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Eye Infections
[ Mycotic keratitis |
Endogenous oculomycosis |
Extension oculomycosis ]
Mycotic keratitis
Mycotic keratitis refers to the corneal infection caused by either filamentous fungi (moulds) or yeast. There are important epidemiological and clinical differences (see table below) between these two forms. The most important risk factors related to fungal keratitis include trauma (generally with plant material), chronic ocular surface diseases, contact lens usage, surgery, corneal anesthetic abuse, and immunodeficiencies [432, 1139, 1963, 2223]. Interestingly, fungal keratitis is a condition related to warm climates [1341]. In the southernmost states of the United States, fungal keratitis explains up to 35% of microbial keratitis cases compared with 1% in New York or Minnesota [135, 610, 1340, 1963].
| Fungi type |
Moulds |
Yeasts |
| Predisposing factors |
- Outdoor or vegetable-related trauma
- Contact lens usage
- Eye surgery
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| Clinical features |
- Stromal infiltrates have minimal cellular reaction and rough texture.
- The epithelial surface looks dry, gray and may be either above the level of the corneal surface or ulcerated.
- Feathery infiltrates. Sometimes pigmented fungal elements can be recognized
- Satellite lesions or multifocal microabscesses are also seen.
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- Small, oval, sharply demarcated ulcerations with a "color button" configuration
- Extensive stromal inflammation and edema
- May be indistinguishable from Gram-positive bacterial keratitis
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| Most common etiologic agents |
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Fungal keratitis is a serious condition that requires prolonged treatment and close follow-up. Natamycin (Pimaricin) appears to be the drug of choice and amphotericin B a second alternative [1341]. Chlorhexidine has emerged as a potential inexpensive option but current data are limited [1866]. Systemic therapy with azoles, particularly fluconazole should be considered when yeasts are involved [2223]. Surgery may be necessary, depending upon the degree of damage to the eye. Interventions range from simple scraping of ulcerative lesions to superficial or lamellar keratectomy [2026, 2111]. Animal models suggest that excimer laser may have a role in the future [880]. Anecdotal experience with liposomal preparations of amphotericin B have suggested their potential role in refractory cases [861].
The lesions typically advance into the deep stroma of the cornea and contain hyphae that are 3-4 um in diameter with some swollen cells. The fungus usually develops throughout the entire depth of the cornea. It is not uncommon for hyphae to be only in the middle and deeper layers. Early in the disease, there is an acute suppurative inflammatory process accompanied by coagulative necrosis. Hyphae are typically aligned parallel to the lamellae of the cornea.
Direct examination
The diagnosis of mycotic keratitis must include the demonstration of the fungus in corneal scrapings and the recovery of a compatible fungus. Clinical material can be mounted in 10% KOH or stained by the Gram, PAS, GMS, Giemsa or calcofluor techniques. Fungi are usually deep within the corneal structure, not on the surface. Extensive debridement may be necessary to obtain satisfactory clinical material. Swabs are unsatisfactory.
Isolation
Inoculate the specimens onto Sabouraud glucose agar, inhibitory mould agar or brain heart infusion agar with 10% sheep blood and incubate at 30°C. Cycloheximide may inhibit the growth of many of the etiologic agents of mycotic keratitis. A medium containing cycloheximide, if used, cannot be used alone.
- Acremonium spp.
- Aspergillus flavus
- Aspergillus fumigatus
- Aspergillus niger
- Bipolaris spp.
- Candida albicans
- Curvularia spp
- Exserohilum spp.
- Fusarium oxysporum
- Fusarium solani
- Lasiodiplodia theobromae
Endogenous oculomycosis
This form of eye infection results from hematogenous dissemination of a systemic fungal disease. Eye involvement is typically a late event following widespread dissemination. The mycosis may involve the orbit, retina, optic nerve, sclera, conjunctiva, and adjacent tissue. The diseases in order of frequency are: candidiasis, cryptococcosis,
coccidioidomycosis,
blastomycosis,
sporotrichosis,
paracoccidioidomycosis,
histoplasmosis, and
aspergillosis.
The most common of these forms of endogenous disease is Candidal endophthlamitis, and the reader should refer to our detailed discussion of this entity.
Amphotericin B is in general the drug of choice. Surgery (vitrectomy) is frequently needed. For details, consult the chapter on each condition as listed above.
Extension oculomycosis
Extension oculomycosis represents a special form of rhinocerebral zygomycosis in the diabetic patient. The infection starts in the upper portion of the nasal septum and extends into the orbit of the eye, frontal sinuses, major cerebral vessels, and subsequently the central nervous system. Rhizopus arrhizus is the most common etiologic agent. Symptoms include orbital pain, ophthalomoplegia, localized anesthesia, proptosis, limitation of movement, fixation of the pupil, and loss of vision.
Control of diabetes is the most important factor. Systemic, local amphotericin B, or both and surgery are typically required.
Direct examination
Clinical material, especially from the tissue surrounding the eye if the eye is not enucleated, is mounted in 10% KOH and/or Calcofluor and then examined for sparsely septate, irregularly branching hyphae that are 6-15 um in diameter.
Isolation
Techniques for Zygomycetes
The techniques that apply to any of the Zygomycetes would be appropriate.
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References
135. Asbell, P., and S. Stenson. 1982. Ulcerative keratitis. Survey of 30 years' laboratory experience. Arch Ophthalmol. 100:77-80.
432. Chern, K. C., D. M. Meisler, K. R. Wilhelmus, D. B. Jones, G. A. Stern, and C. Y. Lowder. 1996. Corneal anesthetic abuse and Candida keratitis. Ophthalmology. 103:37-40.
610. Doughman, D. J., N. M. Leavenworth, R. C. Campbell, and R. L. Lindstrom. 1982. Fungal keratitis at the University of Minnesota: 1971-1981. Trans Am Ophthalmol Soc. 80:235-47.
861. Goldblum, D., B. E. Frueh, S. Zimmerli, and M. Bohnke. 2000. Treatment of postkeratitis fusarium endophthalmitis with amphotericin B lipid complex [In Process Citation]. Cornea. 19:853-6.
880. Gottsch, J. D., M. L. Gilbert, D. F. Goodman, M. E. Sulewski, J. D. Dick, and W. J. Stark. 1991. Excimer laser ablative treatment of microbial keratitis. Ophthalmology. 98:146-9.
1139. Jones, D. B. 1978. Therapy of postsurgical fungal endophthalmitis. Ophthalmology. 85:357-73.
1340. Liesegang, T. J., and R. K. Forster. 1980. Spectrum of microbial keratitis in South Florida. Am J Ophthalmol. 90:38-47.
1341. Liesengag, T. J. 1999. Fungal keratitis. In H. E. Kaufman, B. A. Barron, and M. B. McDonald (ed.), Cornea. Butterworth-Heinermann, Woburn.
1866. Rahman, M. R., G. J. Johnson, R. Husain, S. A. Howlader, and D. C. Minassian. 1998. Randomised trial of 0.2% chlorhexidine gluconate and 2.5% natamycin for fungal keratitis in Bangladesh. Br J Ophthalmol. 82:919-25.
1963. Rosa, R. H., Jr., D. Miller, and E. C. Alfonso. 1994. The changing spectrum of fungal keratitis in south Florida. Ophthalmology. 101:1005-13.
2026. Sanitato, J. J., C. G. Kelley, and H. E. Kaufman. 1984. Surgical management of peripheral fungal keratitis (keratomycosis). Arch Ophthalmol. 102:1506-9.
2111. Singh, G., and S. R. Malik. 1972. Therapeutic keratoplasty in fungal corneal ulcers. Br J Ophthalmol. 56:41-5.
2223. Tanure, M. A., E. J. Cohen, S. Sudesh, C. J. Rapuano, and P. R. Laibson. 2000. Spectrum of fungal keratitis at Wills Eye Hospital, Philadelphia, Pennsylvania. Cornea. 19:307-12.
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