7 Contact lens infections Flashcards
Microbial/infectious keratitis:
Inflammation of cornea by bacteria, fungus, protist
Often following CL wear/corneal damage
Microbial keratitis risks:
CL overnight/extended wear
Inadequate hygiene
Ocular/systemic disease (diabetes/mellitus)
Extended corticosteroid use
Surgery / trauma
Acanthamoeba keratitis:
Rare protist corneal infection
Present in air, soil, fresh/tap water, hospital equipment, chlorinated pools
80% from CL wear (night/extended/submerged)
Acanthamoeba structure:
The ancan. Trophozoite has amoeboid shape with spike acanthopodia
Acanthamoeba protist survival:
Phenotypic switch into cyst form withstands environment (feeding /replication stage)
Extreme conditions (antimicrobials) > double walled cyst (no metabolism)
Difficult treatment
Acanthamoeba keratitis clinical presentation:
Extreme pain, redness, epiphora, FBS, photophobia
Progression > ring infiltrates (inflammtory in stroma) > Corneal ulceration /stromal abscess > enucleation
Acanthamoeba pathogenesis:
Adhesion to cornea epithelium
Cytopathic desquamation of epithelium > bowman’s penetration
Stromal invasion via collagenolytic enzyme
Neuritis (focus nerve damage)
Acanthamoeba adhesion
Binding to mannose glycoproteins via adhesin expressed on trophozoite mannose-binding protein
Abrasion / CLs increase mannose expression
Acanthamoeba Cytopathic effect
Cytolysis, phagocytosis, apoptosis of corneal epithelium
Inhibition of proteins > increase Ca channel activity
Acanthamoeba Stromal invasion:
Collagenolytic enzyme (serine/MMPs) release, damage collagen type 1
Causes corneal lesions, stromal ring infiltrates
Acanthamoeba treatment:
Topical drug cocktail against cysts
Biguanides (polyhexamethylese: PHMB) + diamidines (Hexamidine)
Hourly 0.2% of each then tapered
Mycotic keratitis
Corneal fungal infection of damaged epithelium
Filamentous (tropical): Fusarium
Yeast like (temperate): Candida
Mycotic keratitis risks:
CLs, Agriculture, defective eye closure, systemic diseases (diabetes)
Mycotic keratitis clinical presentation:
Abrupt pain, photophobia, discharge, blur, ulcer, feathery satellite infiltrates
IOP increase from iris fungal mass
Mycotic keratitis mechanism:
Adhesion to damaged epithelium via adhesins
Invasion past immune via fungal load
Morphogenesis to evade antimicrobials
Toxigenicity via mycotoxin production
Mycotic adhesion
Adhesins bind to cells/glycoproteins via mannoprotein
Glycoproteins upregulation by epithelium damage
Mycotic keratitis treatment:
Chemotherapy (topical + systemic)
Antifungals:
Polyenes (Natamycin)
Azoles (Triazoles)
Fluorinated pyrimidines (Flucytosine)
Dangerous in developing countries
Bacterial keratitis:
90% of microbial keratitis, mainly from CLs
Caused by Pseudomonas aeruginosa (most common), Strep p. (ulcer in developing countries), Staph a. , serratia
Bacterial keratitis clinical presentation:
Pain, redness, photophobia, ulceration
Ring infiltrates
IOP increase / glaucoma
Bacterial keratitis mechanism
Adhesion via adhesins
Invasion via proteases
Cytotoxic cornea damage
Stromal Necrosis and ring infiltrates
Bacterial keratitis adhesion:
Flagella mobilize microbe (non-virulent without)
Pili / Fimbriae > bind damaged epithelium carbohydrates/proteins
Staph a. > MASCRAMMS bind to collagen
Bacterial keratitis invasion
Exotoxin proteases degrade basement membrane
Metalloprotease and immune stimulation > RO presence
P Aeru. Contains many proteases which melt cornea
Bacterial keratitis drug treatments:
Broad spectrum antibiotics
Analgesics for pain
Cycloplegics for ciliary spasm
Antiglaucoma for IOP
Therapeutic CL for ulceration
Avoid NSAIDs (risk corneal melting)
Bacterial keratitis antibiotic treatments:
Broad spectrum antibiotics > Fluroquinolone mono/combination therapy
Aminoglycosides > gram-neg
Cephalosporin > gram-pos
Fluroquinolones > both bacteria via DNA/topisomerase inhibition