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ACANTHAMOEBA KERATITIS

KERATITIS
It refers to the INFLAMMATION OF CORNEA
It is characterized by:
(A) Corneal Oedema
(B) Cellular Infiltration 
(C) Ciliary Congestion

Acanthamoeba

It is a Pathogenic Free Living Amoeba.
Species:   1)A.castellanii
                     2)A.culbertsoni
                     3)A.polyphagia
                     4)A.astromyx
Acanthamoeba Castellanii is responsible for Acanthamoeba keratitis
Morphology
It exists in two forms
1.Active Trophozoite form
2.Resistant Cystic form
Life Cycle

HabitatSoil, Fresh water, Well water, Sea water, Sewage, Air
Infective Form : Both Trophozoites and cysts
Mode of transmission:  Direct contact with cornea
Other infections:   Granulomatous Amoebic Encephalitis(GAE)(Inhalation or Ingestion)

ACANTHAMOEBA KERATITIS

Recently gained importance because of
1.Increasing incidence
2.Difficulty in Dx
3.Unsatisfactory Rx

ETIOLOGY

Causative agent: Acanthamoeba castellani : a pathogenic free living Amoeba
Habitat: soil, fresh water, sea water, well water, sewage , air
Mode of infection: Direct corneal contact with any material or water contaminated with the organism
CLINICAL FEATURES


Symptoms:
1.Foreign Body Sensation
2.Mild pain to Severe pain ( out of proportion to degree of inflammation)
3.Watering
4.Photophobia
5.Blurring of Vision
6.Blepharospasm

EPITHELIAL LESIONS
Epithelial roughening and irregularities: often mistaken for Punctate epitheliopathy
Epithelial ridges
Radial keratoneuritis:
Pathognomic of Acanthamoeba keratitis
Seen in 50% of cases
It is the inflammatory response of corneal nerves associated with perineural infiltrates.
These infiltrates are found in the midstroma, beginning paracentrally, and extending to the limbus in a radial pattern.
This is the cause of severe pain disproportionate to inflammation.
Trophozoites selectively cluster around corneal nerve fibres
Also seen in P. aeruginosa ulcerative keratitis
Psedodendrites:
mistaken of Herpes simplex keratitis


STOMAL LESIONS
Patchy and satellite stromal infiltrates
Ring infiltrates:
Central or Paracentral
Overlying epithelial defect
Underlying Keratic precipitates
Ring abscess:
Stromal necrosis+Hypopyon @ later stages

Differential diagnosis

Viral Keratitis
Fungal Keratitis
Suppurative Keratitis

    
DIAGNOSIS
Clinical Dx:
Difficult to diagnose due to overlapping features
Dx by exclusion in non responsive pt.s being treated for herpetic, bacterial and viral keratitis
Confocal microscopy:
Direct visualization of cysts in cornea
Laboratory Dx:
KOH mount: Detection of cysts
Calcofluor white stain: Cysts appear Bright apple green.
LPCB film: Demonstration of cysts in corneal scrapings
Culture on E.coli enriched non nutrient agar:Trophzoites within 48 hrs which turn into cysts.
PCR: Amoebic DNA
Corneal Biopsy: non conclusive cases; cyst detection

TREATMENT

Quite unsatisfactory.
1.Non specific Rx:
ØCycloplegics: 1% Atropine eye drops     
ØReduce pain from ciliary spasm
ØPrevents formation of post. synechiae from secondary iridocyclitis
ØIncrease blood supply to ant. uvea by relieving pressure in ant. ciliary artery; thereby bringing more antibodies to aqueous humor
ØReduces exudation by decreasing hyperemia and permeability
ØSystemic analgesics: Paracetamol or Ibuprofen
ØVitamins: A,B and C: Helps in healing
2)Specific Rx:
a.Topical antiamoebic agents include:
Diamidines: Propamidine isethionate (0.1 %), and
   hexamidine (0.1%).
Biguanides : Polyhexamethylene biguanide
   (PHMB), 0.02% and chlorhexidine, 0.02%.
Aminoglycosides: Neomycin and Paromycin
Imidazoles: Clotrimazole and miconazole.
Multiple drug therapy is needed for a long time (3–4
months) for early epithelial lesions and 6–12 months
for stromal lesions. Any of the following combination
may be choosen:
Propamidine or hexamidine + PHMB or
Chlorhexidine + Neomycin or
Paromycin + clotrimazole or miconazole or
itraconazole.
• Frequency of instillation: hourly for a week, then
taper slowly over 3–4 months for epithelial lesions
and 6–12 months for stromal lesions.
b. Oral ketoconazole 200 mg BID, or itraconazole 100mg BD may be added in advanced cases.

3. Long-term prophylactic therapy with PHMB, twice a day for a year is recommended.
4. Penetrating keratoplasty is frequently required in non-responsive cases. Surgery should be performed after a full course of maximum medical therapy and a quiescent phase of at least six months.


                     



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