Adenovirus (same family as respiratory disease, distinct ocular picture — see RSV/Parainfluenza/Adenovirus topic). KEY CONTRAST vs bacterial: WATERY discharge (not purulent) + conjunctival injection + PREAURICULAR LYMPHADENOPATHY (tender node anterior to ear) — bedside distinguishing sign, characteristic of viral not bacterial.
Specific virulent adenovirus serotypes. Conjunctivitis → progresses to KERATITIS → SUBEPITHELIAL CORNEAL INFILTRATES → visual blurring/photophobia persisting WEEKS-MONTHS after acute phase resolves (testable: prolonged recovery despite self-limited viral cause). HIGHLY CONTAGIOUS — healthcare-associated outbreaks well documented. Transmission: direct contact, fomites (esp. ophthalmic instruments/equipment), prolonged surface survival → strict hand hygiene + instrument disinfection between patients = key IC point in ophthalmology.
HSV-1 mostly. Latency in TRIGEMINAL GANGLION (same pattern as HSV/VZV topic) → reactivation → recurrent episodes (not single illness). PATHOGNOMONIC: DENDRITIC ULCER — branching tree-like corneal epithelial defect, seen with FLUORESCEIN stain + slit-lamp/cobalt blue light. High-yield unique sign.
CRITICAL MANAGEMENT POINT: TOPICAL STEROIDS CONTRAINDICATED (or extreme caution + antiviral cover) in active HSV epithelial keratitis — local immunosuppression → unchecked live virus replication → WORSENS disease. Contrast vs steroid-inclusive management elsewhere in curriculum (bacterial meningitis, PCP, neurocysticercosis) where steroids target host inflammation without this live-pathogen-replication risk.
Recurrent HSV keratitis → progressive corneal scarring/vision loss — important cause of infectious corneal blindness, distinct from EKC.
Adenoviral/EKC: SUPPORTIVE only (cool compresses, lubrication, strict hygiene/isolation) — NO specific approved antiviral. Self-limited (weeks), though EKC infiltrates persist longer. HSV keratitis: SPECIFIC effective antiviral (topical/oral aciclovir) — central to management. Key contrast: adenovirus = no specific antiviral; HSV = specific effective antiviral exists.
Viral conjunctivitis/keratoconjunctivitis is, genuinely and specifically, most commonly caused by Adenovirus (the same viral family covered generally under Respiratory Syncytial Virus/Parainfluenza and Adenovirus Infections for its respiratory manifestations, here causing a genuinely distinct, ocular-predominant clinical picture) — a real, high-yield point of contrast with bacterial conjunctivitis’s discharge character established under Bacterial Conjunctivitis, Keratitis and Uveitis: viral conjunctivitis characteristically produces watery, rather than purulent, discharge, alongside prominent conjunctival injection, and, genuinely importantly, is typically accompanied by preauricular lymphadenopathy — a palpable, tender lymph node just anterior to the ear on the affected side, a specifically useful, testable clinical sign that helps distinguish viral from bacterial conjunctivitis at the bedside, since preauricular adenopathy is far more characteristic of viral than bacterial conjunctival infection.
Epidemic keratoconjunctivitis, caused by specific, particularly virulent adenovirus serotypes, represents the more severe end of the adenoviral ocular disease spectrum — genuinely notable for its combination of conjunctivitis progressing to corneal involvement (keratitis), producing characteristic subepithelial corneal infiltrates that can, genuinely importantly, cause visual blurring and photophobia persisting for weeks to months after the acute conjunctival phase has resolved, a real, specifically testable point about this disease’s potential for a genuinely prolonged visual recovery despite its viral, ultimately self-limited underlying cause. EKC is, additionally, genuinely notable for its high contagiousness and well-documented capacity for healthcare-associated outbreaks — transmission occurs readily via direct contact, contaminated fomites (including, notably, ophthalmic equipment and instruments used in eye clinics), and, importantly, the virus can survive on surfaces for a genuinely prolonged period, making strict hand hygiene and instrument disinfection between patients a real, practically important infection-control point specifically emphasized in ophthalmology practice settings.
Herpes simplex virus (HSV), most commonly HSV-1, causes a genuinely distinct form of viral keratitis worth holding separately from the adenoviral picture above, given its fundamentally different underlying biology: following primary infection, HSV establishes latency in the trigeminal ganglion (the same general neuronal latency-and-reactivation pattern covered under Herpes Simplex and Varicella-Zoster Virus Infections), with reactivation producing recurrent episodes of ocular disease rather than a single self-limited illness. The classic, genuinely pathognomonic corneal finding is the dendritic ulcer — a branching, tree-like corneal epithelial defect, visible with fluorescein staining under slit-lamp/cobalt-blue-light examination — a real, specifically high-yield diagnostic sign worth remembering precisely, since this dendritic pattern is essentially unique to HSV keratitis among the causes of corneal ulceration covered in this section. A genuinely critical, specifically testable management point: topical corticosteroids are contraindicated (or require extreme caution combined with antiviral cover) in active HSV epithelial keratitis, since steroid-induced immunosuppression at the local corneal level can allow the live, replicating virus to proliferate essentially unchecked, worsening rather than improving the disease — a real, important contrast with the corticosteroid-inclusive management approaches seen elsewhere in this curriculum (e.g., adjunctive steroids in bacterial meningitis, PCP, neurocysticercosis), where steroids target host-inflammation rather than risk enabling ongoing live pathogen replication the way they genuinely can here. Recurrent HSV keratitis, over multiple episodes, risks progressive corneal scarring and vision loss, making this a genuinely important cause of infectious corneal blindness distinct from the acute EKC picture above.
Adenoviral conjunctivitis/EKC is managed supportively (cool compresses, lubrication, and strict hygiene/isolation precautions to limit transmission), since no specific approved antiviral treatment exists for adenoviral eye disease, with the condition generally self-limited over one to a few weeks (though EKC’s subepithelial infiltrates, as noted, can affect vision for considerably longer). HSV keratitis, by genuine contrast, does have a specific, effective antiviral treatment — topical or oral aciclovir/related antivirals — reflecting the real, practical difference between adenovirus (no specific antiviral available in routine practice) and HSV (specific, effective antiviral therapy exists and is central to management) as a genuinely important point of therapeutic contrast between the two viral causes covered in this topic.
Personal revision notes, mnemonics and reminders.
