diagnosis was confirmed by finding amastigotes of Leishmania sp. in bone marrow smears and biopsy specimens. In 4 patients, the initial diagnosis of VL was made fortuitously in gastrointestinal biopsies performed systematically (3 patients) or in case of diarrhea (1 patient). In one duodenal biopsy, Leishmania sp. and Mycobacteria sp. were associated. Liver biopsy allowed the diagnosis of VL in 3 cases. Autopsy was performed in 9 patients, showing a disseminated leishmaniasis with very unusual localizations (adrenal and heart) in 2 cases. Cutaneous leishmaniasis involvement was noted before (4 patients), at the same time (2 patient), or after (1 patient) the diagnosis of VL. Inflammatory infiltrates noted with Leishmania sp. infection were made by CD68 macrophages with (8 patients) or without (8 patients) associated CD8 positive lymphocytes. Immunoperoxidase study using polyclonal anti-Leishmania sp. antibodies contributed to the diagnosis in all cases. Electron microscopy of 2 digestive biopsy specimens showed the ultrastructural characteristics of Leishmania sp. amastigotes. The zymodeme MON-1 of L infantum was identified by isoenzyme electrophoresis in all patients. The mean of CD4 counts was 37/mm3 at the time of diagnosis, and the mean duration before the death was 8 months. As shown in this study, VL in AIDS can be diagnosed in gastrointestinal or liver biopsies. Diagnosis of VL was made when the CD4 count was very low and was correlated with a poor prognosis.Human Pathlogy 02/2000; 31(1):75-84. DOI:10.1016/S0046-8177(00)80202-6 · 2.81 Impact Factor
Article: Gastric disease in AIDS[Show abstract] [Hide abstract]
ABSTRACT: In contrast to the esophagus and colon, the stomach is a less common site for the occurrence of primary opportunistic infections in AIDS. Most gastric opportunistic infections in AIDS occur as part of a generalized gastrointestinal or systemic syndrome (ie, secondary involvement). Besides infections, opportunistic neoplasms such as Kaposi's sarcoma and non-Hodgkin's lymphoma can also involve the stomach in AIDS patients. Since the introduction of highly active antiretroviral therapy, the incidence of gastrointestinal disorders has decreased in HIV-infected patients and the incidence of nonopportunistic gastrointestinal disorders, including Helicobacter pylori infection and peptic ulcer disease, has risen. The main diagnostic tool for AIDS patients with suspected gastric pathology is upper endoscopy with biopsies. The article presents the various gastric pathologies that can occur in AIDS and focuses on their clinical and endoscopic approach.Techniques in Gastrointestinal Endoscopy 04/2002; 4(2):66-70. DOI:10.1053/tgie.2002.33013
- Clinical Microbiology and Infection 06/2003; 9(5):421, 463-6. DOI:10.1046/j.1469-0691.2003.00749.x · 5.20 Impact Factor