7 Contact lens infections Flashcards

1
Q

Microbial/infectious keratitis:

A

Inflammation of cornea by bacteria, fungus, protist
Often following CL wear/corneal damage

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2
Q

Microbial keratitis risks:

A

CL overnight/extended wear
Inadequate hygiene
Ocular/systemic disease (diabetes/mellitus)
Extended corticosteroid use
Surgery / trauma

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3
Q

Acanthamoeba keratitis:

A

Rare protist corneal infection
Present in air, soil, fresh/tap water, hospital equipment, chlorinated pools
80% from CL wear (night/extended/submerged)

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4
Q

Acanthamoeba structure:

A

The ancan. Trophozoite has amoeboid shape with spike acanthopodia

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5
Q

Acanthamoeba protist survival:

A

Phenotypic switch into cyst form withstands environment (feeding /replication stage)
Extreme conditions (antimicrobials) > double walled cyst (no metabolism)
Difficult treatment

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6
Q

Acanthamoeba keratitis clinical presentation:

A

Extreme pain, redness, epiphora, FBS, photophobia
Progression > ring infiltrates (inflammtory in stroma) > Corneal ulceration /stromal abscess > enucleation

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7
Q

Acanthamoeba pathogenesis:

A

Adhesion to cornea epithelium
Cytopathic desquamation of epithelium > bowman’s penetration
Stromal invasion via collagenolytic enzyme
Neuritis (focus nerve damage)

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8
Q

Acanthamoeba adhesion

A

Binding to mannose glycoproteins via adhesin expressed on trophozoite mannose-binding protein
Abrasion / CLs increase mannose expression

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9
Q

Acanthamoeba Cytopathic effect

A

Cytolysis, phagocytosis, apoptosis of corneal epithelium
Inhibition of proteins > increase Ca channel activity

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10
Q

Acanthamoeba Stromal invasion:

A

Collagenolytic enzyme (serine/MMPs) release, damage collagen type 1
Causes corneal lesions, stromal ring infiltrates

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11
Q

Acanthamoeba treatment:

A

Topical drug cocktail against cysts
Biguanides (polyhexamethylese: PHMB) + diamidines (Hexamidine)
Hourly 0.2% of each then tapered

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12
Q

Mycotic keratitis

A

Corneal fungal infection of damaged epithelium
Filamentous (tropical): Fusarium
Yeast like (temperate): Candida

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13
Q

Mycotic keratitis risks:

A

CLs, Agriculture, defective eye closure, systemic diseases (diabetes)

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14
Q

Mycotic keratitis clinical presentation:

A

Abrupt pain, photophobia, discharge, blur, ulcer, feathery satellite infiltrates
IOP increase from iris fungal mass

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15
Q

Mycotic keratitis mechanism:

A

Adhesion to damaged epithelium via adhesins
Invasion past immune via fungal load
Morphogenesis to evade antimicrobials
Toxigenicity via mycotoxin production

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16
Q

Mycotic adhesion

A

Adhesins bind to cells/glycoproteins via mannoprotein
Glycoproteins upregulation by epithelium damage

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17
Q

Mycotic keratitis treatment:

A

Chemotherapy (topical + systemic)
Antifungals:
Polyenes (Natamycin)
Azoles (Triazoles)
Fluorinated pyrimidines (Flucytosine)
Dangerous in developing countries

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18
Q

Bacterial keratitis:

A

90% of microbial keratitis, mainly from CLs
Caused by Pseudomonas aeruginosa (most common), Strep p. (ulcer in developing countries), Staph a. , serratia

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19
Q

Bacterial keratitis clinical presentation:

A

Pain, redness, photophobia, ulceration
Ring infiltrates
IOP increase / glaucoma

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20
Q

Bacterial keratitis mechanism

A

Adhesion via adhesins
Invasion via proteases
Cytotoxic cornea damage
Stromal Necrosis and ring infiltrates

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21
Q

Bacterial keratitis adhesion:

A

Flagella mobilize microbe (non-virulent without)
Pili / Fimbriae > bind damaged epithelium carbohydrates/proteins
Staph a. > MASCRAMMS bind to collagen

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22
Q

Bacterial keratitis invasion

A

Exotoxin proteases degrade basement membrane
Metalloprotease and immune stimulation > RO presence
P Aeru. Contains many proteases which melt cornea

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23
Q

Bacterial keratitis drug treatments:

A

Broad spectrum antibiotics
Analgesics for pain
Cycloplegics for ciliary spasm
Antiglaucoma for IOP
Therapeutic CL for ulceration
Avoid NSAIDs (risk corneal melting)

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24
Q

Bacterial keratitis antibiotic treatments:

A

Broad spectrum antibiotics > Fluroquinolone mono/combination therapy
Aminoglycosides > gram-neg
Cephalosporin > gram-pos
Fluroquinolones > both bacteria via DNA/topisomerase inhibition

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25
Bacterial keratitis treatment procedure:
Broad-spec antibiotics every half hour for a day Severe cases use loading doses 5 minutes for 30 minutes
26
Innate defences of cornea:
Tears > lactoferrin/lysozyme, immunoglobins (IgA/G), filtration Epithelia > Cytokine secretion (IL-a) on damage > immune response Keratocytes > IL-6 synthesis > anti-microbial / healing Corneal nerves > sensory reflex via substance P/Calcitonin > IL-8 > Neutrophils Complement > Protein cascade in limbus Interferons (IFN) > Antiviral proteins
27
Interferon corneal defence:
IFN-a from leucocytes IFN-b from fibroblasts IFN-y from T/NK cells MHC assist IFNs IFN-a/b activate NK cells to target viral cells
28
Cells of innate immunity:
Neutrophils Eosinophils Macrophages NK cells
29
Neutrophils:
Pass endothelial cells via diapedesis (adhesion receptors on endothelum) Phagocytoses microbes
30
Eosinophils:
With IgE receptors and complement components Activated via IL-3/5 > granulation
31
Macrophages in corneal defence:
Phagocytic / antigen presenting / Cytokine secretion
32
NK cells in corneal defence:
Large granular lymphocytic cells without antigen receptors Recognize MHC1 > inhibition Lyse cells poorly expressing MHC Secrete TFN-a / IFN-a
33
Cells of acquired immunity
Langerhans cells Cytokines
34
Langerhans cells of cornea:
Antigen presenters with MHC-2/1 antigens in limbal cornea Recognize nonself antigen > processed > MHC transport to surface > T cell activation MHC1 > CD8+ Cytotoxic T cell (kill microbe) MHC2 > CD4+ T Helper cell (secrete cytokines)
35
Cytokine release in cornea:
TH1 > IL-2 / IFN-y, IgG/M/A synthesis TH2 > IL-4/5, IgE synthesis
36
Immunologic differences from limbus to central cornea:
Peripheral: Langerhans / IgM / C1 (complement cells) Antigen-antibody complexes activate complement easier in periphery
37
Immune response to pseudomonas aeruginosa:
Bacterial lipopolysacchride (LPS) presence > Toll receptor 4 activation > Platelet adhesion molecule > increased diapedesis of neutrophils
38
Contact lens complications:
Hypoxia Microbial keratitis Allergic / Toxic reaction CL DED/Discomfort CL-induces papillary conjunctivitis Mechanical damage
39
Corneal oxygen supply with CLs:
Disrupts O2 (Dk/t) / nutrient flow from tear film Disrupts tear flow Exacerbated by poor fit/extended wear
40
CL Hypoxia induced changes:
Ocular/limbal erythema (redness) Stromal oedema, vascularization, epithelial thinning, endothelial polymegethism (change in cell size), weakened immune defence.
41
Treatment for CL hypoxia:
Silicone hydrogel / rigid gas-permeable CL change Intermittent wear, CL discontinuing
42
Inflammatory CL changes/clinical presentation:
CL infiltrative events (CIE) Contact lens-induced red ere (CLARE) Pain, photophobia, keratitis, peripheral ulcers
43
Risk of non-infective CL inflammation:
30 day extended wear, Silicone hydrogel CLs, poor eye closure, tight lenses Smoking > Infiltrates Toxicity from CL solution
44
Non-infective CL inflammation treatment:
Self resolving in 21 days after cessation Corticosteroids / antibiotics increase speed CL hygiene education
45
CL induced papillary conjunctivitis (CLPC) types:
Local > CL too thick > chemotactic factor release > inflammatory response Generalized > denatured tear film > lens deposits > antigenic stimulus
46
CL induced papillary conjunctivitis CLPC risks:
Soft CLs (silicone-hydrogel) Mechanical stimuli from poor CL fit Long term wear > accumulation of lens deposits
47
Cl induced papillary conjunctivitis (CLPC) clinical presentation:
Papules, palpebral conjunctival erythema (redness) Itching, mucus discharge
48
CL induced papillary conjunctivitis (CLPC) treatment:
Daily CL change Hydrogen peroxide CL solution Enforce rinse-rub cleaning Topical mast cell stabilizers / antihistamines > steroids Cessation of CLs
49
Allergic / Toxic reaction to CL pathophysiology:
Uptake of small molecules from hydrogel material and CL solution > immune response
50
Manifestations of allergic / toxic CL reaction:
Toxic keratitis / conjunctivitis with conj. Hyperemia, corneal irritation/infiltrates Pain, CL intolerance, photophobia, tearing Leads to Limbal stem cell deficiency (LSCD) and limbal corneal staining (after 2-4h)
51
Causes of allergic / toxic CL reaction:
Irritate / cause LSCD / Stain limbal cornea Preservatives (Thiomersal) Overnight wear/hypoxia
52
Definition of CL related discomfort and dryness
Episodic or persistent adverse ocular sensation related to lens wear Symptoms must subside after cessation, unlike DED
53
Physical clinical signs of CL related discomfort/dryness:
Lid wiper epitheliopathy and lid parallel conj. Folds
54
Lid wiper epitheliopathy
CL friction on blink > palpebral conj. Irritates > abrasion on blink with ocular surface/CL > lissamine stain parallel to marx's line (lid rim facing eye)
55
Lid parallel conj. Folds
Bulbar conj. Stretching and folding at lower lid margin At 4 and 8 o'clock on bulbar conj.
56
CL wear and dry eye
12 fold risk factor, 50% CL users experience EDE symptoms Caused by meibomian blockage via mechanical trauma
57
Treatment of CL related discomfort/dryness
EDE treatment > lipid lubricant, lid hygiene, compress, suppliments Without EDE > Daily CL change, non-preseritive solution, manage Demodex
58
Mechanical changes with CLs:
Blinking / eye rubbing / CL dislocation / insertion / removal / CL damage Long term wear > Corneal sensitivity loss (with low O2) Sup. Epithelial arcuate lesions (SEAL) > upper cornea lesion Corneal warpage from poor fitting hard CLs
59
CL microbial keratitis epidemiology and risk
Risk increases 80 fold, 2-5 per 10000 users 10% with MK lose 2 lines of vision Smoking, poor hygiene, unlicensed lens use
60
Treatment of CL microbial keratitis:
CL cessation, broad spectrum antimicrobials, cycloplegics (synechiae prevention), doxycycline (corneal melting prevention)
61
Types of microbes in CL related microbial keratitis:
Bacterial > most common Pseudomonas sp. Fungal > commonly in tropical and agriculture Acanthamoeba > Protozoan in water