A mouse model reproducing the pathophysiology of neonatal group B streptococcal infection

• Published in: Nature communications Vol. 9; no. 1; pp. 3138 - 13
• Main Authors: Andrade, Elva Bonifácio, Magalhães, Ana, Puga, Ana, Costa, Madalena, Bravo, Joana, Portugal, Camila Cabral, Ribeiro, Adília, Correia-Neves, Margarida, Faustino, Augusto, Firon, Arnaud, Trieu-Cuot, Patrick, Summavielle, Teresa, Ferreira, Paula
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 07.08.2018; Nature Publishing Group; Nature Portfolio
• Subjects: 13/105; 13/2; 13/21; 13/31; 13/51; 14; 14/63; 59; 631/250/255/1638; 631/326/41/2531; 64; 64/60; 82/51; Animals; Animals, Newborn; Bacteriology; Behavior, Animal; Body Weight; Developmental disabilities; Disease control; Disease Models, Animal; Disease transmission; Female; Hemolysin Proteins; Hemolysin Proteins - chemistry; Humanities and Social Sciences; Infections; Infectious Disease Transmission, Vertical; Inflammation; Learning; Life Sciences; Lungs; Male; Maze Learning; Medicin och hälsovetenskap; Memory; Meningitis; Meningitis - microbiology; Meningitis, Bacterial; Mice; Mice, Inbred BALB C; Microbiology and Parasitology; multidisciplinary; Neonates; Perforin; Perforin - chemistry; Pregnancy; Pregnancy, Animal; Science; Science (multidisciplinary); Streptococcal Infections; Streptococcal Infections - physiopathology; Streptococcal Infections - transmission; Streptococcus; Streptococcus agalactiae; Streptococcus agalactiae - pathogenicity; Vagina; Vagina - microbiology
• ISSN: 2041-1723; 2041-1723
• DOI: 10.1038/s41467-018-05492-y

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. Animal models of group-B streptococcal infections are needed to develop effective therapies. Here, Andrade et al. present a mouse model in which the bacteria are transmitted from vaginally colonised pregnant females to their offspring, causing neonatal meningitis and neurological developmental disabilities.