Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Shigella flexneri 2a was isolated from a patient with Reiter's syndrome (RS) following a family outbreak of traveler's diarrhea. Among 3 members at risk, only the patient was positive for HLA-B27. Data from 3 similar families support the hypothesis that susceptibility to RS is genetically transmitted. It is urged that every effort be made to culture and subtype Shigella and other enteric pathogens in RS following diarrhea. Concurrently, the patient had hepatitis, interpreted as a parallel enteric infection.
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PMID:Reiter's syndrome following Shigella flexneri 2a: a sequel to traveler's diarrhea. Report of a case with hepatitis. 31 5

During 1986-87 this continuing survey showed 15 specific infections in the staff of 235 laboratories, representing 28,524 person years of exposure. The community was the probable source of four of the five cases of tuberculosis and one of the five cases of salmonellosis. Occupational exposure was the probable cause of four infections by Shigella flexneri, three by Salmonella typhimurium, and one by S typhi, all affecting medical laboratory scientific officers (MLSOs) in microbiology. Occupational exposure was also the probable cause of one case of tuberculosis in a mortuary technician and one of probable non-A, non-B hepatitis in a medical laboratory scientific officer haematology worker. The overall incidence of reported infections was 52.6/100,000 person years (35/100,000 for infections of probable occupational origin). The highest rates of laboratory acquired infections related to MLSO microbiology workers and mortuary technicians. No additional infections were seen as a result of extending the survey to forensic laboratories.
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PMID:Infections in British clinical laboratories, 1986-87. 250 46

Apoptosis is a physiological process critical for tissue homeostasis. It is essential for the regulation of immune responses. A series of molecules transduce apoptoic signals and induce the characteristic morphological appearances of apoptotic cells. Infectious diseases modulate apoptosis and this contributes to disease pathogenesis. Infection with HIV results in enhanced levels of CD4 T-lymphocyte apoptosis in both directly infected cells and in uninfected bystander cells. A variety of HIV proteins including gp120 contribute to this process. A number of different pathways induce HIV-associated CD4 T-lymphocyte apoptosis and apoptosis of uninfected bystander cells is particularly associated with increased susceptibility to Fas. Other viruses including hepatitis viruses and the human herpesviruses also modulate apoptosis. Bacterial infection induces apoptosis which is frequently mediated by the direct activation of caspases in the absence of death receptor ligation. Bacterial induction of apoptosis may either be due to bacterial factors such as the invasin IpaB of Shigella flexneri or be the result of host immune responses which control infection as demonstrated in infections due to Mycobacterium spp. Apoptosis may be modulated by therapeutic strategies, such as antiretroviral therapy, and an improved understanding of infection-associated apoptosis modulation will aid the design of novel therapeutic approaches to control infectious diseases.
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PMID:Apoptotic cell death in the pathogenesis of infectious diseases. 1154 64