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)

A chart review of 73 human immunodeficiency virus (HIV)-infected patients with enteric microsporidiosis was conducted to define the natural history of microsporidiosis. A substantial proportion of patients remained symptomatic after 6 months (54.8% with persistent diarrhea and 51.2% with weight loss). Predictors for persistent diarrhea included high HIV RNA viral load and no initiation of protease inhibitor therapy.
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PMID:Natural history of intestinal microsporidiosis among patients infected with human immunodeficiency virus. 1048 25

Among 1454 persons whose stool samples (n=5692) were submitted to a reference laboratory for microsporidia assessment from 1993 to 1996, microsporidia were identified in 338 persons: 261 persons infected with human immunodeficiency virus (HIV), 16 transplant patients, and 61 others. Intestinal microsporidiosis appears to be an endemic disease in HIV-positive persons (prevalence, 0.1%) and a sporadic disease in HIV-negative persons (prevalence, <1/1 million). A waterborne outbreak in 200 persons (attack rate, 1% in HIV-positive patients/month) occurred in the 1995 summer, without evidence of fecal contamination of water. No explanation was found before the outbreak ended, several months before the antiprotease era. Factors associated with microsporidiosis diagnosis were HIV infection, male homosexuality, low CD4 cell counts, and diarrhea. The major factor associated with a diagnosis of microsporidiosis during the outbreak was living in an area corresponding to one of the three water distribution subsystems of the town. Lake contamination was suspected.
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PMID:Waterborne outbreak of intestinal microsporidiosis in persons with and without human immunodeficiency virus infection. 1088 35

The ribosomal DNA internal transcribed spacer sequences of 13 unrelated Encephalitozoon intestinalis isolates obtained from human immunodeficiency virus (HIV)-infected patients with intestinal microsporidiosis were analyzed by gene amplification and DNA sequencing. Among these isolates, we found only one genetic lineage which suggests that E. intestinalis may have a clonal distribution in HIV-infected patients.
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PMID:Genetic homology among thirteen Encephalitozoon intestinalis isolates obtained from human immunodeficiency virus-infected patients with intestinal microsporidiosis. 1083 11

Human microsporidiosis is a parasitic infection due to species of four different genera: Encephalitozoon; Enterocytozoon; Nosema; and Pleistophora. Although well known as a cause of disease in animals, microsporidiosis was only occasionally reported in humans. Recently, in human immunodeficiency virus (HIV)-infected patients, microsporidia belonging to Encephalitozoon and Enterocytozoon species have proved to be important opportunistic pathogens. Enterocytozoon bieneusi is associated with chronic intermittent diarrhea, cholangiopathy and sinusitis whereas Encephalitozoon intestinalis, Encephalitozoon hellem and Encephalitozoon cuniculi, the three Encephalitozoon species found in humans, are associated with diarrhea, rhinosinusitis, keratoconjunctivitis, nephritis and hepatitis. Diagnosis of microsporidial infections in humans was until recently an invasive, laborious procedure including electron microscopy of small intestine biopsies. However, new simple staining methods using Uvitex 2B or modified trichrome stain for feces and other body fluids have facilitated clinical diagnosis as well as drug evaluation and epidemiological studies. The application of monoclonal antibodies and molecular techniques such as the polymerase chain reaction have further improved microsporidial diagnosis. Treatment of Entero. bieneusi has, until now, been unsuccessful whereas albendazole has proved to be an effective treatment for Encephalitozoon species infection. Identification of effective treatment for Entero. bieneusi infections and further study of the pathogenicity of these microsporidial infections in immunocompetent hosts are important future challenges.
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PMID:Human microsporidiosis: Clinical, diagnostic and therapeutic aspects of an increasing infection. 1186 34

We report what is, to our knowledge, the first study in which microsporidial infection was detected in elderly human immunodeficiency virus (HIV)--negative patients. Of the 60 elderly patients studied, 47 had diarrhea. Intestinal microsporidiosis due to Enterocytozoon bieneusi was diagnosed in 8 patients (17.02%) by use of Weber's chromotrope-based stain and polymerase chain reaction with species-specific primers. The mean age of these 8 patients was 75 years; 7 had chronic diarrhea and 1 had nonchronic diarrhea. Six of the patients with chronic diarrhea had no other pathogens isolated. In our opinion, elderly patients, because of their special immunological characteristics, should be considered a group at risk for the acquisition of intestinal microsporidiosis.
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PMID:Intestinal microsporidiosis due to Enterocytozoon bieneusi in elderly human immunodeficiency virus--negative patients from Vigo, Spain. 1188 Sep 56

Disseminated microsporidiosis is diagnosed uncommonly in patients not infected with human immunodeficiency virus (HIV). We present a case of disseminated microsporidiosis in a renal transplant recipient who was seronegative for HIV. Chromotrope-based stains were positive for microsporidia in urine, stools, sputum, and conjunctival scrapings. Electron microscopy, immunofluorescence, polymerase chain reaction, and cultures of renal tissue identified the organism as Encephalitozoon cuniculi. The patient was treated with oral albendazole and topical fumagillin with clinical improvement. In addition, she underwent a transplant nephrectomy and immunosuppressive therapy was withdrawn. Follow-up samples were negative for microsporidia. However, the patient developed central nervous system manifestations and died. An autopsy brain tissue specimen demonstrated E. cuniculi by immunofluorescent staining. Disseminated microsporidiosis must be considered in the differential diagnosis of multiorgan involvement in renal allograft recipients.
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PMID:Disseminated microsporidiosis in a renal transplant recipient. 1222 Feb 48

Enterocytozoon bieneusi is an agent of intestinal microsporidiosis leading to malabsorption syndrome and diarrhea in AIDS patients. Respiratory tract microsporidiosis due to Encephalitozoon spp. has been reported. To date, however, only two cases of pulmonary involvement of E. bieneusi have been documented for patients with intestinal microsporidiosis. We report here another pulmonary localization of E. bieneusi in a human immunodeficiency virus-infected patient. Clinical features of these three cases are reviewed. E. bieneusi can colonize the respiratory tract but could be considered a simple carriage associated with an intestinal infection.
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PMID:Pulmonary localization of Enterocytozoon bieneusi in an AIDS patient: case report and review. 1245 1

Microsporidia are obligate intracellular parasites that cause opportunistic infections in AIDS and other immunocompromised patients. Eight simian immunodeficiency virus (SIV)-infected rhesus macaque monkeys (Macaca mulatta) were inoculated orally with Enterocytozoon bieneusi spores isolated from intestinal lavage fluid of an AIDS patient (genotype D) to study the natural history of this infection. Four monkeys were already naturally infected with E. bieneusi (also genotype D), and were included to determine if a second inoculum affected the course of illness. Spore shedding was detected in feces of all eight monkeys within the first week of experimental infection. Five monkeys died within 3.5 months of experimental E. bieneusi inoculation. Three of these five monkeys began the study with CD4+CD29+ T cell levels well below 20% of total T lymphocytes. Deaths were due to a variety of AIDS-related manifestations. Microsporidia did not appear to directly contribute to mortality but may have contributed to morbidity. At necropsy, microsporidia were found in bile and tissue sections of the gallbladder but not in the gut, kidneys, or liver. The percent CD4+CD29+ levels of the last three monkeys remained near the level observed at the time of inoculation. These monkeys lived more than 2 years after the end of the study and continued to shed spores. This study corroborates previous reports that E. bieneusi can be reliably transmitted to SIV-infected rhesus monkeys but indicates that the use of SIV-infected monkeys for the study of microsporidiosis is complicated by the confounding effect of other opportunistic or AIDS-related infections.
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PMID:Natural and experimental infection of immunocompromised rhesus macaques (Macaca mulatta) with the microsporidian Enterocytozoon bieneusi genotype D. 1534 31

We studied microsporidiosis in human immunodeficiency virus-positive patients in 2 Lima hospitals. Of 2652 patients, 66% were male, 6% received antiretroviral therapy (ART), and the median CD4 lymphocyte count was 131 cells/microL. Sixty-seven patients (3%) had microsporidiosis; stool specimens from 56 were identified as having Enterocytozoon bieneusi of 10 different genotypes. The 2 most common genotypes, Peru-1 and Peru-2, were not associated with significant increases in chronic diarrhea; other genotypes were associated with a 4-fold increased risk. Risk factors for E. bieneusi infection segregated by genotype: contact with duck or chicken droppings and lack of running water, flush toilet, or garbage collection with genotype Peru-1 and watermelon consumption with other genotypes. Shortened survival was associated with low CD4 lymphocyte count (P<.0001), no ART (P<.0001), and cryptosporidiosis (P=.004) but not with microsporidiosis (P=.48). Our data suggest the possibility of zoonotic E. bieneusi transmission and an association with poor sanitary conditions.
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PMID:The epidemiology of intestinal microsporidiosis in patients with HIV/AIDS in Lima, Peru. 1583 92

Immune reconstitution might not be the only factor contributing to the low prevalence of microsporidiosis in human immunodeficiency virus (HIV)-infected patients treated with protease inhibitors, as these drugs may exert a direct inhibitory effect against fungi and protozoa. In this study, we developed a cell culture-quantitative PCR assay to quantify Encephalitozoon intestinalis growth in U-373-MG human glioblastoma cells and used this assay to evaluate the activities of six HIV aspartyl protease inhibitors against E. intestinalis. A real-time quantitative PCR assay targeted the E. intestinalis small-subunit rRNA gene. HIV aspartyl protease inhibitors were tested over serial concentrations ranging from 0.2 to 10 mg/liter, with albendazole used as a control. Ritonavir, lopinavir, and saquinavir were able to inhibit E. intestinalis growth, with 50% inhibitory concentrations of 1.5, 2.2, and 4.6 mg/liter, respectively, whereas amprenavir, indinavir, and nelfinavir had no inhibitory effect. Pepstatin A, a reference aspartyl protease inhibitor, could also inhibit E. intestinalis growth, suggesting that HIV protease inhibitors may act through the inhibition of an E. intestinalis-encoded aspartyl protease. These results showed that some HIV protease inhibitors can inhibit E. intestinalis growth at concentrations that are achievable in vivo and that the real-time quantitative PCR assay that we used is a valuable tool for the in vitro assessment of the activities of drugs against E. intestinalis.
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PMID:Inhibitory activity of human immunodeficiency virus aspartyl protease inhibitors against Encephalitozoon intestinalis evaluated by cell culture-quantitative PCR assay. 1591 34


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