Introduction

• Inflammatory reaction of vascular choroid and secondarily the neurosensory retina (NSR) (chorioretinitis) or retina first and subsequently the choroid (retina choroiditis).
• Cause: all causes of uveitis including infectious agents (bacteria, viruses), trauma, neoplasia, reflex uveitis secondary to corneal surface disease, septicemia, penetrating injury, immune mediated.
• Signs: in absence of anterior uveitis, chorioretinitis diagnosed only ophthalmoscopically.
• Diagnosis: ophthalmoscopic signs confirm clinical entity, underlying cause may be identified by full clinical examination, history, hematology and/or biochemistry. Vitreocentesis may be helpful with PCR or bacteriological culture.
• Treatment: attempt to identify and treat underlying cause.
• Prognosis: depends on extent/distribution of lesions and underlying cause. Often even large lesions appear to have little effect on vision.

Pathogenesis

Etiology

• Bacteria:Leptospira,Brucella Brucellosis ,Borrelia Borrelia burgdorferi.
• Parasites:Toxocara canis Toxocara canis (chronic inflammatory retinal granuloma).
• Viruses: Canine distemper Canine distemper disease (most common cause of retinochoroiditis).
• Protozoa:Toxoplasma gondii Toxoplasmosis andLeishmania donovaniand migrating Dipteran larvae (retinal inflammation).
• Rickettsia: Tropical canine pancytopenia and Rocky Mountain spotted fever (retinitis and retinal hemorrhage).
• Fungi: Blastomycosis , Histoplasma, coccidiodes, protothecocis and Cryptococcus (retinal inflammation).
• Neoplasia.
• Trauma.
• Foreign bodies.

Pathophysiology

• Choroid usually focus of inflammation.
• Retina and vitreous usually secondarily affected. Choroiditis alone is rare.
• Vitreal haze may preclude visualization of fundus in active chorioretinitis.
• Acute inflammation is followed by resolution and retinal scarring, usually seen as increased reflectivity (in tapetum) with or without ectopic pigment deposition . Scars referred to as post-inflammatory retinopathy/chorioretinitis.
• UDS = auto-immune reation to melanin, resulting in:
  • Uveitis.
  • Vitiligo (depigmentation of skin especially mucocutaneous junctions - lids, lips, nose).
  • Poliosis (whitening of hair).
• Nomenclature reflects structure where inflammation commences:
  • Chorioretinitis = choroid primarily involved, seconday spread to nsr (most common).
  • Retinochoroiditis = nsr primarily involved, secondary spread to choroid (seen with neurotropic viruses such as distemper.)
  • Retinitis = NSR only involved.
  • Choroiditis (or posterior uveitis) = choroid only involved.
• Distinctions difficult to make clinically, usually made on histology.

• Early in inflammatory process, exudates accumulate around retinal blood vessels, forming perivascular opacities .
• As exudates increase in quantity, retina becomes edematous, nsr may separate from retinal pigment epithelium (RPE) retinal detachment, exudate may extend into vitreous → vitreal opacification may preclude visualization of fundus.
• Hemorrhage may accompany severe inflammation . Shape of hemorrhage defines its location: subretinal - diffuse (between nsr and rpe); deep retinal - 'dot and blot' (confined by cell bodies and axons); superficial retinal - flame shaped (following distribution of fibers in nerve fiber layer); preretinal - keel shaped, following gravitational forces (between nsr and vitreal face).
• Healing is mediated by tissue macrophages and rpe. Connective tissue elements may proliferate leading to folding in retina. Nsr atrophies, causing hyper-reflectivity in tapetal region, pallor in nontapetal. In atrophic area, there may be inceased pigmentation. Borders of lesion usually very distinct. Blood vessls crossing lesion may be attenuated or tortuous.
• UDS: autoimmune response to melanin pigment.

Diagnosis

Treatment

Prevention

Outcomes