Ординатура / Офтальмология / Учебные материалы / Uveitis Text and Imaging Text and Imaging Text and Imaging 2009

revealed that she was an agricultural labourer and the systemic episode occurred during a busy harvest time. She was seen by a local physician who obtained a complete blood count, a chest X-ray, Widal test and peripheral smear for malarial parasites, all of which were negative. The patient was treated empirically with broad spectrum antibiotics and the general condition of the patient slowly improved. One month later she developed pain, redness, and decreased vision in each eye and she was referred to Aravind Eye Hospital. Initial examination revealed a best corrected vision of 6/18 in both eyes. Intraocular pressure by applanation was 12 mm Hg bilaterally. Slit lamp examination revealed moderate, bilateral nongranulomatous panuveitis. Posterior segment signs of both eyes were remarkable with severe vitreous reaction, vitreous membranes, disc oedema, and vitreous exudates in the form of string of pearl appearance (Figures 2 and 3). Laboratory investigations including syphilis serologies, skin testing with PPD were negative. Microagglutination for Leptospira

Figure 2: Fundus photograph RE showing marked vitreous membranes and disc oedema

Figure 3: Fundus photograph LE showing marked vitreous membranes and string of pearl appearance

Figure 4: Rapid progression of cataract with posterior synechiae

was positive for L. autamonalis at 1:100 dilution. The patient was treated with oral doxycycline, 100 mg twice daily for 10 days, topical corticosteroids, mydriatic agent and oral prednisolone, 40 mg daily for 1 week with a slow tapering over two months. After two months, the inflammation was found under control, however, the left eye showed mature cataract with posterior synechiae (Figure 4). The left fundus was not visible. The left eye cataract was operated and a posterior chamber intraocular lens was implanted. One month after surgery in the left eye, the lens in the right eye showed a rapid progression of cataract and it became pearly white. The vision in her right eye dropped to 2/60, for which an extracapsular cataract extraction with posterior chamber lens implantation was performed. Vision stabilised at 20/20 in each eye following surgery.

KEY POINTS

•Water borne spirochaetal illness spread from animal to human.

•Leptospirosis is one of the common tropical diseases, it remains underdiagnosed, mainly because of its varying clinical manifestations.

•Leptospirosis is a multisystem disorder with a wide range of clinical manifestations.

•Leptospirosis commonly affects the young and middleaged men mainly because of the increased risk of exposure to leptospiral-contaminated water or soil.

•MAT is currently considered a gold standard test. However, methodological complexities limit its use in several ophthalmic hospitals.

•Nongranulomatous panuveitis, hypopyon, membranous vitreous opacities, papillitis and vasculitis are important clinical signs of leptospiral uveitis.

•Corticosteroids are the mainstay of treatment for leptospiral uveitis.

•Leptospiral uveitis carries good prognosis.

REFERENCES

1.Faine S, Adler B, Bolin C, Perolat P. Leptospira and Leptospirosis. (2nd edn). Medi Sci, Melbourne, Australia: 1999;1-230.

2.Vinetz JM, Leptospirosis. Curr Opin Infect Dis 2001; 14:527-38.

3.Levett PN. Leptospirosis. Clin Microbiol Rev 2001;14:296326.

4.Feigin RD, Anderson DC. Human leptospirosis. Crit Rev Clin Lab Sci 1975;5:413-67.

5.Bharti AR, Nally JE, Ricaldi JN, et al. Leptospirosis: a zoonotic disease of global importance. Lancet Infect Dis 2003;3:757-71.

6.Edwards GA, Domm BM. Human leptospirosis. Medicine 1960;39:117-56.

7.Rathinam SR, Namperumalsamy P. Leptospirosis. Ocular Immunol Inflamm 1999;7:109-18.

8.Smythe L. Leptospirosis worldwide, 1999. Wkly Epidemiol Rec 1999;74:237-42.

9.Ratnam S. Leptospirosis: an Indian perspective. Ind J Med Microbiol 1994;12:228-39.

10.Centers for Disease Control and Prevention. Case definitions for infectious conditions under public health surveillance. Morb Mortal Wkly Rep 1997;46:49.

11.Terpstra WJ, Ligthart GS, Schoone GJ. Serodiagnosis of human Leptospirosis by Enzyme-Linked ImmunosorbentAssay (ELISA) Zentralbl Bakteriol A 1980;247:400-5.

12.Rathinam SR. Ocular Leptospirosis. Curr Opin Ophthalmol 2002;13:381-6.

13.Martins MG, Matos KTF, da Silva MV, de Abreu MT. Ocular manifestations in the acute phase of leptospirosis. Ocu Immunol Inflam 1998;6:75-9.

14.Mancel E, Merien F, Pesenti L, Salino D, Angibaud G, Perolat P. Clinical aspects of ocular leptospirosis in New Caledonia (South Pacific). Aust N Z J Ophthalmol 1999;27:380-6.

15.Rathinam SR, Ratnam S, Selvaraj S, et al. Uveitis associated with an epidemic outbreak of leptospirosis. Am J Ophthalmol 1997;124:71-9.

16.Barkay S, Garzozi H. Leptospirosis and uveitis. Ann Ophthalmol 1984;16:164-8.

17.Rathinam SR, Namperumalsamy P, Cunningham ET Jr. Spontaneous cataract absorption in patients with leptospiral uveitis. Br J Ophthalmol 2000;84:1135-41.

18.Woods AC. Endogenous uveitis. Baltimore: Williams and Wilkins 1960;76-8.

19.Duke-Elder S (Ed). Diseases of the Uveal Tract System of Ophthalmology, London Hendry Kimpton 1966;II:322-5.

20.Sturman RM, Laval J, Weil VJ. Leptospiral uveitis. Arch Ophthalmol 1959;61:633-40.

21.Van Thiele. The Leptospirosis Leiden 1948 Universiitaive pers Leiden. Cited by Edwards GA, Domm BM Human leptospirosis Medicine 1960;39:117-55.

22.Oksala A, Salminen A. Leptospiral Uveitis Acta. Ophthalmologist 34:185, 1956 Cited by Edwards GA, Domm BM Human leptospirosis Medicine 1960;39:117-55.

23.Rowen GE, City M. Leptospiral uveitis. Ophthalmology 1957;58:754-7.

24.Gsell O, Rehsteiner K, Verrey F. Iridocyclitis following leptospirosis. Am J Ophthalmol 1947;30:801.

25.Hanno HA, Cleveland AF. Leptospiral uveitis. Am J Ophthalmol 1949;32:1564-6.

26.Alexander A, Baer A, Fair JR, et al. Leptospiral uveitis Report of a Bacteriologically verfied case. Arch Ophthalmol 1952;48:292-7.

27.Doret M, Rohm A. Augenkomplikationen bei benignen Leptospirosen, Klin. Monatsbl. Augenh 1951;118:51-66.

28.Brand N, Benmoshe H. Human leptospirosis associated with eye complications. Isr Med J 1963;22:182-4.

29.Waitkins SA. Leptospirosis as an occupational disease. Br J Ind Med 1986;43:721-5.

30.David R, Barkay S. Anterior uveitis and leptospirosis. Ann Ophthalmol 1976;8:958-62.

31.Zhu sp. Analysis of 137 cases of leptospiral Uveitis Zhonghua Yan Ke Za Zhi 1979;15:247-9.

32.Levin N, Nguyen-Khoa JL, Charpentier D, Strobel M, Fournie-Amazouz E, Denis P. Panuveitis with papillitis in leptospirosis. Am J Ophthalmol 1994;117:118-9.

33.Rathinam S, Ratnam S, Suresh Babu L, Natarajan Sreenivasan K. Leptospiral antibodies in patients with recurrent ophthalmic involvement. Indian J Med Res 1996;103:66-8.

34.Chu KM, Rathinam R, Namperumalsamy P, Dean D. Identification of Leptospira species in the pathogenesis of uveitis and determination of clinical ocular characteristics in south India. J Infect Dis 1998;177:1314-21.

35.Moro F. Sulle uveitis leptospirosiche, Ann ottal e clin. Ocul. 1953;79:531-54: abstracted, excerpta. Med XII 1954;8:717.

36.Millin J, Milletto G. A propos des complications ocularies de la. Leptospirose. Ann ocul 1956;189:591.Cited by Sturman RM, Laval J, Weil VJ. Leptospiral uveitis. Arch Ophthalmol 1959;61:633-9.

37.Priya CG, Bhavani K, Rathinam SR, Muthukkaruppan VR. Identification and evaluation of LPS antigen for serodiagnosis of uveitis associated with leptospirosis. J Med Microbiol 2003;52:667-73.

38.Ray S, Gragoudas E. Neuroretinitis. Int Ophthalmol Clin 2001;41:83-102.

39.King JH. Ocular manifestations of leptospirosis symposium on the leptospirosis medical science publication No1 P 72 Washington 2 D.C 1953 US. Cited by Edwards GA, Domm BM Human leptospirosis Medicine 1960;39:117-55.

40.Alston JN, Broom JC. Leptospirosis in man and animals E Edinburgh 1953 E and S Livingstone Ltd, Cited by Edwards GA, Domm BM Human leptospirosis Medicine 1960;39:117-55.

41.McClain JB, Ballou WR, Harrison SM, et al. Doxycycline therapy for leptospirosis. Ann Intern Med 1984;100:696- 8.

42.Panaphut T, Domrongkitchaiporn S, Vibhagool A, Thinkamrop B, Susaengrat W. Ceftriaxone compared with sodium penicillin g for treatment of severe leptospirosis. Clin Infect Dis 2003;36:1507-13.

DEFINITION

Cat scratch disease (CSD), or ocular Bartonellosis, is a self-limited, systemic illness caused by a gram-negative bacillus, Bartonella henselea. It usually presents as a benign tender lymphadenitis involving the lymph nodes draining dermal or conjunctival sites of inoculation. The disease entity was first described in 1950 by Debré et al1 but the causative agent was not discovered until 1983, when Wear and associates2 identified pleomorphic bacilli in lymph node biopsy specimens prepared with Warthin–Starry silver stain. The bacilli were shortly identified in skin at the primary inoculation site3 and in the conjunctiva of patients with Parinaud oculoglandular syndrome.4 The organism was cultured in 1988 by English and associates5 from the lymph nodes of 10 of 19 patients with cat scratch disease.

EPIDEMIOLOGY

Cat-scratch disease has been shown to be a worldwide zoonotic infection.6 Cats are the primary mammalian reservoir for B. henselae7 and infection rates in cats appear to be higher in areas with more fleas.8 The cat flea (Ctenocephalides felis) has been shown to be a transmission vector among cats7,9 and possibly on occasion to humans. The prevalence of CSD in the United Sates is approximately 22,000 cases per year.10 The prevalence in other countries is unknown. The transmission of B.henselae from cats to humans usually occurs via scratches or by the contamination of surface wounds.11,12 The infection is not known to be transmitted from human to human. CSD follows a

seasonal pattern, with peaks in the fall and winter months, although cases have been reported at all times of the year.13,14 Children and young adults are reported to be at increased risk for systemic B. henselae infection.

SYSTEMIC DISEASE

Primary inoculation often results in a systemic infection. The infected individual often develops an erythematous papule, vesicle, or macule at the site of inoculation followed by a systemic reaction within few weeks. The symptoms include regional lymphadenitis, low-grade fever, chills, malaise, night sweats, headache, and fatigue.15,16 Most patients experience localized disease with mild systemic symptoms that resolve within several months.17 Other less common manifestations of cat scratch disease include encephalitis (1 to 2%), osteomyelitis (less than 1%), and hepatosplenic disease (less than 1%).18

OPHTHALMIC MANIFESTATIONS

The eye can be involved either with the primary inoculation complex, resulting in the so-called Parinaud oculoglandular syndrome or by haematogenous spread, leading to an array of ocular and neuroophthalmic complications. Ocular involvement occurs in 5 to 10 percent of patients with cat scratch disease.13

ADNEXAL AND ANTERIOR SEGMENT MANIFESTATIONS

Parinaud oculoglandular syndrome appears to be the most common ocular complication of cat scratch

disease, affecting approximately 5 percent of symptomatic patients.13 It represents the regional lymphadenopathy associated with infection of the conjunctiva, eyelid, or adjacent skin surface.19 Transmission to the eye is likely to be from hand-to-eye contact, or possibly from aerosol of cat flea feces.20 Patients with Parinaud oculoglandular syndrome typically complain of unilateral eye redness, with sparse and mucoid conjunctival exudates. Lid swelling is usually mild. Conjunctival granulomas are usually tarsal in location. The regional lymphadenopathy involving the preauricular, submandibular, or cervical lymph nodes slowly resolves over several months. Intraparotid node involvement is occasionally associated with parotid swelling.20

CSD has been occasionally associated with conjunctival involvement simulating rhabdomyosarcoma,21 orbital abscess,22 stromal keratitis,23,24 anterior uveitis,25 and neovascular glaucoma.26

NEURORETINITIS

CSD is the most common identifiable cause of neuroretinitis. The condition is usually unilateral but may be bilateral.14 The onset of visual symptoms usually follows the onset of systemic symptoms by 2 to 3 weeks. The most common complaint is decreased vision.27 Visual acuity at the time of initial examination varies from 20/20 to light perception. A relative afferent papillary defect, dyschromatopsia, and a visual field defect are usually present.20 Anterior chamber cells and flare are seen at times and vitreous cells are common. Ophthalmoscopy typically shows optic disc oedema and lipid exudation in the macula arranged in a partial or complete star configuration (Figure 1).28 The optic disc is the primary target of inflammation in neuroretinitis.29 The optic disc oedema occurs approximately 1 week prior to the development of stellate maculopathy, which therefore may be absent at the time of initial presentation. The optic nerve involvement leads to peripapillary retinal thickening and, frequently, an exudative retinal detachment (Figure 2A).30 Intraretinal haemorrhages may be seen.31 Fluorescein angiography shows leakage from the optic disc with no evidence of capillary abnormality in the macular area (Figure 2B).32 Indocyanine green angiography also may show optic disc

Figure 1: Typical neuroretinitis with optic disc oedema associated with a complete macular star

hyperfluoresecence (Figure 2C). OCT may be helpful in detecting macular serous detachment.

Neuroretinitis usually has a self-limited course. Most patients usually recover excellent visual acuity over a period of several weeks to months.14 The macular star usually resolves in approximately 8 to 12 weeks, but it may be present for up to 1 year. A few patients may be left with mild pallor of the optic disc.20 Retinal pigment epithelium changes also may develop after resolution of a prominent macular star.

Cat scratch disease may occasionally present with a large inflammatory mass or exudate of the optic nerve head (Figures 3 and 4).33

CHORIORETINAL INVOLVEMENT

There may be one or more white areas of inner retinitis or chorioretinitis typically juxtavascular in location that may accompany neuroretinitis (Figure 2D)14,34 or occur in the absence of obvious optic disc involvement (Figure 5).14,27,35 These retinal lesions were found to be more common than neuroretinitis by some authors.27 They are a good clue for the diagnosis of CSD in patients with neuroretinitis.They may be associated with an angiomatous-like proliferation of retinal capillaries (Figure 6),36,37 which is more clearly characterized by fluorescein angiography. The abnormal vascular network is characteristic of HIV positive patients,38 but vascular abnormalities can also occur close to the optic disc in immunocompetent patients.

Figures 4A and B: Optic disc inflammatory mass associated with dense hard exudates surrounding the optic disc (A) and vitreous traction on OCT (B)

The inner white retinal lesions may simulate cottonwool ischemic spots, but their distribution in the fundus is not necessarily associated with the distribution of a first-order arteriole as is the case with cotton-wool spots.

Branch retinal arteriolar occlusion27,34,39 or branch retinal venous occlusion20,38 may be associated with an area of focal retinitis.

Less common chorioretinal manifestations of CSD include large inflammatory retinal mass in the posterior pole,33 choroidal mass with or without an associated abnormal vascular network (Figure 7), intermediate uveitis with retinal vasculitis,40 unilateral panuveitis with clinical and fluorescein angiographic features simulating Vogt-Koyanagi-Harada disease,41 isolated serous macular detachment,42 serous macular detachment simulating central serous chorioretinopathy,43 macular hole,44 and vitreous haemorrhage.45

Figures 5A and B: Small retinal infiltrates without associated neuroretinitis in a patient with CSD

PATHOGENESIS

Bartonella are gram-negative, oxidase-negative, fastidious, and aerobic bacilli.46 Bartonella henselae has been demonstrated to be the principal cause of CSD.47,48 The predominant mode of transmission of B. Henselae is through a cat scratch or bite. Cat fleas may act as a vector of transmission of the bacilli from cat to human.7,9 It is unknown whether fundus changes are the direct result of optic nerve or intraocular infection by Bartonella or if the ocular findings represent a parainfectious inflammatory response.17 A retinal biopsy performed from a focus of retinitis in a patient with human immunodeficiency virus, had isolated a B henselae.49

Figure 6: Chorioretinitis associated with abnormal vascular network characteristic of CSD in HIV-positive patients

Figure 7: Ocular CSD presenting as solitary choroidal granuloma

Bartonella organisms are known to establish and maintain an intimate relationship with vascular endothelium. This relationship has been suggested to be important for the production of local vasoproliferative response, especially in immunocompromised patients.39

DIAGNOSIS

CSD may be suspected in patients with a regional lymphadenopathy with mild fever and malaise. Traditionally, the diagnosis of CSD was made when 3 out of the following 4 criteria were present, i.e.

(1)contact with a cat and a scratch or inoculation site,

(2)no other causes of the lymphadenopathy identified,

(3)a positive skin test in response to cat scratch disease antigen, or (4) the characteristic histopathological changes in a lymph node biopsy.46

The blood culture isolation of B. henselae is difficult and expensive. The diagnosis of CSD is now possible through 2 serologic tests currently available.16 An indirect fluorescent antibody (IFA) test was developed to detect the humoral response to the organism. The sensitivity and specificity of this assay appear to be 90 percent or better for immunocompetent patients.11 Enzyme-linked immunoassays (EIA) and Western blot procedures were later developed, and EIA was shown to have IgG sensitivity of 86 to 95 percent and specificity of 96 percent compared with IFA.50 More recently, A polymerase chain reaction–based assay for the detection of B. henselae 16S ribosomal RNA gene

in a very small sample of serum or other body fluids have been employed for diagnosis purposes.51

DIFFERENTIAL DIAGNOSIS

The differential diagnosis for Parinaud’s oculoglandular syndrome includes tularemia, tuberculosis, syphilis, rickettsiosis, infectious mononucleosis, sporotrichosis, and acute Chlamydia trachomatis infection.52

Although CSD is the most common cause of neuroretinitis, other infectious and inflammatory conditions have been identified as causes of neuroretinitis, including tuberculosis, sarcoidosis, toxoplasmosis, syphilis, toxocariasis, Lyme disease, rickettsiosis, leptospirosis, mumps, varicella, and herpes simplex.28,29 Other causes of optic disc oedema and a macular star include vascular disorders such as systemic hypertension,53 diabetes mellitus,28 increased intracranial pressure,54 branch retinal vein occlusion, and anterior ischemic optic neuropathy.20

Retinitis and chorioretinitis associated with CSD can be distinguished from other infectious or noninfectious entities on the basis of history, systemic signs and symptoms, and the pattern of ocular involvement.

TREATMENT

There are no clear recommendations for the treatment of CSD or its ocular complications. Immunocompetent

patients with B. henselae infections generally resolve completely without treatment. Many physicians do not treat mild to moderate systemic CSD. They treat severe ocular or systemic complications of B. henselae infection in immunocompetent patients, and all immunocompromised patients. They often use doxycycline, erythromycin, ciprofloxacin, azithromycin, trimethoprim-sulfametoxazole, rifampin, or intramuscular gentamicin.16,55 The duration of treatment is usually 2 to 4 weeks in immunocompetent patients and 4 months for immunocompromised patients.56 HIV positive patients may show recurrences of intraocular CSD,38 and treatment may be maintained until CD4+ reach good levels. The role of oral corticosteroid in the management of ocular CSD in immunocompetent patients is unknown.

To prevent CSD, it is recommended to wash and disinfect any wounds immediately after a cat scratch or bite, and ovoid contact with stray felines. Immunocompromised patients should be especially careful to avoid scratches and to control flea infestation.

PROGNOSIS

Most patients with CSD neuroretinitis recover normal or near-normal visual acuities. Macular exudates may take months to resolve. There may be mild residual colour vision abnormalities, subnormal contrast sensitivity, and abnormal evoked potentials.29

REFERENCES

1.Debré R, Lamy M, Jammet ML, et al. La maladie des griffes de chat. Bull Mem Soc Med Hosp Paris 1950;66:76-9.

2.Wear DJ, Margileth AM, Hadfield TL, et al. Cat scratch disease: a bacterial infection. Science 1983;221:1403-5.

3.Margileth AM, Wear DJ, Hadfield Tl, et al. Cat-scratch disease: bacteria in skin at the primary inoculation site. JAMA 1984;252:928-31.

4.Wear DJ, Malaty RH, Zimmerman LF, et al. Cat-scratch disease bacilli in the conjunctiva of patients with Parinaud’s oculoglandular syndrome. Ophthalmology 1985;92:1282-7.

5.English CK, Wear DJ, Marigleth AM, et al. Cat-scratch disease. Isolation and culture of the bacterial agent. JAMA 1988;259:1347-52.

6.Kordick DL, Wilson KH, Sexton DJ, et al. Prolonged Bartonella bacteremia in cats associated with cat-scratch disease patients. J Clin Microbiol 1995;33:3245-51.

7.Koehler JE, Glaser CA, Tappero JW. Rochalimaea henselae infection: a new zoonosis with the domestic cat as reservoir. JAMA 1994;271:531-5.

8.Jameson P, Greene C, Regnery R, et al. Prevalence of Bartonella henselae antibodies in pet cats throughout regions of North America. J Infect Dis 1995;172:1145-9.

9.Chomel BB, Kasten RW, Floyd-Hawkins K, et al. Experimental transmission of Bartonella henselae by the cat flea. J Clin Microbiol 1996;34:1952-6.

10.Jackson LA, Perkins BA, Wenger JD. Cat-scratch disease in the United States: an analysis of three national databases. Am J Public Health 1993;83:1707-11.

11.Dalton MJ, Robinson LE, Cooper J, et al. The use of Bartonella antigens for serologic diagnosis of cat-scratch disease at a national referral center. Arch Intern Med 1995; 155:1670-6.

12.Warwick WJ. The cat scratch syndrome: many diseases or one disease? Prog Med Virol 1967;9:256-301.

13.Carithers HA. Cat-scratch disease: an overview based on a study of 1,200 patients. Am J Dis Child 1985;139:112433.

14.Reed JB, Scales KD, Wong MT, et al. Bartonella henselae neuroretinitis in cat scratch disease: diagnosis, management, and sequelae. Ophthalmology 1998;105:459-66.

15.Midani S, Ayoub EM, Anderson B. Cat-scratch disease. Adv Pediatr 1996,43:397-422.

16.Spach DH, Koehler JE. Bartonella-associated infections. Infect Dis Clin North Am 1998;12:137-55.

17.Chorich LJ III. Bartonella. In: Foster CS, Vitale AT, (Eds): Diagnosis and Treatment of Uveitis. W.B Saunders Company, 2002;260-3.

18.Cunningham ET, Koehler JE. Ocular bartonellosis. Am J Ophthalmol 2000;130:340-9.

19.Carithers HA. Oculoglandular disease of Parinaud: a manifestation of cat scratch disease. Am J Dis Child 1978; 132:1195-1200.

20.Ormerod LD, Dailey JP. Ocular manifestations of catscratch disease. Curr Opin Ophthalmol 1999;10:209-16.

21.Marr BP, Shields CL, Shields JA, Eagle RC Jr. Conjunctival cat-scratch disease simulating rhabdomyosarcoma. J Pediatr Ophthalmol Strabismus 2003;40(5):302-3.

22.Mirakhur B, Shah SS, Ratner AJ, Goldstein SM, Bell LM, Kim JO. Cat scratch disease presenting as orbital abscess and osteomyelitis. J Clin Microbiol 2003;41(8):3991-3.

23.Lohmann CP, Gabler B, Kroher G, Spiegel D, Linde HJ, Reischl U. Disciform keratitis caused by Bartonella henselae: an unusual ocular complication in cat scratch disease. Eur J Ophthalmol 2000;10(3):257-8.

24.Gabler B, Linde HJ, Reischl U, Lohmann CP. Disciform keratitis caused by Bartonella henselae infection: detection of a rare ocular complication of cat-scratch disease with PCR. Klin Monatsbl Augenheilkd 2000;217(5):299-302.

25.Rehman SU, Metcalfe TW, Barnham M. Anterior uveitis associated with cat scratch disease. Br J Ophthalmol 1998; 82:587-8.

26.Gray AV, Michels KS, Lauer AK, Samples JR. Bartonella henselae infection associated with neuroretinitis, central retinal artery and vein occlusion, neovascular glaucoma, and severe vision loss. Am J Ophthalmol 2004;137(1):187- 9.

27.Solley WA, Martin DF, Newman NJ, et al. Cat scratch disease: posterior segment manifestations. Ophthalmology 1999;106:1546-53.

28.Williams N, Miller NR. Neuroretinitis. In: Pepose JS, Holland GN, Wilhelmus KR, (Eds): Ocular infection and immunity. St. Louis: Mosby Year Book, 1996;601-08.

29.Gass JD. Diseases of the optic nerve that may simulate macular disease. Trans Am Acad Ophthalmol 1977;83:766.

30.Wade NK, Levi L, Jones MR, Bhisitkul R, Fine L, Cunningham ET Jr. Optic disk edema associated with peripapillary serous retinal detachment: an early sign of systemic Bartonella henselae infection. Am J Ophthalmol 2000;130(3):327-34.

31.Bar S, Segal M, Shapira R, et al. Neuroretinitis associated with cat scratch disease. Am J Ophthalmol 1990;110:703- 5.

32.Lombardo J. Cat-scratch neuroretinitis. J Am Optom Assoc. 1999;70(8):525-30.

33.Cunningham ET Jr, McDonald HR, Schatz H, et al. Inflammatory mass of the optic nerve head associated with systemic Bartonella henselae infection. Arch Ophthalmol 1997;115:1596-7.

34.Ormerod LD, Skolnick KA, Menosky MM, et al. Retinal and choroidal manifestations of cat-scratch disease. Ophthalmology 1998;105:1024-31.

35.Zacchei AC, Newman NJ, Sternberg P. Serous retinal detachment of the macula associated with cat scratch disease. Am J Ophthalmol 1995;120:796-7.

36.Gray AV, Reed JB, Wendel RT, Morse LS. Bartonella henselae infection associated with peripapillary angioma, branch retinal artery occlusion, and severe vision loss. Am J Ophthalmol 1999;127(2):223-4.

37.Fish RH, Hogan RN, Nightingale SD, et al. Peripapillary angiomatosis associated with cat-scratch neuroretinitis. Arch Ophthalmol 1992;110:323.

38.Curi AL, Machado DO, Heringer G, Campos WR, Orefice F. Ocular manifestation of cat-scratch disease in HIVpositive patients. Am J Ophthalmol 2006;141(2):400-1.

39.Cohen SM, Davis JL, Gass JDM. Branch retinal arterial occlusions in multifocal retinitis with optic nerve edema. Arch Ophthalmol 1995;113:1271-6.

40.Soheilian M, Markomichelakis N, Foster CS. Intermediate uveitis and retinal vasculitis as manifestations of cat scratch disease. Am J Ophthalmol 1996;122:582-4.

41.Khurana RN, Albini T, Green RL, Rao NA, Lim JI. Bartonella henselae infection presenting as a unilateral panuveitis simulating Vogt-Koyanagi-Harada syndrome. Am J Ophthalmol 2004;138(6):1063-5.

42.Asensio-Sánchez VM, Rodríguez-Delgado B, GarcíaHerrero E, Cabo-Vaquera V, García-Loygorri C. Serous

macular detachment as an atypical sign in cat scratch disease. Arch Soc Esp Oftalmol 2006;81(12):717-9.

43.Matsuo T, Kato M. Submacular exudates with serous retinal detachment caused by cat scratch disease. Ocul Immunol Inflamm 2002;10(2):147-50.

44.Albini TA, Lakhanpal RR, Foroozan R, Holz ER. Macular hole in cat scratch disease. Am J Ophthalmol 2005;140(1): 149-51.

45.Degueldre F, Bonnet S. Cause inhabituelle d’une hémorragie du vitré : La neurorétinite de la maladie des griffes du chat. À propos d’un cas. Bull Soc Belge Ophtalmol 2002;285:37-40.

46.Anderson BE, Neuman MA. Bartonella spp. As emerging human pathogens. Clin Microbiol Rev 1997;10:203-19.

47.Anderson B, Sims K, Regnery R, et al. Detection of Rochalimaea henselae DNA in specimens from cat scratch disease patients by PCR. J Clin Microbiol 1994;32:942-8.

48.Litwin CM, Martins TB, Hill HR. Immunologic response to Bartonella henselae as determined by enzyme immunoassay and Western blot analysis. Am J Clin Pathol 1997; 108:202-9.

49.Warren K, Goldstein E, Hung VS, et al. Use of retinal biopsy to diagnose Bartonella (formerly Rochalimaea) henselae retinitis in an HIV-infected patient. Arch Ophthalmol 1998;116:937-40.

50.Barka NE, Hadfield T, Patnaik M, et al. EIA for detection of Rochalimaea henselae–reactive IgG, IgM, and IgA antibodies in patients with suspected cat-scratch disease (letter). J Infect Dis 1993;167:1503.

51.Relman DA, Loutit JS, Schmidt TM, et al. The agent of bacillary angiomatosis. An approach to the identification of uncultured pathogens. N Engl J Med 1990;323:1625-7.

52.Jones DB. Cat-scratch disease. In: Pepose JS, Holland GN, Wilhelmus KR, (Eds): Ocular infection and immunity. St Louis: Mosby Year Book, 1996;1389-97.

53.Noble KG. Hypertensive retinopathy simulating Leber idiopathic stellate neuroretinitis. Arch Ophthalmol 1997;115:1594-5.

54.Maitland CG, Miller NR. Neuroretinitis. Arch Ophthalmol 1984;102:1146-50.

55.Margileth AM. Antibiotic therapy for cat-scratch disease: clinical study of therapeutic outcome in 268 patients and a review of the literature. Pediatr Infect Dis J 1992;11:474- 8.

56.Koehler JE, Relman DA. Bartonella species. In: Yu WL, Merigan TC Jr, Barriere SL, (Eds): Antimicrobial therapy and vaccines. Baltimore: Williams and Wilkins, 1999;578-3.

INTRODUCTION

Herpes viruses represent a major etiology of retinitis and their implication should always be taken into consideration in typical clinical presentations. Primary infection by members of this family is usually efficiently controlled by the immune system. However, the immune system does not completely clear the virus. Herpes viruses have developed a love-hate relationship with their hosts, which they have maintained for over 30 × 106 years. Herpes virus genomes persist in a latent form at specific sites in the infected host. The status of the host’s immune system largely defines the outcome of viral infections and their complications. The majority of the population is seropositive for at least 4 (Varicella, Cytomegalovirus, Herpes simplex type I, Epstein-Barr virus) of the 8 human herpesviruses. Initial infection with these herpes viruses is usually clinically inapparent. And the viruses become latent without causing any pathologic condition during the subject’s lifetime. In a small percentage of people, cytopathogenicity with subsequent inflammation may occur after the acute phase of viral disease or upon recurrences. This may induce retinitis with subsequent complications in the absence of adequate therapeutic strategy. Any delay may worsen the final prognosis and highlights the importance of an energetic diagnostic approach based on thorough clinical and virological examination.1,2 Diagnostic confirmation is a major issue and allows specific therapeutic strategies based on antivirals and, sometimes corticosteroids. The use of molecular biological techniques is particularly informative.

Detection of viral DNA by PCR from patients with retinitis is a rapid, sensitive and accurate procedure. Systemic antiviral drugs should be proposed rapidly in order to control viral replication before the use of corticosteroids. Maintenance therapy based on low dose antivirals can reduce the rate of recurrence and should be considered.

EPIDEMIOLOGY

Herpes viruses can be transmitted to a susceptible individual following close contact with the secretions, skin, or mucous membranes of an infected person shedding virus. Infections with herpes viruses are very common in the general population, but in most cases they do not cause clinically apparent disease. Ocular herpes simplex virus type 2 infection seems to spread via an oculogenital route in the majority of cases. The prevalence of seropositivity increases with age and varies geographically. In the United States, positive serology against HSV-1 is generally detected in 50 percent of high-status and 80 percent of low-status socioeconomic persons by the age of 303 and prevalence increases with age. VZV seroconversion has been reported in the US in nearly 90 percent of the population by the age of 60 years.4 Herpes virus infections involving the posterior segment of the eye are less common than other ocular viral infections and include CMV retinitis or progressive outer retinal necrosis in immunocompromised hosts and acute retinal necrosis or non necrotizing viral retinopathies mainly in immunocompetent patients. The prevalence of herpetic retinitis has been found to be closely sex-