REVIEW ARTICLE
Year : 2015 | Volume
: 3 | Issue : 1 | Page : 3--5
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
Correspondence Address:
Honaida Elshiek
Makkaha Eye Complex, Sudan Eye Center Alryaid, Alnus Street, Alryaid, Khartoum
Sudan
Abstract
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.
How to cite this article:
Elshiek H, Pineda R. Fungal keratitis.Albasar Int J Ophthalmol 2015;3:3-5
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How to cite this URL:
Elshiek H, Pineda R. Fungal keratitis. Albasar Int J Ophthalmol [serial online] 2015 [cited 2023 Sep 27 ];3:3-5
Available from: https://www.bijojournal.org/text.asp?2015/3/1/3/169310 |
Full Text
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 keratitisContact lens wear [6] is another risk factor for the development fungal keratitisTopical 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 infectionCandida species cause ocular infections in immunocompromised host and corneas with chronic erosions/ulceration from other causesOther 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 surfaceFilamentous keratitis: Gray or yellow-white stromal infiltrate with indistinct fluffy margins. Progressive infiltration is often associated with satellite lesionsFeathery branch-like extension or a ring-shaped infiltrate may developRapid progression with necrosis and thinning can occurPenetration 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 presentOther 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 suggestiveLack of response to conventional antibacterial therapy.Corneal scraping [9] for staining with gram, Giemsa, Gomori methenamine silver, and calcofluor white stainsCulture 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 culturesCorneal biopsy may be required if smear and cultures are negative and is indicated in the absence of clinical improvement after 3–4 daysOther 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 agentsTopical 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 comfortSubconjunctival 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 mgTetracycline (e.g., doxycycline) may be given for its anti-collagenase effect when there is significant thinningIOP 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 diseasePeripheral keratitis definition.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
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