The bacterial plant pathogen Xanthomonas campestris pv. campestris, the causal agent of Black Rot in Brassicaceae, has a unique entry strategy via hydathodes, which are specialized water pores on the leaf blade. From here the bacterium colonizes the vasculature and spreads systemically. Whereas bacterial host entry via wounds or stomata is well understood, surprisingly little is known on the resistance and virulence mechanisms that operate in these natural openings. We study immunity in the Xanthomonas-Arabidopsis thaliana interaction focusing on a guttation-based natural entry”assay that permits hydathode colonization and in a compatible interaction outbreak to the xylem. We find that BAK1/BKK1-dependent immunity against Xanthomonas operates both in hydathodes and the xylem. Furthermore, hydathodal immunity requires EDS1/PAD4 and salicylic acid. During early infection stages, this immunity controls bacterial levels in hydathodes, while later it prevents bacterial spread into the vasculature. As immunity was independent of type III effectors, it can be classified as a Pattern-triggered immunity (PTI). However, effectors were essential for hydathode ingress, even in a hypersusceptible or immunocompromised background, eluding that they are required for full pathogenicity. To our knowledge, this is the first evidence that PTI operates in hydathodes to contain and restrict bacterial proliferation.