[West Nile fever (West Nile encephalitis)].
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
West Nile virus was first detected in North America in 1999 and has spread throughout the United States and Canada and into Mexico and the Caribbean. The cases of encephalitis in New York were diagnosed as Saint Louis encephalitis which was endemic in the North America. However, dead crows and dead flamingo were found around the same time in New York. American birds seldom die by Saint Louis encephalitis virus infection. According to viral isolation and sequencing of the genome, the causative agent of unknown encephalitis was West Nile virus which was a member of Flaviviridae which cause fever, meningitis and encephalitis. West Nile virus is still active in North America in summer season, 1999 -2005. CDC enlightens people how to protect themselves and their community from West Nile virus. There are some reports that West Nile viral infections were occurred by blood transfusion, biologic products from blood and organ transfusion.
West Nile virus is a mosquito-borne flavivirus, and maintained in mosquito-bird cycle in nature. Humans are a dead-end host in West Nile virus infection. Symptoms are developed in approximately 20% of West Nile virus-infected humans. Encephalitis and meningitis are developed in about 1 out of 150 infected humans, especially in elderly populations. It has recently been reported that West Nile virus causes polio-like, acute flaccid paralysis and polyneuritis. These symptoms occur in patients without central nervous system symptoms as well as in those with encephalitis. Thus, West Nile virus causes various types of illness in humans. West Nile virus has not entered Japan yet. However, West Nile virus should be considered to be one of the causative agents for patient with a febrile illness, meningitis, encephalitis or acute flaccid paralysis who came back from West Nile endemic or epidemic areas of the world.
Explore the source record for details and available documents.
BACKGROUND: West Nile fever, considered a nonsevere manifestation of West Nile virus infection, has not been clinically well described in the United States. In 2002, Illinois had 884 documented cases of West Nile virus infection with 66 associated deaths. OBJECTIVE: To describe the symptoms and functional outcomes of West Nile fever. DESIGN: Case series. SETTING: Illinois. PATIENTS: 98 community-dwelling patients with laboratory evidence of West Nile virus infection but no history of clinical evidence of meningitis, encephalitis, or acute flaccid paralysis. INTERVENTION: Outpatient interviews. MEASUREMENTS: Presence and duration of patient-reported symptoms of infection, symptom-associated absenteeism, health care use, and impact on daily activities. RESULTS: Of 98 patients, 96% had fatigue for a median of 36 days, 81% had fever for a median of 5 days, 71% had headache for a median of 10 days, 61% had muscle weakness for a median of 28 days, and 53% had difficulty concentrating for a median of 14 days. Thirty respondents reported hospitalization, with a median stay of 5 days. At 30 days after onset, 63% of respondents continued to have symptoms. Duration did not vary significantly with increased age. Among the 72 patients who normally attended work or school, 57 (79%) could not attend because of illness (median absence, 10 days). LIMITATIONS: Recall bias could have been introduced by the delay between illness onset and interview and by self-reporting of illness information. CONCLUSIONS: West Nile fever is a more severe illness than has previously been documented. Mandatory reporting of West Nile fever cases in addition to West Nile meningoencephalitis cases could allow more accurate and timely recognition of the geographic distribution of West Nile virus infections and could inform public health interventions.
West Nile Fever (WNF) is caused by a B arbovirus, which was first isolated in 1937 in Uganda. In Israel the disease bears an epidemic character, and during 1950-1957 several widespread outbreaks of WNF were described in detail. It emerged from obscurity in 1999 when the first incursion of the virus in North America caused 62 cases of encephalitis and 7 deaths in New York. In 1996 an outbreak in Romania signaled that WNF had emerged as clinically important disease in Europe. The virus is transmitted by a mosquito vector. Wild birds serve as amplifying hosts. Human and some domestic animals such as horses, can be infected incidentally. While neurological disease has been prominent in some epidemics, the West Nile virus infection is usually asymptomatic in areas of the world where the virus is endemic. This is a case study of the first patient diagnosed and treated for West Nile Fever in the Western Galilee, Israel. The epidemiology, pathogenesis, clinical manifestations, diagnosis and treatment of the disease are presented in detail.
The West Nile fever is a viral disease transferred by a mosquito bite. It is well known in the world for the last 70 years. Recently, there was an outbreak of this disease in Israel. We will describe case reports of 2 patients who were afflicted by the disease. The first one was hospitalized with an unusual presentation including paralysis to the lower limbs, while the second one was admitted with meningitis. In both, the course was quite dramatic, and one of them expired. Reviewing the literature revealed that neurological manifestations are quite frequent among these patients (90%), while in elder people, they were fatal.
Some emerging infectious diseases have recently become endemic in Germany. Others remain confined to specific regions in the world. Physicians notice them only when travelers after infection in endemic areas present themselves with symptoms. Several of these emerging infections will be explained. HIV is an example for an imported pathogen which has become endemic in Germany. SARS and avian influenza are zoonoses with the potential to spread from person to person. Avian influenza in humans provides a possibility for the reassortment of a potential new pandemic strain. Outbreaks of dengue fever in endemic areas are reflected in increased infections in travelers returning from these areas. Currently, West-Nile-virus infections are only imported into Germany. The timely implementation of diagnostic, therapeutic and infection control measures requires physicians to include these diseases in their differential diagnosis. To achieve this goal, good cooperation between physicians, laboratories and the public health service is essential.
Over the past few decades, the geographical distribution of arthropod-borne zoonoses has dramatically expanded. The influence of human-induced or ecological changes on the risk of disease outbreaks is undeniable. However, few hypotheses have been proposed which address the re-emergence of these diseases, the spread of these viruses to previously uninfected areas and their establishment therein. Host and vector movements play an important role in the dissemination of pathogens, and the ability of these diseases to colonise previously uninfected areas may be explained by the diversity of hosts and vectors, the presence of favourable ecological conditions, and the successful adaptations of vectors or pathogens to new ecosystems. The objective of this paper is to describe the epidemiological processes of the vector-borne diseases Rift Valley fever, West Nile fever, Japanese encephalitis and Crimean-Congo haemorrhagic fever.
BACKGROUND: The arbovirus infections West Nile fever (WNF) and sandfly fever (SFF) are both endemic in the Middle East. Despite the fact that the mosquito and sandfly vectors of these viruses are still found in Israel, SFF has not been reported since 1948, whereas outbreaks of WNF occur periodically. It is suspected that some of the cases of nonspecific febrile illnesses in Israel may in fact be either WNF or SFF. AIM: To determine the extent of past arbovirus infections in subgroups of Israeli soldiers. METHODS: Sera from random samples of three groups of healthy soldiers aged 18-20 (n=273), 21-30 (n=497), and 40-55 years (n=285) were examined for IgG and IgM antibodies to West Nile virus (WNV), sandfly fever Sicilian virus (SFSV), and sandfly fever Naples virus (SFNV), using an ELISA method. RESULTS: The prevalence of antibodies increased with age for all three viruses examined, and ranged from 7.0%, 0, and 2.8%, for WNV, SFSV, AND SFNV, respectively, in soldiers aged 18-20 years, to 41.9%, 23.7%, and 30.8%, in those aged 40-55 years. The percentage of seropositives for IgG who were also IgM positive were 1.0%, 5.9%, and 3.4%, for WNV, SFSV, AND SFNV, respectively. 17.5% of the seropositives for WNV were also positive for SFSV, as compared with 5.7% among the WNV-seronegatives. Among the seropositives for WNV, 23.99% were positive for SFNV, compared with 9.1% of WNV seronegatives. 48.2% of seropositives for SFSV were positive for SFNV, as compared with 8.4% for SFSV-seronegatives. In the age agroup 40-55 years, there were significantly higher prevalence rates in those born in Israel compared with those born abroad. CONCLUSIONS: There is still significant exposure to WNV, SFSV, and SFNV in Israel. Arborviruses are probably responsible for many cases of non-specific febrile illness in this region.
West Nile virus (WNV) is a member of the Flaviviridae family, genus Flavivirus. Its reservoir hosts are wild birds. Infection is transmitted to humans by infected mosquitoes of the genus Culex. In most cases, it is either asymptomatic or manifests itself as mild fever. Typically, WNV illnesshas a sudden onset with fever above 39 degrees C and accompanying symptoms such as chills, headache, arthralgia, myalgia, back ache, cough and sore throat. Gastrointestinal symptoms are frequently reported. Generalized lymphadenopathy and conjunctivitis may develop. In some patients the infection can progress to meningoencephalitis. Diagnosis is currently based on detection of IgM antibodies in blood and cerebrospinal fluid or direct detection of WNV RNA.
Explore the source record for details and available documents.
West Nile fever has now spread to much of the United States. This disease can be diagnosed using one of several laboratory tests, notably an immunoglobulin M enzyme-linked immunosorbent assay. It can cause devastating neurologic damage, including an unusual polio-like syndrome. Magnetic resonance imaging is an important imaging tool in such patients. Treatment is largely supportive, although antiviral agents are under investigation.
Explore the source record for details and available documents.
West Nile (WN) virus is endemic in Israel. The last reported outbreak had occurred in 1981. From August to October 2000, a large-scale epidemic of WN fever occurred in Israel; 417 cases were confirmed, with 326 hospitalizations. The main clinical presentations were encephalitis (57.9%), febrile disease (24.4%), and meningitis (15.9%). Within the study group, 33 (14.1%) hospitalized patients died. Mortality was higher among patients >70 years (29.3%). On multivariate regressional analysis, independent predictors of death were age >70 years (odds ratio [OR] 7.7), change in level of consciousness (OR 9.0), and anemia (OR 2.7). In contrast to prior reports, WN fever appears to be a severe illness with high rate of central nervous system involvement and a particularly grim outcome in the elderly.
An experimental infection of mice with West Nile Virus (WNFV) showed pronounced dystrophic changes in the hepatic parenchyma and expression of WNV antigens in the endothelium of hepatic capillaries and in hepatocyte cytoplasm, which testifies to the tropic action of WNFV to hepatic tissue.
An experimental infection of mice with West Nile virus (WNV) showed pronounced dystrophic changes in tissues of the kidneys and myocardium as well as expression of WNV antigens in cells of the lungs, kidneys and myocardium, which can denote tropism of WNV to tissues of the lungs, kidneys and myocardium.
The recent epizootic of West Nile fever in Israel affected predominantly young domestic geese between three and eight weeks old. Clinically, the birds presented paralytic signs while morbidity and mortality were severe in affected flocks. The condition was encountered from early September through late November on goose farms located throughout the country. Losses incurred by goose flocks were sufficiently great as to warrant investigation of ways to protect young geese against the neurological form of the disease. We have conducted a series of vaccination trials in which three-week old geese were immunized with an attenuated, commercial flavivirus vaccine derived from Israel turkey meningoencephalitis virus (TME). Birds were challenged two weeks later with a low Vero cell passage of West Nile virus by the intracerebral route. In a second group of experiments, inactivated and live TME vaccines were given in tandem at an interval of two weeks and challenged two weeks later. The third vaccination trial was based on West Nile virus (WNV) harvested from infant mouse brain, inactivated with formalin and oil adjuvanted. A single injection given either subcutaneously or intramuscularly resulted in 75% protection of the vaccinated groups, while two injections spaced two weeks apart resulted in 94% protection. Groups of geese, vaccinated at the farms and challenged under controlled conditions in the laboratory, showed levels of protection ranging from 39% to 72% for TME vaccine and 52% and 80% for WNV vaccine. The lower levels of protection are attributable to flocks being affected with intercurrent infections at the time of vaccination.