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| REVIEW ARTICLE |
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| Year : 2015 | Volume
: 3
| Issue : 1 | Page : 3-5 |
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Fungal keratitis
Honaida Elshiek1, Roberto Pineda2
1 Department of Cornea, Makkaha Eye Complex, Sudan Eye Center, Alryaid, Alnus St, Alryaid, Khartoum, Sudan
2 Massachusetts Eye and Ear Infirmary, 243 Charles St, Boston, MA 02114, USA
| Date of Web Publication | 10-Nov-2015 |
Correspondence Address:
Honaida Elshiek
Makkaha Eye Complex, Sudan Eye Center Alryaid, Alnus Street, Alryaid, Khartoum
Sudan
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1858-6538.169310
Fungal keratitis is a very serious and potentially sight-threatening corneal infection that most commonly develops in patients after trauma or in those with a compromised corneal surface. Although it is relatively rare but due the extensive use of topical antibiotics and Steroids there have been a noticeable increase in fungal keratitis. Keywords: Candida; Canthamoeba keratitis; fungal corneal infection; keratomycosis
How to cite this article:
Elshiek H, Pineda R. Fungal keratitis. Albasar Int J Ophthalmol 2015;3:3-5 |
| Definition | |  |
Candida keratitis is a potentially sight-threatening corneal infection that most commonly develops in patients after trauma or in those with a compromised corneal surface.
| Intruduction | | |
Fungal keratitis causes severe ocular morbidity and blindness worldwide,[1] especially in developing countries.[2] Yeast (genus Candida)[3] and Filamentous fungi [4] (genera Fusarium [4] and Aspergillus)[5] are the main two types of fungi causing keratitis. Candida keratitis [3] is a potentially sight-threatening corneal infection that most commonly develops in patients after trauma [5] or in those with a compromised corneal surface. Fungi gain access to the corneal stroma through a defect in the epithelial barrier.
| Etiology | | |
Fungi are a group of microorganism that has rigid walls and a distinct nucleus with multiple chromosomes containing both DNA and RNA. The two main types of fungi causing keratitis are:
- Yeast (e.g., genus Candida), ovoid unicellular organism that reproduce by budding, is responsible for most cases of fungal keratitis in temperate climates. It is a common offender in the northern and coastal regions of the United States, constituting 32–43% of the keratomycoses, and commonly occurs in eyes with predisposing alterations in host defenses
- • Filamentous fungi (e.g., genera Fusarium and Aspergillus), multicellular organisms that produce tubular projection known as hyphae, are the most common pathogens in tropical climates
Fungi gain access to the corneal stroma through a defect in the epithelial barrier. Once in the stroma, they multiply and cause tissue necrosis, leading to a host inflammatory reaction. Organisms can penetrate deep into the stroma and through an intact Descemet's membrane. It is thought that once organisms gain access to the anterior chamber, eradication of the organisms becomes extremely difficult. Likewise, fungi that extend from the cornea into the sclera become difficult to treat.
Risk factors
- Trauma [5] to the cornea with plant or vegetable material is the leading risk factor for fungal keratitis
- Contact lens wear [6] is another risk factor for the development fungal keratitis
- Topical corticosteroids [7] are a major risk factor as well as they appear to activate and increase the virulence of fungal organisms by reducing the cornea's resistance to infection
- Candida species cause ocular infections in immunocompromised host and corneas with chronic erosions/ulceration from other causes
- Other common risk factors include corneal surgery (e.g., penetrating keratoplasty)[1] and chronic keratitis (e.g., herpes simplex virus, herpes zoster).
| Clinical Presentation | | |
The presentation is with a gradual onset of pain, grittiness, photophobia, blurred vision, and watery or mucopurulent discharge.
Signs
- Candida keratitis: Yellow-white densely suppurative infiltrate and collar-stud morphology may be seen. Candida ulcers occasionally have distinct oval outlines with a plaque-like surface
- Filamentous keratitis: Gray or yellow-white stromal infiltrate with indistinct fluffy margins. Progressive infiltration is often associated with satellite lesions
- Feathery branch-like extension or a ring-shaped infiltrate may develop
- Rapid progression with necrosis and thinning can occur
- Penetration of an intact Descemet's membrane may occur and lead to endophthalmitis without evident perforation
- An epithelial defect is not invariable and is sometimes small when present
- Other features include anterior uveitis, hypopyon, endothelial plaque, increased intraocular pressure (IOP), scleritis, and sterile or infective endophthalmitis.
| Diagnostics (Lab Diagnostics) | | |
[8]
- History of trauma involving vegetative matter is highly suggestive
- Lack of response to conventional antibacterial therapy.
- Corneal scraping [9] for staining with gram, Giemsa, Gomori methenamine silver, and calcofluor white stains
- Culture media [10] include sheep blood agar, chocolate agar and thioglycolate broth. Initial growth occurs within 72 hours in 83% of cultures and within 1 week in 97% of cultures
- Corneal biopsy may be required if smear and cultures are negative and is indicated in the absence of clinical improvement after 3–4 days
- Other less widely used methods for identification of fungi include electron microscopy and polymerase chain reaction.
| Differential Diagnosis | | |
Differential diagnosis includes [8] bacterial, herpetic, and acanthamoeba keratitis. It is important to be aware of co-infection, including with an additional fungal species.
| Prophylaxis | | |
The patient's chief concern should be noted, and a complete systemic and ocular history, eliciting specific risk factors for infection of the external eye, should be obtained. A detailed history and physical examination are essential to the proper diagnosis of external eye infections.
| Therapy | | |
Initially, the fungal infection should be treated medically, potentially, and surgically, as fungal infection can be rapidly destructive to the integrity of the eye. Hospital admission may be necessary. Topical and systemic treatment usually lasts for several weeks to months. Lack of disease progression is the first therapeutic response.
Medical therapy
- Removal of the epithelium over the lesion may enhance penetration of the antifungal agents
- Topical treatment of the antifungal agents [11] should initially be given hourly for 48 h, and then reduced as signs permit. Because most antifungals are fungistatic, successful treatment should be continued for prolonged periods;at least 12 wk)[11]
- Candida is treated with amphotericin B 0.15% or econazole 1%; alternatives include natamycin 5%, fluconazole 2%, and clotrimazole 1%
- Filamentous infection is treated with natamycin 5% or econazole 1%; alternatives are amphotericin B 0.15% and miconazole 1%
- A broad-spectrum antibiotic prevent bacterial co-infection
- Cycloplegia for comfort
- Subconjunctival fluconazole may be used in severe cases.
- Systemic antifungals may be given for severe cases when lesions are near the limbus or for suspected endophthalmitis, options include oral voriconazole, itraconazole, or fluconazole 200 mg
- Tetracycline (e.g., doxycycline) may be given for its anti-collagenase effect when there is significant thinning
- IOP should be monitored
Surgical therapy
Debridement and superficial keratectomy, [12] although mostly of diagnostic benefit, may enhance the effectiveness of medical treatment.
Conjunctival flaps have been advocated for non-healing ulcers and are often effective. Therapeutic keratoplasty (penetrating or deep anterior lamellar) [12] is considered when medical therapy is ineffective or following perforation or impending scleral extension.
| Prognosis | | |
The prognosis varies depending on the depth and size of the lesion and the causative organism. In general, small superficial infections respond well to topical therapy. Deep stromal infections and infections with concomitant scleral or intraocular involvement are much more difficult to eradicate. [13]
Three factors significantly associated with treatment failure of fungal keratitis such as large ulcer size (>14 mm), the presence of hypopyon, and Aspergillus as causative organism.
| Epidemiology | | |
Fungi may be part of the normal external ocular flora; they have been isolated from the conjunctival sac in 3–28% of healthy eyes in various series and can be recovered from diseased eyes with greater frequency (17–37%).
Aspergillus species are the most common organism responsible for fungal keratitis worldwide. However, in the United States, Candida species is the most common etiology.
Overall, the incidence of fungal keratitis is low (6–20%). More reports of fungal keratitis originate from the Southern United States, and it continues to be a disease most commonly encountered in patients who come from a rural setting.
| Cross-References | | |
- Necrotizing keratitis disease
- Non-necrotizing keratitis disease
- Peripheral keratitis definition.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 2. | Chowdhary A, Singh K. Spectrum of fungal keratitis in North India. Cornea 2005;24:8-15. |
| 3. | Sun RL, Jones DB, Wilhelmus KR. Clinical characteristics and outcome of Candida Keratitis. Am J Ophthalmol 2007;143:1043-5. |
| 4. | Hagan M, Wright E, Newman M, Dolin P, Johnson G. Causes of suppurative keratitis in Ghana. Br J Ophthalmol 1995;79:1024-8. |
| 5. | Basak SK, Basak S, Mohanta A, Bhowmick A. Epidemiological and microbiological diagnosis of suppurative keratitis in Gangetic West Bengal, eastern India. Indian J Ophthalmol 2005;53:17-22. [ PUBMED]  |
| 6. | Khor WB, Aung T, Saw SM, Wong TY, Tambyah P, Tan AL. Outbreak of fusarium keratitis associated with contact lens wear in Singapore. JAMA (Impact Factor: 35.29) 2006;295:2867-73. |
| 7. | Peponis V, Herz JB, Kaufman HE. The role of corticosteroids in fungal keratitis: A different view. Br J Ophthalmol 2004;88:1227. |
| 8. | Dalmon C, Porco TC, Lietman TM, Prajna NV, Prajna L, Das MR, et al. The clinical differentiation of bacterial and fungal keratitis: A photographic survey. Invest Ophthalmol Vis Sci 2012;53:1787-91. |
| 9. | Sharma S, Kunimoto DY, Gopinathan U, Athmanathan S, Garg P, Rao GN. Evaluation of corneal scraping smear examination methods in the diagnosis of bacterial and fungal keratitis: A survey of eight years of laboratory experience. Cornea 2002;21:643-7. |
| 10. | Bhadange Y, Sharma S, Das S, Sahu SK. Role of liquid culture media in the laboratory diagnosis of microbial keratitis. Am J Ophthalmol 2013;156:745-51. |
| 11. | Mravičić I, Dekaris I, Gabrić N, Romac I, Glavota V, Mlinarić- Missoni E. An Overview of Fungal Keratitis and Case Report on Trichophyton Keratitis, Keratitis. In: Srinivasan M, editor. ISBN: 978-953-51-0568-8, InTech. 2012. Available from: http://www.intechopen.com/books/keratitis/fungalkeratitis. [Last accessed on 2015 Sep 30]. |
| 12. | SudanR, Sharma YR. Keratomycosis: Clinical diagnosis, Medical and Surgical Treatment. JK SCIENCE 2003;5:9. Jall1l3ly-March 2003. |
| 13. | Nielsen SE, Nielsen E, Julian HO, Lindegaard J, Højgaard K, Ivarsen A, et al. Incidence and clinical characteristics of fungal keratitis in a Danish population from 2000 to 2013. Acta Ophthalmol 2015;93:54-8. |
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