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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
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↗
PubMed1995

Therapy of penicillin-resistant pneumococcal meningitis.

Antimicrobial therapy of pneumococcal meningitis has been altered in recent years based on changes in pneumococcal susceptibility patterns, with emergence of strains that are either relatively or highly resistant to penicillin G (minimal inhibitory concentrations of 0.1-1.0 micrograms/ml and > or = 2 micrograms/ml, respectively. In areas of the world where relatively penicillin-resistant strains of Streptococcus pneumoniae are present, the third generation cephalosporins (either cefotaxime or ceftriaxone) should be used as empiric therapy, and for highly penicillin-resistant pneumococcal strains, vancomycin (with or without rifampin) is recommended. It is imperative that susceptibility testing be performed on all cerebrospinal fluid pneumococcal isolates to guide the choice of antimicrobial therapy. Vaccination recommendations with the 23-valent pneumococcal vaccine should also be strictly enforced for use in appropriate populations that are at increased risk of pneumococcal infections.

Bacterial Vaccines↗
PubMed1999

Prevention of hearing loss in experimental pneumococcal meningitis by administration of dexamethasone and ketorolac.

Pneumococcal meningitis remains a significant cause of morbidity, particularly sensorineural hearing loss. Recent literature has suggested that a vigorous host immune response to Streptococcus [corrected] pneumoniae is responsible for much of the neurologic sequelae, including deafness, after bacterial meningitis. This study used a rabbit model of hearing loss in experimental pneumococcal meningitis to evaluate the therapeutic effect of two anti-inflammatory agents, dexamethasone and ketorolac, coadministered with ampicillin. Both adjunctive drugs minimized or prevented sensorineural hearing loss compared with placebo. Dexamethasone, administered 10 min before ampicillin, was particularly effective in minimizing mean hearing threshold change compared with placebo for both clicks (dexamethasone: 6.7-dB sound pressure level [SPL] vs. placebo: 33. 4-dB SPL, P=.0078) and 10-kHz tone bursts (dexamethasone: 8.4-dB SPL vs. placebo: 53.4-dB SPL, P=.0003). These findings support the beneficial role of anti-inflammatory agents in reducing the incidence of hearing loss from pneumococcal meningitis, especially if therapy is instituted early in the course of infection.

Acoustic Stimulation↗
PubMedDate not supplied

Therapeutic efficacy of cefozopran in a murine model of haematogenous pneumococcal meningitis.

Antimicrobial regimens for the treatment of pneumococcal meningitis are not established. We have produced a murine model of haematogenous pneumococcal meningitis and have examined its usefulness for determining the required dosage and term of antimicrobial agents. Streptococcus pneumoniae serotype 6 was injected intraperitoneally (inoculum: about 1 x 10(4) CFU) into mice. Although half of the mice died within 2 days, the surviving mice showed positive bacterial cultures, increase of the protein level, decrease of the glucose level and infiltration of polymorphonuclear leucocytes into cerebrospinal fluids (CSF). When cefozopran was administered subcutaneously twice a day for 1-3 days starting 2 days after infection, dose- and duration-dependent effects were observed and all mice treated with 20 mg/kg of cefozopran for 3 days survived. The penetration rate of cefozopran from blood to CSF in infected mice was 44.7%, which was 6 times higher than that obtained in uninfected mice. This model may be useful for investigating the pathogenesis of haematogenous pneumococcal meningitis and its therapy.

Animals↗
PubMed1978

Experimental pneumococcal meningitis. IV. The effect of methyl prednisolone on meningeal inflammation.

This study was undertaken to determine whether adrenal corticosteroids suppress meningeal inflammation in experimental pneumococcal meningitis in rabbits and, if so, whether the mechanism of suppression involves inhibition of chemotactic activity in CSF or modification of granulocyte responses to inflammation mediators. It was found that methyl prednisolone, administered intramuscularly in doses of 15 or 30 mg/kg 24 hr and 48 hr after induction of meningitis, significantly reduced (p less than 0.01) the mass of granulocytes present in the meninges 72 hr after infection, the time of maximum meningeal inflammation. The larger dose of steroid produced approximately twice the suppressive effect of the smaller dose (p less than 0.05). The regime of methyl prednisolone that produced maximal suppression of meningeal inflammation (30 mg/kg/day) did not alter CSF chemotactic activity or chemotactic responsiveness and phagocytic activities of granulocytes from rabbits with meningitis. However, steroid therapy inhibited an increase in granulocyte adherence that was observed in untreated animals with meningitis (p less than 0.05). Thus methyl prednisolone in doses of 15 and 30 mg/kg given daily to rabbits with pneumococcal meningitis produced a suppressive effect on meningeal inflammation that was dose-dependent and was possibly mediated by inhibition of granulocyte adherence.

Animals↗