Experimental Cerebro-Spinal Meningitis in Monkeys

Flexner, Simon

doi:10.1084/jem.9.2.142

Cited by 47 publications

(13 citation statements)

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“…In this regard, pneumococcal infection in mice was uniformly lethal (25), whereas 60 to 70% of patients with pneumonia recovered without therapy (Table 1). Similarly, intraspinal meningococcal infection produced a fulminant meningitis in monkeys (48), whereas 20 to 50% of patients with meningitis recovered without therapy ( Table 2). The monkey intratracheal model for pneumococcal pneumonia was more useful for demonstrating the therapeutic efficacies of antibodies, and the beneficial effects of serum could be shown as late as 4 days after infection (19).…”

Section: Infectionsmentioning

confidence: 98%

“…A pandemic in the early 1900s with a mortality rate of 70 to 80% provided a major impetus for the development of serum therapy for meningococcal meningitis. Serum therapy for meningococcal infections was developed by Jochmann (64) (48). Administration of antimeningococcal serum directly into the subarachnoid space shortly after infection cured the majority of treated monkeys (46,47,97).…”

Section: Infectionsmentioning

confidence: 99%

“…In the intratracheal model, direct administration of pneumococci into the lower airways circumvents defenses in the nose and upper airways. Similarly, antimeningococcal sera were developed primary by using the monkey model of intraspinal infection (46)(47)(48)(49)(50), which cannot be considered physiological because the bacteria and the serum were introduced directly into the subarachnoid space. Despite little relevance to the pathogenesis of disease in humans, each of these models was effective at identifying potentially useful antibodies for human therapy.…”

Section: Infectionsmentioning

confidence: 99%

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Serum therapy revisited: animal models of infection and development of passive antibody therapy

Casadevall

Scharff

1994

Antimicrob Agents Chemother

216

157

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Section: Infectionsmentioning

confidence: 98%

Section: Infectionsmentioning

confidence: 99%

Section: Infectionsmentioning

confidence: 99%

See 1 more Smart Citation

Serum therapy revisited: animal models of infection and development of passive antibody therapy

Casadevall

Scharff

1994

Antimicrob Agents Chemother

216

157

View full text Add to dashboard Cite

“…They unsuccessfully injected several irritant solutions (glycerin, urine, acids, adrenal extracts) to produce hydrocephalus. Further, several possible ways to trigger chronic hydrocephalus from the obstruction of the cerebral aqueduct by cotton injection 5 , blood 6 , bacteries 7 , kaolin-aluminum silicate 8 , and others were described. The first structure that suffers because of the increase in CSF pressure and ventricular expansion is the ependyma, followed by the white matter 9,10 .…”

Section: Introductionmentioning

confidence: 99%

Changes caused by hidrocephalus, induced by kaolin, in the corpus callosum of adult dogs

Cardoso¹,

Lachat²,

Lopes³

et al. 2011

Acta Cir. Bras.

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PURPOSE:To analyze the ventricular enlargement and myelination of the corpus callosum in adult dogs after four and eight weeks of kaolin-induction of hydrocephalus. METHODS: 36 dogs were randomly divided into 3 groups: 1 -without hydrocephalus, 2 -kaolin-induction of hydrocephalus until the fourth week, and 3 -kaolin-induction of hydrocephalus until the eighth week. Ventricular ratios and volumes were calculated using magnetic resonance images, and myelination of the corpus callosum were histologically evaluated using solocromo-cianin stain. RESULTS: Radiological hydrocephalus was observed in 93.75% and overall mortality was 38.4%. Ventricular volumes and ratios were higher in groups 2 and 3 compared to group 1 and similar when measures in the fourth and eighth weeks were compared in the group 3. Indices of luminescence in the knee and in the splenium of the corpus callosum were higher in group 2 than in group 1 indicating that there was loss of myelin in group 2, and similar in groups 1 and 3, showing a tendency to remyelination after 8 weeks. CONCLUSION: The corpus callosum of dogs with kaolin-induced hydrocephalus responds with demyelination of the knee and splenium by the fourth week with a tendency to remyelination by the eighth week. Key words: Hydrocephalus. Corpus Callosum. Myelin Sheath. Dogs. RESUMO OBJETIVO:Analisar a dilatação ventricular e a mielinização do corpo caloso em cães adultos após quatro e oito semanas da indução de hidrocefalia por caulin. MÉTODOS: 36 cães foram aleatoriamente divididos em 3 grupos: 1-sem hidrocefalia, 2-quatro semanas de hidrocefalia induzida por caulin, 3-oito semanas de hidrocefalia induzida por caulin. As razões e volumes ventriculares foram calculados utilizando imagens de ressonância magnética, e, a mielinização do corpo caloso por estudo histológico (coloração com solocromo-cianina). RESULTADOS: Hidrocefalia foi observada radiologicamente em 93,75% e a mortalidade global foi de 38,4%. Os volumes e as razões ventriculares foram maiores nos grupos 2 e 3 em relação ao grupo 1 e semelhantes nas quarta e oitava semanas no grupo 3. Índices de luminescência no joelho e no esplênio do corpo caloso foram maiores no grupo 2 em relação ao grupo 1, indicando que houve perda de mielina no grupo 2, e semelhantes nos grupos 1 e 3, mostrando uma tendência à remielinização em torno de 8 semanas. CONCLUSÃO: O corpo caloso de cães com hidrocefalia induzida por caulin responde com desmielinização no joelho e esplênio em torno de quatro semanas com tendência à remielinização em torno da oitava semana. Descritores: Hidrocefalia. Corpo Caloso. Bainha de Mielina. Cães. Changes caused by hidrocephalus, induced by kaolin, in the corpus callosum of adult dogsActa Cirúrgica Brasileira -Vol. 26 (Suppl. 2) 2011 -9

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“…The long history of animal models of meningococcal disease dates back to 1907, when meningitis was induced in monkeys (10). Presently, two rodent models (mouse and rat) and two routes of infection (intraperitoneal [i.p.]…”

mentioning

confidence: 99%

The Meningococcal ABC-Type l -Glutamate Transporter GltT Is Necessary for the Development of Experimental Meningitis in Mice

Colicchio

Ricci²,

Lamberti

et al. 2009

Infect Immun

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Experimental animal models of bacterial meningitis are useful to study the host-pathogen interactions occurring at the cerebral level and to analyze the pathogenetic mechanisms behind this life-threatening disease. In this study, we have developed a mouse model of meningococcal meningitis based on the intracisternal inoculation of bacteria. Experiments were performed with mouse-passaged serogroup C Neisseria meningitidis. Survival and clinical parameters of infected mice and microbiological and histological analysis of the brain demonstrated the establishment of meningitis with features comparable to those of the disease in humans. When using low bacterial inocula, meningococcal replication in the brain was very efficient, with a 1,000-fold increase of viable counts in 18 h. Meningococci were also found in the blood, spleens, and livers of infected mice, and bacterial loads in different organs were dependent on the infectious dose. As glutamate uptake from the host has been implicated in meningococcal virulence, mice were infected intracisternally with an isogenic strain deficient in the ABC-type L-glutamate transporter GltT. Noticeably, the mutant was attenuated in virulence in mixed infections, indicating that wild-type bacteria outcompeted the GltT-deficient meningococci. The data show that the GltT transporter plays a role in meningitis and concomitant systemic infection, suggesting that meningococci may use L-glutamate as a nutrient source and as a precursor to synthesize the antioxidant glutathione.

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Experimental Cerebro-Spinal Meningitis in Monkeys

Cited by 47 publications

References 0 publications

Serum therapy revisited: animal models of infection and development of passive antibody therapy

Serum therapy revisited: animal models of infection and development of passive antibody therapy

Changes caused by hidrocephalus, induced by kaolin, in the corpus callosum of adult dogs

The Meningococcal ABC-Type l -Glutamate Transporter GltT Is Necessary for the Development of Experimental Meningitis in Mice

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