Mycoplasma hyopneumoniae (Mhp) is a pathogen of swine that causes large economic losses to swine production. Mhp is often regarded as an extracellular pathogen that binds to the epithelial cilia lining the respiratory tract where it causes ciliostatis and epithelial cell death. Its small genome is consistent with it having evolved by genome reduction and adopting a parasitic lifestyle. Consistent with this view, Mhp has no other known host and is not known to survive for extended periods in the environment. Notably, studies have reported the isolation of Mhp from extrapulmonary tissue sites such as the liver, spleen, kidneys and lymph nodes of infected swine. While Mhp is well adept at colonising respiratory epithelium and transmitting to naïve host via the expulsion of microaerophilic mucosal droplets within the crowded confines of modern day production facilities, we suggest that it has also 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. We investigated the ability of Mhp to invade a porcine epithelial monolayer (PK-15) using confocal microscopy, scanning electron microscopy and transmission electron microscopy. Gentamicin protection assays were used to quantify the proportion of Mhp cells that invade PK-15 cells. Developmental markers on the surface of the vesicles were assessed using confocal microscopy demonstrating that Mhp is trafficked via the complete endocytic pathway. A proportion of intracellular Mhp cells appear to escape lysosomal fusion to phagolysosomes, and reside free within the cytoplasm. We also show that Mhp is capable of being exocytosed back to the extracellular milieu. 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.