Tuberculoid leprosy and cytomegalovirus retinitis as immune restoration disease in a patient with AIDS.

Here we report a unique case of tuberculoid leprosy and cytomegalovirus retinitis in a 27-year-old female patient with AIDS, suggestive of highly active antiretroviral therapy (HAART)-induced immune restoration disease. After initiation of HAART, the patient presented with decreased visual acuity, hypoesthetic patch with local nerve thickening, and an increase in her CD4+ T cell count. On further investigations cytomegalovirus retinitis and tuberculoid leprosy were confirmed. To our knowledge no case with such a co-existence has previously been reported.

Indentificação dos alelos HLA de classe I e classe II em pacientes co-infectados com hanseniase e AIDS / Identification of alleles HLA of classroom I and classroom II in patients co-infectedes with leprosy and AIDS

A imunidade celular do hospedeiro e quem determina a evoluçao e o quadro clinico do paciente, tanto na hanseniase como na infecçao pelo virus da imunodeficiencia adquirida (HIV). O virus HIV, assim como o Micobacterium leprae (M. leprae) sao antigenos intracelulares que estimulam a resposta imune celular e o perfil Th1. Os linfocitos T (LT) reconhecem esses antigenos quando apresentados juntamente com as moleculas do complexo HLA na superficie da celula apresentadora de antigeno (APC), desencadeando a resposta imune especifica. Muitos estudos tem sido realizados na tentativa de associar o complexo HLA com as diversas patologias. Na hanseniase, o complexo HLA tem sido amplamente estudado, na tentativa de elucidar os mecanismos que levam ao direcionamento da forma clinica, uma vez que estes alelos atuam de forma direta na resposta imune atraves da apresentaçao do peptideo antigenico para celula T. Estudos realizados com os alelos HLA de classe I apresentaram resultados controversos enquanto que a maioria das pesquisas de classe II, os resultados sao mais concordantes revelando associaçoes positivas dos alelos HLA-DR2 e HLA-DR3, com a forma tuberculoide (HT) e do alelo HLA-DQ1, com a forma virchoviana (HV). No HIV os alelos HLA parecem estar mais fortemente associados a deterioraçao imunologica que com a manifestaçao clinica da doença. Varios estudos associam consistentemente os alelos de classe I, HLA-B35 e HLA-Cw4 com a aceleraçao da progressao para a aids enquanto os alelos HLA-A1, HLA-B8, HLA-B27, HLA-Cw7 e os de classe II, HLA-DR3 e HLA-DQ2 estao associados a progressao lenta...

Co-infeccao pelo virus da imunodeficiencia humana (HIV) e o Mycobacterium leprae: aspectos imunologicos e caracterizacao anatomopatologica e imunofenotipica de lesoes de pele / ?

O aumento de susceptibilidade a infecções por micobactérias, notadamente Mycobacterium avium e Mycobacterium tuberculosis, é uma conseqüência bem conhecida da infecção pelo Vírus da Imnudeficiência Humana (HIV) refletindo em maior morbi/letalidade nos pacientes co-infectados. À medida que o HIV se dissemina em regiões tropicais e subtropicais endêmicas para a hanseníase, como é o caso do Brasil, os efeitos do HIV na hanseníase deveriam ser aparentes. No entanto, várias questões, como as listadas, ainda não estão totalmente esclarecidas. A infecção pelo HIV: constitui fa or de risco para a hanseníase? Agravaria a hanseníase pré-existente? Altera a progressão da resposta imune para o Mycobacterium leprae e as manifestações da doença levando a amior incidência de formas multibacilares? Altera a histoarquitetura e a compisição celular da pele? Favorece maior número de reações tipo 2? Representa fator de risco para incapacidades? Infuência o tratamento MDT-hansênico? Aumenta a letalidade? Relatos de casos isolados ou pequenas casuísticas de pacientes co-infectados descritos indicam que a interação HIV-M. leprae é incerta, pouco conhecida e representa um enigma do ponto de vista imunológico. A imunidade celular, gradativamente comprometida na infecção pelo HIV, representa o mecanismo protetor crucial para ambos patógenos. Embora pudéssemos prever um resultado desfavorável à medida que a imunossupressão se instala e a imunidade celular diminui, não está definido até que ponto a infecção por um patógeno influencia o curso da outra infecção. No contexto de uma região de alta endemicidade para a hanseníase e média endemicidade para o HIV, como é o Estado de Goiás, o presente estudo se propôs a avaliar a situação de co-infecção HIV-M. leprae entre os pacientes atendidos no centro de referência HAA/HDT. Dezoito pacientes co-infectados, atendidos no HAA/HDT, Goiânia, Goiás, no período de 1986 a 2001, que assinaram consentimento informado, tiveram biópsias de lesões de pele disponíveis para a análise histopatológica (HE e Fite-Faraco) e imunofenotípica (imuno-histoquímica). Utilizaram-se os critérios de classificação de Ridley-Jopling. A metade das biópsias analisadas era de pacientes virgens de tratamento e as demais, de pacientes em tratamento (n=3), em lesão residual pós tratamento (n=3) e nos casos de retratamento (n=3). Contagens de linfócitos T CD8+ periféricos (Citometria de Fluxo, FACSCount, BD) e valores de carga viral (NASBA, Organon), obtidos

In vitro susceptibility studies of Cryptococcus neoformans isolated from patients with no clinical response to amphotericin B therapy.

The in vitro activities of three antifungal drugs alone and in combination were evaluated against five isolates of Cryptococcus neoformans using time-kill curves (TKC). The isolates were from AIDS patients who had either died or had failed to show a clinical response during amphotericin B (AMB) treatment. AMB, fluconazole (FCZ) and flucytosine (5FC), and combinations of the drugs (AMB plus 5FC, AMB plus rifampicin (RIF) and FCZ plus 5FC), were evaluated. With all five isolates AMB did not show fungicidal activity; instead, a persistent or tolerant effect was observed. Combinations of AMB plus 5FC and AMB plus RIF showed a clear synergic effect, except for one isolate tested with AMB plus RIF. In contrast, the FCZ plus 5FC combination did not inhibit growth of any isolate.

AIDS and tuberculosis/leprosy in Nigeria: the urbanisation factor.

A study was conducted between February and June 1994 on the influence of urbanisation on the seroprevalence of human immunodeficiency virus (HIV) amongst tuberculosis (TB) and leprosy patients in the 4 Primary Health Care Zones in Nigeria. Results indicate that 71.4% of all smear positive TB patients and 75% of all multibacillary (MB) leprosy patients that are HIV seropositive in this study are resident in the urban areas. This study emphasizes the need for careful sample selection in studies involving HIV and tuberculosis/leprosy, and for careful monitoring of the HIV/leprosy interactions.

Activities of sparfloxacin, azithromycin, temafloxacin, and rifapentine compared with that of clarithromycin against multiplication of Mycobacterium avium complex within human macrophages.

The activities of sparfloxacin, azithromycin, temafloxacin, and rifapentine against two virulent strains of the Mycobacterium avium complex isolated from patients with AIDS were evaluated in a model of intracellular infection and were compared with that of clarithromycin. Human monocyte-derived macrophages were infected with the M. avium complex at day 6 of culture. The intracellular CFU was counted 60 min after inoculation. The intracellular and supernatant CFU was counted on days 4 and 7 after inoculation. The concentrations used, which were equal to peak levels in serum, were 10 micrograms of rifapentine per ml (MICs for the two strains, 4 and 16 micrograms/ml), 4 micrograms of clarithromycin per ml (MICs, 8 and 4 micrograms/ml), 1 microgram of azithromycin per ml (MICs, 32 and 16 micrograms/ml), 4 micrograms of temafloxacin per ml (MICs, 2 and 16 micrograms/ml), and 1 microgram of sparfloxacin per ml (MICs, 0.5 and 2 micrograms/ml). Compared with controls on day 7 after inoculation, clarithromycin (P less than 0.001), sparfloxacin (P less than 0.001), and azithromycin (P less than 0.001 for the first strain, P less than 0.02 for the second) slowed intracellular replication. Rifapentine (P less than 0.001) and temafloxacin (P less than 0.001) slowed intracellular replication of the first strain but not of the second strain. Azithromycin plus sparfloxacin was as effective as sparfloxacin alone. In this macrophage model, sparfloxacin or clarithromycin (difference not significant) exhibited a better efficacy than rifapentine, azithromycin, or temafloxacin against intracellular M. avium complex infection.

Transmissible lymphoma and simian acquired immunodeficiency syndrome in rhesus monkeys.

Four rhesus monkeys (Macaca mulatta) were inoculated with a homogenate of a cutaneous lepromatous leprosy lesion from a mangabey monkey (Cercocebus atys). One died of B-cell lymphoma, and another died of an immunodeficiency syndrome. Cell suspensions prepared from the tumor and spleen of the monkey with lymphoma induced lymphoma or an immunodeficiency syndrome when inoculated into additional young rhesus monkeys. The immunodeficiency syndrome was similar to simian acquired immunodeficiency syndrome and consisted of opportunistic infections, lymphoid hyperplasia or atrophy, wasting, and syncytial cell formation. Mitogen responses and percentages of T4- and T8-positive lymphocytes were normal until the animals were moribund. Lymphoblastoid cell lines became established in vitro from tumor cell suspensions. These cells were infected with a herpesvirus related to Epstein-Barr virus. In addition, a retrovirus morphologically similar to human T-cell lymphotrophic virus type III (HTLV-III) and simian T-lymphotrophic virus type III (STLV-III) was isolated from one of the lymphoblastoid cell lines (LCL). Type D retroviruses could not be demonstrated in the monkeys in the transmission study; however, a retrovirus similar to that in the LCL was isolated from 4 animals by coculture of peripheral blood lymphocytes with the human cell line H9. These results suggest that this retrovirus, STLV-III/Delta, may be associated with the immunodeficiency syndrome in these macaques and may be of mangabey origin.