Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During autumn 1992, we observed two unrelated family outbreaks of Chlamydia pneumoniae infection. Family A consisted of grandmother (aged 77 yrs), father (aged 41 yrs), mother (aged 38 yrs), daughter (aged 10 yrs), and two sons (aged 6 yrs and 3 months, respectively). The grandmother and daughter suffered from pneumonia, father from pharyngitis and bronchitis and the older son from mild bronchitis. No symptoms were recorded in the mother and younger son. Symptomatic subjects showed a fourfold increase in immunoglobulin G (IgG) titre for Chlamydia pneumoniae, determined by a microimmunofluorescence test with specific antigen (TW-183). Other serological studies against Mycoplasma pneumonia, Legionella pneumophila, influenza virus type A and B, adenovirus and respiratory syncytial virus (RSV) were negative. Sputum culture gave a positive result for Haemophilus influenzae, colony forming units (cfu) = 10(4).ml-1 in the grandmother. No serum positivity was recorded in the mother and younger son, who remained asymptomatic. All symptomatic patients were successfully treated with macrolides. Family B consisted of mother (aged 63 yrs) and daughter (aged 36 yrs). Both suffered from Chlamydia pneumoniae pneumonia. Diagnosis was made by means of serological microimmunofluorescence test, and direct identification using an indirect immunofluorescence test on pharyngeal swab. Sputum culture and other serological tests remained negative. Both patients were successfully treated with macrolides. These observations emphasize the relevance of Chlamydia pneumoniae in family cluster respiratory infections.
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PMID:Two family outbreaks of Chlamydia pneumoniae infection. 814 7

Bacterial infection of the lower respiratory tract can impact on the etiology, pathogenesis, and the clinical course of COPD in several ways. Several recent cohort studies suggest that lung growth is impaired by childhood lower respiratory tract infection, making these individuals more vulnerable to developing COPD on exposure to additional injurious agents. Impairment of mucociliary clearance and local immune defense in smokers allows bacterial pathogens to gain a foothold in the lower respiratory tract. These pathogens and their products can cause further impairment of mucociliary clearance due to enhanced mucus secretion, disruption of normal ciliary activity, and airway epithelial injury, and thus persist in the lower respiratory tract. This chronic colonization of the lower respiratory tract by bacterial pathogens could induce a chronic inflammatory response with lung damage. Nontypeable Haemophilus influenzae, usually regarded as an extracellular mucosal pathogen, has been demonstrated to cause intracellular infections of the upper and lower respiratory tract respiratory tissue. Increased incidence of chronic Chlamydia pneumoniae infection of the respiratory tract has been associated with COPD. These chronic infections of respiratory tissues could contribute to the pathogenesis of COPD by altering the host response to cigarette smoke or by inducing a chronic inflammatory response. Application of newer molecular and immunologic research techniques is helping us define precisely the role of bacterial infection in COPD.
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PMID:Bacterial infection and the pathogenesis of COPD. 1084 57