Science1 publisher3 min readPublished
Sweden's birth registers tie 975 congenital infections to a threefold autism risk
Karolinska researchers followed 3.7 million births for up to 30 years and found that raised autism and intellectual disability risks held even when infected children were compared with their own uninfected siblings.
The Scientist · Science desk

What happened
- Karolinska Institutet researchers followed 3.7 million people born in Sweden between 1987 and 2021 through national health, psychiatric and educational registers for up to 30 years.
- Only 975 children in that cohort were diagnosed at birth with a congenital TORCH infection, the group covering toxoplasma, syphilis, rubella, cytomegalovirus and herpes simplex.
- Comparing infected children with their own uninfected full siblings left the raised autism and intellectual disability risks intact. The sibling design is the study's check on family genetics and household environment.
Compiled by The ScientistSomething wrong?How this is made
Why it matters
- decision A congenital infection detected at delivery now comes with a quantified 30-year outlook, including the sevenfold intellectual disability figure. Neonatal teams can schedule developmental follow-up against a number.
- exposure The affected group is larger than the counted group, because infected children who never reached a diagnostic threshold still averaged lower school grades. That part shows up in education records, not psychiatric ones.
- constraint Preventing every one of these diagnosed infections would have removed on the order of 195 autism cases from 3.7 million births. That is the most congenital infection control could contribute to population autism totals.
That case count comes to roughly one diagnosed congenital TORCH infection per 3,800 births [13]. Apply the one-in-five autism estimate to that group and about 195 children, across three and a half decades of Swedish births, had both a diagnosed congenital infection and an autism diagnosis [14]. Renee Gardner, a co-author at Karolinska Institutet's Department of Global Public Health, put both scales in one sentence. "They account for a very small proportion of all cases of autism in the population, but for those children who are actually affected, we see a clearly elevated risk of both autism and intellectual disability," she said [10].
Full siblings share half their genome and usually a household, so comparing an infected child with an uninfected brother or sister holds constant the family-level factors registers measure badly. The raised autism and intellectual disability risks held in that comparison [6]. The comparison cannot correct for how the 975 children were found: every one of them was diagnosed at birth [2]. Congenital infections that leave no visible sign at delivery are unlikely to be in the count. So the one-in-five figure describes infants whose infection was detected, not every fetus one of these pathogens reached.
The researchers reported no notable association with ADHD or obsessive-compulsive disorder [7]. If infected newborns were simply watched more closely by clinicians for the next thirty years, that extra attention should have shown up in those columns as well. It did not.
Hugo Sjoqvist, the lead author and a doctoral researcher at Karolinska, said the autism side of this literature has been thin. "It has long been known that these infections can cause intellectual disability. However, the link to autism has been less clear in previous research, which has often been based on small patient groups," he said [11].
Two of the headline numbers are different kinds of measure. The threefold figure is a relative risk and the one in five is an absolute estimate [3][5]. Divide the second by the first and the implied autism risk among comparison children is about 7 percent [15]; the two are reported separately, so that 7 percent is a calculation, not a figure the study reports.
Infected children who never received a neurodevelopmental diagnosis still averaged lower school grades [8]. Intellectual disability risk, by contrast, was the sharpest signal in the paper: more than seven times higher overall, and up to 30 times higher for severe to profound cases [4].
The study does not measure prevention. The cohort tracks what followed an infection detected at birth [2]. It does not compare children born under one screening or vaccination regime with children born under another, so these data cannot estimate what a prenatal programme would prevent. The paper is in JAMA Pediatrics [9].
What to watch
- How many of the 975 infected children had an uninfected sibling in the within-family analysis; that count sets the precision of the sibling estimate.
- Pathogen-specific splits: cytomegalovirus, toxoplasma and syphilis have different prevention routes, and a pooled TORCH estimate leaves open which one to act on.
- Whether a cohort with universal newborn screening reproduces the one-in-five autism figure, given that detection at birth selects the symptomatic infections.