West nile virus meningo-encephalitis: Possible sexual transmission.
West Nile virus (WNV), a flavivirus, (1) is generally arthropod-borne and is currently the most common cause of epidemic meningo-encephalitis in North America. (2) It has an incubation period of 3 to 14 days following infection. Transmission has been reported via transfusion of blood products, through solid organ transplantation, and transplacental transmission. (1) No documented cases of sexual transmission of WNV have been previously reported although sexual transmission of Zika virus, another flavivirus, has been reported. (3) We report a 44-year-old previously healthy woman who developed a neuroinvasive form of WNV following unprotected sexual intercourse with her husband one day before he developed symptoms of serologically confirmed WNV infection.
This is a 44-year-old right-handed white woman, in previously excellent health, who presented on August 28, 2014 with confusion, lethargy, and distorted vision. She and her husband reside in Mandeville, Louisiana. Her husband reported she experienced mild fever, malaise, nausea, and vomiting and minor headache over the preceding 4 days and was being treated for a presumptive urinary tract infection with nitrofurantoin. He reported having a flu-like illness two weeks before her presentation, which consisted of malaise, cough, rash, as well as myalgias, and arthralgias. Neither he nor his wife was aware of any mosquito bite exposure although he works as a supervisor in a heavily mosquito-infested area. Just prior to his illness becoming manifest, they had had unprotected vaginal intercourse. His illness lasted roughly one week with full recovery.
Her maximum temperature was 100.2[degrees] F. Her complete blood count revealed a white blood cell count of 13,300 with 8 percent polymorphonuclear cells. Both CT and MRI brain scan were normal. Cerebrospinal fluid (CSF) was reported to be "hazy" in appearance with an protein (148.2 mg/ml), glucose 50 mg/ml and the serum glucose 117 mg/ml . The CSF contained 1000 white blood cells/[mm.sup.3] (73 percent neutrophils, 24 percent lymphocytes, and 3 percent monocytes) and 0 red blood cells/[mm.sup.3]. The gram stain was negative for organisms, but positive for white blood cells. She received a course of antibiotic therapy, which included vancomycin and ceftriaxone, along with acyclovir. CSF bacterial cultures were negative as was the herpes simplex virus polymerase chain reaction. Her CSF WNV IgG was negative but the IgM was positive. HIV 1 and 2 serology were nonreactive. Her husband's blood test was positive for West Nile virus IgM, titer not reported, performed by the Louisiana State Lab in Baton Rouge. During the hospital course, she developed significant weakness of her lower extremities with no explanation by MR imaging of the brain and entire spine.
Examination on August 31, 2014 revealed her to be alert and she interacted in an appropriate fashion, but was irritable complaining of significant burning pain in both legs. Cranial nerve exam as well as motor and cerebellar function of the upper extremities was normal. There was reduced tone in both lower extremities with strength in the 2-3/5 range with somewhat variable effort attributed to pain. Sensation was intact with no sensory level noted and normal sacral sensation with superficial abdominal reflexes present. Deep tendon reflexes were 1 + for both biceps, 2+ for both triceps, 2+ for both knees and 1+ for both ankles with the Babinski response negative on the right and positive on the left.
Repeat CSF exam, on October 24, 2014, revealed clear and colorless fluid with 13 white blood cells, 100 percent lymphocytes, 2 red blood cells, a protein of 74.9 mg/dl and a glucose of 58 mg/dl. Both the CSF WNV IgG and IgM were positive. An electromyogram revealed diffuse denervation changes in both lower extremities with normal nerve conduction velocities. On re-examination, at four months follow-up, she had mild persistent paraparesis as her only sequela.
This patient we report was somewhat unique in terms of the virulence of the CSF findings. (4) Sexual transmission of WNV has never previously been reported. However, there has been the observation of a related viral infection, namely Zika, by presumed sexual transmission. (3) In this instance, an American scientist working in Senegal became infected, presumably through a mosquito bite. In addition to extreme fatigue, maculopapular rash, headache and arthralgia, he developed symptoms of prostatitis with hematospermia upon his return to Colorado. His wife developed a similar clinical picture of headache, malaise, maculopapular rash, and arthralgia, within several days of sexual intercourse, with positive Zika virus titer. In addition, Musso et al. (5) reported a 44-year-old male in Tahiti who developed Zika virus infection in association with hematospermia and the virus was isolated from his semen. Although, we are not aware of detection of WNV in the seminal fluid of humans, it has been detected in the urine of infected humans (6) and hamsters. (7) In addition, the dengue 2 virus, another flavivirus, has been found in the reproductive system of the carrier male mosquito. (8) The timeframe of contact, the lack of mosquito bite exposure as reported by the patient, and such suggestive information raises the distinct, but clearly not documented, possibility that our patient was infected through sexual intercourse. Calling attention to this possibility is of potential clinical relevance.
(1.) Petersen LR, Brault A, Nasci RS. West Nile virus: Review of the literature. JAMA 2013; 310:308-315
(2.) DeBiasi RL, Tyler KL. West Nile virus meningoencephalitis. Nat Clin Pract Neurol 2006; 2: 264-275
(3.) Foy BD, Kobylinski KC, Chilson Foy JL, et al. Probable non-vector borne transmission of Zika virus, Colorado, USA Emerg Infect Dis 2011; 17:880-882
(4.) Tyler KL, Pape J, goody RJ, Corkill M, Kleinschmidt-DeMasters BK. CSF findings in 250 patients with serologically confirmed West Nile virus meningitis and encephalitis. Neurology 2006; 66:361-365
(5.) Musso D, Roche C, Robin E, Nhan T, Teisser A, Cao-Lormeau V-M. Potential sexual transmission of Zika virus. Emerg Infect Dis 2015; 21:359-361
(6.) Murray K, Walker C, Herrington E, et al. Persistent infection with West Nile virus years after initial infection. J Infect Dis 2010; 201:2-4
(7.) Tonry JH, Xiao SY, Siirin M, Chen H, da Rosa AP, Tesh RB. Persistent shedding of West Nile virus in urine of experimentally infected hamsters. Am J Trop Med Hyg 2005; 72:320-324
(8.) Tu WC, Chen CC, Hou RF. Ultrastructural studies on the reproductive system of male Aedes aegypt (Diptera: Culicidae) infected with dengue 2 virus. J Med Entomol 1998; 35:71-76
Dr. Kelley is Professor and Chairman of Neurology at Tulane University School of Medicine, Dr. Berger is Professor and Chairman emeritus of the Department of Neurology at the University of Kentucky School of Medicine and is presently Professor of Neurology at University of Pennsylvania School of Medicine, Mr. Brian Kelley is a first year medical student at Tulane.
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|Author:||Kelley, Roger E.; Berger, Joseph R.; Kelley, Brian P.|
|Publication:||The Journal of the Louisiana State Medical Society|
|Article Type:||Clinical report|
|Date:||Jan 1, 2016|
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