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Mothers carrying S. aureus during third trimester more likely to have babies who are colonized
Mothers who are colonized with Staphylococcus aureus during their third trimester of pregnancy or at the time of delivery are more likely to have infants who carry the bacteria, according to a recent study.
Researchers from the division of pediatric infectious diseases at the Vanderbilt University Medical Center in Nashville enrolled women between 34 and 37 weeks of gestation during 2007 and 2009, resulting in 476 and 471 mother-infant pairs for a prospective study to examine maternal-fetal Staphylococcus transmission.
The researchers, including Infectious Diseases in Children Editorial Board Member C. Buddy Creech, MD, MPH, used nasal and vaginal swabs of women at the time of enrollment and nasal swabs for both mother and child at delivery as well at the 2-month and 4-month visits to determine if the infant was colonized with S. aureus.
The researchers reported that methicillin-resistant S. aureus (MRSA) colonization occurred in 10% to 17% of mothers when they enrolled in the study. At 2 months of age, when infant MRSA colonization peaked, 20.9% of infants were colonized. The researchers concluded that maternal staphylococcal colonization at the time of study enrollment and at delivery did increase the chance of similar colonization of the infant at birth, at discharge, and at 2 and 4 months of age. Of colonized infants, researchers reported that only two infants developed staphylococcal disease.
According to the study results, 50 maternal-infant pairs had concurrent MRSA colonization: 76% shared isolates of the same pulsed-field type and 30% shared USA300 isolates.
The researchers encouraged future research that would “seek to elucidate the potential role of maternally derived antibodies in modifying staphylococcal carriage/infection risk in infants.”
Disclosure: Dr. Creech reports no relevant financial disclosures. The study was funded by the National Institutes of Health.
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Staphylococcus aureus causes both local and serious systemic infections in otherwise healthy full-term neonates and infants. Local infections include pustulosis, abscesses or cellulitis; invasive infections include osteomyelitis, pneumonia and even meningitis. Methicillin-resistant S. aureus is now commonly isolated from such neonates and infants as it has been in older children over the past decade or so. In particular, the evaluation of otherwise healthy infants less than 30 days of age with even simple pustulosis often leads to a full sepsis evaluation and even hospitalization pending culture results. Preventing these infections with onset in the community would be ideal but where and how neonates and young infants acquire S. aureus and become colonized needs to be understood first. As opposed to S. aureus infections occurring in the neonatal intensive care unit, little information is available relating to the acquisition of S. aureus by healthy babies and the subsequent development of community-onset S. aureus infections in the first several months of life.
Jimenez-Truque and colleagues have now shed some light on the relationship of maternal colonization by S. aureus and subsequent colonization in the infant. Babies born to women who were colonized with S. aureus in the nose or vagina during pregnancy or in the nose at the time of delivery were more likely to be colonized with S. aureus at birth and up to 4 months of age compared with babies born to women not colonized. Using molecular techniques, the investigators were able to determine that colonization was more commonly related to horizontal compared with vertical transmission. This finding means that measures targeted at delivery to prevent colonization of neonates whose mothers are colonized with S. aureus during pregnancy are not likely to be very effective (such as with group B streptococcus).
Another interesting finding was related to the carriage of genes encoding Panton-Valentine leukocidin (PVL), which have been found in the vast majority of the community-associated MRSA isolates in the United States, typically the USA300 pulsotype. USA300 accounted for 34% of all the MRSA isolates from mothers and the babies; 27% of the USA300 isolates did not carry the genes encoding PVL. The significance of this finding is not clear. But, as with most studies, the findings raise many more questions to address and I suspect that Buddy Creech and his colleagues will be busy for many more years studying the pathogenesis of S. aureus infections in infants and children.