Ocular toxocariasis is a clearly defined disease. However, much remains to
be learned concerning the migratory route, ocular changes, diagnosis and tr
eatment. Studies in paratenic hosts have contributed to our understanding a
nd will yield more information. Various experimental animals have been used
, such as mice, rabbits, guinea pigs, primates, hamsters and gerbils. Of th
ese, the last appear to be the most appropriate model due to their high sus
ceptibility to ocular infection. Results obtained from different animal mod
els are often not comparable due to the fact that dose and routes of inocul
ation are diverse. Early stages in the pathogenesis of ocular toxocariasis
are manifested by haemorrhages in the anterior chamber and iris, replaced i
n time by accumulations of white cells. Ocular migration produces an early
cell reaction, formed by an infiltration of neutrophils accompanied by vasc
ulitis and retinal microinfarcts. Over a period of time, an increase of mac
rophages and the distribution of the infiltrates is observed. Later, granul
omatous lesions are formed. These do not necessarily contain a larva and th
eir appearance varies in different animal models. Local production of IgE a
nd the presence of specific IgG have been described.