A sexually dichotomous, autistic-like phenotype is induced by Group B Streptococcus maternofetal immune activation.
Maternal GBS infection in late pregnancy can trigger autism-like brain and behavior changes in male rat pups.
01Research in Context
What this study did
Scientists infected pregnant rats with Group B Strep late in pregnancy. They then watched the pups for autism-like behaviors and checked their brains for changes. Only male pups were studied for behavior.
What they found
Male pups born to infected moms showed clear autism-like signs. They had repetitive movements and unusual social responses. Their brains also showed inflammation and structural changes. Female pups were not affected in the same way.
How this fits with other research
Thirtamara Rajamani et al. (2013) used a similar method. They exposed pregnant mice to diesel exhaust instead of GBS. Both studies saw male-only increases in repetitive behaviors. This pattern strengthens the idea that male fetal brains are more vulnerable to prenatal stress.
Three human studies measured GABA levels in autism. Fatemi et al. (2014), Taylor et al. (2017), and Harada et al. (2011) all found lower GABA in autism brains. The rat study adds a possible cause: maternal infection can trigger brain changes that mirror this GABA loss.
Song et al. (2024) seems to disagree. They found no GABA difference between autistic and typical children. The key difference is age and method. Yulu looked at older kids with MRI. The rat study and the other human work looked at younger brains or post-mortem tissue. Timing and technique matter.
Why it matters
You cannot change a child's sex or paternal age, but you can screen and treat GBS during pregnancy. This study gives pediatric BCBAs a talking point for prenatal care teams. When a boy shows early repetitive behaviors, ask about maternal infection history. It may explain part of the profile and guide family-centered education.
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02At a glance
03Original abstract
Group B Streptococcus (GBS) is a commensal bacterium present in the lower genital tract of 15-30% of healthy pregnant women. GBS is the leading cause of chorioamnionitis and cerebral injuries in newborns, occurring most often in the absence of maternofetal pathogen translocation. Despite GBS being the most frequent bacterium colonizing pregnant women, no preclinical studies have investigated the impact of end-gestational maternal GBS exposure on the offspring's brain development and its behavioral correlates. Our hypothesis is that GBS-induced gestational infection/inflammation has a deleterious neurodevelopmental impact on uninfected offspring. Our goal was to study the impact of maternal GBS infection on the placental and neurodevelopmental features in the offspring using a new preclinical rat model. GBS-exposed placentas exhibited chorioamnionitis characterized by the presence of Gram-positive cocci and polymorphonuclear cells, with the latter being significantly more prominent in the labyrinth of male offspring. GBS-exposed male offspring had reduced thickness of periventricular white matter. In addition, they exhibited autistic-like behaviors, such as abnormal social interaction and communication, impaired processing of sensory information and hyperactivity. Overall, these data show for the first time that gestational exposure to GBS plays an important role in the generation of neurodevelopmental abnormalities reminiscent of human autism spectrum disorders (ASD). These results provide new evidence in favor of the role of a common and modifiable infectious/inflammatory environmental factor in human ASD pathophysiology. Autism Res 2017, 10: 233-245. © 2016 International Society for Autism Research, Wiley Periodicals, Inc.
Autism research : official journal of the International Society for Autism Research, 2017 · doi:10.1002/aur.1647