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Enterococcal meningitis: a clinical study of 39 cases and review of the literature.

To describe the clinical features and outcome of enterococcal meningitis, we retrospectively reviewed the charts of 39 cases seen at 2 tertiary hospitals during a 25 years and collected 101 additional, previously reported cases for review. Among these 140 cases, there were 82 cases (59%) of postoperative meningitis and 58 cases (41%) of spontaneous meningitis. Eighty-six patients (61%) were adults and 54 (39%) were children. Patients with spontaneous meningitis had a higher frequency of community-acquired infection (50% versus 18%; p < 0.01), severe underlying diseases (67% versus 22%; p < 0.01), and associated enterococcal infection (29% versus 8%; p < 0.01) than patients with postoperative meningitis. The clinical presentation was similar in both groups, but patients with spontaneous infection had a higher frequency of bacteremia (58% versus 12%; p < 0.01), and a lower frequency of mixed infection (9% versus 29%; p < 0.01). Spontaneous meningitis in children was associated with a significantly lower frequency of fever, altered mental status, headache, and meningeal signs (p < 0.01), probably explained by the high proportion of neonates in this age-group. Most infections were caused by Enterococcus faecalis, which accounted for 76% of the isolates identified at the species level. Fifteen of the 25 cases due to Enterococcus faecium were produced by vancomycin-resistant strains. Most patients were treated with ampicillin, penicillin, or vancomycin, with or without aminoglycosides, for a median period of 18 days (range, 1-85 d). Overall mortality was 21%. The mortality rate was higher in spontaneous than in postoperative meningitis (33% versus 12%; p < 0.01), but was similar in patients treated with beta-lactams (18%), glycopeptides (14%), or other antibiotics (25%), as well as in patients treated with monotherapy (16%) or combination therapy (22%). An adverse outcome correlated significantly with advanced age, the presence of severe underlying diseases, associated enterococcal infection, bacteremia, septic shock, and the absence of fever at presentation. Shunt removal was associated with a lower mortality. Multivariate analysis showed that the presence of severe underlying diseases was the only prognostic factor associated with mortality (odds ratio = 6.8, 95% confidence intervals = 2.7-17.5, p < 0.01).

Adolescent↗

Strategies to prevent neuronal damage in paediatric bacterial meningitis.

PURPOSE OF REVIEW: The mortality of bacterial meningitis can reach 30%, and up to 50% of survivors suffer from persisting neurological deficits as a consequence of the disease. The incidence of neurological sequelae of bacterial meningitis has not improved over the last decade. Adjunctive therapeutic options are limited, and ongoing research into the pathophysiology of brain damage in bacterial meningitis aims at providing the scientific basis for future development of more efficient adjunctive options. RECENT FINDINGS: In a population with good access to health care, dexamethasone given before or at the time of initiation of antibiotic therapy acts beneficially in paediatric pneumococcal meningitis, but not in meningococcal meningitis. In experimental animal models, brain-derived neurotrophic factor protected against brain injury and improved hearing while melatonin, which has antioxidant properties among other effects, reduced neuronal death. Transgene technology can be used to provide new insights into the pathophysiology of the disease and to identify potential therapeutic targets. SUMMARY: Although dexamethasone improves outcome of bacterial meningitis under defined circumstances, the morbidity of bacterial meningitis still remains unacceptably high. Experimental models may help to identify new therapeutic strategies to further improve the neurological outcome in young children suffering from bacterial meningitis.

Animals↗

Altered brain exposure of morphine in experimental meningitis studied with microdialysis.

BACKGROUND: During pathologic conditions such as meningitis and traumatic brain injury the function of the blood-brain barrier (BBB) is disturbed. In the present study we examined the cerebral pharmacokinetic pattern of morphine in the intact brain and during experimentally induced meningitis using a pig model. Secondly, the use of intracerebral microdialysis as a potential tool for monitoring damage in the BBB by studying the pharmacokinetics of morphine is addressed. METHODS: Six pigs were studied under general anaesthesia. One occipital and two frontal microdialysis probes and one pressure transducer were inserted into the brain tissue. Another probe was placed into the jugularis interna. Morphine 1 mg kg(-1) was administered as a 10-min infusion, and morphine concentrations were then measured for 3 h. Meningitis was subsequently induced by injecting lipopoly-saccharide into the cisterna magna. When meningitis was established, the morphine experiment was repeated. RESULTS: The unbound area under the concentration-time curve (AUCu) ratio of morphine in brain to blood was 0.47 (0.19) during the control period, and 0.95 (0.20) (P < 0.001) during meningitis. The increase in the brain/blood AUCu ratio during meningitis implies decreased active efflux and increased passive diffusion of morphine over the BBB. The half-life of morphine in brain was longer than in blood during both periods, and was unaffected by meningitis. CONCLUSION: This study demonstrates that the morphine exposure to the brain is significantly increased during meningitis as compared with the control situation.

Analysis of Variance↗

Potential of environmental models to predict meningitis epidemics in Africa.

OBJECTIVES: Meningococcal meningitis is a major public health problem in Africa. This report explores the potential for climate/environmental models to predict the probability of occurrence of meningitis epidemics. METHODS: Time series of meningitis cases by month and district were obtained for Burkina Faso, Niger, Mali and Togo (536 district-years). Environmental information (1989-1999) for the continent [soil and land-cover type, aerosol index, vegetation greenness (NDVI), cold cloud duration (CCD) and rainfall] was used to develop models to predict the incidence of meningitis. Meningitis incidence, dust, rainfall, NDVI and CCD were analysed as anomalies (mean minus observed value). The models were developed using univariate and stepwise multi-variate linear regression. RESULTS: Anomalies in annual meningitis incidence at district level were related to monthly climate anomalies. Significant relationships were found for both estimates of rainfall and dust in the pre-, post- and epidemic season. While present in all land-cover classes these relationships were strongest in savannah areas. CONCLUSIONS: Predicting epidemics of meningitis could be feasible. To fully develop this potential, we require (a) a better understanding of the epidemiological and environmental phenomena underpinning epidemics and how satellite derived climate proxies reflect conditions on the ground and (b) more extensive epidemiological and environmental datasets. Climate forecasting tools capable of predicting climate variables 3-6 months in advance of an epidemic would increase the lead-time available for control strategies. Our increased capacity for data processing; the recent improvements in meningitis surveillance in preparation for the distribution of the impending conjugate vaccines and the development of other early warning systems for epidemic diseases in Africa, favours the creation of these models.

Aerosols↗

Interleukin-1alpha, interleukin-6 and tumor necrosis factor-alpha levels in children with sepsis and meningitis.

BACKGROUND: Cytokines are thought to be important endogenous mediators of the host immune response to infection. The purpose of the present study was to evaluate the utility of serum levels of interleukin (IL)-1alpha, IL-6 and tumor necrosis factor (TNF)-alpha in the prediction and differentiation of sepsis and meningitis in children. METHODS: Blood was collected from 50 children admitted to hospital for suspicion of infection. On the basis of predetermined criteria and investigation, the children were classified into sepsis (n = 30) and meningitis (n = 20) groups, as well as into healthy controls (n = 24) and non-infected sick controls (n = 12). The sepsis group was subdivided according to culture results into S1 (proven sepsis, n = 11) and S2 (clinical sepsis, n = 19). Serum IL-1alpha, IL-6 and TNF-alpha were measured by enzyme-linked immunosorbent assay (ELISA) while C-reactive protein (CRP) was measured by nephelometer. RESULTS: In non-infected sick controls, sepsis and meningitis groups, levels of CRP (P < 0.001, P < 0.05 and P < 0.01, respectively), IL-1alpha (P < 0.001 for all), and IL-6 (P < 0.01, P < 0.001, P < 0.001, respectively) were significantly elevated compared to healthy controls. In sepsis, levels of IL-1alpha increased in the S2 subgroup (P < 0.001) and IL-6 increased in the S1 and S2 subgroups (P < 0.05, P < 0.001, respectively) compared with healthy controls. In meningitis, IL-1alpha had the highest sensitivity and negative predictive value, while IL-6 had the highest specificity and positive predictive value in non-infected sick controls, sepsis and meningitis groups. CONCLUSION: Interleukin-1alpha, IL-6 and CRP are increased in non-infected sick controls, sepsis and meningitis patients but it is not possible to differentiate between them. IL-1alpha had the highest sensitivity in meningitis while IL-6 had the highest specificity in prediction of sepsis and meningitis and their assessment together may improve accuracy in the diagnosis of childhood infection.

C-Reactive Protein↗

Group B streptococcal meningitis in adults: recent increase in Southeast Asia.

BACKGROUND: Meningitis caused by Streptococcus agalactiae (Group B Streptococcus) is rare in adults and usually affects patients with predisposing conditions. AIMS: To describe an increase in adult group B streptococcal meningitis occurring in parallel in Hong Kong and Singapore. METHODS: All cases of bacterial meningitis admitted to the Prince of Wales Hospital, Hong Kong and Singapore General Hospital in 1998, aged 15 years or above, were reviewed. Medical records for the previous ten years were searched for previous cases of adult group B streptococcal meningitis. RESULTS: In 1998, 29 adult patients with bacterial meningitis were admitted to the two hospitals. S. agalactiae was isolated in 11 cases, Streptococcus pneumoniae in three cases, Klebsiella pneumoniae in two cases, and Pseudomonas pseudomallei in one case. In 11 cases no bacteriological diagnosis could be made. Two patients with adult group B streptococcal meningitis had predisposing conditions for infection. One patient died before a definite diagnosis could be established. A ten year review of records revealed one previous case of adult group B streptococcal meningitis in a patient with multiple risk factors. CONCLUSIONS: An increase of group B streptococcal meningitis has occurred among adults admitted to two major hospitals in two Southeast Asian cities. In the majority of cases there were no identifiable predisposing conditions. The cause of this increase of group B streptococcal remains unclear.

Adult↗

Phospholipase B in the brains and meninges of nonsensitized and sensitized rats after challenge with Angiostrongylus cantonensis.

After a primary infection with 100 Angiostrongylus cantonensis larvae, infected rats showed elevated phospholipase B activity in meningeal and brain homogenates beginning with the first week and continuing through the first month of infection. The rise in phospholipase B values through the first 4 weeks, with a prolonged peak spanning days 30 to 31, coincided with the invasion and maturation of the parasites in the brain, and the ensuing sharp decline in phospholipase B levels, shown by the readings on day 45, coincided in turn with the known migration of the worms from the brain to the lungs, which begins about 5 weeks after infection. In the meninges, the pattern of enzyme elevation was generally similar to that in the brain samples except that the highest activity was seen earlier at days 8 to 9, followed by a gradual decline by days 30 to 31 and a sharper drop by day 45. Rats challenged with 100 larvae 53 days after the primary infection exhibited an almost immediate rise of phospholipase B activity in both the brain and meninges; the peaks of activity occurred at day 1 for the meninges and day 25 for the brain, and levels above control values were still present at day 50. Comparison of the total enzymatic content of the cerebral tissue and meninges revealed that a remarkably high proportion of the phospholipase B activity was contained in the meninges. The inference that elevated levels of this enzyme in the cerebral tissue of A. cantonensis-infected rats are due to inflammatory reactions within the meningeal envelopes was confirmed by histochemical demonstration of specific sites of enzymatic activity limited to the meninges. It is of interest that 80% of the cells positive for the enzyme were clearly identifiable as eosinophils since an association of bone marrow eosinophilia and high phospholipase B levels in rats infected with A. cantonensis was shown in our earlier study of rats infected with this parasite.

Angiostrongylus↗

Meningitis in infancy in England and Wales: follow up at age 5 years.

OBJECTIVE: To describe important sequelae occurring among a cohort of children aged 5 years who had had meningitis during the first year of life and who had been identified by a prospective national study of meningitis in infancy in England and Wales between 1985 and 1987. DESIGN: Follow up questionnaires asking about the children's health and development were sent to general practitioners and parents of the children and to parents of matched controls. The organism that caused the infection and age at infection were also recorded. SETTING: England and Wales. PARTICIPANTS: General practitioners and parents of children who had had meningitis before the age of 1 year and of matched controls. MAIN OUTCOME MEASURES: The prevalence of health and developmental problems and overall disability among children who had had meningitis compared with controls. RESULTS: Altogether, 1584 of 1717 (92.2%) children who had had meningitis and 1391 of 1485 (93.6%) controls were successfully followed up. Among children who survived to age 5 years 247 of 1584 (15.6%) had a disability; there was a 10-fold increase in the risk of severe or moderate disability at 5 years of age among children who had had meningitis (relative risk 10.3, 95% confidence interval 6.7 to 16.0, P<0.001). There was considerable variation in the rates of severe or moderate disability in children infected with different organisms. CONCLUSION: The long term consequences of having meningitis during the first year of life are significant: 32 of 1717 (1.8%) children died within five years. Not only did almost a fifth of children with meningitis have a permanent, severe or moderately severe disability, but subtle deficits were also more prevalent.

Age Factors↗

Tumor necrosis factor in mediating experimental Haemophilus influenzae type B meningitis.

Tumor necrosis factor (TNF) could possibly be instrumental in mediating injury to the CNS during bacterial meningitis. In CSF of rabbits with meningitis induced with Haemophilus influenzae type b (Hib) lipooligosaccharide (LOS), TNF activity was first detected 45 min after intracisternal (IC) injection of 20 ng Hib LOS and white blood cells (WBC) first appeared 75 min later. The peak TNF activity (45 ng/ml) was observed at 120 min after IC and persisted for 5 h. When 1-2 X 10(7) CFU of Hib was used to induce meningitis, peak CSF TNF activity was comparable with that after 20 ng Hib LOS, but the activity persisted for 14 h. Dexamethasone (DXM) (1 mg/kg per i.v.) given 1 h before or simultaneously with IC Hib LOS reduced significantly TNF activity and meningeal inflammation. Goat anti-human TNF alpha antibodies given IC with 20 ng Hib LOS or 2 X 10(6) CFU of Hib resulted in a significant reduction in CSF TNF concentrations, which was also associated with reduced meningeal inflammation in Hib LOS-inoculated animals. We conclude that TNF participates in mediating meningeal inflammation associated with Hib experimental meningitis, and that DXM, when given before or with Hib LOS, inhibits CSF TNF production and modulates the meningeal inflammatory response.

Animals↗

Clinical outcomes of neonatal meningitis in very-low birth-weight infants.

We sought to describe the clinical presentation and consequences of meningitis among 64 very-low-birth-weight (VLBW <1.5 kg) infants who had 67 culture-proven episodes of meningitis over an 18-year period, 1977 through 1995. Demographic and neonatal descriptors of meningitis and later outcomes were retrospectively examined and neurodevelopmental outcomes of 39 of 45 (87%) meningitis survivors were compared to those of nonmeningitis survivors followed up to 20 months corrected age. Causes of meningitis included coagulase-negative Staphylococcus in 43% of episodes, other gram-positive bacteria in 19%, gram-negative bacteria in 17%, and Candida species in 20% of episodes. Spinal fluid abnormalities were sparse, regardless of etiologic organism. Of 38 nonbloody spinal fluid taps (<1,000 erythrocytes/mm3), 6 had >30 leukocytes/mm3, 5 protein >150 mg/dL%, and 6 glucose <30 mg/dL (1.67 mmol/L). Only 10 infants (26%) had 1 or more of these spinal fluid abnormalities. Meningitis survivors had a higher rate of major neurologic abnormality (41% vs 11%, p<0.001) and subnormal (<70) Mental Development Index (38% vs 14%, p<0.001) than nonmeningitis survivors. Impairment rates did not differ by etiologic organism. The effect of meningitis on neurologic outcome persisted even after controlling for birth weight, intraventricular hemorrhage, chronic lung disease, and social risk factors (odds ratio 2.27 [95% CI 1.02, 5.05]). We conclude that despite a sparsity of abnormal spinal fluid findings, culture-proven neonatal meningitis among VLBW infants has a detrimental effect on neurologic outcome, which persists even after controlling for other risk factors.

Blindness↗

3-Aminobenzamide, a poly (ADP-ribose) synthetase inhibitor, attenuates the acute inflammatory responses and brain injury in experimental Escherichia coli meningitis in the newborn piglet.

The aim of the present study was to evaluate the anti-inflammatory and neuroprotective effects of a poly (ADP-ribose) synthetase inhibitor 3-aminobenzamide during the early phase of experimental bacterial meningitis in the newborn piglet. Meningitis was induced by intracisternal injection of 10(8) colony forming units of Escherichia coli in 100 microl of saline. 3-Aminobenzamide, given 30 mg kg(-1) as a bolus i.v. injection 30 min before induction of meningitis, significantly attenuated the meningitis-induced acute inflammatory responses such as increased cerebrospinal fluid (CSF) lactate concentration, CSF leukocytosis and increased CSF tumor necrosis factor-alpha level. However, meningitis-induced increase in intracranial pressure and decrease in CSF glucose level were not significantly improved. Increased cerebral cortical cell membrane lipid peroxidation products (conjugated dienes) and decreased brain ATP/phosphocreatine levels observed in the meningitis group were also significantly improved with 3-aminobenzamide treatment. However, the improvement of reduced Na+, K+-ATPase activity did not reach a statistical significance (p = 0.06). In summary, 3-aminobenzamide significantly attenuated the acute inflammatory responses and the ensuing brain injury during the early phase of neonatal bacterial meningitis. These findings suggest that poly (ADP-ribose) synthetase inhibitors such as 3-aminobenzamide might be a promising novel anti-inflammatory and neuroprotective adjuvant therapy in neonatal bacterial meningitis.

Acute Disease↗

N(omega) -nitro-L-arginine methyl ester (L-NAME) attenuates the acute inflammatory responses and brain injury during the early phase of experimental Escherichia coli meningitis in the newborn piglet.

We evaluated the anti-inflammatory and neuroprotective effect of nonselective NOS inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), in experimental bacterial meningitis in the newborn piglet. Meningitis was induced by intracisternal injection of 10(8) colony forming units of Escherichia coli. L-NAME 10 mg kg(-1) was given intravenously 30 min before induction of meningitis. L-NAME significantly attenuated the increase in intracranial pressure and decrease in cerebrospinal fluid glucose concentration observed in the meningitis group. Systemic and cerebral perfusion pressure were even higher compared to the control and meningitis groups. However, the meningitis-induced increase in tumor necrosis factor-alpha level, leukocyte numbers and lactate level in the cerebrospinal fluid was not significantly attenuated with L-NAME administration. Reduced cerebral cortical cell membrane Na+, K+ -ATPase activity and increased lipid peroxidation products, indicative of meningitis-induced brain cell membrane dysfunction, were significantly improved with L-NAME treatment. Decreased brain glucose and ATP levels were also significantly improved with L-NAME treatment. These findings suggest that L-NAME was effective in attenuating the acute inflammatory responses and brain injury in neonatal bacterial meningitis.

Animals↗

Method for inducing experimental pneumococcal meningitis in outbred mice.

BACKGROUND: Streptococcus pneumoniae is the leading cause of bacterial meningitis. Pneumococcal meningitis is associated with the highest mortality among bacterial meningitis and it may also lead to neurological sequelae despite the use of antibiotic therapy. Experimental animal models of pneumococcal meningitis are important to study the pathogenesis of meningitis, the host immune response induced after infection, and the efficacy of novel drugs and vaccines. RESULTS: In the present work, we describe in detail a simple, reproducible and efficient method to induce pneumococcal meningitis in outbred mice by using the intracranial subarachnoidal route of infection. Bacteria were injected into the subarachnoid space through a soft point located 3.5 mm rostral from the bregma. The model was tested with several doses of pneumococci of three capsular serotypes (2, 3 and 4), and mice survival was recorded. Lethal doses killing 50 % of animals infected with type 2, 3 and 4 S. pneumoniae were 3.2 x 10, 2.9 x 10 and 1.9 x 10(2) colony forming units, respectively. Characterisation of the disease caused by the type 4 strain showed that in moribund mice systemic dissemination of pneumococci to blood and spleen occurred. Histological analysis of the brain of animals infected with type 4 S. pneumoniae proved the induction of meningitis closely resembling the disease in humans. CONCLUSIONS: The proposed method for inducing pneumococcal meningitis in outbred mice is easy-to-perform, fast, cost-effective, and reproducible, irrespective of the serotype of pneumococci used.

Animals↗

Nosocomial outbreak of neonatal Salmonella enterica serotype Enteritidis meningitis in a rural hospital in northern Tanzania.

BACKGROUND: Clinicians at Haydom Lutheran Hospital, a rural hospital in northern Tanzania noted an unusually high case-fatality rate of pediatric meningitis and suspected an outbreak of an unknown agent or an organism resistant to the empirical therapy. METHODS: We established a provisional microbiology laboratory to investigate the suspected outbreak. Blood and spinal fluid specimens were taken from children below the age of seven years with suspected meningitis. The blood and spinal fluid specimens were inoculated in commercial blood culture bottles and locally prepared Thayer-Martin medium in slanted tubes, respectively. The bacterial isolates were sent to Norway for further investigation, including susceptibility testing and pulsed-field gel-electrophoresis (PFGE). RESULTS: Among 24 children with suspected meningitis and/or septicemia, five neonates had meningitis caused by Salmonella enterica serotype Enteritidis, all of whom died. Two children had S. Enteritidis septicemia without meningitis and both survived. Genotyping with PFGE suggested a clonal outbreak. The salmonella strain was resistant to ampicillin and sensitive to gentamicin, the two drugs commonly used to treat neonatal meningitis at the hospital. CONCLUSION: The investigation reminds us that nontyphoidal salmonellae can cause meningitis associated with very high case-fatality rates. Resistance to multiple antimicrobial agents increases the risk of treatment failure and may have contributed to the fatal outcome in all of the five patients with salmonella meningitis. The investigation indicated that the outbreak was nosocomial and the outbreak subsided after hygienic measures were instituted. Establishing a provisional microbiological laboratory is a valuable and affordable tool to investigate and control outbreaks even in remote rural areas.

Bacteremia↗

Production of interleukin-10 in the cerebrospinal fluid in aseptic meningitis of children.

IL-10 is a cytokine that has antiinflammatory properties. We investigated IL-10 using ELISA and a reverse-transcribed polymerase chain reaction in the cerebrospinal fluid (CSF) of children with or without aseptic meningitis. When the patients with aseptic meningitis had meningeal symptoms, IL-10 in the CSF was detectable in 14 of 22 patients (88 +/- 146 ng/L, n = 31). The IL-10 levels decreased as meningeal symptoms disappeared. In 20 of 21 control children without meningitis, CSF samples had no detectable levels of IL-10 (< 10 ng/L). Serum IL-10 levels were lower than the corresponding levels in the CSF from the same individuals with aseptic meningitis. Significant correlations were found between IL-10 levels and mononuclear cell counts in the CSF of the affected patients (r = 0.644, p < 0.001). The IL-10 mRNA was detected by reverse-transcribed polymerase chain reaction-assisted amplification in the CSF cells in four of seven patients with the disease. The culture of CSF mononuclear cells produced high levels of IL-10 (152-485 ng/L) in all of five patients. Cytokine kinetics in the CSF showed that mean IL-10 levels reached the peak on the 2nd to 3rd d of the illness, although all mean levels of IL-6, IL-8, and granulocyte colony-stimulating factor were the highest on the 1st d of the illness. In summary, IL-10 is produced in the CSF in aseptic meningitis, and may increase relatively late compared with the proinflammatory cytokines. IL-10 may play an immunoregulatory role in the meningeal inflammatory network.

Adolescent↗

Dexamethasone increases hippocampal neuronal apoptosis in a rabbit model of Escherichia coli meningitis.

Mortality and long-term sequelae rates are high among adults and children with acute bacterial meningitis. Adjunctive treatment with dexamethasone has been shown to reduce systemic complications in bacterial meningitis patients, but corticosteroid treatment may have detrimental effects on hippocampal function. We evaluated the effect of dexamethasone treatment in addition to antibiotic therapy in a rabbit model of Escherichia coli meningitis. A moderate anti-inflammatory effect of dexamethasone could be demonstrated with respect to the inflammatory mediator prostaglandin E2, whereas no significant effect of dexamethasone on tumor necrosis factor-alpha, cerebrospinal fluid pleocytosis, protein, lactate, indicators of global neuronal damage, or blood gas analysis was found. Dexamethasone, however, increased the rate of apoptotic neurons in the granular layer of the hippocampal dentate gyrus. In view of the proapoptotic effect of adjunctive dexamethasone on hippocampal neuronal cells in animal models of Gram-positive and Gram-negative meningitis, the application of dexamethasone should be considered carefully in those forms of bacterial meningitis for which no evidence-based data of beneficial effect in humans are available, such as neonatal meningitis, bacillary Gram-negative meningitis or nosocomial forms of meningitis (e.g. following neurosurgery).

Animals↗

Age of meningitis or encephalitis is independently predictive of outcome from anterior temporal lobectomy.

BACKGROUND: The occurrence of meningitis or encephalitis in early childhood, i.e., < or =4 years of age, may be associated with both the development of medial temporal lobe epilepsy (MTLE) and an excellent operative outcome following an anterior temporal lobectomy (ATL). However, whether the predictive value of this risk factor for partial epilepsy is independent of the finding of mesial temporal sclerosis (MTS) on MRI is not known. METHODS: Consecutive patients (n = 39) with a remote history of meningitis or encephalitis who underwent an ATL were compared with 78 sex- and age-matched control subjects who had not experienced a CNS infection before ATL. All patients in both groups had nonlesional temporal lobe epilepsy and were followed up for at least 12 months postoperatively. RESULTS: There was a trend for the patients with a history of meningitis or encephalitis to have a lower frequency of class I postoperative outcome (61.5% vs 73.1%, p = 0.21). In the meningitis or encephalitis group, a class I outcome was more frequent in those with a history of meningitis or encephalitis at a young age (<4 years) (19/23 vs 5/16, p = 0.002), those with MTS detected on a preoperative MRI (22/31 vs 2/8, p = 0.04), and those with a history of meningitis (16/21 vs 8/18, p = 0.05). Multivariate logistic regression analysis found that a history of meningitis or encephalitis at a young age (b = 2.0, O.R. = 7.5, p = 0.048) was predictive of a class I outcome independent of the presence of MRI-identified MTS (b = 2.0, O.R. = 7.3, p = 0.07). CONCLUSION: The age of occurrence of a remote history of meningitis or encephalitis, but not the type of infection, is predictive of outcome after an ATL independent of the finding of MTS on the preoperative MRI.

Adolescent↗

Possible trimethoprim/sulfamethoxazole-induced aseptic meningitis.

OBJECTIVE: To report a case of trimethoprim/sulfamethoxazole (TMP/SMX)-induced aseptic meningitis. CASE SUMMARY: An 18-year-old woman diagnosed with acute myeloid leukemia was admitted for a bone marrow transplant. She had already attained remission with daunorubicin, thioguanine, and high-dose cytarabine. A routine lumbar puncture performed on admission revealed an abnormally elevated leukocyte count, and meningitis was suspected. The patient had been taking TMP/SMX (trimethoprim 120 mg) twice daily on Monday, Tuesday, and Wednesday for the past 3 months; no other medication was being used. Upon examination, the patient mentioned having had headaches for the past few weeks. Since viral, bacterial, and fungal cultures were negative, a diagnosis of aseptic meningitis was made. According to the Naranjo probability scale, TMP/SMX was a possible cause of the aseptic meningitis. Eleven days after discontinuation of TMP/SMX, lumbar puncture results had returned to normal. DISCUSSION: Many drugs have been associated with aseptic meningitis. Antibiotics are often linked with aseptic meningitis, with TMP/SMX being the most frequently associated antibiotic. Many cases of TMP/SMX-induced aseptic meningitis have been reported, while few cases have been reported with trimethoprim and sulfamethoxazole given separately. CONCLUSIONS: Despite the widespread use of TMP/SMX and the years of experience we have had with the drug, it is important to remain vigilant regarding possible adverse effects, particularly aseptic meningitis.

Adolescent↗