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PubMed1985

Selective destruction of meningeal cells by 6-hydroxydopamine: a tool to study meningeal-neuroepithelial interaction in brain development.

The effects of 6-hydroxydopamine (6-OHDA) on meningeal cells were studied at different ages in conjunction with blockade of the neuronal uptake 1 for catecholamines using nomifensine (NMF) and of the extraneuronal uptake 2 using normetanephrine (NMN). Our results show that maximal numbers of meningeal cells over the cerebellum of the newborn rat are destroyed by a threshold dose of 6-OHDA of 25 micrograms. The morphological characteristics which mark the time course of degeneration of meningeal cells were used to assess the effects of 6-OHDA given in conjunction with either NMF or NMN to differentiate between neuronal (uptake 1) and extraneuronal (uptake 2) effects of 6-OHDA. Uptake of 6-OHDA into meningeal cells and their subsequent degeneration was prevented by pretreatment with NMN but not with NMF. This finding indicates that meningeal cells have uptake 2 capacity but no uptake 1 membrane pump and explains both their uptake of 6-OHDA and their extreme sensitivity to the toxic effects of this drug. Application of this pharmacological regimen using NMF and NMN in conjunction with 6-OHDA thus allows selective destruction of meningeal cells which may be used experimentally to study the contribution of meningeal cells to brain development.

Animals↗
PubMed1985

Meningeal cells are involved in foliation, lamination, and neurogenesis of the cerebellum: evidence from 6-hydroxydopamine-induced destruction of meningeal cells.

In the present paper we report on experiments conducted to find out if there is a positive correlation between the destruction of meningeal cells over the newborn rat cerebellum by 6-hydroxydopamine (6-OHDA) and the subsequent development of abnormalities in cerebellar fissuration, lamination, and granule cell number. Both destruction of meningeal cells and quality and magnitude of 6-OHDA-induced cerebellar defects show the same threshold sensitivity without further dose responsiveness. Blockade of neuronal uptake 1 for catecholamines with nomifensine prevents neither destruction of meningeal cells nor the development of abnormalities in cerebellar structure after 6-OHDA treatment. Blockade of extraneuronal uptake 2 for catecholamines with normetanephrine prevents both destruction of meningeal cells and the development of typical cerebellar abnormalities after 6-OHDA treatment. All three parallel experiments suggest that there is a positive correlation between the destruction of meningeal cells and the development of abnormal cerebellar structure, indicating that meningeal cells are involved in these defective morphogenetic processes, i.e., fissuration, lamination, and cell proliferation in the external granular layer. The preferential localization of defects in cerebellar fissures indicates that, in analogy to the mesenchyme surrounding other epithelia with a branching morphogenesis, the role of meningeal cells could be the production of interstitial collagen which is necessary to stabilize the epithelial basal lamina in the fissures.

Animals↗
PubMed2026

How Do Climatic Factors Directly Influence the Incidence and Risk of Meningococcal Meningitis Across the African Meningitis Belt? A Narrative Literature Review.

Globally, the highest incidence of meningococcal meningitis occurs within the African meningitis belt, spanning 26 countries across sub-Saharan Africa. Meningococcal meningitis incidence is highly seasonal in this region specifically, with outbreaks mostly occurring during the dry season, characterized by low rainfall and atmospheric humidity, high temperature, and increased dust and wind speed. The strong seasonality of meningococcal outbreaks coincides with seasonal variation in climatic factors. This multicollinearity can make it difficult to identify environmental drivers of disease and the mechanisms by which they operate. This review aims to collate existing evidence to better clarify the mechanisms by which climatic variables influence meningococcal meningitis incidence. We examined the impact of dust, wind speed, temperature, rainfall, and land cover on meningococcal meningitis outbreaks. Within the literature, atmospheric dust and wind speed had the strongest statistical association with meningococcal outbreaks and demonstrated greater predictive probability than other climatic variables. However, several climatic factors have demonstrable influences on one another, reflected in the seasonality of meningococcal meningitis. Atmospheric dust can reduce precipitation levels in part through its radiative properties. Decreased rainfall and increasing temperatures can dry out soil, increasing its availability to be uplifted as dust. Alongside, this lower atmospheric humidity increases evaporative demand, leading to faster soil moisture loss and enhanced surface drying. We argue that rainfall, temperature, and land cover variability may act as part of a broader climatic mechanism, increasing atmospheric dust. This increases the incidence and risk of meningococcal meningitis.

Africa↗
PubMed2002

Recurrent herpes simplex virus type 2 meningitis: a case report of Mollaret's meningitis.

It is well known that herpes simplex virus (HSV) type 2 produces acute meningitis, while HSV type 2 rarely causes recurrent meningitis (Mollaret's meningitis). We report the history of a 40-year-old patient with recurrent HSV type 2 meningitis (Mollaret's meningitis). The patient had seven episodes of meningeal symptoms within a 7-year period. In the seventh episode, HSV type 2 DNA was confirmed by nested polymerase chain reaction (PCR) with the cerebrospinal fluid (CSF). A real-time quantitative PCR study of the first CSF sample detected 2,000 copies of the HSV genome, which rapidly disappeared following treatment with acyclovir. The present case may be the first case of HSV type 2 Mollaret's meningitis to be documented in Japan. In our case, HSV serum antibody titers were at low levels during the whole course of the disease. The possible pathophysiology of this case is discussed.

Acyclovir↗
PubMedDate not supplied

[Fatality rates of bacterial meningitis from current health databases suggest a different case definition. Results of a follow-up study of bacterial meningitis in Lazio Region, Italy, 1996-2000].

OBJECTIVES: To describe mortality and case fatality rate due to bacterial meningitis in the Lazio Region from 1996 to 2000, and to compare these estimates with those from Cause-of-death Registry (CDR) and Hospital Discharge Registry (HDR). METHODS: A follow-up study of mortality was conducted through Registry Offices for bacterial meningitis cases reported to surveillance in 1996-2000 among residents in the Lazio Region. Death due to bacterial meningitis was defined as a patient who died during a hospitalization for meningitis or who died within 30 days after hospitalization and whose underlying cause of death was bacterial meningitis (ICD-9: 036.0, 036.1, 036.2,320.0, 320.1, 320.2, 320.3, 320.7, 320.8, 320.9, 027.0). Case fatality rates estimated from follow-up study were compared with estimates from CDR and HDR of the same period. RESULTS: 525 bacterial meningitis cases were reported among residents in the whole period; 98 deaths were detected with a case fatality rate (CFR) of 18.7% (CI 95% 15.4-22.5); estimates were higher in patients 64+ year old (44.6%; CI 95% 33.7-55.9) and in meningitis due to Streptococcus pneumoniae (27.5%; CI 95% 20.3-35.6) or Listeria (32.0%; CI 95% 14.9-53.5). The CFR was 10.1% according to the CDR and 10.9% according to the HDR. CONCLUSIONS: CFRs differ according to the database used. Differences may be partially due to a selective lower sensitivity in reporting deceased cases, but the most important factor seems to be the case definition used in follow-up study and other sources of data.

Adolescent↗
PubMed1982

[The passage of mezlocillin into the cerebrospinal fluid. An experimental study in dogs with normal meninges and with Staphylococcus aureus meningitis (author's transl)].

The passage of mezlocillin into the CSF was investigated in normal dogs and in dogs with experimentally induced Staphylococcus aureus meningitis. The areas under the curves (AUC) of mezlocillin concentrations in blood and CSF were compared. The antibiotic was administered by slow (1 hour) intravenous infusion in doses of 100, 200 and 400 mg/kg bodyweight. Samples of blood and CSF were collected simultaneously 30, 40, 60, 75, 90, 105, 120, 180 and 240 minutes after the infusion. The penetration of mezlocillin into the CSF of dogs with non-inflamed meninges was poor (peak less than or equal to 2 micrograms/ml, CSF/serum AUC ratio : 0.9 %), but it was very substantial in dogs with meningitis. After the 200 mg/kg dose, the mean CSF peak was 43 micrograms/ml (range : 33-60 micrograms/ml) and the CSF/serum AUC ratio was 26.6 %. Similar experiments were performed with other beta-lactam antibiotics. In dogs with healthy meninges the CSF/serum AUC ratios were 0.52 % with amoxycillin, 0.75 % with cefuroxime, 1.05 % with cefamandole, 1.18 % with cefoxitin and 3.6 % with cefotaxime. In dogs with meningitis, the corresponding ratios were 16.3 % with cefotaxime, 17.4 % with cefamandole, 18.5 % with cefoxitin, 18.6 % with amoxycillin and 18.7 % with cefuroxime. These results suggest that cefotaxime penetrates best across normal meninges and mezlocillin across inflamed meninges.

Animals↗
PubMed1994

Chronic meningitis: the role of meningeal or cortical biopsy.

Meningeal and cortical biopsies were evaluated in 37 patients (25 men and 12 women; mean age, 54 yr) who had chronic meningitis of an unknown cause between 1985 and 1993 (the era of magnetic resonance imaging). Magnetic resonance imaging with gadolinium contrast was the most useful diagnostic imaging technique, demonstrating meningeal enhancement in 15 of 32 patients (47%). Only 2 of 32 (6%) computed tomographic scans revealed enhancement. A definitive diagnosis was made in 16 of 41 biopsies (39%), but in cases where enhancement was present on either magnetic resonance imaging or computed tomography, a diagnosis was obtained in 80% (12 of 15 cases). Only 2 of 22 biopsies (9%) from nonenhancing regions were diagnostic. Although the locations of enhancement were distributed evenly, biopsies through suboccipital and pterional craniotomies gave the highest diagnostic yields (50%). Furthermore, if the biopsies were obtained from enhancing regions, the yield of these two approaches increased to 84 and 100%, respectively. Of 18 cases in which biopsy samples were taken from both the meninges and cortex, only 1 had cortical involvement alone. The meninges were therefore diagnostic in 15 of the 16 definitive diagnostic cases (94%). Second biopsies were necessary in four cases, of which the three biopsies from enhancing regions were diagnostic. The most frequent causes of chronic meningitis were sarcoid (31%) and metastatic adenocarcinoma (25%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Bacterial meningitis in the United States, 1978 through 1981. The National Bacterial Meningitis Surveillance Study.

From 1977 to 1981, 18,642 cases of bacterial meningitis were reported to the Centers for Disease Control. We analyzed data from 27 states with full participation from 1978 through 1981. Hemophilus influenzae was the most frequent cause of bacterial meningitis (48.3%), followed by Neisseria meningitidis (19.6%) and Streptococcus pneumoniae (13.3%). Overall attack rates for males were greater than for females (3.3 v 2.6 cases per 10(5) population per year). Attack rates were highest in children under 1 year of age (76.7 per 10(5) population per year). Case-fatality ratios were highest for gram-negative and miscellaneous causes of bacterial meningitis (33.7%) and lowest for meningitis caused by H influenzae (6.0%). Neisseria meningitidis and S pneumonia meningitis occurred preponderantly during the winter, while H influenzae meningitis had peak activity in the spring and fall. Ampicillin resistance among H influenzae increased from 18.7% in 1978, to 23.9% in 1981. Serogroup B Neisseria meningitidis was the most common serogroup identified during the reporting period (51.1%), followed by serogroup C (22.3%), serogroup Y (5.8%), and serogroup A (4.7%) infections.

Adolescent↗
PubMed2000

Polysaccharide vaccines for preventing serogroup A meningococcal meningitis.

BACKGROUND: Controlled trials over two decades ago showed that the polysaccharide vaccine prevented meningococcal meningitis. Subsequent observational studies suggested variations in the level and duration of protection, particularly among young children. OBJECTIVES: To determine the effect of polysaccharide serogroup A vaccine for preventing serogroup A meningococcal meningitis. SEARCH STRATEGY: MEDLINE and the Cochrane Controlled Trials Register. SELECTION CRITERIA: Randomised and other prospective controlled trials. DATA COLLECTION AND ANALYSIS: One reviewer collected data and assessed the methodologic quality of the trials. Data were pooled using the Exact method to assess vaccine efficacy at one, two and three years post-vaccination. MAIN RESULTS: The protective effect within the first year was consistent across all eight trials, including one with participants exclusively under six years of age (in Finland); overall vaccine efficacy was 95% (Exact 95% CI 87%, 99%). The Finnish trial lacked statistical power to assess the effect of a booster dose given to children less than 18 months old. In the three other trials that included children less than six years old (one in Sudan and two in Nigeria), none of the vaccinated children developed meningitis, but the statistical significance of this finding was undetermined. Protection extended into the second (in two studies) and third (in one study) years after vaccination, but these results were also not statistically significant. REVIEWER'S CONCLUSIONS: When compared with current recommendations, the methodological quality and relative incompleteness of the published reports could arguably render the trials invalid for this review. However, it was unlikely that the results of the trials in such diverse settings would have been biased towards a strong and consistent protective effect. Immunogenicity trials were not included in this review. Stage two of the review will assess the vaccine effect from observational studies.

Humans↗
PubMed2003

Clinical data and cerebrospinal fluid findings in Lyme meningitis versus aseptic meningitis.

The purpose of this study was to characterise Lyme meningitis (LM) in a Belgian paediatric population and to suggest findings that could allow early distinction from aseptic meningitis (AM). The medical records of patients hospitalised between 1993 and 2000 and with a discharge diagnosis of LM (n=14) or AM (n=16) were retrospectively reviewed. The Kruskal-Wallis test was used to compare data. Of the patients, 16 were identified with AM and 14 with LM, amongst which 7 presented with isolated LM and 7 with associated peripheral facial palsy (PFP). Patients with AM, when compared with LM, complained of more pronounced signs and symptoms of meningitis (fever, headaches, and neck stiffness); they statistically displayed a shorter period of symptoms before admission (1.6 vs 15 days), higher neutrophilic component (mean 56% vs 2.4%), and lower protein levels (mean 0.39 vs 1.12 g/l) on cerebrospinal fluid analysis. In the neuroborreliosis group, the duration of symptoms was shorter and the cerebrospinal protein level was lower in cases of LM associated with PFP compared to isolated LM (mean 1.3 vs 15 days; mean 0.55 g/l vs 1.12 g/l). Conclusions. Our results suggest that some clinical data and laboratory findings may help the physician to diagnose aseptic or Lyme meningitis before completion of serologic testing. LM should be suspected in cases of meningitis with very low CSF neutrophilic counts and high protein levels associated with prolonged duration of symptoms, low grade fever, and absence of pronounced signs of meningitis.

Adolescent↗
PubMed1982

Bacterial meningitis without clinical signs of meningeal irritation.

A clinical diagnosis of meningitis in neonates is difficult because of paucity of physical findings. In older infants and children, nuchal rigidity, Kernig's or Brudzinski's sign, or bulging fontanelles are sought. A review of 1,064 cases of bacterial meningitis beyond the neonatal period revealed that 16 (1.5%) patients had none of those meningeal signs during the entire hospitalization, despite CSF pleocytosis. Eight patients (50%) were 2 years old or older. Lumbar punctures were done because of unexplained fever, changes in behavior or mental status,, seizures, or occurrence of skin petechiae in febrile patients. These patients frequently had moderate pleocytosis and all survived. The meningitis was caused by Neisseria meningitidis in seven patients, Haemophilus influenzae in six, Streptococcus pneumoniae in two, and Salmonella enteritidis in one patient. CSF should be examined in a patient of any age whenever meningitis is a consideration, even if patients lack meningeal signs.

Child↗
PubMed2000

Neurotrophin-3 levels in cerebrospinal fluid from children with bacterial meningitis, viral meningitis, or encephalitis.

Neurotrophin-3 levels were measured in the cerebrospinal fluid of 35 patients with bacterial meningitis, viral meningitis, or encephalitis by two-site enzyme immunoassay. Elevated cerebrospinal fluid levels of neurotrophin-3 were demonstrated in 8 of 18 patients with bacterial meningitis. Follow-up examination of the eight patients at the convalescent stage showed diminished cerebrospinal fluid levels of neurotrophin-3. In contrast, none of the 17 patients with viral meningitis or encephalitis showed an elevation of neurotrophin-3 levels in cerebrospinal fluid. No relationships were observed between neurotrophin-3 levels and cerebrospinal fluid cell numbers, cerebrospinal fluid protein levels, serum C-reactive protein concentrations, or outcome in bacterial meningitis. Since neurotrophin-3 is involved in the survival of neurons and the modulation of the immune system, neurotrophin-3 could play a neuroprotective or immunomodulatory role in bacterial meningitis.

Adolescent↗
PubMed1991

[Recurrent aseptic meningitis in periodic disease or Mollaret's meningitis?].

A 33 year-old Sephardic Jewish man with familial mediterranean fever (FMF), presented during a 7 year period, 6 episodes of aseptic meningitis, improving within less than 24 h after spinal tap. Cerebrospinal fluid analysis showed a mixed leucocytic pleocytosis ranging from 100 to 1,000 cell/mm3. Spinal fluid cultures for bacteria, viruses and viral antibodies were always negative. Our case supports other reports showing that recurrent aseptic meningitis, although rare, may occur in FMF. It usually responds to treatment with colchicine, like other manifestations of the disease. FMF meningitis has been compared to Mollaret's meningitis whose cause is undetermined. However, Mollaret's meningitis, unlike FMF, is sporadic and ubiquitous, is not transmitted genetically and affects men and women equally. Moreover, in Mollaret's meningitis transient neurological abnormalities, such as signs of encephalitis have often been reported: polyserositis or associated amylosis are absent, there is no biological inflammatory syndrome, and in 65% of the patients the CSF contains specific large mononuclear-derived cells called endothelial cells. Such abnormalities have not been described in FMF.

Adult↗
PubMed1990

Bacterial meningitis in the United States, 1986: report of a multistate surveillance study. The Bacterial Meningitis Study Group.

A prospective, laboratory-based surveillance project obtained accurate data on meningitis in a population of 34 million people during 1986. Haemophilus influenzae was the most common cause of bacterial meningitis (45%), followed by Streptococcus pneumoniae (18%), and Neisseria meningitidis (14%). Rates of H. influenzae meningitis varied significantly by region, from 1.9/100,000 in New Jersey to 4.0/100,000 in Washington state. The overall case fatality rates for meningitis were lower than those reported in several studies from the early 1970s, suggesting that improvements in early detection and antibiotic treatment may have occurred since that time. Concurrent surveillance was also performed for all invasive disease due to the five most common causes of bacterial meningitis. Serotypes of group B streptococcus other than type III caused more than half of neonatal group B streptococcal disease and mortality, suggesting that an optimal vaccine preparation must be multivalent. Of the organisms evaluated, group B streptococcus was the second most common cause of invasive disease in persons greater than 5 years old.

Adolescent↗
PubMed1999

[Meningitis (II)--acute bacterial meningitis].

Acute meningitis is a medical emergency, particularly in patients with rapidly progressing disease, mental status changes or neurological deficits. The majority of cases of bacterial meningitis are caused by a limited number of species, i.e. Streptococcus pneumoniae, Neisseria meningitis, Listeria monocytogenes, group B Streptococci (Streptococcus agalactiae), Haemophilus influenzae and Enterobacteriaceae. Many other pathogens can occasionally cause bacterial meningitis, often under special clinical circumstances. Treatment of meningitis includes two main goals: Eradication of the infecting organism, and management of CNS and systemic complications. Empiric therapy should be initiated without delay, as the prognosis of the disease depends on the time when therapy is started. One or two blood cultures should be obtained before administering the first antibiotic. Empiric therapy is primarily based on the age of the patient, with modifications if there are positive findings on CSF gram stain or if the patient presents with special risk factors. It is safer to choose regimens with broad coverage, as they can usually be modified within 24-48 hours, when antibiotic sensitivities of the infecting organism become available. Adjunctive therapy with dexamethasone is also administered in severely ill patients concomitantly with the first antibiotic dose. In patients who are clinically stable and are unlikely to be adversely affected if antibiotics are not administered immediately, including those with suspected viral or chronic meningitis, a lumbar puncture represents the first step, unless there is clinical suspicion of an intracerebral mass lesion. Findings in the CSF and on CT scan, if performed, will guide the further diagnostic work-up and therapy in all patients.

Acute Disease↗
PubMed1990

Pentoxifylline modulates meningeal inflammation in experimental bacterial meningitis.

Pentoxifylline has been shown to decrease endotoxin-induced tumor necrosis factor alpha production and reverse the inflammatory actions of interleukin-1 (IL-1) and tumor necrosis factor on leukocyte function. Because of the potential role of this cytokine-leukocyte interaction in the pathogenesis of bacterial meningitis, we investigated the ability of pentoxifylline to modulate meningeal inflammation in the rabbit meningitis model. Pentoxifylline treatment (initially an intravenous injection of 20 mg/kg followed by 6 mg/kg per h) started 20 min before intracisternal injection of 20 ng of Haemophilus influenzae type b lipooligosaccharide (endotoxin) reduced significantly concentrations in cerebrospinal fluid of leukocytes (P less than 0.0001), protein (P less than 0.001), and lactate (P less than 0.001) during the 9-h infusion compared with values in intravenous-saline-treated rabbits. When pentoxifylline was given 1 h after H. influenzae type b endotoxin, the mean peak lactate and leukocyte concentrations in cerebrospinal fluid were significantly lower than those in control animals. Pentoxifylline also significantly decreased lactate and protein concentrations (P less than 0.05) and tended to diminish leukocyte counts (P = 0.08) compared with results in control animals after antibiotic-induced release of endotoxin in animals with H. influenzae meningitis. In this regard, dexamethasone was superior to pentoxifylline and no synergism was observed when the drugs were combined. Additionally, pentoxifylline attenuated meningeal inflammatory changes induced by intracisternal inoculation of 10 ng of rabbit recombinant IL-1 beta compared with results in either dexamethasone- or saline-treated animals. We conclude that pentoxifylline is effective in this animal model in modulating the meningeal inflammatory response following intracisternal inoculation of H. influenzae type b endotoxin or organisms or rabbit recombinant IL-1beta.

Animals↗
PubMed1991

Enhanced attenuation of meningeal inflammation and brain edema by concomitant administration of anti-CD18 monoclonal antibodies and dexamethasone in experimental Haemophilus meningitis.

Antiinflammatory therapy has been shown to reduce the adverse pathophysiological consequences that occur in bacterial meningitis and to improve outcome from disease. In the present study, modulation of two principal steps of the meningeal inflammatory cascade was accomplished by concomitant administration of dexamethasone to diminish overproduction of cytokines in response to a bacterial stimulus and of a monoclonal antibody directed against adhesion-promoting receptors on leukocytes to inhibit recruitment of white blood cells into the subarachnoid space. Dexamethasone and antibody therapy produced a marked attenuation of all indices of meningeal inflammation and reduction of brain water accumulation after H. influenzae-induced meningitis in rabbits compared with results of each agent given alone and of untreated animals. In addition, the enhanced host's meningeal inflammatory reaction that follows antibiotic-induced bacterial lysis was profoundly ameliorated when dual therapy was administered without affecting clearance rates of bacteria from cerebrospinal fluid and vascular compartments. The combination of both therapeutic approaches may offer a promising mode of treatment to improve further the outcome from bacterial meningitis.

Animals↗
PubMed2006

Influence of the blood bacterial load on the meningeal inflammatory response in Streptococcus pneumoniae meningitis.

BACKGROUND: Despite bacteraemia is present in the majority of patients with pneumococcal, little is known about the influence of the systemic infection on the meningeal inflammatory response. METHODS: To explore the role of systemic infection on the meningeal inflammation, experimental meningitis was induced by intracisternal injection of approximately 1 x 10(6) CFU Streptococcus pneumoniae, type 3, and the 26 rabbits were either provided with approximately 1 x 10(6) CFU S. pneumoniae intravenously at 0 hour ("bacteraemic" rabbits, n = 9), immunized with paraformaldehyde-killed S. pneumoniae for 5 weeks prior to the experiment ("immunized" rabbits", n = 8), or not treated further ("control" rabbits, n = 9). WBC and bacterial concentrations were determined in CSF and blood every second hour during a 16 hours study period together with CSF IL-8 and protein levels. We also studied CSF and blood WBC levels in 153 pneumococcal meningitis patients with and without presence of bacteraemia. RESULTS: As designed, blood bacterial concentrations were significantly different among three experimental groups during the 16 hours study period (Kruskal Wallis test, P < 0.05), whereas no differences in CSF bacterial levels were observed (P > 0.05). Blood WBC decreased in bacteraemic rabbits between approximately 10-16 hours after the bacterial inoculation in contrast to an increase for both the immunized rabbits and controls (P < 0.05). The CSF pleocytosis was attenuated in bacteraemic rabbits as compared to the two other groups between 12-16 hours from time of infection (P < 0.017), despite accelerated CSF IL-8 levels in bacteraemic rabbits. In patients with pneumococcal meningitis, no significant difference in CSF WBC was observed between patients with or without bacteraemia at admission (n = 103, 1740 cells/microL (123-4032) vs. n = 50, 1961 cells/microL (673-5182), respectively, P = 0.18), but there was a significant correlation between CSF and blood WBC (n = 127, Spearman rho = 0.234, P = 0.008). CONCLUSION: Our results suggest that a decrease in peripheral WBC induced by enhanced bacteraemia in pneumococcal meningitis results in an attenuated CSF pleocytosis.

Animals↗