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)

Three hundred eighty-six isolates of Propionibacterium sp. were recovered from 2,003 specimens studied for the identification of anaerobic bacteria in children during a 15-year period. Three hundred forty-three (89%) of these were Propionibacterium acnes. A total of 50 (13%) Propionibacterium isolates identified from 45 patients were considered to cause infection. Clinically significant infections caused by Propionibacterium sp. were associated with bacteremia in 10 children; ear infection in eight; abscesses in seven; adenitis and central nervous system infection in five each; burns in four; wounds in three; tumors and bone in two each; and cysts, eye, sinus, and mastoid in one each. Predisposing or underlying conditions were present in 33 children (73%). These included the presence of a foreign body (17), immunodeficiency (six), malignancy (five), diabetes (five), previous surgery (four), and steroid therapy (two). Antimicrobial therapy was given to 41 (91%) children. Surgical drainage was concomitantly performed in 22 (49%). Four patients died. This study highlights the importance of Propionibacterium sp. as an unusual, but potentially important, pathogen in children.
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PMID:Infection caused by Propionibacterium in children. 795 90

Experimental intravenous challenge of 8-week-old kittens with the feline immunodeficiency virus Maryland isolate (FIV-MD) was investigated for its ability to infect the central nervous system (CNS) and induce neurologic abnormalities. Six cats were inoculated with 1,000 TCID50 units of FIV-MD isolate, with six age-matched cats serving as uninfected controls. Clinical and immunological evaluation documented that challenged cats developed immunodeficiency and growth delay. Neurologic examination revealed an abnormal stereotypic motor behavior consisting of repetitive, compulsive roaming that developed as early as 4 weeks postinfection (PI) and persisted throughout the 16-month study in three cats. Serial neuroelectrodiagnostic evaluation revealed persistent abnormal electroencephalographic recordings in three infected cats. Serial evoked potential (EP) recordings at 3, 8, and 12 months PI demonstrated significantly prolonged interpeak latencies III-V at 3 months PI and I-III at 12 months PI for brainstem EP recordings. Alterations of visual EPs were detected only at the 3-month time period. Retinocortical time, however, was significantly different from that in control cats at 3 and 12 months PI. Magnetic resonance imaging evaluation of FIV-MD-infected cats at 12 months PI revealed cortical atrophy, mild ventricular enlargement, and discrete white matter lesions. At 16 months PI, however, histopathological examination of brain tissue indicated only mild lesions limited to satellitosis and perivascular lymphocytic infiltrates. Virus was detected in the CNS by reverse transcriptase, immunofluorescence, and antigen capture. Evaluation of the cerebrospinal fluid revealed intrathecal anti-FIV-MD antibody despite lack of detectable viremia in five challenged cats. Collectively, these findings demonstrate the induction of virus-associated neurologic disease following parenteral FIV challenge in conjunction with an immunodeficiency state. The nature of the nervous system infection is analogous to HIV-1 pediatric encephalopathy.
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PMID:AIDS-associated encephalopathy with experimental feline immunodeficiency virus infection. 838 49

Entry of human immunodeficiency virus type 1 (HIV-1) into target cells requires both CD4 (ref. 1, 2) and one of a growing number of G-protein-coupled seven-transmembrane receptors. Viruses predominantly use one, or occasionally both, of the major co-receptors CCR5 or CXCR4, although other receptors, including CCR2B and CCR3, function as minor co-receptors. CCR3 appears critical in central nervous system infection. A 32-base pair inactivating deletion in CCR5 (delta 32) common to Northern European populations has been associated with reduced, but not absolute, HIV-1 transmission risk and delayed disease progression. A more commonly distributed transition causing a valine to isoleucine switch in transmembrane domain I of CCR2B (64I) with unknown functional consequences was recently shown to delay disease progression but not reduce infection risk. Although we confirm the lack of association of CCR2B 64I with transmission, we cannot confirm the association with delayed progression. Although subjects with CCR5 delta 32 defects had significantly reduced median viral load at study entry, providing a plausible explanation for the association with delayed progression, this association was not seen with CCR2B 64I. Further studies are needed to define the role of CCR2B64I in HIV pathogenesis.
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PMID:The role of CCR5 and CCR2 polymorphisms in HIV-1 transmission and disease progression. 958 7

Neurologic abnormalities involving the central and peripheral nervous system are common in patients infected with the human immunodeficiency virus (HIV). Evidence of central nervous system infection (cerebrospinal fluid abnormalities) occurs early; however, evidence of central and peripheral nervous system dysfunction usually occurs at later stages. Neurologic manifestations may be due to chronic immunosuppression, direct neurotropic effect of HIV, or medication effects. It is important to recognize that brain and spine imaging studies are highly sensitive in detecting abnormal pathologic processes, but these studies have low specificity for establishing a specific pathologic diagnosis.
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PMID:Neurologic abnormalities in human immunodeficiency virus infection. 1128 12

Intravenous infection of cats with feline immunodeficiency virus was used as a model system to study activation of virus replication in brain-resident microglial cells in vitro. Virus release by ramified microglial cells isolated from subclinically infected animals was detectable in cell-free tissue culture supernatant only by reverse transcription and nested PCR of gag-specific RNA sequences and not by virion-associated reverse transcriptase activity. In contrast, cocultivation of in vivo-infected microglial cells with mitogen-activated peripheral blood mononuclear cells (PBMC) regularly allows detection of high virus yields in cell-free tissue culture fluid. Besides uptake and multiplication of microglia-derived virus in PBMC, release of virus from microglia is stimulated by cell contact with PBMC. The data suggest that T lymphocytes patrolling the central nervous system could reactivate the semilatent state of lentiviruses in microglial cells in the course of clinically silent central nervous system infection.
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PMID:In vitro activation of feline immunodeficiency virus in ramified microglial cells from asymptomatically infected cats. 1148 54

Since the advent of pandemic of the human immunodeficiency virus infection, the possible pathogens responsible for acute meningoencephalitis have broadened. Human immunodeficiency virus itself can cause acute meningoencephalitis, and the immunocompromise associated with human immunodeficiency virus infection predisposes the infected patients to acute meningoencephalitis caused by a variety of other infectious or non-infectious etiologies. Here reported are 2 cases of acute meningoencephalitis with history of blood transfusion and travel to southeast Asia; both are positive for screening tests of human immunodeficiency virus infection. One of the pathogen causing central nervous system infection, Mycobacterium tuberculosis, was identified by polymerase chain reaction; the other left undiagnosed. It is known that patients of human immunodeficiency virus infection or acquired immunodeficiency syndrome can present with acute central nervous system infection. The need for routine screening of human immunodeficiency virus antibody is currently under debate; nevertheless, the possibility of human immunodeficiency virus infection has to be kept in mind in patients with acute meningoencephalitis.
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PMID:Acute meningoencephalitis as initial presentation of human immunodeficiency virus infection: report of two cases. 1238 Jul 95

A retrospective analysis of 326 clinically diagnosed cases with meningitis over a period of five-and-a-half years was carried out to determine the prevalence of cryptococcal infection, its associated risk factors and therapeutic outcome. Fifty-four (16.6%) patients with cryptococcal meningitis were identified by smear examination, culture and/or cryptococcal antigen latex agglutination test. Records of 45 cryptococcal meningitis patients were available; 18 (40%) of them were apparently healthy immunocompetent individuals, 13 (28.9%) had human immunodeficiency virus (HIV) infection, 9 (20%) were renal transplant recipients, 4 (8.9%) were diabetic and 1 (2.2%) had systemic lupus erythematosus. Ten (22.2%) patients died and 11 (24.4%) patients (all HIV-positive) left against medical advice. The present study indicates that cryptococcal infection is associated with high mortality. Presenting symptoms being indistinguishable from other causes of central nervous system infection, all patients with a clinical diagnosis of meningitis, irrespective of their immune status should be investigated for cryptococcal infection.
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PMID:Cryptococcal infection in patients with clinically diagnosed meningitis in a tertiary care center. 1465 40

We aimed to evaluate the diagnostic value of lumbar puncture in excluding nosocomial meningitis as the cause of mental status changes in medical intensive care unit patients. We retrospectively reviewed the records of all patients admitted to the medical intensive care unit at our institution over a four-year period who had a lumbar puncture performed during their stay. Patients with central nervous system devices were excluded. During the study period 63 lumbar punctures were performed, 31 to exclude nosocomial meningitis. Of these 31 patients, 25 (80.6%) received antimicrobials during hospitalization before performance of lumbar puncture. In one patient with human immunodeficiency virus (HIV) infection, Gram stain demonstrated yeast; in the remainder, Gram stain was negative. Cultures were negative for pathogenic bacteria in all 30 of these patients (overall yield: 0%, 95% CI: 0-10.0%). Five patients (16.1%) had a cerebrospinal fluid leucocytosis (>10 leukocytes/mm3); of these, all had received prior antibiotics, two had positive cryptococcal antigen results, and three had central nervous system infection suspected clinically without an evident alternative diagnosis. In no non-HIV subject did lumbar puncture alter management. Lumbar puncture performed in the medical intensive care unit to exclude nosocomial meningitis as the cause of mental status changes has a low yield and rarely changes management. These findings should not be generalized to patients who have sustained head trauma, have undergone neurosurgical procedures, or may be immunosuppressed.
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PMID:The yield of lumbar puncture to exclude nosocomial meningitis as aetiology for mental status changes in the medical intensive care unit. 1649 44

A variety of autoantibodies have been identified with complex neurological disorders including limbic encephalitis. The underlying trigger for the immune-mediated process and the role of autoantibodies in the pathogenesis of limbic encephalitis remain to be clarified. Here, we report a 16-year-old female who was diagnosed with acute-onset non-neoplastic limbic encephalitis. The initial treatment with pulse doses of i.v. methylprednisolone improved the neurological symptoms. During the next 12 months, progressive decline was reported in her academic functioning and seizure control. Additional diagnostic evaluation revealed no evidence of malignancy or central nervous system infection but circulating anti-GAD antibodies were present in the serum and cerebrospinal fluid. Intravenous gammaglobulin infusion was initiated and continued monthly. Intravenous and oral steroids were added to the intravenous immunoglobulin treatment because of the worsening course and seizures, despite treatment with antiepileptic medications. Screening for quantitative immunoglobulins demonstrated hypogammaglobulinaemia with low immunoglobulin M and G in addition to low immunoglobulin A levels. There was a lack of protective pneumococcal antibody titers before and after immunization. Therefore, common variable immunodeficiency was suspected despite there being no history of recurrent infections. To our knowledge, this is the first report describing a possible link between immune-mediated limbic encephalitis and immune deficiency.
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PMID:Limbic encephalitis associated with anti-GAD antibody and common variable immune deficiency. 1953 23

Cryptococcus neoformans meningoencephalitis is the most common fungal central nervous system infection, in people affected by the human immunodeficiency virus. It is rare in inmunocompetent children and it is often fatal. It predominates in males at a ratio of 3 to 1. We describe the cases of two school children, one male and one female, with history of contact with pigeons (Columba livea), whose clinical symptoms were fever, headache, photophobia, diplopia, ataxia and meningeal signs, with unilateral involvement of cranial nerve VI. The diagnosis was established by the isolation of Cryptococcus neoformans in culture, staining with India ink and evidence of latex antigen agglutination in the cerebrospinal fluid. The determination of antibodies to human immunodeficiency virus and quantification of CD4, CD8 and T lymphocyte cells, were normal. In the first case, a chest X-ray showed a round mass, circumscribed in the bottom half of the left lung. A brain MRI revealed an image compatible with a nodular cryptococcoma in the parietal region. A pattern of intracranial hypertension was established, with papilledema and bilateral amaurosis, that evolved unsatisfactorily, with the subsequent death of the patient. Both were treated with amphotericin B (1 mg/Kg/day) or fluconazole (6 mg/Kg/day). The second case had a favorable evolution. The Crypotococcus neoformans is not a common fungus in inmunocompetent children. Early detection of the disease and appropriate treatment is essential to achieve a better prognosis ot the disease.
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PMID:[Cryptococcus neoformans meningoencephalitis in immunocompetent schoolchildren]. 1966 18


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