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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neisseria meningitidis, the meningococcus, remains a major cause of bacterial meningitis. Previously developed animal models for this infection do not adequately mimic its natural pathogenesis in humans. We have investigated a number of different potential animal models and describe a neonatal mouse model. Meningococci were instilled intranasally into five-day-old mice; invasiveness was measured by blood cultures and cisternal puncture, and colonization was determined by nasal cultures. Fifty two percent of mice became bacteremic after instillation of strains which are virulent for humans. Human carrier strains were avirulent in this model. Iron dextran enhanced the nasal colonization, invasiveness and mortality due to disease-associated isolates but had no effect on carrier strains. Colonization rates were similar for all strains. There was a marked age-related change in susceptibility to infection which was inversely correlated with levels of serums C3. Immunization of Swiss CD1 dams with N. meningitidis serotype 2 vaccine protected their litters from meningococcal infection. Protective levels of serum antibody were acquired by neonatal mice after suckling immunized dams. The neonatal mouse meets most of the criteria for an appropriate animal model for meningococcemia.
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PMID:A neonatal mouse model of meningococcal disease. 308 62

Bacterial meningitis due to Streptococcus pneumoniae is associated with an significant mortality rate and persisting neurologic sequelae including sensory-motor deficits, seizures, and impairments of learning and memory. The histomorphological correlate of these sequelae is a pattern of brain damage characterized by necrotic tissue damage in the cerebral cortex and apoptosis of neurons in the hippocampal dentate gyrus. Different animal models of pneumococcal meningitis have been developed to study the pathogenesis of the disease. To date, the infant rat model is unique in mimicking both forms of brain damage documented in the human disease. In the present study, we established an infant mouse model of pneumococcal meningitis. Eleven-days-old C57BL/6 (n = 299), CD1 (n = 42) and BALB/c (n = 14) mice were infected by intracisternal injection of live Streptococcus pneumoniae. Sixteen hours after infection, all mice developed meningitis as documented by positive bacterial cultures of the cerebrospinal fluid. Sixty percent of infected C57BL/6 mice survived more than 40 h after infection (50% of CD1, 0% of BALB/c). Histological evaluations of brain sections revealed apoptosis in the dentate gyrus of the hippocampus in 27% of infected C57BL/6 and in 5% of infected CD1 mice. Apoptosis was confirmed by immunoassaying for active caspase-3 and by TUNEL staining. Other forms of brain damage were found exclusively in C57BL/6, i.e. caspase-3 independent (pyknotic) cell death in the dentate gyrus in 2% and cortical damage in 11% of infected mice. This model may prove useful for studies on the pathogenesis of brain injury in childhood bacterial meningitis.
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PMID:An infant mouse model of brain damage in pneumococcal meningitis. 1793 41