Botryomycosis in acquired immunodeficiency syndrome

The first case, to our knowledge, of an integumentary form of botryomycosis is reported in a homosexual man with acquired immunodeficiency syndrome. Anal fistula and ischiorectal and gluteal abscesses developed following severe cryptosporidial diarrhea. Grains composed of gram-positive cocci were identified in the suppurative exudate. The grains had attached to multinucleated macrophages, many of which contained clusters of cocci in their cytoplasm. It is postulated that the cocci were able to survive and probably replicate in the cytoplasm of multinucleated macrophages, and were subsequently extruded as grains. These observations suggest a defect in intracellular killing of cocci by the monocyte-macrophage system. This may relate to failure in induction of control of macrophage activity by T4-inducer subsets.     

Pituitary pathology in acquired immunodeficiency syndrome

Pituitary morphology was studied in 49 autopsied patients with acquired immunodeficiency syndrome. Direct infectious involvement was noted in six adenohypophyses (12%), including five cases by cytomegalovirus and one by Pneumocystis carinii. Two cases with neurohypophysial lesions presumably caused by cytomegalovirus and one questionable case of Toxoplasma gondii were also observed. In all instances these changes were associated with generalized and/or cerebral infection by these same agents. Neither Kaposi's sarcoma nor malignant lymphoma was encountered in the pituitary glands. Acute necrotic foci, presumably due to infarction, were noted in four cases. Four pituitary microadenomas (8%) and four hyperplastic nodules were identified. The incidence of such noninfectious lesions, as well as the prevalence and distribution of the various immunoreactive adenohypophysial cell types, were similar to those seen in the pituitary glands of age-matched male control patients.     

Cytomegalovirus adrenalitis in acquired immunodeficiency syndrome

Seventy-three adrenal glands of 44 patients with acquired immunodeficiency syndrome (AIDS) were examined and graded histologically to reveal cytomegaloviral (CMV) adrenalitis. The number of CMV inclusion bodies (IB) were evaluated and compared with 3 methods in 58 adrenal glands of 40 patients: histological sections, immunocytochemistry for early antigens of CMV, and in situ hybridization with biotinylated probes for CMV DNA All 73 adrenal glands contained foci of lymphocytic infiltrate. Forty (55%) showed CMV adrenalitis and necrosis, which were more extensive in the medulla than in the cortex. The number of CMV IB increased with the severity of necrosis and fibrosis (grades I, 1.0; II, 3.6; III, 27.8 IB/ thousand cells counted in 20 fields). More than 85 percent of both glands were necrotic in0 only I patient (2.3%). For the 3 methods, the means of the number of CMV IB were as follows: in situ hybridization with biotinylated probe, 17.7; immunocytochemistry, 12.9; and H&E, 8.1. However, using multivariant analysis, there was no statistically significant difference. Thirty-three (45%) adrenal glands contained no CMV IB by any of the 3 methods. We conclude that CMV adrenalitis is a common finding in patients with AIDS. Destruction of adrenal tissue is usually not widespread enough to result in adrenocortical insufficiency.     

Intestinal leishmaniasis in acquired immunodeficiency syndrome

In endemic regions, visceral leishmaniasis is one of the most common opportunistic infections in HIV positive patients. Simultaneous infection with Leishmania and HIV has been reported in some countries but this is the first report of such a case in Iran. Our patient was a 27 years old man with intermittent night fever, abdominal pain, loss of appetite, vomiting, watery diarrhea and severe weight loss for 6 months. He had low socio-economic status with an imprisonment history. The patient was quite cachectic and had low grade fever. Physical exam and upper GI endoscopy revealed oropharyngeal candidiasis. Microscopic evaluation of duodenal biopsy material showed Leishmania amastigotes in macrophages of lamina propria. Leishman bodies were also observed in bone marrow aspiration specimen. Serologic tests were positive for Leishmania infantum. HIV antibody was also positive with a CD4+cell count of 80/μl. The diagnosis was acquired immunodeficiency syndrome with simultaneous visceral leishmaniasis involving intestinal mucosa.     

Myositis and acquired immunodeficiency syndrome

Clinical and pathologic observations made in a patient with inflammatory myopathy associated with the acquired immunodeficiency syndrome (AIDS) are presented. Multinucleated giant cells were a prominent histopathologic feature in the muscle biopsy samples. The findings indicate that in some patients with AIDS myositis, inflammatory myopathy may be the direct result of infection with the human immunodeficiency virus.     

Tuberculosis and acquired immunodeficiency syndrome

India has the largest HIV-infected population in the world with over 4 million infected. The current evidence indicates that the doubling time of the epidemic in India is less than 2 years. Those infected with Mycobacterium tuberculosis add to the gravity of the situation enhancing both morbidity and mortality in these dually infected patients. With the incomprehensive diagnostic facilities available, it is wise to exploit the situation with utilization of tuberculin test with a different cut off criterion for the early diagnosis of mycobacterial infection amongst HIV positive population, especially when there are financial constraints and lack of diagnostic facilities to get CD4 cell count.     

Pulmonary aspergillosis in the acquired immunodeficiency syndrome

BACKGROUND AND METHODS. Symptomatic pulmonary aspergillosis has rarely been reported in patients with the acquired immunodeficiency syndrome (AIDS). We describe the predisposing factors, the clinical and radiologic features, and the therapeutic outcomes in 13 patients with pulmonary aspergillosis, all of whom had human immunodeficiency virus (HIV) infection and 12 of whom had AIDS. RESULTS. Pulmonary aspergillosis was detected a median of 25 months after the diagnosis of AIDS, usually following corticosteroid use, neutropenia, pneumonia due to other pathogens, marijuana smoking, or the use of broad-spectrum antibiotics. Two major patterns of disease were observed: invasive aspergillosis (in 10 patients) and obstructing bronchial aspergillosis (in 3). Cough and fever, the most common symptoms, tended to be insidious in onset in patients with invasive disease (median duration, 1.3 months before diagnosis). Breathlessness, cough, and chest pain predominated in the three patients with obstructing bronchial aspergillosis, who coughed up fungal casts. Radiologic patterns included upper-lobe cavitary disease (sometimes mistaken for tuberculosis), nodules, pleural-based lesions, and diffuse infiltrates, usually of the lower lobe. Transbronchial biopsies were usually negative, but positive cultures were obtained from bronchoalveolar-lavage fluid or percutaneous aspirates. Dissemination to other organs occurred in at least two patients, and direct invasion of extrapulmonary sites was seen in two others. The results of treatment with amphotericin B, itraconazole, or both were variable. Ten of the patients died a median of 3 months after the diagnosis (range, 0 to 12 months). CONCLUSIONS. Pulmonary aspergillosis is a possible late complication of AIDS; if diagnosed early, it may be treated successfully.     

Thymus involution in the acquired immunodeficiency syndrome

Acquired immunodeficiency syndrome (AIDS) is a severe disorder of unknown etiology and pathogenesis, predominantly affecting homosexual males and other high-risk groups and characterized by profound alterations in T-lymphocyte function. The authors have examined thymus tissue from 14 patients who died of AIDS and compared the results with findings in five control groups: healthy age-matched controls, elderly individuals, patients with chronic or debilitating illnesses other than AIDS, infants with conditions causing "stress atrophy," and patients with myasthenia gravis. The AIDS group included 11 homosexual males, 1 Haitian, 1 homosexual who was also a drug abuser, and a 10-month-old infant believed to have contracted AIDS following blood transfusion. All the AIDS cases showed marked thymus involution with severe depletion of both lymphocytes and epithelial elements. The latter component consisted primarily of thin cords and nests of primitive-appearing epithelial cells that could be defined by positive immunohistochemical staining for keratin. Many cases showed a variable plasma cell infiltration, and the majority exhibited distinct vascular changes in the form of hyalinization and/or onion-skin patterns, primarily in the adventitia. Most striking of all was the marked paucity of Hassall's corpuscles; four patients had none at all, while in the other ten patients all the Hassall's corpuscles were calcified. These changes were far more extensive than those seen in any of the control groups, which retained most of their complement of Hassall's corpuscles even in the face of marked overall involution. The physiologic function of Hassall's corpuscles is not known, but recent immunohistochemical studies have implicated them in the synthesis of "facteur thymique serique" (FTS, thymulin) and other thymic hormones known to play a role in regulating T-helper and suppressor cell activity. It is conceivable that the extensive destruction of Hassall's corpuscles observed in AIDS may be a crucial element in the pathogenesis of this syndrome.     

Neuropathology of the acquired immunodeficiency syndrome

This review attempts to assess critically the literature on the neuropathology of acquired immunodeficiency syndrome in light of our experience with 172 patients with acquired immunodeficiency syndrome who underwent extensive postmortem examinations of the central and peripheral nervous systems. The neuropathologic manifestations of the disease can be divided into three categories: (1) primary or putative/indirect effects of the human immunodeficiency virus, (2) opportunistic infections, and (3) neoplasms. We discuss the known etiologic agents and postulated pathogenetic mechanisms responsible for the broad range of neurologic diseases observed in patients with acquired immunodeficiency syndrome.     

Neuropathology of the acquired immunodeficiency syndrome

Neuropathology of acquired immunodeficiency syndrome. The Central Nervous System (CNS) has been examined at autopsy in 60 patients who died of AIDS in a 6-year period in our hospital. Most of the patients were intravenous drug abusers, the mean age was of 34 years, with a high prevalence of males. Neurologic symptoms were present in 62% of patients, while histologic lesions have been observed in 51 cases (85%). Opportunistic infections were found in 27 patients, the commonest being T. gondii (12) and Cytomegalovirus (7); Progressive Multifocal Leukoencephalopathy was observed in 2 cases. HIV-associated lesions included 21 cases of Multifocal Giant Cell Encephalitis (MGCE), 15 of Progressive Diffuse Leukoencephalopathy (PDL) and 7 cases of Vacuolar Myelopathy. Primary CNS lymphoma was noted in 8 patients and secondary deposits were observed in 3 cases. Simultaneous CNS lesions by more than one pathogen were frequently encountered. The main pathogenetic mechanisms for characterization of all the lesions and their relationship with clinical features of the disease are discussed. It is supposed that MGCE and PDL represent two different patterns of HIV-encephalopathy.