We experienced a cluster of 3 cases of culture-proved infectious keratitis
that, although caused by different organisms, each had a white plaque attached
to the corneal surface without the typical findings associated with an infectious
A 68-year-old woman visited our clinic complaining of a foreign body
sensation and epiphora for 3 weeks in her right eye. She had no history of
ocular disease or trauma. On slitlamp examination, a white plaque of gelatinous
texture with sharply demarcated and elevated margins was seen on the nasal
paracentral cornea in conjunction with a pterygium (Figure 1A). There was no epithelial defect, stromal infiltration
around the plaque, or cellular reaction in the anterior chamber. Specimens
were collected from the periphery of the plaque for smear and culture, and
hourly administration of fortified antibiotic eyedrops was initiated. However,
no resolution of the corneal plaque was observed for 1 week. Plaque removal
was tried and the lesion was easily removed, leaving an almost clear stromal
bed underneath. Assuming a diagnosis of a sterile corneal ulcer because of
the quiet ocular findings and negative culture report, the fortified topical
antibiotic regimen was changed to ofloxacin, 4 times daily, with hourly nonpreserved
artificial tears. An epithelial defect at the plaque removal site persisted
for 2 weeks, so we applied human amniotic membrane (HAM) and removed the pterygium.
However, the epithelial defect slowly enlarged into the central cornea despite
a lateral tarsorrhaphy. A white plaque reappeared on the epithelial defect
during the next 3 months. Four months after her initial examination, we repeated
removal of the corneal plaque and microbiologic testing from the stromal bed.
The corneal plaque showed a roughened surface that appeared calcific in nature
(Figure 1B) and was easily detached.
The culture result disclosed Comamonas acidovorans
with susceptibility to several antibiotics, including cefotaxime sodium, ceftriaxone
sodium, ceftazidime, imipenem, and pefloxacin, although the patient did not
return during the follow-up for treatment. Three months later, she sought
care for a corneal perforation at another clinic and underwent evisceration
A, A white plaque of gelatinous
texture with sharply demarcated and elevated margins is seen on the nasal
paracentral cornea in conjunction with a pterygium. B, The corneal plaque,
which slowly reappeared after the removal of the original plaque in part A,
exhibits a roughened surface and an apparently calcific nature and was easily
detached. C, Perforation is seen in the central cornea where the white plaque
was attached in part B.
A 66-year-old woman was referred to us for a 1-month history of a foreign
body sensation in her left eye. Initial slitlamp examination showed a white,
calcific-appearing plaque with an elevated and well-outlined border (Figure 2). The cornea was otherwise quiet
with no cellular reaction in the anterior chamber. The plaque was removed
surgically and scraping for culture was performed from the underlying stromal
bed. HAM was transplanted with the basement membrane layer up to prevent a
persistent epithelial defect. Corneal epithelium, initially growing over the
periphery of the HAM, failed to cover the center of the HAM, which showed
signs of dissolution. At that time, pathologic examination of the plaque disclosed
suspicious filamentous organisms embedded within severely degenerative tissue,
and the microbiology laboratory reported the growth of Microsporum species. Treatment was begun with 0.15% amphotericin B
eyedrops, and the HAM was covered slowly with epithelium, with no sign of
recurrence at 3 months after discontinuation of treatment.
A white plaque, apparently calcific
in nature, is seen with elevated and well-defined margins. Otherwise, the
cornea appears to be quiet and the anterior chamber is clear.
A 57-year-old man was referred for a possible corneal ulcer. He had
complained of a gritty sensation in his left eye for 3 weeks. He also had
a white and apparently calcific plaque, which had a well-demarcated and elevated
margin (Figure 3A). A mild cellular
reaction (1+) was seen in the anterior chamber. Excisional biopsy of the plaque,
scrapings from the stromal bed for smear and culture, and transplantation
of HAM over the denuded stroma were performed, followed by initiation of treatment
with fortified antibiotics. One week later, the HAM started to dissolve, revealing
a puslike fluid accumulation underneath. Natamycin eyedrops were added according
to the biopsy result, which showed many filamentous fungal organisms within
the plaque (Figure 3B). Acremonium species were cultured from the stromal bed. The corneal
lesion improved gradually without any sequelae except for opacity that was
limited to the HAM.
A, A white and apparently calcific
plaque shows a well-demarcated and elevated margin. B, The filamentous fungal
organisms that were within the excised plaque (Gomori methenamine silver,
original magnification ×200).
Although caused by different organisms, our 3 cases of infectious keratitis
were characterized by the shared manifestations of a white corneal plaque,
slow progression, and mild clinical inflammatory features relative to most
cases of infectious keratitis. Entrapment of less virulent microorganisms
within the plaques, which were formed by an unknown mechanism, might be the
reason for the slow and mild clinical features. However, corneal perforation
is possible if the correct diagnosis and proper management are delayed as
in case 1, where pathological examination of the plaque was not performed
owing to our inexperience.
We performed immediate HAM transplantation in cases 2 and 3 because
of the problem of the persistent epithelial defect in case 1, where the initial
negative microbiologic report influenced us not to be suspicious of an infection
in cases 2 and 3. In retrospect, we do not think that HAM transplantation
was essential to healing. In fact, the HAM might have acted to some extent
as a barrier against the penetration of antimicrobial eyedrops. The best management
option would probably be an excisional biopsy of the plaque and the administration
of antibiotics guided by an in vitro drug sensitivity test, without HAM transplantation.
HAM could be used later if an epithelial defect persists after treatment of
the infectious component.
As for the cultured microorganisms in this report, C acidovorans is a ubiquitous gram-negative rod and is generally considered
nonpathogenic. Keratitis caused by C acidovorans
has been rarely reported, and no reported cases showed clinical features that
were similar to our case 1.1,2Microsporum, although one of the most common causative
organisms for dermatomycoses, has not been reported to cause infectious keratitis
to the best of our knowledge. Acremonium-caused keratitis
is also rare compared with other fungal infections.3
Further microbiologic evidence may be needed to confirm the true role of these
organisms in corneal ulcers. We believe, however, that corneal perforation,
as in case 1, and a healing response to antifungal drops, as in cases 2 and
3, suggest the infectious nature whatever the actual causative organism might
In conclusion, these were all cases of indolent corneal infections that
manifested as white plaques on the cornea. It is important to perform culture
and histopathologic studies on the plaque in addition to the stromal bed for
this kind of atypical infectious keratitis.
Corresponding author and reprints: Beom-Jin Cho, MD, Department of
Ophthalmology, College of Medicine, University of Ulsan, Asan Medical Center,
#388-1, Poongnap-dong, Songpa-gu, Seoul 138-040, South Korea.
Cho B, Lee YB. Infectious Keratitis Manifesting as a White Plaque on the Cornea. Arch Ophthalmol. 2002;120(8):1091-1093. doi: