Viral & Chlamydial Conjunctivitis

Adenoviral Conjunctivitis

Adenovirus causes more infectious conjunctivitis than any other organism, accounting for most viral cases and a large share of conjunctivitis presentations overall. Two features of the virus explain that dominance: it survives for extended periods on inanimate surfaces, and it spreads efficiently through direct contact with contaminated fingers and ocular secretions. Towels, doorknobs, and clinical equipment all serve as fomites, which is why adenoviral conjunctivitis is a recurring source of clinic-based outbreaks.

The classic presentation is watery discharge with mild conjunctival injection, often following or accompanying an upper respiratory infection. A tender, palpable preauricular lymph node on the affected side is a hallmark finding. It reflects a lymphatic drainage response to viral antigen and is typically absent in bacterial conjunctivitis or allergic conjunctivitis, making it one of the more reliable bedside clues pointing toward a viral cause.

Epidemic Keratoconjunctivitis

Epidemic keratoconjunctivitis (EKC) is the severe end of the adenoviral spectrum, classically caused by adenovirus serotypes 8, 19, and 37. Its defining clinical triad is follicular conjunctivitis, keratitis, and preauricular lymphadenopathy. The keratitis is what separates EKC from ordinary adenoviral conjunctivitis, and it's responsible for the disease's most troublesome late complication.

Subepithelial Infiltrates

Weeks after the acute infection resolves, patients can develop persistent blurred vision from subepithelial corneal infiltrates. These represent an immune-mediated response to residual adenoviral antigen rather than ongoing active infection, but they can still cause glare and blurred vision severe enough to warrant topical corticosteroids for symptom and visual-quality control.

Contagiousness is another reason EKC is treated with more caution than routine conjunctivitis. It remains contagious for up to 10–14 days from onset, and because the virus persists on surfaces and instruments such as tonometer tips, it is a classic cause of nosocomial outbreaks within ophthalmology clinics.

Other Viral Conjunctivitis

Herpetic Conjunctivitis

As with EKC, corticosteroids carry a specific risk in suspected herpetic conjunctivitis. Without a confirmed diagnosis and antiviral coverage on board, steroids can worsen herpes keratitis and promote corneal ulceration by suppressing local immune defenses against active viral replication. Topical steroids should generally be withheld until the diagnosis is secure and antiviral therapy is already in place.

Molluscum Contagiosum-Associated Conjunctivitis

Molluscum contagiosum lesions on the eyelid margin don't infect the conjunctiva directly. Instead they shed viral particles and toxic material into the tear film, producing a chronic secondary follicular conjunctivitis. Recognizing the causative eyelid lesion, rather than treating the conjunctivitis in isolation, is the key to resolving it.

Pharyngoconjunctival Fever

Pharyngoconjunctival fever is a separate adenoviral syndrome, driven by serotypes 3, 4, and 7 rather than the 8, 19, and 37 that cause EKC. Fever, pharyngitis, and preauricular lymphadenopathy dominate the picture, often in children during a pool or school outbreak, and the keratitis that defines EKC is usually mild or absent. Most cases clear without the corneal complications or extended contagious period that make EKC harder to manage.

Management

Supportive care is the mainstay of treatment for uncomplicated viral conjunctivitis: cool compresses, artificial tears, and hygiene measures to limit spread. Most cases resolve on their own, and no specific antiviral is routinely necessary for garden-variety adenoviral disease.

Trachoma

Trachoma is the leading infectious cause of blindness worldwide, driven by repeated conjunctival infection with Chlamydia trachomatis serotypes A, B, Ba, and C. These are distinct from the D–K serotypes responsible for genital infection and adult inclusion conjunctivitis. The disease spreads via eye-seeking flies, shared fomites like towels, and direct contact, and it concentrates in communities with poor water access and sanitation.

Repeated infection over years leads to conjunctival scarring, trichiasis, and eventual corneal opacification. Field severity is tracked using the WHO simplified grading system: five signs abbreviated TF (trachomatous inflammation–follicular), TI (trachomatous inflammation–intense), TS (trachomatous scarring), TT (trachomatous trichiasis), and CO (corneal opacity). It was built for rapid field surveillance, not a full slit-lamp exam.

The staging system feeds directly into the WHO's SAFE strategy for trachoma control. Surgery addresses trichiasis in patients already at risk of corneal scarring. Antibiotics means mass azithromycin distribution across an entire endemic district, repeated annually for three to five years in high-prevalence areas. Facial cleanliness and Environmental improvement, better access to water and latrines, target the transmission cycle itself rather than treating disease that has already occurred.

Chlamydial Conjunctivitis Beyond Trachoma

Neonatal

Chlamydial conjunctivitis in neonates presents later than gonococcal disease, typically 5–14 days after birth compared to gonococcus's 2–5 day window. That timing difference is often the first clue to etiology, well before any culture returns. Unlike routine bacterial conjunctivitis, neonatal chlamydial conjunctivitis must be treated with systemic therapy (oral erythromycin or azithromycin) rather than topical treatment alone. Topical therapy alone fails to clear the organism from the nasopharynx and respiratory tract, leaving the infant at risk for chlamydial pneumonia.

Adult Inclusion Conjunctivitis

In sexually active adults, chronic unilateral follicular conjunctivitis unresponsive to topical antibiotics should raise suspicion for chlamydial inclusion conjunctivitis, an extension of genital chlamydial infection to the eye (serotypes D–K). The treatment principle is the same as in neonates: systemic therapy, a single dose of oral azithromycin or a course of doxycycline, clears the genital reservoir and prevents recurrence in a way topical treatment alone cannot.

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