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Show Journal of Clinical Neuro- ophthalmology 9( 4): 229- 233, 1989. © 1989 Raven Press, Ltd., New York Herpes Zoster Ophthalmicus, Contralateral Hemiplegia, and Recurrent Ocular Toxoplasmosis in a Patient with Acquired Immune Deficiency Syndrome- Related Complex Sasikala Pillai, M. D., Muneera A. Mahmood, M. D., and Suresh R. Limaye, M. D. A 42- year- old man presented with herpes zoster ophthalmicus on the right side. He was found to have acquired immune deficiency syndrome- related complex. Two weeks later he developed toxoplasmic retinochoroiditis in the left eye. He also presented later with left hemiplegia, which was probably caused by herpes zoster arteritis. Nine months after the retinal lesion resolved he developed another area of toxoplasmic retinochoroiditis adjacent to the first lesion. Herpes zoster may be the first presentation of acquired immune deficiency syndrome- related complex in a young healthy individual. Ophthalmologists are encountering patients with acquired immune deficiency syndrome who may have multiple organisms as the cause for their ocular infections and this might pose a treatment dilemma. The combination of herpes zoster ophthalmicus and ocular toxoplasmosis in this patient makes this case unusual. Key Words: Acquired immune deficiency syndromeHerpes zoster ophthalmicus- Contralateral hemiplegia- Ocular toxoplasmosis. From the Department of Ophthalmology, D. C. General Hospital, Georgetown University Medical Center, Washington, ~ C., U. S. A. . Address correspondence and reprint requests to Dr. Sasikala Pillai at D. C. General Hospital, Ophthalmology ServICe, Rm. 3325, Core Bldg., 19th St. & Massachusetts Ave., S. E., Washington, D. C. 20003, U. S. A. 229 Acquired immune deficiency syndrome ( AIDS) is an infection caused by human T- celllymphotropic virus ( HTLV) and is characterized by a severe disturbance of cell- mediated immunity that leads to opportunistic infections in previously healthy individuals. The occurrence of systemic toxoplasmosis in AIDS is common, but only nine reports of ocular toxoplasmosis in AIDS have been published. We are presenting a patient diagnosed as having herpes zoster ophthalmicus and AIDSrelated complex ( ARC) who later developed recurrent ocular toxoplasmosis in the other eye. CASE REPORT On September 9, 1985, a 42- year- old man presented with a I- week history of painful vesicles on the right side of face and scalp. He gave a history of an upper respiratory tract infection with cough and a " rundown feeling" for 2 weeks. He had chicken pox during childhood. He admitted to occasional marijuana use and gave a history of one episode of homosexual activity at the age of 15 years, but also had many female sexual contacts. On initial examination the best corrected visual acuity was 00 20/ 20, as 20/ 20. There were small vesicular lesions in the distribution of the ophthalmic division of the fifth cranial nerve on the right side. There were conjunctival hyperemia and old keratitic precipitates on the same side. A clinical diagnosis of right herpes zoster ophthalmicus was made. Topical gentamicin drops were prescribed. He was also seen by the dermatologist who prescribed 60 mg prednisone daily for 5 days, reduced 230 S. PILLAI ET AL. thereafter by 5 mg daily. Three days later he presented with acute granulomatous anterior uveitis in the right eye and was prescribed 2% homatropine and 1% Pred Forte eyedrops four times daily. Two weeks after the initial presentation with herpes zoster ophthalmicus he complained of malaise and developed swelling of both knees. His visual acuity was 00 20/ 20 and OS 20/ 80. He now had granulomatous anterior uveitis in the left eye. There were 2+ cells in the vitreous with a peripheral necrotizing retinal lesion in the superior temporal quadrant of the retina and a small chorioretinal scar nasally; these findings were consistent with a clinical diagnosis of toxoplasmic retinochoroiditis. Oral prednisone was discontinued. Physical examination at this time revealed axillary and inguinal lymphadenopathy. Laboratory test results showed a corrected sedimentation rate of 27 ( normal 0- 10); white blood cell count ( WBC) was 4.1 x 103 . Fluorescent treponemaI antibodyabsorption reactive and microhemagglutination assay for antibodies to T. pallidum ( MHA- TP) were reactive; rapid plasma reagin nonreactive, fluorescent anti- nuclear antibody, and rheumatoid factor tests were negative. The patient had been treated for syphilis many years ago. Serum toxoplasmosis titer ( IgG immunofluorescent antibody) was 1: 3,192. The patient's serum was positive for HTLV III antibody by enzyme- linked immunosorbent assay and he had an abnormal helperto- suppressor T- lymphocyte subset ratio. He was anergic to cutaneous mumps and purified protein derivative ( PPO) injections. Radiologic examination of the chest showed changes that suggested emphysema in both lungs. He was treated with 150 mg Oaraprirn oral loading dose followed by 25 mg twice daily, 3 g Sulfadiazine loading dose followed by 1 g four times daily and 3 mg folinic acid once a week for 6 weeks. Topical use of 1% Pred Forte and 2% Homatropine was continued in 00 and started in OS. One week after commencing treatment the retinal lesion became flatter and pigmentation was noted at the edge of the lesion. Two months after his initial presentation he developed nerve fiber layer infarcts in both eyes ( Fig. 1). On November 15, 1985 he presented to the emergency room with left sided facial weakness and left hemiplegia. He was admitted to the hospital. A FIG. 1. OD showing nerve fiber layer infarcts in the retina. H20 AND OCULAR TOXOPLASMOSIS WITH ARC 231 cerebrospinal fluid tap showed protein 43 mgldl, glucose 47 mgldl, WBC 9/ mm3 , RBC 5/ mm3, differential 25% polymorphonuclear cells and 75% lymphocytes. Gram stain, India ink preparation, venereal disease reference test ( VORL) and routine cultures from the cerebrospinal fluid were negative. Because VORL was negative in cerebrospinal fluid, the neurologist felt that the patient did not require intravenous aqueous penicillin. Computed axial tomography ( CAT) scan of the brain was normal. T- Iymphocyte helper- to- suppressor ratio ( T41T8) was 0.43 ( normal 1.2- 8.8). Serum toxoplasmosis titer ( IgG immunofluorescent antibody) was 1: 16,384. Blood cultures were negative but urine cultures were positive for candida. The patient refused to have a carotid angiogram at this time. His clinical condition improved, and he was discharged from the hospital after 13 days. On February 27, 1986 he had 20/ 25 vision au. The toxoplasmic retinochoroiditis had resolved. Serum toxoplasmosis titer was negative. He still had some residual motor and sensory deficit on the left side. A carotid angiogram done 6 months after the onset of hemiplegia showed no abnormality. On October 1, 1986 a fluffy white 1V2 disc diameter retinal lesion was noted adjacent to the healed toxoplasma lesion in the superotemporal quadrant of the left eye. The vitreous reaction was moderate. Serum toxoplasmosis titer was 1: 16. Since the lesion looked clinically like toxoplasmosis he was again treated with daraprim, sulfonamides, and folinic acid. The repeat T4IT8 ratio was 0.14 ( normal 1.2- 3.8). After treatment the vitreous appeared less hazy and the retinal lesion had regressed, showing pigmentation. The ocular findings remained the same until the time of his death in March, 1987. He died from complications arising from Pneumocystis carinii pneumonia and atypical mycobacterial pulmonary infection. COMMENT AIDS patients are susceptible to a variety of opportunistic infections, which include Pneumocystis carinii pneumonia, candidiasis, cytomegalovirus infections, herpes simplex infections, hepatitis B virus infections, toxoplasmosis, cryptococcosis, and atypical mycobacterial infections ( 1). Cone and Schiffman ( 2) suggested that the development of herpes zoster ophthalmicus in a previously healthy individual indicated an immunologic aberration that could ultimately evolve into AIDS. Two of their four patients with herpes zoster had reduction in T- helper cells and a reversal of T- cell helper/ suppressor ratio. Sandor et aI. ( 3) evaluated 25 consecutive cases of herpes zoster ophthalmicus and identified a subgroup of persons distinguishable by the presence of AIDS risk factors in association with a diminished helper T- cell population and polyclonal elevation in gamma globulin. Cole et al. ( 4) described four cases of herpes zoster ophthalmicus in homosexual men; two of them had AIDS and two had ARC. In a prospective investigation of 54 consecutive cases of herpes zoster ophthalmicus, Sandor et aI. ( 5) found that over a 2- year period, 21% of the AIDS- risk subgroup developed AIDS. He suggested that systemic corticosteroids for treatment of herpes zoster ophthalmicus should be avoided in individuals with risk factors associated with AIDS. None of their patients showed any of the ocular manifestations associated with AIDS during the acute phase of herpes zoster ophthalmicus. During the 2V2- year followup one patient had necrotizing retinitis and died of central nervous system toxoplasmosis. Manifestations of herpes zoster encephalitis may appear between 1 week before and 8 weeks after the onset of the cutaneous eruption. Most cases occur within 2 weeks after the rash is seen ( 6). Laboratory findings in the cerebrospinal fluid include an increase in the leukocyte count, mostly mononuclear cells, and moderate elevations of protein. Mackenzie and colleagues ( 7) suggested that the virus spreads along the intracranial branches of the fifth nerve to the intracranial portions of the internal carotid artery, and to the first 2 cm of the middle cerebral artery, the first 3 cm of the anterior cerebral artery, and to the large arteries at the base of the brain. Hilt et aI. ( 8), in his review of patients with herpes zoster ophthalmicus and contralateral hemiparesis, found that although the neurological manifestations were usually monophasic, some patients had recurrent episodes of angiitis in the distribution of the middle cerebral artery. Segmental narrowing of the proximal middle cerebral, anterior cerebral, and distal internal carotid artery have been documented by Walker et aI. ( 9), Mackenzie et aI. ( 7), and Bourdette et al. ( 10). CAT scans have shown lesions consistent with infarction in the distribution of the middle cerebral artery ( 8,11). Postmortem examination has revealed fulminant vasculitis with viral particles in vascular smooth muscle cells, as shown by Linnemann and Alvira ( 12) and Doyle et aI. ( 13). The occurrence of systemic toxoplasmosis in patients with AIDS is quite common. However, there have been only nine reports of ocular toxoplasmosis in patients with AIDS ( Table 1). Our patient is unusual in that he presented with herpes zoster ophthalmicus and was diagnosed to have I Gill Neuro- ophthalmol, Vol. 9, No. 4, 1989 232 Reference Sandor et al. ( 5) Parke and Font ( 14) Schuman and Friedman ( 15) Boyer ( 16) Alonso et al. ( 17) Weiss et al. ( 1 B) Snider et al. ( 19) Friedman ( 20) S. PILLAI ET AL. TABLE 1. Findings in patients with AIDS and ocular toxoplasmosis Associated CNS Ocular Method conditions toxoplasmosis toxoplasmosis of diagnosis AIDS Encephalitis Necrotizing retinitis Unknown AIDS, cryptococcal Negative Unilateral acute After enucleation meningitis retinal necrosis: no scars Case no. 1 Brain abscess Unilateral After enucleation AIDS, retinochoroiditis: Pneumocystis no scars carinii pneumonia Case No, 2 Negative Unilateral Clinical features AIDS, retinochoroiditis Pneumocystis with healed carinii pneumonia pigmented lesions AIDS, Encephalitis Retinochoroiditis: After enucleation Cytomegalovi rus no scars AIDS Lesion in right Retinochoroiditis Vitreous cu Itu re basal ganglia initially Toxoplasma cysts in brain AIDS, Candida Negative Retinochoroiditis After enucleation initially: no scars AIDS Lesion in right Bilateral Vitreous culture basal ganglia retinochoroiditis AIDS, Pneumocystis Frontal abscess Retinochoroiditis: After enucleation carinii pneumonia initially no scars ARC He received oral prednisone ( 615 mg total dose) to prevent postherpetic neuralgia, While he was taking oral steroids he developed toxoplasmic retinochoroiditis in the other eye. Nozik and O'Conner ( 21) attempted to reactivate healed, experimentally induced toxoplasmic retinochoroiditis in the rabbit with systemically administered corticosteroids, and were unsuccessful. Kaufman ( 22) suggested that acute disseminated infection ( as in congenital toxoplasmosis) in the absence of effective immunity is made lethal by corticosteroids, but that the ocular disease of chronic toxoplasmosis does not exacerbate or become lethal with steroid therapy. Our patient developed hemiplegia, which was presumed to be due to viral cranial vasculitis. Since a carotid angiogram was not done during the acute phase it was not possible to confirm the diagnosis. After that time he developed nerve fiber layer infarcts in both eyes and reactivation of toxoplasmosic retinochoroiditis in the left eye. The most recent serum toxoplasmosis titer was only 1: 16, which may indicate further worsening of his immune deficiency. Although his Tlymphocyte helper- to- suppressor ratio decreased further, he remained free from opportunistic infections associated with AIDS until the time of his death in March 1987. The possibility of AIDS or ARC should be considered in young patients who present with herpes zoster ophthalmicus. Ocular toxoplasmo<; i~ is h':' ing mnre lrequently reported in patients with ARC or AIDS. J Clin NeUflO · ophlh"/;" tli. Vol 4. No. 4. 1989 REFERENCES 1. Centers for Disease Control: Update on AIDS- United States. Morbid Mortal Weekly Rep 1982; 31: 507- 514. 2. Cone LA. Schiffman MA. Herpes zoster and the acquired immune deficiency syndrome. Ann Intern Med 1984; 100: 462. 3. Sandor E. Croxson TS. Millman A. et aL Herpes zoster ophthalmicus in patients at risk for AIDS. N Engl J Med 1984; 310: 111&- 1119. 4. Cole LE, Meisler OM, Calabrese LH, et aL Herpes zoster ophthalmicus and AIDS. Arch Ophthalmol 1984; 102: 10271029. 5. Sandor EV, Millman A, Croxson TS, et aL Herpes zoster ophthalmicus in patients at risk for AIDS. Am J Ophthalmol 1986; 101: 153- 155. 6 Appelbaum E, Kreps SI, Sunshine A. Herpes zoster encephalitis. Am J Med 1962; 32: 25- 31. 7. Mackenzie RA. Forbes GS, Karnes WE. Angiographic findings in herpes zoster arteritis. Ann NeuroI1981; 10: 458- 464. 8. Hilt DC, Buchholz 0, Krumholz A, et aL Herpes zoster ophthalmicus and delayed contralateral hemiparesis caused by cerebral angiitis: diagnosis and management approaches. A, m Neurol 1983; 14: 543- 553. 9. Walker RJ, Gammal TE, Allen MB. Cranial arteritis associated with herpes zoster. Radiology 1973; 107: 109- 110. IO Bourdette ON, Rosenberg NL, Yatsu FM. Herpes zoster ophthalmicus and delayed ipsilateral cerebral infarction. Neurology 1983; 33: 142&- 1432. 11. Menkes DB, Samir BN, Corbett AJ. Hemispheric infarction after herpes zoster ophthalmicus. J Neurol Neurosurg Psychiatrv 1983; 46: 786- 788. 12. Linn~ mann CC, Alvira MM. Pathogenesis of varicellazoster angiitis in the central nervous system. Arch Neurol 1980; 37: 239- 240. 13. Doyle PW, Gibson G, Dolman CL. Herpes zoster ophthalmicus with contralateral hemiplegia: identification of cause. All/! NeuroI1983; 14: 84- 85. 14. Parke OW, Font RL. Diffuse toxoplasmic retinochoroiditis in a patient with AIDS. Arch Ophthalmol 1986; 104: 571- 575. 15. Schuman jS, Friedman AH. Retinal manifestations of the AIDS: cytomegalovirus, Candida albicans, Cryptococcus, Tox- H20 AND OCULAR TOXOPLASMOSIS WITH ARC 233 oplasffiosis and Pnellmocystis carini;. Trails 0I'I, tllal"", 1 Soc UK 1983; 103: 177- 190. 16. Boyer OS. Discussion of AIDS: ocular manifestations: Ophthalmology 1983; 90: 872-- 873. 17. Alonso R, Heiman- Patterson T, Mancall EL. Cerebraltoxoplasmosis in acquired immune deficiency syndrome. Arch Neurol 19& 1; 41: 321- 323. 18. Weiss A. Margo CE, Ledford OK. et al. Toxoplasmic retinochoroiditis as an initial manifestation of the acquired immune deficiency syndrome. Am / 0l'htJIll/"", 1 1986; 101: 24S- 249 .. 19. Snider WD, Simpson OM, Nielsen SL, et al. Neurologic complications of acquired immune deficiency syndrome. Analysis of 50 patients. Ann Neurol 1983; 14: 403- 418. 20. Friedman AH. Retinal lesions in the acquired immune deficiency syndrome. Trans Am Ophthalmol Soc 1984; 82: 447491. 21. Nozik RA, O'Connor RG. Studies on experimental ocular toxoplasmosis in the rabbit. Arch Ophthalmol 1979; 84: 78S791. 22. Kaufman HE. The effect of corticosteroids on experimental ocular toxoplasmosis. Am I Ophtha/ mol 1960; 50: 919- 925. / elin Neu",- ophthalmol, Vol. 9, No. 4, 1989 |
