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Summary Table

Category	Details
Risk Factors	Contact lens wear (especially overnight/extended use), corneal trauma or foreign body, dry eye syndrome, immunosuppression, herpes simplex virus reactivation, recent eye surgery, contaminated water exposure (Acanthamoeba)
Etiology	Bacterial (Pseudomonas aeruginosa, Staphylococcus aureus), viral (HSV, VZV), fungal (Fusarium, Aspergillus after organic matter trauma), parasitic (Acanthamoeba from contaminated water/contact lens solution)
Patient Presentation	Acute eye pain, photophobia, tearing, blurred vision, foreign body sensation, red eye
Classic Physical Exam	Ciliary (circumcorneal) injection, corneal opacity or infiltrate on slit-lamp exam, possible hypopyon (layered white blood cells in anterior chamber), dendritic ulcer with fluorescein staining (HSV)
Key Diagnostic Results	Slit-lamp examination showing corneal infiltrate or ulceration, fluorescein staining pattern (dendritic = HSV, ring infiltrate = Acanthamoeba), corneal scraping with culture and Gram stain for bacterial cases
Management	Bacterial: topical fluoroquinolone drops (moxifloxacin or gatifloxacin) every 1 hour initially. HSV epithelial: oral valacyclovir or topical ganciclovir. Fungal: topical natamycin or voriconazole. Acanthamoeba: topical polyhexamethylene biguanide (PHMB) + propamidine. Refer to ophthalmology urgently for all suspected keratitis
Keywords	"Contact lens wearer with painful red eye," "dendritic ulcer," "corneal infiltrate," "hypopyon," "ring-shaped infiltrate," "pain out of proportion" (Acanthamoeba)

1. Pathophysiology

The cornea is an avascular, transparent structure that depends on the tear film, blinking reflex, and intact epithelium as its primary defense barriers. When any of these are compromised, pathogens can invade the corneal stroma and trigger an inflammatory cascade.

In bacterial keratitis, disruption of the corneal epithelium (most commonly from contact lens wear or trauma) allows organisms to adhere, colonize, and produce proteolytic enzymes that degrade the stromal collagen. Pseudomonas aeruginosa is the organism most strongly associated with contact lens-related keratitis because it produces exotoxins and elastase that cause rapid, aggressive stromal necrosis. This explains why bacterial keratitis can progress to corneal perforation within 24 to 48 hours if untreated.

In HSV keratitis, the virus resides in a latent state within the trigeminal ganglion and reactivates along the ophthalmic division (V1). During epithelial disease, the virus replicates within corneal epithelial cells, producing the characteristic dendritic ulcer with terminal bulbs visible on fluorescein staining. When stromal involvement occurs, the mechanism shifts from direct viral cytopathic damage to an immune-mediated process: CD4+ T cells and complement activation cause stromal inflammation and neovascularization. This distinction is critical because epithelial HSV keratitis is treated with antivirals alone, while stromal disease requires antivirals combined with topical corticosteroids to suppress the immune response.

Fungal keratitis occurs most often after trauma with organic or vegetable matter (tree branches, soil). Fungi penetrate deep into the stroma, producing satellite lesions and feathery borders due to hyphal extension between stromal lamellae. The indolent course and poor response to antibacterial agents are distinguishing features.

Acanthamoeba keratitis develops in contact lens wearers exposed to contaminated water (swimming, showering, or using tap water to rinse lens cases). The organism exists in both trophozoite and cyst forms; the cyst form is extremely resistant to standard disinfection, which explains the notoriously difficult and prolonged treatment course. The pathognomonic finding is perineural infiltration, which causes severe pain disproportionate to clinical findings, and a characteristic ring-shaped stromal infiltrate on examination.

2. Classification and Clinical Manifestation

Type	Risk factors	Onset	Clinical Features	Distinguishing Finding
Bacterial	Contact lens wearer, corneal trauma	Acute (hours to 1-2 days)	Purulent discharge, dense stromal infiltrate, possible hypopyon	Rapid progression, mucopurulent exudate, single dense infiltrate
HSV Epithelial	History of prior HSV or cold sores, stress/UV triggers	Subacute (days)	Tearing, photophobia, decreased corneal sensation	Dendritic ulcer with terminal bulbs on fluorescein stain
HSV Stromal	Recurrent HSV keratitis	Gradual	Stromal haze, edema, possible neovascularization, intact epithelium	Disciform (disc-shaped) stromal edema, immune rings
Fungal	Agricultural worker, trauma with plant material	Indolent (days to weeks)	Gray-white infiltrate, feathery margins	Satellite lesions, raised edges, slow progression despite antibiotics
Acanthamoeba	Contact lens wearer with water exposure	Subacute to chronic	Severe pain out of proportion to exam findings	Ring-shaped infiltrate, radial keratoneuritis (perineural infiltrates)
Exposure/ Neurotrophic	Facial nerve palsy (CN VII), post-trigeminal ablation	Gradual	Central or inferior corneal epithelial defect	Incomplete lid closure (lagophthalmos) or absent corneal reflex

3. Diagnostic Workup

Test	Purpose	When to Order
Slit-lamp biomicroscopy	Best initial test; visualizes corneal infiltrate, ulcer morphology, anterior chamber reaction	All suspected cases
Fluorescein staining	Highlights epithelial defects; reveals dendritic pattern (HSV) or ring pattern (Acanthamoeba)	All suspected cases
Corneal scraping with Gram stain and culture	Gold standard for identifying the causative organism	Moderate-to-severe ulcers, central ulcers, non-responsive cases, suspected fungal/Acanthamoeba
KOH preparation / Calcofluor white stain	Identifies fungal hyphae	Suspected fungal keratitis
Confocal microscopy	Non-invasive identification of Acanthamoeba cysts and fungal elements	Suspected Acanthamoeba or fungal keratitis
Viral PCR (corneal swab)	Confirms HSV or VZV DNA	Atypical presentations of suspected herpetic keratitis

The workup begins with slit-lamp examination, which is the best initial step for any patient presenting with a painful red eye and suspected corneal pathology. The slit lamp reveals the location, depth, and morphology of the infiltrate, and allows assessment of anterior chamber inflammation (cells and flare) and hypopyon.

Fluorescein staining under cobalt blue light is performed concurrently. This is the test that reveals the classic patterns: a dendritic ulcer with terminal bulbs is virtually diagnostic of HSV epithelial keratitis, while a ring-shaped infiltrate raises strong suspicion for Acanthamoeba. A geographic ulcer (larger, amoeboid shape without terminal bulbs) suggests advanced or treated HSV disease.

Corneal scrapings for Gram stain, culture, and sensitivity should be obtained before starting empiric antibiotics in all cases with a central or large ulcer (greater than 2 mm), suspected fungal or parasitic etiology, or failure to respond to initial therapy. The scraping is taken from the leading edge and base of the ulcer using a Kimura spatula or blade. Blood agar, chocolate agar, and Sabouraud agar (for fungi) are standard culture media. For Acanthamoeba, a non-nutrient agar with E. coli overlay is the required culture medium.

Confocal microscopy has emerged as a valuable non-invasive tool that provides near-histologic resolution of the cornea in vivo, allowing direct visualization of Acanthamoeba cysts (bright, round, double-walled structures) and fungal hyphae without the need for scraping.

4. Management and Treatment

Condition	First-Line Treatment	Duration / Notes
Bacterial (mild-moderate)	Topical fluoroquinolone: moxifloxacin 0.5% or gatifloxacin 0.3%, 1 drop every 1-2 hours while awake	Taper over 1-3 weeks based on clinical response
Bacterial (severe / vision-threatening)	Fortified topical antibiotics: cefazolin 50 mg/mL + tobramycin 14 mg/mL, alternating every 30 minutes initially	Adjust based on culture sensitivity; ophthalmology co-management required
HSV epithelial	Oral valacyclovir 500 mg three times daily for 7-10 days, OR topical ganciclovir 0.15% gel five times daily	Do NOT use topical corticosteroids in epithelial disease (will worsen viral replication)
HSV stromal	Oral valacyclovir 500 mg three times daily + topical prednisolone acetate 1% (slow taper)	Corticosteroid must always be covered by antiviral; taper steroids gradually over weeks to months
HSV prophylaxis (recurrent)	Oral acyclovir 400 mg twice daily for at least 12 months	Reduces recurrence rate by approximately 50% (HEDS trial)
Fungal	Topical natamycin 5% every 1-2 hours (filamentary fungi) or topical voriconazole 1% (yeast)	Treat for 6-12 weeks minimum; poor penetration requires prolonged course
Acanthamoeba	Topical PHMB 0.02% or chlorhexidine 0.02% + propamidine 0.1% (Brolene), every 1 hour initially	Treatment for months; cyst form is resistant, so dual therapy targeting both trophozoites and cysts is essential
Exposure keratitis	Aggressive lubrication, taping eyelid shut at night, consider tarsorrhaphy	Address underlying cause (e.g., Bell palsy)

Acute stabilization for any suspected infectious keratitis involves initiating empiric broad-spectrum topical antibiotics immediately after corneal cultures are obtained. Do not delay treatment waiting for culture results. For contact lens wearers, the lens must be removed and also sent for culture.

The most tested treatment principle is the distinction between HSV epithelial vs. stromal keratitis. In epithelial disease, the damage is from direct viral replication, so the treatment is antiviral therapy alone. Corticosteroids are contraindicated in epithelial HSV keratitis because they suppress local immune defenses and promote viral proliferation, potentially leading to geographic ulceration and perforation. In stromal disease, however, the damage is immune-mediated, so topical corticosteroids are indicated to control the inflammatory response, but they must always be paired with concurrent antiviral coverage to prevent viral reactivation.

For Acanthamoeba, treatment is prolonged and challenging. The cyst form is resistant to almost all antimicrobials, which is why dual antiseptic therapy (a biguanide plus a diamidine) is used. Therapy often continues for 3 to 6 months, and recurrence is common if treatment is stopped prematurely.

Patients who progress to corneal perforation or who fail medical therapy may require corneal transplantation (penetrating keratoplasty).

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Conjunctivitis (bacterial/viral)	Red eye, tearing, discharge	No corneal infiltrate or ulceration on slit lamp; vision is preserved; diffuse conjunctival injection rather than circumcorneal (ciliary) injection
Anterior uveitis (iritis)	Painful red eye, photophobia, ciliary flush	Cornea is clear on slit lamp; cells and flare are in the anterior chamber without corneal infiltrate; consensual photophobia (pain when light is shone in the opposite eye)
Acute angle-closure glaucoma	Painful red eye, blurred vision, photophobia	Elevated intraocular pressure, mid-dilated and fixed pupil, hazy cornea (edema, not infiltrate), halos around lights; no fluorescein uptake
Corneal abrasion	Pain, foreign body sensation, positive fluorescein staining	Epithelial defect without underlying stromal infiltrate or opacity; no anterior chamber reaction; heals within 24-48 hours
Episcleritis / Scleritis	Red, painful eye	Sectoral redness (episcleritis) or deep boring pain (scleritis); cornea is clear; no infiltrate or staining
Endophthalmitis	Pain, decreased vision, hypopyon	Typically follows intraocular surgery or penetrating trauma; vitreous involvement; diffuse intraocular inflammation beyond just the cornea
Corneal foreign body / rust ring	Pain, tearing, foreign body sensation, focal fluorescein uptake	Visible foreign body on slit lamp; infiltrate develops only if secondary infection occurs

6. Traps and High-Yield Pearls

The single most common trap on this topic is the student who sees "red eye + contact lens wearer" and jumps to conjunctivitis. Contact lens wear combined with pain, photophobia, and a corneal infiltrate or opacity is keratitis, and the answer is empiric topical fluoroquinolone, not observation or topical erythromycin.

The second major trap is the corticosteroid question in HSV keratitis. Students must recognize the dendritic ulcer as epithelial HSV disease and know that topical steroids are absolutely contraindicated. The vignette may describe a well-meaning provider who prescribes steroid drops for a "red eye," and the question will ask what complication follows (answer: worsening ulceration and potential perforation). Conversely, if the vignette describes a patient with stromal haze, no epithelial defect, and prior HSV history, the answer is topical steroids plus antiviral.

A third pearl involves Acanthamoeba: the classic vignette is a contact lens wearer who swims in a lake or uses tap water to rinse the lens case, presenting with pain out of proportion to findings on exam and a ring-shaped infiltrate. This presentation is designed to test whether the student can distinguish it from bacterial keratitis, which would be more fulminant with purulent discharge.

Finally, always remember the corneal reflex pathway: sensation is carried by the ophthalmic division of the trigeminal nerve (V1), and the efferent limb is the facial nerve (VII). Reduced corneal sensation should raise suspicion for HSV keratitis (virus damages corneal nerves), while inability to close the eye (CN VII palsy) causes exposure keratitis. Both are commonly tested neuroanatomy connections.

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