**6. Intraocular infections**

Intraocular infections may involve different intraocular structures. Primarily they affect the uveal tissues (choroid, ciliary body and iris), the retina and secondarily the vitreous [12, 13]. Therefore, they may be manifesting as uveitis and/or choroidal and/or retinal lesions and the differential diagnosis is from inflammation (sterile) disorders.

Uveitis may be divided either by location to anterior; intermediate (pars planitis) and posterior, by clinical features: granulomatous versus non‐granulomatous and etiology: bacterial, viral, fungal, protozoan and helmintic.

Patients may complain of ocular pain, decreased vision and/or ocular redness. The clinical signs vary. In uveitis, the anterior uvea is affected and white cells and flare are encountered in the anterior and posterior chamber and in the anterior third of the vitreous (behind the lens). Keratic precipitates (inflammatory cells and debris) over the endothelium and hypopyon may exist. The precipitates may be fine as in nongranulomatous uveitis or large and coarse (mutton fat) in granulomatous uveitis. In intermediate uveitis, the pars plana may be covered by inflammatory white band and vitreous veils resembling snowballs may be found. In posterior uveitis, white cells and flare involve the posterior 2/3 of the vitreous. They may be accompanied by retinal, choroidal or chorioretinal lesions. These lesions are key element in clinical diagnosis, which may be made by the involved tissues (retina, choroid or both), location (posterior pole, peripapillary or periphery), size, color and number of lesions (**Table 1**). For definitive diag‐ nosis, laboratory tests are usually required.

**Figure 11.** Toxocara retinochoroiditis. Note the active white lesion. It may appear adjacent to a chorioretinal scar.

Treatment should be first aimed at the offending microorganism. Topical and systemic antimicrobial are being used. Topical corticosteroids may be added in the absence of corneal ulcer. Systemic corticosteroids are being added if the offending microorganism is covered and the center of the macula is being threatened or involved by the infectious process.

penetrating ocular trauma injury is by intravenous broad‐spectrum antibiotics (e.g. ciproflox‐ acin 400 mg bid) for 3 days. The data about treatment of endophthalmitis are based mainly on postoperative (cataract extraction) endophthalmitis. When endophthalmitis is suspected, vitreous samples for smears, cultures and sensitivity should be obtained before commencing antibiotic treatment. Treatment includes intravenous broad‐spectrum antibiotics such as vancomycin 1 gr bid and ceftazidime 1 gr tid or moxifloxacin 400 mg/day IV as well as periocular injections and topical. Topical and/or systemic corticosteroids may be added only

Intraocular infections may involve different intraocular structures. Primarily they affect the uveal tissues (choroid, ciliary body and iris), the retina and secondarily the vitreous [12, 13]. Therefore, they may be manifesting as uveitis and/or choroidal and/or retinal lesions and the

Uveitis may be divided either by location to anterior; intermediate (pars planitis) and posterior, by clinical features: granulomatous versus non‐granulomatous and etiology: bacterial, viral,

Patients may complain of ocular pain, decreased vision and/or ocular redness. The clinical signs vary. In uveitis, the anterior uvea is affected and white cells and flare are encountered in the anterior and posterior chamber and in the anterior third of the vitreous (behind the lens). Keratic precipitates (inflammatory cells and debris) over the endothelium and hypopyon may exist. The precipitates may be fine as in nongranulomatous uveitis or large and coarse (mutton fat) in granulomatous uveitis. In intermediate uveitis, the pars plana may be covered by inflammatory white band and vitreous veils resembling snowballs may be found. In posterior uveitis, white cells and flare involve the posterior 2/3 of the vitreous. They may be accompanied by retinal, choroidal or chorioretinal lesions. These lesions are key element in clinical diagnosis, which may be made by the involved tissues (retina, choroid or both), location (posterior pole, peripapillary or periphery), size, color and number of lesions (**Table 1**). For definitive diag‐

**Figure 11.** Toxocara retinochoroiditis. Note the active white lesion. It may appear adjacent to a chorioretinal scar.

after the regression of the endophthalmitis.

differential diagnosis is from inflammation (sterile) disorders.

**6. Intraocular infections**

12 Advances in Common Eye Infections

fungal, protozoan and helmintic.

nosis, laboratory tests are usually required.


**Table 1.** TRD—traction retinal detachment; DD—disc diameter.

**Figure 12.** Toxocara chorioretinitis. Note the whitish lesion that may represent shrinked larva. Traction retinal detach‐ ment may occur.

**Figure 13.** Cytomegalovirus (CMV) retinitis. Note the white lesions and intraretinal hemorrhages.

**Figure 14.** Acute retinal necrosis. Note the whitish lesion without retinal hemorrhages. The lesion is blurred by the inflammation in the vitreous.
