Acanthamoeba keratitis

Overview

Rare but sight-threatening corneal infection caused by a free-living amoeba; notorious for being misdiagnosed as herpes simplex keratitis (HSK) or bacterial keratitis, leading to delayed treatment and worse outcomes.

Presentation

•Severe ocular pain disproportionate to clinical signs - caused by perineural invasion of corneal nerves (hallmark feature)
•Radial perineuritis - inflammatory infiltrate along corneal nerves; highly suggestive of Acanthamoeba keratitis
•Ring-shaped (annular) corneal stromal infiltrate - classic late sign on slit lamp
•Pseudo-dendrites - branching epithelial lesions in early disease; mimic HSK but more ragged, less defined terminal bulbs
•Photophobia, foreign body sensation, watering, redness, blurred vision

Investigations

🥇 First-line

•Slit lamp examination with fluorescein staining - identifies epithelial defects, ring infiltrate, pseudo-dendrites, perineuritis
•Corneal scraping for microscopy - calcofluor white staining fluoresces cysts under UV light; Giemsa stain also used
•Confocal microscopy (in vivo) - non-invasive; visualises cysts and trophozoites in stroma; preferred at specialist centres
•PCR of corneal scraping - highly sensitive and specific

🏆 Gold standard

•Corneal scraping cultured on non-nutrient agar overlaid with E. coli - Acanthamoeba feeds on bacteria, leaving visible tracks on agar
💡
Acanthamoeba does NOT grow on standard blood or chocolate agar - it requires non-nutrient agar with E. coli (or Enterobacter aerogenes) overlay. This is a classic exam detail.

Management

•Treatment duration typically 6-12 months - cyst form is resistant to most antimicrobials; premature cessation risks relapse

🥇 First-line

•Topical polyhexamethylene biguanide (PHMB) 0.02% - disrupts amoebic cell membranes of trophozoites and cysts; applied hourly initially then tapered
•First-line (adjunct): Topical chlorhexidine 0.02% - combined with PHMB for synergistic effect in moderate-severe disease

🥈 Second-line

•Topical propamidine isethionate (Brolene) 0.1% - diamidine; added to biguanide therapy, particularly in early/mild disease
•Topical hexamidine - alternative diamidine
•Adjunct: Immediate and permanent cessation of contact lens wear until infection resolved

🥉 Third-line

•Oral or topical voriconazole - refractory or severe cases with deep stromal involvement
•Penetrating keratoplasty (corneal transplant) - only after infection eradicated; reserved for corneal scarring with significant visual loss
⚠️
Do NOT use topical steroids in suspected Acanthamoeba keratitis - they suppress the inflammatory response and allow the organism to proliferate unchecked. This is a common and serious pitfall when the presentation has been misdiagnosed as HSK.

Key Risk Factors

•Contact lens wear in water - swimming, showering, or hot tub use with lenses in (>85% of cases occur in contact lens wearers)
•Rinsing lens cases with tap water
•Corneal trauma

Distinguishing from Herpes Simplex Keratitis

Acanthamoeba keratitis vs herpes simplex keratitis
FeatureAcanthamoeba keratitisHerpes simplex keratitis
Dendrites on slit lampPseudo-dendrites - ragged, no clear terminal bulbsTrue dendrites with terminal bulbs - diagnostic
PainSevere, out of proportion to signsModerate, proportionate to signs
PerineuritisRadial perineuritis - highly suggestiveAbsent
Ring infiltratePresent (late sign)Absent
Key risk factorContact lens wear in waterCold sores / skin lesions (HSV)
Topical steroidsContraindicated - worsens infectionUsed in stromal disease
🎯
The exam question above illustrates the classic differentiator: true dendrites with terminal bulbs on fluorescein slit lamp = HSK, not Acanthamoeba. Acanthamoeba produces pseudo-dendrites that are more ragged and lack terminal bulbs.