PanOph

Bacterial keratitis

Cornea

Key Points

  • •Bacterial keratitis is an ophthalmic emergency — delay in treatment can lead to corneal perforation within 24–48 hours
  • •Always perform corneal scraping for smear and culture BEFORE starting antibiotics in sight-threatening ulcers
  • •Contact lens wear is the leading risk factor in developed nations; Pseudomonas is the most common organism in CL wearers
  • •Fortified dual therapy (cefazolin + tobramycin) is standard for sight-threatening ulcers; monotherapy fluoroquinolone for mild cases
  • •The SCUT trial showed adjunctive steroids may benefit deep central ulcers and Pseudomonas keratitis but do not improve overall outcomes
1. Definition

Bacterial keratitis is an infection of the corneal stroma caused by bacterial organisms, characterised by a corneal epithelial defect with underlying stromal infiltrate and suppuration. It is an ophthalmic emergency that can rapidly progress to corneal perforation and endophthalmitis if untreated.

2. Epidemiology

Incidence: 2.5–11 per 100,000 population per year in developed nations; significantly higher (up to 799 per 100,000) in developing countries.

Contact lens wear is the leading risk factor in developed nations (accounting for 30–60% of cases), while ocular trauma predominates in agricultural economies. Extended-wear CL carry ~4x higher risk than daily disposable (~1 in 2,500 vs ~1 in 10,000 annual incidence).

No sex predilection. Peak incidence in young adults (contact lens users) and the elderly (ocular surface disease).

Pseudomonas aeruginosa is the most common organism in contact lens wearers; Staphylococcus aureus and Streptococcus pneumoniae predominate in non–contact-lens-related cases.

3. Aetiology and causes

Gram-positive cocci:

  • Staphylococcus aureus — most common overall (non-CL); round/oval infiltrate, moderate suppuration
  • Staphylococcus epidermidis — frequently cultured from contact lenses (often a contaminant; clinically significant in post-surgical/immunocompromised)
  • Streptococcus pneumoniae — aggressive central ulcer with hypopyon, undermined (serpiginous) edges

Gram-negative rods:

  • Pseudomonas aeruginosa — most common in CL wearers; rapidly progressive liquefactive necrosis, ring infiltrate, green discharge
  • Neisseria gonorrhoeae — hyperacute onset; can penetrate INTACT corneal epithelium (classic exam differentiator); copious purulent discharge
  • Serratia marcescens — CL-associated, indolent
  • Moraxella spp. — indolent, paracentral-inferior, debilitated/alcoholic patients

Other gram-negatives:

  • Haemophilus influenzae — more common in children; associated with concurrent upper respiratory infection

Gram-positive rods:

  • Corynebacterium — opportunistic, mild
  • Bacillus cereus — post-traumatic (especially soil/metal), fulminant

Atypical:

  • Nocardia — indolent, 'wreath-like' infiltrate with satellite lesions
  • Mycobacterium (NTM) — post-LASIK or trauma, chronic non-healing keratitis
4. Pathogenesis
  1. Breach of the corneal epithelium (trauma, contact lens wear, surgery, epithelial disease) allows bacterial adherence to exposed stroma. Exception: Neisseria gonorrhoeae and Corynebacterium diphtheriae can penetrate intact epithelium.
  2. Bacterial adhesins bind to exposed extracellular matrix proteins (fibronectin, laminin). In CL wearers, Pseudomonas forms biofilms on the lens surface, creating a micro-environment that facilitates adhesion even without gross epithelial defect.
  3. Bacteria proliferate and elaborate toxins and proteases (e.g., Pseudomonas exotoxin A, elastase, alkaline protease) that cause direct stromal lysis. Pseudomonas type III secretion system injects cytotoxins (ExoS, ExoU) directly into host epithelial cells — ExoU is associated with more severe, rapidly progressive ulcers.
  4. Host inflammatory response: neutrophil infiltration → release of matrix metalloproteinases (MMP-2, MMP-9) → further stromal melting.
  5. Inflammatory mediators increase vascular permeability → anterior chamber reaction → hypopyon (sterile collection of inflammatory cells in early stages).
  6. Uncontrolled infection → descemetocele → perforation → endophthalmitis.
5. Classification

By pathological type (Jones classification):

  • Suppurative (purulent) — Pseudomonas, Pneumococcus, Gonococcus
  • Non-suppurative — Nocardia, Mycobacterium, Moraxella

By morphology:

  • Central ulcer — typically Pseudomonas, Pneumococcus
  • Paracentral/peripheral ulcer — Moraxella, Staphylococcus
  • Ring infiltrate — Pseudomonas (infectious ring abscess, suppurative) vs Acanthamoeba (differential); distinguish from Wessely immune ring (sterile, represents antigen-antibody complex at diffusion front)

By severity (Wills Eye Hospital grading):

  • Non-sight-threatening: infiltrate <2 mm, peripheral, no AC reaction
  • Sight-threatening: infiltrate ≥2 mm, central (within 3 mm of visual axis), deep stromal involvement, AC reaction, hypopyon

By organism type: Gram-positive vs Gram-negative vs Atypical

6. Risk factors and associations
  • Contact lens wear (especially extended/overnight wear, poor hygiene, swimming/tap water exposure with lenses) — strongest risk factor in developed nations.
  • Bandage contact lens use post-surgery.
  • Ocular surface disease: dry eye, blepharitis, neurotrophic keratopathy, bullous keratopathy.
  • Ocular trauma: agricultural injury, foreign body.
  • Prior ocular surgery: especially refractive surgery (LASIK, PRK — interface keratitis risk), PK.
  • Topical corticosteroid use.
  • Systemic immunosuppression: diabetes, HIV, malnutrition.
  • Lid abnormalities: lagophthalmos, entropion, trichiasis.
  • Contaminated ocular medications.
7. Clinical features

Symptoms: acute onset pain, photophobia, tearing, decreased vision, mucopurulent discharge.

Signs:

  • Corneal epithelial defect with underlying stromal infiltrate (white-yellow opacity)
  • Stromal oedema and necrosis; may have ring infiltrate (Pseudomonas)
  • Mucopurulent/purulent discharge — greenish in Pseudomonas
  • Anterior chamber reaction; hypopyon in severe cases
  • Conjunctival injection, chemosis, lid oedema
  • Corneal thinning, descemetocele, or perforation in advanced cases
  • Corneal sensation is NORMAL — reduced sensation suggests HSV or Acanthamoeba (important differentiating sign)

Organism-specific clues:

  • Pseudomonas: rapid onset, soupy liquefactive necrosis, green discharge, ring infiltrate, central
  • Pneumococcus: aggressive, central deep ulcer, undermined (serpiginous) edges, dense hypopyon
  • Moraxella: indolent, oval, paracentral-inferior, thin/malnourished/alcoholic patient
  • Nocardia: wreath-like pattern with satellite lesions, indolent course
  • Staphylococcus: round/oval infiltrate, moderate suppuration, well-defined edges
  • Neisseria: hyperacute, copious purulent discharge, can penetrate intact epithelium
  • Bacillus: fulminant post-trauma (especially soil/metal), ring abscess, rapid perforation

Red flags for severe disease:

  • Infiltrate ≥2 mm or within central 3 mm
  • Hypopyon present
  • Descemetocele or corneal thinning >50%
  • Scleral involvement or extension
  • Worsening on adequate therapy at 48h
  • Only eye / monocular patient
8. Investigations

Corneal scraping (MANDATORY before starting treatment in sight-threatening ulcers):

  • Technique: scrape base and edges of ulcer with Kimura platinum spatula (preferred instrument — common MCQ answer) or #15 Bard-Parker blade under slit lamp. Inoculate culture plates directly at the bedside using the C-streak technique (a 'C' pattern on each plate allows distinguishing true growth from contaminants).
  • Smear: Gram stain (most important initial test — identifies cocci vs rods, Gram +/−; results in ~30 minutes), Giemsa stain (morphology, intracellular organisms), KOH/calcofluor white (to rule out fungal).
  • Culture: blood agar (most bacteria), chocolate agar (Neisseria, Haemophilus), Sabouraud dextrose agar (fungi), thioglycolate broth (anaerobes), non-nutrient agar with E. coli overlay (Acanthamoeba).

Additional:

  • Corneal biopsy: if cultures negative and not responding to treatment.
  • Confocal microscopy: to exclude Acanthamoeba or fungal co-infection.
  • Anterior segment OCT: assess depth of infiltrate, stromal thinning.
  • B-scan ultrasound: if view is hazy, to rule out endophthalmitis.
9. Differential diagnosis

Fungal keratitis:

  • Feathery/serrated margins, satellite lesions, dry raised surface
  • Indolent course over days to weeks
  • History of vegetative/organic trauma
  • Corneal sensation: normal

Acanthamoeba keratitis:

  • Ring infiltrate, perineural infiltrates (pathognomonic)
  • Severe pain disproportionate to clinical signs
  • Contact lens + water exposure (swimming, tap water)
  • Corneal sensation: reduced

Herpes simplex keratitis:

  • Dendritic/geographic ulcer with terminal bulbs
  • Reduced corneal sensation (key differentiator from bacterial)
  • Recurrent episodes, unilateral
  • May have history of perioral cold sores

Marginal keratitis:

  • Peripheral, near limbus with clear lucid interval between infiltrate and limbus
  • Associated blepharitis/meibomian gland disease
  • Culture-negative (immune-mediated, not infectious)
  • Responds to topical steroids

Mooren ulcer:

  • Peripheral, progressive, juxtalimbal
  • No stromal infiltrate (distinguishing feature)
  • Chronic, painful, autoimmune
  • Diagnosis of exclusion

Sterile corneal infiltrate:

  • Small (<1 mm), multiple, peripheral
  • Minimal symptoms (mild irritation, no severe pain)
  • Contact lens–related immune reaction
  • Culture-negative, responds to steroid after ruling out infection
10. Complications

Early:

  • Corneal thinning → descemetocele → perforation
  • Iris prolapse through perforation
  • Endophthalmitis (intraocular spread of infection)
  • Secondary glaucoma (from inflammation, synechiae, or pupillary block)

Late:

  • Corneal scarring and vascularisation → permanent visual loss
  • Irregular astigmatism
  • Cataract (from inflammation or prolonged steroid use)
  • Symblepharon formation (in severe cases with conjunctival involvement)
  • Phthisis bulbi (end-stage)

Treatment-related:

  • Drug toxicity from prolonged intensive fortified antibiotics (epithelial toxicity, punctate keratopathy)
  • Steroid-related complications (secondary infection, glaucoma, delayed healing)
11. Management
  1. Corneal scraping for smear and culture BEFORE starting antibiotics (in sight-threatening ulcers). Scrape → start empirical antibiotics immediately — do NOT wait for Gram stain results before initiating therapy. Gram stain guides adjustment, not initial treatment.
  2. Loading dose protocol: instill the chosen antibiotic drops every 5 minutes for 5 doses (30 minutes), then transition to the maintenance schedule below.
  3. Empirical therapy — intensive fortified antibiotic drops:
  • Monotherapy: Fluoroquinolone (moxifloxacin 0.5% or gatifloxacin 0.3%) q1h around the clock — for non-severe ulcers. Evidence from Ofloxacin Treatment Study (OTS) showed equivalence to fortified combination.
  • Dual therapy (sight-threatening): Fortified cefazolin 5% (or vancomycin 5%) + fortified tobramycin 1.3–1.5% (or gentamicin 1.4%), alternating q30min–1h for first 48h then taper.
  • Note on antibiotic resistance: rising fluoroquinolone-resistant Pseudomonas and MRSA strains underscore the importance of culture-guided therapy. Empirical dual fortified therapy remains the safer choice for sight-threatening ulcers.
  1. Contact lens management: discontinue CL wear immediately. Culture the contact lens AND storage case immediately (lens case often grows the causative organism before corneal cultures turn positive). Do not resume CL wear until fully healed and cleared by ophthalmologist.
  2. Adjunctive therapy:
  • Cycloplegic: atropine 1% or homatropine 2% TID (reduce pain, prevent synechiae).
  • Topical anaesthetics (e.g., proparacaine 0.5%): use sparingly for examination and corneal scraping only — chronic/repeated use delays epithelial healing and is contraindicated.
  • Oral analgesics for pain.
  • Avoid topical steroids in first 48–72h; may consider after culture-positive response to antibiotics (per SCUT trial: no significant overall benefit, but beneficial in subgroups — central/deep ulcers, Pseudomonas keratitis, and vision worse than counting fingers at baseline; NOT beneficial in Nocardia or NTM keratitis).
  • Avoid patching (promotes anaerobic environment and bacterial proliferation).
  • PACK-CXL (photoactivated chromophore for keratitis corneal cross-linking): riboflavin 0.1% is applied to the debrided cornea and activated by UV-A (365 nm, 3 mW/cm²) — generates reactive oxygen species that damage microbial DNA and cross-link stromal collagen. Emerging adjunctive therapy for drug-resistant bacterial keratitis; Level 2 evidence (RCTs) shows potential benefit as an add-on, not a replacement for antibiotics.
  1. Modify treatment based on culture and sensitivity results at 48–72h. Switch from dual therapy to targeted monotherapy once organism and sensitivity are confirmed.
  2. Taper antibiotics as infiltrate resolves and epithelium heals (over 2–4 weeks).
  3. Surgical intervention if medical failure:
  • Tissue adhesive (cyanoacrylate glue) for small perforations/descemetoceles (<1.5–2 mm); bandage CL placed over glue.
  • Therapeutic penetrating keratoplasty (TPK) for uncontrolled infection or large perforation (>2 mm or progressive despite maximal medical therapy).
  • Amniotic membrane transplant for persistent epithelial defect.
  • Evisceration/enucleation in blind painful eye with panophthalmitis.

Red flags for severe disease (consider urgent referral/hospitalisation):

  • Infiltrate ≥2 mm or within 3 mm of visual axis
  • Descemetocele or perforation
  • Hypopyon
  • Scleral involvement
  • Non-compliant patient unable to self-administer hourly drops
  • Unilateral eye or only seeing eye
  • Worsening despite 48h of appropriate therapy
12. Prognosis

Visual outcome depends on size, depth, location of ulcer and virulence of organism.

Central ulcers carry worse visual prognosis due to scarring in the visual axis; peripheral ulcers generally have better outcomes as scarring does not affect central vision.

Typical healing times: Pseudomonas 2–3 weeks, Pneumococcus 3–4 weeks, Moraxella 4–6 weeks (indolent), Staphylococcus 2–4 weeks.

Pseudomonas ulcers: aggressive but respond well to appropriate antibiotics; 60–70% achieve ≥6/18 with early treatment.

Pneumococcal ulcers: moderate prognosis; deeper ulcers may require surgery.

Moraxella ulcers: indolent but may perforate if untreated.

Overall, approximately 50% of bacterial keratitis eyes achieve BCVA ≥6/12 with appropriate treatment.

Recurrence risk: 10–15%, higher in those with persistent risk factors (dry eye, CL wear).

Therapeutic keratoplasty graft survival: approximately 50–60% at 5 years.

Clinical Pearls

1
A contact lens wearer with a red eye must remove the lens and bring it (plus the case) for culture — the lens case often grows the causative organism before corneal cultures turn positive.
2
Corneal sensation is NORMAL in bacterial keratitis — if reduced, think HSV or Acanthamoeba. This single test can change your entire differential.
3
Sterile infiltrates in CL wearers are small (<1 mm), multiple, peripheral, and culture-negative — do not confuse with infectious keratitis. They respond to steroids, infectious ulcers do not.
4
Moraxella keratitis in a thin, malnourished, or alcoholic patient is a classic viva scenario — look for indolent oval paracentral-inferior ulcer.
5
If a bacterial ulcer worsens despite 48h of fortified antibiotics, consider fungal or Acanthamoeba co-infection and re-scrape — mixed infections account for up to 10% of culture-positive keratitis.
6
Neisseria gonorrhoeae can penetrate INTACT corneal epithelium — the only common bacterium that does so. Hyperacute onset + copious purulent discharge = think gonococcal.
7
Never patch a bacterial corneal ulcer — patching creates a warm, moist, dark environment that promotes bacterial proliferation.
8
Exam trap — When to culture: Scraping and culture are indicated for: corneal infiltrate >2mm, central location, deep stromal involvement, chronic/non-responding ulcer, suspected fungal/Acanthamoeba, history of contact lens wear, and any ulcer in a single-eyed patient. Small peripheral infiltrates in contact lens wearers can be treated empirically.
9
Exam trap — Fortified antibiotics recipe: Fortified cefazolin (50mg/mL): reconstitute 500mg vial, dilute with artificial tears. Fortified tobramycin/gentamicin (14mg/mL): add injectable to commercial drops. These cover Gram-positive (cefazolin) + Gram-negative (aminoglycoside). For Pseudomonas: fortified tobramycin + fluoroquinolone provides dual anti-pseudomonal coverage.
10
Exam trap — Contact lens keratitis: Pseudomonas aeruginosa is the most common organism in contact lens-related keratitis. It produces a rapidly progressive, suppurative ulcer with greenish mucopurulent discharge and ring infiltrate. Treatment: intensive fortified tobramycin + fluoroquinolone (ciprofloxacin/moxifloxacin). Never patch a contact lens ulcer — promotes bacterial growth.
11
Exam trap — Steroids in bacterial keratitis: The SCUT trial (Steroids for Corneal Ulcers Trial) showed that adjunctive topical prednisolone started 48 hours after antibiotics did NOT significantly improve overall outcomes but may benefit central, deep ulcers with baseline VA <6/60. Never start steroids before 48 hours of antibiotics and never in fungal keratitis (steroids worsen fungal infections).

Oral-exam questions

  • What instrument is used for corneal scraping? — Kimura platinum spatula (not a blade). The C-streak inoculation technique is used to distinguish true growth from contaminants.
  • Name one bacterium that can penetrate intact corneal epithelium — Neisseria gonorrhoeae. Also Corynebacterium diphtheriae (less commonly asked).
  • What is the Wessely immune ring? — A sterile ring infiltrate caused by antigen-antibody complex deposition at the diffusion front. Distinguish from infectious Pseudomonas ring abscess.
  • When would you add steroids in bacterial keratitis? — Per SCUT trial: only after 48–72h of culture-positive response to antibiotics. Beneficial in central/deep ulcers and Pseudomonas; NOT in Nocardia or NTM.
  • How do you prepare fortified cefazolin 5%? — Reconstitute 500 mg cefazolin powder with 10 mL artificial tears. Final concentration = 50 mg/mL (5%). Shelf life: 24h at room temperature, 4 days refrigerated.
  • What is the significance of a non-healing ulcer despite 48h of fortified antibiotics? — Consider mixed infection (fungal or Acanthamoeba co-infection in up to 10%), resistant organism, or incorrect diagnosis. Re-scrape and broaden workup.
  • What is the significance of a 'ring infiltrate' in corneal ulcers? — A ring-shaped stromal infiltrate indicates an antigen-antibody (Wessely immune ring) reaction in the corneal stroma. It is seen in: Pseudomonas keratitis (aggressive), Acanthamoeba keratitis (pathognomonic ring infiltrate), and some fungal infections. In the context of a contact lens wearer with ring infiltrate — think Acanthamoeba first (if indolent, painful out of proportion) or Pseudomonas (if aggressive, suppurative).
  • How do you manage a corneal perforation from infectious keratitis? — Immediate: tissue adhesive (cyanoacrylate glue) + bandage contact lens for small perforations (=<2mm). Patch graft (lamellar or penetrating) for larger perforations. Therapeutic penetrating keratoplasty if extensive perforation or uncontrolled infection. Continue intensive antibiotics. Never use steroids in a perforating ulcer==.

Mnemonics

SPEAKS

S — Staphylococcus (most common non-CL) P — Pseudomonas (most common in CL wearers) E — Epithelial defect + stromal infiltrate A — AC reaction / hypopyon K — Kimura spatula for scraping S — SCUT trial (steroids controversy)

TICS

T — Tobramycin (Gram-negative) I — Intensified q30min–1h C — Cefazolin (Gram-positive) S — Sight-threatening ulcers

Comparison Tables

Organism-Specific Features of Bacterial Keratitis
Pseudomonas aeruginosa
Onset
Rapid (hours)
Morphology
Central, ring infiltrate, liquefactive necrosis
Distinguishing Clue
Green discharge, soupy stromal melt
Associated Risk Factor
Contact lens wear
Perforation Risk
HIGH
Staph. aureus
Onset
Moderate
Morphology
Round/oval, well-defined, moderate suppuration
Distinguishing Clue
Most common non-CL organism
Associated Risk Factor
Ocular surface disease, elderly
Perforation Risk
LOW
Strep. pneumoniae
Onset
Rapid
Morphology
Central, deep, undermined (serpiginous) edges
Distinguishing Clue
Dense hypopyon, serpiginous margin
Associated Risk Factor
Dacryocystitis, debilitated
Perforation Risk
HIGH
Moraxella spp.
Onset
Indolent
Morphology
Oval, paracentral-inferior
Distinguishing Clue
Malnourished/alcoholic patient
Associated Risk Factor
Malnutrition, alcoholism
Perforation Risk
MODERATE
Neisseria gonorrhoeae
Onset
Hyperacute
Morphology
Rapidly progressive, full-thickness
Distinguishing Clue
Penetrates INTACT epithelium
Associated Risk Factor
STI, neonatal
Perforation Risk
HIGH
Nocardia
Onset
Indolent
Morphology
Wreath-like, satellite lesions
Distinguishing Clue
Wreath pattern, NTM-like course
Associated Risk Factor
Trauma, immunosuppression
Perforation Risk
LOW
Bacillus cereus
Onset
Fulminant
Morphology
Ring abscess, rapid perforation
Distinguishing Clue
Soil/metal trauma, devastating course
Associated Risk Factor
Post-traumatic (soil/metal)
Perforation Risk
HIGH
Culture Media for Corneal Scraping
Blood agar
Target Organism
Most bacteria
Key Feature
General-purpose, supports most aerobic/facultative organisms
Chocolate agar
Target Organism
Neisseria, Haemophilus
Key Feature
Enriched — lysed RBCs provide X and V factors
Sabouraud dextrose agar
Target Organism
Fungi
Key Feature
Acidic pH selects for fungal growth
Thioglycolate broth
Target Organism
Anaerobes
Key Feature
Liquid enrichment, reduced oxygen environment
Non-nutrient agar + E. coli overlay
Target Organism
Acanthamoeba
Key Feature
Trophozoites feed on bacterial lawn, leaving tracks
Monotherapy vs Dual Fortified Therapy
Indication
Monotherapy (Fluoroquinolone)
Non-sight-threatening ulcer
Dual Fortified (Cefazolin + Tobramycin)
Sight-threatening ulcer
Evidence
Monotherapy (Fluoroquinolone)
OTS trial — equivalent efficacy
Dual Fortified (Cefazolin + Tobramycin)
Gold standard for severe keratitis
Advantages
Monotherapy (Fluoroquinolone)
Commercially available, no compounding, better compliance
Dual Fortified (Cefazolin + Tobramycin)
Broader spectrum, synergistic, targets resistant organisms
Disadvantages
Monotherapy (Fluoroquinolone)
Emerging fluoroquinolone resistance
Dual Fortified (Cefazolin + Tobramycin)
Requires compounding, frequent instillation, epithelial toxicity
Dosing
Monotherapy (Fluoroquinolone)
q1h around the clock
Dual Fortified (Cefazolin + Tobramycin)
Alternating q30min–1h × 48h, then taper
Cost/Access
Monotherapy (Fluoroquinolone)
Affordable, widely available
Dual Fortified (Cefazolin + Tobramycin)
Higher cost, needs hospital pharmacy

Self-Assessment (5)

MCQ

A 22-year-old contact lens wearer presents with a rapidly progressive central corneal ulcer with ring infiltrate and greenish discharge. What is the most likely causative organism?

MCQ

Which instrument is the preferred choice for performing a corneal scraping in bacterial keratitis?

MCQ

A bacterial corneal ulcer with infiltrate size ≥2 mm, located within the central 3 mm of the visual axis, and associated with hypopyon is classified as:

MCQ

Which bacterium can penetrate INTACT corneal epithelium?

MCQ

According to the SCUT trial, adjunctive topical corticosteroids in bacterial keratitis showed benefit in which subgroup?

References

  1. AAO Preferred Practice Pattern: Bacterial Keratitis (2018)
  2. Srinivasan M, et al. The Steroids for Corneal Ulcers Trial (SCUT): secondary 12-month clinical outcomes of a randomized controlled trial. Am J Ophthalmol. 2014;157(2):327-333.
  3. Hyndiuk RA, et al. Comparison of ciprofloxacin ophthalmic solution 0.3% to fortified tobramycin-cefazolin in treating bacterial corneal ulcers (Ofloxacin Treatment Study). Ophthalmology. 1996;103(11):1854-1863.
  4. Krachmer JH, Mannis MJ, Holland EJ. Cornea and External Disease: Clinical Diagnosis and Management, 4th Edition
  5. Kanski JJ, Bowling B. Clinical Ophthalmology: A Systematic Approach, 8th Edition
  6. Ehlers JP, Shah CP. The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease, 7th Edition

Related Content

SCUT — Steroids for Corneal Ulcers TrialOTS — Ofloxacin Treatment StudyFungal KeratitisHSV KeratitisCorneal Ulcer with HypopyonDry Eye Disease
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