Impact of deltamethrin impregnated mosquito nets on the transmission of malaria in the coastal lagoon area, Benin]

Neopterin has been determined in blood as a marker of cellular immune system activation. We studied cerebrospinal fluid (CSF) neopterin levels in children with neurologic diseases, and the following results were obtained: (1) CSF neopterin levels markedly increased at the acute phase of bacterial meningitis, aseptic meningitis, and encephalitis as compared with those in patients without neurologic diseased. (2) In the CSF of patients with bacterial meningitis and aseptic meningitis, neopterin levels decreased more rapidly than the total cell count and 2'5' oligoadenylate synthetase (2-5 AS) did. (3) CSF neopterin in patients with non-infectious neurologic diseases was almost equal to that in patients without neurologic diseases. (4) There was no correlation between CSF neopterin and other CSF values, such as total cell count, mononuclear cell count, protein, and 2-5 AS. These results suggest that CSF neopterin is a useful marker of inflammatory central nervous diseases.     

Increased creatine kinase brain isoenzyme concentration in cerebrospinal fluid with meningitis

CPK-BB (CK-BB) isoenzyme is an intracellular enzyme released in various neurologic conditions, including central nervous system (CNS) infections. Activity of CK-BB in cerebrospinal fluid (CSF) was determined in 80 children by electrophoresis and densitometry. The possible correlation between CNS infection and CK concentrations was assessed. Significantly elevated concentrations of CK activity (P < 0.01) in the CSF were found in children with bacterial meningitis as compared with children with either aseptic meningitis or normal CSF findings. The data suggest the possibility of utilizing CSF CK activity to differentiate between bacterial and viral meningitis in situations where a routine CSF examination is inconclusive.     

The soluble 60-kDa tumour necrosis factor receptor: no difference found between patients with relapsing-remitting multiple sclerosis and controls: increasing levels are associated with the recovery from Guillain-Barré syndrome

We determined serum and cerebrospinal fluid (CSF) levels of the soluble 60-kDa tumour necrosis factor (TNF) receptor (sTNF-R p60) in 50 patients with relapsing-remitting multiple sclerosis (MS) and in 18 patients with Guillain-Barré syndrome (GBS). Neither in serum nor in CSF samples was there a statistically significant difference between mean receptor concentrations of patients with MS (serum: 1064, SD 262 pg/ml; CSF: 555, SD 130 pg/ml), with other noninflammatory neurological diseases (serum: 1008, SD 248 pg/ml; CSF: 530, SD 112 pg/ml) and with healthy control subjects (serum: 918, SD 180 pg/ml). In order to determine disease activity, magnetic resonance imaging (MRI) of the brain was performed in all MS patients. The mean sTNF-R p60 levels of patients who showed gadolinium DTPA enhancement on MRI were not different from those without enhancement (1034, SD 274 pg/ml vs 1099, SD 248 pg/ml in serum samples and 546, SD 109 pg/ml vs 565, SD 152 pg/ml in CSF samples). In GBS, the sTNF-R p60 levels of serum and CSF samples were significantly higher than in MS and all control groups except for the group with viral meningitis (VM) (GBS: 1544, SD 834 pg/ml in serum, 882, SD 147 pg/ml in CSF; VM: 1518, SD 375 pg/ml in serum, 1131, SD 611 pg/ml in CSF; P < 0.001 for serum samples and P < 0.005 for CSF samples). Serial serum sTNF-R p60 measurements in 13 patients with GBS showed an increase in receptor levels parallel with the recovery from the disease (1276, SD 374 pg/ml at the time of disease onset, 1554, SD 482 pg/ml 14-24 days later and 1787, SD 525 pg/ml after 28-32 days). From our results and the conflicting data of previous studies, we could not agree with the suggestion that the assessment of sTNF-R p60 in MS patients is a useful marker for disease activity. In GBS, subsequently increasing sTNF-R p60 levels are associated with recovery from the disease. It remains to be shown whether they might represent a relevant pathogenetic factor during this stage of GBS.     

The aseptic meningitis syndrome: a complication of posterior fossa surgery

The syndrome of aseptic meningitis is characterized by spiking fever and meningismus. CSF analysis generally shows increased pleocytosis, hypoglycorrhachia, elevated protein and negative cultures. In an earlier series, 70% of children with posterior fossa operations developed the syndrome. In a new review the incidence was slightly more than 30%. The incidence of aseptic meningitis following operation for structural lesions was 44%, which was higher than the tumor group, where the meningitic syndrome was seen in 25% of the children. It is the purpose of this paper to reexamine the impact that steroids have made on the prevalence of the aseptic meningitis syndrome, and to review recent studies that have attempted to distinguish between aseptic and bacterial meningitis.     

The value of C-reactive protein for the differentiation of bacterial meningitis from viral meningitis

In order to differentiate bacterial meningitis versus viral meningitis, we have comparatively tested the efficacy of the following tests: C-reactive protein (CRP), erythrocytes sedimentation rate (ESR), fever, level of glucose in cerebro-spinal fluid (CSF), glucose in CSF/glycemia ratio, number of white blood cells in peripheric blood, percentage of neutrophils in peripheric blood, level of proteins in CSF and number of nucleated cells in CSF for a group of 49 patients, both children and adults with central nervous system infection (37 patients with bacterial meningitis and 12 with viral meningitis) hospitalised between May 1993 and July 1994 in Clinical Hospital for Infectious Diseases in Ia?i. The mean value of CRP in bacterial meningitis patients was 8.78 mg%, contrasting with the mean value of CRP = 1.92 mg% recorded in patients with viral meningitis. Ten out of 37 bacterial meningitis patients presented a CRP concentration < 1.85 mg%. All these 10 patients have already had an antibiotic treatment at the moment of the assay. One out of 12 cases of viral meningitis had a value of CRP = 3.3 mg%, all the remainder cases having values under 1.85 mg%. We recorded highly significant differences between the two patient groups for CRP (p < 0.001), ESR (p < 0.01), protein concentration in CSF (p < 0.001) and number of nucleated cells in CSF (p < 0.001). Differences recorded for fever, concentration of glucose in CSF, glucose in CSF/glycemia ratio, number of leucocytes in peripheric blood and percentage of neutrophils in peripheric blood, were not significant (p > 0.5). Data were analysed also by box-plot method which facilitates the visual appraisal of the differences recorded between the two aetiological groups. In conclusion, assays of CRP and ESR may be used as differentiation tests for bacterial meningitis versus viral meningitis, when assay is done before the antibiotic treatment, being sufficient sensitive, and easy to perform.     

Serum levels of basic fibroblast growth factor in acute myocardial infarction

As it has been reported that basic fibroblast growth factor (bFGF) is a circulating peptide and bFGF gene expression is increased after myocardial ischemia, this study was designed to investigate the serum levels of bFGF in patients with acute myocardial infarction (AMI). Using a bFGF enzyme-linked immunoassay, bFGF levels were determined in venous blood of 15 patients with AMI on admission, at 10 days, and 30 days after infarction, and of 15 age-matched healthy volunteers who were used as controls. bFGF serum levels on admission were similar to normal values (7.48 +/- 2.3 vs 8.14 +/- 2.9 pg/ml). However, they significantly increased (16.82 +/- 3.4 pg/ml; p <0.05) 10 days after the onset of AMI, and at 30 days they returned to baseline (7.07 +/- 2.9 pg/ml). The increased bFGF levels at the second week post AMI suggest that bFGF plays an important role in mediating the development of coronary collateral circulation after myocardial ischemia in humans.     

Basic fibroblast growth factor reduces lactic acid-induced neuronal injury in rat hippocampal neurons

OBJECTIVE: To evaluate the long-term effects of lactic acidosis and to examine a potential neuroprotective role of basic fibroblast growth factor (bFGF) on hippocampal neurons. DESIGN: Long-term observation in a cell-culture study. SETTING: University research laboratory. SUBJECTS: Adult, differentiated, primary rat hippocampal neurons. INTERVENTIONS: Neurons were exposed to medium acidified with 20 mM lactic acid, pH 6.2, for a 10-min period, and maintained untreated or in the presence of bFGF (500 pg/mL, 1 ng/mL, 10 ng/mL, 20 ng/mL) applied after exposure. MEASUREMENTS AND MAIN RESULTS: Viability was analyzed by a dye inclusion/enzyme activity test and morphology by phase contrast and immunofluorescence microscopy. [3H]Arachidonic acid (AA) release was measured by liquid scintillation spectrometry. All cultures appeared to be unchanged during the first days after exposure to lactic acidosis. Neurodegeneration became apparent within 3 days. Seven days after exposure, cell survival decreased to 60% in lactic acidosis-injured, untreated cultures. Morphologic damage appeared as a 50% reduction in axonal and 25% reduction in dendritic arborizations. AA release increased to four-fold enhanced levels relative to control values. bFGF (1, 20, and 10 ng/ mL) enhanced neuronal viability (p < .05), and 10 ng/mL bFGF induced a maximal increase in live cells to 80% of controls. Axonal arborizations increased to 50% and dendritic arborizations to 75% of controls after 10 ng/mL bFGF (p< .05). bFGF in a dose of 20 ng/ mL enhanced axonal branching to 40% and dendrites in number and branching to 50% of controls (p< .05). bFGF (500 pg/mL, and 1 and 10 ng/mL) decreased enhanced AA (p < .05), and 10 ng/mL bFGF maximally reduced increased AA to two-fold enhanced values relative to controls. CONCLUSIONS: In vulnerable neurons, exposure to moderate lactic acidosis induces a process of cell injury with long latency. bFGF applied postinjury reduces the delayed neurodegeneration and may have neuroprotective efficacy in new therapeutic strategies to ischemia-induced cerebral injury.     

Activation of protein phosphatase 5 by limited proteolysis or the binding of polyunsaturated fatty acids to the TPR domain

In the urine of patients with bladder cancer, levels of the angiogenio peptide basic fibroblast growth factor (bFGF) may be elevated 100-fold. To date, levels of expression of bFGF in bladder tumor tissue have not been determined, nor has the cellular source of the urinary bFGF been identified. bFGF mRNA expression was quantified using RNase protection analysis in 32 primary bladder tumors and 8 normal bladder specimens. In addition, bFGF protein expression in the tumor cytosol was determined using a Quantikine ELISA, and bFGF protein expression was localized with immunohistochemistry. bFGF mRNA expression was absent in 28 of 32 (87%) bladder cancers despite detectable expression in 7 of 8 (87%) normal bladder specimens (P = 0.0001). In only one tumor was bFGF mRNA expression higher than in normal bladder tissue. Median bFGF protein expression was also higher in the normal bladder specimens than in the superficial tumors (3800 pg/g protein versus 1140 pg/g protein; P < 0.02), but there was no statistically significant difference between protein expression in normal bladder and invasive cancers (3800 pg/g versus 3600 pg/g). Median bFGF protein expression was higher in invasive cancers than in superficial tumors (P < 0.05). Intense bFGF immunoreactivity was seen in the basal lamina of normal transitional epithelium, in normal human detrusor muscle, and in vessels within tumors. Tumor cell immunoreactivity was rare and was usually weak. Only in the tumor which strongly overexpressed bFGF mRNA and protein was cytoplasmic staining detectable in the neoplastic cells. There are two mechanisms of bFGF-induced angiogenesis in bladder cancer. Rarely, neoplastic cells synthesize bFGF but more commonly bFGF is released by degradation of epithelial basement membranes and detrusor muscle, from where it can diffuse into the tumor microenvironment and bind to blood vessels. Mechanisms of extracellular matrix degradation may be important in bladder cancer angiogenesis and progression and as such are potential therapeutic targets.     

Cytokine response in cerebrospinal fluid after birth asphyxia

Experimental studies suggest that cytokine-mediated inflammatory reactions are important in the cascade leading to hypoxic-ischemic brain injury. The purpose was to study the content of pro- and antiinflammatory cytokines in cerebrospinal fluid (CSF) of asphyxiated and control infants. Samples of CSF were obtained from 20 infants who fulfilled the criteria of birth asphyxia and from seven newborn control subjects. The concentrations of IL-1beta, IL-8, IL-10, tumor necrosis factor (TNF)-alpha, and granulocyte/monocyte colony-stimulating factor (GM-CSF) were determined with ELISA and of IL-6 using a bioassay. The concentration of IL-6 (pg/mL) was higher in asphyxiated (250, 35-543; median, interquartile range) than in control (0, 0-18) infants (p = 0.001). There was also a significant relationship between IL-6 and the degree of HIE, and between IL-6 and outcome. In addition, the content of IL-8 (pg/mL) was higher (p = 0.009) in the asphyxia group (170, 70-1440), than in the the control group (10, 0-30) and there was an association between IL-8 and degree of HIE. The levels of IL-10, TNF-alpha, GM-CSF, and IL-1beta did not differ between groups. In conclusion, the proinflammatory cytokines IL-6 and IL-8 were markedly elevated in CSF of asphyxiated infants, and the intrathecal levels of these cytokines corresponded to the degree of HIE.     

Effects of aspirin treatment on survival in non-insulin-dependent diabetic patients with coronary artery disease. Israeli Bezafibrate Infarction Prevention Study Group

We studied seizures that occur during the acute phase of aseptic and bacterial meningitis in childhood. Of the 108 children with aseptic meningitis, five had seizures (4.7%). Four patients developed them within 24 hours of the onset of the initial symptom (fever in 3 cases), and three had repeated seizures on the first day. One case had SIADH complication, but another neurologic abnormalities were not observed. On the 18 children with bacterial meningitis, three cases (16.7%) had seizure, which occurred on the second day of illness. Disturbance of consciousness and cerebral hypertension were observed in 2 cases each, and abnormal cerebral CT findings in all the three. The NSE level in the cerebrospinal fluid was elevated in 2 cases. Thus, seizures occurring in the acute phase of aseptic meningitis may reflect transient cerebral functional abnormality accompanying fever or SIADH, whereas those in bacterial meningitis may result from neural tissue damage due to encephalopathy or angitis. In aseptic and bacterial meningitis, the presence of seizures in the acute phase was not correlated with the neurological outcome.     

Inhibition of peripheral blood mononuclear cell proliferation by cardiac glycosides

We prospectively studied the epidemiologic, clinic signs and outcome of bacterial meningitis in 125 children who were admitted into a PICU (Pediatric Intensive Care Unit) of 11 hospitals of Spain and whose meningitis was diagnosed between May 1994 and April 1995. RESULTS: The median age of the children was 3.55 +/- 3.32 years (range 1 month to 16.5 yrs). Eighty-eight were bacterial meningitis, probably bacterial 30 and aseptic 7. The most frequently isolated organisms were N. meningitidis (52), H. influenza type b (17) and S. pneumoniae (8). Twenty-five percent of N. meningitidis had C serotype. Incidence rate of each germen was depending of age. All patients diagnosed of H. influenza type b meningitis were less than 3 years old. H. influenza type b and meningococcus had similar incidence rate during the first year of life (27% versus 31%). During the first three years of life H. influenza type b produced one third of bacterial meningitis. A mortality rate of 5.6% (seven patients: 3 S. pneumoniae, 1 N. meningitidis, 1 H. influenza type b and 2 unknown germen) was observed. Patients who die had lower Glasgow coma score (p = 0.034) and seizures (p = 0.001) at admission. At discharge of PICU, 9 survivors (7.2%) had sequelae: mental retardation in 7 patients and hearing loss in two. One third of patients needed hemodynamic support and a 15% of them ventilatory support. CONCLUSIONS: Age is an important epidemiological factor in the etiology of pediatric acute meningitis. H. influenza type b and N. meningitidis had similar incidence rate during the first year of life. S. pneumoniae had the highest mortality rate (37.5%). The presence of coma and seizures at admission were associated with mortality.     

Experimental reproduction of a spiking mortality syndrome of turkeys

We measured the levels of interleukin-6 (IL-6), albumin, C-reactive protein (CRP) and alpha 2 macroglobulin (alpha 2M), all of which have different spectrums of molecular weight, in the cerebrospinal fluid (CSF) and serum in 121 patients to evaluate damage to the blood-cerebrospinal fluid barrier (BCB) in meningitis. There was an extraordinary high level of IL-6 in the CSF when patients had bacterial or viral meningitis, but the level returned to a normal range within a week in almost all of these cases. There were no significant differences in CSF albumin levels among the different disease groups. The CRP level in CSF is considered to correlate with the serum level, and CSF CRP was higher in bacterial meningitis than in viral meningitis, however, CRP in CSF was increased in some of the infectious diseases without meningitis. The alpha 2M in CSF, which tends to be at extraordinarily high levels when there is damage to the BCB, correlated highly with CSF cell counts. CSF IL-6 seemed to be a useful indicator to identify the acute active phase of meningitis. CRP and alpha 2M in CSF are considered to be useful to differentiate bacterial meningitis, bacterial infection without meningitis and viral meningitis. Extraordinarily high levels of alpha 2M, which has a high molecular weight, in CSF is indicative of BCB damage.     

Elevated levels of basic fibroblast growth factor in patients with limb ischemia

Basic fibroblast growth factor (bFGF), a prototypic member of a family of heparin-binding growth factors, is angiogenic both in vitro and in vivo. Increased levels and activity of bFGF have been documented in a variety of diseases, including tumors. We sought to determine whether bFGF might be similarly elevated in patients with clinical evidence of limb ischemia. Serum was obtained at the time of percutaneous revascularization from patients with symptomatic peripheral vascular disease (46 procedures were performed on 40 patients). An enzyme-linked immunoassay specific for bFGF was used (limit of detection, 1 pg/ml; range in normal subjects, 0 to 5 pg/ml). Among the 40 patients (28 men, 12 women, mean age 70 years) studied, elevated circulating bFGF (> or = 10 pg/ml) was detected in 36 samples (78%); levels ranged from 10 to 310 pg/ml (mean +/- SEM = 62 +/- 12). In 16 (89%) of 18 patients with both rest pain and nonhealing ischemic ulcers, serum bFGF levels were elevated up to 30 times normal values. In conclusion, circulating levels of bFGF are elevated in patients with vascular insufficiency and may reflect a physiologic response to limb ischemia.     

Diagnostic value of atypical lymphocytes in cerebrospinal fluid from adults with enteroviral meningitis

We have noted two morphologically distinct types of atypical lymphocytes (AL) in the cerebrospinal fluid (CSF) of adult patients with meningitis: one, which we designate type-I AL, with multilobulated nuclei resembling those of the abnormal cells in adult T-cell leukaemia (ATL); and another, type-II AL, characterized by large lymphocytes with basophilic cytoplasm and nuclei containing coarse chromatin. Type-I AL were detected in 25 of 39 patients (64%) with enteroviral and in 11 of 109 (11%) with aseptic meningitis presumed to be caused by other viruses, but not in meningitis resulting from Cryptococcus neofirmans (n = 14), Mycobacterium tuberculosis (n = 19) or acute bacterial infection (n = 49). Type-I AL were not seen in herpes zoster (n = 15) aseptic meningeal reactions (n = 15), or in leptomeningeal carcinomatosis (n = 14). Type-II AL were often present in meningitis of various aetiologies and in aseptic meningeal reactions, but not in leptomeningeal carcinomatosis. The presence of type-I AL in the CSF was found to be indicative of enteroviral meningitis with the highest predictive value (69%), while type-II AL had a lower diagnostic positive predictive value in meningitis of the five aetiologies above. Type-I AL immunostained for CD4, while type-II AL were stained for CD8. The presence of type-I AL in CSF strongly suggests enteroviral meningitis, which warrants careful follow-up without antifungal, antituberculous or antibacterial agents. However, type-I AL, which are likely to be virally transformed lymphocytes, must be distinguished from ATL cells, which frequently involve the meninges.     

Evaluation of intracranial cysts by intraoperative MR

Eleven patients with intracranial cystic collections were evaluated in the open-bore intraoperative MR system. In each case, the cystic collection or the surrounding cerebrospinal fluid (CSF) space was injected with .02 to .5 cc of .5 mol/l gadopentetate dimeglumine. Serial imaging was performed using T1-weighted imaging. In seven patients, free communication was demonstrated between the cystic collection and the surrounding CSF spaces. In four cases, the cyst did not communicate with the CSF; two of these were drained in the intraoperative MR system with reduction in symptoms. One patient developed an aseptic meningitis 10 days after the study, which was successfully treated with steroids; no other complications were noted. We conclude that the communication of intracranial cystic collections with the cisterns and ventricles can be safely and effectively elucidated with gadolinium injection in the intraoperative MR system.     

Decreased melatonin levels in postmortem cerebrospinal fluid in relation to aging, Alzheimer's disease, and apolipoprotein E-epsilon4/4 genotype

Sleep disruption, nightly restlessness, sundowning, and other circadian disturbances are frequently seen in Alzheimer's disease (AD) patients. Changes in the suprachiasmatic nucleus and pineal gland are thought to be the biological basis for these behavioral disturbances. Melatonin is the main endocrine message for circadian rhythmicity from the pineal. To determine whether melatonin production was affected in AD, melatonin levels were determined in the cerebrospinal fluid (CSF) of 85 patients with AD (mean age, 75 +/- 1.1 yr) and in 82 age-matched controls (mean age, 76 +/- 1.4 yr). Ventricular postmortem CSF was collected from clinically and neuropathologically well defined AD patients and from control subjects without primary neurological or psychiatric disease. In old control subjects (>80 yr of age), CSF melatonin levels were half of those in control subjects of 41-80 yr of age [176 +/- 58 (n = 29) and 330 +/- 66 (n = 53) pg/mL, respectively; P = 0.016]. We did not find a diurnal rhythm in CSF melatonin levels in control subjects. In AD patients the CSF melatonin levels were only one fifth (55 +/- 7 pg/mL) of those in control subjects (273 +/- 47 pg/mL; P = 0.0001). There was no difference in the CSF melatonin levels between the presenile (42 +/- 11 pg/mL; n = 21) and the senile (59 +/- 8 pg/mL; n = 64; P = 0.35) AD patients. The melatonin level in AD patients expressing apolipoprotein E-epsilon3/4 (71 +/- 11 pg/mL) was significantly higher than that in patients expressing apolipoprotein E-epsilon4/4 (32 +/- 8 pg/ml; P = 0.02). In the AD patients no significant correlation was observed between age of onset or duration of AD and CSF melatonin levels. In the present study, a dramatic decrease in the CSF melatonin levels was found in old control subjects and even more so in AD patients. Whether supplementation of melatonin may indeed improve behavioral disturbances in AD patients should be investigated.     

The biologic activities of peptidoglycan in experimental Haemophilus influenzae meningitis

While gram-positive bacterial cell walls are known to incite inflammation, the contribution of gram-negative peptidoglycan to disease has not been characterized. The ability of cell wall, purified peptidoglycan, and soluble peptidoglycan subcomponents from Haemophilus influenzae to provoke inflammation was determined in a rabbit model of meningitis. Haemophilus peptidoglycan, with or without associated proteins, produced brain edema at > or = 0.1 micrograms/mL of cerebrospinal fluid (CSF); leukocytosis and protein accumulation in CSF occurred only at > or = 10.0 micrograms/mL of CSF. Solubilized peptidoglycan was 10-fold more active than intact cell wall. The bioactivity of peptidoglycan from ampicillin-resistant H. influenzae was at least twofold greater than that of ampicillin-sensitive strains. Consistent with these pathologic effects of purified peptidoglycan, ampicillin-induced bacterial lysates in which endotoxin was neutralized induced brain edema and protein influx but little leukocytosis. Thus, peptidoglycan seems to contribute to the pathology of gram-negative meningitis, particularly brain edema.     

PGG-Glucan activates NF-kappaB-like and NF-IL-6-like transcription factor complexes in a murine monocytic cell line

Basic fibroblast growth factor (bFGF) and FGF receptors have been localized to photoreceptors and retinal pigmented epithelium (RPE), but the function of bFGF in adult retina and RPE is unknown. Exogenous bFGF has a neuroprotective effect in retina and brain and its expression is increased in some neurons in response to cytokines or stress. In this study, we investigated the effect of light, other types of stress, neurotrophic factors, and cytokines on bFGF levels in cultured human RPE. Some agents that protect photoreceptors from the damaging effects of constant light, including brainderived neurotrophic factor (BDNF), ciliary neurotrophic factor, and interleukin-1 beta, increase bFGF mRNA levels in RPE cells. Intense light and exposure to oxidizing agents also increase bFGF mRNA levels in RPE cells and cycloheximide blocks the increase. An increase in bFGF protein levels was demonstrated by ELISA in RPE cell supernatants after incubation with BDNF or exposure to intense light or oxidizing agents. These data indicate that bFGF is modulated in RPE cells by stress and by agents that provide protection from stress and support the hypothesis that bFGF functions as a survival factor in the outer retina.     

Trimethoprim-sulphamethoxazole-induced meningitis

Drug-induced meningitis is rarely included in the differential diagnosis of aseptic (usually recurrent) meningitis. A 74-year-old man who suffered from recurrent aseptic meningitis following re-exposures to trimethoprim-sulphamethoxazole (Resprim) is presented. The clinical and laboratory findings resembled those found in bacterial meningitis, excluding normal glycorrachia. Extensive microbiological, serologic and imaging studies did not disclose any relevant findings. All symptoms and signs resolved rapidly following drug withdrawal, and findings on follow-up lumbar puncture were normal.