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Summary Table

Feature	Detail
Risk Factors	Recent upper respiratory infection (URI), close contact with infected individuals (schools, dormitories, healthcare settings), immunocompromised states, swimming pools (particularly for adenovirus)
Etiology	Adenovirus (most common cause, responsible for up to 90% of cases), enterovirus, herpes simplex virus (HSV), varicella-zoster virus (VZV), measles, influenza
Patient Presentation	Acute-onset eye redness, watery (serous) discharge, foreign body sensation, tearing; often starts unilaterally then spreads to the contralateral eye within 24 to 48 hours
Classic Physical Exam	Diffuse conjunctival injection, follicular reaction on the inferior palpebral conjunctiva (small, pale, dome-shaped elevations), watery discharge, tender preauricular lymphadenopathy, eyelid edema
Key Diagnostic Results	Clinical diagnosis in most cases; adenoviral rapid antigen testing (immunochromatography) if confirmation needed; fluorescein staining to rule out corneal involvement
Management	Supportive care: cool compresses, artificial tears, strict hygiene and contact precautions; antivirals reserved for herpetic etiology only
Keywords	"Watery discharge," "follicular reaction," "preauricular lymphadenopathy," "recent cold/URI," "spread to the other eye," "red eye with no purulent discharge"

1. Pathophysiology

Viral conjunctivitis results from direct viral invasion of the conjunctival epithelium, most commonly by adenovirus serotypes 3, 4, 7, 8, 19, and 37. The virus gains entry through contact with infected secretions, fomites, or contaminated water, then replicates within the epithelial cells of the conjunctiva. This triggers a cell-mediated immune response involving T-lymphocytes and monocytes, which aggregate beneath the conjunctival epithelium to form the characteristic follicles seen on the tarsal conjunctiva. These follicles are the histologic hallmark that distinguishes viral from bacterial conjunctivitis.

The immune reaction produces serous (watery) exudate rather than the purulent, thick discharge seen in bacterial infection, because the inflammatory infiltrate is predominantly lymphocytic rather than neutrophilic. This explains why the discharge in viral conjunctivitis is thin, clear, and copious.

The involvement of the preauricular lymph node reflects lymphatic drainage from the conjunctiva. Viral antigens are transported to this regional node, causing reactive lymphadenopathy. This finding is a strong clinical discriminator because bacterial conjunctivitis rarely produces palpable preauricular nodes.

The disease typically begins unilaterally, and the contralateral eye becomes involved within days due to autoinoculation from hand-to-eye contact. Adenoviral conjunctivitis can also produce subepithelial corneal infiltrates (small, round, whitish opacities) that appear 1 to 3 weeks after symptom onset. These represent antigen-antibody complexes deposited in the anterior corneal stroma and can cause prolonged photophobia and blurred vision.

Two well-recognized clinical syndromes deserve attention. Pharyngoconjunctival fever (PCF), caused by adenovirus serotypes 3 and 7, presents with conjunctivitis, pharyngitis, and fever, often in children. Epidemic keratoconjunctivitis (EKC), caused by serotypes 8, 19, and 37, is more severe with prominent corneal involvement, and is highly contagious in healthcare and institutional settings.

2. Classification and Clinical Manifestation

Syndrome	Serotypes	Key Features	Corneal Involvement	Systemic Symptoms
Pharyngoconjunctival fever (PCF)	Adenovirus 3, 7	Follicular conjunctivitis + pharyngitis + fever; common in children and outbreaks at swimming pools	Mild or absent	Fever, sore throat, cervical lymphadenopathy
Epidemic keratoconjunctivitis (EKC)	Adenovirus 8, 19, 37	Severe follicular conjunctivitis, often with pseudomembranes; extremely contagious	Subepithelial infiltrates (can persist for weeks to months)	Minimal systemic symptoms
Acute hemorrhagic conjunctivitis	Enterovirus 70, Coxsackievirus A24	Rapid onset, subconjunctival hemorrhages, lid edema	Rare	May be associated with polio-like paralysis (enterovirus 70)
Herpetic conjunctivitis (HSV)	HSV-1 (primary or recurrent)	Unilateral, vesicular lesions on eyelid/periorbital skin, dendritic ulcer on fluorescein staining	Dendritic or geographic corneal ulcer (pathognomonic)	May have systemic HSV signs in primary infection
Measles keratoconjunctivitis	Measles virus (paramyxovirus)	Conjunctivitis as part of the measles prodrome, accompanied by Koplik spots, coryza, and cough	Superficial keratitis	High fever, maculopapular rash

3. Diagnostic Workup

Test	Role	Key Findings
Clinical examination	Best initial approach	Follicular reaction, watery discharge, preauricular lymphadenopathy, often bilateral
Fluorescein staining with slit lamp	Rule out corneal involvement	Subepithelial infiltrates in EKC; dendritic ulcer if HSV (rules in herpetic etiology)
Adenoviral rapid antigen detection (RPS Adeno Detector)	Confirmatory when diagnosis is uncertain	Point-of-care immunochromatographic test; sensitivity around 90%, high specificity
Viral culture	Gold standard (rarely needed clinically)	Identifies the exact viral serotype; slow turnaround, primarily for epidemiologic purposes
PCR	Most sensitive confirmatory test	Detects viral DNA/RNA; reserved for atypical or severe cases, immunocompromised patients
Gram stain and culture of discharge	To exclude bacterial conjunctivitis	Should be negative for bacteria; ordered when purulent discharge raises concern for bacterial etiology

Viral conjunctivitis is overwhelmingly a clinical diagnosis. The combination of watery discharge, follicular conjunctival reaction, and preauricular lymphadenopathy in the setting of a recent URI or known contact is sufficient to establish the diagnosis in most scenarios.

Fluorescein staining with slit-lamp examination should be performed when there is concern for corneal involvement. In EKC, subepithelial infiltrates appear as scattered whitish opacities. If a dendritic ulcer is identified, the diagnosis shifts to HSV keratoconjunctivitis, which fundamentally changes management (antivirals become mandatory, and corticosteroids are contraindicated without antiviral coverage).

When the clinical picture is ambiguous or in outbreak settings, an adenoviral rapid antigen test provides point-of-care confirmation within minutes. This is particularly useful in emergency departments or ophthalmology clinics to guide infection control decisions. Viral culture remains the traditional gold standard but is slow and primarily used for public health surveillance rather than bedside decision-making.

Gram stain and bacterial culture of the discharge are not routinely needed but should be obtained when the discharge appears mucopurulent, when there is no improvement after 7 to 10 days (suggesting bacterial superinfection), or in neonates and contact lens wearers where bacterial keratitis must be excluded.

4. Management and Treatment

Setting	Intervention	Details
All cases	Supportive care	Cool compresses 3 to 4 times daily, preservative-free artificial tears every 2 to 4 hours
All cases	Infection control	Strict hand hygiene, avoid sharing towels/pillows, stay home from school/work for at least 10 to 14 days while symptomatic, disinfect surfaces
Symptomatic relief	Topical antihistamines or vasoconstrictors	May reduce discomfort but do not shorten disease course
Herpetic etiology (HSV)	Topical antiviral	Ganciclovir 0.15% ophthalmic gel, 5 times daily until ulcer heals, then 3 times daily for 7 days; OR trifluridine 1% drops every 2 hours (max 9 drops/day)
Herpetic etiology (HSV)	Oral antiviral	Acyclovir 400 mg 5 times daily for 7 to 10 days, or valacyclovir 500 mg to 1 g three times daily for 7 to 10 days
EKC with pseudomembranes	Membrane removal + short-course topical corticosteroids	Performed by ophthalmology; corticosteroids only under close follow-up to prevent complications
Subepithelial infiltrates (post-EKC)	Low-dose topical corticosteroids	Only if infiltrates impair vision; tapered slowly over weeks under ophthalmologic supervision
Contraindicated	Topical corticosteroids without antiviral cover in HSV	Risk of viral replication, corneal melting, perforation
Not indicated	Topical antibiotics	No role in confirmed viral conjunctivitis; do not prescribe "just in case"

The cornerstone of management for adenoviral conjunctivitis is supportive care. There is no effective antiviral therapy against adenovirus; the disease is self-limited and resolves within 7 to 21 days. Cool compresses reduce lid edema and provide symptomatic relief. Preservative-free artificial tears help dilute the viral load on the ocular surface and reduce irritation.

Infection control is a critical and highly testable component. Adenovirus can survive on dry surfaces for weeks, and patients remain contagious for up to 14 days after symptom onset. In healthcare settings, instrument decontamination and strict contact precautions are essential to prevent nosocomial outbreaks.

Topical antibiotics should not be prescribed for viral conjunctivitis. This is a common clinical error and a frequent test point. Unnecessary antibiotic use promotes resistance, can cause allergic reactions, and delays appropriate management if herpetic etiology is missed.

When the etiology is HSV, the management changes entirely. Topical ganciclovir gel or trifluridine drops are first-line, and oral acyclovir or valacyclovir should be added for more extensive disease or immunocompromised patients. Topical corticosteroids are strictly contraindicated in HSV keratitis unless concurrent antiviral therapy is given, because steroids suppress the local immune response and can cause explosive viral replication, stromal necrosis, and corneal perforation.

For persistent subepithelial infiltrates following EKC, low-dose topical corticosteroids (such as fluorometholone or loteprednol) may be used cautiously under ophthalmologic supervision. These infiltrates are immunologic rather than infectious, so steroids address the underlying mechanism, but they carry the risk of steroid-induced glaucoma and cataract formation with prolonged use.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Bacterial conjunctivitis	Red eye, discharge, bilateral involvement	Discharge is thick, purulent, and yellow-green; eyes often "stuck shut" in the morning; papillary (not follicular) reaction; no preauricular lymphadenopathy
Allergic conjunctivitis	Red eye, bilateral, tearing	Intense itching is the dominant symptom; papillae (cobblestoning) on upper tarsal conjunctiva; chemosis; history of atopy; no lymphadenopathy, no URI
Gonococcal conjunctivitis	Severe red eye, copious discharge	Hyperacute onset (within 12 to 24 hours); profuse purulent discharge; often in sexually active adults or neonates (ophthalmia neonatorum); corneal perforation risk; Gram stain shows gram-negative intracellular diplococci
Chlamydial conjunctivitis (inclusion conjunctivitis)	Follicular reaction, chronic red eye	Chronic course (weeks to months); concurrent STI symptoms (urethritis, cervicitis); superior tarsal follicles and eventual scarring; diagnosed by PCR or Giemsa stain showing intracytoplasmic inclusion bodies
Anterior uveitis (iritis)	Red eye, photophobia	Ciliary flush (perilimbal injection), not diffuse conjunctival injection; miotic pupil; cells and flare on slit lamp in the anterior chamber; no discharge
Acute angle-closure glaucoma	Red eye, tearing	Severe pain, nausea/vomiting; mid-dilated fixed pupil; elevated intraocular pressure; corneal edema (steamy cornea); this is an emergency
Keratitis (bacterial/fungal)	Red eye, tearing, foreign body sensation	Corneal opacity or infiltrate visible on slit lamp; pain out of proportion to exam findings; hypopyon may be present; history of contact lens use or trauma

6. Traps and High-Yield Pearls

The most common way students lose points on viral conjunctivitis questions is by prescribing topical antibiotics for a clearly viral presentation. When the vignette describes watery discharge, follicular reaction, preauricular lymphadenopathy, and a recent cold, the answer is supportive care only. Selecting antibiotic drops is the classic wrong answer choice designed to test whether you can differentiate viral from bacterial conjunctivitis at the bedside.

The second major trap involves missing HSV keratoconjunctivitis. If the vignette mentions vesicular lesions on the eyelid, a dendritic pattern on fluorescein staining, or recurrent unilateral episodes, the diagnosis is HSV and the management must include antivirals. Answering "supportive care only" for herpetic disease is a high-penalty error. Equally dangerous is selecting topical corticosteroids alone for any red eye with corneal involvement without first ruling out HSV, as this can lead to corneal perforation.

A third common mistake is confusing follicles with papillae. Follicles (pale, dome-shaped, avascular) point toward viral or chlamydial conjunctivitis. Papillae (red, flat-topped, with a central vascular core and "cobblestone" appearance) point toward bacterial or allergic conjunctivitis. This distinction drives the differential, and test-writers exploit it frequently.

Finally, remember that preauricular lymphadenopathy is the single most reliable physical exam finding that separates viral conjunctivitis from bacterial and allergic etiologies. If the vignette includes this finding, it is almost certainly pointing you toward a viral cause. The core competency being tested across all these questions is pattern recognition: identifying the viral triad of watery discharge, follicles, and preauricular node, resisting the urge to prescribe antibiotics, and recognizing the red flags that shift the diagnosis to HSV.

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