Ocular tuberculosis (TB) commonly causes severe inflammation and vision loss in TB-endemic countries. The mechanism by which tuberculous infection becomes established in the eye is poorly understood. We have developed the zebrafish larva infected with Mycobacterium marinum as a model to study the early pathogenesis of ocular TB. We find that hematogenous bacterial seeding of the eye occurs despite a functional blood retinal barrier. Prototypical early granulomas form in response to bacteria in the eye. These granulomas involve the retinal vasculature and retinal pigment epithelium-choroid complex which are characteristic locations for human ocular TB. We find that peripheral blood monocytes are recruited to the nascent ocular granuloma further suggesting that the immune privileged nature of the eye is breached by this inflammatory focus.