Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are quite a few pathogens which can cause pneumonia. Identifying the agent of infection simplifies therapy by allowing the appropriate treatment to be targeted with a minimum amount of toxic drugs. Empirical therapy is ideally reserved for settings in which the patient is not acutely ill, there is a high probability of a single, easily treated pathogen, and rapid diagnostic facilities are available if treatment fails. Empirical therapy, however, is often necessary in many AIDS-endemic regions where diagnostic tests are unavailable due to limited resources. In such circumstances, a treatment algorithm independent of extensive diagnostic testing and targeted against locally prevalent pathogens is called for. Malin and colleagues have reported finding Pneumocystis carinii pneumonia (PCP) among 33% of 64 patients in Zimbabwe observed with diffuse pneumonia unresponsive to penicillin. Untreated PCP is lethal. Further, despite three negative sputum smears for Mycobacterium tuberculosis, the organism was the most common pathogen ultimately identified, confirming previous reports and highlighting the importance of anti-TB therapy. The high incidence of PCP raises concerns that in certain parts of Africa treatment algorithms which do not consider PCP may need to be re-evaluated. Different patient selection criteria among studies with discordant results may partially explain the differences in the incidence of PCP in different parts of Africa. Otherwise, regional environmental differences, host genetic variation, and differences in the virulence of various strains of P. carinii may play a role. Data on the incidence of PCP in HIV-infected infants in Africa would provide insights into the role of P. carinii as a pathogen. The authors note that if the incidence of PCP is rising, even in selected areas, then prophylaxis in such areas with co-trimoxazole may be a cost-effective management approach which may also decrease the incidence of bacterial infections. Alternatively, early empirical therapy with co-trimoxazole at high doses may be an effective approach for treating both PCP and bacterial infections before the initiation of empirical anti-TB therapy.
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PMID:Pneumocystis carinii in Africa: an emerging pathogen? 747 17

A 76-year-old man with parkinsonism and dementia was reported. He developed resting tremor at age 69 followed by hypokinesia, rigidity and small step gait. L-dopa ameliorated his symptoms with no hallucinations for the initial 5 years. His mental level did not decrease during that period. He was admitted to our hospital because of dehydration and fever at age 74. Subsequently, his cognitive function deteriorated, with visual hallucination. Serial brain CT studies displayed a progressive cerebral cortical atrophy without focal lesions. He died of respiratory distress syndrome and disseminated coagulopathy resulting from pneumonia, dehydration and syndrome malin. Postmortem examination revealed a marked bilateral loss of melanin-containing neurons with Lewy bodies in the substantia nigra and locus ceruleus. Lewy bodies were also in the basal nucleus of Meynert, with moderate neuronal cell loss. The distribution of Lewy bodies was widespread in the cerebral cortical areas, corresponding to the neocortical subtype according to the consensus guideline for the pathologic diagnosis of dementia with Lewy bodies. According to the criteria of the Consortium to Establish a Registry for Alzheimer's Disease, the age-related plaque score in the present case suggested Alzheimer's disease, although cortical neurofibrillary changes corresponded to stage II by the criteria of Braak and Braak. These pathological findings established the diagnosis of dementia with Lewy bodies from the quantitative and distributional viewpoints. Based on recent neuropathological evidence, a spectral theory, which presents idiopathic Alzheimer's disease and Parkinson's disease as the two extremes of a spectrum of neurodegeneration, has been proposed. Dementia with Lewy bodies is located in the middle of this spectrum. Pathological evaluation based on quantitative consensus guidelines is important to establish the diagnosis in patients with parkinsonism and dementia, since neuropathological changes of Alzheimer's disease, Parkinson's disease and dementia with Lewy bodies are often observed in a mixed manner in these patients.
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PMID:[An autopsy case of dementia with Lewy bodies who showed the typical parkinsonism in the initial five years]. 1120 Nov 92

Lafora disease (LD) is a severe, autosomal recessive, latechildhood- to teenage-onset, progressive myoclonic epilepsy. It is due to either EPM2A or NHLRC1 mutations. We describe a patient with homozygous deletion encompassing the entire NHLRC1 gene, not previously reported, and with clinical course more progressive than in the most patients with NHLRC1 mutations. The diagnosis of LD in our patient was based on the typical clinic, neurophysiological presentation, as well as skin biopsy followed by molecular genetics findings. She developed normally until the age of 15, when she had her first occipital and generalized seizures. Four years after the first seizure the patient became bedridden, demented and presented with severe clinical condition. She died of pneumonia at age 20. This report is the first case of homozygosity for NHLRC1 deletion and thus adds to mutational heterogeneity of LD. Besides, it widens the spectrum of LD patients with severe phenotype and NHLRC1 mutations.
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PMID:Lafora disease: severe phenotype associated with homozygous deletion of the NHLRC1 gene. 2331 23