A Case of Chronic Acanthamoeba Keratitis

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Transcript A Case of Chronic Acanthamoeba Keratitis

A 12 year history of
Chronic, Culture-confirmed
Acanthamoeba Keratitis
Elmer Y. Tu, MD
Joel Sugar, MD
Charlotte E. Joslin, PhD
Lisa M. Nijm, JD, MD
The authors have no financial interest in the subject
matter of this poster
Purpose
 To
report a case of chronic, recalcitrant
Acanthamoeba keratitis (AK) persisting for
over 12+ yrs.
Clinical Presentation (12/27/1995)

32 y.o female physician contact lens wearer
seen in consultation at the University of Illinois
Eye and Ear Infirmary (IEEI) for chronic keratitis
of the right eye of 2 years duration.

Herpetic keratitis 1989 OD
• Recurrent dendritic disease 1994



Dendritic disease resolved with topical trifluridine alone
Development of persistent stromal edema, subsequent immune
ring
June 1995 – Recurrence tx with topical
corticosteroids, trifluridine.
• Persistent inflammation required continued medications as
above. Oral acyclovir was added 200 mg q.i.d.
Clinical Presentation (12/27/1995)
 OS
Normal
 OD VA 20/40-2
 Slit lamp examination


Mild central stromal edema
Fine KP over the central corneal endothelium
• AC quiet

Partial, superficial anterior stromal immune
crescent extending between 3 and 7 o’clock
paracentrally.
Clinical course
 Waxing
and waning course of corneal
inflammation


Visual acuity fluctuates between 20/20 and
20/50.
Chronic very low dose topical corticosteroids
and occasional trifluridine
 Referred

to the University of Iowa
Confocal microscopy and epithelial biopsy
performed
• Acanthamoebae identified
Clinical course

Initial anti-acanthamoebal
treatment


Chlorhexidine 0.02% Q2h for 3
weeks
Continued for 11 months Q2-qid
dosing.
• Discontinued because of
pregnancy
• Maintained on topical steroids

Subsequent 8 years


Intact endothelium
Extended treatment with topical
chlorhexidine, polyhexamethyl
biguanide (PHMB), desmodine,
oral itraconazole without significant
change in inflammatory
recurrences or activity.
Visual acuity largely maintained
20/20-20/25 BSCVA
Stromal haze, scarring No
organisms appreciated
2001 Nidek Confoscan 2
Clinical Course

Follow up at an outside facility without change in
therapy
 November, 2006






Increasing severity and frequency of episodes of
inflammation
Prednisolone acetate 1% Q1h
Decreasing vision – 20/60
Corneal thickness – 576 OD, 618 OS
IOP normal
Slit lamp examination – Large KP, moderate corneal
haze
Intervention

Vision declined to 20/200
despite hourly topical
corticosteroids, topical
chlorhexidine, oral
voriconazole


Full thickness Penetrating
keratoplasty 1.9.2007
Pathology – endothelial cell
attenuation, stromal
infiltration
Microcystic epithelial
edema
• No organisms seen

Culture – Positive for
acanthamoeba
Acanthamoeba cysts in
deep stroma – bright
centered thick walled
structures (arrow)
2006 Nidek Confoscan 3
Follow-up
 August,




2009
Visual acuity BSCVA 20/30
Topical loteprednol QD
No adjunctive anti-acanthamoebal therapy
No further episodes of inflammation
Discussion

To our knowledge, our patient represents the
longest sustained corneal infestation with
recoverable Acanthamoebae reported to date.
 The stromal inflammation seen in our patient is
not uncommon in AK, but usually subsides with
preferred therapy which our patient received for
years often at high sustained frequencies.


Indicates that this organism was clinically resistant
Persistence of inflammation has been suggested
to represent either persistent infection, reported
lasting a year or more, or a sterile reaction to
persistent amoebic antigens.
Discussion
 Persistence


of infection is not surprising.
Acanthamoebal cysts may survive in harsh
environments, remaining viable for decades.
Host immune response is likely ineffective in
aiding clearance of Acanthamoebae
• The use of corticosteroids has not been associated
with poorer outcomes in AK, and it is unclear what
role it may have had here, but was successful in
maintaining ~ 20/25 vision for over a decade
Conclusion

Clinicians need to be aware that AK may manifest as a
chronic recurrent stromal keratitis lasting >10 years


Chronic, persistent inflammation should not be interpreted as
sterile until otherwise proven
Course further mimics HSV keratitis
• May also coexist with HSV keratitis

Should be suspected in any at-risk individuals with this clinical
picture
• Contact lens wearers

Confocal microscopy has adjunctive utility in deep AK


Identified both at epithelial and deep stromal stage
Surgical intervention may be necessary and curative
when medical therapy fails

Oral voriconazole was added late, earlier, more aggressive
medical therapy may be indicated