INFECTIVE KERATITIS

 Infective keratitis is an uncommon but important infection because it

has the potential to cause blindness. It can be caused by a wide
variety of microorganisms. Most children with corneal infections
come to medical attention because of a painful red eye.
Distinguishing infectious keratitis from other causes of red eye
accurately and promptly is extremely important.

PATHOGENESIS
 Trauma caused by the use of contact lenses is the most common
factor predisposing to bacterial and fungal keratitis in children

RISK FACTORS:
Trauma
 Corneal foreign body
 Corneal abrasion or laceration
 Contact lens wear
 Trichiasis or distichiasis
 Prior ocular or eyelid surgery
Corneal exposure
 Congenital and acquired disorders of the eyelids globe proptosis
 Facial palsy
 Moribund or sedated state
Abnormalities of the ocular surface
 Dry-eye syndrome
 Mucin deficiency from loss of goblet cells malnutrition
 Corneal anesthesia

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 Ocular rosacea
Immunodeficiency states
 Topical corticosteroid therapy immunosuppressive therapy
 Immune deficiency syndrome
 Atopy

CLINICAL PRESENTATION
 Severe pain is the hallmark of infective keratitis. Reflex tearing,
redness of the eye, photophobia, and decreased vision are
prominent symptoms.
 Keratitis usually is distinguished by the presence of greyish corneal
opacification. Loss of the epithelium over the corneal infiltrate dulls
the corneal light reflex and permits topically applied fluorescein dye
to stain the area.
 Progressive destruction can lead to corneal thinning and eventual
perforation. The anterior chamber can contain dispersed
inflammatory cells or visible aggregates of neutrophils layering
inferiorly (hypopyon).
 In an uncooperative child, examination of the eye is facilitated by the
use of a topical anesthetic and a lid speculum.

ETIOLOGY
Herpes Simplex Virus:
 Keratoconjunctivitis caused by herpes simplex virus (HSV) usually is
mild and, during the primary episode of infection, is indistinguishable
from other causes of viral conjunctivitis except by the presence of
skin or corneal lesions.

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 The most common manifestations are unilateral follicular
conjunctivitis, watery ocular discharge, and preauricular adenopathy.
Inspection of the swollen lids often reveals the presence of vesicles
or lid margin ulcerations.
 Most episodes of herpetic keratitis represent recurrent disease after
primary infection that has resulted in latent infection of the cornea or
trigeminal ganglion.

Varicella-Zoster Virus
 Infection caused by varicella-zoster virus (VZV) can be associated
with small vesicular or papular eruptions at the limbus. These
lesions usually resolve without sequelae, but the affected
conjunctiva often is red and painful.
 Herpes zoster ophthalmicus refers to reactivation of VZV along the
sensory distribution of the ophthalmic division of the trigeminal
nerve.

Other Viruses
 Measles, mumps, rubella, adenovirus, coxsackievirus A24, and
enterovirus 70 are associated commonly with a self-limited punctate
epithelial keratitis
 Epstein-Barr virus can invade all layers of the cornea. Superficially
there can be multiple epithelial dendrites.

Bacteria
 Bacterial infection of the cornea is considered a medical emergency
because it can progress rapidly and lead to severe visual loss. The

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 presence of a dense greyish infiltrate and surface ulceration in an
actively inflamed eye should be considered bacterial infection until
proved otherwise
 The most common causes of bacterial keratitis in children are
staphylococci and streptococci, seen in children who have chronic
bacterial blepharokeratoconjunctivitis. These children often have
itchy and burning eyes, photophobia, and tearing.
 On examination, debris on the eyelashes (“scurf”) is seen, which
represents protein exudate from inflamed eyelids. Lid margins are
red, the myeibomian glands are inspissated with thickened oil,
telangiectasia may be seen in ocular rosacea, and there is
inflammation of the conjunctiva and cornea. The cornea may have
infiltrates at the lid margins, and ulceration and neovascularization
can result from chronic inflammation.

Fungi
 Fungal keratitis is rare in childhood and usually is the consequence
of ocular trauma, especially with vegetable matter. The prior use of
topical corticosteroid agents, systemic immunosuppression,
preexisting corneal disease, and tropical environment increase the
risk for fungal infection.
 Typically, the ulcer has a subacute onset and progresses
insidiously. Slit-lamp examination commonly reveals a yellow-white
infiltrate with feathery edges; a dry, raised surface; and satellite
lesions.

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 Acanthamoeba Keratitis
 Acanthamoeba causes a recalcitrant keratitis that frequently leads to
visual loss. It usually occurs in contact lens wearers or in persons
exposed to contaminated water.
 Severe pain, out of proportion to the severity of the keratitis, is
common.

Interstitial and Marginal Keratitis

 Interstitial keratitis usually is a delayed manifestation of a systemic
infection from a variety of bacterial, viral, and parasitic pathogens.
Congenital syphilis historically was the predominant cause of
interstitial keratitis.
 Pain, photophobia, and reflex tearing are the major symptoms.
Examination reveals an intact corneal epithelium with underlying
cellular infiltration of the superficial or deep stroma.
 Staphylococcal lid disease is associated with a marginal keratitis in
which infiltrates form in the peripheral cornea, often where the lid
margins cross the limbus (at 2, 4, 8, and 10 o’clock). Cultures of the
infiltrates are sterile, suggesting that they result from hypersensitivity
reactions to staphylococcal antigens or exotoxins deposited on the
ocular surface

DIAGNOSTIC PROCEDURES
 Evaluation of infectious keratitis should include corneal scrapings for
smears and cultures.

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 Children often require sedation or examination under anesthesia to
allow thorough evaluation and collection of appropriate specimens.
 Corneal specimens are obtained by scraping the leading edge and
base of the ulcer with a sterilized Kimura spatula or Calgi swab.
 Staining of corneal scrapings is important for the early identification
of bacteria, fungi, and Acanthamoeba and may provide the sole
etiologic evidence in culture-negative cases.
 Microbial antigens can be detected using immunodiagnostic
methods.
 Lumbar puncture should be performed in neonates with suspected
herpetic eye disease. Diagnosis is done by polymerase chain
reaction testing of cerebrospinal fluid and plasma for HSV.

TREATMENT
 The mainstay of treatment for corneal infections is the intensive use
of topical anti-infective agents.
 Corneal ulcers are medical emergencies.

Viruses
 Except herpesvirus eye disease, the treatment of viral infections is
symptomatic because infections are self-limited, and no effective
therapy is currently available.
 Children with recurrent episodes of herpetic keratitis may benefit
from long-term prophylactic use of acyclovir to prevent recurrence,
but resistance to acyclovir can develop over time.

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 Herpes zoster keratouveitis is unresponsive to available topical
antiviral agents and is best managed with frequent application of
corticosteroid topically and acyclovir (80 mg/kg/day) orally.

Bacteria
 The mainstay of treatment for bacterial keratitis is a combination of a
cephalosporin (50 mg/mL) drops and a fortified aminoglycoside,
either tobramycin (15 mg/mL) or gentamicin (14 mg/mL).45
Cefazolin is selected for gram-positive coverage, and ceftazidime is
used when there is concern about P. aeruginosa.
 Because of their rapid clearance, topical antibiotics should be
administered frequently, beginning with 1 drop every minute for 5
minutes, followed by doses every 15 to 30 minutes until culture
results are available.71 Subsequent therapy is modified according to
culture results and clinical course, but treatment usually is continued
for 7 to 14 days.
 A favorable therapeutic response is indicated by diminished pain,
healing of the epithelium, decrease in size and density of the corneal
infiltrate, and decrease in corneal edema and inflammation in the
anterior chamber.

Fungi
 Fungal keratitis is treated with topical natamycin, flucytosine,
amphotericin B, miconazole, or flucytosine.
 Frequent (hourly) initial instillation is slowly reduced over several
weeks. Adequate treatment requires 6 to 12 weeks owing to poor

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 corneal penetration and the slow growth of fungi. Lack of a
therapeutic response should prompt the addition of parenteral
therapy or consideration of excisional keratoplasty.
 Subconjunctival fluconazole can be helpful in severe fungal keratitis
unresponsive to topical and systemic therapy.

Acanthamoeba Keratitis
 Treatment of Acanthamoeba keratitis often is complicated by
delayed diagnosis. Early and aggressive therapy with cationic
disinfectants (poly-hexamethylene biguanide or chlorhexidine),
combined with dibrompropamidine isethionate (Brolene) and
neomycin, can be curative.7
 Corneal transplantation is only recommended when the infection
continues, and anti-infectives will be required long term to prevent
recurrence in the graft.

COMPLICATIONS
 Long-term complications usually are related to loss of corneal
transparency and refractive changes.
 Although the severity of scarring tends to diminish over time, even
short periods of visual deprivation in children younger than 8 years
of age can result in development of amblyopia.
 Although corneal transplants can restore vision,81 corneal grafting
in children may fail because of graft rejection.