Phytophthora austrocedri was identified as the primary pathogen causing the “Mal del ciprés” disease in Patagonian forests, which leads to the mortality of the endemic conifer Austrocedrus chilensis. Trees present withering foliage and defoliation, as well as root necrosis that may extend to the stem. This study aimed to describe the histological alterations occurring during P. austrocedri infection of roots of A. chilensis seedlings. Inoculations were performed by placing agar plugs colonized with the pathogen mycelium in direct contact with the roots. Histological studies of root sections were performed four weeks post-inoculation. Safranin-fast green, phloroglucinol-HCl, toluidine blue, lugol and diaminobenzidine stains were used to describe and compare anatomo-histological features observed in roots of non-inoculated versus inoculated seedlings. In healthy tissues, the presence of lignified Phi thickenings in radial and tangential walls of cortical cells was evidenced. These structures are reported for the first time for A.chilensis. The presence of hyphae and oospores in inoculated plants confirmed the success of colonization of the pathogen in roots. In inoculated roots, a disorganization of tissues with collapse of parenchymal cells was evidenced. In addition, it was observed necrosis of the epidermis and of the cortical parenchyma, and alterations in parenchyma cells (loss of turgor and content, cells without starch, and abnormal accumulation of phenolic compounds). Lignin content was not affected by the presence of the pathogen. The area occupied by Phi thickenings was smaller in P.austrocedri-colonized tissues, and these structures showed an accumulation of phenolic compounds, that was absent in healthy tissues. Parenchymal cells, the first rows of tracheids, as well as rays, showed an active production of hydrogen peroxide in areas invaded by the pathogen. Results evidenced that A. chilensis triggers mechanisms to restrict and resist the infection, but P. austrocedri manages to evade them and finally colonizes and degrades host tissues.