Symbiotoxicity refers to the capacity of environmental stressors to alter not only the host organism, but also the microbiomes with which it lives in symbiosis. Applied to infectious diseases, this concept suggests that drug, chemical, or environmental exposure could promote certain infections by disrupting the protective functions of the microbiome. Intestinal, respiratory, skin, and vaginal microbiomes contribute to colonization resistance, maintenance of epithelial barriers, maturation of anti-infective immunity, and structuring of the resistome.

Antibiotics provide the best-established model, particularly through recurrent Clostridioides difficile infection, alteration of the neonatal microbiome, and enrichment of the resistome. More recent data suggest that non-antibiotic drugs, industrial or agricultural contaminants, metals, air pollutants, and plasticizers may likewise modify microbial communities. This issue is particularly relevant in newborns and preterm infants, whose microbiome, barriers, and immune system are still maturing. Intestinal colonization preceding some neonatal bloodstream infections illustrates a possible continuum from ecological disruption to pathobiont dominance and invasive infection. However, infectious symbiotoxicity should be regarded as a conceptual framework rather than an established diagnostic entity. It represents an integrative approach linking the exposome, microbiome, resistome, immune maturation, and infection risk, which remains to be confirmed by longitudinal, mechanistic, and interventional studies.