Mycoplasma hyopneumoniae (Mhp) is a genome-reduced and metabolically-deficient pathogen of swine that incurs significant losses to global pork production. Mhp is often regarded as an extracellular pathogen that binds to the epithelial cilia lining the respiratory tract where it causes ciliostasis and epithelial cell death and evokes a sustained inflammatory response. Several studies reported the isolation of Mhp from extrapulmonary tissue sites such as the liver, spleen, kidneys and lymph nodes of infected swine suggesting it may have evolved the capacity to invade epithelial tissue and disseminate to distal tissue sites; possibly as a means to survive long term by evading host immune responses. Here we provide a detailed account of Mhp invading a porcine epithelial monolayer (PK-15) using 3D-structured illumination microscopy, confocal microscopy, scanning electron microscopy and transmission electron microscopy. Mhp causes cytoskeletal rearrangements and the formation of a phagolysosome that envelop the invasive cells. Gentamicin protection assays performed after blocking integrin β1 (ITGβ1) sites demonstrated that Mhp cells engage ITGβ1 on the PK-15 surface to initiate engulfment. Confocal microscopy of fibronectin and/or ITGβ1 in conjunction with various endocytic developmental markers showed that Mhp cells are trafficked intracellularly alongside fibronectin and ITGβ1, providing Mhp with a mechanism to gain access to the host cytoplasm. Intracellular Mhp cells were also observed in the vicinity of degraded lysosomes and free in the cytosol, suggesting that Mhp can survive fusion with lysosomes. The ability to disseminate to distal tissue sites represents a mechanism for persistent long term survival in the host and provides new avenues to lessen the economically devastating consequences of this pathogen.