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Human immunodeficiency virus (HIV) infection is increasing worldwide, and several reports indicate …


Biology Articles » Virology » Oral ulcer as an unusual feature of visceral leishmaniasis in an AIDS patient » Discussion

Discussion
- Oral ulcer as an unusual feature of visceral leishmaniasis in an AIDS patient

VL is being reported with increased frequency in HIV patients. Investigators from Spain have reported 16 cases of HIV disease, in which the patients developed VL with typical clinical presentation.[2]

Fever, diarrhea and loss of weight are the presenting features of VL. Hepatosplenomegaly, anemia, hemorrhagic manifestations, lymphadenopathy are the other signs in patients with VL.[7] This case had fever, diarrhea and loss of weight for the past 6 years. She also had hepatosplenomegaly, lymphadenopathy, bleeding per rectum and anemia.

The white retinal necrosis heavily pointed towards cytomegalovirus retinitis. The possibility of other causes of oral ulcer in HIV patients, like herpes simplex, aphthous ulcers and atypical Mycobacterium tuberculosis , was excluded by history and clinically by Tzanck smear examination and histopathology respectively.

Although the course of leishmaniasis with HIV has not been determined as yet, extensive gastrointestinal infiltration by leishmania can cause malabsorption and thus emaciation of the patient.[8] Death ultimately occurs in 3 to 20 months in untreated cases of leishmaniasis. The history of blood transfusion (BT) 4 years prior to the onset of these symptoms and keeping in mind that it takes 15 to 20 years for AIDS to manifest itself completely,[9] it is justified to presume that the patient acquired HIV infection by mode of BT. Professional blood donors are migrant people from endemic areas; with this in mind, VL can very well be presumed to have been acquired through transfusion in this case, in the absence of any focal outbreak in the area or absence of travel to endemic areas. It is common knowledge that the course of leishmania spread depends on cellular immunity of the host and development of hypersensitivity to the parasite antigen; thus, the HIV status perhaps contributed to the leishmania spread as and when infection occurred during the period of 10 years. Furthermore, the progression of disease has to be related to the development of suppressor T lymphocyte in the host. Thus, it seems very likely that this patient did suffer from both HIV disease and VL at the same time.

VL could have mimicked the symptoms and signs of abdominal tuberculosis, for which she got the treatment inadvertently without any improvement. The frequency, morbidity and presentation of infections vary with the degree of immunosuppression of the patient, as well as the prevalence of infectious organisms in a given individual or environment.[8]

Oral ulceration in this patient as one uncommon clinical manifestation of VL, along with splenomegaly and lymph node enlargement, is indeed a very significant presentation along with HIV infection. Secondly, BT as a mode of HIV transmission still exists in highly populated countries like India. VL with oral ulceration was the first presentation of HIV in this case, and to the best of our knowledge only one such case has been reported earlier from India.[6] This case belonged to the endemic area of Bihar, and there were nodular lesions, which showed dense cellular infiltrates with lymphocytes, histiocytes and plasma cells on histopathology. Our case was from a non-endemic area and had an oral ulcer, which had macrophages full of leishmania amastigotes. Milian has reported a similar case, in which the patient was ex-intravenous drug abuser and suffered from HIV, hepatitis C and oral leishmaniasis.[10] His case presented with a painful vegetating tumor on the hard palate. Lesional biopsy confirmed the diagnosis of leishmaniasis; bone marrow aspirate, however, was negative.

Our case belonged to a non-endemic area, thus highlighting the fact that leishmaniasis can manifest in an unusual manner in HIV-infected people and may at times be the only presentation of HIV disease, even in non-endemic areas. The overlapping geographical distribution of VL and AIDS is increasing due to (a) spread of AIDS pandemic in suburban and rural areas of the world and (b) the simultaneous spread of VL from rural to suburban areas.

The incidence of VL among Indian AIDS cases might be higher but remains undetected for want of proper laboratory support in interior areas. The health care providers should have a high index of suspicion for VL in all HIV-infected cases with lymphadenopathy and hepatosplenomegaly.


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