A vaccine for horses (ATCvet code: QI05AA10 (WHO)) based on killed viruses exists; some zoos
have given this vaccine to their birds, although its effectiveness is
unknown. Dogs and cats show few if any signs of infection. There have
been no known cases of direct canine-human or feline-human transmission;
although these pets can become infected, it is unlikely they are, in
turn, capable of infecting native mosquitoes and thus continuing the
disease cycle.[76] AMD3100, which had been proposed as an antiretroviral drug for HIV, has shown promise against West Nile encephalitis. Morpholino antisense oligos conjugated to cell penetrating peptides have been shown to partially protect mice from WNV disease.[77] There have also been attempts to treat infections using ribavirin, intravenous immunoglobulin, or alpha interferon.[78] GenoMed, a U.S. biotech company, has found that blocking angiotensin II can treat the "cytokine storm" of West Nile virus encephalitis as well as other viruses.[79]
A vaccine called Chimerivax-WNV is being actively researched and has undergone phase II Clinical trials in 2011.[80][81] [needs update]
Monday, March 27, 2017
Epidemiology
WNV was first isolated from a feverish 37-year-old woman at Omogo in the West Nile District of Uganda in 1937 during research on yellow fever virus.[71] A series of serosurveys
in 1939 in central Africa found anti-WNV positive results ranging from
1.4% (Congo) to 46.4% (White Nile region, Sudan). It was subsequently
identified in Egypt
(1942) and India (1953), a 1950 serosurvey in Egypt found 90% of those
over 40 years in age had WNV antibodies. The ecology was characterized
in 1953 with studies in Egypt[72] and Israel.[73] The virus became recognized as a cause of severe human meningoencephalitis
in elderly patients during an outbreak in Israel in 1957. The disease
was first noted in horses in Egypt and France in the early 1960s and
found to be widespread in southern Europe, southwest Asia and Australia.
The first appearance of WNV in the Western Hemisphere was in 1999[4] with encephalitis reported in humans, dogs, cats, and horses, and the subsequent spread in the United States may be an important milestone in the evolving history of this virus. The American outbreak began in College Point, Queens in New York City and was later spread to the neighboring states of New Jersey and Connecticut. The virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence.[74] West Nile virus is now endemic in Africa, Europe, the Middle East, west and central Asia, Oceania (subtype Kunjin), and most recently, North America and is spreading into Central and South America.
Recent outbreaks of West Nile virus encephalitis in humans have occurred in Algeria (1994), Romania (1996 to 1997), the Czech Republic (1997), Congo (1998), Russia (1999), the United States (1999 to 2009), Canada (1999–2007), Israel (2000) and Greece (2010).
Epizootics of disease in horses occurred in Morocco (1996), Italy (1998), the United States (1999 to 2001), and France (2000), Mexico (2003) and Sardinia (2011).
Outdoor workers (including biological fieldworkers, construction workers, farmers, landscapers, and painters), healthcare personnel, and laboratory personnel who perform necropsies on animals are at risk of contracting WNV.[75]
The first appearance of WNV in the Western Hemisphere was in 1999[4] with encephalitis reported in humans, dogs, cats, and horses, and the subsequent spread in the United States may be an important milestone in the evolving history of this virus. The American outbreak began in College Point, Queens in New York City and was later spread to the neighboring states of New Jersey and Connecticut. The virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence.[74] West Nile virus is now endemic in Africa, Europe, the Middle East, west and central Asia, Oceania (subtype Kunjin), and most recently, North America and is spreading into Central and South America.
Recent outbreaks of West Nile virus encephalitis in humans have occurred in Algeria (1994), Romania (1996 to 1997), the Czech Republic (1997), Congo (1998), Russia (1999), the United States (1999 to 2009), Canada (1999–2007), Israel (2000) and Greece (2010).
Epizootics of disease in horses occurred in Morocco (1996), Italy (1998), the United States (1999 to 2001), and France (2000), Mexico (2003) and Sardinia (2011).
Outdoor workers (including biological fieldworkers, construction workers, farmers, landscapers, and painters), healthcare personnel, and laboratory personnel who perform necropsies on animals are at risk of contracting WNV.[75]
Treatment
No specific treatment is available for WNV infection. In severe cases
treatment consists of supportive care that often involves
hospitalization, intravenous fluids, respiratory support, and prevention of secondary infections.
Prognosis
While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60–90 days to recover.[12][67] People with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple long term (>1+ years) somatic complaints such as tremor, and dysfunction in motor skills and executive functions. People with milder illness are just as likely as people with more severe illness to experience adverse outcomes.[68] Recovery is marked by a long convalescence with fatigue. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.[69][70]Monitoring and control
West Nile virus can be sampled from the environment by the pooling of trapped mosquitoes via ovitraps, carbon dioxide-baited light traps, and gravid
traps, testing blood samples drawn from wild birds, dogs, and sentinel
monkeys, as well as testing brains of dead birds found by various animal
control agencies and the public.
Testing of the mosquito samples requires the use of reverse-transcriptase PCR (RT-PCR) to directly amplify and show the presence of virus in the submitted samples. When using the blood sera of wild birds and sentinel chickens, samples must be tested for the presence of WNV antibodies by use of immunohistochemistry (IHC)[60] or enzyme-linked immunosorbent assay (ELISA).[61]
Dead birds, after necropsy, or their oral swab samples collected on specific RNA-preserving filter paper card,[62][63] can have their virus presence tested by either RT-PCR or IHC, where virus shows up as brown-stained tissue because of a substrate-enzyme reaction.
West Nile control is achieved through mosquito control, by elimination of mosquito breeding sites such as abandoned pools, applying larvacide to active breeding areas, and targeting the adult population via lethal ovitraps and aerial spraying of pesticides.
Environmentalists have condemned attempts to control the transmitting mosquitoes by spraying pesticide, saying the detrimental health effects of spraying outweigh the relatively few lives that may be saved, and more environmentally friendly ways of controlling mosquitoes are available. They also question the effectiveness of insecticide spraying, as they believe mosquitoes that are resting or flying above the level of spraying will not be killed; the most common vector in the northeastern United States, Culex pipiens, is a canopy feeder.
Testing of the mosquito samples requires the use of reverse-transcriptase PCR (RT-PCR) to directly amplify and show the presence of virus in the submitted samples. When using the blood sera of wild birds and sentinel chickens, samples must be tested for the presence of WNV antibodies by use of immunohistochemistry (IHC)[60] or enzyme-linked immunosorbent assay (ELISA).[61]
Dead birds, after necropsy, or their oral swab samples collected on specific RNA-preserving filter paper card,[62][63] can have their virus presence tested by either RT-PCR or IHC, where virus shows up as brown-stained tissue because of a substrate-enzyme reaction.
West Nile control is achieved through mosquito control, by elimination of mosquito breeding sites such as abandoned pools, applying larvacide to active breeding areas, and targeting the adult population via lethal ovitraps and aerial spraying of pesticides.
Environmentalists have condemned attempts to control the transmitting mosquitoes by spraying pesticide, saying the detrimental health effects of spraying outweigh the relatively few lives that may be saved, and more environmentally friendly ways of controlling mosquitoes are available. They also question the effectiveness of insecticide spraying, as they believe mosquitoes that are resting or flying above the level of spraying will not be killed; the most common vector in the northeastern United States, Culex pipiens, is a canopy feeder.
Prevention
Personal protective measures can be taken to greatly reduce the risk of being bitten by an infected mosquito:
- Using insect repellent on exposed skin to repel mosquitoes. EPA-registered repellents include products containing DEET (N,N-diethylmetatoluamide) and picaridin (KBR 3023). DEET concentrations of 30% to 50% are effective for several hours. Picaridin, available at 7% and 15% concentrations, needs more frequent application. DEET formulations as high as 30% are recommended for children over two months of age.[58] Protect infants less than two months of age by using a carrier draped with mosquito netting with an elastic edge for a tight fit.
- When using sunscreen, apply sunscreen first and then repellent. Repellent should be washed off at the end of the day before going to bed.
- Wear long-sleeve shirts, which should be tucked in, long pants, socks, and hats to cover exposed skin. Insect repellents should be applied over top of protective clothing for greater protection. Do not apply insect repellents underneath clothing.
- The application of permethrin-containing (e.g., Permanone) or other insect repellents to clothing, shoes, tents, mosquito nets, and other gear for greater protection. Permethrin is not labeled for use directly on skin. Most repellent is generally removed from clothing and gear by a single washing, but permethrin-treated clothing is effective for up to five washings.
- Be aware that most mosquitoes that transmit disease are most active during twilight periods (dawn and dusk or in the evening). A notable exception is the Asian tiger mosquito, which is a daytime feeder and is more apt to be found in, or on the periphery of, shaded areas with heavy vegetation. They are now widespread in the United States, and in Florida they have been found in all 67 counties.[59]
- Staying in air-conditioned or well-screened housing, and/or sleeping under an insecticide-treated bed net. Bed nets should be tucked under mattresses and can be sprayed with a repellent if not already treated with an insecticide.
Diagnosis
Diagnosis
An immunoglobulin M antibody molecule: Definitive diagnosis of WNV is obtained through detection of virus-specific IgM and neutralizing antibodies.
Diagnosis of West Nile virus infections is generally accomplished by serologic testing of blood serum or cerebrospinal fluid (CSF), which is obtained via a lumbar puncture. Initial screening could be done using the ELISA technique detecting immunoglobulins in the sera of the tested individuals.
Typical findings of WNV infection include lymphocytic pleocytosis, elevated protein level, reference glucose and lactic acid levels, and no erythrocytes.
Definitive diagnosis of WNV is obtained through detection of virus-specific antibody IgM and neutralizing antibodies. Cases of West Nile virus meningitis and encephalitis that have been serologically confirmed produce similar degrees of CSF pleocytosis and are often associated with substantial CSF neutrophilia.[55] Specimens collected within eight days following onset of illness may not test positive for West Nile IgM, and testing should be repeated. A positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavavirus infection and is not by itself evidence of an acute West Nile virus infection.[56]
If cases of suspected West Nile virus infection, sera should be collected on both the acute and convalescent phases of the illness. Convalescent specimens should be collected 2–3 weeks after acute specimens.
It is common in serologic testing for cross-reactions to occur among flaviviruses such as dengue virus (DENV) and tick-borne encephalitis virus; this necessitates caution when evaluating serologic results of flaviviral infections.[57]
Four FDA-cleared WNV IgM ELISA kits are commercially available from different manufacturers in the U.S., each of these kits is indicated for use on serum to aid in the presumptive laboratory diagnosis of WNV infection in patients with clinical symptoms of meningitis or encephalitis. Positive WNV test results obtained via use of these kits should be confirmed by additional testing at a state health department laboratory or CDC.
In fatal cases, nucleic acid amplification, histopathology with immunohistochemistry, and virus culture of autopsy tissues can also be useful. Only a few state laboratories or other specialized laboratories, including those at CDC, are capable of doing this specialized testing.
Differential diagnosis
A number of various diseases may present with symptoms similar to those caused by a clinical West Nile virus infection. Those causing neuroinvasive disease symptoms include the enterovirus infection and bacterial meningitis. Accounting for differential diagnoses is a crucial step in the definitive diagnosis of WNV infection. Consideration of a differential diagnosis is required when a patient presents with unexplained febrile illness, extreme headache, encephalitis or meningitis. Diagnostic and serologic laboratory testing using polymerase chain reaction (PCR) testing and viral culture of CSF to identify the specific pathogen causing the symptoms, is the only currently available means of differentiating between causes of encephalitis and meningitis.Vertical transmission
Vertical transmission,
the transmission of a viral or bacterial disease from the female of the
species to her offspring, has been observed in various West Nile virus
studies, amongst different species of mosquitoes in both the laboratory
and in nature.[48] Mosquito progeny infected vertically in autumn, may potentially serve as a mechanism for WNV to overwinter and initiate enzootic horizontal transmission the following spring, although it likely plays little role in transmission in the summer and fall.[49]
A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene CCR5 gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of CCR5 made up 4.0 to 4.5% of a sample of West Nile disease sufferers, while the incidence of the gene in the general population is only 1.0%.[53][54]
Risk factors
Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation.[50] For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension, and diabetes mellitus.[51][52]A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene CCR5 gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of CCR5 made up 4.0 to 4.5% of a sample of West Nile disease sufferers, while the incidence of the gene in the general population is only 1.0%.[53][54]
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