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Diagnostic Approach to Rash and Fever in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Lee S. Engel, Charles V. Sanders, Fred A. Lopez
West Nile viral symptomatic infections range from West Nile fever to neuroinvasive disease. Most patients with symptoms have self-limited West Nile fever. West Nile fever is characterized by acute onset of fever, headache, fatigue, malaise, muscle pain, difficulty concentrating, and neck pain [118,119]. Approximately 57% of patients with West Nile fever will have a transient macular rash on the trunk of the body [118].
Neurological manifestations of West Nile virus
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Daniel E. Smith, J. David Beckham, Daniel M. Pastula, Kenneth L. Tyler
After a typical incubation period of 3–8 days, but potentially as long as 28 days after infection, systemic symptoms can develop. West Nile fever develops in about 20% of patients characterized as non-specific “flu-like” symptoms consisting of fever, headache, malaise, anorexia, abdominal pain, sore throat, back pain, and/or diarrhea [24,25,27]. In one series of patients, it was noted that the most commonly reported symptoms were fever (100%), generalized fatigue (74%), nausea/vomiting (44%), headache (48%), and back/limb pain (35%) [28]. A maculopapular rash occurs in ~25%–50% of patients.24 This is morbilliform, nonpruritic, and predominantly involves the torso and proximal extremities, sparing the palms and soles. For unclear reasons, the rash tends to be seen more frequently in both younger patients as well as in those without neuroinvasive disease [12,29,30].
Marburg and Ebola Virus Infections
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
Pyrexia, rash, myalgia, and hemorrhage form the main basis for the following list of conditions to be considered in the differential diagnosis: Arbovirus infections, including Chikungunya fever, Sindbis fever, yellow fever, dengue, West Nile fever, Rift Valley fever, Congo hemorrhagic fever, Kyasanur Forest disease, and Omsk hemorrhagic feverRodent-borne virus infections, represented by hemorrhagic fever with renal syndrome, Argentinian and Bolivian hemorrhagic fevers, and Lassa feverOther virus infections such as those caused by Marburg and Ebola viruses, smallpox, measles, and herpesvirusesRickettsial infections, especially the louse- and tick-borne varietiesBacterial infections, especially meningococcal, streptococcal, staphylococcal and plague septicemia, typhoid, and leptospirosisProtozoal infections comprising mainly falciparum malaria and acute African trypanosomiasis.
The knowns and unknowns of West Nile virus in Europe: what did we learn from the 2018 outbreak?
Published in Expert Review of Anti-infective Therapy, 2020
Jeremy V Camp, Norbert Nowotny
Whereas WNV is associated with a febrile illness in humans (‘West Nile fever’, WNF), two successful genetic lineages – lineage 1 in North America and lineages 1 and 2 in southern, central, and eastern Europe, respectively – are associated with a neuroinvasive disease (‘West Nile neuroinvasive disease’, WNND) in humans, horses, and birds [4, 5]. In general, it is thought that 80% of human infections are asymptomatic, with only 20% resulting in mild febrile illness [6]. Epidemiological data from Europe reported by the European Centre for Disease Prevention and Control (ECDC) over the last 3 years suggest that approximately 65–73% of reported WNF cases will develop WNND, although this figure likely underestimates the number of unreported WNF cases, and therefore overestimates the proportion of infections which develop WNND, as revealed through blood-donor screening in endemic countries [7,8,9]. Of those patients who develop WNND, the case fatality ratio is approximately 10% [10]. Thus, for every fatal case of WNND, there are at least 40 total cases, with only 10 displaying signs of disease. As the risk groups for WNND include people over 50 years old, and immunocompromised patients (e.g. organ transplant recipients), these asymptomatic cases pose a threat to the donor organ and blood supply [7, 11, 12].
Emerging and threatening vector-borne zoonoses in the world and in Europe: a brief update
Published in Pathogens and Global Health, 2019
West Nile Fever (WNF) is caused by a flavivirus transmitted by mosquitoes of the genus Culex. WNF is endemic in large areas of Africa, south Asia, the Middle East and in warmer parts of Europe, such as France, Greece, Romania and Italy [62,63]. The main reservoir hosts are wild migratory birds. Due to the avian transmission cycle, WNF can spread very fast on long distances [64]. For a long time, WNF was considered to be an infection typical for the Old World, but in 1999, due to its extremely high transmission potential, it appeared for the first time on the western hemisphere – at the northeast coast of the USA [65]. The extremely good spreading abilities were confirmed when WNF was detected 2 years later in Canada [66] and Mexico [67]. In Europe, an increasing number of WNF outbreaks has been observed over the last 20 years [68] and the last one was recorded in 2018 in southern and central Europe [69]. It can be explained by hot summers and mild winters, which support both increased density and biting activity of temperature-sensitive Culex mosquitoes and high replication rate of flavivirus [10,70,71]. The strong influence of temperature on WNF transmission was clearly confirmed by WNF outbreaks and spreading to previously unaffected areas in years with abnormally high temperatures [10,72]. It was confirmed that the distribution of the main European WNF vector – Culex molestus has expanded to the north [73]. There are multiple vaccines potentially preventing WNF in humans, however, the sufficiently effective vaccine without any side effects is still lacking [49].
Phosphonate inhibitors of West Nile virus NS2B/NS3 protease
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2019
Marcin Skoreński, Aleksandra Milewska, Krzysztof Pyrć, Marcin Sieńczyk, Józef Oleksyszyn
The West Nile virus (WNV) belongs to the flavivirus genus (Flaviviridae family) and is a mosquito-borne human pathogen of global occurrence. WNV was first isolated from humans in 1937 in the West Nile district of Uganda1. In 1953, it was identified in birds of the Nile delta region. Until 1997, WNV was not considered pathogenic to birds when a more virulent strain appeared in Israel and caused fatal disease with signs of encephalitis and paralysis in various bird species. In 1999, a pathogenic WNV strain was transferred to New York leading to its rapid spread throughout the USA, Canada and in the following years, the virus further spread, reaching northern countries of South America2. The virus also became a relevant human pathogen in Eurasia, causing large outbreaks in Greece, Israel, Romania, and Russia3–6. Although the lifecycle of WNV involves the transmission of viruses between birds and mosquitoes, various mammalian species, including humans, and horses, are susceptible to the virus. However, mammals are generally dead-end hosts, being infected through the bites of infected mosquitoes7. Although infections with WNV are mainly asymptomatic, one-fifth of the infected humans develops symptoms of the milder West Nile fever or more severe neuroinvasive diseases (meningitis and encephalitis). Unfortunately, no vaccine or effective antiviral therapy against WNV is available8.