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Clinicopathologic Reports, Case Reports, and Small Case Series
January 1, 2005

Bilateral Multifocal Choroiditis With Serous Retinal Detachment in a Patient With Brucella Infection: Case Report and Review of the Literature

Arch Ophthalmol. 2005;123(1):116-118. doi:10.1001/archopht.123.1.116

Brucellosis is a zoonotic disease caused by the gram-negative bacteria Brucella melitensis or Brucella abortus. It is transmitted from animals to man through the ingestion of unpasteurized milk, milk products, or uncooked meat.1 The diagnosis of systemic brucellosis is clinically suggested in patients with fever, arthralgia, myalgias, anorexia, sweating, headache, and malaise. The onset can be acute or insidious, generally beginning within 2 to 4 weeks after inoculation.1 A variety of ocular complications have been reported in patients with brucellosis.2,3 Ocular inflammations are generally a late manifestation consisting variably of dacryoadenitis, episcleritis, chronic iridocyclitis, nummular keratitis, multifocal choroiditis, exudative retinal detachment, and optic neuritis.46 Rare cases of endogenous endophthalmitis have been reported in which Brucella species have been isolated from vitreous humor.7

The purpose of this case report is to describe a case of multifocal choroiditis associated with serous retinal detachment in both eyes, without any other general symptoms, as the initial sign of brucellosis. Fluorescein and indocyanine green (ICG) angiographies of this disease are, to our knowledge, described for the first time.

Report of a Case

The patient was a 39-year-old man of Arab-Bedouin origin with a severe reduction of vision in the right eye. He had had “dust” in his left eye for 1 week and in the right eye for 4 days before admission. There were no other symptoms, known diseases, or known allergies. The patient admitted intake of raw, unpasteurized goat’s milk in the past.

On examination, visual acuity was 6/240 OD and 20/20 OS. Results of slitlamp examination of the anterior chamber and vitreous of both eyes were normal. Results of ophthalmoscopic examination of the right eye showed hyperemic optic disc with serous retinal detachment of the posterior pole that included the macula, associated with multiple, deep creamy whitish yellow choroidal lesions (Figure 1A). Similar lesions sparing the macula were seen in the left eye (Figure 1B).

Figure 1.
A, Fundus photograph of the right eye shows a hyperemic optic disc with serous retinal detachment of the posterior pole that includes the macula, and multiple, deep creamy whitish yellow choroidal lesions. B, Fundus of left eye with similar findings not involving the macula.

A, Fundus photograph of the right eye shows a hyperemic optic disc with serous retinal detachment of the posterior pole that includes the macula, and multiple, deep creamy whitish yellow choroidal lesions. B, Fundus of left eye with similar findings not involving the macula.

Fluorescein angiography demonstrated multiple hyperfluorescent lesions in the middle phase and late leakage of the lesions. Minimal staining of both optic nerves was seen, with no significant leakage (Figure 2). Results of ICG angiography were notable for multiple hyperfluorescent and hypofluorescent spots in the early and intermediate phases. The late phase showed multiple hot spots with large areas of hypofluorescence (Figure 3). The A and B scan ultrasonography showed shallow peripapillary retinal detachments without choroidal thickness.

Figure 2.
A, Middle-phase fluorescein angiography shows multiple hyperfluorescent lesions in the right eye. B, Late-phase fluorescein angiography in the same eye shows late leakage of the lesions with minimal staining of the optic nerve. C, Middle-phase fluorescein angiography in the left eye shows multiple hyperfluorescent lesions. D, Late-phase fluorescein angiography in the same eye shows late leakage of the lesions (not involving the macula) with minimal staining of the optic nerve.

A, Middle-phase fluorescein angiography shows multiple hyperfluorescent lesions in the right eye. B, Late-phase fluorescein angiography in the same eye shows late leakage of the lesions with minimal staining of the optic nerve. C, Middle-phase fluorescein angiography in the left eye shows multiple hyperfluorescent lesions. D, Late-phase fluorescein angiography in the same eye shows late leakage of the lesions (not involving the macula) with minimal staining of the optic nerve.

Figure 3.
A and B, Early-phase indocyanine green (ICG) angiography (55 and 83 seconds, respectively, after dye injection) in the right eye shows multiple hyperfluorescent and hypofluorescent spots in the posterior pole. C and D, Late-phase ICG angiography (20 and 30 minutes, respectively, after dye injection) in the same eye shows multiple hot spots associated with large hypofluorescent areas. E and F, Early-phase ICG angiography (35 seconds after dye injection) in the left eye shows multiple hyperfluorescent and hypofluorescent spots in the posterior pole. G, Middle-phase ICG angiography (90 seconds after dye injection) in the same eye shows multiple hyperfluorescent and hypofluorescent spots in the posterior pole. H, Late-phase ICG angiography (30 minutes after dye injection) in the same eye shows multiple hot spots associated with large hypofluorescent areas.

A and B, Early-phase indocyanine green (ICG) angiography (55 and 83 seconds, respectively, after dye injection) in the right eye shows multiple hyperfluorescent and hypofluorescent spots in the posterior pole. C and D, Late-phase ICG angiography (20 and 30 minutes, respectively, after dye injection) in the same eye shows multiple hot spots associated with large hypofluorescent areas. E and F, Early-phase ICG angiography (35 seconds after dye injection) in the left eye shows multiple hyperfluorescent and hypofluorescent spots in the posterior pole. G, Middle-phase ICG angiography (90 seconds after dye injection) in the same eye shows multiple hyperfluorescent and hypofluorescent spots in the posterior pole. H, Late-phase ICG angiography (30 minutes after dye injection) in the same eye shows multiple hot spots associated with large hypofluorescent areas.

Results of the physical examination were entirely normal. Results of the systemic workup, including serologic testing for syphilis, tuberculosis, and antinuclear antibody, were normal. Brucella infection was also considered because of the history of intake of raw unpasteurized goat’s milk. Results of serologic testing for Brucella species using the agglutination method were positive at a titer of 1:160. Brucella blood cultures were negative.

The patient started therapy consisting of streptomycin sulfate, 1 g/d in an intramuscular injection for 2 weeks, and doxycycline hyclate, 100 mg orally twice daily for 6 weeks. After 1 week of treatment, mild anterior uveitis, expressed as fine keratic precipitates with 1+ flare and 1+ cells, developed in both eyes. Serous detachment of the fovea developed in the left eye, with a drop in visual acuity to 6/120 OS. He started therapy consisting of dexamethasone phosphate drops 4 times a day in both eyes and oral prednisone at a dose of 1 mg/kg.

One month after the patient’s initial symptoms, visual acuity had improved to 20/30 OU and choroidal lesions had disappeared. Fluorescein angiography demonstrated multiple peripapillary window defects without late leakage. The prednisone dose was tapered and stopped during a 2-month period. Three months after presentation, visual acuity remains 20/30 OU.

Comment

Brucellosis uveitis generally develops after the acute phase and is considered a noninfectious immune response4,5 or a form of septic choroiditis with low-virulence live organisms in the choroid. Choroiditis due to brucellosis is usually multifocal and nodular8 or geographic.2 Nodular choroiditis with adjacent retinal edema and hemorrhage is said to be characteristic of brucellosis.9 Tabbara and Al-Kassimi2,10 described geographic choroiditis in 3 of 5 patients. All of the patients responded to systemic antibiotic therapy and experienced complete recovery from the uveitis.

The initial clinical findings in our patient consisted of bilateral multifocal geographic choroiditis with serous retinal detachments and papillary congestion. After 1 week of systemic antibiotic therapy, choroiditis in the left eye expanded to the fovea with a corresponding severe drop in visual acuity (6/120 from 20/20). After systemic corticosteroid therapy was begun, visual acuity returned to 20/30 OU, with improvement of the choroiditis. This result supports the concept that the ocular manifestations of brucellosis have an immune component.

The diagnosis of ocular brucellosis may pose some problems because findings may mimic other causes of infectious and noninfectious uveitis. Therefore, it is important to obtain a detailed history that includes occupation, exposure to animals, travel to enzootic areas, and ingestion of high-risk foods (eg, unpasteurized dairy products).

It is difficult to isolate the organism in the chronic stages of the disease. In the absence of an isolate of the infecting organism from blood or tissues, a serologic investigation is of paramount importance to the diagnosis and management.1,3

In the case reported herein, early anti-Brucella therapy and treatment with corticosteroids resulted in complete recovery and return of visual acuity.

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Article Information

Correspondence: Dr Rabinowitz, Tabenkin 25 St, Beer-Sheva, Israel 84750 (ronenrab@netvision.net.il).

Financial Disclosure: None.

References
1.
Young  EJ Brucella species. Mandel  GLBennett  JEDolin  RPrinciples and Practice of Infectious Diseases. New York, NY Churchill Livingstone Inc2002;2386- 2393
2.
Tabbara  KF Brucellosis and nonsyphilitic treponemal uveitis. Int Ophthalmol Clin 1990;30294- 296
PubMedArticle
3.
al-Kaff  AS Ocular brucellosis. Int Ophthalmol Clin 1995;35139- 145
PubMedArticle
4.
Walker  JSharma  OPRao  NA Brucellosis and uveitis. Am J Ophthalmol 1992;114374- 375
PubMed
5.
Abd Elrazak  M Brucella optic neuritis. Arch Intern Med 1991;151776- 778
PubMedArticle
6.
Gungur  KBekir  NANamiduru  M Ocular complications associated with brucellosis in an endemic area. Eur J Ophthalmol 2002;12232- 237
PubMed
7.
al-Faran  MF Brucella melitensis endogenous endophthalmitis. Ophthalmologica 1990;20119- 22
PubMedArticle
8.
Woods  AC Endogenous Inflammations of the Uveal Tract.  Baltimore, Md Williams & Wilkins1961;
9.
Duke-Elder  SPerkins  ES Disease of the uveal tract. Duke-Elder  SSystem of Ophthalmology. Vol 9 London, England Kimpton1966;236- 242
10.
Tabbara  KFal-Kassimi  H Ocular brucellosis. Br J Ophthalmol 1990;74249- 250
PubMedArticle
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