Part 4 • Infectious Uveitic Conditions
Chapter 10 Spirochetal Diseases
and facial nerve paresis. Between 10% and 44% of patients with leptospirosis experience uveitis,140 which is typically an acute, often bilateral, iridocyclitis with fine keratic precipitates, posterior synechiae, occasional vitreous opacities, and rarely retinal exudates. Patients often have blurred vision and mild ocular irritation, but respond well to treatment with mydriatics and topical steroids. More severe cases of uveitis have been reported and may occur long after the disease has appeared to subside. Barkay and Garzozi132 reported on 16 patients with predominantly anterior uveitis secondary to leptospirosis with positive serologic results. Leptospirosis should be considered as a possible cause of uveitis of unknown cause, especially in patients with occupational or recreational risk factors for the disease.
Diagnosis
The white blood cell count is normal to slightly elevated in most cases of leptospirosis; values >15 000 cells/mm3 suggest the presence of hepatic disease. Differential counts usually reveal >70% neutrophils, a finding that may differentiate leptospirosis from viral infection. In patients with liver involvement, intravascular hemolysis may cause anemia and elevated serum bilirubin levels.
A definitive diagnosis of leptospirosis requires isolation of the spirochete from a clinical specimen, usually blood or CSF, or seroconversion (a fourfold or greater rise in antibody titer) in the presence of clinical illness. The organism is present in blood and CSF for only 8–10 days after infection, and the spirochete quickly disappears as antibodies appear in the serum. The leptospires can be identified by darkfield examination, but this technique requires expertise. Leptospiruria occurs during the immune phase, although leptospires are easily confused with cellular debris in urine sediment. Tissue samples may also be examined, but tissue analysis for leptospires is predominantly limited to postmortem examination. Detection of leptospira DNA by PCR in the aqueous humor of a patient with uveitis has been reported.141
In practice, laboratory diagnosis of leptospirosis is usually made serologically. The macroscopic slide agglutination test uses a boiled suspension of leptospires and is used mostly as a screening test. The microscopic agglutination test uses live or formalin-treated antigens, is more specific, and can be used to determine both antibody titer and serotype. Sensitive and specific complement fixation tests and ELISAs for the detection of IgM antibody against leptospiral antigens have been developed. They are both inexpensive and easy to use and are playing an increasing role in the diagnosis of leptospirosis. Agglutinins appear on the 6th to 12th day of illness, and the maximum titer is reached during the 3rd and 4th weeks. Early treatment with antibiotics may delay or suppress development of the antibody response, but if initial serologic test results are negative the tests should be repeated 2 weeks later.
Prognosis
Patients with anicteric leptospirosis usually recover uneventfully within 2–6 weeks, although convalescence may extend up to 1 month. Death occurs in 5–30% of untreated patients and is usually attributable to acute renal failure. Uveitis occurs in 10% of patients from 2 weeks to 1 year after initial infection, but the prognosis for these patients is generally good.
Table 10-10 Treatment of leptospirosis
MILD INFECTION
Doxycycline 100 mg PO bid × 7 days OR
Amoxicillin 500 mg PO q6h × 7 days OR
Ampicillin 500–750 mg PO q6h × 7 days
MODERATE TO SEVERE INFECTION
Penicillin G 1.5 million units IV q6h × 10 days OR
Ampicillin 0.5–1g IV q6h × 10 days OR
Ceftriaxone 1g IV qd × 10 days
SEVERE UVEITIS OR NEUROLOGIC ABNORMALITIES OR ARTHRITIS
Ceftriaxone 2 g/day IV × 14–21 days
Treatment
Recommendations for the treatment of leptospirosis can be found in Table 10-10. Chemotherapeutic trials were conducted during outbreaks of leptospirosis in military personnel training in Panama. Doxycycline, 200 mg orally once a week and at the end of training, prevented infection.142 Antibiotics have been shown to reduce disease complications if they are given by the fourth day of infection; however, administration is still recommended for severe infections, even if diagnosis is made after 4 days after infection.
In severe cases of leptospirosis, recommended therapy is penicillin G, 1.5 million units, or ampicillin, 500–1000 mg, administered intravenously every 6 hours for 10 days. Intravenous ceftriaxone has also been used to treat severe leptospirosis. Less severe cases may be treated with a 7-day course of doxycycline, 100 mg orally twice a day; ampicillin, 500–750 mg orally every 6 hours; or amoxicillin, 500 mg orally every 6 hours.143,144 Supportive therapy is given for renal failure, hypotension, and hemorrhage.
Prevention of leptospirosis centers on the elimination of large animal reservoirs of disease, including livestock and pets. In fact, cattle-associated leptospirosis is a problem in the British Isles, and at least 4% of all British dairy farmers are at risk for infection.128
The ophthalmologist must be diligent in pursuing the clinical history for evidence of previous or persistent lowgrade infection that is suggestive of leptospirosis when evaluating patients with a uveitis of unknown cause, especially in dairy farmers. Because many cases are unrecognized, it is not possible to state definitively how many cases of uveitis are secondary to leptospirosis; however, one report indicated that only 17% of 483 proven cases of leptospirosis were initially diagnosed correctly.145 In an editorial, Watt146 suggested that a history of water or animal contact in a patient with severe myalgias and conjunctival suffusion suggests the presence of leptospirosis, particularly in someone returning from travel in Asia or Latin America. The ophthalmologist can confirm the diagnosis by sending a serum sample to a reference laboratory for the microscopic agglutination test or for an ELISA for leptospirosis.
Case 10-1
A 59-year-old HIV-positive white man developed a sudden decrease in vision in both eyes. Visual acuity was 20/400 OU. Examination revealed bilateral hypopyons (see Fig. 10-9), dense
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References
vitritis, and patchy areas of retinal infiltrates in both eyes (see Fig. 10-2A). The patient was referred to the National Institutes of Health with a presumed diagnosis of cytomegalovirus retinitis. Laboratory evaluation at the National Institutes of Health revealed positive VDRL and FTA-ABS test results. A diagnosis of syphilis was made, and the patient was treated with intravenous penicillin G. Within 2 weeks visual acuity improved to 20/40 OU. The retinal infiltrates also resolved, and the patient was left with a pigmentary retinopathy characteristic of resolved syphilitic retinitis (see Fig. 10-2B).
Figure 10-9. Hypopyon uveitis in a patient with syphilis (see Case 10-1).
References
1.Schaudin FR, Hoffman E. Vorlüfger Berichtüber das Vorkommen von Spirochaeten in syphilitschen Krankheitsproducten und bei Papillomen. Arb Gesundheitsamte 1905; 22: 527.
2.Mahoney JF, Arnold RC, Harris A. Penicillin treatment of syphilis: A preliminary report. J Vener Dis Inform 1943; 24: 355–357.
3.Continuing increase in infectious syphilis – United States. MMWR Morb Mortal Wkly Rep 1988; 37: 35–38.
4.Congenital syphilis – New York City, 1986–1988. MMWR Morb Mortal Wkly Rep 1989; 38: 825–829.
5.Primary and secondary syphilis
– United States, 2003–2004. MMWR Morb Mortal Wkly Rep 2005; 55: 269–273.
6.Berry CD, Hooton TM, Collier AC, et al. Neurologic relapse after benzathine penicillin therapy for secondary syphilis in a patient with HIV infection. N Engl J Med 1987; 316: 1587–1589.
7.Johns DR, Tierney M, Felsenstein D. Alteration in the natural history of neurosyphilis by concurrent infection with the human immunodeficiency virus. N Engl J Med 1987; 316: 1569–1572.
8.Sparling PF. Natural history of syphilis. In: Holmes KK, Per-Anders M, Sparling PF, Wiesner PJ, eds. Sexually transmitted diseases. New York: McGraw-Hill, 1990, p 214.
9.Chapel TA. The variability of syphilitic chancres. Sex Transm Dis 1978; 5: 68–70.
10.Pulido JS, Corbett JJ, McLeish WM. Syphilis. In: Gold DH, Weingeist TA, eds. The Eye and Systemic Disease. Philadelphia, JB Lippincott, 1990,
p 234.
11.Tramont EC. Syphilis in adults: From Christopher Columbus to Sir Alexander Fleming to AIDS. Clin Infect Dis 1995; 21: 1361–1371.
12.Chapel TA. The signs and symptoms of secondary syphilis. Sex Transm Dis 1980; 7: 161–164.
13.Woods AC. Syphilis of the eye. Am J Syph Gonorrhea Vener Dis 1943; 27: 133–186.
14.Wilhelmus KR. Syphilis. In: Insler MS, ed. AIDS and Other Sexually Transmitted Diseases and the Eye. Orlando, FL, Grune & Stratton, 1987, pp 73–104.
15.Lukehart SA, Hook EW, Baker-Zander SA, et al. Invasion of the central nervous system by Treponema pallidum: Implications for diagnosis and treatment. Ann Intern Med 1988; 109: 855–862.
15a. Marra CM. Update on neurosyphilis. Curr Infect Dis Rep 2009; 11: 127–134.
16.Lowenfeld IE. The Argyll Robertson pupil, 1869–1969: A critical survey of the literature. Surv Ophthalmol 1969;
14:199–299.
17.Dorfman DH, Glaser JH. Congenital syphilis presenting in infants after the newborn period. N Engl J Med 1990;
323:1299–1302.
18.Duke-Elder S. System of Ophthalmology, vol XIII, The Ocular Adnexa, Part II, Lacrimal, Orbital, and Paraorbital Diseases. St. Louis, CV Mosby, 1974, p 615.
19.Arruga J, Valentines J, Mauri F, et al. Neuroretinitis in acquired syphilis. Ophthalmology 1985; 92: 262– 270.
20.Morgan CM, Webb RM, O’Connor GR. Atypical syphilitic chorioretinitis and vasculitis. Retina 1984; 4: 225–231.
21.Mendelsohn AD, Jampol LM. Syphilitic retinitis. A cause of necrotizing retinitis. Retina 1985; 4: 221–234.
22.Jumper JM, Machemer R, Gallemore RP, et al. Exudative retinal detachment and retinitis associated with acquired syphilitic uveitis. Retina 2000; 20: 190–194.
23.Halperin LS, Lewis H, Blumenkranz MS, et al. Choroidal neovascular membrane and other chorioretinal complications of acquired syphilis. Am J Ophthalmol 1989; 108: 554–562.
23a. Tsimpida M, Low LC, Posner E, et al. Acute syphilitic posterior placoid chorioretinitis in late latent syphilis. Int J STD AIDS 2009; 20: 207–
208.
24.Tramont EC. Treponema pallidum
(syphilis). In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett’s Principles and Practice of Infectious Diseases, 6th ed. New York, Churchill Livingstone, 2005, pp 2768–2785.
24a. Syphilis testing algorithms using treponemal tests for initial screening
– Four laboratories, New York City, 2005–2006. MMWR Morb Mortal Wkly Rep 2008; 57: 872–875.
25.Guidelines for the prevention and control of congenital syphilis. MMWR Morb Mortal Wkly Rep 1988; 37(Suppl 1): 1–13.
26.Riedner G, Rusizoka M, Todd J, et al Single-dose azithromycin versus penicillin G benzathine for the treatment of early syphilis. N Engl J Med 2005; 353: 1236–1244.
27.Johns DR, Tierney M, Felsenstein D. Alterations in the natural history of neurosyphilis by concurrent infection with the human immunodeficiency virus. N Engl J Med 1987; 316: 1569–1572.
28.Tramont EC. Syphilis in the AIDS era. N Engl J Med 1987; 316: 1600– 1601.
29.Stoumbos VD, Klein ML. Syphilitic retinitis in a patient with acquired immunodeficiency syndrome-related complex. Am J Ophthalmol 1987; 103: 103–104.
30.Passo MS, Rosenbaum JT. Ocular syphilis in patients with human immunodeficiency virus infection. Am J Ophthalmol 1988; 106: 1–6.
157
Part 4 • Infectious Uveitic Conditions
Chapter 10 Spirochetal Diseases
31.Levy JH, Liss RA, Maguire AM. Neurosyphilis and ocular syphilis in patients with concurrent human immunodeficiency virus infection. Retina 1989; 9: 175–180.
32.Zaidman GW. Neurosyphilis and retrobulbar neuritis in a patient with AIDS. Ann Ophthalmol 1986; 18: 260–261.
33.Markowitz DM, Beutner KR, Maggio RP, et al. Failure of recommended treatment for secondary syphilis. JAMA 1986; 255: 1767–1768.
34.Richards BW, Hessburg TJ, Nussbaum JN. Recurrent syphilitic uveitis. [Letter] N Engl J Med 1989; 320: 62.
35.Hicks CB, Benson PM, Lupton GP, et al. Seronegative secondary syphilis in a patient infected with the human immunodeficiency virus (HIV) with Kaposi sarcoma. Ann Intern Med 1987; 107: 492–495.
36.Hollander H. Cerebrospinal fluid normalities and abnormalities in individuals infected with human immunodeficiency virus. J Infect Dis 1988; 158: 855–858.
37.Recommendations for diagnosing and treating syphilis in HIV-infected patients. MMWR Morb Mortal Wkly Rep 1988; 37: 600–608.
38.Pace JL, Csonka GW. Endemic non-venereal syphilis (bejel) in Saudi Arabia. Br J Vener Dis 1984; 60: 293–297.
39.Tabbara KF, Al Kaff AS, Fadel T. Ocular manifestations of endemic syphilis (bejel). Ophthalmology 1989;
96:1087–1091.
40.Smith JL. Neuro-ophthalmological study of late yaws: I. An introduction to yaws. Br J Vener Dis 1971; 47: 223–225.
41.Smith JL, David NJ, Indgin S, et al. Neuro-ophthalmological study of late yaws and pinta: II. The Caracas project. Br J Vener Dis 1971; 47: 226–251.
42.Roman GC, Roman LN. Occurrence of congenital, cardiovascular,
visceral, neurologic, and neuroophthalmologic complications in late yaws: a theme for future research. Rev Infect Dis 1986; 8: 760–770.
43.Steere AC, Malawista SE, Snydman DR, et al. Lyme arthritis: An epidemic of oligoarticular arthritis in children and adults in three Connecticut communities. Arthritis Rheum 1977;
20:7–17.
44.MacDonald AB. Lyme disease: A neuro-ophthalmologic view. J Clin Neuroophthalmol 1987; 7: 185– 190.
45.Burgdorfer W, Barbour AG, Hayes SF, et al. Lyme disease: A tick-borne spirochetosis? Science 1982; 216: 1317–1319.
46.Berger BW, Kaplan MH, Rothenberg IR, et al. Isolation and characterization of the Lyme disease spirochete from the skin of patients with erythema chronicum migrans. J Am Acad Dermatol 1985; 13: 444–449.
47.Barbour AG. Isolation and cultivation of Lyme disease spirochetes. Yale J Biol Med 1984; 57: 521–525.
48.Barbour AG, Hayes SF. Biology of Borrelia species. Microbiol Rev 1986;
50:381–400.
49.Levine JF, Wilson ML, Spielman A. Mice as reservoirs of the Lyme disease spirochete. Am J Trop Med Hyg 1985;
34:355–360.
50.Wilson ML, Adler GH, Spielman A. Correlation between abundance of deer and that of the deer tick, Ixodes dammini (Acari: Ixodidae). Ann Entomol Soc Am 1986; 23: 172– 176.
51.Steere AC. Lyme disease. N Engl J Med 1989; 321: 586–596.
52.Tsai TS, Bailey RE, Moore PS. National surveillance of Lyme disease 1987– 1988. Conn Med 1986; 53: 324–326.
53.Surveillance for Lyme Disease
– Unites States, 1992–2006. MMWR Morb Mortal Wkly Rep 2008; 57(SS10): 1–9.
54.Lastavica CC, Wilson ML, Berardi VP, et al. Rapid emergence of a focal epidemic of Lyme disease in coastal Massachusetts. N Engl J Med 1989;
320:133–137.
55.Steere AC, Bartenhagen NH, Craft JE, et al. The early clinical manifestations of Lyme disease. Ann Intern Med 1983; 99: 76–82.
56.Pachner AR, Steere AC. The triad of neurologic manifestations of Lyme disease: Meningitis, cranial neuritis, and radiculoneuritis. Neurology 1985;
35:47–53.
57.Clark JR, Carlson RD, Sasaki CT, et al. Facial paralysis in Lyme disease. Laryngoscope 1985; 95: 1341–
1345.
58.Steere AC, Batsford WP, Weinberg M, et al. Lyme carditis: Cardiac abnormalities of Lyme disease. Ann Intern Med 1980; 93: 8–16.
59.Bertuch AW, Rocco E, Schwartz EG. Eye findings in Lyme disease. Conn Med 1987; 51: 151–152.
60.Baum J, Barza M, Weinstein P, et al. Bilateral keratitis as a manifestation of Lyme disease. Am J Ophthalmol 1988; 105: 75–77.
61.Orlin SE, Lauffer JL. Lyme disease keratitis. Am J Ophthalmol 1989;
107:678–680.
62.Schlesinger PA, Duray PH, Burke BA, et al. Maternal–fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. Ann Intern Med 1985;
103:67–69.
63.Weber K, Bratzke HJ, Neubert U, et al.
Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. Pediatr Infect Dis J 1988; 7: 286–289.
64.Markowitz LE, Steere AC, Benach JL, et al. Lyme disease during pregnancy. JAMA 1986; 255: 3394–3396.
65.Williams CL, Benach JL, Curran AS, et al. Lyme disease during pregnancy: A cord blood serosurvey. Ann NY Acad Sci 1988; 539: 504–506.
66.Aaberg TM. The expanding
ophthalmologic spectrum of Lyme disease. Am J Ophthalmol 1989; 107: 77–80.
67.Flack AJ, Lavoie PE. Episcleritis, conjunctivitis, and keratitis as other manifestations of Lyme disease. Ophthalmology 1990; 97: 973– 975.
68.Steere AC, Duray PH, Kauffmann DJ, et al. Unilateral blindness caused by infection with the Lyme disease spirochete, Borrelia burgdorferi. Ann Intern Med 1985; 103: 382–
384.
69.Kornmehl EW, Lesser RL, Jaros P, et al. Bilateral keratitis in Lyme disease. Ophthalmology 1989; 96: 1194–1197.
70.deLuise VP, O’Leary MJ. Peripheral ulcerative keratitis related to Lyme disease. [Letter] Am J Ophthalmol 1991; 111: 244–245.
71.Suttorp-Schulten MSA, Kuiper H, Kijlstra A, et al. Long-term effects of ceftriaxone treatment on intraocular Lyme borreliosis. Am J Ophthalmol 1993; 116: 571–575.
72.Karma A, Seppala I, Mikkila H, et al. Diagnosis and clinical characteristics of ocular Lyme borreliosis. Am J Ophthalmol 1995; 119: 127–135.
73.Bialasiewicz AA, Ruprecht KW, Naumann GOH, et al. Bilateral diffuse choroiditis and exudative retinal detachments with evidence of Lyme disease. Am J Ophthalmol 1988; 105: 419–420.
74.Koch F, Augustin AJ, Boker T. Neuroborreliosis with retinal pigment epithelium detachments. Ger J Ophthalmol 1996; 5: 12–15.
75.Scholes GN, Teske M. Lyme disease and pars planitis. Ophthalmology 1989; 107(Suppl): 126.
76.Copeland RA Jr, Nozik RA, Shimokaji G. Uveitis in Lyme disease. Ophthalmology 1989; 107(Suppl): 127.
77.Winward KE, Smith JL, Culbertson WW, et al. Ocular Lyme borreliosis. Am J Ophthalmol 1989; 108:
651–657.
78.Leys AM, Schonherr U, Lang GE, et al. Retinal vasculitis in Lyme borreliosis. Bull Soc Belge Ophthalmol 1995; 259: 205–214.
79.Vine AK. Retinal vasculitis. Semin Neurol 1994; 14: 354–360.
80.Logigian EL, Kaplan RF, Steere AC. Chronic neurologic manifestations of Lyme disease. N Engl J Med 1990; 323: 1438–1444.
81.Wu G, Lincoff H, Ellsworth RM, et al. Optic disc edema and Lyme disease. Ann Ophthalmol 1986; 18: 252– 255.
82.Jacobson DM, Frens DB. Pseudotumor cerebri syndrome associated with Lyme disease. Am J Ophthalmol 1989; 107: 81–82.
83.Federowski JJ, Hyman C. Optic disk edema as the presenting sign of Lyme disease. Clin Infect Dis 1996; 23: 639–640.
84.Scott IU, Silva-Lepe A, Siatkowski RM.
158
Chiasmal optic neuritis in Lyme disease. Am J Ophthalmol 1997; 123: 136–138.
85.Schecter SL. Lyme disease associated with optic neuropathy. Am J Med 1986; 81: 143–145.
86.Reik L Jr, Burgdorfer W, Donaldson JO. Neurologic abnormalities in Lyme disease without erythema chronicum migrans. Am J Med 1986;
81:73–78.
87.Seidenberg KB, Leib M. Orbital myositis with Lyme disease. Am J Ophthalmol 1990; 109: 13–16.
88.Balcer LJ, Winterkorn JM, Galetta SL. Neuro-ophthalmic manifestations of Lyme disease. J Neuroophthalmol 1997; 17: 108–121.
89.Stanek G, Strle F. Lyme borreliosis. Lancet 2003; 362: 1639–1647.
90.Schwartz BS, Goldstein MD, Ribeiro JMC, et al. Antibody testing in Lyme disease: A comparison of results in four laboratories. JAMA 1989; 262: 3431–3434.
91.Luger SW, Krauss E. Serologic tests for Lyme disease: Interlaboratory variability. Arch Intern Med 1990;
150:761–763.
92.Barbour AG. The diagnosis of Lyme disease: Rewards and perils. Ann Intern Med 1989; 110: 501–502.
93.Dattwyler RJ, Volkman DJ, Lugt BJ, et al. Seronegative Lyme disease dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi. N Engl J Med 1988; 319: 1441–1446.
94.Russell H, Saampson JS, Schmid GP, et al. Enzyme-linked immunosorbent assay and indirect immunofluorescence assay for Lyme disease. J Infect Dis 1984; 149: 465–470.
95.Craft JE, Grodzicki RL, Steere AC. Antibody response in Lyme disease: Evaluation of diagnostic tests. J Infect Dis 1984; 149: 789–795.
96.Magnarelli LA, Anderson JF, Johnson RC. Cross-reactivity in serological tests of Lyme disease and other spirochetal infections. J Infect Dis 1987; 156: 183–188.
97.Hunter EF, Russell H, Farshy CE, et al. Evaluation of sera from patients with Lyme disease in the fluorescent treponemal antibody test for syphilis. Sex Transm Dis 1986; 13: 232–236.
98.Duffy J, Mertz LE, Wobig GH, et al. Diagnosing Lyme disease: The contribution of serologic testing. Mayo Clin Proc 1988; 63: 1116–1121.
99.Grodzicki RL, Steere AC. Comparison of immunoblotting and indirect enzyme-linked immunosorbent assay using different antigen preparations for diagnosing early Lyme disease. J Infect Dis 1988; 157: 790–797.
100.Mandell H, Steere AC, Reinhardt BN, et al. Lack of antibodies to Borrelia burgdorferi in patients with amyotrophic lateral sclerosis. N Engl J Med 1989; 320: 255–256.
101.Nocton JJ, Dressler F, Rutledge BJ,
et al. Detection of Borrelia burgdorferi
DNA by polymerase chain reaction in synovial fluid from patients with Lyme arthritis. N Engl J Med 1994;
330:229–234.
102.Hilton E, Sood S. Ocular Lyme borreliosis diagnosed by polymerase chain reaction on vitreous fluid. Ann Intern Med 1996; 125: 424–425.
103.Steere AC, Grodzicki RL, Kornblatt AN, et al. The spirochetal etiology of Lyme disease. N Engl J Med 1983;
308:733–740.
104.Guidelines Wormser GP, Nadelman, RB, Dattwyler RL, et al Practice guidelines for the treatment of Lyme disease. Clin Infect Dis 2000; 31(Suppl 1): S1–14.
105.Verdon ME, Sigal LH. Recognition and management of Lyme disease. Am Fam Phys 1997; 56: 427–
436.
106.Steere AC, Taylor E, McHugh GL, et al. The overdiagnosis of Lyme disease. JAMA 1993; 269: 1812– 1816.
107.Rosenbaum JT, Rahn DW. Prevalence of Lyme disease among patients with uveitis. Am J Ophthalmol 1991; 112: 462–463.
108.Breevald J, Kuiper H, Spanjaard L,
et al. Uveitis and Lyme borreliosis. Br J Ophthalmol 1993; 77: 480–481.
109.Preac-Mursic V, Pfister HW, Spiegel H, et al. First isolation of Borrelia burgdorferi from an iris biopsy. J Clin Neuroophthalmol 1993; 13: 155–161.
110.Schubert HD, Greenebaum E, Neu HC. Cytologically proven seronegative Lyme choroiditis and vitritis. Retina 1994; 14: 39–42.
110a. Hilton E, Smith C. Sood S. Ocular Lyme borreliosis diagnosed by polymerase chain reaction on vitreous fluid. Ann Intern Med 1996; 125: 424–425.
111.Dattwyler RJ, Halperin JJ, Volkman DJ, et al. Treatment of late Lyme borreliosis – Randomised comparison of ceftriaxone and penicillin. Lancet 1988; 1: 1191–1194.
112.Bryceson ADM, Parry EHO, Perine PL, et al. Louse-borne relapsing fever: A clinical and laboratory study of 62 cases in Ethiopia and a reconstruction of the literature. QJ Med 1970; 39: 129–170.
113.Southern PM Jr, Sanford JP. Relapsing fever: A clinical and microbiological review. Medicine (Baltimore) 1969, 48: 129–149.
114.Rhee KY, Johnson WD Jr. Borrelia species (relapsing fever). In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett’s Principles and Practice of Infectious Diseases, 6th edn. New York: Churchill Livingstone, 2005, pp 2795–2796.
115.Meader CN. Five cases of relapsing fever originating in Colorado, with positive blood findings in two.
Colorado Med 1915; 12: 365– 368.
116.Burgdorfer W. The enlarging spectrum
References
of tick-borne spirochetoses: RR Parker memorial address. Rev Infect Dis 1986; 8: 932–940.
117.Horton JM, Blaser MJ. The spectrum of relapsing fever in the Rocky Mountains. Arch Intern Med 1985;
145:871–875.
118.Perine PL, Parry EHO, Vukotich D, et al. Bleeding in louse-borne
relapsing fever I. Clinical studies in 37 patients. Trans Roy Soc Trop Med Hyg 1971; 65: 776–781.
119.Quin CE, Perkins ES. Tick-borne relapsing fever in East Africa. J Trop Med 1946; 49: 30–32.
120.Hamilton JB. Ocular complications in relapsing fever. Br J Ophthalmol 1943; 27: 68–80.
121.Sciotto CG, Lauer BA, White WL, et al. Detection of Borrelia in acridine orange-stained blood smears by fluorescence microscopy. Arch Pathol Lab Med 1982; 107: 384–386.
122.Schwan TG, Schrumpf ME, Hinnebusch BJ, et al. GlpQ: an antigen for serological discrimination between relapsing fever and Lyme borreliosis. J Clin Microbiol 1996; 34: 2483–2492.
123.Kazragis RJ, Dever LL, Jorgensen JH, et al. In vivo activities of ceftriaxone and vancomycin against Borrelia spp. in the mouse brain and other sites.
Antimicrob Agents Chemother 1996;
40:2632–2636.
124.Warell DA, Perine PL, Krause DW, et al. Pathophysiology and immunology of the Jarisch– Herxheimer-like reaction in louse-
borne relapsing fever: Comparison of tetracycline and slow-release penicillin. J Infect Dis 1983; 147: 898–908.
125.Weil A. Über eine Eigenümliche, mit Milztumor. Ikterus and Nephritis einhergehende, akute Infektionskrankheit. Deutsch Arch Klin Med 1886; 39: 209–232.
126.Barkay S, Garzozi H. Leptospirosis. In: Gold DH, Weingeist TA, eds. The Eye in Systemic Disease. Philadelphia, JB Lippincott, 1990, pp 226–228.
127.Palmer MF. Laboratory diagnosis of leptospirosis. Med Lab Sci 1988; 45: 174–178.
128.Waitkins SA. Update on leptospirosis. Br Med J 1985; 290: 1502–1503.
129.Graphs and maps for selected notifiable diseases in the United States. MMWR Morb Mortal Wkly Rep 1994; 42: 13–64.
130.Sasaki DM, Pang L, Minette HP, et al. Active surveillance and risk factors for leptospirosis in Hawaii. Am J Trop Med Hyg 1993; 48: 35–43.
130a. Priya CG, Rathinam SR, Muthukkaruppan V. Evidence for endotoxin as a causative factor for leptospiral uveitis in humans. Invest Ophthalmol Vis Sci 2008; 49: 5419–5424.
131.Bernard N, Moshe H. Human leptospirosis associated with eye complications. Israel Med J 1963; 22:
159
Part 4 • Infectious Uveitic Conditions
Chapter 10 Spirochetal Diseases
182. |
1995; 207: 1327–1331. |
132.Barkay S, Garzozi H. Leptospirosis and uveitis. Ann Ophthalmol 1984; 16: 164–168.
133.Murdoch D. Leptospiral uveitis. Trans Ophthalmol Soc NZ 1980; 32: 73–75.
134.Duke-Elder S. System of Ophthalmology, vol VIII, Diseases of the Outer Eye. London: Henry Kimpton, 1965, pp 201–203.
135.Outbreak of acute febrile illness among athletes participating in triathlons – Wisconsin and Illinois, 1998. JAMA 1998; 280: 1473–1474.
136.Rathinam SR, Rathnam S, Slevaraj S, et al. Uveitis associated with an epidemic outbreak of leptospirosis. Am J Ophthalmol124: 71–79. 1997.
137.Dwyer AE, Crockett RS, Kalsow CM. Association of leptospiral seroreactivity and breed with uveitis and blindness in horses: 372 cases (1986–1993). J Am Vet Med Assoc
138.Rathinamsivakumar, Ratnam S, Sureshbabu L, et al. Leptospiral antibodies in patients with recurrent ophthalmic involvement. Indian J Med Res 1996; 103: 66–68.
139.Levin N, Nguyen-Khoa JL, Charpentier D, et al. Panuveitis with papillitis in leptospirosis. Am J Ophthalmol 1994; 117: 118–119.
140.Duke-Elder S. System of Ophthalmology, vol IX, Disease of the Uveal Tract. London: Henry Kimpton, 1966, pp 322–325.
141.Merien F, Perolat P, Manel E, et al. Detection of Leptospira DNA by polymerase chain reaction in aqueous humor of a patient with unilateral uveitis. J Infect Dis 1993; 168: 1335–1336.
142.Takafuji ET, Kirkpatrick JW, Miller RN, et al. An efficacy trial of doxycycline chemoprophylaxis against
leptospirosis. N Engl J Med 1984;
310:497–500.
143.Levett PN. Leptospirosis. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett’s Principles and Practice of Infectious Diseases, 6th ed. New York, Churchill Livingstone, 2005, pp 2789–2795.
144.Farr RW. Leptospirosis: State-of-the-art clinical article. Clin Infect Dis 1995;
21:1–8.
145.Heath CW Jr, Alexander AD, Galton MM. Leptospirosis in the United States. N Engl J Med 1965; 273: 857–922.
146.Watt GW. Leptospirosis as a cause of uveitis. Arch Intern Med 1990; 150: 1130–1132.
160