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)

Microsporidia are obligate, intracellular, spore-forming protozoal parasites. Their host range is extensive and includes most invertebrates and all classes of vertebrates. Five microsporidial genera (Enterocytozoon, Encephalitozoon, Septata, Pleistophora, and Nosema) and unclassified microsporidia have been associated with human disease, which appears to manifest primarily in immunocompromised persons. The clinical manifestations of microsporidiosis are diverse and include intestinal, pulmonary, ocular, muscular, and renal disease. The majority of microsporidial infections in persons infected with human immunodeficiency virus (HIV) are attributed to Enterocytozoon bieneusi, an important cause of chronic diarrhea and wasting. Four cases of microsporidial infection among persons not infected with HIV who had documented or presumed cellular immunodeficiency and four cases of corneal stroma infection due to microsporidia in immunocompetent patients have been described. Furthermore, the first case of traveler's diarrhea due to E. bieneusi in an immunocompetent and otherwise healthy patient is reported in this issue. The sources of human microsporidial infections and modes of transmission are unknown.
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PMID:Microsporidial infections in immunodeficient and immunocompetent patients. 781 72

Microsporidia are obligate intracellular spore-forming protozoal parasites belonging to the phylum Microspora. Their host range is extensive, including most invertebrates and all classes of vertebrates. More than 100 microsporidial genera and almost 1,000 species have now been identified. Five genera (Enterocytozoon spp., Encephalitozoon spp., Septata spp., Pleistophora sp., and Nosema spp.) and unclassified microsporidia (referred to by the collective term Microsporidium) have been associated with human disease, which appears to manifest primarily in immunocompromised persons. The clinical manifestations of microsporidiosis are diverse and include intestinal, pulmonary, ocular, muscular, and renal disease. Among persons not infected with human immunodeficiency virus, ten cases of microsporidiosis have been documented. In human immunodeficiency virus-infected patients, on the other hand, over 400 cases of microsporidiosis have been identified, the majority attributed to Enterocytozoon bieneusi, an important cause of chronic diarrhea and wasting. Diagnosis of microsporidiosis currently depends on morphological demonstration of the organisms themselves. Initial detection of microsporidia by light microscopic examination of tissue sections and of more readily obtainable specimens such as stool, duodenal aspirates, urine, sputum, nasal discharge, bronchoalveolar lavage fluid, and conjunctival smears is now becoming routine practice. Definitive species identification is made by using the specific fluorescein-tagged antibody (immunofluorescence) technique or electron microscopy. Treatment options are limited, but symptomatic improvement of Enterocytozoon bieneusi infection may be achieved with the anthelmintic-antiprotozoal drug albendazole. Preliminary observations suggest that Septata intestinalis and Encephalitozoon infections may be cured with albendazole. Progress is being made with respect to in vitro propagation of microsporidia, which is crucial for developing antimicrosporidial drugs. Furthermore, molecular techniques are being developed for diagnostic purposes, taxonomic classification, and analysis of phylogenetic relationships of microsporidia.
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PMID:Human microsporidial infections. 783

Five cases of intestinal microsporidiosis are reported, including one case of a heterosexual female acquired immunodeficiency syndrome (AIDS) patient, three homosexual males, and one bisexual male AIDS patients with detailed description of their clinical course. These five cases underscore the severity of immunodeficiency in patients with microsporidiosis. All patients had multiple opportunistic infections and a CD4 cell count below 100/microliters long before diarrhea developed. This is the first kinetic study of helper T-lymphocytes in cases of microsporidiosis. Diagnosis was made by duodenal biopsies stained with Brown and Brenn or Gram-Weigert technique (confirmed by electron microscopy) and by stool smears stained with a modified trichrome technique. However, the best preparation was plastic sections stained with toluidine blue, which demonstrated both the spores and plasmodia clearly. In our evaluation, Giemsa stain was also acceptable for identification of microsporidian spores in both intestinal biopsies and stool smears, but there was a failure to identify the organism on hematoxylin and eosin, acid-fast, periodic acid-Schiff, and Gomeri's methenamine silver stained preparations. Therapeutic attempts using albendazole, metronidazole, octreotide, and zidovudine (AZT) failed to eradicate microsporidia in these patients.
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PMID:Intestinal microsporidiosis. Report of five cases. 784 80

Microsporidia cause opportunistic infections in AIDS patients and commonly infect laboratory animals, as well. Euthymic C57B1/6 mice experimentally infected with intraperitoneal injections of 1 x 10(6) Encephalitozoon cuniculi Levaditi, Nicolau et Schoen, 1923, Encephalitozoon hellem Didier et al., 1991, or Nosema corneum Shadduck et al., 1990 displayed no clinical signs of disease. Athymic mice, however, developed ascites and died 8-16 days after inoculation with N. corneum, 21-25 days after inoculation with E. cuniculi, and 34-37 days after inoculation with E. hellem. All athymic mice displayed hepatomegaly, dilated intestine and accumulation of ascites fluid. Granulomatous lesions are primarily located in the liver, lung, pancreas, spleen, and on serosal surfaces of abdominal organs. The murine microsporidiosis model also was used to examine immune response that inhibit microsporidia growth in vitro. Recombinant murine interferon-gamma (mIFN-gamma, 100 mu/ml) alone or in combination with lipopolysaccharide (LPS; 10 ng/ml) could activate thioglycollate-induced peritoneal murine macrophages to destroy E. cuniculi. The production of the nitrogen intermediate, NO2-, correlated with parasite destruction. Inhibition of NO2- generation by addition of the L-arginine analogue, NG-monomethyl L-arginine (NMMA), inhibited microsporidia killing, as well. Since microsporidiosis is becoming an important opportunistic infection in AIDS patients, a microsporidiosis model is being developed using SIV/DeltaB670-infected rhesus macaque monkeys (Macaca mulatta). SIV-infected immunocompetent monkeys given E. cuniculi or E. hellem per os developed specific antibodies, and microsporidia could be detected sporadically by calcofluor or antibody fluorescence staining of stool and urine sediment smears. As immunodeficiency progressed, monkeys developed diarrhoea, cachexia, and anorexia, and organisms were detected in urine and stool with greater frequency. Immunodeficient SIV-infected monkeys died approximately 27 days after receiving E. hellem by intravenous inoculation, and approximately 110 days after receiving E. hellem per os. Lesions typical for SIV-infection were observed in both groups of monkeys and microsporidia were detected in kidney and liver of the intravenously-injected monkeys. The murine microsporidiosis model provides an efficient means for studying protective immune responses to microsporidiosis, and may prove useful for screening immunological and chemotherapeutic agents. The pathogenesis of Encephalitozoon microsporidiosis in SIV-infected monkeys appears to parallel encephalitozoonosis in AIDS patients, suggesting that simian microsporidiosis may provide a useful model for evaluating diagnostic methods and therapeutic strategies during various stages of progressing immunodeficiency.
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PMID:Experimental microsporidiosis in immunocompetent and immunodeficient mice and monkeys. 805 Jul 48

Several trends in clinical medicine have converged recently and placed intestinal protozoan infections in a position of increasing importance to health professionals. These trends include the pandemic of human immunodeficiency virus (HIV) infections that cause the acquired immunodeficiency syndrome (AIDS) and result in associated opportunistic infections. The increasing use of powerful chemotherapeutic and immunosuppressive agents to prevent rejection of transplanted tissues in human allograft recipients has predisposed these patients to intestinal parasitic infections, which often become chronic and debilitating. Large numbers of people engage in business, philanthropic work, and vacation travel on a worldwide basis. The number of susceptible, potential human hosts for parasitic infections will continue to increase in the coming years. We reviewed 4 protozoan infections that have recently attracted the interest of clinicians, either because they are newly discovered or because they are increasingly prevalent. These infections include cryptosporidiosis and recently described infections due to Cyclospora species. The AIDS pandemic has also been associated with both the discovery and the rapid emergence of human microsporidiosis. Isospora belli has received renewed attention because of chronic infections now observed in HIV-infected hosts.
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PMID:New parasites on the block: emerging intestinal protozoa. 805 39

Enterocytozoon bieneusi is a newly described microsporidia in humans thought to be responsible for chronic diarrhoea in acquired immunodeficiency syndrome (AIDS) patients. The epidemiology of this parasite is still unknown; it could be a strictly opportunistic agent or a human enteropathogen. E. bieneusi spores were searched for in stool smears of two populations using a modified chromotrope 2R staining. The first population consisted of 60 patients infected by the human immunodeficiency virus (HIV) and the second of 990 children aged from one month to six years consulting two primary care centers in Niamey, Niger. E. bieneusi spores were found in 4 out of the 60 HIV-positive patients (7%). These 4 patients belonged to a subgroup of 35 patients with < 50 CD4 cells/microliters. Out of 990 children, 8 shed E. bieneusi spores in their stools; the presence of spores was not associated with a particular clinical phenotype (diarrhoea, fever, dehydration, vomiting). Although HIV status could not be evaluated, the HIV prevalence rate among women consulting the same care centers was low (0.5%) and it is therefore unlikely that all eight children were HIV-infected. The results show for the first time that E. bieneusi can infest HIV-negative subjects. Microsporidiosis is frequent in AIDS patients with low CD4 cell counts. Further work is needed to define the prevalence and the possible pathogenic effect of E. bieneusi in immunocompetent subjects.
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PMID:[Prevalence of Enterocytozoon bieneusi spores in the stool of AIDS patients and African children not infected by HIV]. 812 4

The microsporidian Enterocytozoon bieneusi has been recognized as an important cause of chronic diarrhea in severely immunodeficient adults infected with human immunodeficiency virus (HIV). We report the first case of intestinal E. bieneusi infection in a child. The 9-year-old boy with connatal HIV infection presented with failure to thrive, chronic diarrhea, and intermittent abdominal pain. His CD4 lymphocyte count was 0.05 x 10(9)/L and dropped to 0.01 x 10(9)/L. No HIV-associated opportunistic infection other than oral hairy leukoplakia and oral candidiasis had been found before microsporidia were detected. Treatment of microsporidiosis with albendazole was of no benefit. During follow-up, the boy also developed intestinal cryptosporidiosis. Evaluation of chronic diarrhea in severely immunodeficient HIV-infected children should include examination for intestinal microsporidia. We recommend the use of a new coprodiagnostic technique that allows detection of microsporidial spores in stool specimens. Furthermore, consideration of dual or even multiple parasitic infections in the differential diagnosis of chronic diarrhea may have both important clinical and epidemiological implications.
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PMID:Intestinal coinfection with Enterocytozoon bieneusi and Cryptosporidium in a human immunodeficiency virus-infected child with chronic diarrhea. 821 93

Eighteen patients infected with human immunodeficiency virus and with chronic unexplained diarrhea were prospectively studied to investigate the prevalence and clinical and biologic features of intestinal microsporidiosis. All patients underwent extensive evaluation for bacterial, viral, and parasitic pathogens. Enterocytozoon bieneusi was found in 9 patients (50%; 95% confidence interval, 27-73) in stools and duodenal and jejunal biopsies. In 8 patients, it was the sole pathogen found. Other pathogens were also isolated from the intestinal tracts of 4 patients, but diarrhea remained unexplained in 6. Patients with intestinal microsporidiosis had significantly lower mean Karnofsky scores (69.4 vs. 85.5, P = .009), CD4 cell counts (18.6 vs. 209.8/microL, P = .02), and D-xylose absorption tests (0.13 vs. 0.36 g/L, P < .001) than did patients without intestinal microsporidiosis. Intestinal microsporidiosis appears to be a frequent cause of unexplained chronic diarrhea in patients with AIDS and is associated with diminished D-xylose absorption.
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PMID:Intestinal microsporidiosis in human immunodeficiency virus-infected patients with chronic unexplained diarrhea: prevalence and clinical and biologic features. 841 71

Microsporidiosis is a common finding in HIV-infected patients who have diarrhoea. The species most commonly causing gastrointestinal disease is Enterocytozoon bieneusi. Recently Septata intestinalis has been described as a cause of diarrhoea and disseminated infection in patients with AIDS. A 44-year-old homosexual man with severe immunodeficiency (CD4 cell count 40/microliters) had a history of watery diarrhoea for 2 weeks. Microsporidian spores measuring 1.2 to 1.5 x 2.5 to 3.0 microns were found in stool samples. Electron microscopy of duodenal biopsies confirmed the diagnosis of intestinal microsporidiosis and showed parasitophorous vacuoles with the typical ultrastructure of S. intestinalis. The patient was treated with albendazole (400 mg twice daily) and became asymptomatic within 4 days. No spores could be detected in stool samples after a treatment period of 14 days. About 25 infections with S. intestinalis have been reported to date, and the case presented here is the first in a German patient.
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PMID:Intestinal microsporidiosis with Septata intestinalis in a patient with AIDS--response to albendazole. 858 46

Sinusitis in patients with human immunodeficiency virus (HIV) infection usually arises from the same organisms that are infective in the nonimmunosuppressed population. The authors of this article report that optimal antimicrobial treatment and functional endoscopic sinus surgery failed to eradicate sinonasal disease in three of five patients with acquired immunodeficiency syndrome (AIDS) and refractory sinusitis. The sinonasal disease was manifested by congested, edematous, and polypoid mucosa, often with a superimposed bacterial infection from ostial obstruction. After tissue was sent for electron microscopy (EM), the patients were eventually diagnosed with microsporidiosis of the sinonasal cavities. Microsporidia are obligate intracellular protozoans that have been seen in AIDS patients with diarrhea. These protozoans have only recently been identified in sinonasal tissue. Microsporidia are often missed on routine histopathology. The authors present case reports on their five AIDS patients with refractory sinusitis. The management of refractory sinusitis in the HIV-infected population, including mandatory EM of sinonasal tissue, is also discussed.
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PMID:Microsporidian sinusitis in patients with the acquired immunodeficiency syndrome. 869 10


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