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)

Free-living amebas of the genera Acanthamoeba and Naegleria are allied in basic cell biology, ecology, and human disease-producing potential. However, several enigmas surrounding these amebas need further intellectual and scientific scrutiny. For instance, a clearer differentiation is needed of factors delineating pathogenic species--those most frequently associated with human infections--from nonpathogenic species. Further, have the pathogenic species bridged the gap in a step-wise fashion between their habitat and the human host to express their disease-producing potential? Second, what attributes of amebas account for the spectrum of disease caused by Acanthamoeba and Naegleria? In the brain, Naegleria is highly destructive of tissue in the course of a rapidly evolving, hemorrhagic primary meningoencephalitis in normal individuals. Central nervous system invasion by Acanthamoeba, however, occurs only in compromised hosts, and is a more slowly evolving subacute to chronic encephalitis. Further, the epidemiology of the infections are disparate. Naegleria is acquired from exposure to contaminated fresh water; this epidemiologic link is absent in Acanthamoeba meningoencephalitis. Naegleria invades the central nervous system via the olfactory nerve; Acanthamoeba is deposited in the central nervous system via hematogenous spread from a pulmonary or cutaneous focus. Additionally, Naegleria is apparently restricted to the brain; Acanthamoeba is not so bridled, and invades more sites in the human body. Finally, Acanthamoeba are beginning to appear opportunistically more frequently in patients infected with the human immunodeficiency virus. To avoid the same lack of effective therapeutics we still face in treating cryptosporidium infections in these patients, more emphasis must be placed on clinical trials dealing with the management of Acanthamoeba infections in patients with AIDS.
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PMID:Free-living amebas of the genera Acanthamoeba and Naegleria: an overview and basic microbiologic correlates. 823 68

We report the case of a 52-year-old male heterosexual patient with acquired immunodeficiency syndrome (AIDS) and reactivation of Chagas' disease manifested by meningoencephalitis and myocarditis, diagnosed post-mortem. Unexplained reactivation of Chagas' disease should be included among the diagnostic criteria of AIDS in human immunodeficiency virus positive patients. On the other hand, AIDS should be considered in the differential diagnosis of patients with unexplained reactivation of Chagas' disease.
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PMID:Trypanosoma cruzi meningoencephalitis and myocarditis in a patient with acquired immunodeficiency syndrome. 828 7

Four weeks after an attack of pneumonia of unknown aetiology a 40-year-old woman was hospitalized because of a nonpurulent, predominantly basal meningoencephalitis and infratentorial abscesses. She had dysarthria, mild right-sided motor hemiparesis and central paresis affecting the 7th cranial nerve. An area of fluctuating resistance, about 3 cm in diameter, was noticed over the left thigh. Serology indicated inflammatory disease, but there was no immunodeficiency. The CSF showed lymphocytic pleocytosis with mild protein increase but no evidence of infective agent. As tubercular meningitis was suspected she was treated with rifampicin (300 mg i.v. twice daily), isoniazid (300 mg i.v. once daily), streptomycin (800 mg i.m. once daily), cefotaxime (2.0 g i.v. three times daily), fluconazole (200 mg i.v. once daily) and dexamethasone (16-8-8 mg i.v.). She suddenly died two days after admission, probably as the result of central regulatory failure. Generalized nocardiosis involving lung, subcutaneous tissue and brain was revealed at autopsy. Although nocardiosis occurs predominantly in patients under immunosuppression, this infection should be considered in the differential diagnosis of treatment-resistant pneumonia and meningoencephalitis without obvious predisposition.
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PMID:[Generalized nocardiosis with meningoencephalitis in a nonimmunosuppressed female patient]. 837 98

Mycotic complications were registered in 21 out of 37 HIV-infected subjects. Oropharyngeal candidiasis was most common. It occurred prior to or concurrently with esophageal and skin candidiasis, fungemia, meningoencephalitis and disseminated lesions. With immunodeficiency progression, the prevalence and severity of mycosis go up. The causing fungi vary in great range: Candida albicans, Candida krusei. Candida tropicalis, Candida pseudotropicalis, Candida parapsilosis. Cryptococcus neoformans, Rhodotorula rubra, Penicillium chrysogenum.
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PMID:[The clinical picture of mycotic complications in HIV-infected patients]. 857 7

In this autopsy series of cryptococcal meningoencephalitis (CME), the authors analyzed neuropathologic lesions in 13 human immunodeficiency virus (HIV) and 14 non-HIV-related cases. Most non-HIV patients did not have immunosuppressive predisposing illness. Analysis of pathological findings revealed significant differences in the inflammatory response to CME in patients with and without HIV infection. None of the acquired immunodeficiency syndrome (AIDS) patients had granulomatous inflammation, whereas most non-HIV-associated cases had granulomas, supporting a role for cell-mediated immunity in CME. Lymphocytic infiltrate in both groups consisted of T cells (CD45RO+). In some non-HIV-associated cases, CME was undiagnosed and untreated. In most HIV-associated cases, CME had an encephalitic component, resulting in grossly or microscopically visible accumulations of fungi within the brain parenchyma, whereas in non-HIV-associated cases, CME was often confined to the subarachnoid space and large perivascular spaces (Virchow-Robin spaces). In non-HIV-associated cases, yeast forms were fewer and showed a more limited distribution. In contrast, many extracellular fungi were present in many cases of HIV-associated CME. The principal reactive cell in CME in AIDS was brain macrophages and microglia, especially those in the perivascular and juxtavascular locations. Reactive astrocytes were limited to large destructive lesions and subpial regions. In several patients with HIV-associated CME, large parenchymal cryptococcomas contained Crytococcus neoformans (CN) with cell wall pigmentation, suggestive of melanin. The authors suggest that in AIDS patients altered immune functions allow CN to accumulate within the brain, predominantly extracellularly, and that deficient macrophage/microglial effector function may be responsible for the altered pathology. In addition, coexisting CNS processes in HIV-associated CME may contribute to the altered pathology. The authors conclude that cryptococcal meningitis is not a disease limited to the cerebrospinal fluid (CSF) space but affects the brain more significantly than suspected. Therapeutic strategies that enhance the effector function of glial cells at the CNS-CSF barrier may be useful for improving the response to therapy.
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PMID:Pathology of cryptococcal meningoencephalitis: analysis of 27 patients with pathogenetic implications. 876 20

Amplification of viral nucleic acids from the cerebrospinal fluid (CSF) has considerably improved the diagnosis of several acute, subacute and chronic viral infections of the nervous system. In herpes simplex virus (HSV) encephalitis (HSE) the polymerase chain reaction (PCR) has become the method of choice for the rapid, non invasive diagnosis. Other herpes virus associated diseases which can now be reliably diagnosed are encephalitis, ventriculoencephalitis, polymyeloradiculitis, myelitis and an inflammatory polyradiculoneuropathy caused by cytomegalovirus (CMV), HSV, varicella-zoster virus (VZV) or Epstein-Barr virus (EBV), EBV associated primary B-cell-lymphoma of the brain, acute aseptic meningitis in young adults allied with VZV, and meningoencephalitis with recurrent seizures due to human herpes virus type 6 (HHV-6). In AIDS patients, PCR has helped to differentiate lesions either due to the human immunodeficiency virus (HIV) itself or to opportunistic infections such as progressive multifocal leukoencephalopathy (PML) caused by JC virus (JCV) or CMV related complications. HIV can be detected early in the course of infection in the CSF and the amount of proviral DNA in CSF cells seems to be correlated with the severity and/or progression of neurological signs and symptoms. Acute epidemic aseptic meningitis caused by enterovirus infections can now be reliably diagnosed and typed by reverse transcriptase PCR (RT-PCR). Meningitis cases caused by vaccination with the Jeryl Lynn and Urabe vaccine strain of mumps virus have been identified using RT-PCR and sequencing of the amplified products (amplicon).
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PMID:Clinical implications of nucleic acid amplification methods for the diagnosis of viral infections of the nervous system. 879 10

An infectious molecular clone of simian immunodeficiency virus SIVsm was derived from a biological isolate obtained late in disease from an immunodeficient rhesus macaque (E543) with SIV-induced encephalitis. The molecularly cloned virus, SIVsmE543-3, replicated well in macaque peripheral blood mononuclear cells and monocyte-derived macrophages and resisted neutralization by heterologous sera which broadly neutralized genetically diverse SIV variants in vitro. SIVsmE543-3 was infectious and induced AIDS when inoculated intravenously into pig-tailed macaques (Macaca nemestrina). Two of four infected macaques developed no measurable SIV-specific antibody and succumbed to a wasting syndrome and SIV-induced meningoencephalitis by 14 and 33 weeks postinfection. The other two macaques developed antibodies reactive in Western blot and virus neutralization assays. One macaque was sacrificed at 1 year postinoculation, and the survivor has evidence of immunodeficiency, characterized by persistently low CD4 lymphocyte subsets in the peripheral blood. Plasma samples from these latter animals neutralized SIVsmE543-3 but with much lower efficiency than neutralization of other related SIV strains, confirming the difficulty by which this molecularly cloned virus is neutralized in vitro. SIVsmE543-3 will provide a valuable reagent for studying SIV-induced encephalitis, mapping determinants of neutralization, and determining the in vivo significance of resistance to neutralization in vitro.
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PMID:A molecularly cloned, pathogenic, neutralization-resistant simian immunodeficiency virus, SIVsmE543-3. 899 88

Chimeric simian-human immunodeficiency viruses (SHIVs) carrying envelope glycoproteins derived from a T cell-macrophage dual-tropic primary isolate (human immunodeficiency virus type 1 [HIV-1] strain DH12) were constructed. When inoculated into macaque monkeys, SHIV(MD14) carrying simian immunodeficiency virus-derived nef established significantly higher virus loads than did SHIV(MD1), which contains the HIV-1 nef gene. Three patterns of CD4 cell depletion were observed in infected monkeys: exponential and irreversible loss to undetectable levels within 10 weeks of infection; marked reduction during acute infection followed by partial recovery and stabilization (lasting from 10 weeks to > 1 year), with a later decline to undetectable levels in some animals; and a transient loss during acute infection. The induced immunodeficiency was accompanied by CD4 cell counts of < 50 cells/microL and was associated with Pneumocystis carinii pneumonia, cytomegalovirus meningoencephalitis, lymphoid depletion, and thymic atrophy.
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PMID:Infection and pathogenicity of chimeric simian-human immunodeficiency viruses in macaques: determinants of high virus loads and CD4 cell killing. 923 1

Due to the worldwide AIDS pandemic, HIV-1 has become the major factor for central nervous system (CNS) diseases. Two major disorders of the CNS caused by HIV-1 have been described, a meningoencephalitis which occurs in 30-50% of patients early after infection and the AIDS dementia complex (ADC, also known as HIV-associated dementia) which is characterized by a predominantly subcortical dementia. The pathophysiology of these clinical syndromes still remains an enigma. However, since monocytes/macrophages may represent the major place of virus replication in the CNS, a hematogenous invasion of HIV-1 into the brain may be crucial to the neuropathogenesis of ADC. One of the most valuable animal models for the study of neuro-AIDS is the infection of macaque monkeys with the simian immunodeficiency virus (SIV). In about 50% of infected rhesus monkeys with an AIDS-like disease, neuropathological lesions similar to ADC in men have been observed. This animal model contributes to our understanding of the mechanisms of viral neuroinvasion early after infection and in the development of neurological disease. In this review we will summarize the state of the art and will focus on further questions concerning the neuropathogenesis of HIV/SIV.
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PMID:Infection of macaque monkeys with simian immunodeficiency virus: an animal model for neuro-AIDS. 945 Feb 28

In this short review, the Author evaluates the most important diagnostic problems about tuberculous meningoencephalitis. Any inadequate therapy can alternate the clinical picture and the results of the cerebrospinal fluid examination, and the clinical evaluation may become very difficult. The neuroradiological findings (CT and MRI), even when correlated to the typical neuropathological features of the disease, could be very sensitive but not specific. An accurate evaluation of the clinical context and, above all, of the clinical history, is the best way to avoid a tardive diagnosis and inappropriate therapies, and to choose which diagnostic procedures must be performed. In the latest years, the immunodeficiency status related to HIV infection, and the mobility of many persons from geographic areas endemic for TBC stressed the importance of this diagnosis. The extreme variability of the clinical picture is discussed, and the author describes the common manifestations as well as the rare syndromes associated with this disorder. The review indicates also the diseases with which the neurologist must challenge for a differential diagnosis. Some practical suggestions indicate how to minimize a diagnostic and therapeutic delay, for a disorder that in many cases is still lethal or leading to serious neurological complications or sequelae.
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PMID:[Clinical evaluation in the early diagnosis of tuberculous meningoencephalitis]. 952 6


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