Keratomycoses: causes, symptoms, diagnosis, treatment

Fungal diseases of the cornea, which have become more frequent in recent years and often proceed severely and with a bad outcome, are of leading importance in the pathology of the organ of vision caused by fungi. Their diagnosis and treatment are difficult. In the development of these diseases, the first place belongs to aspergilli, followed by cephalosporium, candida, fusarium, penicillium and other fungi. In most patients, fungal keratitis is primary, since the parasite enters from outside, and its introduction is often facilitated by minor injuries to the cornea by plant and other damaging agents.

The disease occurs more easily and is more severe in people with reduced resistance of the body due to diabetes, anemia, liver cirrhosis, radiation therapy, leukemia, and also with chronic irritation of the conjunctiva. Sometimes fungal infection is superimposed on herpetic keratitis, spring catarrh, other diseases of the cornea, aggravating their severity and complicating diagnosis.

The clinical picture of mycotic processes occurring in the cornea largely depends on the type of pathogen that preceded its introduction, the condition of the eye and the body, their reactivity, and the stage of the disease.

The most common and therefore best known type of fungal ulcer of the cornea is caused by mold and other fungi. Occupying a particular part of the cornea, most often its center or paracentral area, such an ulcer begins with the appearance of a disc-shaped yellowish-gray infiltrate in the subepithelial or deeper layers of the stroma, which quickly turns into a disk-shaped, ring-shaped or oval-shaped ulcer with a diameter of 2-3 to 6-8 mm. The edges of the ulcer are raised and protrude as a grayish-yellow shaft, and the center looks gray, uneven, dry, sometimes with a mound of crumbly particles or a whitish cheesy coating. When stained with fluorescein, a deeper tissue defect is revealed along the inner perimeter of the shaft surrounding the ulcer. Sometimes, infiltration radiates from this shaft in all directions, giving the ulcer its most characteristic appearance. However, more often there is no such radiance, and biomicroscopically a translucent zone of intracorneal infiltrate is determined around the ulcer, folds of Descemet's membrane and precipitates are visible.

In 1/3-1/2 of patients, the ulcer is accompanied by hypopyon. Eye irritation is expressed sharply from the very beginning of the disease, often serous-plastic or plastic iridocyclitis occurs. Later, the ulcer acquires a chronic course, does not tend to spontaneous healing, and does not respond to antibacterial therapy. In some cases, with or without such treatment, the ulcer spreads in depth, perforates the cornea, and can end in endophthalmitis.

For quite a long time the disease proceeds without the ingrowth of vessels into the cornea, then sooner or later, if antifungal therapy is not started, vessels appear in different layers of the stroma, surround the ulcer and grow into the cornea. The danger of perforation in such cases decreases, but vascularized leukoma gradually forms.

The sensitivity of the diseased cornea is impaired quite early, especially around the ulcer, but remains in the healthy eye, which distinguishes a fungal infection from a viral one.

In some patients, a fungal corneal ulcer from the very beginning appears to be similar to a creeping ulcer: an undermined infiltrated edge is formed, the tissue defect quickly spreads in width and depth. The similarity with ulcus serpens is enhanced by a high viscous hypopyon, a sharply expressed irritation of the eye.

Superficial keratomycosis, most often caused by Candida albicans, is milder and leaves fewer traces. According to G. Kh. Kudoyarov and M. K. Karimov (1973), such patients develop grayish-white infiltrates on the cornea that rise above the epithelium, resemble dust particles, are larger dots, or are loose lumps of bizarre outlines. They are easily removed with a damp cotton wool pad, but the epithelium underneath them is thinned or exfoliated. Eye irritation is moderate; without treatment, infiltrates quickly reappear. They may also appear as dense white plaques that grow deep and become necrotic, forming fistulas of the cornea.

In diagnosing keratomycosis, the anamnesis and clinical picture of the disease, its torpidity, resistance to antibacterial and other therapy are of great importance. The ethnology is most accurately recognized based on the results of microscopic examination of smears, scrapings, biopsies, trephinatops during keratoplasty, sowing this material on special media, and infection of animals.

Histologically, corneal mycoses are characterized by signs of chronic inflammation, in particular predominantly lymphocytic infiltration between the stromal layers, where fungal mycelium may also be found. Most often, the pathogen is detected, identified, and tested for sensitivity to drugs in growing cultures, and infection of animals confirms its pathogenesis. If such a diagnosis is impossible, trial treatment with antifungal agents can help to recognize a fungal infection.

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Treatment of conjunctival mycosis

Treatment is carried out with the above-mentioned fungicidal antibiotics, iodine and other drugs, which are prescribed locally and orally, and less often administered parenterally. Only ophthalmic forms of these drugs are suitable for local therapy, and various schemes can be followed when using them. For example, some ophthalmologists recommend instilling a nystatin solution (100,000 IU in 1 ml) every 2 hours during the day, applying 1% pimaricin ointment in the evening, and instilling an antibiotic solution three times a day to affect possible accompanying bacterial flora. When the pathogen is isolated, agents are used to which it is sensitive. However, it should be remembered that the fungus detected is not always to blame for the eye disease; it may only be one of the conjunctival saprophytes, which are found here quite often. Thus, B. Aniey et al. (1965) found such saprophytes in 27.9% of patients admitted for cataract extraction and in 34.6% of patients with non-mycotic conjunctival and corneal diseases.

Treatment of keratomycosis

Treatment consists of therapeutic and other effects on the foci of infection in the cornea and the general administration of mycostatics. Scraping out fungal ulcers and infiltrates or removing them by other mechanical methods, which has been used since the beginning of the century, has not lost its significance. During scraping (removal with a trephine, tampon, etc.), the area of the cornea cleared of the mycotic substrate and necrotic masses is smeared with a 5-10% alcohol solution of iodine or iodoform, powdered with amphotericin B powder. Sometimes they resort to cauterization of the ulcer. Already the first smearing brings relief to the patient and stops the process. Scraping is preceded and continued after by instillation of a 0.15-0.3% solution of amphotericin B into the conjunctival sac every 0.5-1 hour during the first 2-3 days, then 4 times a day. Nystatin is given orally in a dose of up to 1,500,000-2,000,000 IU per day, levorin. In severe cases, intravenous administration of amphotericin B is indicated. Potassium iodide remains an old, proven remedy for treating mycoses of the cornea, from 2 to 10 g of which is prescribed orally daily. A 10% solution can be administered intravenously, huh? A 1-2% solution can be instilled into the conjunctival sac. Treatment is carried out in a hospital for 4-6 weeks.

For actinomycetes, broad-spectrum antibiotics and sulfonamides are indicated.

The effectiveness of local therapy can be increased by electrophoresis of mycostatics, in particular sodium nystatin and sodium levorin through baths (10,000 U in 1 ml, from the cathode at a current of 0.5-4 mA, 10-15 min, daily, for a course of 15 procedures). As reported by M. K. Karimov and A. R. Valiakhmetova (1980), who developed and applied this method of treatment in 45 patients, it is much more effective than instillations of the same agents. With phoresis, the analgesic effect, fungicidal action, stimulation of immunogenesis are more noticeable, the drugs penetrate deeper into the corneal tissue. In addition to antifungal therapy, patients with keratomycosis receive symptomatic treatment (mydriatics, keratoplastic agents, etc.). Heat, as well as hypertonic solutions of sodium chloride under the conjunctiva, are indicated only in case of pronounced manifestations of iridocyclitis complicating the disease. To eliminate possible bacterial flora, antibiotics should be administered in the first week of treatment. Therapeutic or therapeutic in combination with mechanical treatment is most successful in case of superficial lesions of the cornea by fungi. Penetration of infection deeper than 2/3 of its stroma requires more active measures. As L. K. Parfenov and M. K. Karimov, FM Polack et al., G. Giinther and many other authors testify, only layer-by-layer or penetrating, partial or total keratoplasty can save the eye from death in case of deep corneal mycosis, provided that it is undertaken in a timely manner, carried out with complete elimination of the lesions and in combination with antimycotic therapy. Less often, conjunctival corneal coating is used or supplemented with keratoplasty.