- Email: [email protected]
Ocular involvement in patients infected by the West Nile virus
PUBLIC HEALTH
Ocular involvement in patients infected by the West Nile virus Steven B. Koevary, Ph.D.
The New England College of Optometry, Department of Biomedical Sciences and Disease, Boston, Massachusetts
West Nile virus (WNV), a mosquito-borne RNA virus for which there is no treatment, began emerging as a threat to health in the United States in 1999. Since then, its frequency and apparent clinical severity have increased. Patients with severe disease may experience ocular complications that include pain, vitreous inflammation, nonrelapsing chorioretinitis, retinal vasculitis, chorioretinal scarring, optic neuritis, and retinal hemorrhages. Age appears to be a risk factor for the development of ocular symptoms. Most patients with ocular involvement report floaters or decreased vision. Many ocular inflammatory conditions with an associated underlying systemic cause often present with chorioretinitis. However, the characteristic distribution and linear array or scattered pattern of the chorioretinal lesions seen in WNV is distinctive. The foregoing notwithstanding, other multifocal choroidopathies must be considered including syphilis, ocular histoplasmosis, multifocal choroiditis, tuberculosis, and sarcoid. Although topical steroids were reported to resolve WNV-induced uveitis and its associated keratic precipitates, most cases resolved irrespective of treatment, and relapses were uncommon. It is important for the eye care professional to be alert to the possible presence of WNV, particularly in older patients who present with ocular symptoms during mosquito season. Thus, a thorough ocular evaluation should include a dilated fundus examination and, when indicated, fluorescein angiography should be performed in patients suspected of being infected with WNV. Key Words: West Nile virus, Centers for Disease Control, vitreous inflammation, nonrelapsing chorioretinitis, chorioretinal lesions, retinal vasculitis, optic neuritis, retinal hemorrhages
Koevary, SB. Ocular involvement in patients infected by the West Nile virus. Optometry 2005;76:609-12.
Epidemiology West Nile virus (WNV) is a mosquito-borne single-stranded RNA flavivirus, belonging to the Japanese encephalitis virus antigenic complex, which was first isolated and identified in 1937 in the blood of a febrile woman who lived in the West Nile district of Uganda.1 Until recently, this disease-causing pathogen was found nearly exclusively in the Eastern Hemisphere, with a notable presence in West Asia, Africa, and the Middle East.2 In 1957, it was the cause of an outbreak of human meningoencephalitis in Israel and was first recognized as the causative agent in equine disease in the early 1960s.3 Since its emergence in North America in 1999, it has steadily expanded its movement westward to California and southward into the Caribbean.4,5 Of concern to public health officials is the fact that in the last decade, the frequency and apparent clinical severity of WNV outbreaks have increased, with some patients now experiencing severe neurologic disease and vision loss. The total number of symptomatic patients with WNV infection as reported to the Centers for Disease Control (CDC), the number of states affected, and some other clinical data, are shown in Table 1. Interestingly, the number of WNV cases decreased last year for the first time in 5 years, from its high of nearly 10,000 in 2003, possibly owing to more public awareness regarding its transmission. The principal vectors for the WNV are mosquitoes from the genus Culex, with wild birds, particularly crows, acting as the amplifying hosts,3,6 as evidenced by the initial human epidemic in New York City in 1999.4 The peak incidence of human disease in North America occurs in late August and early September. Infected hosts were reported to transmit WNV transplacentally, by transfusion, 609
VOLUME 76 / NUMBER 10 / OCTOBER 2005
OPTOMETRY
PUBLIC HEALTH
Table 1. West Nile virus activity in the United States in 2004 as reported by the CDC Number of states affected
Neuroinvasive disease
40
900
Fever
Other clinical/ unspecified
Total cases reported to the CDC
Deaths
1,017
553
2,470
88
and by organ transplantation.7 Currently, there is no established treatment for WNV infection. The CDC recommends the following advice for reducing the chances of being bitten by a mosquito carrying WNV: 1. apply insect repellent containing DEET; 2. when possible, wear long sleeves, long pants, and socks when outdoors; 3. avoid outdoor activities from dusk to dawn, which are peak mosquito-biting times for many species of mosquitoes; and 4. install or repair screens to keep mosquitoes out of your home.
Clinical Manifestations Systemic Most individuals who become infected with the WNV remain asymptomatic. Thus, as reported by the CDC, in previous outbreaks in the Northern Hemisphere, an estimated 80% of people who became infected never had symptoms attributable to the infection. Like many other viruses, the incubation time in humans for WNV ranges between 2 and 14 days. The clinical features of the disease itself, termed West Nile fever, are fever, headache, fatigue, and, in more severe cases, skin rash and retro-orbital pain. Symptoms, which usually have a rapid and sudden onset, last about a week.8,9 Severe disease, which occurs in a small percentage of patients, is characterized by central nervous system (CNS) symptoms that take the form of West Nile meningitis, encephalitis, or poliomyelitis. Patients may experience a stiff neck, altered mental state, flaccid paralysis, ataxia, Guillain-Barre syndrome, or cranial nerve palsies. Patients with CNS involvement show cerebrospinal fluid (CSF) pleocytosis and increased protein levels.8 Hepatitis, pancreatitis, and myocarditis can also complicate the illness.10 By far, the patients that are most susceptible to encephalitis and death are the elderly4,10; there have not been many reported cases of illness in children, although of the 4 recent cases reported, 1 did have ocular involvement.11 A diagnosis of WNV is deter-
mined by serologic testing for the presence of specific IgM in the CSF and serum using an enzyme-linked immunosorbent assay (ELISA) kit12 and by polymerase chain reaction (PCR), which is an in vitro technique that can be used to rapidly synthesize large quantities of, in this case, viral genome.
Ocular Patients with severe disease may experience ocular complications that include vitreous inflammation, nonrelapsing chorioretinitis, retinal vasculitis, chorioretinal scarring, optic neuritis, and retinal hemorrhages.13-17 Age appears to be a risk factor for ocular signs of WNV, and one study in which 14 cases were reviewed reported that 5 patients with WNV-associated chorioretinitis had diabetes mellitus.18 Most patients with ocular involvement report floaters or decreased vision. Many ocular inflammatory conditions with an associated underlying systemic cause often present with chorioretinitis. However, the characteristic distribution and linear array or scattered pattern of the chorioretinal lesions seen in WNV is distinctive.19 This unique pattern of multifocal chorioretinal lesions in patients with systemic symptoms was suggested as a means of establishing a diagnosis of WNV while serologic testing is pending.19 However, other multifocal choroidopathies must be considered including syphilis, ocular histoplasmosis, multifocal choroiditis, tuberculosis, and sarcoid. Patients have generally presented with floaters or clouded vision, in addition to other systemic symptoms, and ocular findings were unilateral or bilateral and included conjunctivitis, uveitis, and nongranulomatous lesions.7 Vasculopathy in the form of retinal vasculitis can accompany the intraocular inflammation or may be present with meningoencephalitis. Many patients also complained of ocular pain. While topical steroids were reported to resolve the uveitis and
610 OPTOMETRY
VOLUME 76 / NUMBER 10 / OCTOBER 2005
PUBLIC HEALTH
Table 2. Ocular and visual findings in 8 patients with WNV Study
Sex
Age
Ocular and visual findings
Vandenbelt et al.22
M
64
Adelman et al.23
M
81
Adelman et al.14
F
62
Hershberger et al.16
F
61
Hershberger et al.16
M
56
Kuchtey et al.15
F*
56
Anninger et al.13
F
55
Kaiser et al.17
F*
46
Blurred vision, floaters, flare, prepapillary vitritis, chorioretinal lesions Reduced visual acuity, vitreous cells, chorioretinal lesions Reduced visual acuity, floaters, vitreous cells, keratic precipitates, chorioretinal lesions, intraretinal hemorrhages Blurred vision, anterior chamber cells and flare, chorioretinal lesions Decreased visual acuity, floaters, anterior chamber cells and flare, vitreous cells, mild disc edema, chorioretinal lesions Reduced visual acuity, iritis, vitreitis, trace conjunctival hyperemia, keratic precipitates, moderate anterior chamber and vitreous inflammation, inferior arcuate visual field defect Reduced visual acuity, chorioretinal lesions, optic neuritis, reduced color vision, keratic precipitates, vitreous cells, diffuse visual field depression Retinal artery occlusions, retinal edema, capillary nonperfusion
* Patients had preexisting nonproliferative diabetic retinopathy.
associated keratic precipitates, most cases resolved irrespective of treatment7,20 and relapses were uncommon. It has been noted that patients with ocular symptoms did not have flaccid paralysis. However, because it is difficult to assess vision in severely ill individuals, it is not clear whether other nonparalytic patients had vision loss. 7 Optic neuritis is also observed in patients with WNV, and increased intracranial pressure from meningoencephalitis could result in papilledema. A summary of the ocular symptoms in 8 recently reported cases of WNV appears in Table 2. In a representative case of WNV infection with ocular complications, Hershberger et al.16 reported the case of a 61-year-old woman who had a headache, high fever, anorexia, profound generalized weakness, and difficulty performing fine motor movements. As is most typical in these patients, she developed ocular symptoms in addition to a skin rash almost a week after the onset of her presenting symptoms. In her case, ocular symptoms took the form of cells and flare in the anterior chamber and vitreous in the right eye, and multiple creamy to partially atrophic nummular chorioretinal lesions in both eyes. The differential diagnosis in this case included
multifocal choroiditis, birdshot choroiditis, and atypical primary vitreoretinal lymphoma. These physicians referred the patient to ocular oncology for further evaluation after placing her on topical prednisone. At the time of her oncology followup, which took place 3 weeks later, she was still experiencing headaches, weakness, anorexia, and visual blurring. Results of slit lamp biomicroscopy showed cells and flare as well as multiple deep chorioretinal lesions (see Figure 1). The patient’s systemic and ocular symptoms resolved completely over the ensuing 2 to 3 weeks. Examination of the patient after 4 months found the presence of mildly increased pigmentation in her chorioretinal lesions, with complete resolution of her other ocular findings. There has been only one report of intrauterine transmission of WNV,21 as alluded to above. In that case, the mother, a 20-year-old AfricanAmerican woman, had WNV 2 months before delivery of a full-term infant girl. The neonate’s blood tested positive for WNV, and, interestingly, she exhibited a large chorioretinal scar involving the macula in her right eye and granularity but no frank chorioretinal scarring in the macula of her left eye. She also displayed mild 611
VOLUME 76 / NUMBER 10 / OCTOBER 2005
OPTOMETRY
PUBLIC HEALTH
Figure 1
Arteriovenous phase of the fluorescein angiogram of the right eye of a 61-year-old woman infected with the WNV. Note the presence of chorioretinal lesions with central hypofluorescence and peripheral hyperfluorescence. (Reprinted with permission from Hershberger et al.16)
chorioretinal scarring in the far temporal periphery of her left eye.
Summary Whereas ocular complications only appear to affect older individuals with severe WNV, the number of such patients will likely increase over time, because this disease, which first appeared on the east coast in 1999 and has since extended to the Pacific, continues to advance. Epidemiologists predict that WNV will become epidemic and cause annual outbreaks in the foreseeable future.7 The eye care professional should be alert to the possible presence of WNV, particularly in older patients who present with ocular symptoms during mosquito season. Thus, a thorough ocular evaluation should include a dilated fundus examination and, when indicated, fluorescein angiography in patients suspected of being infected with WNV.19
References 1. Smithburn KC, Hughes TP, Burkw AW, et al. A neurotropic virus isolated from blood of a native Ugandan. Am J Trop Med Hyg 1940;20:37-43. 2. Guharoy R, Gilroy SA, Noviasky JA, et al. West Nile virus infection. Am J Health-Syst Pharm 2004;61:1235-41. 3. Brown D, Lloyd G. Zoonotic viruses. In: Cohen J and Powderly WG, eds. Infectious Diseases, 2nd ed. Edinburgh: Mosby, 2004:2098-9. 4. Nash D, Mostashari F, Fine A, et al. The outbreak of West Nile infection in the New York City area in 1999. N Engl J Med 2001;344:1807-14.
5. Marfin AA, Gubler DJ. West Nile encephalitis in the United States. Clin Infect Dis 2001;33:1713-9. 6. Mitchell CJ. Arthropod vector and vertebrate associations of West Nile virus. In: Morilla A, Yoon K-J, Zimmerman JJ, eds. Trends in emerging viral diseases of swine. Ames, Iowa State University Press, 2002:269-79. 7. Granwehr BP, Lillibridge KM, Higgs S, et al. West Nile virus: where are we now? Lancet Infect Dis 2004;4:547-56. 8. Tsai TF, Khan AS, McJunkin JE. Togaviridae, Flaviviridae, and Bunyaviridae. In: Long, ed. Principles and practice of pediatric infectious diseases, 2nd ed, New York: Churchill Livingstone, 2003:1111. 9. Garg S, Jampol LM. Systemic and intraocular manifestations of West Nile virus infection. Surv Ophthalmol 2005;50:3-13. 10. Craven RB, Roehrig JT. West Nile virus. JAMA 2001; 286:651-3. 11. Yim R, Posfay-Barbe KM, Nolt D, et al. Spectrum of clinical manifestations of West Nile virus infection in children. Pediatrics 2004;114:1673-5. 12. Petersen LR, Marfin AA. West Nile virus: a primer for the clinician. Ann Intern Med 2002;137:173-9. 13. Anninger WV, Lomeo MD, Dingle J, et al. West Nile virus-associated optic neuritis and chorioretinitis. Am J Opthalmol 2002;136:1183-5. 14. Adelman HS, Jampol LM, Caughron MC, et al. Vitritis and chorioretinitis in a patient with West Nile virus infection. Arch Opthhalmol 2003;121:205-7. 15. Kuchtey RW, Kosmorsky GS, Martin D, et al. Uveitis associated with West Nile virus infection. Arch Opthalmol 2003;121:1648-9. 16. Hershberger VS, Augsburger JJ, Hutchins RK, et al. Chorioretinal lesions in nonfatal cases of West Nile virus infection. Opthalmology 2003;110:1732-6. 17. Kaiser PK, Lee MS, Martin DA. Occlusive vasculitis in a patient with concomitant West Nile virus infection. Am J Opthalmol 2003;136:928-30. 18. Nash D, Mostashari F, Fine A, et al. Outbreak of the West Nile virus in the New York City area in 1999. N Eng J Med 2001;344: 1807-14. 19. Khairallah M, Yahia SB, Ladjimi A, et al. Chorioretinal involvement in patients with West Nile virus infection. Ophthalmology 2004;111:2065-70. 20. Bakri SJ, Kaiser PK. Ocular manifestations of West Nile virus. Curr Opinion Ophthalmol 2004;15:537-40. 21. Alpert SG, Fergerson J, Noel L-P. Intrauterine West Nile virus: ocular and systemic findings. Am J Ophthalmol 2003;136:733-5. 22. Vandenbelt S, Shaikh S, Capone A Jr, et al. Multifocal choroiditis associated with West Nile virus encephalitis. Retina 2003;23:97-9. 23. Adelman R, Membreno JH, Afshari NA, et al. West Nile chorioretinitis. Retina 2003;23:100-1.
Corresponding author: Steven B. Koevary, Ph.D. The New England College of Optometry Department of Biomedical Sciences and Disease 424 Beacon Street Boston, Massachusetts 02459 [email protected]
612 OPTOMETRY
VOLUME 76 / NUMBER 10 / OCTOBER 2005
Ocular involvement in patients infected by the West Nile virus Steven B. Koevary, Ph.D.
The New England College of Optometry, Department of Biomedical Sciences and Disease, Boston, Massachusetts
West Nile virus (WNV), a mosquito-borne RNA virus for which there is no treatment, began emerging as a threat to health in the United States in 1999. Since then, its frequency and apparent clinical severity have increased. Patients with severe disease may experience ocular complications that include pain, vitreous inflammation, nonrelapsing chorioretinitis, retinal vasculitis, chorioretinal scarring, optic neuritis, and retinal hemorrhages. Age appears to be a risk factor for the development of ocular symptoms. Most patients with ocular involvement report floaters or decreased vision. Many ocular inflammatory conditions with an associated underlying systemic cause often present with chorioretinitis. However, the characteristic distribution and linear array or scattered pattern of the chorioretinal lesions seen in WNV is distinctive. The foregoing notwithstanding, other multifocal choroidopathies must be considered including syphilis, ocular histoplasmosis, multifocal choroiditis, tuberculosis, and sarcoid. Although topical steroids were reported to resolve WNV-induced uveitis and its associated keratic precipitates, most cases resolved irrespective of treatment, and relapses were uncommon. It is important for the eye care professional to be alert to the possible presence of WNV, particularly in older patients who present with ocular symptoms during mosquito season. Thus, a thorough ocular evaluation should include a dilated fundus examination and, when indicated, fluorescein angiography should be performed in patients suspected of being infected with WNV. Key Words: West Nile virus, Centers for Disease Control, vitreous inflammation, nonrelapsing chorioretinitis, chorioretinal lesions, retinal vasculitis, optic neuritis, retinal hemorrhages
Koevary, SB. Ocular involvement in patients infected by the West Nile virus. Optometry 2005;76:609-12.
Epidemiology West Nile virus (WNV) is a mosquito-borne single-stranded RNA flavivirus, belonging to the Japanese encephalitis virus antigenic complex, which was first isolated and identified in 1937 in the blood of a febrile woman who lived in the West Nile district of Uganda.1 Until recently, this disease-causing pathogen was found nearly exclusively in the Eastern Hemisphere, with a notable presence in West Asia, Africa, and the Middle East.2 In 1957, it was the cause of an outbreak of human meningoencephalitis in Israel and was first recognized as the causative agent in equine disease in the early 1960s.3 Since its emergence in North America in 1999, it has steadily expanded its movement westward to California and southward into the Caribbean.4,5 Of concern to public health officials is the fact that in the last decade, the frequency and apparent clinical severity of WNV outbreaks have increased, with some patients now experiencing severe neurologic disease and vision loss. The total number of symptomatic patients with WNV infection as reported to the Centers for Disease Control (CDC), the number of states affected, and some other clinical data, are shown in Table 1. Interestingly, the number of WNV cases decreased last year for the first time in 5 years, from its high of nearly 10,000 in 2003, possibly owing to more public awareness regarding its transmission. The principal vectors for the WNV are mosquitoes from the genus Culex, with wild birds, particularly crows, acting as the amplifying hosts,3,6 as evidenced by the initial human epidemic in New York City in 1999.4 The peak incidence of human disease in North America occurs in late August and early September. Infected hosts were reported to transmit WNV transplacentally, by transfusion, 609
VOLUME 76 / NUMBER 10 / OCTOBER 2005
OPTOMETRY
PUBLIC HEALTH
Table 1. West Nile virus activity in the United States in 2004 as reported by the CDC Number of states affected
Neuroinvasive disease
40
900
Fever
Other clinical/ unspecified
Total cases reported to the CDC
Deaths
1,017
553
2,470
88
and by organ transplantation.7 Currently, there is no established treatment for WNV infection. The CDC recommends the following advice for reducing the chances of being bitten by a mosquito carrying WNV: 1. apply insect repellent containing DEET; 2. when possible, wear long sleeves, long pants, and socks when outdoors; 3. avoid outdoor activities from dusk to dawn, which are peak mosquito-biting times for many species of mosquitoes; and 4. install or repair screens to keep mosquitoes out of your home.
Clinical Manifestations Systemic Most individuals who become infected with the WNV remain asymptomatic. Thus, as reported by the CDC, in previous outbreaks in the Northern Hemisphere, an estimated 80% of people who became infected never had symptoms attributable to the infection. Like many other viruses, the incubation time in humans for WNV ranges between 2 and 14 days. The clinical features of the disease itself, termed West Nile fever, are fever, headache, fatigue, and, in more severe cases, skin rash and retro-orbital pain. Symptoms, which usually have a rapid and sudden onset, last about a week.8,9 Severe disease, which occurs in a small percentage of patients, is characterized by central nervous system (CNS) symptoms that take the form of West Nile meningitis, encephalitis, or poliomyelitis. Patients may experience a stiff neck, altered mental state, flaccid paralysis, ataxia, Guillain-Barre syndrome, or cranial nerve palsies. Patients with CNS involvement show cerebrospinal fluid (CSF) pleocytosis and increased protein levels.8 Hepatitis, pancreatitis, and myocarditis can also complicate the illness.10 By far, the patients that are most susceptible to encephalitis and death are the elderly4,10; there have not been many reported cases of illness in children, although of the 4 recent cases reported, 1 did have ocular involvement.11 A diagnosis of WNV is deter-
mined by serologic testing for the presence of specific IgM in the CSF and serum using an enzyme-linked immunosorbent assay (ELISA) kit12 and by polymerase chain reaction (PCR), which is an in vitro technique that can be used to rapidly synthesize large quantities of, in this case, viral genome.
Ocular Patients with severe disease may experience ocular complications that include vitreous inflammation, nonrelapsing chorioretinitis, retinal vasculitis, chorioretinal scarring, optic neuritis, and retinal hemorrhages.13-17 Age appears to be a risk factor for ocular signs of WNV, and one study in which 14 cases were reviewed reported that 5 patients with WNV-associated chorioretinitis had diabetes mellitus.18 Most patients with ocular involvement report floaters or decreased vision. Many ocular inflammatory conditions with an associated underlying systemic cause often present with chorioretinitis. However, the characteristic distribution and linear array or scattered pattern of the chorioretinal lesions seen in WNV is distinctive.19 This unique pattern of multifocal chorioretinal lesions in patients with systemic symptoms was suggested as a means of establishing a diagnosis of WNV while serologic testing is pending.19 However, other multifocal choroidopathies must be considered including syphilis, ocular histoplasmosis, multifocal choroiditis, tuberculosis, and sarcoid. Patients have generally presented with floaters or clouded vision, in addition to other systemic symptoms, and ocular findings were unilateral or bilateral and included conjunctivitis, uveitis, and nongranulomatous lesions.7 Vasculopathy in the form of retinal vasculitis can accompany the intraocular inflammation or may be present with meningoencephalitis. Many patients also complained of ocular pain. While topical steroids were reported to resolve the uveitis and
610 OPTOMETRY
VOLUME 76 / NUMBER 10 / OCTOBER 2005
PUBLIC HEALTH
Table 2. Ocular and visual findings in 8 patients with WNV Study
Sex
Age
Ocular and visual findings
Vandenbelt et al.22
M
64
Adelman et al.23
M
81
Adelman et al.14
F
62
Hershberger et al.16
F
61
Hershberger et al.16
M
56
Kuchtey et al.15
F*
56
Anninger et al.13
F
55
Kaiser et al.17
F*
46
Blurred vision, floaters, flare, prepapillary vitritis, chorioretinal lesions Reduced visual acuity, vitreous cells, chorioretinal lesions Reduced visual acuity, floaters, vitreous cells, keratic precipitates, chorioretinal lesions, intraretinal hemorrhages Blurred vision, anterior chamber cells and flare, chorioretinal lesions Decreased visual acuity, floaters, anterior chamber cells and flare, vitreous cells, mild disc edema, chorioretinal lesions Reduced visual acuity, iritis, vitreitis, trace conjunctival hyperemia, keratic precipitates, moderate anterior chamber and vitreous inflammation, inferior arcuate visual field defect Reduced visual acuity, chorioretinal lesions, optic neuritis, reduced color vision, keratic precipitates, vitreous cells, diffuse visual field depression Retinal artery occlusions, retinal edema, capillary nonperfusion
* Patients had preexisting nonproliferative diabetic retinopathy.
associated keratic precipitates, most cases resolved irrespective of treatment7,20 and relapses were uncommon. It has been noted that patients with ocular symptoms did not have flaccid paralysis. However, because it is difficult to assess vision in severely ill individuals, it is not clear whether other nonparalytic patients had vision loss. 7 Optic neuritis is also observed in patients with WNV, and increased intracranial pressure from meningoencephalitis could result in papilledema. A summary of the ocular symptoms in 8 recently reported cases of WNV appears in Table 2. In a representative case of WNV infection with ocular complications, Hershberger et al.16 reported the case of a 61-year-old woman who had a headache, high fever, anorexia, profound generalized weakness, and difficulty performing fine motor movements. As is most typical in these patients, she developed ocular symptoms in addition to a skin rash almost a week after the onset of her presenting symptoms. In her case, ocular symptoms took the form of cells and flare in the anterior chamber and vitreous in the right eye, and multiple creamy to partially atrophic nummular chorioretinal lesions in both eyes. The differential diagnosis in this case included
multifocal choroiditis, birdshot choroiditis, and atypical primary vitreoretinal lymphoma. These physicians referred the patient to ocular oncology for further evaluation after placing her on topical prednisone. At the time of her oncology followup, which took place 3 weeks later, she was still experiencing headaches, weakness, anorexia, and visual blurring. Results of slit lamp biomicroscopy showed cells and flare as well as multiple deep chorioretinal lesions (see Figure 1). The patient’s systemic and ocular symptoms resolved completely over the ensuing 2 to 3 weeks. Examination of the patient after 4 months found the presence of mildly increased pigmentation in her chorioretinal lesions, with complete resolution of her other ocular findings. There has been only one report of intrauterine transmission of WNV,21 as alluded to above. In that case, the mother, a 20-year-old AfricanAmerican woman, had WNV 2 months before delivery of a full-term infant girl. The neonate’s blood tested positive for WNV, and, interestingly, she exhibited a large chorioretinal scar involving the macula in her right eye and granularity but no frank chorioretinal scarring in the macula of her left eye. She also displayed mild 611
VOLUME 76 / NUMBER 10 / OCTOBER 2005
OPTOMETRY
PUBLIC HEALTH
Figure 1
Arteriovenous phase of the fluorescein angiogram of the right eye of a 61-year-old woman infected with the WNV. Note the presence of chorioretinal lesions with central hypofluorescence and peripheral hyperfluorescence. (Reprinted with permission from Hershberger et al.16)
chorioretinal scarring in the far temporal periphery of her left eye.
Summary Whereas ocular complications only appear to affect older individuals with severe WNV, the number of such patients will likely increase over time, because this disease, which first appeared on the east coast in 1999 and has since extended to the Pacific, continues to advance. Epidemiologists predict that WNV will become epidemic and cause annual outbreaks in the foreseeable future.7 The eye care professional should be alert to the possible presence of WNV, particularly in older patients who present with ocular symptoms during mosquito season. Thus, a thorough ocular evaluation should include a dilated fundus examination and, when indicated, fluorescein angiography in patients suspected of being infected with WNV.19
References 1. Smithburn KC, Hughes TP, Burkw AW, et al. A neurotropic virus isolated from blood of a native Ugandan. Am J Trop Med Hyg 1940;20:37-43. 2. Guharoy R, Gilroy SA, Noviasky JA, et al. West Nile virus infection. Am J Health-Syst Pharm 2004;61:1235-41. 3. Brown D, Lloyd G. Zoonotic viruses. In: Cohen J and Powderly WG, eds. Infectious Diseases, 2nd ed. Edinburgh: Mosby, 2004:2098-9. 4. Nash D, Mostashari F, Fine A, et al. The outbreak of West Nile infection in the New York City area in 1999. N Engl J Med 2001;344:1807-14.
5. Marfin AA, Gubler DJ. West Nile encephalitis in the United States. Clin Infect Dis 2001;33:1713-9. 6. Mitchell CJ. Arthropod vector and vertebrate associations of West Nile virus. In: Morilla A, Yoon K-J, Zimmerman JJ, eds. Trends in emerging viral diseases of swine. Ames, Iowa State University Press, 2002:269-79. 7. Granwehr BP, Lillibridge KM, Higgs S, et al. West Nile virus: where are we now? Lancet Infect Dis 2004;4:547-56. 8. Tsai TF, Khan AS, McJunkin JE. Togaviridae, Flaviviridae, and Bunyaviridae. In: Long, ed. Principles and practice of pediatric infectious diseases, 2nd ed, New York: Churchill Livingstone, 2003:1111. 9. Garg S, Jampol LM. Systemic and intraocular manifestations of West Nile virus infection. Surv Ophthalmol 2005;50:3-13. 10. Craven RB, Roehrig JT. West Nile virus. JAMA 2001; 286:651-3. 11. Yim R, Posfay-Barbe KM, Nolt D, et al. Spectrum of clinical manifestations of West Nile virus infection in children. Pediatrics 2004;114:1673-5. 12. Petersen LR, Marfin AA. West Nile virus: a primer for the clinician. Ann Intern Med 2002;137:173-9. 13. Anninger WV, Lomeo MD, Dingle J, et al. West Nile virus-associated optic neuritis and chorioretinitis. Am J Opthalmol 2002;136:1183-5. 14. Adelman HS, Jampol LM, Caughron MC, et al. Vitritis and chorioretinitis in a patient with West Nile virus infection. Arch Opthhalmol 2003;121:205-7. 15. Kuchtey RW, Kosmorsky GS, Martin D, et al. Uveitis associated with West Nile virus infection. Arch Opthalmol 2003;121:1648-9. 16. Hershberger VS, Augsburger JJ, Hutchins RK, et al. Chorioretinal lesions in nonfatal cases of West Nile virus infection. Opthalmology 2003;110:1732-6. 17. Kaiser PK, Lee MS, Martin DA. Occlusive vasculitis in a patient with concomitant West Nile virus infection. Am J Opthalmol 2003;136:928-30. 18. Nash D, Mostashari F, Fine A, et al. Outbreak of the West Nile virus in the New York City area in 1999. N Eng J Med 2001;344: 1807-14. 19. Khairallah M, Yahia SB, Ladjimi A, et al. Chorioretinal involvement in patients with West Nile virus infection. Ophthalmology 2004;111:2065-70. 20. Bakri SJ, Kaiser PK. Ocular manifestations of West Nile virus. Curr Opinion Ophthalmol 2004;15:537-40. 21. Alpert SG, Fergerson J, Noel L-P. Intrauterine West Nile virus: ocular and systemic findings. Am J Ophthalmol 2003;136:733-5. 22. Vandenbelt S, Shaikh S, Capone A Jr, et al. Multifocal choroiditis associated with West Nile virus encephalitis. Retina 2003;23:97-9. 23. Adelman R, Membreno JH, Afshari NA, et al. West Nile chorioretinitis. Retina 2003;23:100-1.
Corresponding author: Steven B. Koevary, Ph.D. The New England College of Optometry Department of Biomedical Sciences and Disease 424 Beacon Street Boston, Massachusetts 02459 [email protected]
612 OPTOMETRY
VOLUME 76 / NUMBER 10 / OCTOBER 2005