Introduction & epidemiology

Infectious keratitis (IK) is the leading cause of corneal blindness worldwide and the fifth cause of blindness from all causes. Its incidence varies widely by region — from 2.5 to 799 cases per 100,000 population/year — with the heaviest burden falling on low- and middle-income countries ^[1,2].

The causative pathogen depends closely on the geographic and climatic setting and on the patient's risk factors. In industrialized countries, contact lens wear is the main risk factor and increases the risk of corneal infection by a factor of up to 6 ^[3].

IK are severe infections of the corneal stroma, commonly called abscesses. They most often follow an ocular surface injury and may be caused by bacteria, fungi, amoebae or, more rarely, viruses; polymicrobial infection is found in 2 to 15% of cases ^[1].

Pathophysiology of corneal infection

A corneal infection almost always implies a compromised cornea: damaged epithelium and impaired defense system. At least one of these factors is nearly always present and must be sought systematically:

• Altered eyelid kinetics or position;
• Reduced corneal sensation;
• Qualitative or quantitative abnormality of the tear film, which is rich in antibacterial proteins (lysozyme, lactoperoxidase, lactoferrin, beta-lysin, alpha- and beta-defensins, secretory IgA, complement);
• Local or systemic iatrogenic factors.

Most micro-organisms colonize only an already compromised cornea. A few bacteria are, however, directly invasive on a healthy cornea — Neisseria gonorrhoeae, Corynebacterium diphtheriae, Haemophilus influenzae, Listeria and certain strains of Pseudomonas aeruginosa. They adhere to the epithelium and then to the stroma via surface adhesins and secrete proteases and toxins that degrade the extracellular matrix and allow stromal penetration ^[2].

In the contact lens wearer, the lens and its case promote biofilm formation and bacterial adhesion (particularly P. aeruginosa), while chronic hypoxia, epithelial microtrauma, and reduced tear clearance impair the surface defenses ^[3].

Clinical examination & ulcer semiology

3.1 History

Seek risk factors (contact lenses and their care regimen, trauma — particularly vegetal —, recent corneal or refractive surgery, pre-existing corneal disease, immunosuppression) and characterize the pain and the drop in acuity, which varies with the location of the abscess. On a compromised ocular surface, consider Gram-positive cocci and yeasts.

3.2 Clinical diagnosis

Slit-lamp examination after instillation of fluorescein refines the diagnosis and guides assessment of severity. The clinical appearance points toward the etiology but cannot, on its own, reliably identify the organism: distinguishing bacterial from fungal keratitis on examination alone remains poor ^[2,7]. The very definition of an abscess combines a fluorescein-staining epithelial defect and a localized or diffuse infiltrate, with conjunctival hyperemia and a perilimbal (ciliary) flush.

The Wessely ring (immune ring) is an annular stromal infiltrate surrounding a central abscess.

Severity criteria — the 1-2-3 rule

Severity criteria trigger microbiological sampling and intensive treatment. The first landmark is a mnemonic:

Other severity criteria:

• Associated scleritis;
• Associated endophthalmitis;
• Impending or established perforation;
• Suspected Pseudomonas or Neisseria;
• Worsening despite 24 h of antibiotic therapy;
• Bilateral involvement;
• Corneal graft;
• Postoperative setting (refractive or corneal surgery);
• Host: child, immunosuppression.