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Show f. Clin. Neuro-ophthalmol. 3: 197-203, 1983. Ocular Syphilis Acute and Chronic THOMAS C. SPOOR, M.D., M.5. PAULA WYNN, M.D. WALTER C. HARTEL, M.D. CHARLES S. BRYAN, M.D. Abstract We describe our experience over the past 2 years with the ocular manifestations in 32 patients with acute and chronic syphilis. We urge that syphilis be considered in evaluating those patients with recurrent iritis, chorioretinitis, papillitis, optic atrophy, or abnormal pupillary findings. Specific serologic testing (FTAABS) must be obtained. Screening serologies (VORL) are inadequate. We suggest that patients with evidence for CSF involvement or active ocular disease be treated by continuous intravenous infusion of 24 million units penicillin G daily for 10 days. Introduction Syphilis is controversial. Its reported incidence is increasing, 1.2 as are the reports in the ophthalmic literature:l - 7 Ocular involvement by syphilis is often misdiagnosed in the active stages and underdiagnosed during its late stages. Visual complications may be devastating. The limitations of standard, screening non-Treponemal serologic testing have been recently publicized in both the medical and ophthalmologic literature. 3 • M Although these limitations have been recognized and the need for specific serologic testing has been advocated for more than 15 years/ 9 . 10 it is often difficult to obtain a serum FTA-ABS test at many institutions in the face of a nonreactive screening serologic test (VORL, RPR). Ocular manifestations of syphilis are being described with increased frequency. Acute ocular inflammation may be associated with infectious (primary and secondary) syphilis. These patients may present with anterior and posterior uveitis,:l optic neuritis," or perineuritis."' 7 Most are sexually active adults and up to 70% may be homosexual or bisexual.M A second type of ocular involvement is characteristic of late syphiliS and present in the older From the Division of Ophthalmology (TCS). Universitv of South Alabama College of Medicine. Mobile, Alabama;' Department of Ophthalmology (rw. WCH). and Department of Medicine (CSS). University of South Carolina School of Medicine. Columbia. South Carolina. September 1983 population. These patients are often poor and out of the mainstream of medical care. Here syphilis is a diagnosis of exclusion based upon otherwise unexplained clinical findings (chorioretinitis, optic atrophy, pupillary abnormalities) and a reactive serum FTA-ABS test. The initial infection may often have been treated inadequately. Visual loss may be progressive and severe. The reported incidence of syphilis is increasing and most agree that its true incidence is much higher (Table 1).1 Acute (primary and secondary) syphilis is often found in homosexual or bisexual males with no history of a visible chancre due to the nature of their sexual contact (Table 2).2. MTable 3 describes the regional incidence of syphilis in the United States. 1. 2 The characteristic lesion of primary syphilis is the chancre-a painless, indurated, often eroded ulcer found on skin or mucous membranes. In heterosexual men, it is usually located on the penis, hence visible to both patient and physician. In women and homosexual men, the lesions appear in the anal canal, mouth, cervix or labia, concealed from both patient and casual examiner. Hence, no history of a primary lesion is elicited, and there is no suspicion of a recent primary infection. Subsequently, no treatment is given and transmission continues. Chancres heal spontaneously in 2-12 weeks. During the primary stage, the disease may be serologically silent (sic) both VORL and FTAABS may be nonreactive; however, 90% of patients will have reactive FTA-ABS and 70% reactive VORL tests (Table 4).M Secondary syphilis follows 6-8 weeks after the primary stage. Its systemic manifestations are protean and well-reviewed elsewhereH The classic manifestation is a maculopapular rash accompanied by constitutional symptoms. The rash will also disappear without treatment in 2-6 weeks. All serologic tests (specific and nonspecific) are said to be reactive at this stage. Both primary and secondary syphilis are transmissible. Table 5 describes the reported incidence of primary and secondary syphiliS In the United States in 1980. 1 Ocular manifestations of secondary syphilis may include an- 197 Ocular Syphilis Number of Cases a Estimated prevalence of untreated cases, all stages-325,000.' TABLE 1. Reported Incidence of Syphilis in the United States· TABLE 3. Relative Regional Incidence of Syphilis-19B1· Case Reports Case 1 A 47-year-old man with insulin-dependent diabetes mellitus presented to the emergency room in ,February 1982, complaining of a red right eye, Conjunctivitis was diagnosed and treated with topical sulfacetamide. He returned 3 days later complaining of photophobia with pain and swelling about his right eye. He was referred to the eye clinic for further evaluation. He had an episode of iritis in his right eye 3 years previously. Visual acuity was 20/30 in the right eye and 20/20 in the left eye. Extraocular motility was normal. Pupillary reactions were normal. The right upper lid was swollen and the lacrimal gland enlarged. Mild proptosis was present. The conjunctiva was mod-terior uveitis, chorioretinitis, optic neuritis, and perineuritis.3, 5, 6, 7. 9 latent syphilis is a serologic diagnosis characterized by a reactive specific treponemal antibody test (FTA-ABS), normal CSF examination, and lacking clinical manifestations of syphilis. Nonspecific, reaginic antibody testing (VORL) may be nonreactive in 30% of those patients.8 late or tertiary syphilis includes benign gummatous syphilis, cardiovascular syphilis, and neurosyphilis, 3,8 Many late syphilitics have nonreactive, nonspecific antibody tests (VORL), but all are said to have a reactive specific treponemal antibody test (FTA-ABS or TPI).8 A patient with a reactive FTA-ABS, no clinical manifestation of neurosyphilis, but CSF abnormalities, i.d. elevated protein, pleocytosis, or a reactive VORL, has asymptomatic neurosyphilis. Symptomatic neurosyphilis classically includes meningovascular syphilis, general paresis, and tabes dorsalis. The classic clinical pictures are rarely seen, Most patients present with mixed or incomplete syndromes due to partial treatment during the infectious stage.8. 11 Ocular manifestations of late syphilis include iritis, chorioretinitis, optic atrophy, and pupillary abnormalities,3, 9,11 These are the patients we designate as having chronic ocular syphilis. Table 4 summarizes the temporal courses and serologic reactions during the various stages of syphilis.8 Table 6 summarizes reported ocular and adnexal manifestations of syphilis. 12 - 19 We describe herein six cases illustrating both acute and chronic ocular syphilis and review our experience over the last 2 years with the ocular manifestations of this disease in 26 additional patients. Heightened clinician awareness of this disease and its ocular manifestations may avert acute or chronic, progressive visual loss from this preventable and potentially treatable cause of blindness, 97 100 91 100 97 31,266 21,033 20,168 287 45 72,799 73 77 20,767 6,437 % Positive (Serum) 72 100 73 VORL FTA-ABS 12,609 2,148 9,819 22,925 27,204 20,297 20,979 277 75 68,832 1980 1981 2 yrs. Louisiana Georgia Texas Florida Mississippi 3 wks. 9-12 wks. 0-12 yrs. Time Postinfection 5-10 yrs. 20 yrs. 25-30 yrs. 10-40 yrs. Male Female a See reference. 2 Heterosexual Bisexual Homosexual Not stated Primary and secondary syphilis Early latent Late latent Congenital Not states All stages Stage of Syphilis Number 1 Number 2 Number 3 Number 4 Number 5 a See reference.] TABLE 5. Reported Incidence of Primary and Secondary Syphilis-19BO· USee references,H TABLE 2. Sexual Preference Primary, Secondary, and Early Latent Syphilis-19BO· TABLE 4. Stages of Syphilis· Infectious Primary Secondary Early latent Noninfectious Late latent Tertiary syphilis Neuro-syphilis Meningovascular General paresis Tabes dorsalis Cardiovascular a See references." Journal of Clinical Neuro-ophthalmology TABLE 6. Ocular Manifestations of Syphilis· Lids Chancre Gumma Tarsitis Ulcerative blephartis Conjunctive Chancre Papular syphilides Gumma Orbit Periostitis Gumma Cornea Interstitial keratitis Ulcers Deep, punctate keratitis Keratitis profunda Keratitis punctata profunda Keratitis pustuliformis profunda Keratitis linearis migrans Gumma Sclera Episcleritis Scleritis Gumma Anterior Chamber Hypopyon a See references. 12 - 19 erately injected, the cornea uninvolved. Cell and flare were present in the anterior chamber. The conjunctiva, cornea, anterior chamber and lens were normal in the left eye. Applanation tonometry was normal in both eyes. Dilated fundus examination revealed clear vitreous and normal discs, vessels and maculae, and peripheral retina in both eyes. The patient was admitted with the diagnosis of idiopathic orbital inflammation with iritis in the right eye. Orbital x-rays were normal. Computed tomography demonstrated lacrimal gland enlargement. CBC, ANA, LE prep, and sedimentation rate were normal. The patient was begun on scopolamine 1/4% in the right eye twice daily, and 1% prednisolone acetate in the right eye every 2 hours. The VORL was reported reactive at 1:8 with a reactive FTAABS. The Health Department documented a nonreactive VORL obtained 3 years earlier. Lumbar puncture revealed one lymphocyte, total protein of 29 mg/dI, a glucose of 127 mg/dI, and a nonreactive VORL. The patient, therefore, received intramuscular benzathine penicillin G 2.4 million units which was repeated twice at weekly intervals. Over the next few days, visual acuity returned to 20/20 in both eyes with resolution of periorbital swelling and conjunctival injection. At discharge, the anterior chamber was clear without cell or flare. He returned for his injections and continued to improve as the topical steroids were tapered. September 1983 Spoor, Wynn, Hartel, Bryan Iris and Ciliary Body Roseolae Papules Gumma Pupils Light-near dissociation Lens Capsular rupture and necrotizing cortical inflammationcongenital syphilis Dislocation Optic Nerve Neuritis Perineuritis Neuroretinitis Gumma Motility Dysfunction Oculomotor, abducens, trochlear paresis-associated with basilar meningitis Periodic alternating nystagmus Retina and Vitreous Chorioretinitis-pseudoretinitis pigmentosa, salt and pepper fundus Perivasculitis Central retinal artery/vein occlusion Cystoid macular edema Vitritis Case 2 A 34-year-old man presented in October 1981, with a 2-week history of decreased vision and pain upon movement of the right eye. Six months earlier, he was treated with benzathine penicillin for a penile lesion and a rash diagnosed as syphilitic. Visual acuity was 20/40 in the right eye and 20/20 in the left eye. A right afferent pupil defect was present and he complained of a subjective visual field defect in the temporal quadrant. Fundus examination revealed a swollen right optic disc with splinter hemorrhages. The left fundus was normal. Computed tomography of the head and orbits was normal. Serologic testing revealed a reactive VORL of 1:64 and a reactive FTA-ABS. The CSF contained 937 WBCs with 99% lymphs, 1% polys, a protein of 94 mg/dI, glucose of 78, and a VORL reactive of 1:16. He was treated with intravenous aqueous penicillin G 24 million units/day for 10 days. His ocular exam and visual function improved markedly. He has not returned for followup examination or repeat lumbar puncture. Case 3 A 32-year-old asymptomatic man was noted to have constriction of his left visual field during a routine ophthalmologic examination. Skull x-rays and computed tomography were negative, and he was referred for neuro-ophthalmologic consultation. 199 Ocular Syphilis Medical and ocular history were unrevealing. There was no previous ocular trauma. Visual acuity was 20/20 in both eyes. There were no localizing pupillary or motility findings. Goldmann perimetry was normal in the right eye. A peripheral nasal defect was present in the left eye. Slit lamp examination and intraocular pressure were normal. The right fundus was normal. Retinal pigment clumping, droupout, and vascular sheathing adjacent to the temporal arcades were present in the left eye. The peripheral fundi were normal. The electroretinogram was not extinguished. VORL was reactive at a titer of 1:2, FTA-ABS was reactive. VORL in the cerebrospinal fluid was nonreactive; chemistries and cytology were normal. The patient denied homosexual or extramartial sexual activity; but allowed that he had an episode of"clap" treated with penicillin several years prior to his marriage. His wife of 10 years and 9-yearold child had nonreactive serologies. Case 4 A 61-year-old man presented for routine ophthalmologic examination in February 1981. Best-corrected visual acuity was 20/40+ in the right eye and 20/25 in the left eye. Examination revealed bilateral ptosis. The remainder of the examination was normal, including dilated fundus examination. He returned in November 1981, complaining of decreased visual acuity of the right eye. Visual acuity at that time was 20/40 in the right eye and 20/25 in the left eye. The anterior segment was normal bilaterally. Pupils were equal and reactive. Dilated fundus examination revealed multiple microvascular infarctions of the posterior pole and retinal pigment epithelial changes in the right eye. The left fundus was normal. Additional history revealed that as an adolescent, after sexual exposure, he developed a sore on his penis which was treated with an injection. Since this was before World War II, the injection could not have been penicillin. However, he did receive penicillin for a tooth abcess 2 months prior to presentation. Multiple laboratory examinations were performed, including antinuclear antibody, complete blood count, sedimentation rate, blood sugar, and urinalysis; all of which were normal. The VORL was reactive at 1:32 as was the FTA-ABS. A CSF examination revealed a WBC count of 14 cells/mcl (100% lymphocytes) with an elevated protein of 94 mg/dl, a normal glucose, and reactive VORL at 1:16. He was treated with intravenous aqueous penicillin G 24 million units daily for 10 days. He has not returned for follow-up examination or repeat lumbar puncture. Case 5 A 74-year-old woman presented to her ophthalmologist in July 1981, complaining of decreased VISIOn in both eyes, progressing over the past 8 months. Examination revealed a visual acuity of no light perception in the right eye and 20/40 in the left eye, best-corrected. The right pupil was amaurotic. Slit lamp examination was normal in both eyes, as was applanation tonometry. Dilated fundus examination revealed pale, atrophic discs bilaterally with slight retinal pigment epithelium disruption in both maculae. Skull x-rays and sedimentation rate were normal; however, VORL was reactive at 1:4,096 with a reactive FTA-ABS. The CSF contained 21 WBCs/mcl with 5% monocytes and 95% IY.I!lphocytes. Protein and glucose were normal. The CSF VORL was reactive at 1:32. She was treated with 24 million units intravenous aqueous penicillin G daily for 10 days. She returned for repeat lumbar puncture on December 29, 1981. At that time, the CSF contained 4 WBCs, protein and glucose remained normal, and the VORL reactive at 1:32. Case 6 A 69-year-old man presented to the eye clinic in June 1980, complaining of progressive bilateral visual loss over the past year. Best-corrected visual acuity was 20/25 in the right eye and 20/200 in the left eye. Applanation tensions were 12 in both eyes. Motility testing revealed a 10-diopter comitant left exotropia. An afferent pupillary defect was present in the left eye, as was dyschromatopsia. Light/near dissociation was demonstrable. Cup to disc ratio was 0.4 in both eyes, with mild disc pallor in the left eye. Goldmann perimetry revealed a generally constricted field with an enlarged blind spot in the right eye and an island of vision inferiorly present only with the V. test object in the left eye. Initial evaluation included normal skull films and a reactive serum FTA-ABS. The patient was treated with benzathine penicillin 2.4 million units weekly for 3 weeks. However, computed tomography of the brain and orbits was obtained since the visual loss was out of proportion to the optic nerve appearance. A large, enhancing, suprasellar mass was demonstrated. Selective cerebral angiography could not be performed due to vessel tortuosity. The patient subsequently underwent bifrontal craniotomy for excision of his tuberculum sella meningioma. Discussion Syphilis remains a "great imitator" in ophthalmology as well as neurology and medicine. Our experience has taught us that syphilis should be considered in the evaluation of a sexually active patient presenting with anterior uveitis, orbital inflammation, chorioretinitis, or swelling of the optic discs, accompanying symptoms of visual dysfunchon. In the older patient, chronic syphilis should Journal of Clinical Neuro-ophthalmology be suspected when evaluating complaints of visual loss from optic atrophy, chorioretinitis, or abnormal pupillary findings. However, it should remain a diagnosis of exclusion. Cases 1 and 2 represent recently acquired syphilis in sexually active patients. Ocular manifestations include acute uveitis, chorioretinitis, papillitis, perineuritis, and idiopathic orbital inflammation. 3. 5- 7 Attention has been recently drawn to syphilis as a possible etiology of acute and chronic uveitis of unknown etiology,3 as has the value of specific serologic testing in establishing this diagnosisa . 4 To our knowledge, this is the first report of active syphilis mimicking idiopathic orbital inflammation presenting with pain, proptosis, and lacrimal gland enlargement. We have recently seen another patient-a 24year- old female-with similar signs of ocular inflammation and previously undetected syphilis. We cannot state with certainty whether these inflammatory signs represent manifestations of active syphilis or coincident idiopathic orbital inflammation. Case 1 had negative serologies documented by the health department 3 years prior to our examination. It is reasonable to assume that he had been infected during that interval. Both patients responded rapidly to topical corticosteroids and intramuscular benzathine penicillin. Posterior orbital inflammation presenting as optic nerve perineuritis and uveitis has been reported by others.6 . 7 In view of the negative CSF studies and a prompt response to treatment, we believe our treatment was appropriate. Syphilitic optic neuritis has been recognized for many years,20. 21 and has been recently redescribed.." At a recent symposium/9 Weinstein, Newman, and Morgan described three cases of acute, unilateral optic neuritis as part of the meningeal inflammation accompanying secondary syphilis. 22 All three patients had acute disc swelling and visual loss. None had significant intraocular inflammation. Visual acuity usually improves after appropriate treatment with penicillin. When central nervous system involvement is documented by positive CSF serology, treatment consisting of 2-4 million units of intravenous aqueous penicillin every 4 hours for 8-10 days has been suggested.2 . 1 The older regiment for treatment of secondary and tertiary syphilis consisting of 2.4 million units of intramuscular benzathine penicillin once weekly for 3 weeks may result in inadequate levels of penicillin in the cerebrospinal fluid. 24 - 26 Syphilitic optic neuritis may accompany active secondary syphilis or occur during a Jarisch-Herxheimer reaction following penicillin treatment of primary syphilis. Cases 3 and 4 represent chorioretinitis that we attribute to syphilis. Case 3 had normal CSF serology, cytology, and chemistries, and would by September 1983 Spoor, Wynn, Hartel, Bryan TABLE 7. Characteristics of Ocular Findings Associated with Positive FTA-ABS: N = 26 Patients Percent Ages-32-74 years Chorioretinitis 8 30.8 Optic atrophy 11 423 Meningioma 1 3.8 Chromophobe adenoma 1 3.8 Normal examination 5 19.3 VORL + Serum 18/26 69.2 CSF 3/8 37.5 definition have latent syphilis except for his chorioretinitis. Case 4 had reactive CSF serology, pleocytosis, and elevated protein, documenting active neurosyphilis with chorioretinitis. We believe that ocular involvement by late syphilis may occur with or without abnormal CSF findings and must be diagnosed based upon suspicion and a reactive FTA-ABS test. We elected to treat case 3 with high-dose intravenous penicillin in spite of his negative CSF serology due to the proximity of his chorioretinitis to his macula, and his young age. Table 7 describes the ocular findings associated with positive FTA-ABS tests in 26 additional patients ages 43-74 years. We designate these patients as having "chronic syphilis," diagnosed by suspicion and positive FTA-ABS testing. Chorioretinitis and optic atrophy are the most priminent ocular findings in these patients. Two of our patients had visual loss (Table 7), optic atrophy, and a reactive FTA-ABS test. They also had surgically treatable intracranial masses. Although acute and chronic syphilis are significant etiologies for visual loss, we believe that this should remain a diagnosis of exclusion. The diagnosis of neurosyphilis as the etiology for visual loss and optic atrophy should only be made after a negative neuroradiologic examination has ruled out a compressive mass lesion. Both optic atrophy (case 5) and chorioretinitis (cases 3 and 4) may be manifestations of active neurosyphilis requiring treatment with high-dose intravenous penicillin, rather than a residua of a chronic syphilitic infection. Although many of our patients (6/9) had nonreactive CSF serology, we believe the CSF should be examined for evidence of active neurosyphilis prior to treatment in those patients with ocular stigmata of syphilis and visual dysfunction. Approximately 30% of our patients with chorioretinitis or optic atrophy had nonreactive serum VORLs. This is in agreement with previously reported figures (Table 1).:1. H. llJ We again stress the limitations of nonspecific serologic testing such as VORL and RPR when evaluating a patient with suspected late syphilis. 201 Ocular Syphilis Syphilis is not only elusive diagnostically; however, recent reports make us wonder whether we can even properly treat it. Cohen et al. 26 described a patient with a 3-week course of intramuscular procaine penicillin (600,000 units/day) who continued to deteriorate neurologically and manifest clinical, serologic, and CSF evidence for active neurosyphilis. These authors suggested high-dose, intravenous penicillin for the treatment of neurosyphilis. Collart and Poitevin25 recently deduced that it was impossible to establish a standard treatment regimen for patients with syphilis due to variations in dividing time of the organisms and tissue levels of penicillin. Furthermore, they postulated that it may well be impossible to obtain bacteriologic sterilization in secondary, latent, and tertiary syphilis; and it is probably highly unlikely even in primary syphilis. Despite the standing and seemingly authoritative recommendations for therapy by (for example) the United States Public Health Service concerning treatment regimens for syphilis, it should be emphasized that no prospective, controlled studies have addressed the optimum dosage or duration or therapy for any form of this disease. Neurosyphilis poses a unique challenge for three reasons. First, penicillin G penetrates the blood/brain barrier only moderately well in the absence of intense, acute inflammation. Detectable levels are observed rarely after intramuscular benzathine penicillin G. In view of the general assumption that adequate CSF levels of antibiotics are necessary for treatment of infections of the central nervous system, high doses of penicillin would seem necessary. Second, the endpoint of therapy for neurosyphilis is difficult to evaluate, and the reversibility of many of the manifestations is debatable. Third, the different syndromes of neurosyphilis, including the syndromes of ocular syphilis, are sufficiently uncommon that only a massive, multicenter, prospective study could determine the efficacy of one or another regimen. Lacking results of such a study, our preference is to treat neurosyphilis, including the syndromes of ocular syphilis, with 20-24 million units of crystalline penicillin G daily for 10 days.24 The dose should be appropriately decreased in patients with renal impairment,27 since high-dose penicillin G in patients with renal insufficiency can lead to confusion, coma, and seizures. The question arises as to how to treat the patient with optic atrophy or chorioretinitis, a reactive serum FTA-ABS, and normal computed tomography and appropriate x-rays. If there are CSF abnormalities compatible with neurosyphilis, reactive VORL, pleocystosis, or elevated protein, treatment should consist of a full 10-day course of intravenous penicillin G 24 million units/day by continuous infusion. If the CSF is normal and the patient has been adequately treated previously, we recommend observation. If visual acuity or field deteriorate, and there is no other explanation, we suggest a full course of intravenous penicillin despite negative CSF studies. Syphilis remains with us and the ophthalmologist may be confronted with both acute and chronic disease presenting as visual dysfunction. We urge, as others have before US,28. 29 that syphilis be considered in evaluating recurrent or refractory iritis, chorioretinitis, disc swelling, visual loss with optic atrophy, and abnormal pupillary findings. We caution that syphilitic optic neuropathy, acute or chronic, should remain a diagnosis of exclusion in order to avoid missing a surgically amenable lesion. References 1. Sexually treasmitted disease statistical newsletter 1980; and selected veneral disease data. 2. Center for Disease Control, Atlanta, Georgia. Personal Communication. 3. Schlaegel, T.F., and Kao, S.F.: A review of 28 presumptive cases of syphilitic uveitis. Am. f. Ophthalmol. 93: 214, 1982. 4. O'connor, G.R.: An interesting case history. Proc. Bull. 2: 1, 1979. 5. Weinstein, J.M., lexow, S.s., Ho, P., and Spickards, A.: Acute syphilitic optic neuritis. Arch. Ophtha/mol. 99: 1392, 1981. 6. Kline, LB., and Jackson, W.B.: Syphilitic optic perineuritis and uveitis. In Neura-ophthalmology Focus, 1980. J.L Smith, Ed. Masson Publishing USA, New York, 1980, pp. 77-84. 7. Rush, J.A., and Ryna, E.J.: Syphilitic optic perineuritis. Am. f. Ophthalmol. 91: 404, 1981. 8. Holmes, K.K.: Syphilis. In Harrison's Principles of Internal Medicine, G.W. Thorn, RD. Adams, E. Braunwald, K.J, Isselbacher, and R.G. Petersdord, Eds. McGraw-Hill, New York, 1981, pp. 716-726. 9. Smith, J.L, and Israel, C.W.: Optic atrophy and neuro-syphilis. Annu. Rev. Med. 22: 103, 1971. 10. Harner, R.E., Smith, J,L, and Israel, C.W.: The FTAABS test in late syphilis: A serological study in 1,985 cases. f.AM.A. 203: 545, 1968. 11. Hooshmand, H., Escobar, M.R., and Kopf, S.W.: Neurosyphilis, a study of 241 patients. f.AM.A 219: 726,1972. 12. Schwartz, LK., and O'connor, R.: Secondary syphilis with iris papules. Am. f. Ophtha/mol. 90: 380, 1980. 13. Contreraa, F., and Pereda, J.: Congenital syphilis of the eye with lens involvement. Arch. Ophthalmol. 96: 1052, 1978. 14. Jordan, K., Marino, J., and Damast, M.: Bilateral oculomotor paralysis due to neurosyphilis. Ann. Neural. 3: 90, 1978. 15. Davis, D.G., and Smith, J,l.: Periodic alternating nystagmus. Am. f. Ophthalmol. 72: 757, 1971. 16. Smith, J,l.: Acute blindness in early syphilis. Arch. Ophtha/mol. 90: 256, 1973. 17. Crouch, E.R., and Goldberg, M.F.: Retinal periarteritis secondary to syphilis. Arch. Ophtha/mol. 93: 384,1975. Journal of Clinical Neuro-ophthalmology 18. Martin, N.F., and Fitzgerald, CR.: Cystoid macular edema as the primary sign of neurosyphilis. Am. f. Ophthalmol. 88: 28, 1979. 19. Walsh, T.B., and Hoyt, W.F. (Eds): Clinical NeuroOphthalmology. Williams & Wilkins, Baltimore, 1960, pp. 1551-1622. 20. Graveson, G.5.: Syphilitic optic neuritis. f. Neurol. Neurosurg. Psychiatry 13: 216, 1950. 21. Walsh, F.B.: Syphilis of the optic nerve. Trans Am. Acad. Ophthalmol. Otolaryngol. 60: 39, 1956. 22. Frank B. Walsh Society 14th Annual Meeting, February 19-20, 1982. 23. Tramont, E.C: Treponema pallidum (syphilis). In Principles and Practice of Infectious Diseases, B.L. Mandall, Ed. John Wiley & Sons, Inc., New York, 1979, p. 834. 24. Ducas, 1.. and Roosan, H.G.: Cerebrospinal fluid penicillin levels during therapy for latent syphilis. ].A.M.A. 246: 2583, 1981. September 1983 Spoor, Wynn, Hartel, Bryan 25. Collart, P., and Poitevim, M.: Is penicillin therapy always infallible in syphilis? f. Clin. Neuro-Ophthalmol. 2: 77, 1982. 26. Cohen, MS., Gibson, G., and Clarte, M.D.: Lisauer form of paretic neurosyphilis: Forgotten but not gone. Ann. Neurol. 11: 219,1982. 27. Bryan, CS., and Stone, W.].: "Comparable massive" penicillin G therapy in renal failure. Ann. Intern. Med. 82: 189, 1975. 28. Smith, j.L.: Spirochetes in Late Seronegative Syphilis, Penicillin Notwithstanding. Charles C Thomas Springfield, Illinois, 1969. 29. Smith j.L.: The current status of ocular syphilis. Surv. Ophthalmol. 14: 176, 1969. Write for reprints to: Thomas C Spoor, M.D., Department of Surgery, University of South Alabama Medical Center, 2451 Fillingim Street, Mobile, Alabama 36617. 203 |
