Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymph node aspergillosis in an otherwise healthy patient receiving neither antibiotic corticosteroid or immunodepressive drug treatment is an uncommon event. In addition the case reported revealed no deficiency in humoral or cellular immunity. The possibility that aspergillosis may occur in cases without identifiable immunodeficiency is therefore put forward.
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PMID:[A case of lymph node aspergillosis]. 671 32

Pulmonary invasive aspergillosis is a frequent and poor prognosis complication of immunodeficiency and prolonged neutropenia. Its treatment is usually based on amphotericin given as intravenous infusion at 1 to 1.25 mg/kg/d. Use of lipid carriers give the opportunity to administrated higher dose, 5 mg/kg/d, with respect of renal function and good results in the primarily study. Intraconazole is now a good therapy after amphotericin, in the second time of disease.
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PMID:[Curative antifungal treatment of invasive pulmonary aspergillosis]. 750 40

Early in the developmental period of microbiology, Pasteur first observed the phenomenon of dimorphism in fungi when he noticed that the bread mold Mucor grew as a filamentous mold aerobically on the surface of broth cultures but at the bottom of the flask where the environment was anaerobic it reproduced as budding yeast cells. Several infectious fungal pathogens of humans, namely Histoplasma capsulatum, Blastomyces dermatitidis, Paracoccidioides brasiliensis, Sporothrix schenkii, and Coccidioides immitis change from a multicellular filamentous form to an unicellular morphology when they invade tissues. The ability of pathogenic fungi to assume a different shape is referred to as dimorphism. This phenomenon has intrigued clinicians, and medical mycologists since its discovery at the turn of the century. The ability of pathogens to initiate infection, invade host tissues and survive in mammalian hosts is critically linked to the induction of specific gene products. In dimorphic fungi, developmentally regulated gene expression is particularly important, since they may exist in phylogenetically distinct hosts with different body temperatures. Using Histoplasma capsulatum as a model to study parasite-host interactions at the biochemical and molecular level, my laboratory has attempted to relate the clinical spectrum of disease to natural variations in the characteristics of this organism and to adaptations it must make as a saprobe and a parasite. Histoplasma capsulatum is the etiologic agent of histoplasmosis, a respiratory infection that is world-wide in distribution. As a saprobe in soil it is mycelial, but it becomes a budding yeast as a parasite in susceptible hosts. These morphological phases can be reversibly reproduced in vitro by shifting the temperature from 25 degrees C, at which it is mycelial, to 37 degrees C, when it becomes a budding yeast. The process of mycelial-to-yeast conversion is of particular interest since it is triggered by an increase in temperature and conversion to virulence. Viable mycelial fragments and conidia become airborne and enter the pulmonary tract by inhalation after which the fungus rapidly disseminates to other organs. Progressive disseminated histoplasmosis along with candidiasis, cryptococcosis, and invasive aspergillosis are opportunistic fungal infections in patients who are immunosuppressed or otherwise debilitated. Importantly, they are diagnostic hallmarks of acquired immunodeficiency disease syndrome (AIDS). The clinical features of these infections and the genetic characteristics of the etiologic agents present unique parasite-host interactions that make them valuable research models to study. In the infected host, Histoplasma capsulatum encounters various environmental stresses to which it adapts by regulating the expression of specific genes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Unraveling the secrets of Histoplasma capsulatum. A model to study morphogenic adaptation during parasite host/host interaction. 757 55

Surgical consultation is regularly requested for diagnosis and treatment of pulmonary complications of the endemic mycosis, Histoplasma capsulatum, Blastomyces dermatitidis and Coccidioidomycosis immitis, and the yeast Cryptococcus neoformans. All resemble pulmonary malignancies. Histoplasmosis causes pericarditis, mediastinal fibrosis and mediastinal granuloma, which can cause entrapment of vascular structures, the esophagus, and the trachea. Coccidioidomycosis can cause spontaneous pneumothorax and thin wall cavities that can be superinfected with tuberculosis and Aspergillosis. The pathogenesis, diagnosis, and treatment of these organisms are discussed with emphasis on the new oral therapies and complications encountered in persons with human immunodeficiency virus (HIV) infection.
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PMID:The endemic mycoses: surgical considerations. 761 61

A competitive PCR assay involving the use of bronchoalveolar lavage (BAL) samples for the diagnosis of invasive pulmonary aspergillosis (IPA) was developed. For this purpose, a 1-kb mitochondrial DNA fragment of Aspergillus fumigatus was sequenced. The primers used allowed amplification of A. fumigatus, A. flavus, A. terreus, and A. niger DNAs but not DNAs of other fungi and yeasts. BAL samples from 55 consecutively enrolled patients were tested. Three samples were excluded because of failure of correct amplification of the internal competitive control. Of 28 immunocompromised patients, 6 were PCR positive; 3 died of IPA and their BAL cultures yielded A. fumigatus; and 3 were culture negative and did not develop IPA. Of 15 human immunodeficiency virus-positive patients and 9 immunocompetent patients, 5 and 4, respectively, were both PCR positive and culture negative, and none developed aspergillosis. Thus, PCR confirmed IPA in three patients but gave positive results for 25% (12 of 49) of the patients who did not develop aspergillosis. The predictive value of PCR-positive results seems low for patients at risk for aspergillosis. Moreover, the risk of contamination of reaction buffers or biological samples with Aspergillus conidia seems high and has to be weighed in regard to the potential diagnostic benefit of PCR testing as a routine procedure.
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PMID:Detection of Aspergillus species DNA in bronchoalveolar lavage samples by competitive PCR. 761 23

The objective of our study was to evaluate the prevalence of pleural effusions in patients with the acquired immunodeficiency syndrome, to correlate these effusions with any concomitant pulmonary diseases and to evaluate the role of cytologic examination in the diagnosis of the effusions. Twenty-eight of 389 (7.2%) human immunodeficiency virus-infected patients had pleural effusions and 27 of the 28 were suffering from concomitant pulmonary diseases. Those diseases were bacterial pneumonia (9), mycobacterial infection (7), non-Hodgkin's lymphoma (4) and Kaposi's sarcoma (2). Pneumocystis carinii pneumonia was diagnosed in two patients, and cytomegalovirus pneumonitis and pulmonary aspergillosis and small cell carcinoma in one patient each. Cytologic examination of pleural effusions provided conclusive diagnoses of mycobacterial infection in 2 of the 7 patients, of non-Hodgkin's lymphoma in 4 and of P carinii infection in 2.
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PMID:Pleural effusions in human immunodeficiency virus-infected patients. Correlation with concomitant pulmonary diseases. 763 43

A case of acquired immunodeficiency syndrome (AIDS) with preceding aplastic anemia is reported. The patient was a 36 year old female who had been diagnosed as having aplastic anemia 10 years before and thereafter had received multiple transfusions. Human immunodeficiency virus (HIV)-seropositivity was revealed 10 months prior to her death, but no particular clinical signs indicating HIV infection, pre-AIDS or onset of AIDS were recognized before serological diagnosis, although the slow progression of leukopenia was noted along with thrombocytopenia. Her general condition deteriorated during the last 10 months accompanied by an acute decrease in the CD4/CD8 ratio. Autopsy revealed full-blown AIDS: systemic aspergillosis, progressive multifocal leukoencephalopathy, Epstein-Barr virus-related B cell lymphoma arising in the diaphragm and severe lymphocyte depletion in the lymph nodes and spleen. Markedly hypoplastic bone marrow was considered to be primarily attributable to the aplastic anemia but the affection of AIDS was not excluded. The possible transmission route of HIV and the effect of the preceding aplastic anemia on the infection and clinical course of AIDS are discussed.
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PMID:An autopsy case of acquired immune deficiency syndrome (AIDS) with preceding aplastic anemia. 786 68

Based on our prior data suggesting a therapeutic advantage for infusional administration of cyclophosphamide (C), doxorubicin (D), and etoposide (E) in patients with relapsed and resistant non-Hodgkin's lymphoma (NHL), we administered C (750 mg/m2), D (50 mg/m2), and E (240 mg/m2) via continuous intravenous infusion over 96 hours as first line therapy for 21 patients with intermediate- or high-grade non-Hodgkin's lymphoma associated with human immunodeficiency virus (HIV) infection. Treatment was repeated every 28 or more days. The median CD4 count of the study group was 87/ul, and the median serum lactate dehydrogenase was 383 IU/L. Extranodal disease, lymphomatous marrow involvement, and lymphomatous meningitis were present at diagnosis in 90%, 33%, and 10% of patients, respectively. Complete response (CR) occurred in 13 patients (62%, 95% confidence intervals 41%, 81%) and partial response occurred in five patients (24%). The estimated median survival of the study group was 18.0 months. Hematologic toxicity required dose reduction for 47% of cycles and for 79% of patients who received at least two cycles. The mean dose intensity for C, D, and E were 73%, 70%, and 73% of the intended dose intensity, respectively. Opportunistic infection included oral/esophageal candidiasis (N = 7), herpes labialis (N = 3), pulmonary Mycobacterium avium-intracellulare (N = 1), candidemia (N = 1), pneumonitis (N = 1), and disseminated aspergillosis than resulted in a single treatment-related death (5%). Treatment resulted in a significant decrease in the CD4+ lymphocytes, as well as total lymphocytes, T lymphocytes, and CD8+ lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infusional cyclophosphamide, doxorubicin and etoposide in HIV-related non-Hodgkin's lymphoma: a follow-up report of a highly active regimen. 795 Sep 15

A male infant with primary combined immunodeficiency, microcephaly with marked cerebellar hypoplasia, and growth failure of prenatal onset is presented. He developed progressive pancytopenia in the 3rd year of life and died at 42 months from disseminated aspergillosis. Laboratory studies and post mortem examination failed to reveal any known aetiology for his disorder. Hreidarsson et al. [3] previously described a syndrome of progressive pancytopenia with microcephaly, cerebellar hypoplasia and growth failure in three boys, with similar clinical and laboratory findings. Although extensive immunological investigations were not performed in those previous patients, recurrent infections in two of them are suggestive of immunodeficiency. In the light of the immunological findings in our patient, we propose that the condition of the four patients belongs to the same syndrome, which has to be considered as a primary combined immunodeficiency syndrome. This syndrome can be distinguished from the other known immunodeficiency syndromes by its associated characteristic features, namely microcephaly with cerebellar hypoplasia, growth failure of prenatal onset and progressive pancytopenia.
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PMID:A syndrome of primary combined immunodeficiency with microcephaly, cerebellar hypoplasia, growth failure and progressive pancytopenia. 803 21

The relationship of disseminated aspergillosis with human immunodeficiency virus (HIV) infection is unclear. In the initial case definition of acquired immunodeficiency syndrome (AIDS) developed by the Centres for Disease Control (CDC), Atlanta, aspergillosis was included as an AIDS-defining opportunistic infection. In view of the primary relationship of aspergillosis with neutropenia rather than with lymphocyte depletion, as well as the lack of aspergillar infections among reported AIDS cases, aspergillosis was later deleted from the CDC case definition of AIDS. We describe a case of disseminated aspergillosis in a patient with AIDS, with an extensive literature review of the subject.
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PMID:Disseminated aspergillosis in the acquired immunodeficiency syndrome. 814 33


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