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

A case is described of a child of 2.6 years who developed total deafness after acute bacterial meningitis. Rapid obliteration of the cochleas due to osteoneogenesis led to limited cochlear implantation. The case is made for fast tracking these children to cochlear implant teams before neoossification becomes established.
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PMID:Cochlear implantation after bacterial meningitis: the dangers of delay. 906 4

Steroid therapy, in combination with antibiotics for bacterial meningitis in paediatric patients remains controversial. Steroids, and primarily dexamethasone a very potent anti-inflammatory agent, regulate the liberation of various cytokines and inflammatory mediators such as prostaglandins, released during bacterial meningitis and leading to long term complications. Several clinical trials studying infants and children with bacterial meningitis due to Haemophilus influenzae have evaluated the beneficial effects of the administration of dexamethasone at the onset of antibiotherapy and demonstrated that dexamethasone reduced the risk of acquired sensorineural deafness (bilateral moderate or more severe hearing loss) and the incidence of neurological sequelae. Limited information is available for the other bacterial meningitis, although meningococcal meningitis will become more frequent with the use of effective anti-Haemophilus vaccines. In addition some Streptococcus pneumoniae are now resistant to third generation cephalosporins and the use of dexamethasone in that case may be at risk. Finally, no evidence is available for an effective role for dexamethasone in neonatal bacterial meningitis, although it is quite often administered in that age group.
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PMID:[Role of corticoids in purulent meningitis in children: analysis of literature studies]. 908 10

Although the identity of all the variables that may influence speech recognition after cochlear implantation is unknown, the degree of preservation of spiral ganglion cells is generally considered to be of primary importance. A series of experiments in our laboratories, directed at quantification of surviving spiral ganglion cells in the profoundly deaf, evaluation of the predictive value of a variety of clinical parameters, and the evaluation of the consequences of implantation in the inner ear, is summarized. Histologic study of the inner ears of patients who were deafened during life demonstrated that the cause of deafness accounted for 57% of the variability of spiral ganglion cell counts. Spiral ganglion cell counts were highest in individuals deafened by aminoglycoside toxicity or sudden idiopathic deafness and lowest in those deafened by postnatal viral labyrinthitis, congenital or genetic deafness, or bacterial meningitis. Study of the determinants of degeneration of the spiral ganglion revealed that degeneration is most severe in the basal compared with the apical turn and more severe when both inner and outer hair cells are absent. Unlike the findings in some experimental animal studies, no survival advantage of type II ganglion cells could be identified. There was a strong negative correlation between the degree of bony occlusion of the cochlea and the normality of the spiral ganglion cell count. However, even in specimens in which there was severe bony occlusion, significant numbers of spiral ganglion cells survived. A strong positive correlation between the diameter of the cochlear, vestibular, and eighth cranial nerves with the total spiral ganglion cell count (p < 0.001) was found. This would suggest that modern imaging techniques may be used to predict residual spiral ganglion cell population in cochlear implant candidates. Trauma from implantation of the electrode array was studied in both cadaveric human temporal bone models and temporal bones from individuals who received implants during life. A characteristic pattern of damage to the lateral cochlear wall and basilar membrane was identified in the upper basal turn. New bone formation and perielectrode fibrosis was common after cochlear implantation. Despite this significant trauma and reaction, there is no firm evidence that further degeneration of the spiral ganglion can be predicted as a consequence.
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PMID:Patterns of neural degeneration in the human cochlea and auditory nerve: implications for cochlear implantation. 933 69

Haemophilus influenzae is an infrequent etiologic agent of bacterial meningitis in adult patients. In the last 12 years, it was the cause in 12 out of 238 cases (5.0%) of acute bacterial meningitis in adults. There were 5 men and 7 women with a mean age (SD) of 45.4 (16) years (range: 18-68 years). Seven patients (60%) had a communication between subarachnoid space and skin surface or mucosal cavities, and five (41.7%) had otitis or sinusitis. Most of the strains (9/12) were serotype b. Only one patient (8.3%) developed severe neurologic and extra-neurologic complications, and was the one who died. One of the survivors (9.1%) had partial deafness. H. influenzae is not a negligible cause of bacterial meningitis in adults. Moreover, its detection has been increasing in the last years. Patients with a cerebrospinal fluid leak, otitis or sinusitis are at high risk. The outcome is usually favorable if an early adequate therapy is given.
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PMID:[Haemophilus influenzae meningitis in adults: analysis of 12 cases]. 981 May 48

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

A leading cause of morbidity from bacterial meningitis is an irreversible, usually profound sensorineural hearing loss, with an incidence as high as 30% in some studies. Bacterial meningitis remains the most common cause of acquired postnatal sensorineural deafness. Although several clinical studies have examined the long-term outcome of hearing in meningitis, few studies have examined the time course of hearing loss during the acute course of the disease. We have developed an animal model of meningogenic hearing loss in the rat and have plotted the time course of that hearing loss. Serial auditory brain stem responses (ABRs) were measured in rats inoculated in the cisterna magna (subarachnoid space) with Streptococcus pneumoniae (10(5) to 10(7) colony-forming units). All rats injected developed meningitis as evidenced by increased cerebrospinal fluid (CSF) white cell counts and positive CSF cultures. Serial ABR measurements taken 6, 12, 15, 18, 21, and 24 hours after inoculation demonstrated significant threshold shifts and eventual loss of the ABR waveform as compared with measurements in control rats injected with sterile culture medium. Hearing loss began approximately 12 to 15 hours after inoculation and progressed to complete loss by 24 hours (17 of 18 animals). No correlation was found between the magnitude of hearing loss and CSF white cell count or bacterial titer. Temporal bone histology of rats with meningitis shows a dense inflammatory cell infiltrate throughout the subarachnoid space. Labyrinthine inflammatory cells were confined to the scala tympani. The cochlear aqueduct is the proposed route of infection from the meninges to the labyrinth (scala tympani). Endolymphatic hydrops was also noted throughout the cochlea. These experiments both establish a reproducible animal model of meningogenic hearing loss and support the hypothesis that this hearing loss is progressive rather than abrupt in onset and is related to the duration of untreated infection. CSF inflammatory cells appear to enter the cochlea through the cochlear aqueduct. This reliable animal model will enable future studies directed toward further understanding the pathogenesis and pathophysiology of this hearing loss.
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PMID:Time course of hearing loss in an animal model of pneumococcal meningitis. 1022 85

Bacterial meningitis is one of the most common causes of acquired profound sensorineural deafness in children. Measurement of hearing and examination of the cochlea is limited in patients suffering from acute meningitis. A rabbit model of pneumococcal meningitis was developed to identify the temporal bone histopathologic changes that occur in meningogenic labyrinthitis caused by Streptococcus pneumoniae. Light microscopy was previously performed on temporal bones from acutely meningitic rabbits with profound hearing loss as determined electrophysiologically. Extensive inflammation of the cochlea with endolymphatic hydrops was observed. The organ of Corti, however, showed preserved architecture in the majority of these animals. In order to further investigate these findings, a protocol was used to create meningitic rabbits with hearing loss ranging from early high-frequency loss to profound deafness. The temporal bones from 7 rabbits were examined by transmission electron microscopy. In cases of mild hearing loss, partial degeneration of the inner row of outer hair cells, as well as edema of efferent cochlear nerve endings and marginal cells of the stria vascularis, was seen. With increasing degrees of hearing loss, the remainder of the organ of Corti and intermediate cells of the stria showed ultrastructural abnormalities. Spiral ganglion cells and basal cells of the stria vascularis remained intact in all subjects. This study provides unique information regarding the histology and pathophysiology of meningogenic deafness. The clinical implications of these findings are discussed, with an emphasis on potentially reversible changes and therapeutic intervention.
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PMID:Electron microscopic temporal bone histopathology in experimental pneumococcal meningitis. 1037 20

We conducted a retrospective review to specify the frequency, identify the aetiological factors of bacterial meningitis in adults (BMA) and to evaluate the therapeutic protocol used. This study was conducted on 85 (BMA) cases of hospitalised patients between January 1991 and December 1995 (5 years) on our service. The BMA represented 3% of all admissions for infectious diseases at the Foundation Jeanne Ebori in Libreville. It occurred in an endemosporadic fashion. All patients were Black Africans with an average age of 33 years (range: 16-60 years). Males predominated by a ratio of 2.4. Tha patients were seen late in the evolution of the disease, as shown by the folloxing clinical signs: neuropsychic problems (100%), 25 patients (29%) were in a profound coma, 5 (6%) had a hemiplegia, 2 (2%) an hypoacousie and 1 (1%) seizure. Aetiological factors were found in 17 cases (20%) to be in the ORL sphere (sinusitis: n = 8, ear infection: n = 4), pneumopathies (n = 4) and one case of breach dure-mere. The predominant germ was pneumocoque, isolated in 55 cases (65%), 15 cases had a LCR clear (18%). Bacteria gram negative (6%) were identified in the immunocompromised HIV. Third generation cephems had an efficiency higher than beta lactamines: 83% against 73%. The mortality was 18%; 3% of the remaining patients had neurological deafness. The seriousness of the results of this survey calls for the urgent implementation of a surveillance programme.
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PMID:[Bacterial meningitis in the adult. Study of 85 cases observed in the infectious disease unit of the Fondation Jeanne Ebori (F.J.E.), Libreville, Gabon]. 1069 Apr 60

Bacterial meningitis is an important cause of acquired sensorineural deafness in childhood. Deafness following meningitis may be progressive. Previous reports have shown deterioration in hearing up to 12 years after the illness. We present two cases of sensorineural deafness following meningitis. Severe to profound sensorineural hearing losses were detected immediately after meningitis in these patients. The hearing subsequently deteriorated in both cases. Deterioration in hearing thresholds occurred 17 years after the illness in one case. In the other patient the hearing got progressively worse three years after meningitis. She subsequently required a cochlear implant.
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PMID:Delayed deterioration of hearing following bacterial meningitis. 1069 83

Twenty-two children with bacterial meningitis were prospectively studied to follow C-reactive protein (CRP) in serum at admission, 2nd, 5th and 7th days of treatment, and in the cerebrospinal fluid (CSF) at admission, to investigate if there is any relationship of its levels with the clinical evolution. CRP was measured by latex agglutination and/or ELISA techniques with detection limits of 0.15mg/L and 0.9mg/L, respectively. Patients were classified according to clinical evolution in two groups: uneventful recovery (n=12) and complicated evolution (n=10). Clinical complications observed were: relapse of fever (8), persistent fever (4), arthritis (4), ventricle enlargement (2), subdural effusion (1), subdural empyema (1), ataxia (1), cervical hypotonia (1), deafness (1), endophthalmitis (1), acute otitis media (1), secondary skin infection (1) and treatment change due to poor clinical response (1). A significant fall in CRP serum levels was observed among the uneventful recovery group after admission. Distinctly, in the group with a complicated evolution CRP levels showed either secondary elevation or remained high continuously. Mean serum CRP levels were significantly lower in the uneventful recovery group than in the complicated evolution group on 5th day and on 7th day. CRP levels below 20mg/L on 5th and 7th days were associated with an uneventful recovery, and CRP levels higher than 20mg/L on those same days were associated with a complicated clinical evolution (p=0.01* and p=0.0015*, respectively). We conclude that serum CRP levels monitoring in children with bacterial meningitis represents a useful and objective information about the clinical evolution. This procedure is inexpensive and suitable for use in endemic areas lacking sophisticated laboratories.
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PMID:C-reactive Protein Follow-up of Children With Acute Bacterial Meningitis. 1109 88


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