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At least 19 recordsLinked to original sources
PubMed2005

Treatment and prevention strategies to combat pediatric pneumococcal meningitis.

Pneumococcal meningitis is a severe, life-threatening infection of the nervous system affecting infants, children and adults alike. The incidence of pneumococcal meningitis in infants and children less than 2 years of age in Europe is approximately 10 out of 100,000 per year, rising to approximately 148 out of 100,000 per year in Gambian infants. The use of highly sensitive tests such as PCR may increase the likelihood of detecting the infection by 20% or more. Epidemics of serotype 1 pneumococcal meningitis in northern Ghana, have had many of the characteristics of meningococcal meningitis epidemics. Neurologic sequelae may occur in 28-63% of cases, and serotype 3 is associated with a 2.54 relative risk of death. The pathogenic process can be divided into invasion, inflammatory pathways, bacterial toxicity and damage; pneumolysin being particularly associated with apoptosis. In the future, neuroprotection may be achieved, targeting this process at all these levels. Therapeutic guidelines have been published by the Infectious Diseases Society of America. Standard empiric therapy, in those aged greater than or equal to 1 month, is a third-generation cephalosporin plus vancomycin. There is insufficient evidence relating to the use or otherwise of corticosteroids in pneumococcal meningitis to make a firm recommendation. The advent of a pneumococcal conjugate vaccine is the most powerful tool available for the prevention of pneumococcal meningitis in all parts of the world.

Anti-Bacterial Agents↗
PubMed2000

Induced hypothermia in experimental pneumococcal meningitis.

Pneumococcal meningitis resulting from Streptococcus pneumoniae has a death rate of 28% in adults. In severe head injury and stroke, inflammatory changes and intracranial hypertension are improved by induced hypothermia, which also is neuroprotective. We hypothesized that moderate hypothermia ameliorates inflammatory changes in experimental pneumococcal meningitis. Wistar rats were cooled systemically, and meningitis was induced by pneumococcal cell wall components. The increase of regional cerebral blood flow in the meningitis animals was blocked by hypothermia at 6 hours. The reduction of intracranial pressure correlated with temperature. The influx of leukocytes into the cerebrospinal fluid and levels of tumor necrosis factor alpha in the cerebrospinal fluid were decreased. Cooling the animals 2 hours after meningitis induction to 30.5 degrees C was also protective. We conclude that hypothermia is a new adjuvant approach to reduce meningitis-induced changes, in particular intracranial pressure, in the early phase of the disease.

Animals↗
PubMed2004

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↗
PubMed1995

[Protective effect of dexamethasone and phenytoin in the treatment of experimental pneumococcal meningitis].

BACKGROUND: Pneumococcal meningitis has a high morbidity and mortality rate despite effective antibiotherapy, probably due to an exaggerated inflammatory response of the CNS. The use of dexamethasone and phenytoin reduced mortality in adults with pneumococcal meningitis. OBJECTIVE: We sought to determine the effect of dexamethasone, phenytoin or the association of both in several inflammatory parameters in experimental bacterial meningitis. METHODS: The study was performed using a modification of the rabbit model of Dacey and Sande. New Zealand white rabbits were intracisteranly inoculated simultaneously with heat-killed S. pneumoniae R6 dexamethasone, phenytoin or both. CSF leucocytes and concentration of proteins and lactate were determined over 6 hours, as well as the presence of brain edema. RESULTS: Treatment with dexamethasone alone or in association with phenytoin reduced all inflammatory parameters. The administration of phenytoin alone did not prevent an increase of CSF leucocytes or protein concentration, but did prevent the development of brain edema. A trend to wards a protective effect on the lactate concentration was observed. CONCLUSIONS: Our results gives support to the antiinflammatory effect of dexamethasone in experimental pneumococcal meningitis, and suggest that phenytoin may have also a protective effect on brain ischemia. This protective action and the prevention of brain edema could contribute, beyond its anticonvulsivant properties, to the great reduction in the mortality rate observed in some clinical studies in patients with pneumococcal meningitis.

Animals↗
PubMed1987

[Diagnosis of pneumococcal meningitis].

Acute pneumococcal meningitis runs the course of meningoencephalitis morphologically, and when the incidence of meningococcal meningitis is on the increase, this disease may well be mistaken for pneumococcal meningitis (two case reports of such misdiagnosis are presented) or stroke (one case is reported). An effective method for recognizing pneumococcal meningitis at an early stage is bacterioscopic examination of Gram-stained cerebrospinal-fluid smears.

Adult↗
PubMed2006

Gene expression in cortex and hippocampus during acute pneumococcal meningitis.

BACKGROUND: Pneumococcal meningitis is associated with high mortality (approximately 30%) and morbidity. Up to 50% of survivors are affected by neurological sequelae due to a wide spectrum of brain injury mainly affecting the cortex and hippocampus. Despite this significant disease burden, the genetic program that regulates the host response leading to brain damage as a consequence of bacterial meningitis is largely unknown. We used an infant rat model of pneumococcal meningitis to assess gene expression profiles in cortex and hippocampus at 22 and 44 hours after infection and in controls at 22 h after mock-infection with saline. To analyze the biological significance of the data generated by Affymetrix DNA microarrays, a bioinformatics pipeline was used combining (i) a literature-profiling algorithm to cluster genes based on the vocabulary of abstracts indexed in MEDLINE (NCBI) and (ii) the self-organizing map (SOM), a clustering technique based on covariance in gene expression kinetics. RESULTS: Among 598 genes differentially regulated (change factor > or = 1.5; p < or = 0.05), 77% were automatically assigned to one of 11 functional groups with 94% accuracy. SOM disclosed six patterns of expression kinetics. Genes associated with growth control/neuroplasticity, signal transduction, cell death/survival, cytoskeleton, and immunity were generally upregulated. In contrast, genes related to neurotransmission and lipid metabolism were transiently downregulated on the whole. The majority of the genes associated with ionic homeostasis, neurotransmission, signal transduction and lipid metabolism were differentially regulated specifically in the hippocampus. Of the cell death/survival genes found to be continuously upregulated only in hippocampus, the majority are pro-apoptotic, while those continuously upregulated only in cortex are anti-apoptotic. CONCLUSION: Temporal and spatial analysis of gene expression in experimental pneumococcal meningitis identified potential targets for therapy.

Acute Disease↗
PubMed1997

Central nervous system TNFalpha-mRNA expression during rabbit experimental pneumococcal meningitis.

In pneumococcal meningitis inflammatory mediators such as tumor necrosis factor alpha (TNFalpha) are produced in large quantities and play a major role in pathogenesis. It is not known exactly which cells produce these mediators during infection. We investigated the localisation of TNFalpha-mRNA in the central nervous system (CNS) by in situ hybridisation during experimental Streptococcus pneumoniae meningitis. TNF-positive cells were detected only in inflammatory infiltrates within the meninges. Cells within the brain parenchyma and the choroid plexus were completely negative. After monocyte depletion, no TNFalpha-mRNA positive cells were detected in the CNS. These findings suggest that TNFalpha in pneumococcal meningitis is produced in the CNS mainly by blood-derived, infiltrating monocytes.

Animals↗
PubMed2006

Report of two cases of aseptic meningitis with persistence of pneumococcal cell wall components in cerebrospinal fluid after Pneumococcal meningitis.

We describe two cases of aseptic meningitis occurring some time after pneumococcal meningitis. Both cases may have resulted from an inflammatory response to persistent pneumococcal cell membrane components, as the cerebrospinal fluid samples were positive by the Binax NOW Streptococcus pneumoniae antigen test. Potential mechanisms and diagnostic impact are discussed.

Antigens, Bacterial↗
PubMed1994

Effect of dexamethasone on therapy of experimental penicillin- and cephalosporin-resistant pneumococcal meningitis.

Treatment of pneumococcal meningitis has become problematic because of the emergence of penicillin- and cephalosporin-resistant strains and because of the concern that dexamethasone therapy might reduce penetration of antibiotics into the cerebrospinal fluid (CSF). We addressed these issues with our rabbit meningitis model by studying two pneumococcal isolates that were resistant to penicillin and ceftriaxone and susceptible to vancomycin and rifampin. Ceftriaxone, vancomycin, and rifampin were given alone or in combination, with or without coadministration of dexamethasone. Treatment was started 12 to 14 h after intracisternal inoculation of approximately 10(4) CFU of one of the organisms. Rifampin concentrations in serum and CSF were similar, regardless of whether dexamethasone was given, whereas those of ceftriaxone were somewhat lower at each time point in animals given dexamethasone. The penetration of vancomycin into CSF was consistently and substantially reduced with dexamethasone treatment, which resulted in a delay in CSF sterilization not observed in non-dexamethasone-treated animals. When rifampin was used with ceftriaxone for treatment of meningitis caused by the more resistant strain, bacteriologic cure occurred promptly, with or without dexamethasone therapy. In areas with high rates of occurrence of resistant pneumococcal strains, we believe initial empiric therapy of bacterial meningitis should include two antibiotics: ceftriaxone and either rifampin or vancomycin. When dexamethasone is used, the combination of ceftriaxone and rifampin is preferred for therapy.

Animals↗
PubMed1979

[Antibiotic treatment of pneumococcal meningitis (author's transl)].

Pneumococcal meningitis, which represents the third in frequency among the purulent forms of meningitis, continues to be, in spite of antibiotic therapy, a serious problem due to its high mortality rate, which reaches 50 per cent in patients of advanced age. The antibiotic treatment of choice is penicillin G, using chloramphenicol as the substitute antibiotic and the cephalosporins in other instances. This article is a review of the cases of pneumococcal meningitis which were admitted to our hospital in the period between 1969-1977, placing especial stress on the therapy followed. Our experience in the treatment of 28 patients affected with this condition indicates therapeutic success in 45 per cent of the cases treated with penicillin G, and a rate of 70 per cent using cephaloridine. In view of these results we believe that cephaloridine should be considered an important alternative antibiotic in the therapy of pneumococcal meningitis.

Adult↗
PubMed1996

A novel nonpsychotropic cannabinoid, HU-211, in the treatment of experimental pneumococcal meningitis.

Typical features of pneumococcal meningitis have been demonstrated in rats inoculated with Streptococcus pneumoniae. HU-211, a novel noncompetitive N-methyl-D-aspartate antagonist recently demonstrated to inhibit tumor necrosis factor-alpha production under various conditions, improves recovery in some experimental models of brain injury. The present study tested the efficacy of HU-211 in combination with antimicrobial therapy in reducing brain damage in experimental pneumococcal meningitis. S. pneumoniae-infected rats were treated with saline alone, ceftriaxone alone, or with combination of ceftriaxone and HU-211 18 h after inoculation of the bacteria. Brain edema and blood-brain barrier impairment 48 h after infection were significantly (P<.05) reduced suggest that HU-211 when given concomitantly with antibiotics attenuates brain damage in the rat model of pneumococcal meningitis.

Animals↗
PubMed2004

New therapies for pneumococcal meningitis.

The treatment of pneumococcal meningitis remains a major challenge, as reflected by the continued high morbidity and case fatality of the disease. The worldwide increase of penicillin-resistant pneumococci and more recently cephalosporin- and vancomycin-tolerant pneumococci has jeopardised the efficacy of standard treatments based on extended spectrum cephalosporins alone or in combination with vancomycin. This review provides a summary of newly developed antibiotics tested in the rabbit meningitis model. In particular, newer beta-lactam monotherapies (cefepime, meropenem, ertapenem), recently developed quinolones (garenoxacin, gemifloxacin, gatifloxacin, moxifloxacin) and a lipopeptide antibiotic (daptomycin) are discussed. A special emphasis is placed on the potential role of combination treatments with some of the new compounds, which are of interest based on the background of increasing resistance problems due to their often synergistic activity in the rabbit model of pneumococcal meningitis.

Animals↗
PubMed1983

Histochemical demonstration of neuraminidase effects in pneumococcal meningitis.

In three cases of pneumococcal meningitis the in vivo action of pneumococcal neuraminidase could be demonstrated. The removal of sialic acid was demonstrated in necrospy material by the use of labeled peanut agglutinin, which has a high specific affinity for the subterminal disaccharide beta-D-galactopyranosyl-(1-3)N-acetyl-D-galactosamine, thereby exposed. Furthermore, this lectin was used for a rapid in vitro histochemical assay of neuraminidase activity in cerebrospinal fluid and culture medium taken from these cases. From the clinical point of view the exposure of the disaccharide which represents the immunodominant group of the Thomsen-Friedenreich antigen may induce immunologic reactions, because all human sera contain antibodies to this cryptic antigen. Thereby, neuraminidase can contribute to the poor prognosis of pneumococcal meningitis.

Choroid Plexus↗
PubMed1987

Spinal cord dysfunction with quadriplegia complicating pneumococcal meningitis.

A case of pneumococcal meningitis complicated by brain-stem herniation and flaccid quadriplegia is described, from which the patient, an 11 year old boy, made a partial recovery. The patient had suffered a head injury with skull fracture some years previously; this was his third episode of meningitis. The aetiology of the quadriplegia has not been fully established, but is presumed to be of vascular nature at spinal cord level, associated with an acute hypotensive episode. Preventative aspects of recurrent bacterial meningitis and brain-stem herniation following lumbar puncture are stressed.

Child↗
PubMed1994

The pathophysiology of pneumococcal meningitis.

The interactions between pneumococcal surface components and host defence systems that initiate pneumococcal meningitis have been studied in considerable molecular detail over the past decade. In this sense, the pneumococcus has served as a prototype for the unravelling of the genesis of inflammation caused by gram-positive bacteria. This review outlines the progression of these early events involving the cytokine cascade, the coagulation cascade, and leukocyte migration, and relates these processes to the production of blood-brain barrier permeability, the hallmark of injury in meningitis. This new understanding has radically altered the therapy of disease with the promise of greatly improved outcome.

Animals↗
PubMed1998

A possible secondary case of pneumococcal meningitis.

Although institutional outbreaks of pneumococcal infection have been reported, secondary cases of pneumococcal meningitis do not seem to have been described. We report two cases of pneumococcal meningitis involving the same serotype occurring in individuals with direct contact.

Humans↗