Lesioni oculari in corso di leishmaniosi, dalla patogenesi alla lesione

Leishmania spp. infection has been recognized as the causative agent of several ocular and ocular adnexal lesions. Two large comprehensive studies on canine ocular leishmaniosis reported that ocular lesions were detectable, clinically or histologically, in about 25-26% of cases of canine leishmaniosis (Peña et al., 2000; Peña et al, 2008). Most commonly affected sites, in order of frequency, were palpebral or limbal conjunctiva, then anterior uvea (ciliary bodies and iris), cornea, sclera and choroid. Specifically, choroid was never found to be affected alone, but leishmanial choroiditis was present always and only in cases of diffuse intraocular inflammation (panuveitis, endophthalmitis, panophthalmitis). Moreover, Leishmania has been reported to cause lacrimal gland adenitis, possibly with secondary keratoconjunctivitis sicca, and orbital myositis. In all these different intra and extra ocular sites; Leishmania has been associated to severe granulomatous or pyogranulomatous, plasmacell rich infiltration, with a variable number of Leishmania amastigotes within the cytoplasm of infiltrating macrophages. It must be outlined that some authors reported cases of intraocular leishmaniosis in which the parasitic load was so low to require immunohistochemical investigation to pose a definite diagnosis and to locate the parasite. However, cases of ocular leishmaniosis that are submitted for routine diagnostic are most commonly represented by severe diffuse granulomatous or pyogranulomatous inflammation of all eye structures (panophthalmitis) with severe effacement of normal architecture and abundant parasitic load with innumerable intracytoplasmic and free amastigotes detectable. If single case reports and detailed large studies on ocular leishmaniosis are present in the current veterinary literature, very few studies, if any, on the pathogenesis of ocular lesions sustained by Leishmania spp. are currently available. Specifically, how Leishmania infects eye structures is not completely clear. It is obvious that conjunctival mucosa, cornea and sclera can be directly exposed to the infection, and from these sites Leishmania can spread within the eye. But how does amastigotes reach the endo-ocular compartment when surface structures (conjunctiva/cornea) are not affected? Such cases have been reported in the mentioned studies, although the pathogenesis has not been discussed.