In the biotrophic phase of rice blast disease, Magnaporthe oryzae secretes cytoplasmic effectors, which are delivered across the rice plasma membrane into the host cytoplasm, and apoplastic effectors, which are retained in the extracellular compartment between the fungal wall and the rice plasma membrane. Secreted cytoplasmic effectors preferentially accumulate in the biotrophic interfacial complex (BIC), a novel in planta structure that locates beside the tip of the initially filamentous invasive hypha and remains beside the first differentiated bulbous invasive hypha cell. In contrast, secreted apoplastic effectors uniformly surround the bulbous invasive hyphae that grow to fill the invaded cell. We report live cell microscopy of invasive hyphae expressing various fluorescent secretion machinery components and various fluorescent effectors. Localization of Spitzenkörper and polarisome markers confirmed distinct growth and secretion patterns for the filamentous and bulbous invasive hyphae, and suggested that secretion into BICs continued while invasive hyphae grew elsewhere in the host cell. Disruption of the conventional ER-Golgi secretion pathway by Brefeldin A (BFA) treatment blocked secretion of apoplastic effectors, which were retained in the ER, but not secretion of cytoplasmic effectors. Fluorescence Recovery After Photobleaching experiments confirmed that cytoplasmic effectors continued to accumulate in BICs in the presence of BFA. Pathogen mutants that failed to express either of the exocyst complex components MoExo70p or MoSec5p, or the t-SNARE MoSsoIp were defective in secretion of BIC-localized effectors, but not apoplastic effectors. We suggest a model in which exocyst and SNARE complexes play a role in the secretion of cytoplasmic effectors into BICs by an unconventional, Golgi-independent secretory pathway.