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19 December 2023

Are Low Lactose Concentrations a Risk Factor for Staphylococcus aureus-Associated Mastitis? †

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1
School of Biomedical Sciences, The University of Western Australia, Crawley, WA 6009, Australia
2
ABREAST Network, Perth, WA 6000, Australia
3
UWA Centre for Human Lactation Research and Translation, Crawley, WA 6009, Australia
4
International Centre for Genetic Engineering and Biotechnology (ICGEB), Cape Town 7925, South Africa

Abstract

Staphylococcus aureus is a bacterium found in the milk of up to 38% of healthy lactating mothers; however, S. aureus is isolated with increased frequency from colostrum and mastitis milk. Both of these milk types have lower lactose concentrations compared to mature milk from healthy lactating mothers, which may indicate that lactose has a role in determining whether S. aureus can survive in human milk. The aim of this study was (1) to investigate whether the presence of S. aureus in human milk is associated with the milk’s lactose concentration, and (2) to determine whether different lactose concentrations can affect the ability of S. aureus isolates to grow in vitro. Human milk samples were collected at 10 weeks postpartum from mothers participating in the Drakenstein Child Health Study (Cape Town, South Africa) and underwent NMR spectroscopy to determine their metabolome. A subset of these samples (n = 117) was cultured to isolate S. aureus. Milk samples with lactose concentrations of less than 166 mM were more likely to have S. aureus present, compared to samples with lactose concentrations of over 166 mM (p < 0.001). In vitro, the growth of S. aureus was negatively correlated with the lactose concentration of axenic culture. Lactose concentrations associated with human milk appear to have an inhibitory effect on the growth of S. aureus human milk isolates. Therefore, low-lactose human milk could potentially be a risk factor for increased S. aureus growth and the development of S. aureus-associated mastitis.

Author Contributions

Conceptualization, G.C.M., N.-U.-H.G. and M.P.N.; methodology, G.C.M., N.-U.-H.G., A.O.O., S.C., H.J.Z., D.T.G. and M.P.N.; software, G.C.M.; formal analysis, G.C.M., N.-U.-H.G., D.T.G. and M.P.N.; investigation, G.C.M., D.T.G. and M.P.N.; resources, H.J.Z. and M.P.N.; data curation, G.C.M., A.O.O. and S.C.; writing—original draft preparation, G.C.M.; writing—review and editing, G.C.M., N.-U.-H.G., D.T.G. and M.P.N.; supervision, N.-U.-H.G., D.T.G. and M.P.N.; funding acquisition, H.J.Z. and M.P.N. All authors have read and agreed to the published version of the manuscript.

Funding

This work was supported by the Bill and Melinda Gates Foundation (OPP1017641; OPP1017579), and the Australian National Health and Medical Research Council (APP1174455). G.M. is supported by the Sibyl and Wylie Gibbons Scholarship award from the Marshall Centre (The University of Western Australia). D.T.G. is supported by an unrestricted research grant from Medela AG (Switzerland), administered by The University of Western Australia. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Institutional Review Board Statement

The study was conducted in accordance with the Declaration of Helsinki, and approved by the Human Research Ethics Committee of the University of Western Australia (protocol code 2019/RA/5/15/1294 and date of approval 27 May 2020).

Data Availability Statement

Data sharing is not applicable.

Conflicts of Interest

D.T.G. declares participation in the Scientific Advisory Board of Medela AG. D.T.G. is supported by an unrestricted research grant from Medela AG, administered by The University of Western Australia. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. All other authors declare no conflict of interest.
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