Cerebrospinal fluid outflow resistance in rabbits with experimental meningitis. Alterations with penicillin and methylprednisolone.

Scheld, W. Michael; Dacey, Ralph G.; Winn, H. Richard; Welsh, JoEllen; Jane, John A.; Sande, Merle A.

doi:10.1172/jci109850

Cited by 196 publications

(93 citation statements)

References 58 publications

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“…3 Studies in animals have shown that bacterial lysis, induced by treatment with antibiotics, leads to inflammation in the subarachnoid space, which may contribute to an unfavorable outcome. 4,5 These studies also show that adjuvant treatment with antiinflammatory agents, such as dexamethasone, reduces both cerebrospinal fluid inflammation and neurologic sequelae. 4,5 Many controlled trials have been performed to determine whether adjuvant corticosteroid therapy is beneficial in children with acute bacterial meningitis.…”

Section: Methodsmentioning

confidence: 86%

“…4,5 These studies also show that adjuvant treatment with antiinflammatory agents, such as dexamethasone, reduces both cerebrospinal fluid inflammation and neurologic sequelae. 4,5 Many controlled trials have been performed to determine whether adjuvant corticosteroid therapy is beneficial in children with acute bacterial meningitis. The results, however, do not point unequivocally to a beneficial effect.…”

Section: Methodsmentioning

confidence: 86%

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Dexamethasone in Adults with Bacterial Meningitis

2002

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Section: Methodsmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 86%

Dexamethasone in Adults with Bacterial Meningitis

2002

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“…In addition, evidence exists that meningitis is often associated with in-creased intracranial pressure and that this factor may in turn impair cerebral blood flow and thus limit the supply of oxygen and nutrients to the brain [11][12][13]. Increased CSF outflow resistance [14], impaired cerebral circulation [15], increased intracranial pressure, and brain edema [16, 17] have been documented in animal models. These changes are likely to cause the brain to shift its energy production to anaerobic glycolysis and thus increase the production of lactate [18].…”

mentioning

confidence: 99%

Influence of Granulocytes on Brain Edema, Intracranial Pressure, and Cerebrospinal Fluid Concentrations of Lactate and Protein in Experimental Meningitis

Täuber

Borschberg²,

Sande³

1988

Journal of Infectious Diseases

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Brain water content (brain edema), intracranial pressure, and cerebrospinal fluid (CSF) concentrations of lactate and protein increased significantly during 24 h of experimental meningitis due to Streptococcus pneumoniae, but changes were similar in normal and neutropenic rabbits. In sterile meningitis induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP), low and high doses of fMLP were equally effective in inducing CSF pleocytosis, whereas only high doses of fMLP caused brain edema. High doses of fMLP injected intracisternally during pneumococcal meningitis also increased brain water content. The fMLP did not significantly increase intracranial pressure or CSF concentrations of lactate or protein in sterile or pneumococcal meningitis, nor did it cause brain edema in neutropenic animals. Thus, granulocytes may contribute to brain edema during meningitis if adequately stimulated, but intracranial pressure and CSF protein and lactate concentrations appear independent of granulocytes. Stimulation does not appear to occur early in meningitis, when granulocytes were without effect on brain edema.

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“…This is particularly true in regard to the contribution of bacterial components to the induction of the host inflammatory response once bacteria gain access to the cerebrospinal fluid (CSF). An understanding of which bacterial component(s) incites the host response is important since products of inflammation that are released during infection may injure host tissues and be detrimental to the recovery from disease [1][2][3]. This information may provide important clues as to why mortality from pneumococcal disease remains at 20070 despite the development of new, highly bactericidal antibiotics [4].…”

mentioning

confidence: 99%

The Relative Role of Bacterial Cell Wall and Capsule in the Induction of Inflammation in Pneumococcal Meningitis

Tuomanen¹,

Tomasz²,

Hengstler³

et al. 1985

Journal of Infectious Diseases

222

176

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The relative contribution of bacterial components to the induction of inflammation during Streptococcus pneumoniae meningitis is unknown. Several strains of pneumococci with differences in cell surface characteristics (capsule or cell wall) were compared for the effect on the inflammatory response evoked during infection of the cerebrospinal fluid (CSF) in vivo. The presence of bacterial capsular polysaccharide was not necessary for bacterial growth in CSF in vivo but correlated with greater CSF bacterial density. CSF inflammatory changes began to appear when the bacterial concentration exceeded 10 5 cfu/ml, regardless of the pneumococcal strain. CSF inflammatory changes could be invoked by cisternal instillation of 10 5-106 cell equivalents of whole, heat-killed unencapsulated strains or their isolated cell walls but not by similar concentrations of heat-killed encapsulated strains or isolated capsular polysaccharide. Hypoglycorrhachia was observed only during inflammation caused by live bacteria. The inflammatory response characteristic of naturally acquired pneumococcal meningitis can be reproduced by challenge with both encapsulated and unencapsulated bacteria. The bacterial cell wall appears to be the most potent pneumococcal surface component in inducing CSF inflammation.

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Cerebrospinal fluid outflow resistance in rabbits with experimental meningitis. Alterations with penicillin and methylprednisolone.

Cited by 196 publications

References 58 publications

Dexamethasone in Adults with Bacterial Meningitis

Dexamethasone in Adults with Bacterial Meningitis

Influence of Granulocytes on Brain Edema, Intracranial Pressure, and Cerebrospinal Fluid Concentrations of Lactate and Protein in Experimental Meningitis

The Relative Role of Bacterial Cell Wall and Capsule in the Induction of Inflammation in Pneumococcal Meningitis

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