Purpose: Investigations of the course of ocular toxoplasmosis and the
influence of a host's immunological status in an animal model would co
ntribute to our understanding of the pathophysiology underlying this c
ondition. In the current study, these aspects are addressed using naiv
e and primed rabbits infected transvitreally with the non-cyst-forming
BK strain of Toxoplasma gondii. Materials and Methods: Of 45 latex ag
glutination test-negative rabbits, 27 were infected subcutaneously wit
h 5,000 Toxoplasma tachyzoites, and the ensuing infection treated by s
ystemic administration of clindamycin for 20 days. Four of these rabbi
ts died from generalized infection. The remaining 23 primed rabbits we
re then inoculated periretinally with a further 5,000 Toxoplasma tachy
zoites, administered via the transvitreal route; the 18 naive rabbits
were treated likewise. Results: All 18 naive and 21 of the 23 primed r
abbits developed toxoplasmic retinochoroiditis. As regarded progressio
n of the disease, dissemination of the condition (p = 0.0001), degree
of vitreal infiltration (p = 0.0001) and incidence of retinal detachme
nt (p<0.05) were all more pronounced in the naive group. Despite treat
ment, 4 of the 18 (22%) naive rabbits died from generalized infection,
as did 4 of the 27 (15%) subcutaneously infected ones (prior to perir
etinal infection). In the primed (secondarily infected) animal group,
only moderate signs of systemic infection were manifested, and there w
ere no fatalities. Conclusion: The high incidence (> 90%) of retinocho
roiditis achieved even in primed animals, by introducing Toxoplasma ta
chyzoites via the transvitreal route, may reflect the maintenance of a
n intact uveovascular barrier during the early stages of the disease.
The pattern of infection, in being restricted primarily to the retina,
mimics the situation evinced in humans. Regarding propagation of the
disease, the condition manifested in naive rabbits resembles that occu
rring in immunodeficient patients, whereas that evoked in primed anima
ls corresponds to recurrence of infection in immunocompetent patients.