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

The diagnosis and treatment of acute meningitis is a challenge for the primary care physician. Differentiating between bacterial meningitis and aseptic meningitis is not always straightforward. The aseptic meningitis syndrome is usually viral in origin, and enteroviruses account for most cases. The aseptic syndrome also may be caused by unusual bacterial organisms such as Mycobacterium tuberculosis, Leptospira species, Brucella species, Borrelia burgdorferi and others. The classic presentation consists of the acute onset of meningismus, headache, fever, malaise with pleocytosis and normal glucose and slightly elevated protein in the cerebrospinal fluid. Cerebrospinal fluid lactate and serum C-reactive protein measurements may be helpful in differentiating aseptic meningitis from treatable bacterial meningitis. Aseptic meningitis of viral origin usually responds to expectant care. Other causes of aseptic meningitis must be searched for and treated if present.
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PMID:The aseptic meningitis syndrome. 821 11

A retrospective analysis of all patients admitted with the diagnostic codes of aseptic or viral meningitis was performed at two institutions over 3 years. Forty-one patients with cerebrospinal fluid confirmation of aseptic meningitis (increased protein; increased white count; negative gram stain; and negative fungal, tuberculosis, and bacterial cultures) were analyzed. All the patients had headache, which was typically severe and bilateral in 39 of the 41 patients. The headache was of abrupt onset or the worst of the patient's life in 24 of the patients. The quality of the headache, when described, was usually throbbing (11 of 14). Nineteen patients had prodromal symptoms, including malaise, myalgia, gastrointestinal symptoms, and urinary tract infections. All had associated symptoms, including nausea (25), vomiting (23), photophobia (18), stiff neck (25), and back pain (11). Thirty patients were febrile. Lumbar puncture was performed for headache and fever unexplained by systemic illness in 30 patients, meningeal signs in 15, headache of abrupt onset or the worst headache ever in 24, neurologic signs or symptoms in 12, and for other reasons in 2. Computerized tomography, when performed, was negative in all cases. Focal neurologic findings were present in 5 patients, a decreased level of consciousness in 6, and papilledema in 1. A severe headache that worsens, is abrupt in onset, or is the worst of the patient's life could be due to aseptic meningitis, bacterial meningitis, or a subarachnoid hemorrhage. Although not universally present, meningeal signs, fever, and neurologic signs or symptoms should alert one to a possible central nervous system infection.
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PMID:Headache associated with aseptic meningitis. 853 Feb 75

Concentrations of interferon gamma (IFN-gamma) in the lumbar cerebrospinal fluid (CSF) of 30 children (mean age, 27 months) being treated for stage III (16 children) and stage II (14 children) tuberculosis meningitis (TBM) were determined by ELISA. Nine children with stage III TBM and six with stage II TBM received prednisone (4 mg/kg). Concentrations of IFN-gamma in 73 CSF specimens (18 from the first week of therapy, 20 from the second, 19 from the third, and 16 from the fourth) were determined. The mean concentrations were 780 pg/mL in the first week of therapy and 554 pg/mL, 529 pg/mL, and 269 pg/mL in the second, third, and fourth weeks, respectively. Tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) concentrations in 56 specimens from 23 of these same children were determined by ELISA. The mean CSF TNF-alpha concentration in 12 specimens obtained during the first week of therapy was 17 pg/mL, and the mean was 11 pg/mL during each of the subsequent weeks (14 specimens were evaluated in the second week and 15 specimens in the third and fourth weeks of therapy). Mean IL-1beta concentrations in these same groups of specimens were 52 pg/mL, 43 pg/mL, 42 pg/mL, and 18 pg/mL. No correlation could be shown between cytokine concentration and stage of disease, and no differences existed between those who did and those who did not receive prednisone. A significant decline in IL-1beta concentrations was shown during the 4-week period, but none in TNF-alpha or IFN-gamma concentrations was noted. Persistently high CSF INF-gamma concentrations in cases of TBM (as in cases of aseptic meningitis but not bacterial meningitis) at the time of diagnosis suggest an immune response fundamentally different from that in bacterial meningitis.
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PMID:Concentrations of interferon gamma, tumor necrosis factor alpha, and interleukin-1 beta in the cerebrospinal fluid of children treated for tuberculous meningitis. 864 41

The details of 328 patients with bacterial meningitis, admitted from 1984 through 1993, were obtained from 46 departments of pediatrics of large hospitals through questionnaires. The incidence rate per 100,000 child-years was 2.32, being higher in children aged 0-4 years (rate, 7.22) than 5-15 years (rate, 0.49). The disease in the 274 (84%) etiologically diagnosed patients was due to Haemophilus influenzae (95), Streptococcus pneumoniae (56), Group B streptococci (GBS) (41), Escherichia coli (27), and other agents (55), including 7 patients with Mycobacterium tuberculosis infection. The short-term outcome (mean length of follow-up, 2 years, 11 months) of meningitis was death in 26 patients (8.2%) and sequelae in 49 (16.0%), including 26 children with multiple residual impairment. Tuberculous, pneumococcal, and GBS meningitis with a poor outcome increased during the late period (1989-1993) of the 10-year study. The annual infant mortality rate for purulent meningitis decreased from 3.7 to 1.4 per 100,000 population between 1984 and 1993. The incidence of a poor outcome (death and sequelae) in newborns decreased by half during the late period.
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PMID:Epidemiology of bacterial meningitis in children: Aichi Prefecture, Japan, 1984-1993. 873 10

To evaluate the spectrum of meningitis and its impact on human immunodeficiency virus (HIV) infection, 284 adults hospitalized with meningitis in Soweto, South Africa, were studied. Tuberculosis meningitis (TBM) was the most common cause of meningitis (25.4%), followed by acute bacterial meningitis (ABM; 22.5%), acute viral meningitis (AVM; 14.1%), and cryptococcal meningitis (13%). The in-hospital mortality rate exceeded 40% in TBM, ABM, cryptococcal meningitis, the neurosurgery group, and the parameningeal/parenchymal group. Only 56.2% of patients with ABM had positive blood or cerebrospinal fluid cultures. 37.3% of the 193 patients tested for HIV were seropositive. All patients with cryptococcal meningitis and at least 54% of those with TBM were HIV-infected. Moreover, at least 27% of the study population presented with an acquired immunodeficiency syndrome (AIDS)-defining illness such as cryptococcal meningitis or TBM. The high mortality rates observed among meningitis patients in this series reflect immunosuppression associated with HIV infection or malnutrition, late presentation at a hospital, lack of access to medical care, and failure on the part of some primary care providers to consider a diagnosis of meningitis. Underlying HIV infection in increasing numbers of meningitis patients can be expected to produce a need for more hospital beds and increased medical expenditures in South Africa.
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PMID:The spectrum of meningitis in a population with high prevalence of HIV disease. 875 89

Mycobacterial infection has been recognized as a complication in patients with malignancy. Tuberculous (TB) meningitis has not been reported in patients with nasopharyngeal carcinoma (NPC); it may have been overlooked or confused with the underlying malignancy or meningitis caused by other microorganisms. We describe the occurrence of culture-proven TB meningitis in 2 NPC patients. The time lag between the diagnosis of NPC and the occurrence of TB meningitis was 4 years in 1 patient and 6 years in the other. In both patients, the diagnosis of TB meningitis was delayed; they were initially treated for bacterial meningitis. Subsequent antituberculous chemotherapy was successful in 1 patient but failed in the other. Recognition of the infection is important for early diagnosis and proper treatment of this potentially fatal condition in patients with NPC.
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PMID:Tuberculous meningitis in patients with nasopharyngeal carcinoma. 879 91

During the 9 years 1985-1993 a prospective survey of all cases of meningitis in children < 13 years of age presenting to our hospital in the Western Cape Province of South Africa was carried out. Two-thousand-nine-hundred-and-twenty cases of meningitis were identified. The commonest form of bacterial meningitis was tuberculous meningitis (TBM) diagnosed in 282 children (mean age 2.94 years). N. meningitidis identified in 220 children (mean age 2.87 years), Haemophilus influenzae in 156 children (mean age 1.15 years) and S. pneumoniae in 106 children (mean age 2.14) were the next commonest causes of bacterial meningitis diagnosed. One-hundred-and-eighteen cases of bacterial meningitis were confirmed in infants < 1 month of age and the commonest bacteria identified were group B beta-haemolytic Streptococcus in 27, E. coli in 21, Klebsiella species in 11, and Candida species in 15 neonates. The emergence of TBM as the predominant cause of bacterial meningitis in childhood at our hospital is probably a reflection of the worsening tuberculosis situation in the Western Cape Province of South Africa.
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PMID:Pediatric meningitis in the Western Cape Province of South Africa. 893 54

Laboratory techniques for the diagnosis of central nervous system (CNS) infections are rapidly improving but at present have limitations that necessitate our guarded enthusiasm. Enteroviruses are the most common infectious agents of viral meningitis for which an etiology can be determined, and it is anticipated that the use of the reverse transcriptase polymerase chain reaction (RT-PCR) technique should significantly improve the identification of the etiologic agent of aseptic meningitis. The combination of the polymerase chain reaction technique with laboratory methods for the determination of intrathecal antibody production to herpes simplex virus and varicella-zoster virus have improved the rapidity with which these viral infections can be diagnosed. The pearls and pitfalls of the use of these laboratory techniques in the diagnosis of viral meningitis, recurrent meningitis, and focal encephalitis are included. Recommendations for the empiric therapy of bacterial meningitis in children and adults have changed because of the emergence of penicillin and cephalosporin-resistant pneumococcal organisms. The currently recommended antibiotics and their dosages are included. The evidence for the efficacy of dexamethasone therapy in bacterial meningitis is provided. Meningitis due to Mycobacterium tuberculosis is increasingly recognized, and the initiation of empiric antituberculous chemotherapy should not await the results of CSF cultures. Toxoplasma encephalitis and primary CNS lymphoma are the most common cause of mass lesions in patients with HIV, and the diagnostic techniques to distinguish between these two infections is reviewed. A short discussion of the best test for the diagnosis of neurosyphilis is provided.
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PMID:Pearls and pitfalls in the diagnosis and management of central nervous system infectious diseases. 960 16

Drugs offer a simple, cost-effective solution to many health problems, provided they are available, affordable, and properly used. However, effective treatment is lacking in poor countries for many diseases, including African trypanosomiasis, Shigella dysentery, leishmaniasis, tuberculosis, and bacterial meningitis. Treatment may be precluded because no effective drug exists, it is too expensive, or it has been withdrawn from the market. Moreover, research and development in tropical diseases have come to a near standstill. This article focuses on the problems of access to quality drugs for the treatment of diseases that predominantly affect the developing world: (1) poor-quality and counterfeit drugs; (2) lack of availability of essential drugs due to fluctuating production or prohibitive cost; (3) need to develop field-based drug research to determine optimum utilization and remotivate research and development for new drugs for the developing world; and (4) potential consequences of recent World Trade Organization agreements on the availability of old and new drugs. These problems are not independent and unrelated but are a result of the fundamental nature of the pharmaceutical market and the way it is regulated.
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PMID:Access to essential drugs in poor countries: a lost battle? 992 90

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


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