Viral and Fungal Eye Infections: Herpes, Adenovirus and the Moulds

Why antibiotics are the wrong reflex here

A red eye is a symptom, not a diagnosis — and the drug depends entirely on the culprit. The Keratitis chapter builds the general approach to a corneal ulcer; this one narrows to the infections antibacterials cannot reach. Viruses have no cell wall and no bacterial ribosome for a standard antibiotic to attack — they hijack the host cell's own machinery, so an antiviral must instead sabotage viral replication itself. Fungi are eukaryotes, more like our own cells than bacteria are, which is exactly why antifungals are relatively few, relatively toxic, and relatively slow. Giving a broad-spectrum antibacterial to a herpetic or fungal eye simply wastes time while the true pathogen digs deeper. So the first move is always to name the organism: a branching dendrite is herpes; a feathery, satellite-flecked infiltrate after a plant injury is a mould; a florid, follicular, ferociously contagious pink eye is usually adenovirus.

Herpes simplex keratitis — the branching ulcer

Herpes simplex virus (HSV) is a lifelong resident: after a first infection it retreats up the trigeminal nerve to the ganglion and sleeps there, reactivating with stress, illness, ultraviolet light or immunosuppression to travel back down to the cornea. When it attacks the surface epithelium it carves the pathognomonic dendritic ulcer — a fine branching line with terminal end-bulbs that stains brightly with fluorescein. This epithelial disease is treated with topical antivirals: aciclovir 3% ointment or ganciclovir 0.15% gel, dosed five times daily until the ulcer heals. Both are nucleoside analogues — they are the antiviral counterpart of a decoy building block, described in full in the Antimicrobials chapter. Aciclovir must first be activated (phosphorylated) by the virus's own enzyme, thymidine kinase; only inside an infected cell does it become the active triphosphate that jams the viral DNA polymerase. That viral-activation step is the elegant reason aciclovir is so selective — it is switched on chiefly where the virus lives, sparing healthy cells.

When the disease goes deeper than the surface, the treatment changes. If HSV invades the deeper corneal stroma, or recurs repeatedly, oral antivirals come in — aciclovir, or its better-absorbed prodrug valaciclovir, which the gut and liver convert into aciclovir so a smaller, less frequent oral dose reaches the eye. Stromal keratitis is largely an immune reaction to viral antigen rather than live surface virus, so — carefully — a topical corticosteroid may be used to quiet the destructive inflammation, but only ever under specialist supervision and always with an antiviral shield running alongside to stop the steroid from reawakening live virus. Finally, for patients plagued by frequent recurrences, long-term low-dose oral aciclovir prophylaxis roughly halves the recurrence rate — a landmark result from the Herpetic Eye Disease Study (HEDS).

Herpes zoster ophthalmicus — shingles hits the eye

The other herpesvirus that threatens the eye is varicella-zoster (the chickenpox virus). Reactivating decades later from the trigeminal ganglion, it can travel down the first (ophthalmic, V1) division of the trigeminal nerve to produce herpes zoster ophthalmicus — a painful, blistering dermatomal rash across the forehead, upper lid and one side of the nose, stopping crisply at the midline. A vital clue is Hutchinson's sign: vesicles on the tip of the nose. Because the nasociliary nerve supplies both the nose-tip and the eye, involvement there predicts that the globe itself — cornea, uvea, retina — is at risk. Treatment is high-dose oral (or intravenous, if severe or immunocompromised) aciclovir, valaciclovir or famciclovir, started promptly to blunt ocular damage. The disease can smoulder for weeks and its most miserable legacy is post-herpetic neuralgia — a chronic, burning trigeminal pain that lingers long after the rash heals and often needs the neuropathic-pain agents covered in the pain chapters.

CMV retinitis — the price of a failing immune system

Some ocular infections only appear when the immune system can no longer hold them back. Cytomegalovirus (CMV), another herpesvirus, is harmless in a healthy adult but becomes sight-threatening once cell-mediated immunity collapses — classically in advanced, untreated HIV/AIDS (a low CD4 count) or in transplant recipients on heavy immunosuppression, a link back to the Immunosuppression and Toxicology material. It produces a slowly expanding necrotising retinitis, sometimes described as a "pizza-pie" of haemorrhage and creamy exudate on the retina. Treatment is systemic ganciclovir or its oral prodrug valganciclovir, or foscarnet as an alternative; sight-threatening lesions near the macula or optic nerve may also get intravitreal injections to reach a high local drug level fast. But antiviral drugs only buy time. The definitive cure is to rebuild the immune system itself — starting antiretroviral therapy in HIV, or reducing immunosuppression in a transplant patient — so that the body can once again keep CMV asleep. Treat the retina and the immune deficit together, or the retinitis returns.

Adenoviral conjunctivitis — very contagious, no magic bullet

By far the commonest viral eye infection is adenoviral conjunctivitis. In its severe form, epidemic keratoconjunctivitis (EKC), it causes a fiercely red, watery, gritty eye with a follicular reaction, a tender pre-auricular lymph node, and — a week or two in — small corneal infiltrates (subepithelial deposits) that can blur vision for weeks. The sobering truth for a pharmacology chapter is that there is no reliably effective antiviral for it. Management is supportive: cool compresses, artificial tears, and time, since the illness is self-limiting. The most important prescription is not a drug at all but infection-control counselling — it spreads with ferocious ease through contaminated fingers, towels and shared equipment, so scrupulous hand hygiene and keeping the patient away from work, school and swimming pools for the contagious period matters more than anything in a bottle. Antibiotics do nothing except when a rare bacterial co-infection is suspected, and topical steroids are reserved for genuinely vision-threatening corneal infiltrates under ophthalmic supervision — because, as ever, a steroid on an undiagnosed red eye risks unmasking herpes.

Fungal keratitis and endophthalmitis — slow, stubborn, sight-threatening

The eye infection that scoffs at antibiotics and takes weeks to defeat. Fungal keratitis is the great mimic of the corneal-ulcer world: it looks like a slow bacterial ulcer but has a feathery, fluffy edge, sometimes with satellite lesions around the main infiltrate. The classic history is a scratch from vegetable matter — a tree branch, a thorn, a fall onto soil — which seeds a filamentary mould such as Fusarium or Aspergillus. In warm, humid climates and in contact-lens wearers these moulds are a leading cause of infectious blindness. A second group, the yeast Candida, tends to strike an already-diseased or chronically medicated (especially steroid-treated) eye. First-line therapy for filamentary fungal keratitis is topical natamycin, a polyene that — like amphotericin — binds ergosterol in the fungal cell membrane and punches holes in it (the polyene and azole mechanisms are set out in the Antimicrobials chapter). For deeper or resistant disease, or Candida, treatment escalates to topical, oral or intravitreal voriconazole (an azole that blocks ergosterol synthesis) or amphotericin B. When infection breaches into the vitreous cavity — fungal endophthalmitis, sometimes bloodborne in an immunocompromised or intravenous-drug-using patient — intravitreal antifungal injection plus systemic therapy is required, often with surgical vitrectomy. The defining feature of all fungal ocular infection is that it is notoriously slow to respond and hard to eradicate: courses run for many weeks, and — critically — corticosteroids are avoided, because they feed fungal growth just as surely as they feed herpes.