ABSTRACTUnderstanding disease transmission in corals can be complicated given the intricacy of the holobiont and difficulties associated withex situcoral cultivation. As a result, most of the established transmission pathways for coral disease are associated with perturbance (i.e., damage) rather than evasion of immune defenses. Here, we investigate ingestion as a potential pathway for the transmission of coral pathogens that evades the mucus membrane. Using sea anemones (Exaiptasia pallida) and brine shrimp (Artemiasp.) to model coral feeding, we tracked the acquisition of the putative pathogens,Vibrio alginolyticus,V. harveyi, andV. mediterraneiusing GFP-tagged strains.Vibriosp. were provided to anemones using 3 experimental exposures (i) direct water exposure alone, (ii) water exposure in the presence of a food source (non-spikedArtemia), and (iii) through a “spiked” food source (Vibrio-colonizedArtemia) created by exposingArtemiacultures to GFP-Vibriovia the ambient water overnight. Following a 3 h feeding/exposure duration, the level of acquired GFP-Vibriowas quantified from anemone tissue homogenate. Ingestion of spikedArtemiaresulted in a significantly greater burden of GFP-Vibrioequating to an 830-fold, 3,108-fold, and 435-fold increase in CFU mL−1when compared to water exposed trials and a 207-fold, 62-fold, and 27-fold increase in CFU mL−1compared to water exposed with food trials forV. alginolyticus,V. harveyi, andV. mediterranei, respectively. These data suggest that ingestion can facilitate delivery of an elevated dose of pathogenic bacteria in cnidarians and may describe an important portal of entry for pathogens in the absence of perturbing conditions.IMPORTANCEThe front line of pathogen defense in corals is the mucus membrane. This membrane coats the surface body wall creating a semi-impermeable layer that inhibits pathogen entry from the ambient water both physically and biologically through mutualistic antagonism from resident mucus microbes. To date, much of the coral disease transmission research has been focused on mechanisms associated with perturbance of this membrane such as direct contact, vector lesions (predation/biting), and waterborne exposure through preexisting lesions. The present research describes a potential transmission pathway that evades the defenses provided by this membrane allowing unencumbered entry of bacteria as in association with food. This pathway may explain an important portal of entry for emergence of idiopathic infections in otherwise healthy corals and can be used to improve management practices for coral conservation.