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Published on: August 7, 2017
Postnatal antibiotic exposure due to maternal group B streptococcus is associated with childhood asthma
Eyal Kristal1,2, Itamar Ben Shitrit1,3, Yoram Faitelson2
1Saban children's Hospital, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Be'er Sheva, Israel.
Insights
Early antibiotic exposure in infants, even without infection, increases childhood asthma risk. This study highlights the need to consider antibiotic use for maternal indications when assessing asthma development.
Area of Science:
- Pediatrics
- Epidemiology
- Public Health
Background:
- Early-life antibiotic exposure is a known risk factor for childhood asthma.
- Previous studies may be confounded by the indication for antibiotic use (e.g., respiratory infections).
- This study aims to isolate the effect of antibiotics given for maternal reasons in non-infected infants.
Purpose of the Study:
- To assess the unique contribution of postnatal antibiotic therapy to childhood asthma risk.
- To mitigate confounding bias from infant infections in previous studies.
- To investigate the association between non-infectious indication antibiotic use and asthma development.
Main Methods:
- Retrospective cohort study using electronic medical records (2006-2018).
- Identified healthy infants born to mothers with positive Group B Streptococcus (GBS) cultures.
- Excluded infants with respiratory symptoms or positive cultures; used quasi-Poisson regression and propensity score matching for analysis.
Main Results:
- Postnatal antibiotic exposure was associated with increased asthma risk (aRR=1.3, P=.017), validated by propensity model (aRR=1.49, P=.005).
- Antibiotic therapy also linked to increased short-acting beta-agonist use (aRR=1.13, P=.072) and allergic rhinitis diagnosis (aRR=3.00, P=.003).
- The association persisted after controlling for confounders and excluding infants with infections.
Conclusions:
- Postnatal antibiotic therapy for maternal GBS, independent of infant infection, is linked to higher childhood asthma risk.
- Findings suggest a direct impact of certain antibiotic exposures on asthma development.
- Highlights the importance of judicious antibiotic use, even for maternal indications.
Background:
Previous studies identified early-life antibiotic exposure as a risk factor for childhood asthma. However, this association may be confounded by an indication, as antibiotics are often prescribed for respiratory infections, which themselves promote asthma. To mitigate this bias, we aim to assess the unique contribution of postnatal antibiotic therapy, given to non-infected infants for maternal indication, on childhood asthma risk.
Methods:
We screened electronic medical records to identify healthy full-term infants born during 2006-2018 to mothers with a positive group B streptococcus (GBS) vaginal culture. Infants with postnatal respiratory symptoms/pneumonia or positive blood/cerebrospinal fluid cultures were excluded. The primary outcome was an asthma diagnosis by age 6 years. We fitted a multivariable quasi-Poisson regression model to assess the unique contribution of antibiotic treatment to asthma diagnosis. As a validation step, we utilized a propensity model in which infants treated with antibiotics were matched 1:3 with infants not treated.
Results:
The cohort included 14,807 infants, of whom 311 received antibiotics. After controlling for potential confounders, postnatal antibiotic exposure was associated with higher asthma risk (adjusted risk ratio [aRR] = 1.3, 95%; confidence interval [CI] 1.04-1.61, p = .017). Higher asthma risk was validated in the propensity model (aRR = 1.49, 95% CI 1.12-1.96 p = .005). Postnatal antibiotic therapy was also associated with secondary outcomes such as the short-acting beta-ag use (aRR = 1.13, 95% CI 0.99-1.28, p = .072) and allergic rhinitis diagnosis (aRR = 3.00, 95% CI 1.43-6.30, p = .003).
Conclusions:
Postnatal antibiotic therapy administrated for maternal GBS, not confounded by infants' infections, was associated with higher childhood asthma risk.
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