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)

Differences between the two varieties of Cryptococcus neoformans with regard to geographic distribution, epidemiology, and even pathogenicity have been described. None between C. neoformans variety neoformans serotypes A and D have been reported. We reviewed 452 cases of cryptococcosis diagnosed in France, where serotype D is responsible for 21% of the infections. Univariate analysis showed that the frequency of serotype D infections was significantly higher among patients > 60 years of age, those born in Europe, those receiving corticosteroid therapy, and those who had skin lesions. In the multivariate analysis, the risk of serotype D infection was significantly higher for patients with skin lesions, those receiving corticosteroid therapy, and those living in certain regions in France. It was significantly lower for patients with meningitis those coming from Africa, and females. Among the 350 human immunodeficiency virus-infected patients, the risk was significantly higher for those > 60 years old, those who were intravenous drug abusers, and those with skin lesions. The risk was significantly lower for patients from Africa and in cases of meningitis. These results suggest that individual and environmental factors can be associated with the serotype of the infecting strain of C. neoformans.
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PMID:Individual and environmental factors associated with infection due to Cryptococcus neoformans serotype D. French Cryptococcosis Study Group. 914 60

Seventeen asymptomatic individuals positive for human immunodeficiency virus type 1 (HIV-1) and 16 patients with acquired immunodeficiency syndrome (AIDS), all with polymerase chain reaction evidence of HIV-1 DNA, were selected for quantitative analysis to correlate the levels of HIV-1 DNA in brain tissue with the stage of infection. The AIDS patients either were clinically asymptomatic or presented various abnormalities. Neuropathological lesions were assessed by morphological and immunohistochemical methods. To determine the level of HIV-1 DNA, semiquantitative nested polymerase chain reaction was applied using a digoxigenin-labeled primer and chemiluminescence. Serial dilutions of standard HIV DNA were run in parallel with brain DNA samples. Among the 16 AIDS brains studied, 9 showed changes characteristic of HIV encephalitis/leukoencephalopathy while 1 showed focal pontine leukoencephalopathy and 6 showed no obvious neuropathological lesions. Abnormalities in pre-AIDS individuals included meningitis, microgliosis, and astrogliosis. Copy numbers of HIV-1 DNA in the brains of AIDS patients were higher than those in asymptomatic individuals (median, 135 vs 45 copies/150,000 cells). However, there was some degree of overlapping between the two groups, with some AIDS patients showing low figures while 3 asymptomatic individuals had high copy numbers. This suggests that the use of HIV-1 DNA load in the central nervous system as an indicator of progression of the disease should be restricted to large series and not single patients.
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PMID:HIV-1 DNA in brains in AIDS and pre-AIDS: correlation with the stage of disease. 887 81

The FIV (feline immunodeficiency virus) induces in cats brain changes presenting similarities with those observed in human immunodeficiency virus infection. This FIV model was used to study the relationship between viral load in brain, in lymphoid organs and central nervous system (CNS) changes during the early and late stages of infection. Early brain changes were analyzed in animals experimentally infected with two different FIV isolates and sacrificed at 7 and 15 days, 1, 2, 6, and 12 months post inoculation (p.i.). Late CNS abnormalities were analyzed in naturally FIV-infected cats referred to the Veterinary School of Nantes. For each animal, one cerebral hemisphere was fixed and examined using routine techniques. The characterization of FIV replicating cells by in situ hybridization was performed on the other half frozen hemisphere on sections performed in the anterior and the median regions of the brain. During the early stages of infection, moderate gliosis with glial nodules and sometimes white matter pallor and meningitis were associated with few infected cells scattered in the brain. Infection was an early event as infected cells could be detected in brain at 7 p.i. For each cat, these findings were found identical in the two analyzed areas. During the late stages, brain lesions and the number of virus replicating cells increased especially in animals with perivascular infiltrates. The multinucleated giant cells encephalitis was never observed and the number of FIV replicating cells scattered in the whole brain was always low. This discrepancy between the number of replicating cells and the brain lesions, corroborates the hypotheses suggesting that brain injuries may be mediated via diffusive factors and amplification processes through cytokine cascades and cell activations.
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PMID:Virus load and neuropathology in the FIV model. 897 19

Platelet-activating factor (PAF) is a phospholipid synthesized in a variety of cells throughout the body. Platelet-activating factor has been identified in the CNS and has a number of diverse physiological and pathological functions. It has been shown to be a modulator of many CNS processes, ranging from long-term potentiation (LTP) to neuronal differentiation. Excessive levels of PAF appear to play an important role in neuronal cell injury, such as that resulting from ischaemia, inflammation, human immunodeficiency syndrome (HIV) and meningitis. The beneficial effects of PAF receptor antagonists are many and give rise to possible therapeutic strategies for neurotrauma.
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PMID:Platelet-activating factor in the CNS. 901 28

Cryptococcus neoformans causes meningitis in 6 to 8% of individuals with AIDS. Recently, immunotherapeutic modalities including antibody therapy have been proposed for the treatment of cryptococcal meningitis in AIDS patients. This is a rational approach because existing antifungal agents fail to eradicate the infection in the setting of profound immunosuppression. Both murine and human antibodies elicited by the investigational cryptococcal capsular polysaccharide vaccine glucuronoxylomannan-tetanus toxoid (GXM-TT) have been shown to be biologically functional in different model systems. The human immunoglobulin M (lambda) GXM monoclonal antibody (MAb) 2E9 expresses idiotypes that are also found in naturally occurring anti-GXM antibodies and opsonic GXM-TT sera. However, the specificity of human anti-GXM antibodies and their possible role in protection against cryptococcosis are not known. In an effort to discover epitopes that are recognized by human anti-GXM antibodies, we screened a random decapeptide phage display library with the human anti-GXM MAb 2E9. An enzyme-linked immunosorbent assay (ELISA)-based screening method led to the selection of phages with peptide inserts that bound 2E9 and inhibited 2E9-GXM binding. Analysis of the amino acid sequences of these phages revealed an increased frequency of combinations of QTGLD residues. Inhibition ELISAs demonstrated that phages with QTG/TL/D motifs inhibited 2E9-GXM binding better than phages with different motifs. A peptide synthesized from one of the inhibitory phages, peptide 13 (GMDGT QLDRW), inhibited GXM binding to solid-phase 2E9 and 2E9 binding to solid-phase GXM. Peptide 13 also inhibited the GXM binding of GXM-TT immune sera and naturally occurring serum antibodies from human immunodeficiency virus (HIV)-negative, but not HIV-positive, individuals. Taken together, our data indicate that the peptide epitopes selected by 2E9 mimic GXM epitopes and that peptide 13 may be a mimotope of a GXM epitope that is recognized by human anti-GXM antibodies.
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PMID:Peptide epitopes recognized by a human anti-cryptococcal glucuronoxylomannan antibody. 911 46

Streptococcus pneumoniae has become a leading cause of bacteremia, pneumonia, meningitis, and otitis media in the United States. Persons at increased risk include young children, immunocompromised persons, and the elderly. Until 1987, S. pneumoniae was uniformly susceptible to penicillin; since then, in the United States, there has been increased identification of penicillin-nonsusceptible S. pneumoniae (PNSP) (defined as minimum inhibitory concentration [MIC] to penicillin > or = 0.1 microgram/mL), especially penicillin-resistant S. pneumoniae (PRSP) (defined as MIC to penicillin > or = 2.0 micrograms/mL). In addition, PNSP is becoming less susceptible to other antimicrobial drugs, including tetracycline, erythromycin, extended-spectrum cephalosporins, and chloramphenicol; some are susceptible only to vancomycin. Because of the emergence of PNSP, in December 1994, the New York City Department of Health (NYCDOH) amended the New York City health code to require reporting of PNSP to monitor the local prevalence of resistance to penicillin. This report summarizes surveillance findings from NYCDOH's data for 1995, which indicate that the highest case rates were among children aged < 4 years and that, among adults aged 20-44 years with PNSP infections, 71.4% also were infected with human immunodeficiency virus (HIV).
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PMID:Surveillance for penicillin-nonsusceptible Streptococcus pneumoniae--New York City, 1995. 913 81

The purpose of this study was to describe the frequency and duration of clinical features at the time of acute human immunodeficiency virus type 1 (HIV-1) disease in 218 patients with documented symptomatic primary HIV-1 infection. The mean duration of acute HIV-1 disease was 25.1 days (median, 20.0 days) and did not differ by gender, age, and risk factor. The frequency and mean duration of clinical features occurring in >50% of patients were as follows: fever, 77.1% and 16.9 days; lethargy, 65.6% and 23.7 days; cutaneous rash, 56.4% and 15 days; myalgia, 54.6% and 17.7 days; and headache, 50.9% and 25.8 days. Only 15.6% of patients presented with a typical mononucleosis-like illness (MLI) defined as fever, pharyngitis or sore throat, and cervical adenopathy, and 10% had no features of an MLI. A meningitis-like syndrome occurred in 20 patients (9.2%). Acute HIV-1 disease is more diverse than previously reported, and the absence of fever or other MLI features does not rule out acute HIV-1 disease.
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PMID:Acute human immunodeficiency virus type 1 disease as a mononucleosis-like illness: is the diagnosis too restrictive? 914 2

Six men (mean age: 36.3 +/- 29 years) infected with the human immunodeficiency virus (HIV), four Japanese and two from Myammar, were admitted to our hospital for treatment of tuberculosis. In five, HIV positivity on serologic testing was first found when tuberculosis was diagnosed. The mean CD4 cell count was 37.3 +/- 29.6/microliters. Results of tuberculin skin tests were negative in 5 patients. One patient had pulmonary tuberculosis and 5 had miliary tuberculosis. Hilar and mediastinal lymphadenopathy was found on chest X-ray films in 4 patients and superficial lymphadenopathy was found in all patients. All patients had positive mycobacterial cultures of sputum and 2 patients had positive tests for acid-fast bacilli on smears of lymph-node aspirates. In one patient with tuberculosis meningitis, a culture of cerebrospinal fluid for acid-fast bacilli was positive. Epithelioid cell granulomas were found in samples of lung, liver, and bone marrow from 4 patients. Mycobacterium tuberculosis was isolated from all patients, and was not resistant to isoniazid, rifampicin, ethambutol, or streptomycin. Therefore all patients responded well to treatment of tuberculosis.
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PMID:[Tuberculosis in patients with human immunodeficiency virus infection]. 916 41

Tuberculosis in the United States has become primarily an inner-city disease. We examined the epidemiology of culture-confirmed tuberculous meningitis among patients cared for at an urban public hospital in Atlanta. During an 11.5-year period (January 1984-June 1995) cerebrospinal fluid cultures for Mycobacterium tuberculosis were positive in 34 patients, accounting for 1.5% of all culture-confirmed tuberculosis cases. All patients were born in the United States, 31 (91%) were black, 16 (47%) of 34 were human immunodeficiency virus (HIV) seropositive, 9 (26.5%) were HIV seronegative, and 9 (26.5%) had an unknown HIV serostatus. No significant differences were seen in clinical presentation, cerebrospinal fluid, or other laboratory data between HIV seropositive and HIV seronegative/ unknown groups, except for a lower serum white blood cell count among HIV seropositive patients. Mortality was striking; 14 (41.2%) died because of tuberculous meningitis despite appropriate therapy initiated a mean of 3 days after admission. Six survivors had permanent neurologic sequelae. Univariate analysis of outcome was not statistically associated with any measured demographic, laboratory value, stage at presentation, treatment regimen, or HIV serostatus. Multivariate analysis of outcome using 13 independent variables also demonstrated no significant association between these variables and outcome, although a trend was seen for increased mortality for white people (P = 0.09) and increasing age (P = 0.09). Tuberculous meningitis among inner-city residents remains a devastating disease associated with high morbidity and mortality that has changed little during the past 4 decades. HIV infection does not change markedly the clinical presentation or the response to therapy.
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PMID:Tuberculous meningitis at a large inner-city medical center. 918 45

A 2.5-year-old boy with disseminated tuberculosis, highly suspected to be disseminated BCG infection which occurred against a background of secondary immunodeficiency due to measles and malnutrition, is presented. The initial diagnosis was post-measles bronchopneumonia, meningitis and marasmus. The final diagnosis was arrived at only because of a high clinical index of suspicion of tuberculosis which is needed in all communities with a high prevalence of tuberculosis. The absence of AIDS and the extreme rarity of ulceration of a previously healed BCG scar are noted.
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PMID:Ulceration of a previously healed BCG scar in suspected disseminated BCG infection. 923 Sep 76


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