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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sensorineural hearing loss was studied in a rabbit model of experimental bacterial meningitis using electrophysiological and ultrastructural techniques. Hearing impairment was monitored by auditory brain-stem evoked responses (ABERs) and concomitant structural lesions were identified by both transmission (TEM) and scanning (SEM) electron microscopy. Meningitis was induced by intra-cerebrospinal fluid injection of either Escherichia coli (strain 2073 and type K-12) or Haemophilus influenzae type b. Auditory loss of approximately equal to 10 dB occurred in all rabbits by about 10 hours post infection and progressed in severity until by 20 h following infection, hearing losses up to and > 60 dB were obtained. At levels of hearing loss < 20 dB ultrastructural damage to the organ of Corti was barely detectable. With greater levels of hearing loss, patchy structural damage to hair cells, synaptic nerve terminals, supporting cells and inner spiral sulcus cells and cells of the stria vascularis was clearly evident. Bacteria were found in scala tympani, the basilar membrane, the organ of Corti, scala media, the spiral ligament and at the margin of the stria vascularis. Evidence of bleeding was found in some cochleas; erythrocytes were found in scala tympani, scala media, amongst hair cells and beneath the tectorial membrane. The results show that hearing loss is associated with bacterial invasion and damage to the organ of Corti and that the cause of hearing loss is likely to result from multiple lesions within the cochlea. Lesions to sensory cells almost certainly will produce permanent hearing loss. Lesions to supporting cells, nerve terminals and to stria vascularis may well produce only temporary hearing loss.
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PMID:The cochlear lesion in experimental bacterial meningitis of the rabbit. 748 46

A total of 395 Haemophilus influenzae strains from 226 Japanese institutions participating in the Nationwide Surveillance Study Group for Bacterial Meningitis were received from 1999 to 2002. All strains were analyzed by PCR to identify the resistance genes, and their susceptibilities to beta-lactam agents were determined. Of these strains, 29.1% were beta-lactamase nonproducing and ampicillin (AMP) susceptible (BLNAS) and lacked all resistance genes; 15.4% were beta-lactamase producing and AMP resistant and had the bla(TEM-1) gene; 30.6% were beta-lactamase nonproducing and AMP resistant (low-BLNAR) and had a Lys-526 or His-517 amino acid substitution in ftsI encoding PBP 3; 13.9% were beta-lactamase nonproducing and AMP resistant (BLNAR) and had an additional substitution of Thr-385 in ftsI; 9.1% were amoxicillin-clavulanic acid resistant (BLPACR I) and had the bla(TEM-1) gene and a Lys-526 or His-517 amino acid substitution in ftsI; and 1.8% showed resistance similar to that of the BLPACR I group (BLPACR II) but had bla(TEM-1) gene and ftsI substitutions, as was the case for the BLNAR strains. All but three strains were serotype b. The prevalence of BLNAR strains has increased rapidly: 0% in 1999, 5.8% in 2000, 14.1% in 2001, and 21.3% in 2002. The MICs at which 90% of BLNAR isolates were inhibited were as follows: AMP, 16 micro g/ml; cefotaxime, 1 micro g/ml; ceftriaxone, 0.25 micro g/ml; and meropenem, 0.5 micro g/ml. All of these values were higher than those for the BLNAS counterpart strains. The relatively wide distributions of the beta-lactam MICs for BLNAR strains presumably reflect variations in ftsI gene mutations. Pulsed-field gel electrophoresis suggested the rapid spread of specific H. influenzae type b strains throughout Japan. Expedited vaccination, rapid identification, and judicious antibiotic use could slow their spread.
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PMID:Rapidly increasing prevalence of beta-lactamase-nonproducing, ampicillin-resistant Haemophilus influenzae type b in patients with meningitis. 1510 98