Chapter 4

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Mycoses of the Anterior Segment of the Eye

4.1

Prevalence of Fungi in the Conjunctival Flora

In a similar way to bacteria [1, 2], fungi may also occur in the conjunctival flora without necessarily causing any manifest inflammation. A detailed overview is given in table 4.1. The variations in the percentage of positive smears recorded can be explained mainly by diVerences in the ages of the subjects [3, 4]. Fungal colonization of the conjunctiva increased with age, and it is also likely that regional and seasonal factors play a part [5]. In some reports, positive smears were related to individuals rather than to the total number of smears. Some data [5] are diYcult to understand and have not been included in the table. Repeated investigations at intervals of 4 weeks or 1 week [4, 5] seldom found the same species in the 2 smears, which may indicate that fungi in the conjunctiva are mostly airborne microorganisms, i.e. a transient flora. It is also conceivable that the conjunctiva has a fungistatic action. A factor isolated from bovine conjunctiva, which was not described in detail, reduced the number of viable cells of Candida albicans by 80%, while lysozyme had no discernible eVects on the fungi [6].

Topical applications of corticosteroids for 3 weeks were followed by an increase in the prevalence of fungi from 18.8 to 67% [7], though these findings were not confirmed in another study, in which a significant diVerence from the control group was only found after use of betamethasone/neomycin drops [4]. After topical application of hydrocortisone or tetracycline for 4 weeks, fungal colonization rates of the conjunctivae were 41.2 and 28.7%, respectively, in originally fungus-free eyes [8]. Yeasts were isolated from the conjunctival sacs of 13.3% of 37 women with Sjo¨gren’s syndrome, which was a higher prevalence than in a comparable population with normal eyes (same sex and similar age distribution [4]). Fungal colonization rates in patients with nonfungal underlying illnesses were also higher than in those with healthy eyes [9] (see 4.4.1.5).

68

Table 4.1. The prevalence of fungi in the conjunctival flora without inflammation

The lid margins are more often colonized than the conjunctivae [5], as is also the case with bacteria [1, 10]. Of 302 positive fungal smears, 80% were isolated from the lid margin, 15% from the conjunctiva and 5% from both sites [11]. In this study, smears were examined from a group of young native Americans (aged 14–20 years); 36% of 115 smears were positive, and in a similar but younger population (aged 8–15 years) from a diVerent region, fungi were demonstrated even in 86% of 28 smears.

The two largest studies, with 2346 smears [12] and 1106 smears [4] from central Europe showed the incidence of Penicillium spp. to be the highest, followed by Candida spp. and Aspergillus spp. Species from other genera, however, were also isolated, e.g. Scopulariopsis spp. and Cladosporium spp; the latter species were subject to regional variation [12]. A study from India [13] also showed a variety of fungi (including species of Aspergillus, Penicillium, Candida, Fusarium, Alternaria, Hormodendrum and Mucor ).

4.2

Fungal Conjunctivitis

Fungal conjunctivitis is usually found in association with keratomycosis, but it may also occur separately. In a personal experiment, acute conjunctivitis was induced by inoculation with C. albicans [14]. There have been reports of conjunctivitides caused by Candida spp. [15–18] that sometimes caused pseudomembranous exudates, as well as some caused by Blastomyces spp. [19], by Sporotrichum spp. [20, 21] and by Coccidioides spp. [22, 23]. Rhinosporidiosis may, over the course of a few months, lead to vascular proliferations [24–32] and to scleritis [33]. Conjunctivitis due to A. niger has been reported after foreign body injuries [34] and in concomitant trachoma [35]. [36] reported conjunctivitis in 3 children who had received subconjunctival doses of 3% saline because of retinal disease. The saline solutions had been contaminated with yeasts (Endomyopsis fibular ) and moulds (Monoverticillium ramigenum). The conjunctivitis cleared up spontaneously. The injection solutions caused the same symptoms in the eyes of rabbits.

C. neoformans has been isolated from subconjunctival granulomas in patients with AIDS [37, 38].

4.3

Fungal Scleritis

A report by von Graefe [39] in 1857 provided the first description of a case of fungal scleritis after surgery for strabismus carried out by DieVenbach. The ‘fungal granulations’ caused by the condition were described by von Virchow as ‘continuously’ associated with the sclera. A case of fungal scleritis due to A. fumigatus after injury caused by a wood splinter has also been described [40]. The author experimentally induced the same infection in rabbit eyes. Another patient, 2 months after injury caused by the branch of a tree, developed scleritis that healed only after cryotherapy and dura mater grafting;

A. fumigatus was isolated from the biopsy of the scleral nodule [41]. After injury caused by a cow’s tail, a patient developed a scleral abscess with nodules and necrosis and exudative retinal detachment. After 6 months of treatment with flucytosine 1% eye-drops and fluconazole, 200 mg/day orally, the scleral inflammation was completely resolved and the retina was attached [42]. A scleral infection with A. niger , possibly caused by drug abuse or self-mutilation, progressed to endophthalmitis [43]. The reverse – first endophthalmitis, then scleritis – has also been reported [44]. Scleritis due to A. flavus developed after uncomplicated cataract surgery [45]. Resolution of the inflammation was achieved with oral itraconazole after progression to multifocal scleral nodulation and necrosis had occurred during treatment with topical amphotericin B and oral ketoconazole. In a case of uncomplicated phacoemulsification and posterior chamber intraocular lens implantation in the left eye via a 5.5 mm, superior, scleral tunnel incision Rhizopus scleritis developed in a diabetic man. Severe destruction of the globe ensued despite topical, subconjunctival, and intravenous amphotericin B, in combination with hyperbaric oxygen therapy. Histopathological examination of the enucleated globe was consistent with Rhizopus infection [46]. After recurrent pterygium operations with bare scleral technique, one patient developed posterior scleritis, which was found to be caused by P. boydii [47]. The infection mimicked autoimmune posterior scleritis, which prompted the administration of systemic immunosuppressants. A biopsy was required before the condition was correctly diagnosed. Despite oral itraconazole and subconjunctival injections of miconazole, the eye showed no clinical response, necessitating enucleation. In another case Scedosporium prolificans scleritis followed pterygium surgery with b-irradiation (3¶8 Gy) 7 years previously [48]. In a series of intrascleral dissemination of infectious scleritis following pterygium excision one of 18 patients had Aspergillus [49]. The infection could not be cured and the globe was enucleated.

Table 4.2 summarizes published reports on fungal scleritis.

4.4

Keratomycosis

After the first description of a case of Aspergillus keratitis by Leber [50] and others around the turn of the century [51–53], relatively few reports of keratomycoses appeared in the first half of the 20th century. The early 1950s, however, saw a substantial increase. Thus, while [54] found 122 cases in the world literature for the period 1879–1950, they recorded the same number of cases for the period of only 1950–1962. Chick and Conant [55] found 148 cases in the literature, of which 42 had occurred between 1879 and 1916, 84

Table 4.2. Published reports on fungal scleritis

Table 4.2 (continued)

between 1951 and 1962, and only 22 cases in the interval between these 2 periods. Haggerty and Zimmerman [56] noted that only 3 cases of keratomycosis were recorded at the Armed Forces Institute of Pathology in Washington between 1933 and 1952, compared with 13 cases for the period 1952–1956. This represented an incidence of 1 case of mycosis/11,329 corneal infections in the first period, and 1 in 777 in the second. This rapid increase in fungal keratitides in the 1950s and 1960s has obviously not continued exponentially into the 1980s. Nevertheless, there were over 70 references in the literature for the period 1981–1990, and 68 for the period 1991–1997.

4.4.1

Predisposing Factors

4.4.1.1

Corticosteroids

The sudden increase in keratomycoses at the beginning of the 1950s has been attributed to the introduction of corticosteroids [7, 57–72]. This hypothesis was based on the results of animal studies, in which fungal infections

commonly occurred only after additional use of corticosteroids (see p. 162). Corticosteroids suppress the endogenous immune defence [73] and reduce the tolerance limit so that fungal diseases can become established [74, 75]. The term ‘tolerance limit’ represents the number of inoculated blastospores that the body can destroy without manifest signs of disease [76, 77]. The tolerance limit may be reduced by systemic conditions, e.g. diabetes, alcoholism, or malignant tumours, as well as by cytotoxic agents, whole-body irradiation, etc.

Corticosteroids are not known to have direct growth stimulating eVect on fungi [75, 78, 79]. No evidence has been published to support the assumption

[80]that corticosteroids have a direct eVect on the virulence of fungi. Overall, the use of corticosteroids must be regarded as an important risk

factor for the occurrence of keratomycoses.

4.4.1.2

Antibiotics

Antibiotics have also been associated with the occurrence of fungal keratitis [56, 57, 81–85]. In vitro investigations have provided contradictory results. Although tetracyclines were found to have a growth promoting eVect on C. albicans [67, 86], other investigators were unable to confirm this [87]. Tanaka [18] described a stimulant eVect of tetracycline at concentrations below 0.01% and an inhibitory action at 0.25%. In vitro, doxycycline, neomycin and gentamicin reduced the MIC of imidazole derivatives against Candida spp. [88]. Prasad and Nema [89] also found marked in vitro activity of doxycycline against Aspergillus spp., Candida spp., Curvularia spp. and Penicillium spp. In animal experiments, Candida keratitis was exacerbated by tetracyclines [75, 90] and by polymyxin B [91], though when the experiments were repeated polymyxin B had the opposite eVect [92].

The potential mode of a growth-promoting action of antibiotics on fungal growth has been described as a direct growth-stimulating eVect; furthermore, the elimination of bacteria and the change in the bacterial balance was considered to create a ’biological niche’ for the fungi to occupy [69, 75, 78, 79, 93, 94]. Such an eVect of antibiotics has been completely rejected by others [95]. In in vitro experiments, numerous antibiotics (ampicillin, mezlocillin, cefotaxime, tetracycline, chloramphenicol, erythromycin, polymyxin B, sulphamethoxydiazine, etc.) were tested on C. albicans, T. glabrata and A. fumigatus [95]. Apart from tetracycline hydrochloride, the antibiotics exhibited no eVect in experimental candidiasis in mice, leading to the conclusion that: ‘ The sole factor of importance for the development of fungal infections is the condition of the patient who – for any of many reasons – is immunocompromised and thus needs antibiotics, and his impaired immune status also renders him liable to fungal infections.’

Table 4.3. Prevalence of foreign body injuries preceding keratomycosis

4.4.1.3

Foreign Bodies

Corneal foreign bodies have been reported to cause keratomycosis at frequencies varying from about 40 to 90% (table 4.3). The nature of the foreign body is a decisive factor. In many cases they are plant products, such as rice ears, which get into the eye during agricultural work [71, 96–110], but other foreign bodies can also provoke keratomycoses, such as metals, stone fragments, or insects [93, 100, 111–113]. The pathogens can either be introduced into the cornea by the foreign body itself [114], or they may damage the cornea and thus create an opening for the existent transient fungal flora [12, 94].

4.4.1.4

Postoperative Keratomycosis

Keratomycosis following keratoplasty is discussed in chapter 5.1.2 in the context of postoperative fungal endophthalmitis, as these cases generally extend to the deeper sections of the eye. Mention should be made here, however, of 1 case due to C. parapsilosis and 1 due to A. fumigatus after radial keratotomy [115–118].

Table 4.4. Preceding eye diseases of keratomycosis

4.4.1.5

Pre-Existing Eye Diseases

Reports of keratomycoses that have developed in eyes with pre-existing disorders are not uncommon (table 4.4). Four patients have been described with candida keratitis following topical anaesthetic abuse. Three of them had burn of the eye, chronic dry eyes, and corneal abrasion after dirt blew as preceding disease [119]. In a histopathological study including 73 cases of fungal keratitis, [100] found 25 eyes with corneal disorders (herpes zoster ophthalmicus, ocular pemphigoid, lagophthalmos, ulcer and other disorders) as well as 10 with glaucoma (including 7 with bullous keratopathy). As many of these eyes had been treated with corticosteroids or antibiotics for their original disease, it was no longer possible to determine the decisive factor in the development of the fungal infection. Spontaneous C. albicans keratitis has been reported in immunocompromised drug abusers [120].

4.4.1.6

Contact Lenses

Keratomycoses are commonly associated with contact lenses [72, 121–136]. This applies particularly to soft lenses of hydroxyethylmethacrylate, which can be infiltrated by fungi [125, 133]. After prolonged use and with poor hygiene, deposits of epithelial cells and foreign particles may accumulate on the surface of the contact lens and provide a nutrient medium for pathogens [129, 137]. In addition, a moist chamber results between the underside of the contact lens and the surface of the cornea, which provides improved conditions for growth, together with a diminished wipe eVect of the lids and tears.

Fungi were detected in 22 of 312 patients with intolerance reactions after they had worn contact lenses for prolonged periods [125]. The contact lenses

should be examined microscopically in such cases, as the conjunctival smear is usually negative. [132] obtained similar results in an investigation of 11 patients with fungal infections of their contact lenses; 7 of the contact lenses had been heat-disinfected in a medical practice and 3 had been treated with a liquid disinfectant. In this context it has to be borne in mind that because of their toxicity, preservatives are in most cases no longer added to these fluids. Several risk factors may be present together if soft contact lenses are worn on medical reasons with the concurrent use of corticosteroids and antibiotics in already damaged eyes for prolonged periods [124, 130, 131, 133, 138, 139]. Three cases have been reported of fungal corneal ulceration after photorefractive keratectomy with the use of disposable contact lenses [134].

The clinical reports of a contributory eVect of contact lenses to the development of fungal infections, however, have not been supported by the results of animal experiments, in which they had neither a positive nor a negative eVect on the eyes of rabbits [140].

4.4.1.7

Systemic Illness

Systemic illness generally predisposes to additional fungal diseases (see chapter 5.1.1.2), apparently because of reduced immune defences. Keratomycoses have been described in association with diabetes mellitus [69, 72, 81, 98, 100, 124, 141], immunological disorders [124, 142, 143], neoplasms [98, 144] and alcoholism [98]. A syndrome of multiple endocrine deficiency and chronic mucocutaneous candidiasis has been described, in which bilateral keratoconjunctivitis occurs [145, 146], The keratitis, however, is not caused by candidiasis directly [147].

4.4.1.8

Age, Sex, Climate and Season

Keratomycoses occur in all age groups, though children tend to be less commonly aVected [97, 101, 113, 141, 148, 149]. The majority of patients are male, which is attributed to more extensive outdoor activity and the associated greater exposure to foreign bodies [82, 97–100, 113, 149–152]. In contrast, an Indian study showed a predominance of female patients [101], presumably because Indian women are more often employed outside in agriculture.

Keratomycoses occur predominantly in warm, subtropical and damp climates. The incidence correlates with harvest time and the seasonal increase in temperature and humidity [102, 148, 149, 153–155]. However, a higher incidence in the cool, windy months has been found in south Florida [138, 141, 150]. An increase in the incidence of keratitis also seems to be associated with the cool, windy months in the temperate zone [156].

4.4.2

Spectrum of Pathogens Causing Keratomycosis

The literature conveys the impression that the prevalence of individual pathogens is largely dependent on geographical and climatic factors.

Fusarium spp. are the pathogens most commonly isolated in South America [152, 157], Florida [72, 138, 158], Japan [159, 160], Nigeria [99] and South Africa [161]. Aspergillus spp. are more often involved than Fusarium spp. in India [97, 162, 163] and in Vietnam [108]. Candida spp. followed by Aspergillus spp. are the principal pathogens in the temperate zones, e.g. in San Francisco [69], the northern USA [153], the UK [164] and Germany [93]. The predominance of Candida spp. in keratomycosis in Central Europe reflects the frequency of organic and systemic infections in that region [165–169].

Table 4.5 lists the fungi that have been described as causes of keratomycosis.

4.4.3

Clinical Aspects of Keratomycoses

Fungal infections of the cornea start, at first relatively painlessly, about 1–4 weeks after a trauma. There is subepithelial infiltration, which is occasionally associated with recurrent erosion.

The infiltration increases in intensity and extent even if high doses of antibiotics are given (because the condition is mistakenly attributed to bacteria). This is accompanied by violent inflammation in the anterior chamber with endothelial plaques and a hypopyon. The latter initially tends to present the flat, horizontal appearance associated with bacterial origin (fig. 4.1), often followed by a pyramid-like, convex form characteristic of a fungal infection (fig. 4.2, 4.4, 4.6) [170]. At this stage, the hypopyon is no longer fluid and mobile, but viscous and solid. This is presumably due to the hyphae forming a firm skeleton for fibrin and cellular elements. In some cases, inflammation of the anterior chamber with the hypopyon may be so pronounced that secondary glaucoma develops [171, 172]. At this time the patient will complain of severe pain, foreign body sensation and diminished vision. In addition, mixed or deep hyperemia and pseudoptosis will occur. The fungal ulcer developing from the infiltration may show a greater or lesser degree of epithelialization. The margins, however, are mostly covered by epithelium, as the pathogens work their way from there into the subepithelial tissues at the level of the corneal stroma. The ulcer is yellowish-grey in colour and is indistinctly marginated.

Table 4.5. Fungi described as causes of keratomycosis

Table 4.5 (continued)

Table 4.5 (continued)

Table 4.5 (continued)

It is occasionally possible, with adequate magnification, to distinguish hyphae with feathery outward growth (fig. 4.3, 4.4). Another characteristic feature is the geographic form of the ulcer (fig. 4.5). Satellite phenomena are pathognomonic for fungal keratitis, but are not always present. Raised areas within the corneal infiltration are also typical [173] (fig. 4.6). In some cases a white ring is present [174], which may represent an interaction of fungal antigen and host antibody (so called Wessely ring).

The characteristics of keratomycosis are summarized in table 4.6. However, the signs may diVer from those outlined above, and fungal keratitis may present a diVerent appearance, especially if it is a complication of another keratopathy (fig. 4.8). Furthermore, not all the characteristics listed are always present at the same time. If they are seen, however, they should suggest the possibility of keratomycosis. C. albicans and C. parapsilosis may also cause

Fig. 4.1. Case 1. A. fumigatus keratitis with flat, horizontal hypopyon.

Fig. 4.2. The same case as in figure 4.1, 3 weeks later. A pyramid-shaped, convex hypopyon is now visible.

an infectious crystalline keratopathy of the type associated with a bacterial infection [175–181].

If medical treatment is unsuccessful, a descemetocele and perforation may develop in the further course of the disease. Finally, fungal keratitis may lead to endophthalmitis and loss of the eye (see chapter 5.1.2.1.3).

Fig. 4.3. Case 2. Right eye: corneal infiltration without visible or stainable epithelial damage. Radially arranged hyphae protruding from the infiltration (arrow).

Fig. 4.4. Case 2. Left eye: Ulcer with feathery broadening hyphae (white arrow). Pyra- mid-shaped hypopyon (black arrow).

4.4.4

Further Diagnostic Measures in Keratomycosis

The confirmation of a clinically suspected diagnosis of keratomycosis depends on the demonstration of fungi. This requires the collection of material

Fig. 4.5. Geographical infiltration (white arrow), satellite phenomena (black arrow).

Fig. 4.6. Prominent infiltration (white arrow), with a pyramid-shaped hypopyon (black arrow).

that actually contains fungal elements. A positive result, however, is only rarely achieved from a specimen such as a conjunctival smear or a superficial sponge biopsy of the cornea, or from an impression product [182]. In order to include the pathogens lying under the epithelialized ulcer margins, it is necessary to remove, with the aid of a rigid spatula, suYcient corneal tissue (epithelium

Fig. 4.7. Case 3. Secondary fungal infection (by Trichophyton rubrum) complicating recurrent herpes simplex keratitis.

Table 4.6. Characteristics of keratomycosis

Geographical configuration

Poorly marginated feathery infiltration Satellite phenomenon

Infiltrations commonly covered by epithelium

Prominent corneal areas, Kaufman and Wood, 1965 [173]

Viscous, pyramid-shaped, convex hypopyon, Behrens-Baumann, 1991 [170]

and superficial stroma [183]. Ophthalmologists are understandably reluctant to remove corneal substance from the ulcer, but from a diagnostic as well as a therapeutic viewpoint, this reluctance is misplaced (see chapter 4.4.6.1.1). Lemp et al. [184] recommend that where keratomycosis is suspected, several samples should be collected (twice daily for 3 days or until a positive specimen has been obtained). Sometimes even an abrasion with a sharp instrument does not lead to a diagnostic result, and a corneal biopsy (keratectomy) is required to obtain suYcient material for a diagnosis [185–187].

The specimens removed are placed in culture medium and transferred to a mycological laboratory (see chapter 1.8.2). Diagnosis by culturing takes 3–6 days, in the case of some fungi several weeks. It is thus useful to examine part of the specimens under a microscope in order to distinguish primarily between

fungal and bacterial pathogens. Furthermore, the diagnostic positive rate is higher than that achieved by culturing [160]. Suitable stains include a 10% potassium hydroxide solution [188] with ink in the proportions 9:1 [189], gram stain, and Giemsa stain. The best is said to be a modified methenamine-silver stain, which takes 1 h to prepare [190]. An even faster method (2 min) is to stain the fungi with Calcofluor 1% and Evans blue 1% and to observe them under a fluorescence microscope [189, 191–193]. Lactophenol cotton blue mounts of corneal scrapings are also recommended [194]. Confocal microscopy provides a new, noninvasive way of imaging the human cornea in vivo. Fungal hyphae are visualized as high-contrast filaments about 6 lm in diameter and 60–400 lm in length [195–197]. Another technique in identifying fungal elements may be the polymerase chain reaction [198].

In case of an emergency graft, it is useful to divide the corneal disc along the middle of the ulcer. One half can be passed on for microbiological diagnosis whilst the other is used for histopathological examination. In a study in which 61 corneal discs were thus examined, the histopathological examinations were positive in 77.04% and the culturing in 75.4% [199].

4.4.5

Histopathology of the Keratomycoses

The fungal elements can be visualized histologically by periodic acidSchiV reagent, Gridley’s stain for fungi, or Gomori’s methenamine-silver stain [78, 100, 200–203]. A particularly useful method of visualizing fungi is with the use of fluorescein-conjugated lectin concanavalin A [192, 193]. By means of polymerase chain reactions, fungal DNA can be detected even in fixed tissue [204].

Although the fungi penetrate the cornea [110, 205, 206], this is not inevitably associated with necrosis of the overlying tissues [114]. The pathogens are consequently situated deep in the cornea [207] and are thus inaccessible for superficial diagnostic sponge biopsies [100, 208]. For the same reason, it is diYcult for antifungal agents to reach fungal elements [209].

The ‘satellite phenomena’, a clinical characteristic of fungal infections, present a histological picture of microabscesses around fungal elements. They are situated in the periphery of the crater of the ulcer. The granulocytic infiltration is less marked and more focal than in bacterial keratitis [200]. The Wessely immune ring [173, 210], an occasionally observed clinical feature, corresponds histopathologically to a ring abscess [100]. In infectious crystalline keratopathy, the microorganisms produce a ruthenium red-staining glycocalyx, which may be visualized as a biofilm by electron microscopy [176]. The hyphae

may lie parallel to the corneal lamellae, but may also be in a perpendicular position [199]. The perpendicular direction has been interpreted as indicating prior treatment with corticosteroids. In rabbit models, however, this arrangement of the hyphae may be found also without drug treatment [209].

4.4.6

Treatment of Keratomycosis

Fungal keratitis should initially be treated with drugs, provided that the inflammatory process is not too far advanced. Surgical therapies are available as an alternative.

4.4.6.1

Medical Treatment

4.4.6.1.1

Antifungal Agents

Several agents are available for the treatment of keratomycosis, and these have been described in detail in chapter 2. As a rule, they are applied topically, as this results in higher tissue concentrations in the anterior parts of the eye than can be achieved by systemic administration Havener in 1983 [211], and furthermore the risk of systemic side-eVects is low. Therefore, the prescription of oral antifungal agents [161, 212] should be considered only if the topical treatment has been unsuccessful, and endophthalmitis has developed.

A medical treatment regimen for keratomycosis is outlined in table 4.7. The choice of antifungal agent must take account of regional variations in the prevalence of fungi. As in the temperate zone candidal keratomycosis is the most common form (see chapter 4.4.2), amphotericin B is the standard antifungal agent [213, 214]. Drops for instillation are prepared as described in table 2.2. Amphotericin B with its high molecular weight of 924.11 daltons hardly penetrates the corneal epithelium, and a corneal abrasion should thus be carried out. This ‘debridement’ [102], which, depending on the result, should be repeatedly carried out, can serve at the same time to confirm the diagnosis. In Fusarium or Aspergillus keratomycosis, on the other hand, natamycin 5% is more eVective than amphotericin B [164, 215].

Fluconazole has become established as an alternative to amphotericin B, due to its good tolerability and its eVective penetration into the cornea and anterior chamber, even without abrasion [216]. It has been used successfully in candidal keratitis [217, 218], and has also been used orally in this indication [219].

Table 4.7. A medical treatment regimen for keratomycosis

Miconazole 1%, flucytosine 1% and nystatin eye-drops may be used as second-line drugs. Collagen shields have been used as vehicles for medication [220]. Possibly, chlorhexidine gluconate and other antiseptics may be beneficial [221, 222].

4.4.6.1.2

Antifungal Agents plus Corticosteroids

It may seem surprising, in view of the fact that corticosteroids are thought to be predisposing factors for keratomycosis, that these agents are considered for medical treatment of the condition. However, the results of animal experiments (see chapter 7.4.3) suggest that low-dose dexamethasone (at a concentration of 0.01%) may have a beneficial eVect [223]. Subconjunctival injections of 4 mg of dexamethasone every 2 days also proved more eVective in reducing secondary inflammatory reactions in the cornea and anterior chamber and neovascularization in animal experiments than antifungal therapy alone [224]. These results are validated by clinical experience of the combination therapy. Roberts [225] found that use of corticosteroids in addition to antifungal therapy was not followed by any deterioration in the course of Candida keratitis; in fact, he described a definite reduction of iritis. Similar results were reported by O’Day et al. [226] in Aspergillus keratitis; it was not until 4 mg subconjunctival dexamethasone twice daily and hourly drops of prednisolone acetate were added to the antifungal treatment that the corneal oedema and intraocular inflammation were seen to subside.

Nevertheless care should be used in the additional administration of corticosteroids [227], particularly as some authors regard them as contraindi-

cated in fungal keratitis [228, 229]. They should only be given under strict monitoring, and in the later stages when the infiltrative process has been arrested. Considerable importance obviously attaches to the time factor and therefore to the stage of the keratitis (see chapter 7.4.3), which bears out the findings of [72] in 19 patients with fungal keratitis, who were treated with topical steroids for 24 days after a period of antifungal therapy averaging 14 days. Two of the 19 patients received topical corticosteroids within 1–3 days of starting a topical antifungal therapy, and clinical examinations showed their conditions to have worsened. Finally, it is essential that the patient is immunocompetent, as otherwise systemic dissemination of the fungi cannot be ruled out [226].

4.4.6.2

Surgical Treatment

The treatments formerly recommended for keratomycosis included keratectomy, lamellar keratoplasty [98, 230, 231], or a conjunctival graft [98]. In addition, cryotherapy was used in animal experiments [232]. As in the case of corneal ‘abrasion’ or ‘debridement’ [102], keratectomy may be useful for diagnostic purposes and to improve the pharmacokinetics of drug treatment, with the partial removal of the pathogens supporting the medical treatment [113]. A lamellar keratoplasty may also be justified on technical reasons if the focus is situated peripherally at the limbus [106]. As a surgical treatment, however, all of these methods appear to be of little benefit [233]. Either the pathogens are still in the superficial layers of the cornea, in which case medical treatment is likely to be successful and less invasive, or the infection has penetrated so deeply as to be no longer accessible to these methods.

In advanced cases where medical treatment cannot halt the process, it is preferable to carry out an emergency graft [1, 158, 187, 233–246]. In 34 of 125 patients (27%) with fungal keratitis, therapeutic penetrating keratoplasty was performed, typically within 4 weeks of presentation (74%), for medical treatment failure (56%), corneal perforation (32%) and recurrent keratitis while receiving medical therapy (12%) [72]. A repeat keratoplasty was required in 8 patients, 5 for graft failure and 3 for recurrent F. oxysporum keratitis. Keratoplasty has the advantage that it involves removal not only of the pathogenic organisms, but also of the leukocyte and fibrin accumulations that contribute to tissue damage. In addition, it prevents the vascularization that inevitably occurs in prolonged courses and worsens the prognosis of a subsequent, optical keratoplasty [247]. Good results have been obtained in other studies [246, 248], with up to 73% of grafts remaining clear after variable periods of follow-up (1 month to 9 years) and accelerated rehabilita-

Fig. 4.8. The same case as in figure 4.4, 3 weeks after penetrating keratoplasty (6.0/6.1 mm).

tion. Sometimes large penetrating keratoplasties (recipient bed q9.5 mm) are necessary to preserve the structural integrity of the globe [249]. It is thus advisable not to wait too long before performing an emergency graft (fig. 4.8).

However, when emergency grafts in microbial keratitis were compared with a group grafted subsequently for scarring after complete resolution of infection and inflammation, a clear diVerence in graft survival was evident, with a 51% 5-year survival rate for emergency grafts versus 90% for grafts performed in quiet eyes [245].

Topical and systemic corticosteroids should be used in an eVort to reduce inflammation before surgery, when this is indicated, to reduce the incidence of postinflammatory sequelae and improve the prognosis for visual recovery [246]. Corticosteroids are also indicated postoperatively and do not cause recurrences if the fungus-infiltrated area has been surgically removed. As a safety measure, however, postoperative continuation of antifungal treatment is recommended. Failure to seal a perforation with cyanoacrylate adhesive in active keratitis is an absolute indication for penetrating keratoplasty, as irreversible synechial angle closure and secondary glaucoma will result if the anterior chamber remains flat, and there is a significant risk of spontaneous expulsive haemorrhage in the inflamed hypotonic eye [186].

Fig. 4.9. Case 4. Fourteen days after removal of the corneal stitches. Two discrete infiltrations without epithelial defect.

4.4.7

Case Histories

A few examples of keratomycoses are presented below.

4.4.7.1

Case 1

A 40-year-old, generally healthy forester presented after a foreign-body injury of the right eye. He was treated with topical antibiotics (chloramphenicol and kanamycin) for several weeks. On admission he had an ulcer with hypopyon (fig. 4.1), which despite 3 weeks of antibiotic treatment increased in size (fig. 4.2). A conjunctival smear was negative, but A. fumigatus was isolated from a corneal abrasion. With the use of nystatin drops and ointment, with later use of natamycin ointment, the ulcer subsided after 53 days.

4.4.7.2

Case 2

A 60-year-old woman, who had elsewhere undergone extracapsular cataract extraction with posterior chamber lens in both eyes, presented with postoperative recurrent intraocular inflammations, which had been treated with antibiotics and corticosteroids. She was admitted to hospital 6 months after the extractions. The right eye showed corneal infiltration without inflammation of the anterior chamber (fig. 4.3). The left eye showed a corneal ulcer with radial infiltrations and hypopyon (fig. 4.4). C. albicans and Staphylococcus epidermidis were isolated from a smear. Bilateral treatment with topical amphotericin B and antibiotics (polymyxin, neomycin and bacitracin) reversed the infiltration in the right eye. As the left eye failed to improve within one week, penetrating keratoplasty was carried out (fig. 4.8), which was followed by subsidence of the intraocular inflammation.

Fig. 4.10. Case 5. Cryptococcus laurentii corneal ulcer complicating herpes simplex keratitis.

Fig. 4.11. Same case as in figure 4.10. Marked regression of corneal vascularization after 14 months.

4.4.7.3

Case 3

A 10-year-old boy presented with recurrent herpes simplex keratitis in both eyes. Trichophyton rubrum was cultured from a corneal abrasion (fig. 4.7). Onychomycosis of the hands and feet was diagnosed at the same time. Treatment with amphotericin B eye-drops was followed by penetrating keratoplasty.

4.4.7.4

Case 4

A 41-year-old man had undergone penetrating keratoplasty 5 months previously for keratoconus, Amsler stage IV. Since then, he had used topical prednisolone acetate. After removal of the sutures, 2 discrete white infiltrates of the stroma were seen at the margin of the transplant (fig. 4.9). C. albicans was cultured from a conjunctival smear and from the faeces. The infiltrates disappeared within 19 days in response to nystatin eye-drops and natamycin ointment.

4.4.7.5

Case 5

A 33-year-old woman presented with a corneal ulcer and increasing vascularization following recurrent herpes simplex keratitis (fig. 4.10). Cryptococcus laurentii was cultured from a corneal abrasion and treatment started with nystatin eye drops (chapter 2, table 2.4) 10 times daily for 2 months following 4 times daily for 1 month. Subsequently, topical steroids were added, which resulted in regression of corneal vascularization (fig. 4.11).

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