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)

Sensorineural hearing loss is a major sequela of the bacterial meningitis associated in particular with Streptococcus pneumoniae. Recent studies have shown pneumolysin, a toxin elaborated by S. pneumoniae, to be cytotoxic to the guinea pig cochlea. The mechanisms of this cytotoxicity are, however, not fully understood. In the present study this deleterious action of pneumolysin has been shown to be blocked by pretreating the cochlea with NG-methyl-L-arginine, a known inhibitor of nitric oxide synthesis. Furthermore, pretreatment of the cochlea with MK-801, an NMDA receptor antagonist, was also found to confer marked protection from the action of pneumolysin. This latter finding is consistent with previous reports that excess stimulation of NMDA receptors within the cochlea, an event known to lead to excess nitric oxide release, have similar effects on the cochlea as pneumolysin perfusion. It would therefore appear that nitric oxide may represent a significant link in the chain of events leading to the deafness of bacterial meningitis.
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PMID:NG-methyl-L-arginine protects the guinea pig cochlea from the cytotoxic effects of pneumolysin. 754 27

Routine dexamethasone therapy for bacterial meningitis in pediatric patients is controversial. Two experts debated this topic at the 1993 meeting of the Infectious Diseases Society of America. Both experts agreed that for management of Haemophilus influenzae meningitis, dexamethasone significantly reduced sensorineural hearing loss and probably reduced other long-term sequelae. Because relatively few patients with pneumococcal and meningococcal meningitis have been studied, no conclusions could be reached regarding the effectiveness of dexamethasone. Dr. Urs Schaad emphasized the impressive anti-inflammatory effects of dexamethasone in experimental pneumococcal meningitis and the lack of any adverse events when given to children for 2 or 4 days. He recommended routine use of dexamethasone in treating pediatric patients with bacterial meningitis. Dr. Sheldon Kaplan expressed concern regarding the effectiveness of steroids in treating pneumococcal meningitis, especially when penicillin-resistant and cephalosporin-resistant isolates are present, and he addressed the question of the long-term effects of administration of dexamethasone in children with viral meningitis. He advised against the routine use of dexamethasone for non-H. influenzae meningitis.
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PMID:Steroid therapy for bacterial meningitis. 775 96

Hearing impairment as a sequela of acute bacterial meningitis is a well known complication. Dexamethasone therapy in addition to antibiotics is beneficial in the reduction of deafness, implicating that inflammation may be one reason for hearing impairment. The risk of hearing impairment in different types of bacterial meningitis is well studied. In very young children < 1.5 years of life the incidence of hearing loss and the possible correlation of laboratory data with the development of deafness is yet unknown. We therefore examined the brainstem auditory evoked potentials in 25 children between the first month and the 16th month of life who we treated for meningitis during 3 years in our hospital. 11 children were treated with dexamethasone. In 9 children we found abnormal brainstem auditory evoked potentials, which we controlled every 3 months. 7 children had transient conductive hearing impairment with good recovery during the first year after the disease. In 2 cases we found permanent bilateral sensorineural hearing loss. There was a significant relationship between hearing loss and elastase in cerebrospinal fluid. Dexamethasone reduced this relationship. A screening of hearing should be performed as routine control in all patients with acute meningitis. The association of high elastase in cerebrospinal fluid and later hearing impairment indicates a pathophysiological relation between activation of granulocytes and hearing loss.
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PMID:[Hearing disorders in children less than 16 months of age after bacterial meningitis with reference to cerebrospinal fluid elastase]. 788 11

Bacterial meningitis is an important cause of hearing loss in children. Previous studies have shown that a proportion of survivors of childhood bacterial meningitis do not have a formal hearing assessment. To confirm this finding amongst children treated for bacterial meningitis in our hospital, a retrospective audit was performed. The hospital case notes and community audiological records were examined to see how many children were referred for hearing assessment after their illness, and how many actually attended. Between 1984 and 1991, 194 children were directly admitted to our hospital with bacterial meningitis. Thirteen children died, and hearing assessment was carried out on 135 of the 181 survivors (75%), 15 of whom had evidence of sensorineural hearing loss. The major reason for hearing not being assessed was non-referral (31 out of 46 cases), 12 children did not attend for assessment despite referral, and three moved shortly after discharge. Thirty of the children remaining in the area who had no assessment (69.7%) were however seen in hospital out-patients. Routine referral for hearing testing at discharge, with re-referral at out-patient attendance, could help increase the number of children assessed after bacterial meningitis.
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PMID:Children who are seen but not referred: hearing assessment after bacterial meningitis. 805 94

Twenty four children with bacterial meningitis were studied prospectively to ascertain the incidence, type and severity of hearing loss. The incidence of sensorineural hearing loss was 20.8%. Patients with hearing loss were followed-up audiologically for six months to find out the progress of hearing impairment. Of the five patients with sensorineural hearing loss only one showed partial recovery while the other three did not show any improvement. Of the five patients with sensorineural hearing loss only one showed partial recovery while the other three did not show any improvement. One patient was lost to follow-up, therefore, recovery was not known. The degree of hearing loss varied form mild to moderate. Antibiotic treatment and laboratory data were analysed to identify the high risk factors predisposing to hearing impairment. The presence of low CSF sugar level, high protein at the initial lumbar puncture and presence of neurological deficits was associated with a significantly higher risk of hearing loss. However, the nature of antibiotic therapy, duration of illness, age and sex of the patients were not significant risk factors in the development of hearing impairment.
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PMID:Hearing evaluation in children with bacterial meningitis. 807 7

A 10-year-old girl was brought to our ear, nose and throat clinic for consultation on her articulation problem in addition to an attack of bacterial meningitis and cerebrospinal fluid (CSF) rhinorrhea. These problems had bothered her and her family for about 5 years. In August 1988, she had received a bifrontal osteoplastic craniotomy for her CSF leakage, but the procedure was ineffective. Local examination showed bilaterally intact ear drums. The left ear drum looked cloudy and thick with poor mobility under pneumatoscopy. A tympanogram showed that B type. Pure tone audiometry revealed a profound sensorineural hearing loss in the left ear. A CT scan showed widening of the internal auditory canal and dysplasia of the left cochlea and vestibule in addition to fluid accumulation in the mastoid and mesotympanum. Under the impression of CSF otorrhea, an exploratory tympanotomy was performed, revealing an area of leakage in the tympanic cavity. It was sealed with abdominal fat, temporal connective tissue and tissue glue. All of the bothersome symptoms disappeared postoperatively during an 18-month follow-up.
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PMID:[Congenital CSF otitic leakage presenting as rhinorrhea: report of a case]. 810 86

Bacterial meningitis is an infection of the central nervous system involving quite a number of neurological sequelae the most common of which is hearing impairment. To assess the incidence of audiological deficit the authors evaluated retrospectively 20 patients, between 4 months and 11 years of age, observed at the Pediatric Clinic at the University of Pisa between 1988 and 1993. A clinical-neurological examination and a complete auditory assessment (using BAEPs and impedence audiometry) has been performed in every patient between 1 and 18 months after they left hospital. 4 children had persisting neurological sequelae, 3 patients developed sensorineural hearing loss and one child visual impairment and seizures. Haemophilus Influenzae was responsible for 2 cases of sequelae and Streptococcus Pneumoniae for the other 2 cases. The number of days of illness before hospitalization and the institution of an antibacterial treatment, persistence of fever and deviation from the normal level of consciousness and persistence of neck rigidity were not correlated with the presence of sequelae. No correlation has been found between sensorineural hearing loss and the kind of antibacterial therapy. It's advisable that every child, following bacterial meningitis, should undergo a complete and repeated audiological assessment to detect any lesser impairments and/or unilateral losses that may damage the development of speech and language in any way.
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PMID:[Sequelae of bacterial meningitis in childhood: a study of hearing impairment]. 856 40

It is well established that sensorineural hearing loss (SNHL) is an important sequela of acute bacterial meningitis. Previous human temporal bone histopathologic studies have suggested that such hearing loss is due to labyrinthitis. This study involved a detailed and systematic evaluation of the auditory and vestibular end-organs in 41 human temporal bones from patients with acute bacterial meningitis, aimed at describing the spectrum of histopathologic changes within the labyrinth, ascertaining likely routes for spread of infection from the meninges to the inner ear, and comparing the data from humans with those described in a rabbit model of meningogenic labyrinthitis. Our study revealed the following: (a) Suppurative labyrinthitis occurred in 20 (49%) bones. Of these 20 bones, the cochlea was affected in all, whereas the vestibular organs were involved in 10. Eosinophilic staining of inner ear fluids without the presence of inflammatory cells (so-called "serous" labyrinthitis) occurred in 14 of the remaining 21 bones. This staining occurred primarily within the vestibular system. Its significance and pathogenesis remains unknown; (b) Sensory and neural structures of the inner ear appeared intact in the majority of specimens, including bones with suppurative labyrinthitis and those with eosinophilic staining of inner ear fluids. This finding raises the possibility of preventing or reversing SNHL by therapeutic intervention. Spiral ganglion cells were severely degenerated in 12% of bones, indicating a retrocochlear site of hearing loss in addition to the cochlea. This subset of patients may perform poorly after cochlear implantation; (c) It has been traditionally assumed that irreversible and permanent SNHL is caused by suppurative labyrinthitis, whereas reversible SNHL is caused by serous labyrinthitis. Our findings question the validity of these assumptions; (d) The data were consistent with the hypothesis that both the cochlear modiolus and cochlear aqueduct can serve as potential pathways for spread of infection from the meninges to the inner ear; (e) There were many similarities in the histopathology of the inner ear in humans when compared with the rabbit model of meningogenic labyrinthitis. A notable difference was that the cochlear aqueduct appeared to be the sole pathway for spread of infection in the rabbit, whereas in the human, both the modiolus and aqueduct were possible pathways.
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PMID:A human temporal bone study of acute bacterial meningogenic labyrinthitis. 881 13

Here we report a case of pneumococcal meningitis with bilateral sensorineural hearing loss at the onset. The patient was a 60-year-old man who a few days before visiting our hospital experienced common cold-like symptoms, and then he suddenly developed bilateral hearing loss. Examination of the cerebrospinal fluid (CSF) on the day of admission revealed pleocytosis and his CSF culture demonstrated pneumococci. Otorhinolaryngological examinations disclosed bilateral severe sensorineural hearing loss due to cochlear impairment. Many cases of bacterial meningitis concomitant with hearing loss have been reported, but a case of meningitis starting with sudden hearing loss is rare.
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PMID:[A case of adult meningitis with bilateral sensorineural hearing loss at the onset]. 939 67

Pneumococcal meningitis remains a significant cause of morbidity, particularly sensorineural hearing loss. Recent literature has suggested that a vigorous host immune response to Streptococcus [corrected] pneumoniae is responsible for much of the neurologic sequelae, including deafness, after bacterial meningitis. This study used a rabbit model of hearing loss in experimental pneumococcal meningitis to evaluate the therapeutic effect of two anti-inflammatory agents, dexamethasone and ketorolac, coadministered with ampicillin. Both adjunctive drugs minimized or prevented sensorineural hearing loss compared with placebo. Dexamethasone, administered 10 min before ampicillin, was particularly effective in minimizing mean hearing threshold change compared with placebo for both clicks (dexamethasone: 6.7-dB sound pressure level [SPL] vs. placebo: 33. 4-dB SPL, P=.0078) and 10-kHz tone bursts (dexamethasone: 8.4-dB SPL vs. placebo: 53.4-dB SPL, P=.0003). These findings support the beneficial role of anti-inflammatory agents in reducing the incidence of hearing loss from pneumococcal meningitis, especially if therapy is instituted early in the course of infection.
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PMID:Prevention of hearing loss in experimental pneumococcal meningitis by administration of dexamethasone and ketorolac. 984 52


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