Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On June 13, 1991, President George Bush announced in a White House ceremony a local planning effort to break down barriers and provide better access to immunization in six representative localities "to solve the problem of late immunization." (children need to be immunized appropriately by their second birthday, not just in time for school.). The community "Immunization Action Plans" (IAP) are one of several Federal, State, and local responses to an outbreak of measles that produced 27,600 cases and 89 deaths in 1990. The community effort and subsequent early childhood immunization plans around the country are also part of a much broader effort initiated by Secretary Sullivan as a Healthy People Year 2000 goal to increase immunization levels to at least 90 percent for the nation's children by their second birthday. These efforts also respond to 13 recommendations for improving immunization availability made by the National Vaccine Advisory Committee in January 1991. The recommendations focused on improvements in the management of immunization delivery and in methods for measuring immunization status, increasing appropriate consumer demand, and other prevention needs. Although measles prompted the action, the immunization initiative is aimed also at eight other communicable childhood diseases--diphtheria, tetanus, pertussis or whooping cough, poliomyelitis, mumps, rubella, and Haemophilus influenza type b that causes bacterial meningitis, and hepatitis B. Details are described of the immunization action plans developed by Dallas, TX; Maricopa County (Phoenix), AZ; South Dakota; Detroit, MI; San Diego, CA; and Philadelphia, PA, to ensure that children are fully immunized not just by the time they enter school but by age 2 years. The six were chosen by the Centers for Disease Control as representative of many without adequate childhood immunization coverage.
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PMID:Six areas lead national early immunization drive. 159 33

Haemophilus influenzae type b remains the major cause of bacterial meningitis in infants and children. Serum antibodies against the capsular polysaccharide--polyribosylribitolphosphate (PRP)--are protective, but its immunogenicity is poor in children under two years of age. Clinical trials actually in progress concerning an association of PRP with Bordetella pertussis are presented. Other vaccinal preparations are possible, such outer membrane protein, but prospects offered by polysaccharide-protein conjugates appear as the most encouraging.
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PMID:[Prospects for the vaccinal prevention of Haemophilus influenzae type b meningitis]. 634 45

A fourfold or greater increase in titer of complement-fixing (CF) antibodies to Mycoplasma pneumoniae was found in 40.7% of paired sera from 54 patients with bacterial meningitis that had been proven by culture and in 10.3% of 39 patients with other bacteremic infections, but in none of eight patients with whooping cough or 40 patients with mumps meningitis. The CF antigen used was a crude lipid antigen, but comparable antibody increases were found by an enzyme-linked immunosorbent assay using a crude M. pneumoniae protein antigen. Increases were also frequently seen in nonspecific antibodies to the capsular polysaccharide of group A Neisseria meningitidis; these increases were significantly, but not completely, correlated to the nonspecific reactions to the mycoplasmal antigens. The data call for caution in interpreting serologic tests for M. pneumoniae when dealing with diseases not commonly associated with M. pneumoniae.
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PMID:Increase in titers of antibodies to Mycoplasma pneumoniae in patients with purulent meningitis. 680 46

Smoking is associated with an increased risk of respiratory tract infection in adults. In children, exposure to cigarette smoke is a risk factor for respiratory tract infection and bacterial meningitis: Active smoking and passive exposure to cigarette smoke is also associated with carriage of some potentially pathogenic species of bacteria in both adults and children. The aims of the study were to determine the effect of active smoking on: (1) bacterial binding to epithelial cells; (2) expression of host cell antigens that act as receptors for some species; and (3) the effects of passive exposure to water-soluble components of cigarette smoke on bacterial binding. Flow cytometry was used to assess binding to buccal epithelial cells of the following species labelled with fluorescein isothiocyanate: Neisseria meningitidis, Neisseria lactamica, Streptococcus pneumoniae, Bordetella pertussis, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus. Flow cytometry was also used to assess expression of host cell antigens which have been identified as bacterial receptors. For each species, binding to cells of smokers was significantly higher than to cells of non-smokers; however, expression of host cell antigens was similar on epithelial cells of both groups. Non-dilute cigarette smoke extract reduced binding of bacteria to epithelial cells, but dilutions between 1 in 10 and 1 in 320 enhanced binding. We conclude that smokers might be more densely colonised by a variety of potentially pathogenic bacteria. The enhanced bacterial binding to epithelial cells of smokers is not related to enhanced expression of host cell antigens that can act as receptors for some species, but possibly to components in the smoke that alter charge or other properties of the epithelial cell surface. Passive coating of mucosal surfaces with components of cigarette smoke might enhance binding of potentially pathogenic bacteria.
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PMID:The effect of cigarette smoke on adherence of respiratory pathogens to buccal epithelial cells. 1003 May 44