|Year : 2021 | Volume
| Issue : 2 | Page : 532-542
|West nile virus infection: One-Year postkidney transplant
Ali Almajrafi1, Issa Al Salmi2, Faryal Khamis3, Nenad Pandak3, Amina Al-Jardani4, Eskild Petersen5
1 Department of Medicine, Ibri Hospital, Ibri, Oman
2 Department of Renal Medicine, Royal Hospital, Muscat, Oman
3 Department of Medicine, Royal Hospital, Muscat, Oman
4 Central Public Health Laboratories, Ministry of Health, Muscat, Oman
5 Directorate General for Disease Surveillance and Control, Ministry of Health, Muscat, Oman
Click here for correspondence address and email
|Date of Web Publication||11-Jan-2022|
| Abstract|| |
West Nile virus (WNV) infections are a mosquito-borne virus of the Flaviviridae family. The clinical feature of the virus varies between individuals from being asymptomatic in most of the cases to severe central nervous system disease manifested as meningitis, encephalitis, and paralysis. Diabetic nephropathy patient with microvascular and macrovascular complications, who received a kidney transplant a year ago on immunosuppressive therapy, presented with a three-day history of upper respiratory tract infection and fever. He lived in an endemic area of brucella infection. He underwent a thorough and full evaluation with various laboratory and radiological evaluations. The patient was started empirically on ceftriaxone and acyclovir for a presumptive diagnosis of herpes encephalitis and covering also Listeria with ampicillin. The patient did not improve with the initial management, so a T2-weighted magnetic resonance imaging of the brain executed that showed nonspecific hyper-intensity in the left frontal area suggestive of microangiopathic changes. WNV-neutralizing antibodies were positive with a high titer >1:640, whereas WNV RNA was not detected in the plasma sample. In the serum sample, WNV IgM and IgG were both positive. WNV IgM antibodies were detected with 6.55 and 5.97 antibody index and were done by a semiquantitative ELISA. Furthermore, WNV-neutralizing antibodies were positive as well as with a titer of 1:80. As there is no specific antiviral treatment available, the patient management was supportive; reduction in immunosuppressive agents and the use of IV IgG. This is the first reported case of one-year post renal transplant who developed WNV encephalitis and neuropathy with significant response to immunoglobulin after 18 days of infections.
|How to cite this article:|
Almajrafi A, Al Salmi I, Khamis F, Pandak N, Al-Jardani A, Petersen E. West nile virus infection: One-Year postkidney transplant. Saudi J Kidney Dis Transpl 2021;32:532-42
|How to cite this URL:|
Almajrafi A, Al Salmi I, Khamis F, Pandak N, Al-Jardani A, Petersen E. West nile virus infection: One-Year postkidney transplant. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 May 23];32:532-42. Available from: https://www.sjkdt.org/text.asp?2021/32/2/532/335467
| Introduction|| |
West Nile virus (WNV) is a mosquito-borne, single-stranded RNA flavivirus, which was first identified in 1937. Since then, human infection has been reported from many countries worldwide. West Nile fever is a re-emerging disease, caused by a mosquito-borne virus. It is transmitted by over 150 species of mosquitoes as Culex pipiens (Cx. Pipiens), Cx. tarsalis, and Cx. quinquefasciatus. WNV is a zoonotic viral disease that mainly infects humans, horses, and birds. The clinical features of the virus vary between individuals. The majority of the infected individual experiences no symptoms. Approximately 20% of people affected by the virus will experience flu-like symptoms, including fever, headache, nausea, muscle pain, and swollen lymph glands.,,,, Rare presentations, less than 1%, will develop West Nile encephalitis or meningitis, which can lead to coma, tremors, convulsions, paralysis, and even death.,,,,
West Nile Neuroinvasive Disease (WNND), defined as the presence of encephalitis, meningitis or acute flaccid paralysis because of WNV infection, accounted for 43.1% of the total cases. Organ transplant patients are at increased risk of developing WNND.,,,, While seizures have been reported in 3%–16% patients with WNND, status epilepticus because of WNND has been described very rarely.,, It has been reported that 58% of patients with WNND during the 2000 New York epidemic had at least one gastrointestinal symptom or had abnormal abdominal findings., Researchers have suggested that WNV should be considered in the differential diagnosis of patients with gastrointestinal prodromal symptoms, fever, and neurologic symptoms during the summer months in the areas of WNV transmission.,,,, A similar observation was made by various researchers in renal transplant patients who developed WNND.,,,,,,,,
The route of WNV transmission in recent organ recipients can only be deduced by establishing the timing of infection and investigating other possible exposures. To determine the timing and source of infection, paired sera collected immediately before and for several weeks after transplantation should be tested for WNV, and information on blood products administered and mosquito exposures should be obtained.
Diagnosis of WNV in organ transplant recipients may be confounded by the initial attribution of symptoms to immunosuppressive drug toxicity or other infectious etiologies.,, We report a T2DM patient with micro and macrovascular complications and one-year postkidney transplant who developed WNV infection.
| Case Report|| |
A 38-year-old Omani male, with complicated type 2 diabetes mellitus, obesity, post right big toe amputation in December 2017, and received a renal transplant one year ago and now on immunosuppressive medications. His diabetes was well controlled by glargine lantus 36 IU/day and insulin soluble ® 26 IU/day with HbA1c of 59 mmol/mol (7.6%). His immunosuppressive medications were cyclosporine 300 mg/day, prednisolone 5 mg/day, and mycophenolate mofetil 2000 mg/day.
He was admitted to Sultan Qaboos Hospital, in Salalah on August 30, 2018, with a three-day history of upper respiratory tract infection and fever. After admission, he became unconscious with deteriorated Glasgow Coma Scale to 8/15, consequently required intubation for mechanical ventilatory support. His initial cerebral computed tomography (CT) without contrast showed no pathological changes. Lumbar puncture showed pleocytosis with WBC of 81/uL cells (normal range 0–5), lymphocyte-predominant (99% lymphocytes), a high total cerebrospinal fluid (CSF) protein of 146 mg/dL (15–45) and normal CSF glucose of 8 mmol/L (>2.5). The patient was started empirically on ceftriaxone and acyclovir for a presumptive diagnosis of herpes encephalitis and covering also Listeria with ampicilin. The patient did not improve with the initial management, so a T2-weighted magnetic resonance imaging (MRI) brain executed that showed nonspecific hyper-intensity in the left frontal area suggestive of microangiopathic changes. A repeated MRI brain of the same lesion showed no changes after one week [Figure 1]. An EEG showed evidence of both electric nonconvulsive status epilepticus and generalized severe encephalopathy, after which he was started on levetiracetam 500 mg twice daily. Initial viral multiplex polymerase chain reaction (PCR) for the CSF samples came all negative including HSV. [Table 1] shows the full panel result. With the background of endemic brucella in the Dhofar region, he was initiated empirically on neuro-brucellosis treatment with addition of doxycycline and rifampicin. Later on, his medical care was transferred to the Royal Hospital [intensive care unit (ICU), on September 13]. Later in his illness course, brucella serology from CSF sample reported as negative and anti-brucella treatment was stopped. With the supportive measures only, his conscious level returned back slowly. On the 5th day of his ICU stay in Royal Hospital, WNV IgM detected positive in the plasma and CSF samples collected on September 16, 2018. WNV IgM antibodies were detected with 6.55 and 5.97 antibody index and was done by a semiquantitative ELISA. WNV neutralizing antibodies were positive with a high titer >1:640, whereas WNV RNA was not detected in the plasma sample. In the serum sample collected on September 30, 2018; WNV IgM and IgG were both positive. Furthermore, WNV-neutralizing antibodies were positive as well as with a titer of 1:80.
|Figure 1: T2-weighted magnetic resonance imaging showed nonspecific hyper-intensity in the left frontal area.|
Click here to view
|Table 1: Illustrates the viral multiplex in patient cerebrospinal fluid.|
Click here to view
Patients’ kidney function deteriorated upon admission from his previous normal baseline values. At the time of admission, his serum creatinine was 139 umol/L with estimated glomerular filtration rate (eGFR) of 52 mL/ min/1.73 m2. At time of discharge, his serum creatinine was 104 and eGFR 73. His protein creatinine ratio was 54.9 mg/mmol (1.07 g/L) and 9.7 mg/mmol (0.13 g/L) at time of admission and discharge, respectively.
All anti-microbial therapy was stopped. He was extubated on the 6th day of ICU stay. He was found to have a partial motor paresis of the upper and lower limbs (UL) with a power of 3/5) bilaterally and both lower limbs weakness LL with a (power of 1/5) and was started on extensive physiotherapy without significant improvement. He received IV immunoglobulin (Intractect® 50 g/L) 100g × 3 days, after which his power improved significantly over the next two days of the administration. More specifically, UL improved to 5/5 and LL to 4/5. An EMG/NCS was done after 5 days of intravenous immunoglobulin (IVIG) showed absent common peroneal, posttibial and sural nerves and the absence of sensory response of the bilateral ulna and median nerves. Post-rehabilitation, the patient was discharged home on October 31, after 48 days of his admission in RH, with minimal residual weakness of his lower limbs.
The authors obtained all appropriate consent forms from the patient for the publication of this case reports.
| Discussion|| |
This is the first report of WNV infection in a young patient of one-year postkidney transplant. He initially presented with upper respiratory tract infection, progressively deteriorated in consciousness with ultimate WNND. There was progressive recovery of neurological deficit with minimal residual after introduction of IVIG for benefit of doubt after 19 days of his presentation. A high level of clinical suspicion with aggressive evaluation utilizing with appropriate laboratory studies is of paramount importance in the diagnosis of WNV infection in the immunocompromised patients. To the best of our knowledge, there is still no local study demonstrates the type of mosquitoes present in the Dhofar region in Oman. From our regional data; however, the prevalence of WNV in infected horses and birds is considered high. The Culex mosquitoes represented the main vector of the disease in our country and mostly found endemic in backyard poultry.
The virus has a longer history in Europe, Africa, Asia, and the Middle East. Although the mosquito is the vector of disease transmission, human disease has also been acquired through blood transfusion, breastfeeding, transplacental transmission, occupational exposure in laboratory workers, and stem cell and solid organ transplantation.,,,,,
Culex mosquitos are the primary global transmission vectors for WNV. Cx. tarsalis and Cx. pipiens are the main WNV vectors in the United States and Europe but also Cx. quinquefasciatus, Cx. stigmatosoma, Cx. thriambus, Cx. pipiens, and Cx. nigripalpus are shown to be competent vectors for the transmission of WNV. Aedes (stegomyia) albopictus (Ae. albopictus) mosquito is native to Southeast Asia and Oceania hence the popular name “Asian tiger mosquito”. Its worldwide spread started around 40 years ago, but now it is introduced and established in all inhabited continents. In laboratory conditions, Ae. albopictus is a competent vector to 26 arboviruses including WNV., So far, it is unclear if other Aedes mosquitos have any role in WNV transmission., Arabian Peninsula has arid or semi-arid climate resulting in few natural mosquito breeding sites. The Southern part of Arabia, that includes Southern Oman (Dhofar) and Yemen, has a different climate. During July and August, the monsoon covers this coastal region with persistent fog causing some precipitation, high humidity, and lower temperatures thus providing good conditions for mosquito development. Among other mosquito species, Ae. aegypti, Ae. albopictus, Ae. vittatus, Cx. bitaeniorhynchus, Cx. Laticinctus, Cx. quinquefasciatus, Cx. sinaiticus, Cx. sitiens, and Cx. tritaeniorhynchus were detected in the coastal region of Southern Oman confirming that two well-known competent WNV vectors are present in this region: Ae. albopictus and Cx. quinquefasciatus.,
WNV infection is usually transmitted by mosquitoes that acquire the virus from infected wild birds and then spread the virus to humans. Approximately 75% of WNV infections in humans are asymptomatic.,, However, 25% of humans develop a self-limiting febrile illness (West Nile fever), whereas less than 1% experience neuro-invasive disease manifested by encephalitis, meningitis, or acute flaccid paralysis.,,
Transmission of WNV infection has also occurred through blood transfusion, breastfeeding, transplacental exposure, percutaneous injury in the laboratory, and conjunctival exposure to infected avian brain and body fluids., The transmission of WNV by organ transplantation was first reported in 2002 and appears to be associated with a high incidence of severe neuroinvasive disease. Nonetheless, proven organ-derived WNV infection has generally been an uncommon, sporadic occurrence and can easily be overlooked insusceptible patients and their organ donors.,,
The majority of the cases of WNV disease are asymptomatic. WNV infection of immuno-compromised patients is a rare phenomenon and the clinical presentations at this point do not have any characteristic features.,, The immunocompromised incubation period appears to be shorter when compared to the non-immunocompromised patients. The prognostic profile of the disease severity depends on multiple factors such immunocompromised status, diabetic mellitus, and obesity.,,
Most infections are mild; however, people older than 50 years with chronic medical conditions and those receiving immunosuppression are at the highest risk of severe disease, which may include encephalomyelitis and death. Case-fatality rates are low among the general population but ranges between 4% and 29% for hospitalized patients. In the solid organ transplant recipient, the case-fatality rate is quite high. The limited number of documented cases and the lack of routine post-transplant screening in all patients preclude an accurate estimation of this rate. Currently, there is no specific drug treatment or vaccine against the infection.
WNV poses a definite risk to Gulf countries including Oman. The presence of WNV among different animal species in Oman has been known for some time. A limited outbreak occurred in horses in March 2003 in Muscat governorate., In addition, initial serologic surveys in 2012 have detected specific antibodies to WNV in asymptomatic backyard poultry in all Oman regions and governorates with the total flock and the total bird sero-prevalence of 45% and 20.3%, respectively. [Figure 2] demonstrates a summary of reported animal WNV cases in the rest of GCC areas.
|Figure 2: Showed distribution of reported animal West Nile virus cases in GCC.|
Click here to view
Tropical and migratory birds are the main reservoir of the virus, whereas Culex mosquitoes are the main vectors of WNV which can transmit the virus to birds, horses, and humans., On the other hand, infection in chickens and turkeys usually remains subclinical but with the rapid development of high titer antibodies and very low viremia which is unlikely to infect Culex mosquito vectors.,, Horses also do not play a role in the transmission cycle of the virus although they are highly susceptible to WNV infection and occasionally develop symptoms similar to those in humans.,, Hence, regular serological surveys of sentinel chickens and reports of equine cases might potentially provide early warning of corresponding WNV transmission in the human population.,,,, Such one health approach might enable timely anti-epidemic measures in the prevention of mass occurrence of human WNV infections in Oman.
A number of outbreaks have been reported worldwide. There has been a single reported outbreak (19 horses in 2003) in Oman. Consequently, another study conducted in 2015 to estimate the prevalence of WNV in Oman utilizing backyard poultry as sentinel animals. In this study, it was estimated that flock seroprevalence was 45% and the total bird seroprevalence was 20.3%. All tested species showed some WNV seropositive results. Despite the low reporting rate of WN disease both in humans and horses, backyard poultry are at a high risk of exposure in all Oman regions and governorates.
The clinical presentation in the immuno-compromised host appears to be unusual and variable and occasionally may result in death. Outbreak areas are typically found along major bird migratory routes, with the largest outbreaks have occurred in Greece, Israel, Russia, Romania, and the United States. The first serious outbreaks of WNV occurred in the mid-1990s in Algeria and Romania.,
Neuroinvasive disease manifestation is explained by neuronal damage in several regions of the brain. The fatality rate for hospitalized encephalitic cases is approximately 10%, with increased risk for patients with compromised immune systems, advanced age, and underlying conditions such as diabetes mellitus.,
It has been recognized that the elderly and immunocompromised are especially at risk for disseminated WNV infection and for developing fatal encephalitis. In New York City study, researchers found that old age and diabetes mellitus were both shown to be independent risk factors for death. Another group found that patients with both diabetes and hypertension generally have increased morbidity and mortality. Diabetes and hypertension have both been shown to be independent risk factors for increased permeability of the blood–brain barrier (BBB). Increased permeability of the BBB during the viremia period of WNV infection could possibly lead to increased susceptibility of the patient to neuroinvasive disease.,,,
In the present study, our patient was immunocompromised on various immuno-suppression medications. WNV neuroinvasiveness is associated with increased risk among immunosuppressed patients and suggest that an intact immune system is essential for the control of WNV infection. Although peripheral immune responses to WNV can prevent encephalitis, up to 40% of immunocompetent infected with a virulent WNV strain develop lethal neuroinvasive disease.,
Viremia WNV can cross the BBB into the brain and cause meningoencephalitis where the probability of neuroinvasion appeared to correlate with the level and duration of viremia.,
Several mechanisms have been proposed for WNV entry into the central nervous system (CNS): (i) infection or passive transport through the endothelium or choroid plexus epithelial cells, (ii) infection of olfactory neurons and spread to the olfactory bulb, (iii) a “Trojan horse” mechanism in which the virus is transported by infected immune cells trafficking to the CNS, and (iv) direct axonal retrograde transport from infected peripheral neurons.,,
Diagnosis of WNV in organ transplant recipients may be confounded by the initial attribution of symptoms to immunosuppressive drug toxicity or other infectious etiologies.,, Establishing the diagnosis of WNV infection in a transplant recipient may be challenging, as WNV viremia may be prolonged and antibody development may be delayed due to immunosuppressive medications. Overall, these findings suggest that molecular diagnostics may be of value for a longer period after the initial infection and should be considered, in addition to antibody testing, to diagnose WNV infections in organ recipients.,,
Approximately 80% of human WNV infections are asymptomatic. Most symptomatic persons experience an acute systemic febrile illness; less than 1% of infected persons develop neuroinvasive disease, which typically manifests as meningitis, encephalitis, or acute flaccid paralysis.,, Although most WNV infections are acquired through the bite of an infected mosquito, the virus can also be transmitted through transfusion of infected blood products or solid-organ transplantation (SOT). WNV RNA in tissues from donor associated with transmission to organ transplant recipients.,, Most infections are mild, however, people older than 50 years with chronic medical conditions and those receiving immunosuppression are at the highest risk of severe disease, which may include encephalomyelitis and death. Patients present with a variety of neurological symptoms from meningoencephalitis, muscle weakness, diminished reflexes, and even paralysis.,,
The neurological manifestations of the disease vary. For patients with neuroinvasive disease, 35%–40% have meningitis, 55%–60% have encephalitis, and only 5%–10% have myelitis. A prominent finding in West Nile encephalitis is muscular weakness (30%–50% of patients with encephalitis), often with lower motor neuron symptoms, flaccid paralysis, and hyporeflexia with no sensory abnormalities.,, As in our case, the patient had encephalitis manifested by drop in mentation and flaccid paralysis. The complete blood count may be normal or may present with lymphopenia. The cerebrospinal spinal usually has leukocytosis with neutrophilia and increased levels of protein. CT or MRI scans of the brain is usually normal or may show enhancement of the leptomeningeal or periventricular areas. Radiological findings of WNV-infected patients carry prognostic value. Depending on weather, the brain parenchyma, spinal cord, or meningitis are affected, the clinical presentations vary accordingly. The findings of hyperintensities in brain, frontal areas as in our patient, can result in increasing somnolence, agitation, and loss of consciousness., The reported clinical outcome results in such finding may result in severe neurological deficit with some reported mortalities.
WNV infection may persist for longer periods in immunocompromised patients.,, Potentially, these results occur because immunocompromised patients carry a greater viral burden and are less capable of mounting IgM and IgG responses to antigenic challenges. CSF PCR testing therefore may have greater utility for immunocompromised patients. Thus, both CSF PCR and CSF antibody testing should be considered for immunocompromised patients who are being evaluated for WNND. As neither CSF IgM nor PCR is 100% sensitive for WNV, repeat testing of both CSF and sera should be performed if clinical suspicion is high.,,,
WNV infection acquired through SOT can result in severe disease. In five clusters of SOT-associated WNV infections previously reported to public health agencies in the United States, 10 of 13 (77%) organ recipients were infected. Seven of the 10 (70%) infected organ recipients developed encephalitis and three of these patients died. SOT-transmitted WNV infection is difficult to prevent because, unlike blood donors, organ donors are not routinely screened for WNV infection and, even with screening, some infections in donors may not be detected.,,,
The treatment of WNV infection is supportive. Variables trials using IVIG, steroids, interferons, and ribavirin failed to show clinical improvement.,,, Few case reports, however, demonstrated clinical improvement as in our case. It is unclear whether the immunoglobulin administered to the right kidney recipient in the early posttransplantation period to prevent acute antibody-mediated injury may have ameliorated the clinical course of WNV infection, especially because the patient failed to develop severe WNV disease despite a long period during which viral RNA was detectable in blood and urine. The treatment of WNV infection is mainly supportive. Several trials using IVIG, steroids, interferons and ribavirin failed to show clinical improvement. Few case reports, however, demonstrated clinical improvement. Shimoni et al demonstrated successful improvement in muscle power of a patient presented with acute flaccid paralysis due to WNV with IVIG on day 8 of the WNN diagnosis., In our case report, the patient demonstrated clinical benefit after 19 days of initial presentation. Overall, the published human date of IVIG is limited to the case reports only. The majority of the published date described late introduction of IVIG during the illness course.
| Conclusion|| |
Clinicians should have a high index of suspicion for WNV as a cause of systemic febrile illness or encephalitis in organ transplant recipients. Suspected cases should be reported to public health departments in a timely manner to enable a prompt investigation to identify and remove any potentially infected products and enable the identification of other exposed recipients so they may be managed appropriately. Laboratory confirmation and determination of timing of WNV infection is dependent on appropriate testing, which could be improved by the increased use of molecular methods in immunosuppressed patients, WNV infection is confirmed by testing both serum and CSF for WNV RNA and IgM antibody. As there is no specific antiviral treatment available, treatment remains supportive; reduction in immunosuppressive agents and the use of IV IgG and interferon have been reported in the literature, but there is no proven efficacy.
| References|| |
Guharoy R, Gilroy SA, Noviasky JA, Ference J. West Nile virus infection. Am J Health Syst Pharm 2004;61:1235-41.
Watson JT, Pertel PE, Jones RC, S et al. Clinical characteristics and functional outcomes of West Nile Fever. Ann Intern Med 2004;141:360-5.
Davis LE, Beckham JD, Tyler KL. North American encephalitic arboviruses. Neurol Clin 2008;26:727-57.
Davis LE, DeBiasi R, Goade DE, et al. West Nile virus neuroinvasive disease. Ann Neurol 2006;60:286-300.
Frost MJ, Zhang J, Edmonds JH, et al. Characterization of virulent West Nile virus Kunjin strain, Australia, 2011. Emerg Infect Dis 2012;18:792-800.
Sadek JR, Pergam SA, Harrington JA, et al. Persistent neuropsychological impairment associated with West Nile virus infection. J Clin Exp Neuropsychol 2010;32:81-7.
Athar P, Hasbun R, Nolan MS, et al. Long-term neuromuscular outcomes of west nile virus infection: A clinical and electromyographic evaluation of patients with a history of infection. Muscle Nerve 2018;57:77-82.
Bai F, Thompson EA, Vig PJ, Leis AA. Current understanding of west nile virus clinical manifestations, immune responses, neuroinvasion, and immunotherapeutic implications. Pathogens 2019;8:E193.
Sejvar JJ, Marfin AA. Manifestations of West Nile neuroinvasive disease. Rev Med Virol 2006;16:209-24.
Wilson CA, Bale JF Jr. West nile virus infections in children. Curr Infect Dis Rep 2014; 16:391.
Yeung MW, Shing E, Nelder M, Sander B. Epidemiologic and clinical parameters of West Nile virus infections in humans: A scoping review. BMC Infect Dis 2017;17:609.
Martín-Acebes MA, Saiz JC. West Nile virus: A re-emerging pathogen revisited. World J Virol 2012;1:51-70.
Petersen LR, Brault AC, Nasci RS. West Nile virus: Review of the literature. JAMA 2013; 310:308-15.
Sejvar JJ. West Nile virus infection. Microbiol Spectr 2016;4.
Yu A, Ferenczi E, Moussa K, Eliott D, Matiello M. Clinical spectrum of West Nile virus neuroinvasive disease. Neurohospitalist 2020;10:43-7.
Jain N, Fisk D, Sotir M, Kehl KS. West Nile encephalitis, status epilepticus and West Nile pneumonia in a renal transplant patient. Transpl Int 2007;20:800-3.
Parsons AM, Grill MF, Feyissa AM, Britton J, Hocker S, Crepeau A. EEG in WNV neuroinvasive disease. J Clin Neurophysiol 2019;36:135-40.
Wadei H, Alangaden GJ, Sillix DH, et al. West Nile virus encephalitis: An emerging disease in renal transplant recipients. Clin Transplant 2004;18:753-8.
Campbell GL, Marfin AA, Lanciotti RS, Gubler DJ. West Nile virus. Lancet Infect Dis 2002;2:519-29.
Hayes EB, Komar N, Nasci RS, Montgomery SP, O’Leary DR, Campbell GL. Epidemiology and transmission dynamics of West Nile virus disease. Emerg Infect Dis 2005;11:1167-73.
Levi ME. West Nile virus infection in the immunocompromised patient. Curr Infect Dis Rep 2013;15:478-85.
Lindsey NP, Staples JE, Lehman JA, Fischer M; Centers for Disease Control and Prevention (CDC). Surveillance for human West Nile virus disease – United States, 1999-2008. MMWR Surveill Summ 2010;59:1-17.
Mazurek JM, Winpisinger K, Mattson BJ, Duffy R, Moolenaar RL. The epidemiology and early clinical features of West Nile virus infection. Am J Emerg Med 2005;23:536-43.
Nemeth NM, Thomsen BV, Spraker TR, et al. Clinical and pathologic responses of American crows (Corvus brachyrhynchos) and fish crows (C ossifragus) to experimental West Nile virus infection. Vet Pathol 2011;48:1061-74.
Weiss D, Carr D, Kellachan J, et al. Clinical findings of West Nile virus infection in hospitalized patients, New York and New Jersey, 2000. Emerg Infect Dis 2001;7:654-8.
Anesi JA, Silveira FP; AST Infectious Diseases Community of Practice. Arenaviruses and West Nile Virus in solid organ transplant recipients: Guidelines from the American Society of Transplantation infectious diseases community of practice. Clin Transplant 2019; 33:e13576.
Freifeld AG, Meza J, Schweitzer B, Shafer L, Kalil AC, Sambol AR. Seroprevalence of West Nile virus infection in solid organ transplant recipients. Transpl Infect Dis 2010;12:120-6.
Petersen LR. Epidemiology of West Nile virus in the United States: Implications for arbo-virology and public health. J Med Entomol 2019;56:1456-62.
Winston DJ, Vikram HR, Rabe IB, et al. Donor-derived West Nile virus infection in solid organ transplant recipients: Report of four additional cases and review of clinical, diagnostic, and therapeutic features. Transplantation 2014;97:881-9.
Youssef SR, Eissa DG, Abo-Shady RA, et al. Seroprevalence of anti-WNV IgG antibodies and WNV-RNA in Egyptian blood donors. J Med Virol 2017;89:1323-9.
Zanoni F, Alfieri C, Moroni G, et al. Delayed diagnosis of West Nile virus infection in a kidney transplant patient due to inaccuracies in commonly available diagnostic tests. Exp Clin Transplant 2020;18:385-9.
DeSalvo D, Roy-Chaudhury P, Peddi R, et al. West Nile virus encephalitis in organ transplant recipients: Another high-risk group for meningoencephalitis and death. Transplantation 2004;77:466-9.
Eybpoosh S, Fazlalipour M, Baniasadi V, et al. Epidemiology of West Nile virus in the eastern mediterranean region: A systematic review. PLoS Negl Trop Dis 2019;13:e0007081.
Ahlers LR, Goodman AG. The immune responses of the animal hosts of West Nile virus: A comparison of insects, birds, and mammals. Front Cell Infect Microbiol 2018;8:96.
Bażanów B, Jansen van Vuren P, Szymański P, et al. A survey on West Nile and usutu viruses in horses and birds in poland. Viruses 2018;10:E87.
Kolodziejek J, Jungbauer C, Aberle SW, et al. Integrated analysis of human-animal-vector surveillance: West Nile virus infections in Austria, 2015-2016. Emerg Microbes Infect 2018;7:25.
Papa A. West Nile virus infections in Greece: An update. Expert Rev Anti Infect Ther 2012;10:743-50.
Petric D, Petrovic T, Hrnjakovic Cvjetkovic I, et al. West Nile virus ‘circulation’ in Vojvodina, Serbia: Mosquito, bird, horse and human surveillance. Mol Cell Probes 2017;31:28-36.
Zé-Zé L, Proença P, Osório HC, et al. Human case of West Nile neuroinvasive disease in Portugal, summer 2015. Euro Surveill 2015;20:pii=30024.
Goddard LB, Roth AE, Reisen WK, Scott TW. Vector competence of California mosquitoes for West Nile virus. Emerg Infect Dis 2002; 8:1385-91.
Klobucar A, Benic N, Krajcar D, et al. An overview of mosquitoes and emerging arboviral infections in the Zagreb area, Croatia. J Infect Dev Ctries 2016;10:1286-93.
Vilibic-Cavlek T, Savic V, Petrovic T, et al. Emerging trends in the epidemiology of West Nile and usutu virus infections in southern Europe. Front Vet Sci 2019;6:437.
Al Shekaili T. Epidemiological studies on avian influenza and other respiratory viruses in backyard poultry in Oman. Ph.D. Theses. University of Liverpool; 2015. pp. 15–17
Vilibic-Cavlek T, Savic V, Sabadi D, et al. Prevalence and molecular epidemiology of West Nile and Usutu virus infections in Croatia in the ‘One health’ context, 2018. Transbound Emerg Dis 2019;66:1946-57.
Centers for Disease Control and Prevention (CDC). West Nile virus transmission via organ transplantation and blood transfusion – Louisiana, 2008. MMWR Morb Mortal Wkly Rep 2009;58:1263-7.
Martina BE, Koraka P, Osterhaus AD. West Nile virus: is a vaccine needed? Curr Opin Investig Drugs 2010;11:139-46.
Zumla A, Dar O, Kock R, et al. Taking forward a ‘One Health’ approach for turning the tide against the Middle East respiratory syndrome coronavirus and other zoonotic pathogens with epidemic potential. Int J Infect Dis 2016;47:5-9.
Blitvich BJ. Transmission dynamics and changing epidemiology of West Nile virus. Anim Health Res Rev 2008;9:71-86.
Adham D, Moradi-Asl E, Vatandoost H, Saghafipour A. Ecological niche modeling of West Nile virus vector in northwest of Iran. Oman Med J 2019;34:514-20.
Mentoor JL, Lubisi AB, Gerdes T, Human S, Williams JH, Venter M. Full-genome sequence of a neuroinvasive West Nile virus lineage 2 strain from a fatal horse infection in South Africa. Genome Announc 2016;4:e00740-16.
Carroll B, Takahashi R, Reisen W. West Nile virus activity in kern county and the factors leading to the 2007 outbreak. Proc Pap Annu Conf Mosq Vector Control Assoc Calif 2009;76:138-45.
Chaskopoulou A, Dovas CI, Chaintoutis SC, Kashefi J, Koehler P, Papanastassopoulou M. Detection and early warning of West Nile virus circulation in central macedonia, Greece, using sentinel chickens and mosquitoes. Vector Borne Zoonotic Dis 2013;13:723-32.
Kwan JL, Kluh S, Reisen WK. Antecedent avian immunity limits tangential transmission of West Nile virus to humans. PLoS One 2012;7:e34127.
El-Bahnasawy MM, Khater MK, Morsy TA. The mosquito borne West Nile virus infection: is it threating to Egypt or a neglected endemic disease? J Egypt Soc Parasitol 2013;43:87-102.
Mavrouli M, Vrioni G, Kapsimali V, et al. Reemergence of West Nile Virus Infections in Southern Greece, 2017. Am J Trop Med Hyg 2019;100:420-6.
Murray K, Baraniuk S, Resnick M, et al. Risk factors for encephalitis and death from West Nile virus infection. Epidemiol Infect 2006;134:1325-32.
Murray KO, Koers E, Baraniuk S, et al. Risk factors for encephalitis from West Nile virus: A matched case-control study using hospitalized controls. Zoonoses Public Health 2009; 56:370-5.
Nash D, Mostashari F, Fine A, et al. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med 2001;344:1807-14.
Debiasi RL. West Nile virus neuroinvasive disease. Curr Infect Dis Rep 2011;13:350-9.
Hartmann CA, Vikram HR, Seville MT, et al. Neuroinvasive St. Louis encephalitis virus infection in solid organ transplant recipients. Am J Transplant 2017;17:2200-6.
Murray KO, Baraniuk S, Resnick M, et al. Clinical investigation of hospitalized human cases of West Nile virus infection in Houston, Texas, 2002-2004. Vector Borne Zoonotic Dis 2008;8:167-74.
Popescu CP, Florescu SA, Hasbun R, et al. Prediction of unfavorable outcomes in West Nile virus neuroinvasive infection – Result of a multinational ID-IRI study. J Clin Virol 2020;122:104213.
Latif A, Kapoor V, Simmons E, Parekh J, Andukuri V. West Nile virus encephalitis in a young immunocompetent female in Omaha Nebraska. Intractable Rare Dis Res 2019;8:48-51.
Savasta S, Rovida F, Foiadelli T, et al. West-Nile virus encephalitis in an immunocompetent pediatric patient: Successful recovery. Ital J Pediatr 2018;44:140.
Lustig S, Danenberg HD, Kafri Y, Kobiler D, Ben-Nathan D. Viral neuroinvasion and encephalitis induced by lipopolysaccharide and its mediators. J Exp Med 1992;176:707-12.
Miner JJ, Daniels BP, Shrestha B, et al. The TAM receptor Mertk protects against neuro-invasive viral infection by maintaining blood-brain barrier integrity. Nat Med 2015;21:1464-72.
Kakooza-Mwesige A, Mohammed AH, Kristensson K, Juliano SL, Lutwama JJ. Emerging viral infections in sub-saharan africa and the developing nervous system: A mini review. Front Neurol 2018;9:82.
Lim SM, Koraka P, Osterhaus AD, Martina BE. West Nile virus: Immunity and pathogenesis. Viruses 2011;3:811-28.
Roe K, Orillo B, Verma S. West Nile virus-induced cell adhesion molecules on human brain microvascular endothelial cells regulate leukocyte adhesion and modulate permeability of the in vitro blood-brain barrier model. PLoS One 2014;9:e102598.
Koepsell SA, Freifeld AG, Sambol AR, McComb RD, Kazmi SA. Seronegative naturally acquired West Nile virus encephalitis in a renal and pancreas transplant recipient. Transpl Infect Dis 2010;12:459-64.
Hayes C, Stephens L, Fridey JL, et al. Probable transfusion transmission of West Nile virus from an apheresis platelet that screened non-reactive by individual donor-nucleic acid testing. Transfusion 2020;60:424-9.
Inojosa WO, Scotton PG, Fuser R, et al. West Nile virus transmission through organ transplantation in north-eastern Italy: A case report and implications for pre-procurement screening. Infection 2012;40:557-62.
Chinikar S, Javadi A, Ataei B, et al. Detection of West Nile virus genome and specific antibodies in Iranian encephalitis patients. Epidemiol Infect 2012;140:1525-9.
Gyure KA. West Nile virus infections. J Neuropathol Exp Neurol 2009;68:1053-60.
Napoli C, Bella A, Declich S, et al. Integrated human surveillance systems of West Nile virus infections in Italy: The 2012 experience. Int J Environ Res Public Health 2013;10:7180-92.
Shimoni Z, Bin H, Bulvik S, et al. The clinical response of West Nile virus neuroinvasive disease to intravenous immunoglobulin therapy. Clin Pract 2012;2:e18.
Gnann JW Jr., Agrawal A, Hart J, et al. Lack of efficacy of high-titered immunoglobulin in patients with West Nile virus central nervous system disease. Emerg Infect Dis 2019;25: 2064-73.
Issa Al Salmi
Department of Renal Medicine, Royal Hospital, Muscat
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2]
| Article Access Statistics|
| Viewed||1032 |
| Printed||4 |
| Emailed||0 |
| PDF Downloaded||191 |
| Comments ||[Add] |