Chapter 5

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Fungal Endophthalmitis

5.1

Pathogenesis and Clinical Features

Fungal endophthalmitis arises mainly via two pathogenetic pathways. Endogenous (metastatic) endophthalmitis commonly occurs as a result of sepsis, and must be distinguished from exogenously caused endophthalmitis, which can occur as a result of an operation or injury. Persistent keratomycosis may also lead to endophthalmitis.

5.1.1

Endogenous Fungal Endophthalmitis

5.1.1.1

Pathogens

The first description of endogenous endophthalmitis was by von Virchow [1] in 1856, but there was no microbial diVerentiation and the disease may also have had a bacterial cause. Both unilateral and bilateral ‘metastatic ophthalmic diseases’ have been described in the literature [2, 7]. The first description of endogenous fungal endophthalmitis was by Dimmer [2] and not by Miale [5] as mostly reported in the English-language literature. Stock [7] and Kreibig [4] had also published their cases earlier. The fungal species reported as causes of endogenous endophthalmitis are listed in table 5.1. It should be noted here that in the 1990s a change occurred in the causes of candidemia, with non- C. albicans species increasing; this is ominous because of their in vitro resistance to most of the currently available antifungal agents [8].

5.1.1.2

Causes

The causes of endogenous endophthalmitis are varied. A review of the literature reveals the predisposing factors listed in table 5.2. Immunosuppres-

108

Table 5.1. Fungi reported in endogenous endophthalmitis

Table 5.1 (continued)

Table 5.2. Predisposing factors for fungal septicemia and endogenous endophthalmitis

Reduced immune defences, e.g. diabetes, chronic alcoholism, pancreatitis, malignancy Hemodialysis, abdominal surgery

Parenteral hyperalimentation

Organ transplantation, immunosuppressive therapy Indwelling intravenous catheter

Prolonged antibiotic therapy (?) Intravenous drug abuse

AIDS Prematurity

sion, either due to systemic disease or iatrogenically induced through immunosuppressive therapy, seems to be one of the main reasons for fungal septicemia, the prerequisite of fungal endophthalmitis. Such systemic diseases include malignancies, pancreatitis, diabetes mellitus, and alcoholism [9–18]. Iatrogenic factors include hemodialysis [19], systemic (especially gastrointestinal) surgery

and intravenous hyperalimentation [19–29] and transplants [30–37]. One case of C. tropicalis endophthalmitis as the only initial manifestation of pacemaker endocarditis has been described [38]. Three cases of invasive Aspergillus infections complicating coronary artery bypass grafting [39] and several cases of C. albicans endophthalmitis after lithotripsy of a kidney stone have also been reported [40–43].

Indwelling intravenous catheters are often implicated [15, 26, 29, 44–54]. In a series of culture-proven fungal endophthalmitis in 20 eyes of 18 patients, the most common association was long-term intravenous line placement (?2 weeks), which was present in 12 patients (67%). After initial examination, only 2 patients had a systemic culture positive for a fungal organism (none had a positive blood culture) [21]. If a peripheral venous line remains in place for longer than 48 h in patients undergoing intensive care, a 0.1% incidence of sepsis must be expected, and this may rise to 1% with central venous catheters [45]. After Staphylococcus aureus and S. epidermidis, the next most common pathogenic organisms are fungi, which account for 10% of systemic infections. Arteriovenous fistulae used for hemodialysis are also a potential source [50, 55].

The administration of systemic antibiotics is also thought to favor fungal septicemia [50, 51, 56–58], though in vitro and in vivo experimental studies do not support this [59]. It must be remembered that patients with impaired immune defences receive antibiotics, and it is the underlying impairment that allows fungal sepsis to develop.

Another disease category to be considered is drug addiction [60–87]. General fungal diseases have also been described in association with AIDS

[88–101], and include fungal endophthalmitis [88, 91, 102–106]. In 1 case of AIDS, Cryptoccocus sp. was detected in an iris inflammatory mass [107], and 1 patient with limbal nodules was also found to have multifocal choroiditis [108]. Of 235 consecutive autopsies of patients with AIDS, 18 were found to have infectious choroiditis, including C. neoformans, P. carinii, M. tuberculosis, H. capsulatum, Candida spp., A. fumigatus, Toxoplasma gondii and M. aviumintracellulare [109].

The first case of Candida endophthalmitis in premature infants was noted in 1972 [110], and since then additional reports have been published [111–113]. The prevalence of retinal findings in systemic candidiasis in premature infants may reach 50% [114], but this was not confirmed in another study of 15 babies, in whom no retinal involvement was found despite repeated fundoscopic examination [115].

One case of C. albicans endophthalmitis has been reported after anabolic steroid abuse in an athlete [116], and a unique case of A. flavus endophthalmitis associated with periodontitis [117]. C. albicans endophthalmitis after induced abortion has been reported recently [118].

Fungal sepsis is likely to be associated with ocular involvement in 2.8–50% of cases [19, 23, 119, 120]. In a prospective study of 32 patients with positive blood cultures, chorioretinitis was observed in 28% [121], and in another study of 46 candidemic patients was observed in 13% of cases [122]. In a larger study of 108 patients, however, Candida chorioretinitis could only be found in 9% [123]. Fraser et al. [124] reviewed 105 patients with candidemia who underwent ophthalmoscopy and did not diagnose any cases of endophthalmitis. These authors suggest that this may be due to the lack of sequential evaluation by ophthalmologists. In a more recent report [125], a high rate of hematogenous candidal endophthalmitis (50%) was found in patients with postoperative candidemia. In that study, ophthalmoscopy was performed by the same ophthalmologist 5–8 days after the onset of symptoms of sepsis and was repeated after 5 days. Thus, Candida endophthalmitis may be more common than previously thought. Follow-up of patients by qualified personnel should help to identify this complication. In the most recent study of 107 patients, endophthalmitis was found in only 2.8% (3 patients) [119], which was ascribed to the fact that these patients received very early systemic therapy.

In contrast, endophthalmitis may also occasionally be the first sign of fungal septicemia [126, 127]. Of 10 patients with Candida endophthalmitis in an intensive care ward, the 80% mortality rate was clearly increased compared with an overall mortality of 17% for all patients in the surgical intensive care unit of that hospital [128]. It should also be noted that ocular lesions preceded symptomatic meningitis in 6 of 22 patients (27%) with CNS involvement [129].

In patients with the risk factors shown in table 5.2, therefore, regular examinations by an ophthalmologist should be undertaken [15, 127, 130]. This is particularly important in unconscious patients, who are unable to complain of visual symptoms. In addition, detection of antigen by means of a monoclonal antibody or class-specific antibody detection, including amplification procedures has been recommended for the diagnosis of systemic Candida infection [131].

5.1.1.3

Clinical Features

Initially, the eye is externally free of irritation and does not suggest inflammation. Even using a slit-lamp microscope, irritation of the anterior chamber can only be detected later. The patient does not initially complain of pain. After progression of endophthalmitis, blurred vision, photophobia and a red eye may develop (table 5.3). In addition, patients may complain of cobwebs, floaters, or a veil across their vision. Debilitated and extremely

Fig. 5.1. Chorioretinal infiltrates in fungal sepsis. The focus at the temporal side of the macula simulates Roth’s spot.

Table 5.3. Progression of symptoms of endogenous endophthalmitis

Pale and painless in early stage

Creamy, white choroidoretinal lesion(s) with or without intraretinal hemorrhages Blurred vision, floaters

Vitreous opacities (snow balls, string of pearls) Red eye in advanced stage

ill patients may be unable to describe their visual symptoms or may be unaware of them.

The first signs of intraocular infection are white, creamy lesions at the posterior pole [47, 78, 132, 133], which are occasionally prominent (fig. 5.1– 5.3). The lesions may be single or multiple. Both the retina [127, 134, 135] and the chorioidea [133] may be aVected [29, 136]. The foci may be surrounded by hemorrhage and appear similar to Roth’s spots (fig. 5.1) [134, 137].

Cotton-wool spots have also been described [138]. In addition, the vitreous body is infiltrated, where snowball and string-of-pearls formations are characteristic (fig. 5.4–5.7) [127, 139–141]. Long-term observations are necessary, as in 6 cases of Candida endophthalmitis successfully treated with amphotericin B, choroidal neovascularization occurred within 2 weeks to 2 years [142]. There are 2 other case reports of choroidal neovascularization in Candida

Fig. 5.2. The same case as in figure 5.1, 7 days later, showing intensification of the infiltration into the retina and slow absorption of the hemorrhages.

Fig. 5.3. The same case as in figure 5.2, 4 weeks later, showing regression of the infiltration of the fovea.

Fig. 5.4. String-of-pearls infiltration of the vitreous body.

Fig. 5.5. Snowflake infiltration of the vitreous body in Candida endophthalmitis.

endophthalmitis [385, 386]. Papilledema, retinal detachment and iritis with hypopyon may also occur [12]. Finally, episcleritis has been observed [78], and Mucor endophthalmitis has been wrongly diagnosed as Coats’ disease [143].

The above causes and clinical symptoms apply to endogenous endophthalmitis caused by a variety of diVerent fungi, but especially by Candida spp. Infections by some fungi have additional specific features, which are described below.

Fig. 5.6. Combined cord and snowflake infiltration of the vitreous body.

Fig. 5.7. Dense infiltration of the vitreous body in a case of Candida endophthalmitis.

5.1.1.3.1

Endogenous Aspergillus Endophthalmitis

The most common manifestation of aspergillosis is pneumonitis, and this occurs most commonly in immunocompromised hosts [144]. Because blood cultures are often negative for Aspergillus spp., the eye may be the only site

from which a positive culture is obtained. Aspergillus endocarditis has been reported as a particular risk factor for endophthalmitis [145–149]. This is controversial concerning orthotopic liver transplantation [150–153]. Aspergillus spp. are second only to Candida spp. as the etiological agent in endogenous endophthalmitis in drug abusers [71]. These healthy-appearing individuals present with a red, painful eye and decreased vision. Uveitis is a common initial diagnosis and is frequently treated with corticosteroids, resulting in exacerbation of the infection and delay in initiating appropriate treatment. The patient should be questioned about drug abuse and examined for evidence of multiple venepuncture sites. Almost all patients with Aspergillus endophthalmitis have acute anterior uveitis with ocular pain, redness and blurred vision

[154].In a series of 12 eyes with culture-proven endogenous Aspergillus endophthalmitis, 8 eyes revealed a central macular chorioretinal inflammatory lesion

[155].Aspergillus even involves the optic nerve [156]. Sandwich ELISA, which detects Aspergillus galactomannan, may be helpful in establishing an early diagnosis [157].

5.1.1.3.2

Endogenous Cryptococcus Endophthalmitis

When Cryptococcus sp. is the cause, there may be anterior segment inflammatory signs, including keratic precipitates and posterior synechiae [158]. The posterior segment lesions are often elevated and larger than Candida lesions. They may contain overlying retinal telangiectasia [158, 159]. The lesions may be confused with Toxoplasma retinochoroiditis [158, 160], ocular sarcoidosis, or tuberculosis. Histopathological pictures of optic nerve involvement have been shown by Friedenwald et al. [161].

Cryptococcus spp. are an important cause of morbidity and mortality in immunocompromised patients, especially in AIDS [100, 162]. The infection is usually acquired through inhalation. Cryptococcus sp. has been identified in an inflammatory mass in the iris of a patient with AIDS [107], and cryptococcal optic neuropathy has been described in further cases [163, 164]. In a patient with AIDS who had cryptococcal meningitis, sudden simultaneously bilateral blindness occurred. Both optic discs and retinas appeared normal. Lumbar puncture showed an opening pressure of 600 mm H2O. At autopsy, fulminant necrosis of both optic nerves was found, with cryptococcal organisms throughout the basal meninges and in the sheaths of both optic nerves [165].

In a series of 80 patients seropositive for HIV and with cryptococcal infection, papilledema was observed in 26 patients (32.5%) [166]. Papilledema with visual impairment was found in 2 patients with cryptococcal meningitis, and, at autopsy, cryptococcal organisms were found in the optic nerve sheath but not in the optic nerve [167]. Of 6 patients with papilledema, 3 had loss

of visual acuity with multiple cryptococcal abscesses, while the other 3 with normal function had only minimal or no involvement of the visual pathways [168]. In another series of 36 patients with cryptococcal meningitis, papilledema was noted in 12 and extraocular muscle paresis in 5 cases [169]. Most patients with ocular involvement also have CNS infection [37, 158–160, 170–172].

In contrast, patients with cryptococcal meningitis may develop visual loss in the absence of other ocular lesions. There are 2 distinct patterns of visual loss: rapid visual loss within 12 h indicating direct invasion of the optic nerve by C. neoformans, and slow visual loss due to elevated CSF opening pressure [173].

In a patient intubated for 7 days and treated with intravenous methylprednisolone for status asthmaticus, an anterior chamber mass was identified on histopathology as A. fumigatus. Ocular and blood cultures were negative, as were the results of bone marrow biopsy, lung biopsy and anterior chamber paracentesis. Computed tomography showed a solitary lesion in the left lower pulmonary lobe and multiple brain lesions [174]. The patient responded to amphotericin B and flucytosine.

C. neoformans infection can be accurately and rapidly detected with a latex reagent for antigen detection [131].

5.1.2

Exogenous Fungal Endophthalmitis

5.1.2.1

Causes

5.1.2.1.1

Postoperative Fungal Endophthalmitis

Fungal infections following operative procedures on the eye were described early this century, when fungal endophthalmitis was reported after a retinal operation [175] and following cataract extraction [176]. In later publications, the infection was most often described following cataract surgery (table 5.4), even after sutureless small-incision phacoemulsification cataract surgery [177]. In a series of 15 and 13 cases of extracapsular cataract removal, the irrigation fluid was contaminated with C. parapsilosis, respectively [178, 179], and in another series of 13 cases with P. linaceus [180]. In sporadic infections, however, it is more likely that the pathogens originate from the conjunctival sac or the lid margins, particularly as fungi are found there even in healthy individuals (see chapter 4, p. 68). This mode of infection is also likely in the case of bacterial postoperative endophthalmitis [181].

Table 5.4. Fungal endophthalmitis after cataract surgery

Table 5.5. Fungal infections of corneal transplants

Table 5.5 (continued)

a>Aphakia or pseudophakia; b>bullous keratopathy; TP>transplant; MCK>McCarey-Kaufman medium; KP>keratoplasty.

Fungal infections following keratoplasty have been described repeatedly (table 5.5). This is understandable, as bacteria and viruses are also known to be transmitted [182–185]. True transmission from donor to recipient [186–188] must be distinguished, however, from perioperative infection (contamination of the preserving fluid and contamination by local pathogens). Preoperative infection must also be considered. In the case reported by Ross and Laibson [189] of a C. albicans infection following keratoplasty, the operation was performed on an eye that had suVered severe prior damage by descemetoceles, as was also found for the infection of transplants by P. lilacinus described by Gordon and Norton [190] and for 3 cases of Fusarium keratitis [191]. In the case described by Rao and Aquarella [192], a preoperative perforated ulcer was treated with a soft contact lens.

Contamination of the donor material may indeed be considerable. Of 70 transplants, the corneal margin and McCarey-Kaufman medium were contaminated in 14 cases; in two cases of contamination C. parapsilosis and Aspergillus sp. were found, respectively, the other were bacterial pathogens [193]. In a

more recent study of 9,250 organ-cultured corneas, 5% were discarded because of bacterial or fungal contamination [194].

An uncomplicated mitomycin C trabeculotomy with subsequent A. niger endophthalmitis was also recently reported [195].

5.1.2.1.2

Fungal Endophthalmitis following Injury

Fungal infection of the vitreous body following penetrating injury was reported a long time ago [196–199]. Since then, further trauma-induced mycoses have been described [200–207, 387]. Both plant material [161, 208–211] and metal foreign bodies [205, 208, 212–215] have resulted in intraocular fungal infection following penetration of the eyeball.

5.1.2.1.3

Fungal Endophthalmitis following Keratomycosis or Scleritis

In 1896, Schirmer [216] reported a ‘case of mould keratitis’ in which cord formation starting from a corneal ulcer was noted in the eyeball. Further observations have been published [191, 217–222]. A case of keratomycosis with endophthalmitis was reported following a photorefractive keratectomy with the use of a disposable contact lens [223]. In each case of persistent keratomycosis, endophthalmitis may finally develop as pathogens penetrate into the anterior chamber and progress into the deep segments of the eye. Endophthalmitis, leading to enucleation, developed in a similar way from A. niger scleritis [224]. The reverse, i.e. keratomycosis following Candida endophthalmitis, has also been described [225, 226].

5.1.2.2

Clinical Features and Diagnosis

In comparison with acute bacterial infection, a more prolonged period relatively free of inflammation occurs postoperatively or posttrauma. This period is usually about 1–4 weeks [227, 228] but may last much longer [229]. Inflammation of the anterior chamber and visual impairment occur to a variable degree.

Hypopyon may disappear transiently and the fungal inflammation may simulate the Propionibacterium acnes syndrome [230]. Typically, there are graywhite infiltrates in the anterior part of the vitreous body and a fibrinous exudate in the anterior chamber becoming increasingly tougher.

In contrast to this typically insidious course of postoperative fungal infection, bacterial infection may occasionally be confused with intense irritation occurring shortly after trauma. In 2 cases of endophthalmitis caused by C. pa-

rapsilosis, the first clinical symptoms began as early as 3 days after extracapsular cataract extraction with posterior chamber lens [229].

Confirmation of the clinically suspected diagnosis of exogenous endophthalmitis is obtained by aspiration of the anterior chamber, repeated if necessary. In pseudophakia, the material from the anterior part of the vitreous body is positive more often than is an aspirate of the anterior chamber [180]. A microscopic study with gram, Giemsa or 10% potassium hydroxide staining can provide rapid clarification (see chapter 4, p. 87). Mycological diVerentiation may take 1 week or longer (see chapter 1, p. 23). A negative result is obtained in about 50% of samples and does not exclude a fungal infection [180]. On the other hand, negative bacterial cultures, the results of which are available within 2–3 days, suggest a fungal disease. Levels of D-arabinitol, a major metabolite of Candida spp., may be increased in the serum (normal value 4.4×3.1 lmol/l) and vitreous body [231]. In addition, the Candida hemagglutination test may be useful as a screening test and for monitoring the course of the disease [232]. Moreover, polymerase chain reaction may aid in the detection of fungal DNA in small intraocular samples [233].

5.2

Treatment of Fungal Endophthalmitis

The treatment of fungal infections of the interior of the eye is oriented towards the etiology, individual initial findings, and the course of the disease. Although local therapy (drug and/or surgical) may be suYcient in exogenous endophthalmitis, endogenous causes usually require additional systemic administration of 1 or 2 antimycotic agents. Moreover, in endogenous fungal infection one should distinguish between choroiditis and endophthalmitis with regard to an adequate treatment [234].

5.2.1

Drug Treatment

5.2.1.1

Local Antimycotic Therapy

Treatment with drops or subconjunctival application alone is not useful in endophthalmitis, as the antimycotic agents used do not penetrate suYciently into the deep vitreous body. Only in cases in which the infection is limited to the anterior section of the eye may superficial therapy be useful [235, 236]. Intracameral administration [186, 237] in intracapsular aphakia or pseudo-

phakia, or intravitreal injection of an antimycotic agent, is currently the most eVective treatment of endophthalmitis. The main disadvantage (that of performing an intraocular injection) is balanced by the advantage of achieving a high concentration of the drug. This is particularly the case for amphotericin B, which despite the availability of the new azoles, is the antimycotic of choice in many cases. As this drug may have pronounced side eVects when given systemically, it should be applied topically whenever possible. The preparation of amphotericin B solution for intraocular injection is described in chapter 2, table 2.2 (see p. 29). With the development of new agents with more favorable pharmacokinetics and improved fungicidal action, as well as fewer systemic side eVects, oral or parenteral administration alone may be eVective.

Amphotericin B is usually given in a dose of 5 lg to a maximum of 10 lg, injected into the middle of the vitreous body, together with vitrectomy [63, 67, 78, 160, 205, 208, 210, 213, 238, 240]. The opening of the cannula should not be directed towards the retina [241]. The amphotericin B injection can be repeated if necessary [191]. Intraocular amphotericin B has also been shown to be useful in a rabbit model. In unmodified phakic eyes, Candida-infected eyes, aphakic eyes and aphakic vitrectomized eyes of rabbits, the half-lives of drug clearance after a single 10-lg intravitreal injection were 9.1, 8.6, 4.7 and 1.4 days, respectively [242]. In a case of endogenous endophthalmitis caused by A. terreus, only intravitreal and subconjunctival amphotericin B were applied after vitrectomy; the treatment was successful without systemic administration of the antifungal agent [243].

Alternatively, 40 lg of miconazole has been recommended on the basis of experimental data in animals [244], or 25 lg intravitreally and 10 mg subconjunctivally given clinically [245]. Miconazole should be given particularly in P. lilacinus, as resistance of this fungus to amphotericin B can occur [180, 240]. As the therapeutic range of substances administered by the intravitreal route is limited, it is recommended that the relevant injection volume is prepared by the pharmacist rather than by the ophthalmic surgeon [246].

5.2.1.2

Systemic Antimycotic Therapy

In some patients with endogenous Candida endophthalmitis, vitrectomy with intravitreal injection of amphotericin B but without parenteral therapy was successful [238, 243]. However, systemic antimycotic treatment is recommended in endogenous endophthalmitis, because eye involvement usually indicates that further organs are also aVected by the sepsis [12, 15, 19, 247]. In contrast, local treatment alone (operative and drug therapy) may be suYcient in exogenous mycosis.

Amphotericin B has been regarded as the most important antimycotic agent for systemic use [248–251]. Treatment should be administered by an experienced infectious diseases specialist. After administration of a test dose, the dosage is increased daily up to 1 mg/kg body weight/day. Renal function in particular must be monitored (for general information on amphotericin B, see chapter 2, p. 25). After administration of 0.6 mg/kg body weight, the concentration in the vitreous body of 2 patients was 0.1 and 0.23 lg/ml and was therefore within the MIC range for the infecting fungus [252], though in another study it was only 0.04–0.17 lg/ml [253].

As an alternative to amphotericin B, systemic flucytosine, 150 mg/kg body weight/day, is often used, with or without simultaneous vitrectomy [63, 78, 88, 130, 158, 210, 237, 238, 254–257]. A high intravitreal concentration (22.2 lg/ml) could still be measured 18 h after oral administration of flucytosine, 1.5 g [253]. Flucytosine is also prescribed in combination with amphotericin B, as these 2 agents are synergistic [258], and thus the amphotericin B dose may be reduced to 0.5 mg/kg body weight/day. The possibility of development of resistance, even in Candida spp., must, however, be borne in mind [178, 191], and this limits the value of this substance (for general information on flucytosine, see chapter 2, p. 31).

Fluconazole appears to be particularly suitable because of its favorable pharmacokinetics and few side eVects [259, 260]. In C. albicans infections, fluconazole is now used as first-line therapy [261, 262] (see chapter 2, p. 36). Candidal endophthalmitis was cured in 15 of 16 eyes (94%), which included 5 infections complicated by vitreitis; successful treatment required the administration of oral fluconazole, 100–200 mg/day for 2 months [263]. In a case of postoperative endophthalmitis caused by C. parapsilosis, the pathogens could not be eliminated despite 4 weeks of oral treatment with ketoconazole, 100 mg twice daily, and 2 doses of intravitreal amphotericin B, 5 lg; after subsequent oral administration of fluconazole, 100 mg twice daily over 4 months, the pathogens could no longer be isolated, and 1 year later the eye was free from irritation with visual acuity of 20/25 [264]. Other favorable results with few side eVects have been reported [28, 43, 86, 265–271]. Following oral fluconazole, 400 mg/day, the concentrations of the agent were 15 lg/ml in the vitreous cavity and 19 lg/ml in plasma [268]. In 2 cases of P. boydii endophthalmitis, fluconazole produced no additional eVect after miconazole on the progression of the infection in 1 case, and following amphotericin B in the other case [272]. In this report, however, the dose of fluconazole (200 mg/day), was rather low. In a series of 6 patients with Candida endophthalmitis, all eyes were cured by vitrectomy and systemic fluconazole [273]. A report has recently appeared of a case of systemic lupus erythematosus and cryptococcal meningitis with bilateral superior oblique paresis, bilateral optic nerve head swelling and in-

creased intracranial pressure that was treated with oral fluconazole, acetazolamide and dexamethasone, in addition to repeated lumbar punctures to reduce intracranial pressure. This treatment produced a favorable outcome, with recovery of visual acuity from no light perception to 20/20 and normal ocular motility [274].

Oral ketoconazole, 400–600 mg/day, has also been used as an alternative to amphotericin B [191, 238, 257, 275–278]. A concentration of 0.71 lg/ml was found in the aqueous humor and 0.35 lg/ml in the vitreous body 6 h after oral administration of ketoconazole, 600 mg [279]. A disadvantage of this drug is that in vitro resistance of Candida spp. to amphotericin B has developed when both ketoconazole and amphotericin were present simultaneously [280] (for general information on ketoconazole, see chapter 3, p. 34).

Miconazole, 20–30 mg/kg body weight/day, has also been recommended [16, 63, 140, 213, 281, 282]. The concentration in the vitreous body is about 75% of the peak serum concentration [283], however, this agent appears to be less eVective than amphotericin B [140]. It is, nevertheless, preferable against P. lilacinus [191, 240] (for general information on miconazole, see chapter 2, p. 33).

On the basis of animal experiments (see chapter 7) the injection of intravitreal dexamethasone in addition to antifungal agents has been proposed [284] in order to lessen the adverse inflammatory defence mechanisms. This may be helpful; however, steroids should be applicated at least systemically to depress the leukocyte pool in the peripheral systemic vascular system [285].

Based on the available literature, the treatment scheme given in table 5.7 is currently recommended for fungal endophthalmitis, particularly that caused by C. albicans. In cases in which the fungal pathogen has been identified, the antimycotic agent should be selected in accordance with table 2.13 (see chapter 2, p. 40).

5.2.1.3

Surgical Treatment

Numerous reports contain mention of vitrectomy for the treatment of intraocular fungal infection (table 5.6). As in cases of bacterial infection, vitrectomy should not be delayed too long in severe cases of fungal endophthalmitis [139, 191, 237, 257, 286–289].

Pars plana vitrectomy has several advantages. First, suYcient material can be obtained for microbiological confirmation of the diagnosis [290]. The first 40 ml of the aspirate of the vitreous body should be taken up in a sterile syringe, centrifuged and the supernatant examined [205]. Such an examination may be more productive than without centrifugation [60]. Diagnostic vitrectomy is the best technique for culture [291]. Second, a large number of the

Table 5.6. Pars plana vitrectomy for treatment of fungal endophthalmitis

pathogens are simply removed mechanically, so that the host’s natural defences are better able to overcome the remaining pathogens. Third, the undesired abscess of fibrin, macrophages and toxins is removed. Finally, an antimicrobial drug can be placed inside the vitreous cavity at the end of the operation, or even used perioperatively in the irrigation fluid. An intraocular lens does not necessarily have to be removed [191], but central capsule excision is recommended [229]. The fear that pathogenic organisms spread more easily following vitrectomy [111, 255] may be balanced by the fact that the same is true for any antimycotic agent used.

On the other hand, vitrectomy is an additional source of irritation and bleeding risk for the already inflamed eye, and in mild cases and those with little

Table 5.7. Drug treatment regimen of first choice for fungal endophthalmitis, particularly caused by C. albicans : for cases caused by other pathogens, see Chapter 2, table 13 (p. 40)

Endophthalmitis in the anterior section

Topical (hourly) fluconazole 0.2% (chapter 2, tables 2.11 and 2.12, p. 37, 38) for C. albicans or

natamycin 5% for Fusarium sp. or

amphotericin B 0.15–0.5% (chapter 2, tables 2.3 and 2.4, p. 29, 31) after debridement, if no extensive epithelial defect;

appropriate ointment or gel at night

itraconazole, 2¶200 mg, for Candida non-albicans, Aspergillus spp.,

Cryptococcus spp. or

amphotericin B (test dose, increase to a maximum of 1 mg/kg body weight), possibly in combination with flucytosine, 150 mg/kg body weight, then reduce the amphotericin B dose to 0.5 mg/kg body weight

progression drug treatment alone may be successful [74, 254–256, 292–295]. In this context, some authors have not distinguished between choroiditis and endophthalmitis [234]. Spontaneous remission of fungal chorioretinitis has also been described [20, 78]. Thus, the deciding factors for vitrectomy must be the individual’s initial state and course. Recently, a bilateral endogenous Candida endophthalmitis following gastrointestinal operation and use of an indwelling catheter for 10 days has been published demonstrating the value of surgical intervention [54]. Both eyes showed a prominent inflammatory reaction in the anterior chamber. The vitreous was equally infiltrated, visual acuity 5/200 in each eye. Following pars plana vitrectomy on the right eye, both eyes received 5 lg amphotericin B intravitreally. The culture of the vitrectomy fluid yielded C. albicans. Postoperatively the patient was treated systemically with oral fluconazole (200 mg/day). During the first postoperative days,

a marked inflammatory reaction was successfully treated with topical and periocular steroids. Visual acuity improved dramatically in the right eye but remained unchanged in the left eye. Intravitreal injection of amphotericin B was repeated in both eyes. Vitrectomy was scheduled for the left eye, but refused by the patient. After a 9-month follow-up, visual acuity in the right eye was 20/60 despite cystoid macula edema associated with epiretinal membrane. In contrast, the unvitrectomized left eye was functionally lost with complete retinal detachment.

If the endophthalmitis begins from keratomycosis, a penetrating keratoplasty will usually be necessary (see chapter 4, p. 90).

References

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2Dimmer, F., Ein Fall von Schimmelpilzerkrankung des Auges. Klin. Mbl. Augenheilk., 1913. 51:

p.194–204.

3Heinsius, E., Metastatische Ophthalmie durch Blastomyceten. Klin. Mbl. Augenheilk., 1950. 117:

p.136–141.

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