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

Prevalence of progressive sensorineural hearing loss in childhood seems to be extremely variable, as percentages reported range from 4 to 30%. Differences in the criteria employed for identifying the deterioration, in the groups of patients, and the age range, could explain this wide range of reported figures. The etiology of the progressive sensorineural hearing loss in infants can be hereditary or acquired. Hereditary causes are divided into syndromic and non-syndromic, whereas the acquired causes include congenital or acquired infection (syphilis, cytomegalovirus, rubella virus and toxoplasma infections, bacterial meningitis and acquired viral infections) and congenital inner ear anomalies (Mondini's dysplasia, large vestibular aqueduct, large cochlear aqueduct). Other acquired causes such as disorders of the metabolism, chronic use of ototoxic drugs, autoimmune diseases, perilymphatic fistula and head or acoustic trauma are less common. The age of onset of deterioration shows a great variability because even the congenital hearing losses may occur late after birth. The progressive evolution seems to be binaural in most patients, but more commonly it presents interaural differences, and when the hearing deficit is initially asymmetrical the deterioration is usually greater in the ear which appeared least affected in the first audiogram. Furthermore, at the different frequencies, there is a tendency to a greater deterioration at the frequencies initially least affected, but some authors are not in agreement because they report a uniform pattern of progression in the range of 0.5 to 4 kHz with no modification of the audiometric shape in most of the examined patients.
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PMID:[Progressive sensorineural hearing loss in childhood]. 1020 28

The progressive sensorineural hearing loss due to infectious causes can involve different etiological agents like bacteria, viruses, protozoons or mycetes. These infectious agents can act in various ways: directly through a labyrinthitis that may destroy the neuroepithelium; through an ischaemic process secondary to a septic embolus; or through a thrombus. In some cases the damage can occur in a meningitis context, because of the passage of the germ in the inner through the nerves, the vases or the labyrinthine liquids. Bacterial meningitis is one of the causes of progressive sensorinueral hearing loss. Among bacteria, the Mycobacterium Tuberculosis has nowadays acquired a remarkable importance which is also due to its considerable diffusion, despite modern therapy, and to its association with HIV infection. Bacteria can also cause a labyrinthitis acting directly on the inner ear: among these, Treponemas Pallidum, a spirochaete which causes syphilis and Borrelia Burgdorferi, a spirochaete that causes Lyme Disease, must be mentioned. The viruses that are certainly involved in the etiology of progressive sensorineural hearing loss are Cytomegalovirus and Rubella virus. The virus usually causes a labyrinthitis after the viraemia, wich may be due to the passage of the virus from the blood to the endolymph, through the stria vascularis with the consequent infection of the sensorial cells of the organ of Corti. Less frequently the viral damage to the inner ear can occur after a vasculitis, a meningitis or an alteration of the cell-mediated immunity. Progressive sensorineural hearing loss can also occur because of some congenital viral infections such as those caused by Cytomegalovirus and Rubella virus. More recently even the Human Parvovirus B19 seems to have been involved. This virus seems to act through autoimmune and/or immunologic processes, like that causing sudden hearing loss in Lassa fever. Another viral infection which can nowadays more frequently be considered among the cause of progressive hearing loss is HIV. In the HIV infection the neurological toxic lesions due to the administered ototoxic drugs are added up to the damages caused by the opportunistic infectious agents (virus, bacterium, protozoon mycete). However, in these patients HIV itself could be the cause of the auditory and vestibular lesions. More rarely, a progressive hearing loss may be due to the action of a protozoon or mycete only.
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PMID:[Progressive sensorineural hearing loss from infectious agents]. 1020 33

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

Sensorineural hearing loss following acute bacterial meningitis could be caused by hydroxyl radicals generated by the inflammatory response. Obstruction of cerebrospinal fluid circulation through the tela choroidae of the choroid plexuses, with subsequent rupture of the tela choroidae, would expose the auditory nerve to selective radical damage. Acute administration of lipophilic antioxidants might provide the auditory nerve with increased protection.
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PMID:Could antioxidant therapy reduce the incidence of deafness following bacterial meningitis? 1034 76

We evaluated 82 children with bacterial meningitis in 78 institutions in Hokkaido, Japan between 1994 and 1998. The mean number of cases per year was 16.4 (range, 9 to 30). A male predominance occurred with 52 males and 30 females (1.7:1). Median age was 11 months with a range from 1 day to 11 years. Seventy-eight (95%) of the total were less than 5 years old with 55 (67%) less than 2 years old and 45 (55%) less than 1-year old. Four deaths occurred, giving an overall case fatality rate of 4.9%. Sequelae were seen at discharge in 29%, predominantly sensorineural hearing loss, epilepsy and development delay of varying severity. The main causative organisms were Haemophilus influenzae in 49 patients, Streptococcus pneumoniae in 14, Streptococcus agalactiae in 10 and Escherichia coli in 5. The frequency of poor prognosis was 50% for patients with meningitis due to S. pneumoniae or S. agalactiae compared with 27% for patients with meningitis due to H. influenzae.
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PMID:[A study of bacterial meningitis in Hokkaido between 1994 and 1998]. 1083 39

We report a case of a girl with Langerhans cell histiocytosis (LCH) of multifocal bone disease, who developed recurrent bacterial meningitis and unilateral sensorineural hearing loss during the relapsing course of the disease. Mondini dysplasia, a congenital inner ear anomaly, was suspected by high resolution computed tomographic scan and the dysplasia with cerebrospinal fluid leakage was confirmed by surgery in the ipsilateral ear showing hearing loss. Although rare, congenital inner ear anomalies such as Mondini dysplasia should be kept in mind in pediatric patients with hearing impairment and/or recurrent bacterial meningitis during chemotherapy for various types of neoplasms including LCH.
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PMID:Mondini dysplasia and recurrent bacterial meningitis in a girl with relapsing Langerhans cell histiocytosis. 1517 Aug 97

Bacterial meningitis is characterized by an inflammatory reaction to the invading pathogens that can ultimately lead to sensorineural hearing loss, permanent brain injury, or death. The matrix metalloproteinases (MMPs) and tumor necrosis factor alpha-converting enzyme (TACE) are key mediators that promote inflammation, blood-brain barrier disruption, and brain injury in bacterial meningitis. Doxycycline is a clinically used antibiotic with anti-inflammatory effects that lead to reduced cytokine release and the inhibition of MMPs. Here, doxycycline inhibited TACE with a 50% inhibitory dose of 74 microM in vitro and reduced the amount of tumor necrosis factor alpha released into the cerebrospinal fluid by 90% in vivo. In an infant rat model of pneumococcal meningitis, a single dose of doxycycline (30 mg/kg) given as adjuvant therapy in addition to ceftriaxone 18 h after infection significantly reduced the mortality, the blood-brain barrier disruption, and the extent of cortical brain injury. Adjuvant doxycycline (30 mg/kg given subcutaneously once daily for 4 days) also attenuated hearing loss, as assessed by auditory brainstem response audiometry, and neuronal death in the cochlear spiral ganglion at 3 weeks after infection. Thus, doxycycline, probably as a result of its anti-inflammatory properties, had broad beneficial effects in the brain and the cochlea and improved survival in this model of pneumococcal meningitis in infant rats.
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PMID:Doxycycline reduces mortality and injury to the brain and cochlea in experimental pneumococcal meningitis. 1679 Jul 61

The relationship between meningitis and sensorineural hearing loss (SNHL) has long been studied. Many histopathological studies of animal models and human temporal bones with respect to bacterial meningitis have been carried out. However, the relationship between SNHL and tuberculous meningitis was seldom addressed and the pathophysiology remains unclear. We carried out temporal bone studies on material from a 22-year-old patient who developed a right unilateral SNHL before dying from tuberculous meningitis. The histopathological findings for the right temporal bone were as follows: (1) inflammation mainly appeared in the internal auditory canal, modiolus and Rosenthal's canal and extended to the osseous spiral ligament, whereas the perilymphatic spaces were less involved; (2) the organ of Corti, cochlear nerve fibres and spiral ganglion cells were severely degenerated, particularly in the basal and middle turns; (3) the contralateral side (for which the patient had no complaints) showed an inner space free from inflammation, but some granulomatous formations were observed in the middle ear cavity. We conclude that the modiolus and cochlear aqueduct are the main routes for the spread of infection from the meninges to the inner ear. The progression of hearing loss resembles that of bacterial meningitis and shares attributes of retrocochlear SNHL.
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PMID:Tuberculous meningitis-induced unilateral sensorineural hearing loss: a temporal bone study. 1745 85

Sensorineural hearing loss (SNHL) is the most common sequel of bacterial meningitis (BM) and is observed in up to 30% of survivors when the disease is caused by Streptococcus pneumoniae. BM is the single most important origin of acquired SNHL in childhood. Anti-inflammatory dexamethasone holds promises as potential adjuvant therapy to prevent SNHL associated with BM. However, in infant rats, pneumococcal meningitis (PM) increased auditory brainstem response (ABR) thresholds [mean difference = 54 decibels sound pressure level (dB SPL)], measured 3 wk after infection, irrespective to treatment with ceftriaxone plus dexamethasone or ceftriaxone plus saline (p < 0.005 compared with mock-infected controls). Moreover, dexamethasone did not attenuate short- and long-term histomorphologic correlates of SNHL. At 24 h after infection, blood-labyrinth barrier (BLB) permeability was significantly increased in infected animals of both treatment groups compared with controls. Three weeks after the infection, the averaged number of type I neurons per square millimeter of the Rosenthal's canal dropped from 0.3019 +/- 0.0252 in controls to 0.2227 +/- 0.0635 in infected animals receiving saline (p < 0.0005). Dexamethasone was not more effective than saline in preventing neuron loss (0.2462 +/- 0.0399; p > 0.05). These results suggest that more efficient adjuvant therapies are needed to prevent SNHL associated with pediatric PM.
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PMID:Limited efficacy of adjuvant therapy with dexamethasone in preventing hearing loss due to experimental pneumococcal meningitis in the infant rat. 1762 52

Pneumococcal meningitis remains a serious disease with a case fatality rate of 15%-25%. Furthermore, long-term residues affect up to 50% of survivors. One of the most frequent sequelae is sensorineural hearing loss, which occurs in 26% of survivors of pneumococcal meningitis. Unfortunately, sufficient treatment regimens are still missing. New insights into the pathology and pathophysiology of meningitis-associated hearing loss have come from animal models of bacterial meningitis. Most likely, bacteria reach the cochlea through the cochlear aquaeduct. Once arrived in the perilymphatic spaces, they induce a severe suppurative labyrinthitis. The blood-labyrinth barrier breaks, hair cells are damaged, and neurons in the spiral ganglion undergo cell death, leading to meningitis-associated hearing loss. Reactive oxygen and nitrogen species, in particular peroxynitrite, seem to be among the crucial mediators of cochlear damage and hearing loss during meningitis. In our rat model of pneumococcal meningitis, adjunctive therapy with the antioxidants and peroxynitrite scavengers Mn(III)tetrakis(4-bencoic acid)-porphyrin (MnTBAP) and N-Acetyl-L-Cystein (NAC) significantly attenuated acute and long-term hearing loss. In several other animal studies of pneumococcal meningitis, adjunctive antioxidant therapy also protected infected animals from intracranial complications. Therefore, the use of antioxidants seems to be a promising future treatment option in pneumococcal meningitis.
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PMID:Nitrogen and oxygen molecules in meningitis-associated labyrinthitis and hearing impairment. 1808 15


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