BACTERIAL KERATITIS

Signs and Symptoms

The patient with bacterial keratitis will generally present with a

Culture-proven Pseudomonas keratitis
unilateral, acutely painful, photophobic, intensely injected eye. Visual with mucopurulent discharge.
acuity is usually reduced, and profuse tearing is common. There will
be a focal stromal infiltrate with an overlying area of epithelial
excavation. Often, there will be a history of contact lens wear, which is
the most common precipitating condition. Corneal trauma or pre-
existing keratopathy are also common precipitating conditions. 1

Mucopurulent discharge may emanate from the lesion. The cornea

may be edematous. The conjunctival and episcleral vessels will be
deeply engorged and inflamed, often greatly out of proportion to the
size of the corneal defect. In bacterial keratitis, injection is typically 360
degrees rather than sectoral as seen in non-infectious keratitis. A Hypopyon in bacterial keratitis.
pronounced anterior chamber reaction, often with hypopyon, is present
in severe cases. Intraocular pressure may be reduced due to secretory
hypotony of the ciliary body, but may be elevated due to blockage of the trabecular meshwork by the
inflammatory cells. Often, the eyelids will also be edematous.

Pathophysiology

Once the corneal defenses are breached, the cornea is prone to colonization and infection by pathogenic
bacteria. Factors known to compromise corneal defenses include direct corneal trauma, chronic eyelid
disease, systemic immune disease, tear film abnormalities affecting the ocular surface and hypoxic
trauma from contact lens wear.2

Pathogenic bacteria colonize the corneal stroma and immediately become antigenic, both directly and
indirectly, by releasing enzymes and toxins. This sets up an antigen-antibody immune reaction with
chemotactic factors inducing an inflammatory reaction. The body mobilizes polymorphonuclear leukocytes
(PMN), which aggregate at the area of infection, creating an infiltrate. The PMNs phagocytize and digest
the bacteria and damage stromal tissue by releasing numerous enzymes that directly affect and damage
stromal tissue.

The collagen of the corneal stroma is poorly tolerant of the bacterial and leukocytic enzymes, and
undergoes degradation, necrosis and thinning. This leads to scarring of the cornea. As thinning advances,
the cornea may perforate, thus introducing bacteria into the eye with ensuing endophthalmitis.

The most commonly occurring organisms in bacterial keratitis vary depending on the precipitating factors
of the ulcer and the geographic location of the patient. In cases involving contact lens wear and cosmetic
mascara, the most common infective organism is Pseudo-monas aeruginosa. Throughout North America,
the most common infective organism in bacterial keratitis is Staphylococcus aureus, and it appears that
there is an increased incidence of Gram-positive recovery in infectious keratitis. 3

Management

Proper diagnosis and prompt therapy are essential to preserve vision in bacterial keratitis. The first step in
management should be to obtain corneal scrapings for microbiologic studies. The standard of care
describes the use of a platinum spatula with plating directly onto blood and chocolate agar medium.
However, the effectiveness of the fluoroquinolones has led many practitioners away from this standard.
Identification, as well as sensitivity studies, will aid in management. An alternative for treatment of less
severe keratitis is a mini-tip calcium alginate culturette and transport-media-containing carrier. The results
of this technique compared to platinum spatula collection and plating was 83.3% sensitivity and 100%
specificity. The conservative approach supports culturing most, if not all, suspected infectious ulcers. We
advocate obtaining cultures for central lesions that threaten vision, are at risk of perforation, and in
institutionalized patients in nursing homes and hospitals where methicillin-resistant Staph. aureus
infections are possible.4

If the patient has been cultured, initiate broad-spectrum, empirical antibiotic therapy prior to receiving the
results. Monotherapy with fluoroquinolone eye drops has been shown to result in shorter duration of
intensive therapy and shorter hospital stay when compared with combined fortified therapy (tobramycin-
cefazolin). This finding may have resulted from quicker clinical response of healing as a result of less
toxicity found in the patients treated with fluoroquinolones. However, as some serious complications were
encountered more commonly in the fluoroquinolone group, caution should be exercised in using
fluoroquinolones in large, deep ulcers in the elderly. 5

Despite clear efficacy of fluoroquinolones in the management of bacterial keratitis, 2,6-8 consideration must
be given to the increasing resistance to these drugs. Since their inception, there has been a rise in the
incidence of bacterial isolates in keratitis that exhibit resistance to the early generation
fluoroquinolones.2,3,9 One method of combating the increasing problem of fluoroquinolone resistance and
rising level of Gram-positive infections is to use the new fourth-generation topical fluoroquinolones.

Traditional initial monotherapy has utilized the fluoroquinolone Ciloxan (ciprofloxacin, Alcon), two drops
every 15 minutes for six hours, followed by two drops every 30 minutes for 18 hours, and then tapered
depending on patient response. Another second-generation fluoroquinolone, Ocuflox (ofloxacin, Allergan),
is also an effective treatment for bacterial keratitis.7 Both fluoroquinolones have been proven to be as
effective for managing bacterial keratitis as the previously used fortified antibiotics, but with significantly
fewer side effects. Unfortunately, bacterial resistance to the second-generation fluoroquinolones has been
increasing, especially among the Gram-positive organisms. The two most recently available fourth-
generation fluoroquinolones, moxifloxacin (Vigamox, Alcon) and gatifloxacin (Zymar, Allergan), have a
greatly lowered resistance rate while providing much greater Gram-positive activity than previous
generation fluoroquinolones.10 In the future, Zymar or Vigamox dosed on an hourly basis may become the
mainstay therapy for bacterial keratitis.

Strong cycloplegia is also mandatory in order to increase patient comfort and minimize inflammation. The
weakest cycloplegic that should be employed is scopolamine 0.25% tid. If this is insufficient, then atropine
1% bid is indicated. Adjunctive use of cold compresses will also help to reduce inflammation.

The patient should be followed daily until the infection is well controlled. If the results of cultures and
sensitivities show that the initially prescribed antibiotic is appropriate for the infective organism, or if the
patient shows signs of clinical improvement (the ulcer does not worsen, and pain and photophobia are
reduced) at the 24 to 48 hour follow-up visit, a topical corticosteroid such as prednisolone acetate 1% or
loteprednol etabonate 0.5% q2h can be added to speed resolution and decrease corneal scarring.

While steroids have historically been avoided in the management of infectious keratitis, judicious use can
be beneficial. Antibiotics can suppress the infective organism, while corticosteroids can inhibit the
corneotoxic inflammatory response. It has been feared that the immunosuppressive effects of steroids
could enhance bacterial replication and worsen infection. However, if the chosen antibiotic is effective
against the organism, then the concurrent use of steroids will not inhibit the bactericidal effect of the
antibiotic.1117 But note that steroids should not be employed until the antibiotic has been given enough
time to sterilize the ulcer, minimally 24 hours. One also must be certain that there is not a simplex viral,
fungal, or protozoan infection prior to the initiation of topical steroids. Also, steroids should only be used in
conjunction with true bactericidal antibiotics such as fluoroquinolones.

Clinical Pearls
  If a patient presents with a corneal infiltrate without overlying epithelial staining, then the condition
may not be infectious bacterial keratitis.
 The use of strong bactericidal antibiotics will eliminate the infective organisms and sterilize the
ulcer, but will do nothing to quell the inflammatory reaction. In this instance, the inflammatory
reaction is as damaging to the cornea as is the infective organism. If there is evidence that the
antibiotic is suppressing the infective organism, then corticosteroid use will inhibit the
inflammatory reaction and speed healing and reduce corneal scarring.
 For steroids to be most beneficial, prescribe them while the ulcer bed is still open, usually within
the first 24 to 48 hours after you initiate antibiotic therapy. If you wait until the ulcer re-
epithelializes before adding a steroid, the beneficial effects will be reduced. A cautionary note: Be
comfortable that the antibiotic has sterilized the ulcer before instituting the steroid.

PANNUS

Definition: The word "pannus" takes its origin

from the Latin meaning "a piece
of cloth." Relating to the eye, it is
pathologically defined as a superficial
vascularization of the cornea with infiltration
of inflammatory-connective-granulation
tissue. Pannus is not a diagnosis; it is a
finding that results secondary to another
disease process.111 Pannus lesion.

Diseases associated with pannus

 LASIK2
 Allergic conjunctivitis3,11
 Toxic conjunctivitis3
 Neonatal conjunctivitis3
 Chlamydial conjunctivitis3,11
 Fuch's endothelial dystrophy4,5
 Congenital hereditary endothelial dystrophy6
 Superior limbic keratoconjunctivitis of Theodore7
 Terriens marginal degeneration7
 Mycobacterial tuberculos pannus8
 Leprosy8
 Aniridia9
 Keratoconjunctivitis10

1. Friel JP. Pannus. Dorlands Illustrated Medical Dictionary, 26th ed. Philadelphia,
PA; W.B. Saunders Co. 1985: 958959.
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Philadelphia, PA: Mosby International Ltd. 1999: 3.6.13.6.8.
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JS. Ophthalmology. Philadelphia, PA: Mosby International Ltd. 1999: 5.1.1-
5.1.22.
4. Soong HK. Corneal Epithelium. In: Yanoff M, Duker JS. Ophthalmology.
Philadelphia, PA: Mosby International Ltd. 1999: 5.2.15.2.8.
 5. McDermott ML. Corneal Endothelium. In: Yanoff M, Duker JS. Ophthalmology.
Philadelphia, PA: Mosby International Ltd. 1999: 5.3.15.3.10.
6. Sugar J. Stromal Corneal Dystrophies and Ectasias. In: Yanoff M, Duker JS.
Ophthalmology. Philadelphia, PA: Mosby International Ltd. 1999: 5.5.15.5.10.
7. Bouchard CS. Noninfectious Keratitis. In: Yanoff M, Duker JS. Ophthalmology.
Philadelphia, PA: Mosby International Ltd. 1999: 5.7.15.7.12.
8. McLeod S. Bacterial Keratitis. In: Yanoff M, Duker JS. Ophthalmology.
Philadelphia, PA: Mosby International Ltd. 1999: 5.8.15.8.10 .
9. Economou A, Simmons ST. Specific Types of glaucoma: Glaucoma Associated
with Abnormalities of Cornea and Iris, Tumors and Retinal Disease. In: Yanoff
M, Duker JS. Ophthalmology. Philadelphia, PA: Mosby International Ltd. 1999:
12.21.112.21.8.
10. Bachman JA., Gabriel H. A 10-year case report and current clinical review of
chronic beta-hemolytic streptococcal keratoconjunctivitis. Optometry 2002;
73(5):303-10.
11. Ramaesh T, Collinson JM, Ramaesh K, et al. Corneal abnormalities in Pax6+/-
small eye mice mimic human aniridia-related keratopathy. Invest Ophthalmol
Vis Sci 2003; 44(5):871-8.

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