Bacterial & Pseudomonas Keratitis

Pathophysiology & Hypopyon

An intact corneal epithelium resists bacterial invasion well. Most bacterial keratitis needs a break in that barrier before infection can take hold. Trauma, contact lens wear, and dry eye are the classic ways the barrier fails, letting bacteria adhere and invade into the stroma. Bacterial conjunctivitis, by contrast, affects a surface that's still intact; keratitis by definition means the cornea's own defenses already gave way.

Hypopyon, a layered collection of white blood cells in the anterior chamber, is a hallmark of severe bacterial (and fungal) keratitis. It reflects a substantial intraocular inflammatory response, not a purely superficial infection, and its presence should prompt urgent treatment rather than routine follow-up.

Empiric Therapy

Treatment intensity scales with severity. For mild-to-moderate bacterial keratitis, fourth-generation fluoroquinolone monotherapy (e.g. moxifloxacin) is the usual empiric choice. These agents cover common gram-positive and gram-negative pathogens broadly and reach high corneal tissue concentrations, which is what makes single-agent therapy adequate here.

For severe or vision-threatening disease, a fortified antibiotic combination is compounded instead: classically fortified tobramycin plus fortified cefazolin, pairing gram-negative coverage (including Pseudomonas) with gram-positive coverage while culture results are pending.

Neisseria gonorrhoeae causes its own distinct emergency within this category: gonococcal keratoconjunctivitis. Unlike the gradual bacterial infiltrates above, it develops over hours, with copious, reaccumulating purulent discharge and lid swelling, and untreated disease can progress to corneal ulceration and perforation within a day or two. Fluoroquinolone monotherapy isn't the answer here; treatment is a single intramuscular dose of ceftriaxone plus copious saline lavage, often paired with oral azithromycin for likely chlamydial co-infection.

Pseudomonas Keratitis

Pseudomonas aeruginosa gets treated as its own high-risk entity within bacterial keratitis because of how it destroys tissue. It secretes proteolytic enzymes, including elastase and alkaline protease, that degrade corneal stromal collagen directly. The result is rapid, severe stromal melting: an aggressive, fast-moving course that can threaten the globe within days, well ahead of the more gradual progression typical of most other bacterial causes.

Contact lens wear, particularly extended wear, and biofilm formation on lenses and lens cases are the classic risk factors that put Pseudomonas at the top of the differential. The contact lens-related corneal disease page covers those risk factors and lens-hygiene prevention in full. What matters here: any contact lens wearer presenting with keratitis should get empiric coverage adequate for Pseudomonas from the start, not added later once cultures return.

Infectious Keratitis: A Broad Framework

Infectious keratitis is classified by causative organism (bacterial, viral, fungal, or parasitic/Acanthamoeba) because that classification drives antimicrobial therapy directly, not just pathophysiologic understanding. Each category tends to announce itself with characteristic clinical features that narrow the differential before any culture or stain result is back:

• Bacterial: a focal, often rapidly progressive infiltrate with associated hypopyon in severe cases.
• Fungal: feathery, irregular infiltrate margins with satellite lesions; see the fungal keratitis page for full detail.
• Viral (HSV/HZV): a dendritic epithelial ulcer or, in recurrent disease, reduced corneal sensation from nerve involvement; see the HSV & HZV keratitis page.
• Acanthamoeba: pain markedly out of proportion to exam findings, often in a contact lens wearer with water exposure; see the Acanthamoeba keratitis page.

Infiltrate pattern, exposure history, and contact lens status together are usually enough to prioritize an empiric direction at the bedside before smears and cultures return.

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