Ocular Infectious Organisms & Microbiology

Bacterial

Which organism causes bacterial keratitis depends largely on contact lens status. Staphylococcus aureus, a gram-positive coccus, accounts for much of the bacterial keratitis seen in non-lens wearers and after ocular surgery. In lens wearers, Pseudomonas aeruginosa predominates and behaves far more aggressively. Its virulence factors include alkaline protease, elastase (LasB), exotoxin A, and phospholipase C, all of which digest stromal collagen. The result is the classic grey-white ring infiltrate with rapid stromal melt and a real risk of perforation without urgent treatment.

Trachoma is the leading infectious cause of preventable blindness worldwide. It is caused by Chlamydia trachomatis serovars A, B, Ba, and C, an obligate intracellular gram-negative organism. Repeated conjunctival reinfection in endemic areas produces a follicular conjunctivitis that scars over years into cicatricial entropion, trichiasis, and corneal opacification.

Endogenous bacterial endophthalmitis is epidemiologically distinct from the more familiar post-surgical form: the eye is seeded hematogenously from a distant infective focus rather than inoculated directly at surgery. Causative organisms vary by region. Klebsiella dominates in East Asia, often arising from a liver abscess, while Streptococcus, Staphylococcus, and Candida are more common in Western series. Patients typically have a concurrent systemic infection, and visual prognosis is worse than in post-surgical disease.

Viral

Epidemic keratoconjunctivitis (EKC), the adenoviral form, is caused mainly by adenovirus species D serotypes 8, 19, and 37, with 53, 54, 56, and 64 also implicated. Its signature corneal finding is multifocal subepithelial infiltrates (SEIs). These appear 1-2 weeks into the illness as an immune response to residual viral antigen rather than ongoing replication, and they can persist for months, causing photophobia and reduced vision well after the conjunctivitis itself has settled.

HSV-1 produces the single most recognizable lesion in ocular microbiology, the dendritic ulcer: a branching, arborescent epithelial defect with terminal bulbs at the end of each branch. Fluorescein pools in the ulcer base, and rose bengal stains the devitalized cells along its margins.

Herpes zoster ophthalmicus (HZO) follows reactivation of varicella-zoster virus in the trigeminal ganglion. The virus travels down the ophthalmic division (V1) and erupts as vesicles in that dermatome. Vesicles on the tip or side of the nose, Hutchinson's sign, mark nasociliary branch involvement and predict a much higher rate of ocular disease: keratitis, uveitis, and retinitis.

Acute retinal necrosis (ARN) is caused mostly by VZV, and less often by HSV-1 or HSV-2, and occurs even in immunocompetent patients. The triad is rapidly progressive necrotizing retinitis that starts in the periphery and marches centrally, occlusive arteritis, and dense vitritis with anterior uveitis. Retinal detachment risk is high, reported up to 75%.

CMV retinitis has its own fundus signature: full-thickness retinal necrosis with perivascular flame-shaped hemorrhages and white necrotic patches advancing along the vessels. The leading white edge and trailing hemorrhage give the classic "pizza-pie" or "brushfire" appearance.

Molluscum contagiosum, a Poxviridae virus, seeds eyelid margin lesions that shed viral particles into the tear film. The result is a chronic follicular conjunctivitis with micropannus, and removing the lid lesion by curettage or cryotherapy clears the conjunctivitis with it.

Congenital rubella syndrome (Gregg syndrome) causes a posterior segment finding that is milder than its anterior segment manifestations of cataract and glaucoma: salt-and-pepper retinopathy, a fine diffuse pigmentary mottling of the RPE from rubella virus disrupting RPE development in utero. This retinopathy usually spares visual acuity; the anterior segment disease is what sets the visual prognosis.

Fungal

Candida albicans is the most common cause of endogenous fungal endophthalmitis, seeded hematogenously in hospitalized, immunocompromised, or injection-drug-using patients. Risk factors are prolonged IV lines, parenteral nutrition, and immunosuppression. It produces white, fluffy vitreous infiltrates and chorioretinal lesions.

Cryptococcus neoformans reaches the eye by hematogenous spread to the optic nerve and meninges, typically in HIV/AIDS after pulmonary cryptococcosis. Cryptococcal meningoencephalitis raises intracranial pressure and produces papilledema, and the organism can also invade the optic nerve directly to cause visual loss. Its polysaccharide capsule, which stains with India ink, is the key identifying feature.

Parasitic

Toxoplasma gondii is the most common cause of infectious posterior uveitis worldwide. Reactivation produces a focal white necrotizing retinal lesion abutting an old, heavily pigmented scar, the "headlight in the fog" appearance. Disease is usually unilateral in immunocompetent patients but can become multifocal or bilateral when the host is immunocompromised.

Acanthamoeba keratitis is tied almost entirely to contact lens wear, especially with tap water exposure or poor lens hygiene. The free-living amoeba, present in water, soil, and air, adheres readily to lens surfaces, and lens wear breaches the epithelial barrier that would normally keep it out.

Ocular toxocariasis, from Toxocara canis larva migrans, takes two forms in children. A peripheral granuloma sits at the ora serrata with fibrous traction bands running to the disc; a posterior pole granuloma is a white, elevated lesion near the disc or macula. Either can cause leukocoria and must be separated from retinoblastoma.

Diffuse unilateral subacute neuroretinitis (DUSN) is a distinct disease from ocular toxocariasis, though the two can share a causative species. A live nematode larva migrates through the subretinal space. The resulting inflammation produces vitritis, multifocal gray-white outer retinal lesions, and progressive optic atrophy over weeks in an otherwise healthy patient. Toxocara canis and Baylisascaris procyonis are both implicated; Baylisascaris causes the larger-larva form seen across the northern and midwestern United States. Diagnosis rests on directly visualizing the motile worm, and once it's localized, laser photocoagulation of the larva is the only treatment that reliably halts progression.

Onchocerciasis (river blindness) is the leading infectious cause of blindness in sub-Saharan Africa. Onchocerca volvulus microfilariae invade the cornea and uveal tract, but the tissue damage comes from the inflammatory response to dying microfilariae rather than the live organisms. This yields keratitis that begins punctate and progresses to sclerosing, along with anterior uveitis, chorioretinopathy, and optic atrophy.

Loiasis (Loa loa, the African eye worm) is transmitted by deer flies (Chrysops species) in West and Central Africa. Its presentation is unlike any other filarial infection: the adult worm migrates visibly beneath the conjunctiva, producing transient localized swelling and discomfort. That sign alone is diagnostic.

Ocular cysticercosis (Taenia solium larval infection) usually lodges in the vitreous cavity or subretinal space. A live cyst provokes little inflammation and stays viable for years. The danger is cyst death, whether spontaneous or drug-induced, which sets off an intense intraocular inflammatory reaction. For that reason a still-viable vitreous cyst is better removed surgically than treated with antiparasitic drugs.

Orbital trichinosis (Trichinella spiralis) can masquerade as a purely periorbital problem. Larvae migrating through periorbital tissue cause bilateral periorbital edema and conjunctival injection, usually with systemic myalgia, fever, and eosinophilia. That systemic constellation is the cue to send serology for Trichinella antibodies rather than treating a local orbital process.

Microsporidial

Microsporidial keratoconjunctivitis sits in a taxonomic category of its own. Microsporidia are obligate intracellular organisms now placed closest to the true fungi rather than the protozoa, where they were once classified. In HIV-positive patients they cause a bilateral epithelial keratoconjunctivitis with fine punctate epithelial infiltrates. The most specific topical agent is fumagillin; systemic albendazole is often added, and voriconazole has some activity.

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