Microbial Keratitis: The Sight-Threatening Corneal Infection

Why this is an emergency — and not conjunctivitis

Conjunctivitis inflames the surface lining; keratitis destroys the lens you see through. The conjunctiva is a thin, forgiving membrane over the white of the eye; when it gets infected it goes red and weepy and then, almost always, heals without a mark. The cornea is different. It is the eye's clear front lens, avascular and exquisitely ordered so that light passes cleanly to the retina. When bacteria invade the corneal stroma they don't just inflame it — they digest it, releasing enzymes that melt collagen. The body's repair is a scar, and a scar on the cornea is opaque. If that scar lands on the central visual axis, the patient looks out through frosted glass for the rest of their life; if the melt goes deep enough, the cornea can perforate. That is the whole reason keratitis and conjunctivitis, which can look superficially similar to the untrained eye, could not be further apart in urgency. The distinction between them is drawn in detail in the Bacterial conjunctivitis chapter, which carries the map of ocular infections; this chapter is about the one that threatens sight.

Who gets it: the risk factors

A healthy cornea is remarkably resistant; its intact epithelium is a wall that most organisms cannot breach. Keratitis happens when that wall is compromised. By far the dominant risk in the developed world is contact-lens wear — and within that, poor hygiene: sleeping in lenses overnight, topping up old solution, rinsing cases in tap water, swimming or showering in lenses. A lens is a warm, moist, oxygen-starving cap that traps bacteria against the cornea and lets them multiply; overnight wear multiplies the danger several-fold. The other classic doorways are corneal trauma (a scratch, a foreign body, and especially injury with plant or vegetable matter, which points toward fungus), ocular surface disease (dry eye, blepharitis, a poorly closing lid after a facial-nerve palsy — any state that leaves the cornea exposed or poorly lubricated), and — a crucial pharmacological one — topical corticosteroid use, which suppresses local immunity and can turn a smouldering infection into a raging one.

The pharmacological approach: scrape first, then hit hard

This is where keratitis parts ways with conjunctivitis at the level of the prescription itself. For simple bacterial conjunctivitis you can reach for a bottle of chloramphenicol and move on. A corneal ulcer demands something the surface infection never does: identify the organism before you drown it. The first step for any significant ulcer is a corneal scrape — the ophthalmologist scrapes material directly from the edge and base of the ulcer for Gram stain, microscopy and culture. This is done first, at presentation, because once intensive antibiotics start they sterilize the plate and you lose your one chance to name the bug and its sensitivities. Then — often immediately after scraping — comes intensive, broad-spectrum topical therapy. The word to hold onto is intensive: this is not four-times-a-day dosing. The antibiotic is dropped onto the eye as often as every hour, day and night, in the first 48 hours. The cornea has no blood supply, so the drug can only reach the infection from the surface; sheer frequency is how you build a lethal concentration in the tissue. The intensity is the treatment.

Bacterial keratitis: fortified drops and fluoroquinolones

The organisms that matter most are Pseudomonas aeruginosa — the aggressive, fast-melting bug of the contact-lens wearer, capable of perforating a cornea in a couple of days — and the Gram-positives Staphylococcus aureus and Streptococcus. Two treatment strategies exist. The first is fortified antibiotics: standard eye drops are made at concentrations tuned for surface infections, so for a deep corneal ulcer the pharmacy compounds them stronger than any commercial bottle — a fortified aminoglycoside (gentamicin or tobramycin) to cover Gram-negatives like Pseudomonas, paired with a fortified cephalosporin (cefuroxime or cefazolin) to cover Gram-positives. These two are given in alternation, each hourly, so the eye receives a drop every thirty minutes. The second strategy is fluoroquinolone monotherapy: a single broad-spectrum agent such as moxifloxacin (or ciprofloxacin, ofloxacin, levofloxacin), which covers both Gram-positive and Gram-negative organisms in one bottle. Monotherapy is simpler, commercially available and well tolerated, and is standard for most community ulcers; fortified duals are reserved for severe, central or unusually aggressive disease. Both of these agents are covered in depth in the Antimicrobials section — the same fluoroquinolones, aminoglycosides and cephalosporins you meet systemically, here delivered at the surface in extraordinary concentration.

Acanthamoeba: pain out of proportion, the ring infiltrate

When a contact-lens wearer has a keratitis that is not settling on antibacterials, and the pain seems wildly out of proportion to the modest signs on the cornea, think Acanthamoeba — a free-living protozoan found in tap water, soil and hot tubs, which is exactly why rinsing lenses or their cases in tap water is so dangerous. Its two signature clues are that ferocious, disproportionate pain (it attacks the corneal nerves) and, later, a ring-shaped infiltrate in the stroma. It is diagnosed by scrape and culture (on special media) or corneal confocal microscopy, and it is genuinely hard to treat: the mainstay is a biguanide — polyhexamethylene biguanide (PHMB) or chlorhexidine — which disrupts the organism's cell membrane, sometimes combined with a diamidine such as propamidine. Treatment is prolonged, measured in many months, because Acanthamoeba encysts into a dormant, drug-resistant form that must be worn down slowly. It is the keratitis that most rewards early suspicion and most punishes delay.

Fungal keratitis: trauma, vegetation, and a different pharmacy

Fungal keratitis classically follows trauma with plant or vegetable matter — a thorn, a branch, a fall onto soil, common in agricultural work and warm climates — and it comes in two flavours. The filamentary moulds, Fusarium and Aspergillus, produce a dry-looking infiltrate with feathery, branching edges and sometimes satellite lesions around the main ulcer. Candida, a yeast, tends to strike an already compromised ocular surface and looks more like a bacterial ulcer. The pharmacology is entirely its own: topical natamycin 5% is the drug of choice for filamentary fungi, and voriconazole (topical, and oral in deep disease) is the other workhorse. Fungal disease is slow, deep and stubborn, and it carries the single most dangerous steroid trap in all of keratitis — which is why the Viral & Fungal chapter treats it, alongside herpes simplex (HSV) keratitis, in full. The link to HSV is worth flagging here: dendritic (branching) herpetic ulcers share the same absolute rule — steroids can be catastrophic while the organism is live.

The cardinal rule: no steroids until the organism is controlled

A steroid quiets the eye and delights the patient — and can hand the infection the eye. A red, angry, infected eye looks like inflammation, and the reflex to reach for a corticosteroid is powerful because a steroid does dramatically reduce redness and pain. But in active microbial keratitis a steroid suppresses the very local immunity that is fighting the organism, and can convert a controllable ulcer into a rampant one — the effect is most catastrophic in fungal, herpes simplex and Acanthamoeba disease, where steroids are notorious for turning a bad eye into a lost one. So the rule is absolute: control the organism first with the appropriate antimicrobial, and only later — cautiously, under specialist supervision, once the infection is proven to be under control — might a steroid be added to limit scarring. This is the practical, sight-saving edge of the whole steroid-in-infection principle taught in the Inflammation chapter. Two more traps belong here. Do not patch an infected eye: a closed, warm, moist pad is an incubator for bacteria and cuts off the oxygen the cornea needs. And never dispense topical anaesthetic for a patient to take home for the pain: it is toxic to the corneal epithelium, blocks healing and, abused, can melt the cornea — the pain of keratitis is controlled with oral analgesia and by treating the infection, not by anaesthetizing the surface.