Bacteria compete with each other for local supremacy in biologic and environmental niches. In humans, who host an array of commensal bacteria, the presence of one species or strain can sometimes prevent colonization by another, a phenomenon known as “bacterial interference.” We describe how, in the 1960s, infants (and later adults) were actively inoculated with a relatively benign strain of Staphylococcus aureus, 502A, to prevent colonization with an epidemic S. aureus strain, 80/81. This introduced bacterial interference as a clinical approach to disease prevention, but little was known about the mechanisms of interference at that time. Since then, much has been learned about how bacteria interact with each other and the host to establish carriage, compete for niches and shift from harmless commensal to invasive pathogen. We provide an overview of these findings and summarize recent studies in which the genome and function of 502A were compared with those of the current epidemic strain, USA300, providing insight into differences in their invasiveness and immunogenicity. Although staphylococcal vaccines have been developed, none has yet been approved for clinical use. Further studies of staphylococcal strains and the molecular characteristics that lead to exclusion of specific bacteria from some niches may provide an alternative path to disease prevention.
From the *Department of Pediatrics University of Pennsylvania & Pediatric Infectious Diseases, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania
†Department of Pathology, Immunology and Laboratory Medicine, Center for Immunity and Inflammation, Rutgers New Jersey Medical School, Newark, New Jersey
‡RuffDraft Communications LLC Duluth, Minnesota
§Department of Pediatrics, Kaiser Permanente, San Francisco, California (emeritus)
¶Departments of Pediatrics and Dermatology University of California, San Francisco, California (emeritus).
Accepted for publication June 4, 2019.
P.J.P. is supported by a grant from National Institutes of Health (NIH) (R01AI137526-01), and D.P. is supported by grants from NIH (R01HL134870) and the New Jersey Health Foundation (PC 62-19).
The authors have no conflicts of interest to disclose.
P.J.P. and D.P. contributed equally to this work.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.pidj.com).
Address for correspondence: Henry R. Shinefield, MD, 15 East 69th Street Apt. 12A New York, NY 10021. E-mail: firstname.lastname@example.org.