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Production of bacteremia and meningitis in infant rats with group B streptococcal serotypes
Insights
Group B Streptococcus (GBS) infection in infant rats shows high virulence, particularly type III strains. Infant rats are susceptible to GBS, with rapid bacteremia, central nervous system invasion, and mortality.
Area of Science:
- Microbiology
- Infectious Diseases
- Neonatal Research
Background:
- Group B Streptococcus (GBS) is a leading cause of neonatal infections.
- Understanding GBS pathogenesis in a susceptible host is crucial for developing effective interventions.
Purpose of the Study:
- To investigate the virulence and disease progression of GBS in infant rats.
- To evaluate the impact of GBS serotypes and inoculation routes on infection outcomes.
Main Methods:
- Infant rats were inoculated with GBS strains via intranasal, oral, and intraperitoneal routes.
- Bacteremia, mortality, and cerebrospinal fluid (CSF) invasion were monitored.
- Histopathological analysis of brain and meninges was performed.
Main Results:
- Intraperitoneal inoculation regularly caused bacteremia.
- Type III GBS strains demonstrated high virulence, causing bacteremia and death at low inocula.
- CSF invasion occurred in 97% of bacteremic animals, with bacterial concentrations in CSF matching or exceeding blood.
- Susceptibility to GBS infection was age-dependent, with younger rats showing perivascular bacterial distribution and minimal inflammation, while older rats exhibited thickened meninges with immune cell infiltration.
Conclusions:
- Infant rats serve as a valuable model for studying GBS pathogenesis.
- Type III GBS strains exhibit significant virulence, rapidly causing systemic infection and central nervous system invasion.
- Age-related differences in host response influence GBS-induced meningitis pathology.
Abstract:
Group B streptococcal strains, representing the five major serotypes, were inoculated into infant rats by intranasal, oral, and intraperitoneal routes. Bacteremia regularly followed injection by the intraperitoneal route. Four strains (three of type III) isolated from human cerebrospinal fluid appeared more virulent for 5-day-old rats. Injection of fewer than 10 colony-forming units of one strain, a type III, led to bacteremia and death in 27% of animals. The cumulative bacteremia and mortality rate with this strain was 66% in animals given inocula of less than 10 to 10(3) colony-forming units. Bacteremia developed by 24 to 48 h with concentrations of greater than 10(5) colony-forming units per ml of blood, and death occurred soon afterward. Among bacteremic animals, positive cerebrospinal fluid cultures were found in 97%, and cerebrospinal fluid bacterial concentrations were equal to or exceeded bacterial counts in blood. The susceptibility of infant rats to infection with type Ia, Ic, or III strains was age dependent. Histopathological studies of the brain and meninges in 34 bacteremic animals with culture-positive cerebrospinal fluid revealed that 5- to 10-day-old animals had numerous bacteria distributed in a perivascular pattern but, with one exception, no leukocytic infiltration. In contrast, three of the 11- to 12-day-old and two 15-day-old animals had very thickened meninges infiltrated with polymorphonuclear leukocytes, macrophages, and bacteria.