Pr Eric E. GabisonOphthalmology · Cornea & refractive · Paris
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HomePro areaInfectious keratitis › Fungal & Acanthamoeba
Course contents ▾
  1. Introduction & epidemiology
  2. Pathophysiology
  3. Examination & semiology
  4. Severity criteria
  5. Bacterial — overview
  6. Gram-positive cocci
  7. Bacilli & atypical
  8. Fungal keratitis
  9. Acanthamoeba keratitis
  10. Low-risk — empirical
  11. Microbiology & sampling
  12. Targeted therapy & surgery
  13. Synthesis & algorithm
  14. References
Chapitre 08

Fungal keratitis

Fungal keratitis affects more than one million people per year, mainly in Africa and Asia, and is a major cause of corneal blindness in these regions [8]. It predominates in tropical and rural areas and depends on lifestyle (gardeners, farmers). On history, look for: contact lenses, corneal trauma from vegetal matter, topical steroids, immunosuppression.

The prognosis is often unfavorable because of delayed treatment. Fungal virulence is heightened by steroids; fungi penetrate rapidly toward the stroma and endothelium, with a marked anterior chamber reaction and even endophthalmitis.

8.1 Organisms

Two families: filamentous fungi and yeasts. The most frequent are Candida (yeast), Aspergillus and Fusarium (filamentous). Bacterial co-infection can complicate up to 20% of fungal keratitis (particularly Candida).

Yeasts vs filamentous fungi
TypeHost & setting
Yeasts (Candida albicans)Gut/urogenital saprophyte; temperate climates (Europe, United States); requires a compromised cornea (chronic inflammation) and often local or systemic immunosuppression.
Filamentous (Fusarium, Aspergillus)Ubiquitous (plants, soil); infection after vegetal trauma; tropical climates (India, Southeast Asia).

8.2 Presentation

  • Epithelium sometimes intact and fluorescein-negative despite a stromal infiltrate; gray, "dirty," rough surface; ulceration sometimes late;
  • Whitish infiltrate with feathery/cotton-wool, blurred and irregular borders; satellite abscesses; immune ring possible;
  • Penetration to Descemet's membrane: folds, endothelial plaque, flare, hypopyon, fibrin;
  • Often slow course — except under topical steroids, where stromal melt and perforation can occur;
  • Complications: endophthalmitis, purulent melt of the globe, orbital cellulitis.
First-line therapy (MUTT)

Topical natamycin 5% remains the first-line treatment of filamentous keratitis — particularly Fusarium, for which it is superior to voriconazole (MUTT I trial); oral voriconazole provides no additional benefit (MUTT II) [9,10].

Chapitre 09

Acanthamoeba keratitis

Free-living amoebae (Acanthamoeba) are ubiquitous — air, soil, water, especially hard (calcareous) water. They exist in two forms: trophozoites (active, motile) and cysts (dormant), the latter resistant to temperature variation, desiccation, chemical and drug attack, and pH variation.

A rare but serious infection, associated with contact lens wear (found in 85 to 93% of cases [3]) and with misuse (swimming in a pool/hot tub while wearing lenses, overnight wear, rinsing lenses or the case in tap water), water exposure, or trauma.

Onset is often gradual, with signs masked by the lenses, delaying presentation: photophobia, irritation, tearing, then intense pain, characteristically out of proportion to early corneal lesions limited to the epithelium — but this pain is present in only 50% of early cases. Antibiotic, steroid, or antiviral treatment has often already been tried without success. A stromal pseudo-immune ring and an overlying fragile, raised epithelium then appear.

Two phases

Early phase (4-6 weeks, epithelial/subepithelial): superficial punctate keratitis, epithelial irregularity (gelatinous appearance), microcysts, pseudodendrites (differential diagnosis with herpes), epithelial/subepithelial infiltrates, very painful radial keratoneuritis — a pathognomonic but inconstant sign (15%).

Late phase (> 6 weeks, stromal): often after poorly treated infection — persistent/recurrent erosions, disciform stromal infiltrate, immune ring, satellite lesions, stromal melt, thinning, reactive or amoebic scleritis.

Poor prognostic factors
Delayed diagnosis, early topical steroids, trophozoites in "chains" on confocal microscopy (HRT) [12].
Treatment
Prolonged, based on topical biguanides (PHMB). As monotherapy, PHMB 0.08% achieved ~86% medical cure, equivalent to dual therapy with PHMB 0.02% + propamidine 0.1% (ODAK trial) [11].
Major pitfall

Herpetic keratitis is the main differential diagnosis: 66-70% of amoebic keratitis is initially treated as herpes. Amoeba-herpes co-infection is exceptional (2%). Faced with a resistant "herpes" in a contact lens wearer with disproportionate pain: think amoeba.