Infiltration of Erwinia amylovora (Ea) into host leaves induces an oxidative burst similar to that observed during incompatible reactions associated with Hypersensitive Response (HR). However, the subsequent progressive development of necrosis is unlike an incompatible reaction. Type III secretion system (T3SS) hrp genes and effector DspA/E are necessary for disease and eliciting the HR-like response in apple. To understand the mechanism of disease establishment we first compared apple's response to challenges by Ea and the incompatible pathogen Pseudomonas syringae pv. syringae strain B86-6 (Pss). In a second experiment we compared apple's response to Ea, a T3SS and a DspA/E mutant. To identify the transcriptome, we used a two-channel, printed Malus microarray. Leaf tissues were harvested from shoots of fire blight susceptible 'Malling 26' apple rootstock 6 h post-inoculation with either phosphate buffer (Mock), virulent Ea strain Ea273, Pss, or Ea mutants. A total of 2430 differentially expressed genes were identified for the first experiment. Of those, 430 apple genes responded similarly to both compatible and incompatible interactions. In the second experiment 1332 differentially expressed genes were identified. Interesting subsets of genes potentially associated with MAMP-trigger immunity, and with responses to T3 effectors of Ea, including DspA/E-specific responses were further analyzed.