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The Microevolution and Epidemiology of Staphylococcus aureus Colonization during Atopic Eczema Disease Flare.

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Harkins, Catriona P 
Pettigrew, Kerry A 
Oravcová, Katarina 
Gardner, June 
Hearn, RM Ross 


Staphylococcus aureus is an opportunistic pathogen and variable component of the human microbiota. A characteristic of atopic eczema (AE) is colonization by S. aureus, with exacerbations associated with an increased bacterial burden of the organism. Despite this, the origins and genetic diversity of S. aureus colonizing individual patients during AE disease flares is poorly understood. To examine the microevolution of S. aureus colonization, we deep sequenced S. aureus populations from nine children with moderate to severe AE and 18 non-atopic children asymptomatically carrying S. aureus nasally. Colonization by clonal S. aureus populations was observed in both AE patients and control participants, with all but one of the individuals carrying colonies belonging to a single sequence type. Phylogenetic analysis showed that disease flares were associated with the clonal expansion of the S. aureus population, occurring over a period of weeks to months. There was a significant difference in the genetic backgrounds of S. aureus colonizing AE cases versus controls (Fisher exact test, P = 0.03). Examination of intra-host genetic heterogeneity of the colonizing S. aureus populations identified evidence of within-host selection in the AE patients, with AE variants being potentially selectively advantageous for intracellular persistence and treatment resistance.



Anti-Bacterial Agents, Case-Control Studies, Child, Child, Preschool, Clonal Evolution, Dermatitis, Atopic, Drug Resistance, Bacterial, Female, Host Microbial Interactions, Humans, Infant, Male, Phylogeny, Staphylococcal Infections, Staphylococcus aureus, Symptom Flare Up

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Journal of Investigative Dermatology

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Biotechnology and Biological Sciences Research Council (BB/M014088/1)
CPH was supported by Wellcome Trust (grant number 104241/z/14/z). MTGH, KAP, and KO were supported by the Scottish Infection Research Network and Chief Scientist Office through the Scottish Healthcare Associated Infection Prevention Institute consortium funding (CSO reference: SIRN10). Bioinformatics and computational biology analyses were supported by the University of St Andrews Bioinformatics Unit that is funded by a Wellcome Trust ISSF award (grant 097831/Z/11/Z). JP and MTGH were supported by Wellcome Trust grant 098051. AEM is supported by Biotechnology and Biological Sciences Research Council grant BB/M014088/1. SJB is supported by a Wellcome Trust Senior Research Fellowship in Clinical Science (106865/Z/15/Z).