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Updated: Feb 6, 2026
Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat
Published on: October 29, 2014
A mouse model reproducing the pathophysiology of neonatal group B streptococcal infection
Elva Bonifácio Andrade1,2,3,4, Ana Magalhães2,3, Ana Puga1
1ICBAS-Instituto de Ciências Biomédicas de Abel Salazar, Universidade do Porto, 4150-313, Porto, Portugal.
Abstract:
Group B streptococcal (GBS) meningitis remains a devastating disease. The absence of an animal model reproducing the natural infectious process has limited our understanding of the disease and, consequently, delayed the development of effective treatments. We describe here a mouse model in which bacteria are transmitted to the offspring from vaginally colonised pregnant females, the natural route of infection. We show that GBS strain BM110, belonging to the CC17 clonal complex, is more virulent in this vertical transmission model than the isogenic mutant BM110∆cylE, which is deprived of hemolysin/cytolysin. Pups exposed to the more virulent strain exhibit higher mortality rates and lung inflammation than those exposed to the attenuated strain. Moreover, pups that survive to BM110 infection present neurological developmental disability, revealed by impaired learning performance and memory in adulthood. The use of this new mouse model, that reproduces key steps of GBS infection in newborns, will promote a better understanding of the physiopathology of GBS-induced meningitis.
Insights
A new mouse model mimics Group B streptococcal (GBS) meningitis transmission from mother to offspring. This model reveals GBS strain virulence and links infection to long-term neurological deficits in pups.
Area of Science:
- Microbiology
- Infectious Diseases
- Neonatal Health
Background:
- Group B streptococcal (GBS) meningitis is a severe neonatal infection.
- Lack of a suitable animal model hinders understanding and treatment development.
- The natural infection route involves vertical transmission from maternal vaginal colonization.
Purpose of the Study:
- To develop and validate a novel mouse model for GBS meningitis.
- To investigate the role of GBS virulence factors in vertical transmission.
- To assess the long-term neurological consequences of neonatal GBS infection.
Main Methods:
- Vertical transmission of GBS strains (BM110 and BM110∆cylE) from colonized pregnant mice to offspring.
- Monitoring pup mortality, lung inflammation, and neurological development.
- Utilizing a CC17 clonal complex GBS strain and its hemolysin/cytolysin-deficient mutant.
Main Results:
- The virulent GBS strain BM110 caused higher mortality and lung inflammation compared to the attenuated mutant.
- Surviving pups exposed to BM110 exhibited impaired learning and memory in adulthood.
- The model successfully reproduces key aspects of neonatal GBS infection and its sequelae.
Conclusions:
- The developed mouse model effectively replicates vertical GBS transmission and associated pathology.
- Hemolysin/cytolysin production is a key virulence factor in this model.
- Neonatal GBS meningitis can lead to lasting neurological developmental disabilities.
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