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PART 4 CORNEA AND OCULAR SURFACE DISEASES

SECTION 6 Corneal Diseases

Parasitic Keratitis
Jeremy D. Keenan, Stephen D. McLeod 4.14
Definition: Corneal disease caused by protozoal organisms.

Key features
Cellular infiltration of the corneal epithelium or stroma, corneal
inflammation, and necrosis

Associated features
Delay in diagnosis is common.
Pain may be greater than physical findings.
Early cases may demonstrate pseudodendrites.
Later cases may show ring infiltrate in the cornea.

Fig. 4-14-1 Epithelial ridges seen in acanthamoeba keratitis. (Courtesy of Joel Sugar, MD.)
INTRODUCTION
Parasitic infections of the cornea are a significant cause of ocular mor-
bidity. Acanthamoeba keratitis is increasingly recognized in the devel-
oped world as a potentially disastrous complication of contact lens
wear, and one that requires early, aggressive treatment. Onchocerca
infection is still encountered in some parts of the developing world.

ACANTHAMOEBA

EPIDEMIOLOGY AND PATHOGENESIS


Acanthamoebae, found ubiquitously in water, soil, and air, are free-
living protozoans that exist in an active trophozoite form and a dor-
mant cyst form. The trophozoite feeds on microorganisms and
reproduces by binary fission, but if deprived of a food source will encyst.
Cysts are resistant to desiccation, temperature extremes, and various
chemicals, and can remain dormant for years. Acanthamoebae are typi-
cally speciated according to morphologic characteristics, although they Fig. 4-14-2 Perineuritis seen in acanthamoeba keratitis. (Courtesy of Joel Sugar, MD.)
can also be classified into one of 15 genotypes. The vast majority of
keratitis is caused by the T4 genotype.1 perineuritis is thought to be very specific for acanthamoeba keratitis,
Keratitis caused by Acanthamoeba is less common than that caused though it does not appear in many cases (Fig. 4-14-2). Limbitis is com-
by bacteria or fungi, though the incidence of acanthamoeba keratitis mon, and may account for significant pain. Later stages of infection are
increased in the United States for several years in the mid-2000s due characterized by nonspecific stromal infiltration (Fig. 4-14-3) or a char-
to an epidemic related to a contact lens solution.2 The biggest risk fac- acteristic ring infiltrate (Fig. 4-14-4), and uveitis.5 Conjunctival injec-
tor for acanthamoeba keratitis in the developed world is contact lens tion and chemosis are often associated with infection. When present,
wear, with approximately 90% of cases occurring in contact lens wear- fluctuating, nongranulomatous anterior chamber inflammation may
ers.3 Most cases are seen in soft contact lens wearers, though orthok- contribute to the formation of cataract or elevated intraocular pressure.
eratology may convey increased risk. Trauma is the other major risk In the most severe cases, hypopyon, anterior scleritis, or perforation
factor, and accounts for the vast majority of acanthamoeba keratitis (sometimes associated with optic neuritis) can occur.
seen in developing countries.4 Other risk factors include exposure to It has been reported frequently that patients experience severe pain
water, especially fresh water sources, swimming pools or hot tubs, and far out of proportion to clinical findings, but this is an unreliable
homemade contact lens solutions. diagnostic sign, and some patients have reduced or absent corneal
sensation.
CLINICAL FEATURES
DIAGNOSIS
Since a delay in treatment has been shown to adversely affect visual
outcome, clinicians must be acutely aware of the sometimes subtle early As with other forms of infectious keratitis, diagnosis is based on char-
indications of acanthamoeba infection. Early infection is confined to the acteristic clinical findings, and supported by microbiological investiga-
228 epithelium, which demonstrates irregularity and multifocal infiltration, tions. Cysts are visible with routine stains such as Giemsa, Grams, and
pseudodendrites, or elevated epithelial ridges (Fig. 4-14-1). Radial ink-potassium hydroxide, and also with stains that require fluorescent

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Fig. 4-14-5 Light
microscopic view of
a corneal section
4.14
demonstrating
Acanthamoeba cysts.

Parasitic Keratitis
(Courtesy of Joel Sugar, MD.)

Fig. 4-14-3 Nonspecific infiltration of the corneal stroma caused by


Acanthamoeba infection. (Courtesy of Joel Sugar, MD.)

progressively deeper layers of the stroma and eventually penetrate


the anterior chamber. The organism can become encysted in the
corneal stroma, and recrudescence after partially successful treatment
is considered to be due to an inflammatory response to the necrotic
cysts and may not be related to the presence of viable and active
amoebae, as previously thought.9

TREATMENT
Treatment of acanthamoeba keratitis is based on eradication of cysts
from the cornea.10 Although trophozoites are susceptible to many anti-
microbial agents, the cysts are largely resistant. The most effective
medications are the biguanide antiseptic agents chlorhexidine and poly-
hexamethylene biguanide (PHMB), which act by inhibiting membrane
function and are consistently cysticidal (Table 4-14-1).11 Second-line
agents include the diamidines (hexamidine, pentamidine, and propa-
Fig. 4-14-4 Ring infiltrate in corneal Acanthamoeba infection. midine), which inhibit DNA synthesis. Diamidines are also generally
cysticidal, though their activity is more variable. Azole medications
microscopy such as Calcofluor white and acridine orange.6 Scrapings have activity against trophozoites, but are generally not cysticidal.
should also be plated on non-nutrient agar and overlaid with E. coli to There have been reports of effective treatment with oral and topical
assess for growth of trophozoites; plates should be observed for longer voriconazole, though the in vitro susceptibility patterns have not been
than 7 days. If plates are not available, scrapings can be transported to well characterized for this agent. Aminoglycosides such as neomycin
the laboratory in Pages saline. Culture and smear of samples from con- and paromomycin were used in the past, but these agents are not cysti-
tact lens cases and cleaning solutions can also reveal Acanthamoeba. cidal and cause significant corneal toxicity, so there is little rationale to
Polymerase chain reaction (PCR) assays targeting Acanthamoeba support their use.
18S rRNA have been shown to be more sensitive than culture or smear, Little consensus exists on the best way to treat acanthamoeba kera-
but are not currently available at most laboratories.7 titis. A clinical trial compared chlorhexidine monotherapy versus
In vivo confocal microscopy is a relatively new technique that can be PHMB monotherapy, and found no significant differences, with a high
helpful for establishing the diagnosis of acanthamoeba keratitis. Cysts success rate in both groups (78% and 86%, respectively).12 Because cysts
appear as round, hyper-reflective, double-walled structures measuring can be difficult to eradicate, many clinicians treat with multiple agents,
1025m.8 usually with one of the biguanide agents and one of the diamidines. As
Corneal biopsy should be considered for cases with only deep with other types of infectious keratitis, topical therapy should initially
stromal involvement, or when microbiological tests are negative (Fig. be applied frequently (every 3060 minutes), and then the frequency can
4-14-5). Biopsies should be stained with hematoxylin-eosin, periodic be reduced based on the clinical response. Topical medications are gener-
acid-Schiff, and methenamine silver stains. Electron microscopy can ally continued for many months. Pain should be addressed with
also reveal organisms. cycloplegics and oral nonsteroidal anti-inflammatory drugs (NSAIDs).
The role of corticosteroids in the treatment of Acanthamoeba infec-
DIFFERENTIAL DIAGNOSIS tion has not been established. Corticosteroids promote excystment and
proliferation of trophozoites, and may delay healing of acanthamoeba
See Box 4-12-1 (page 221). The pseudodendrites of early disease and keratitis.13 However, corticosteroids also reduce pain and inflamma-
the ring infiltrate of more advanced disease are often mistakenly identi- tion. Several case reports have reported good outcomes in acanthamoe-
fied as representing herpetic keratitis. In those cases that are refractory ba keratitis patients who have used corticosteroids, as long as
to treatment, herpetic keratitis and bacterial superinfection should be anti-acanthamoebic agents were continued after the corticosteroids
considered. were discontinued.10
The role of therapeutic keratoplasty for active acanthamoeba kerati-
PATHOLOGY tis is controversial. Recurrence of Acanthamoeba infection has been
reported to occur in more than half of grafts, leading to poor postopera-
Trophozoites bind to the corneal epithelium and establish infection. tive visual outcomes.14 Others have found much lower rates of recur-
This is followed by thinning and necrosis of the epithelium, which rence, and good visual outcomes.15 Anti-acanthamoebic medications 229
allow the organism to enter the stroma, where it may enter should be continued after keratoplasty.

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4 Agent Trade name Manufacturer
TABLE 4-14-1 ANTIAMEBIC MEDICATIONS

Dosage form Concentration Availability Comment


for ocular use
Cornea and Ocular Surface Diseases

Cationic Antiseptics
Chlorhexidine Solution 0.02% As 20% concentrate Used as disinfectant
Polyhexamethylene Baquacil Zeneca Solution 0.02% As 20% pool disinfectant Used also as a preservative, contact
biguanide (PHMB) lens solutions
Aromatic Diamidines
Propamidine isethionate Brolene Mays & Baker Solution 0.1% w/v 10mL Over-the-counter in UK
Hexamidine Dsomdine Chauvin Solution 0.1% Available in Europe
Azoles
Clotrimazole Lotrimin Schering Suspension 1% As powder from manufacturer Poor suspension; difficult to make
Fluconazole Diflucan Roerig Solution 0.2% As 2mg/mL solution Withdraw from vial with filter needle
Ketoconazole Nizoral Janssen Oil solution 5% As 200mg tablet In mortar, dissolve 2.5 200mg
tablets in 10mL of peanut oil
Miconazole Monistat Janssen Solution 1% As 10mg/mL solution Simple 1:1 solution or directly from
vial via filter
Voriconazole Vfend Pfizer Oral 200mg b.i.d. As 200mg tablet Monitor liver function
Solution 1% As 200mg vial

(Adapted from Richard G. Fiscella, RPh, MPH.)

OUTCOME can be used, with potassium hydroxide plus Calcofluor white, Grams,
and modified ZiehlNeelsen most consistently detecting microsporid-
With timely diagnosis, Acanthamoeba organisms can be eradicated from ia.21 Giemsa staining characteristics are more variable. Microsporidia
the cornea by medical therapy. A minority of patients develop rapidly are difficult to recover in culture. PCR assays that target the 16S rRNA
progressive cataract and glaucoma, presumably from prolonged exposure subunit have been developed but are not performed by most laborato-
to topical medications or to the host inflammatory response.16 Severe ries.22 The confocal microscope can reveal intraepithelial microsporid-
corneal inflammation and necrosis can result in substantial scarring, ia, but these organisms (which measure 15m) approach the
necessitating penetrating keratoplasty for visual rehabilitation. Optical resolution limits of this instrument.23 Electron microscopy performed
keratoplasty performed well after eradication of Acanthamoeba infection on body fluids is considered the gold standard for diagnosis of micro-
carries a good prognosis, but results of therapeutic keratoplasty per- sporidial infection.
formed during active infection are much more variable.14
DIFFERENTIAL DIAGNOSIS
MICROSPORIDIOSIS See Box 4-12-1 (see page 221).

SYSTEMIC ASSOCIATIONS
EPIDEMIOLOGY AND PATHOGENESIS
Microsporidial infection can involve nearly every organ system in
Microsporidia are ubiquitous obligate intracellular parasites closely severely immunocompromised HIV-infected patients (usually CD4 cell
related to fungi.17 Although it is a rare disease, diagnosis of micro- counts <100/L). The gastrointestinal system is most commonly
sporidial keratitis is increasing. This is especially true in Asia, where involved, representing a major cause of malabsorption and diarrhea in
the disease may correspond with the monsoon season.18 Several risk AIDS patients. Ocular infections are second in frequency and may
factors occur for microsporidial keratitis. Immune compromise is the result from nasopharyngeal infection or from urine-to-finger-to-eye
most notable risk factor, especially in persons with HIV. Other states of contamination. When ocular microsporidial infections are diagnosed,
immunosuppression, including local immunosuppression with topical the patient must be fully examined for other areas of involvement.
corticosteroids, make infection more likely. Other major risk factors Other common infections include sinusitis, hepatitis, peritonitis,
include trauma, which is often associated with exposure to water or cholangitis, myositis, bronchiolitis, pneumonia, encephalitis, cystitis,
mud, and contact lens wear.19 Although previously considered to occur and nephritis. Rare manifestations include urethritis, prostatic abscess,
primarily in the setting of HIV, infection is increasingly being observed tongue ulcer, and skeletal and cutaneous involvement.
in immunocompetent persons.
TREATMENT
CLINICAL FEATURES
The optimal treatment regimen for ocular microsporidiosis is not well
Two distinct clinical presentations are possible with ocular micro- defined. Several medications are currently used, including oral agents
sporidial infection: superficial keratoconjunctivitis, which is caused by such as albendazole and itraconazole, and topical agents such as fum-
Encephalitozoon species, and deep stromal keratitis, which is caused by agillin, propamidine, chlorhexidine, polyhexamethylene biguanide
Nosema, Vittaforma, and Trachiplestophora species. The keratocon- (PHMB), voriconazole, and the fluoroquinolones. Fumagillin is one of
junctivitis form was usually seen in immunocompromised persons in the more frequently used medications; a 10mg/mL suspension can be
the past, though this entity is now recognized in immunocompetent applied hourly for 24hours and then tapered based on clinical response.
persons as well.20 Microsporidial keratoconjunctivitis is characterized Albendazole has been used when ocular microsporidiosis was refractory
by minimal conjunctivitis, diffuse punctate epitheliopathy, and coarse to topical therapy.24 A placebo-controlled randomized clinical trial per-
epithelial opacities, some of which stain with fluorescein. Symptoms formed with immunocompetent patients found no benefit of PHMB.25
include pain, photophobia, blurred vision, and foreign body sensation. This trial found that the disease may be self-limited in immunocompe-
Microsporidial stromal keratitis is usually seen in immunocompetent tent patients; the placebo group experienced clinical cure an average of
individuals, where it is often misdiagnosed as herpetic keratitis. Stro- 9 days after diagnosis.
mal infection is characterized by deep stromal infiltrates with or with-
out corneal neovascularization and uveitis. OUTCOME
DIAGNOSIS Treatment of microsporidial keratoconjunctivitis is usually successful,
especially in immunocompetent patients. Immunocompromised per-
230 Diagnosis of microsporidial keratitis is usually made by inspection of sons can develop chronic infections when anti-microsporidial treat-
smears obtained from corneal or conjunctival scrapings. Several stains ment is withdrawn. In such an event, a low maintenance dose of one

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drop a day might be sufficient to control the keratoconjunctivitis. Vis- infection. Serologic tests are available, though some have difficulty
ual acuity improvement is usually seen after the superficial keratitis discriminating O. volvulus from other filarial infections.31 4.14
resolves.25 Disease involving the corneal stroma is difficult to treat, and
recrudescence is common. Some authors advocate full-thickness kerat- DIFFERENTIAL DIAGNOSIS
oplasty in these cases, as microsporidia can invade the anterior cham-

Parasitic Keratitis
ber, and lamellar keratoplasty does not preclude recurrence.26 Similar skin lesions can be seen in association with microfilarial infec-
tion caused by Mansonella perstans. Skin nodules and uveitis can also
be seen with sarcoidosis.
ONCHOCERCIASIS
SYSTEMIC ASSOCIATIONS
EPIDEMIOLOGY AND PATHOGENESIS Besides being present in the skin lesions, the microfilariae can be iden-
tified in blood vessels, visceral organs, the central nervous system,
Onchocerciasis, also known as river blindness, is a major cause of urine, and sputum. Superficial lymph nodes draining areas with cuta-
blindness worldwide. Onchocerciasis affects approximately 18 million neous concentrations of the worms can become painlessly enlarged.
people, of whom 270000 are rendered blind.27 The vast majority of
cases occur in the 34 countries in Africa where the disease is still
endemic. The causative organism, Onchocerca volvulus, is a filarial
PATHOLOGY
nematode that is transmitted by the Simulium black fly, which breeds The destructive inflammation caused by onchocerca infection is stimu-
in the fast-flowing rivers and streams of Africa, Brazil, Mexico, the lated by antigens released by dead and dying organisms. The host
Middle East, and parts of Central America. The fly introduces larvae of immune response results in migration of eosinophils and neutrophils
O. volvulus into the skin during a blood meal, forming a skin nodule of into the corneal stroma. Degranulation of these inflammatory cells
adult worms. After developing into adult worms, females shed hun- releases cytotoxic proteins that disrupt the normal functioning of the
dreds of thousands of microfilariae that migrate through the skin and corneal cells, resulting in corneal opacity.32
have particular affinity for the eyes. Dying microfilariae incite an
inflammatory reaction that results in the cutaneous and ocular clinical
manifestations. An endosymbiont bacteria, Wolbachia, plays an impor-
TREATMENT
tant role in development of larvae, and also possibly in the long-term The skin nodule containing the adult worms should be surgically
survival of adult worms.28 removed. The mainstay of treatment is oral ivermectin given as a single
Eye disease is related to the inflammatory response generated by the dose (150g/kg) repeated annually or biannually. Mass drug adminis-
nematodes, which can be found in the conjunctival epithelium, corneal trations are delivered to entire communities in endemic areas. Ivermec-
stroma, iris, ciliary body, sclera, extraocular muscles, and optic nerve tin kills microfilariae but not adult worms, making it difficult to cure
sheath. The severity of ocular findings depends on the strain of micro- the infection. Oral ivermectin reverses even advanced sclerosing kera-
filariae; strains from the savanna regions of West Africa induce a more titis and iridocyclitis, but treatment is not effective for chorioretinal
severe inflammatory response and sclerosing keratitis, which is typi- lesions, which progress despite treatment.33 A 6-week course of doxycy-
cally absent in infections caused by the rain forest strain.29,30 cline 100200mg per day is used to clear Wolbachia endosymbionts,
and results in long-term sterilization of adult worms.34 Iridocyclitis
CLINICAL FEATURES should be treated with corticosteroids and cycloplegia.
Early infection with the onchocerca worm is marked by a diffuse papu-
lar dermatitis, accompanied by intense pruritus.27 Other cutaneous
OUTCOME
findings can range from lichenification to asymptomatic depigmenta- Although anterior segment inflammation and lesions respond well to
tion to subdermal nodules. Onchocerciasis can involve virtually all treatment, severe visual impairment can result from chorioretinitis
ocular tissues. Lid nodules and edema, chronic conjunctivitis with that, in advanced cases, often continues to progress in spite of treat-
injection, chemosis, and phlyctenule-like conjunctival masses can ment. Health programs are aimed at blindness prevention through
develop. Corneal involvement is marked by a fine interpalpebral epithe- mass treatment, prevention, and vector control. There is evidence that
lial punctate keratitis that overlies white subepithelial flake-like opaci- prolonged repeated mass ivermectin distributions can disrupt trans-
ties and discrete nummular scars, and stromal edema caused by an mission of O. volvulus, suggesting that elimination of disease may
intrastromal worm. These worms can be visualized at the slit lamp on eventually be possible.35
retroillumination at all corneal levels as S- or C-shaped fine, motile
filaments. Sclerosing keratitis represents more severe, blinding corneal
disease. It tends to appear as an anterior stromal haze centered at the
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Descargado para mariana cruz (smarianis_13@hotmail.com) en Univ Antioquia de ClinicalKey.es por Elsevier en noviembre 16, 2017.
Para uso personal exclusivamente. No se permiten otros usos sin autorizacin. Copyright 2017. Elsevier Inc. Todos los derechos reservados.

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