Chapter 6

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Histoplasmosis

6.1

Systemic Histoplasmosis

6.1.1

Epidemiology and Clinical Features

Systemic histoplasmosis occurs predominantly in North America, where it is endemic in the Mississippi Valley and in Arkansas, Kentucky, Missouri and Tennessee [1, 2]. The disease may also be found, however, in Central and South America and in parts of Africa and the Far East [3]. A warmer climate appears to play a role in determining this distribution. The disease occurs in these regions mainly along the larger river basins. It is rare in Europe, and if found has usually been imported from endemic areas [4–6].

In 1906, Darling [7] described for the first time 3 cases of fatal systemic histoplasmosis. He suspected a protozoal disease on the basis of his autopsy examination. He called these structures Histoplasma because they resembled ‘plasmo’-dium-like organisms within ‘histo’-cytes. The fungal nature of the pathogenic organism was subsequently proved in 1934 [8]. Despite its name, H. capsulatum is an unencapsulated organism.

Before the 1940s, histoplasmosis was considered a rare disease in the USA, but during this decade routine radiological examination of soldiers in the 1940s indicated a much higher prevalence. In the USA in the 1960s, an estimated 30 million inhabitants were thought to be infected with H. capsulatum, and it was estimated that about 500,000 new infections and 800 deaths occurred per year [1].

The fungus is present in the superficial layers of the soil and is thought to be associated with bat excrement. Pigeons and poultry are not thought to be carriers [9]. The route of entry into the human body is nearly always the airway. DiVerentiation is made between acute pulmonary histoplasmosis and chronic pulmonary histoplasmosis, and also between a disseminated form and a benign asymptomatic infection [9]. The acute pulmonary form shows the

144

nonspecific symptoms of an acute lung inflammation and is self-limiting within a few weeks. Therefore it generally has a good prognosis. In contrast, chronic pulmonary histoplasmosis leads to cavity formation and is a progressive disease. The disseminated form predominantly aVects the very young or the very old with reduced resistance, and most organs may be aVected. This also occurs in AIDS patients. [2, 10–15]. Over 90% of cases of systemic histoplasmosis lead to the benign, asymptomatic form, which is often not noticed and for which no primary infection can often be recalled.

6.1.2

Diagnosis

6.1.2.1

Histoplasmin Skin Testing

The most important diagnostic test is the histoplasmin skin test. Histoplasmin is an antigen derived from the mycelial phase of the fungus. The test is performed in the same way as the tuberculosis skin test. A positive reaction is shown as a large area of induration of at least 5 mm (diameter) within 48–72 h after injection of 0.1 ml intracutaneously on the volar side of the forearm [9]. Other authors use 2 mm as the critical size and thus obtain a larger number of positive reactions [16]. A positive reaction to this skin test cannot be obtained until 2–4 weeks after Histoplasma infection. The sensitivity is lifelong, except in patients with immunosuppression arising, for example, from use of corticosteroids, severe disease, or advanced age.

The skin test is only positive in 80% of cases of chronic pulmonary histoplasmosis and in 50% of cases of disseminated histoplasmosis [9]. Even in endemic regions, the skin test was no more frequently positive in patients with ocular histoplasmosis syndrome than in a control group [17], probably because a large proportion of the population in such regions are systemically infected without developing ocular symptoms. In a study of 1,417 adults, the overall prevalence was 52.8%, but was higher in men (59.9%) than in women (44.3%); more positive skin tests were obtained in the black population (61.4%) than in the white population (50.7%) [17]. Of this study group, 22 individuals had peripheral symptoms (histo-spots) of ocular histoplasmosis syndrome, and of these 14 responded positively to histoplasmin.

In another study, despite typical ocular histoplasmosis syndrome, falsenegative skin results were found in 11% [18]. In a histologically proven case of disseminated histoplasmosis in a 14-year-old boy who died of histoplasmosis, the skin test was also negative [19]. The percentage of positive reactions can be increased to 83% by using the booster eVect of a second skin

test performed after 3 weeks [16, 20, 21]. This approach is particularly useful in elderly individuals with reduced sensitivity, and shows a clearly enhanced immune response in patients with ocular histoplasmosis syndrome with maculopathy compared with patients who have only peripheral histo-spots [22].

Hemorrhage in the region of the posterior pole of the eye may occur after histoplasmin skin testing [23], and has been reported in 7% of 57 patients [18]. On the other hand, patients in whom a skin test is performed belong to a selected group where the risk of macular hemorrhage is already increased [24].

6.1.2.2

Other Tests

The complement fixation reaction is not generally recommended for diagnosis of histoplasmosis [9], as it is only positive in 16–68% of cases. Despite negative skin tests, however, it may also be increased in proven histoplasmosis [19, 25]. Even when the complement fixation reaction gives a negative result, counter-current immunoelectrophoresis may be positive [6]. A radioimmunoassay, in which antigens may be detected in the urine and serum, has also been recommended [26]. The in vitro stimulation of lymphocytes by H. capsulatum is thought to be diagnostically superior to the complement fixation reaction [22, 27], and has the advantage that macular hemorrhage, possibly brought about by the skin test, is avoided.

HLA-B7 is markedly increased in ocular histoplasmosis syndrome with maculopathy compared with healthy individuals [28–31], but not in patients without maculopathy and peripheral lesions (histo-spots). HLA-DRw2 was increased in 21 of 26 patients (81%) with maculopathy and 8 of 13 patients (62%) with peripheral ocular histoplasmosis syndrome compared with 28% of healthy individuals [31]. Similar patients in Mexico, however, did not show these diVerences [32]. In another series of 4 cases in England, a detailed immunological assessment (including lymphocyte immunophenotyping, flow cytometric analyses, HLA typing and T-cell receptor variable region expression) was carried out in patients and a control group [33]. Analysis of T-cell receptor variable region expression revealed no significant preferential expression. HLA typing also failed to reveal any links. All lymphocyte markers analysed were unremarkable, with the exception of CD38, which was significantly raised compared with controls (p=0.01). This finding was confirmed by the use of 2 diVerent CD38-specific monoclonal antibodies. The raised CD38 in these cases was shown to be persistent when the patients were retested after an interval of several months. Significantly, this may correlate with poor T-cell function, as in common variable immunodeficiency, making these patients more susceptible to various stimuli [33].

Miliary calcifications can be found radiologically in the late stages after pulmonary involvement. Computed tomography [34] and bronchoscopy [35] are also used in diagnosis. Finally, histoplasmosis is proved by identification of H. capsulatum by histological and microbiological criteria. When taking biopsy samples, e.g. from lymph nodes, only a portion of it should therefore undergo fixation, and the remainder should be sent for microbiological examination [6].

6.2

Ocular Histoplasmosis [21]

Ocular histoplasmosis syndrome is a constellation of clinical findings with atrophic, punched-out chorioretinal scars (histo-spots), peripapillary scarring, and absence of inflammation. A small percentage (0–4.5%) of the patients also develop choroidal neovascularization [9, 36–38].

The importance of ocular histoplasmosis syndrome in the 1960s and 1970s is indicated by the observation that in the endemic regions of the USA, 1/1,000 adults developed maculopathy as part of this disease, and without treatment, half of them were legally classified as blind [9]. In Tennessee in particular, with the highest incidence of Histoplasma infection in the USA, 2.8% of new applicants for Aid to the Blind had ocular histoplasmosis syndrome [39].

The prognosis has since improved, and in a 5-year follow-up of 516 patients, the risk of legal blindness was low, even for patients who had bilateral involvement [40]; 81% retained a visual acuity of 20/20 in at least 1 eye and 20% retained this visual acuity in both eyes. Of 252 cases and controls examined in 1970, 216 were still alive in 1985; of these, 202 (94%) were interviewed, 197 (91%) underwent visual acuity measurements, and 173 (80%) were examined by a study ophthalmologist [38]. Both in 1970 and in 1985, cases with disciform macular lesions of ocular histoplasmosis had a higher prevalence of both unilateral and bilateral visual impairment and blindness. Although the prevalence of visual impairment and blindness in 1985 was similar among controls and cases of ocular histoplasmosis without disciform lesions, in 1994 this group of cases had about twice the prevalence of visual impairment as that of controls. The 95% confidence intervals on estimates of relative risks were broad, however, and included unity. No new disciform lesions attributable to ocular histoplasmosis were found in 28 eyes of 18 cases free of these in 1970 or among 148 controls [38].

For many years this syndrome has been referred to as ‘presumed’ ocular histoplasmosis, because Koch’s criteria for ocular histoplasmosis were not

fulfilled in humans. However, in a primate model of ocular histoplasmosis syndrome [41–43], intravascular injection of live yeast-phase H. capsulatum led to the development of typical scars [41]. It has recently been demonstrated that antigenic challenge could result in a reactivation of the inflammatory component of the choroidal scars [43]. This is probably the most compelling evidence for the relationship between H. capsulatum infection and ocular histoplasmosis syndrome, and justifies abandoning the term ‘presumed’ [44], though this is not accepted in general [45].

After a histoplasmosis epidemic, about 6–7% of aVected individuals develop ocular histoplasmosis syndrome [46]. This relatively rare involvement of the eyes explains why no retinal changes could be found in 134 histologically or microbiologically proven cases [47].

After the first description by Krause and Hopkins [23] in 1951, Woods and Wahlen [48], in 1960, unequivocally established ocular histoplasmosis syndrome as an independent disease entity. This provided the impetus for numerous experimental (see chapter 7, p. 187) and clinical studies [9, 17, 18, 37, 46, 49–51]. The fungus has been described in the eyes of patients in numerous histopathological publications [25, 47, 49, 52–63]. In this context, a disseminated form (endophthalmitis) [25, 59, 61, 62] can be diVerentiated from a solitary chorioretinal granuloma [19, 54, 61]. The latter may be up to 5 mm in diameter, which may suggest a tumor. In most patients with ocular histoplasmosis syndrome, however, only chorioretinal scars with occasional lymphocytic infiltration can be found histopathologically. The retinal pigmented epithelium is missing from the center of the scar and is often hypertrophied at the edge, while Bruch’s membrane may show defects. These defects may also be seen in maculopathy with subretinal vessel proliferation [64]. H. capsulatum has been identified in the optic nerve sheath in a patient with AIDS [65].

The pathogen probably spreads from the primary focus in the lung to the choroid, where it produces peripheral ‘histo-spots’ that initially cause no problems. These punched out lesions are prominent as round or oval scars (fig. 6.1), which aVect the retinal pigmented epithelium, and to a greater or lesser extent the choroid, so that the color may appear between yellowish and white. Occasionally, a choroid vessel passes through. Histo-spots are at the posterior pole, reaching to the mid-periphery, and show a variably large diameter. There is sometimes hyperpigmentation at the edge of the scar. Histo-spots may also be arranged in a line in the periphery (fig. 6.2), described as a ‘linear streak of the equator’ [9, 49, 66–68] or ‘peripheral streak lesion’ [69]. By photographic monitoring of the progression, it was established that new histo-spots occurred (26%), some increased in size (46%), and that the foci became narrower and to some extent invisible (45%) without the patient noticing anything [70]. These findings were confirmed in 11 of 81 individuals followed up for a period of 7 years [71]. This

Fig. 6.1. Histo-spots of varying size with and without pigmentation. The choroid is aVected to a variable extent.

is in agreement with experimental findings in primates [41, 43]. Adenocarcinoma of the retinal pigment epithelium arising from a juxtapapillary histoplasmosis scar has been reported in one patient [72]. Acute histoplasmosis choroiditis has recently been reported in 2 immunocompetent brothers [73], whose serial followup examinations will be extremely important for our understanding of the pathogenesis of this syndrome.

Finally, vision suddenly deteriorates, probably after several years. Mental stress was reported by 25% of individuals at the time that this occurred [37]. In 162 patients, the mean age at deterioration was 40 years (range, 16–73 years), and in those with involvement of the other eye 44 years (range, 23–66 years) [74]. Subretinal vessel proliferation is found in the macular region, which can be clearly visualized by fluorescence angiography (fig. 6.3, 6.4), usually with hemorrhage at the edge. Serous or hemorrhagic retinal detachment is found above the neovascularization membrane. A well-circumscribed granuloma containing eosinophils has been identified in this membrane [75]. Inflammatory changes cannot be detected in either the posterior or anterior eye segment. Peripapillary chorioretinal scars (fig. 6.5) have been described, with a prevalence ranging from 16% [51] to 85% [76]. The peripapillary disc scarring consists of choroidal and retinal pigment epithelium atrophy, with a line of pigment at the disc margin of the scar, in contrast to some normal eyes with optic nerve ‘crescents’ that have pigment at the outer border of the scar [77]. In addition, there may be papilledema [78, 79]. Before central subretinal

Fig. 6.2. Linear hyperpigmentation and depigmentation in the periphery (socalled linear streak of the equator or peripheral streak lesion).

Fig. 6.3. Fluorescence angiogram of the other eye of the patient in figure 6.2 with subretinal vessel proliferation (early phase).

Fig. 6.4. Fluorescence angiogram of the other eye of the patient in figure 6.2 with subretinal vessel proliferation (late phase).

Fig. 6.5. Central, hemorrhagic chorioretinopathy. Peripapillary, chorioretinal scar. Other eye of the patient in figure 6.2.

neovascularization develops, minimal choroidal inflammation (minimal recurrence) is thought to occur de novo or at the edge of a scar, initially leading to metamorphopsia [80], which then develops into a hole in Bruch’s membrane with subsequent neovascularization. Alternatively, however, spontaneous remission may occur, and a pigmented limbus around the central focus has been said to be a good prognostic indicator of this [81]. The pigmented limbus consists of pigment-loaded macrophages or represents proliferation of the retinal pigment epithelium [82].

6.3

Treatment of Histoplasmosis

6.3.1

Treatment of Systemic Histoplasmosis

Amphotericin B is available for the treatment of systemic histoplasmosis [9, 83, 84]. The side eVects must be considered, however, and consist predominantly of nephrotoxicity (see chapter 2, p. 27). Thus, the agent is not used in acute pulmonary histoplasmosis with a favorable prognosis, but only in the disseminated and chronic pulmonary progressive forms. A combination of amphotericin B and rifampicin or rifamycin derivatives is thought to be better, as the dose of the single components, and therefore the side eVects can be reduced [85].

Of the newer antimycotic agents, ketoconazole does not appear to have any eVect [86]. Fluconazole shows better in vitro activity against H. capsulatum compared with amphotericin B [87]. Itraconazole is regarded as the treatment of choice [88] (see chapter 2, p. 36).

6.3.2

Treatment of Ocular Histoplasmosis

6.3.2.1

Drug Treatment

Antimycotic therapy of ocular histoplasmosis is not indicated [9] in cases with atrophic scars with or without neovascularization. Apart from the side eVects, this approach is not valid because ocular histoplasmosis syndrome is a consequence of primary infection, and the aVected individuals are generally healthy. As increased stress is reported in association with the development of visual deterioration [37, 89], a reduction in stress has been recommended [9].

Even without hypertensive stress, however, bleeding and detachment of the retina with reduced vision probably occurs at some time after macular neovascularization. Moreover, the development of neovascularization is not aVected by stress reduction, nor by Valsalva’s maneuver or platelet aggregation inhibitors. Subcutaneous interferon alpha, 3¶106 U/m2 4 times daily (mean total dose, 204 MU) did not lead to regression of choroidal neovascularization [90].

The administration of corticosteroids may be appropriate for treatment of minimal recurrences [9, 80]. Using Amsler charts, patients may notice early metamorphopsia, and minimal choroiditis may be suppressed with an intensive course of systemic cortisone. These patients with reactivation of inflammatory lesions may receive additional itraconazole systemically. Perhaps these patients represent a subset of patients with OHS [91]. Previous studies have shown a genetic association in patients with OHS. Both HLA-DRw and HLA-B7 have been found in a high percentage of patients with OHS. In addition, HLA-B7 appeared to be related to the presence of disciform scars. Several, but not all, of these patients have an additional chronic fungal infection of the foot or a history of recurrent vaginal yeast infections. One could speculate that these patients have some immunologic or genetic inability to eradicate fungal infections and that the peripheral fungal infection may somehow trigger an immune response leading to the reactivation of ocular inflammation. This was the rationale in initially treating these patients with itraconazole [91].

6.3.2.2

Photocoagulation and Surgical Treatment

Although some studies found no diVerence in outcome between coagulation treatment of neovascularization and a spontaneous course [92–94], photocoagulation is approved by many authors [74, 95–99]. The subretinal membrane, however, appears to be larger than expected from fluorescence angiography, and either recurrences are frequent, or with suYcient coagulation, damage with a reduction in vision occurs [100]. A meaningful prospective study with regard to the long-term evidence of eYcacy is diYcult in cases with subfoveal localization of the neovascularization [101]. The situation in the case of juxtafoveal or extrafoveal choroidal neovascularization should be assessed diVerently [102, 103]. In a study of 117 patients, the site of recurrence was extrafoveal in 16%, juxtafoveal in 18%, and subfoveal in 66% [104]; 16 eyes were treated with laser photocoagulation, 17 eyes underwent repeat submacular surgery, and 18 eyes were observed. The visual outcome for patients with recurrences amenable to laser treatment was better than for patients who were observed or who underwent surgery.

In a study of 231 patients, 46% had spontaneously suVered considerable reduction in vision at 18 months compared with 13% of cases treated with

argon laser [95]. The entry criteria for this study included subretinal neovascularization within 200–2500 lm of the foveal vessel-free zone, with visual acuity of 0.2 or better. In a retrospective study of 101 eyes with 5–16 years of followup, visual acuity of 20/40 or better was observed in 71% of eyes with treated extrafoveal choroidal neovascularization and in 68% with treated juxtafoveal choroidal neovascularization [105]. Recurrent choroidal neovascularization was observed in 23% of treated eyes during a mean follow-up of 9.6 years.

The other eye of a patient with ocular histoplasmosis with maculopathy should be carefully monitored [106]. As 23% of these eyes with histo-spots in the region of the macula will develop neovascularization within a mean of 4 years (range, 1 week to 36 years) [74], regular monitoring by the patient using the Amsler chart is recommended.

The subretinal vessel membrane was removed for the first time in 2 patients in 1991 and led to an improvement in vision from 1/20 to 0.5 and 1.0 over 3 months and 7 months [107]. The results are encouraging, but long-term followup is not yet available [108–110, 146], including follow-up related to the development of postoperative choriocapillaris atrophy [111]. Operative results are more favorable, however, compared with age-related macular degeneration [112–114], because the new vessels arising in the choroid in postoperative patients usually grow within the subsensory retinal space and not in the subpigment epithelial space, as occurs in patients with age-related macular degeneration [115]. Postoperatively, there may even be a clear improvement in visual acuity [112, 116]. The sagittal arrangement of the neovascular membranes is apparently important [117], rather than the pathological-anatomical structure of the membrane [118]. Ultrastructural findings of idiopathic subfoveal membranes in ocular histoplasmosis syndrome are similar to those in age-related macular degeneration, with the exception of the presence of basal laminar (linear) deposits only in membranes from eyes with age-related macular degeneration [119]. Within these membranes, transforming growth factor beta 1 and basic fibroblast growth factor are present within the major cell types, which suggests a possible pathogenetic role in the development of the neovascular complex [120].

6.4

Differential Diagnosis of Ocular Histoplasmosis

A number of other diseases show some symptoms of ocular histoplasmosis and should be considered in the diVerential diagnosis. These include the diseases described by Nozik and Dorsch [121] and by Dreyer and Gass [122], which, however, like diVuse unilateral subacute neuroretinitis (DUSN) [71] and acute zonal occult outer retinopathy (AZOOR) [123–125], produce in-

flammatory symptoms. The same is true for the cases observed by Doran and Hamilton [126] and Palestine et al. [127]. In contrast to ocular histoplasmosis syndrome, multifocal choroiditis and panuveitis also show active vitritis with chorioretinal lesions during the clinical course [128].

DiVuse subretinal fibrosis is very much more pronounced than ocular histoplasmosis [127, 129]. While the foci in acute posterior multifocal placoid pigment epitheliopathy (APMPPE) [130] can be diVerentiated ophthalmologically and by fluorescence angiography from histo-spots, the foci in ‘birdshot’ [131] and vitiliginous chorioretinopathy [132] are much less clearly defined. Among the findings reported by Watzke et al. [133] and Morgan and Schatz [134] in 21 myopic female patients with punctate inner choroidopathy (PIC), some are reminiscent of ocular histoplasmosis, while others can be clearly distinguished from it. Typical symptoms of punctate inner choroidopathy are photopsia, central or paracentral scotomas, and peripheral field loss. Central and peripheral retinochoroidopathy also occur in cases of trichinosis with the histo-spots tending to be somewhat smaller [135]. Finally, coccidioidomycosis can lead to chorioretinitis that is similar to ocular histoplasmosis [136], though inflammatory signs (paravascular sheathing, vitritis) and much heavier pigmentation are found.

In Europe, cases have been described in which the retina showed the typical signs of ocular histoplasmosis but in which the skin test was negative, and the patients had also never stayed in endemic regions [66, 137, 138, 147]. In 6 of 7 patients from the author’s study, the skin test was negative even after the booster, so that histoplasmosis appeared to be ruled out; in 2 patients, however, chronic reactivation of Epstein-Barr virus was observed [137]. It is thus possible that diVerent organisms produce similar disease pictures [66, 137, 139–142]. Linear streaks of the equator also occur without ocular histoplasmosis [143, 144] (see our case in fig. 6.2). A histopathological study using the polymerase chain reaction with the appropriate primers for H. capsulatum and other organisms is required for such cases [145].

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