Diseases / List of Viral Diseases / West Nile Virus Disease / Detailed Disease Description:
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Editorial Overview of Disease Characteristics for specified SPECIES/TAXA for West Nile Virus Disease: Use sub-contents list below, or simply scroll down the page to view findings. See also: West Nile Virus Disease - Detailed Clinical Signs (Disease Reports)

Overview of Clinical Signs -

SPECIES OVERVIEW
Human
General summary:

Most infections are asymptomatic or so mild as to not be recognised and clinically recorded. In cases with overt clinical disease two main syndromes are recognised, West Nile Fever and West Nile Virus Encephalitis. Pancreatitis, hepatitis and myocarditis associated with WNV infection have also been described. Acute flaccid paralysis is notable in some individuals. The main signs noted may vary between outbreaks. (J84.5.w2, J84.9.w13, J98.358.w2,  J101.64.w1, J123.31.w1, J129.42.w1, B241.49.w49, B242.w1, B243.31.w1, P39.4.w3)

  • West Nile Virus Encephalitis and/or aseptic meningitis:-
    • "Headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, paralysis, and, rarely, death." (W170.Nov01.WNV2)
    • Fever, nuchal rigidity and CSF pleocytosis in cases of meningitis, altered mental status in patients with encephalitis. (P39.4.w3)
    • Additional signs and symptoms seen commonly include fatigue, nausea, vomiting, chills, photophobia and myalgia. (J84.7.w9, J98.352.w1)
    • Profound muscle weakness has been a notable feature of some patients.(J257.168.w2, J257.168.w3, J258.326.w1, P48.1.w2, N7.48.w1)
    • Typical arboviral encephalitis::
      • Symptoms of "fever, malaise, sore throat, nausea and vomiting, lethargy, stupor, coma and convulsions", with signs including "stiff neck, signs of meningeal irritation, tremors, convulsions, cranial nerve palsies, paralysis of extremities, exaggerated deep tendon reflexes, absent superficial reflexes, and pathological reflexes." (B252.32.w32)
      • Patients may present with abrupt onset fever, convulsions and other signs of central nervous system involvement. More typically, non-specific symptoms such as fever, abdominal pain, vertigo, sore throat and respiratory symptoms progress quickly to headache, meningeal signs, photophobia and vomiting. Lethargy, somnolence and intelligence deficits may indicate involvement of deeper structures while more severely affected patients will be obviously disoriented and may be comatose. Common signs include tremors, loss of abdominal reflexes, cranial nerve palsies, hemiparesis, monoparesis, difficulties swallowing and frontal lobe signs. Convulsions and focal signs may be present early in the course of the disease or develop later. (B251.198.w198)
      • "Headache, drowsiness, fever, vomiting and stiff neck are the usual presenting symptoms. Tremors, mental confusion, convulsions and coma may develop rapidly. Paralysis of the extremities occasionally occurs." (B247)
  • West Nile Fever:-

    • Fever and headache, usually with rash (often maculopapular and mainly on the trunk) and/or lympadenopathy. May be accompanied by a variety of other signs and symptoms including:
      • gastrointestinal signs (nausea, vomiting, loss of appetite, diarrhoea), 
      • abdominal pain,
      • arthralgia
      • muscle pains,
      • backache,
      • chills,
      • sore throat, 
      • flushed face,
      • weakness, 
      • ocular pain,
      • congested conjunctiva,
      • splenomegaly,
      • hepatomegaly,
    • (J84.5.w2, J91.5.w1, J101.59.w1, J101.64.w1, J123.31.w1, J129.42.w1, B241.49.w49, B242.w1, B243.31.w1, P31.6.w1, P39.4.w3)
  • West Nile-associated Acute Flaccid Paralysis:-
    • Acute, painless asymmetric flaccid paralysis of one or more limbs, sometimes monoplegia, no numbness, paraesthesia or sensory loss, although occasionally myalgia, often with bowel and/or bladder involvement, often with concurrent encephalopathy. (J84.9.w13, J84.9.w13)
    • Onset during acute infection. (J84.9.w13, P39.4.w3)
    • Four months after onset at least three individuals remained unable to move the affected limbs. (P48.1.w7)

Fever:

  • Usually present in both West Nile Fever and West Nile Virus Encephalitis.
    • Considered a characteristic finding (in 100% of cases) (P31.6.w1, J101.64.w1); in 86% (J91.61.w1); in 90% of 19 cases (J84.7.w9); in 98.3% (J84.7.w14); in all children and 31/37 adults. (J100.93.w1).
    • Sometimes the only clinical sign of infection. (J91.3.w1, J101.64.w1)
    • Commonly 38-40C reported. (J84.7.w32,  J100.93.w1, J101.59.w1, J101.64.w1)
    • Onset, where known, generally sudden. (J84.5.w2, J84.7.w32, J101.59.w1, J103.3.w1B241.49.w49)
    • Sometimes, but not usually, biphasic.(J84.5.w2, J91.3.w1, J100.93.w1, J129.42.w1, B243.31.w1)
    • Sometimes accompanied by chills. (P31.6.w1, J84.5.w2, J84.7.w10, J98.352.w1, J100.93.w1, J101.59.w1, J101.64.w1)
    • May be accompanied by sweating, sometimes profuse. (J91.5.w1)
    • Decline may be gradual. (J91.5.w1, J101.59.w1)
    • Present in 6/7 individuals with acute flaccid paralysis. (J84.9.w13)
    • Present in 91.5% of 188 confirmed cases in Mississippi, 2002. (P48.1.w2)
    • Present in 61/64 (95%) of cases in Ontario, Canada, 2002. (J257.168.w2)
  • (J84.5.w2, J84.5.w3, J84.7.w32, J84.7.w10, J84.7.w14, J84.9.w13, J91.3.w2, J91.5.w1, J96.72.w1, J98.352.w1, J99.54.w1, J99.57.w1, J101.59.w1, J101.64.w1, J102.17.w1, J106.55.w1, J107.36.w1, J111.72.w1, J115.13.w4, J123.31.w1, J129.42.w1, B241.49.w49, B242.w1, B243.31.w1, P31.6.w1)

Rash:

  • Rash has been a common finding in many outbreaks of West Nile Fever and has been described as a characteristic finding. J99.54.w1,J111.72.w1, B241.49.w49, B242.w1, B243.31.w1) and as the second most common finding (after fever). J129.42.w1)
    • In about 50% of cases of West Nile Fever ( B243.31.w1), in 50% (P31.6.w1, J101.64.w1) in 87% of those less than two years old, 73% of those up to five years old, but reducing to 25% and 20% of older children and 14% of adults. (J100.93.w1)
    • In 21.8% of cases during an outbreak in Israel, 2000. (J84.7.w14)
    • In 3/19 cases with encephalitis, meningitis or meningoencephalitis. (J84.7.w9)
    • Rare in outbreak in Volgograd region of Russia, 1999. (J84.7.w32)
    • Sometimes present: "Maculopapular or roseolar rash (in approximately half the cases, spreading from the trunk to the extremities and head)." (J84.5.w2) (J84.5.w2)
    • Present in 25% of 188 confirmed cases in Mississippi, 2002. (P48.1.w2)
    • Present in 17/64 (27%) cases in Ontario, Canada, 2002. (J257.168.w2)
  • Onset: rash may appear during the febrile phase or after it. (J101.64.w1, J129.42.w1, B243.31.w1)
  • Duration: may last for only several hours, commonly for less than a day, but sometimes for several days, even a week. (J101.59.w1, J101.64.w1 J129.42.w1, B243.31.w1)
  • Description: papular (J91.5.w1), maculopapular (J84.5.w2, J84.5.w3, J115.13.w4, B241.49.w49) or roseolar (J84.5.w2, J101.64.w1); characterised as non-painful, non-itching and not followed by desquamation. (J129.42.w1, B243.31.w1)
  • Location: Occurs most commonly on the trunk, less commonly on the face and upper extremities, not normally on the lower extremities. (J84.5.w2, J101.59.w1, J101.64.w1, J129.42.w1)

Lymphadenopathy:

  • Lymphadenopathy (glandular swelling) may be seen.
    • This has been a common or characteristic finding in many outbreaks.
    • It may affect one or more lymph nodes and is sometimes generalised. 
    • (P31.6.w1,J84.5.w3,  J91.23.w1, J99.54.w1, J101.59.w1, J101.64.w1, J107.36.w1, J115.13.w4, J123.31.w1, J129.42.w1, B241.49.w49, B242.w1, B243.31.w1)
    • Sometimes the only clinical sign of infection. (J101.64.w1)
    • Rare in outbreak in Volgograd region of Russia, 1999. (J84.7.w32)
    • Appeared more common in adults than in children during an outbreak in Israel (Maayan Zvi), 1951. (J100.93.w1)
    • Present less commonly than signs such as fever, headache and other pains and rash during an epidemic in South Africa, 1974. (J111.72.w1)
    • Described in only 4.3% of cases during an outbreak in Israel, 2000. (J84.7.w14)
    • Not a feature in patients with encephalitis during an outbreak in and near New York, USA 2000. (J84.7.w9)
    • Present in only 3.7% of 188 confirmed cases in Mississippi, 2002. (P48.1.w2)
    • Present in only 2/64 cases (3%) in Ontario, Canada, 2002. (J257.168.w2)

Malaise and Fatigue:

  • Malaise, fatigue and general weakness are commonly noted, sometimes with drowsiness or somnolence. (J84.5.w2, J84.5.w3, J91.3.w2, J91.5.w1, J101.59.w1, J102.17.w1, J106.55.w1, J115.13.w4, B241.49.w49)
    • Malaise may be noted more frequently in adults than children. (J100.93.w1)
    • General tiredness and weakness commonly accompany the initial fever (J101.64.w1) and may continue during the recovery phase. (J111.72.w1)
    • Generalised weakness is sometimes a prominent sign in patients with encephalitis. (J98.352.w1); e.g. recorded in 8/19 (40% of cases) of individuals with encephalitis, meningitis or meningoencephalitis. (J84.7.w9)
    • Lethargy in 24.6% and general muscle weakness in 56.9% of 188 confirmed cases in Mississippi, 2002. (P48.1.w2)

Headache and other Pain:

  • Severe headache is commonly noted and in many outbreaks has been considered to be one of the main symptoms. (J84.5.w2, J84.5.w3, J84.7.w9, J84.7.w10, J84.7.w32, J91.5.w1, J99.57.w1, J100.93.w1, J102.17.w1, J103.3.w1; J106.55.w1, J111.72.w1, J115.13.w4, J123.31.w1, J129.42.w1, B243.31.w1)
    • In 80% of cases (P31.6.w1); in 51% of cases (J91.61.w1); seen in 78% of adults and 37% of children. (J100.93.w1); in 57.9% of cases during an outbreak in Israel, 2000. (J84.7.w14); in 77% of 352 individuals with acute aseptic meningitis and encephalitis in Romania in 1996. (J98.352.w1
    • Rarely reported in experimental infection of patients with terminal neoplasia but may have been masked by analgesics. (J91.3.w1)
    • Often frontal. (J101.59.w1)
    • May be primarily occipital. (J91.5.w1)
    • Present in 72.3% of 188 confirmed cases in Mississippi, 2002. (P48.1.w2)
  • Ocular pain has been reported in many cases, sometimes with a note that it has been associated with eye movement; it has been a common sign in some outbreaks (e.g. in 45% of cases (P31.6.w1, J101.64.w1)) although it is generally less common than headache. (P31.6.w1, J84.5.w3, J91.3.w2, J100.93.w1 J101.59.w1, J101.64.w1, J102.17.w1; J111.72.w1, J129.42.w1)
  • Myalgia (muscle aches and pains) may be noted, often generalised. In outbreaks myalgia has been noted in e.g. 15.4% (J84.7.w14), 25% (P31.6.w1), 32% (J84.7.w9), 34.6% (P48.1.w2) 55% (J257.168.w2) of patients. (J84.5.w2, J84.5.w3, J84.7.w14, J84.7.w9, J100.93.w1, J111.72.w1, J115.13.w4, J123.31.w1, J257.168.w2, P31.6.w1, P48.1.w2, B241.49.w49, B243.31.w1)
  • Backache or back pain may be noted as a specific symptom. (J84.5.w2, J100.93.w1, J101.59.w1, J107.36.w1, J129.42.w1, B243.31.w1); in one outbreak this was recorded in 40% of individuals (P31.6.w1, J101.64.w1)
  • Abdominal tenderness or pain has been recorded for some patients (J91.3.w2) and noted in variable percentage of patients during outbreaks (20% of cases) (P31.6.w1), 43% (J91.61.w1)
  • Arthralgia (joint pain) may be noted and has sometimes been a common finding (e.g. in 37% of patients in one outbreak (J91.61.w1), in 2/19 (11% of cases) in another (J84.7.w9)), in 24.5% of 188 patients in Mississippi, 2002 (P48.1.w2), in 15/48 (31%) patients in Ontario, Canada, 2002. (J257.168.w2). (J84.7.w9, J91.61.w1, J111.72.w1, J257.168.w2, P48.1.w2)

Muscle weakness/flaccid paralysis:

  • Mild encephalitis and severe myelitis, described as resembling the polio syndrome. In one individual, 68 years old. (J105.135.w1)
  • Flaccid paresis of the left lower extremity with loss of deep tendon reflexes but without any sensory changes. In one individual, 22 years old. (J107.36.w1)
  • Guillain-Barr Syndrome (acute inflammatory demyelinating polyradiculoneuritis). Progressive weakness including proximal and distal muscles, bilateral weakness of facial muscles, and reduced respiration such that ventilatory support was required. In one individual 69 years old. (J106.55.w2)
  • Muscle weakness (3/19 cases, 16% of cases). During an outbreak in and near New York, USA 2000. (J84.7.w9)
  • Acute flaccid paralysis syndrome in six individuals. One or more limbs affected with normal sensation but hyporeflexia or areflexia and asymmetrical weakness, sometimes flaccidity. (N7.51.w1)
  • Acute flaccid paralysis described in seven patients, three of which did not have other findings suggestive of severe central nervous system involvement. In general, acute, painless asymmetric flaccid paralysis of one or more limbs, sometimes monoplegia, no numbness, paraesthesia or sensory loss, although occasionally myalgia, and often with bowel and/or bladder involvement. (J84.9.w13)
    • Four months after onset at least three individuals remained unable to move the affected limbs. (P48.1.w7)
  • Movement disorders reported include tremor (static/kinetic), sometimes with movement, and occasionally disabling and myoclonus, most frequently involving the upper extremity or face. Movement disorders have generally had onset at more than five days after the initial symptoms. In a prospective series of patients tremor was noted in 15 individuals (94%) and myoclonus in 10 (63%). (P39.4.w3)
  • Parkinsonism was noted in 11 of a prospective series of patients (68%), with cogwheel rigidity, bradykinesia and postural instability, but no tremor at rest. This was seen in individuals with meningitis or encephalitis. (P39.4.w3)
  • Bilateral leg weakness (acute flaccid paralysis) with fever and frontal headache. Marked decreases in motor function of both legs, particularly the right leg, and diminished reflexes in both legs, but intact sensation. (J281.181.w1)
  • A review of data from 13 patients with WNV infection found that muscle weakness associated with this infection may vary from acute flaccid paralysis, with or without associated fever or meningitis, through severe muscle weakness to disabling fatigue. (J292.28.w1)

Abdominal and gastro-intestinal signs:

  • Gastro-intestinal signs are sometimes seen and may include nausea, vomiting, diarrhoea, abdominal pain or discomfort, less commonly anorexia, occasionally hepatomegaly or splenomegaly. Severe pancreatitis and hepatitis have been recorded as rare complications. (J84.5.w2, J91.5.w1, J123.31.w1, J129.42.w1, B241.49.w49, B243.31.w1)
    • One or more gastrointestinal symptom(s) or abdominal abnormalities in 11/19 cases (58% of cases). (J84.7.w9)
    • Anorexia or lack of appetite recorded (J91.5.w1, J99.57.w1); in a small proportion of cases (J101.59.w1); in 55% of individuals. (P31.6.w1, J101.64.w1)
    • Gastrointestinal signs have occurred in children without other signs considered more typical. (J99.54.w1)
    • Vomiting in 53% of 352 individuals with acute aseptic meningitis and encephalitis in Romania in 1996. (J98.352.w1)
    • Gastro-intestinal disturbances, anorexia and nausea in a few patients. During an outbreak in Israel, 1952. (J101.59.w1)
    • Nausea noted (J84.5.w3, J102.17.w1, J115.13.w4);  in a small proportion of patients (J101.59.w1); in 25% of cases (P31.6.w1, J101.64.w1);  in8/19 cases, 42%, (J84.7.w9); common during an epidemic in South Africa, 1974. (J111.72.w1)
    • Vomiting noted (J106.55.w1, J115.13.w4)); in 10% (P31.6.w1, J101.64.w1); (8/19 cases, 42% of cases), (J84.7.w9); in 31.3% of cases during an outbreak in Israel, 2000. (J84.7.w14); seen but not common during an epidemic in South Africa, 1974. (J111.72.w1); common in an outbreak in Volgograd region of Russia, 1999. (J84.7.w32)
    • Abdominal pain / diarrhoea:
    • Abdominal pain (4/19, 21% of cases). (J84.7.w9)
    • Diarrhoea (3/19, 16% of cases) (J84.7.w9); diarrhoea (30% of cases), abdominal pain (20% of cases).(P31.6.w1, J101.64.w1)
    • Abdominal pain and/or diarrhoea in 18.5% of cases during an outbreak in Israel, 2000 (J84.7.w14).
    • Abdominal pain and diarrhoea both rare in outbreak in Volgograd region of Russia, 1999. (J84.7.w32)
    • Anorexia, nausea, vomiting and abdominal pain considered common signs, while diarrhoea was less common. Abdominal pains, sometimes with diarrhoea, were noted by 19% of patients; anorexia and nausea were common and vomiting occurred in 45% of children and 19% of adults. (J100.93.w1)
    • Diarrhoea and nausea seen commonly, with vomiting and tenderness of the liver both less common. During an epidemic in South Africa, 1974. (J111.72.w1)
    • Nausea and vomiting. (J115.13.w4)
    • Nausea present in 50.8% and vomiting in 35.8% of 188 confirmed cases in Mississippi, 2002. (P48.1.w2)
    • In Ontario, Canada in 2002, 46/55 (84) patients had anorexia, 40/58 (69%) nausea and 31/58 (53%) vomiting. (J257.168.w2)
  • Splenomegaly: noted (J84.5.w2, J129.42.w1); spleen sometimes enlarged ( J101.59.w1); mild splenomegaly (J107.36.w1); spleen enlargement in 20% of cases. (P31.6.w1, J101.64.w1)
  • Hepatomegaly: slight liver enlargement (J91.3.w2);  liver enlargement in 10% of cases (P31.6.w1, J101.64.w1).
  • Acute pancreatitis with abdominal pain and high blood and urine amylase for several days together with more usual clinical signs of fever (38C), macular rash and enlarged lymph nodes reported in a 20-year-old woman in Israel, 1969. (J91.23.w1)
  • Severe hepatitis in four individuals. (B241.49.w49)

Neurological signs:

  • Until recently most outbreaks of WNV disease have involved mainly West Nile Fever, with neurological signs indicating central nervous system involvement in only a small percentage of affected individuals. During recent outbreaks (late 1990's onwards), a high percentage of clinical cases have involved neurological signs.
    • Meningitis or meningoencephalitis usually occurs at low incidence, "amounting probably to less than 1 in 100 clinical cases." (P31.6.w1)
    • Rare in young adults, e.g. 1/297 cases in soldiers, but more common in the elderly (16/49 cases). (J99.54.w1)
    • Light and transitory meningeal involvement seen in only a few cases, involving "a stiff neck and Kernig's sign." During an outbreak in Israel, 1952. (J101.59.w1)
    •  CNS involvement may occur more frequently in adults than in children. Encephalitic signs include a depressed sensorium (drowsiness to near coma), involuntary twitching, convulsions, hyperactivity followed by decreased activity of tendon reflexes, cogwheel rigidity, paresis and paralysis. (J129.42.w1)
    • 11% of individuals "showed definite or suggestive clinical signs of diffuse encephalitis" including "depressed sensorium, ranging from drowsiness to near-coma; involuntary twitching of hands, and occasionally of face and legs; and irregular variation of deep tendon reflexes, usually hyperactivity followed by diminished activity. Cogwheel rigidity was usually observed. Paralysis or paresis occurred only once and recovery was complete... pyramidal tract signs were observed only in the one patient with paralysis. Cranial nerves and sensory perception were never affected." Experimental infection in patients with terminal neoplasia (J91.3.w1)
    • Encephalitis, apparently mild, seen in some cases. During an epidemic in South Africa, 1974. (J111.72.w1)
    • Insomnia noted in some cases. During an epidemic in South Africa, 1974. (J111.72.w1)
    • Signs of meningitis or encephalitis seen occasionally. (J84.5.w2)
    • Occasionally meningitis. (B242.w1)
    • Meningeal involvement or meningoencephalitis were reported less commonly and more frequently in older patients. (B241.49.w49)
    • Neurological presentations include meningitis or meningoencephalitis in a small proportion of patients (particularly elderly individuals), anterior myelitis and encephalopolyradiculitis. (B243.31.w1)
    • "Occasionally, acute aseptic meningitis or encephalitis (associated with neck stiffness, vomiting, confusion, disturbed consciousness, somnolence, tremor of extremities, abnormal reflexes, convulsions, pareses, and coma), anterior myelitis." (J84.5.w2)
    • Central nervous system involvement (acute aseptic meningoencephalitis or meningitis) involved frequently during an outbreak in Volgograd region of Russia, 1999 with 480 overt cases of infection. (J84.7.w32)
    • Acute aseptic meningitis and encephalitis in 352 individuals during an outbreak in Romania (southeastern Romania including Bucharest) in 1996. (J98.352.w1)
    • Clinical presentations were of diffuse muscle weakness (40%), encephalitis (27%), aseptic meningitis (24%) and fever with headache (9%) during the outbreak in New York, 1999. (P32.1.w2)
    • Encephalitis, meningitis or meningoencephalitis requiring hospitalisation in nineteen individuals during an outbreak in and near New York, USA 2000. (J84.7.w9)
    • Encephalitis. (N7.50.w2)
  • A variety of neurological signs may be seen:
    • Neck stiffness in 57% of 352 individuals with acute aseptic meningitis and encephalitis in Romania in 1996. (J98.352.w1)
    • Confusion in 34% of 352 individuals with acute aseptic meningitis and encephalitis in Romania in 1996. (J98.352.w1)
    • Disturbed consciousness may be a predominant sign in patients with encephalitis. (J98.352.w1)
    • Disorientation may be a predominant sign in patients with encephalitis. (J98.352.w1)
    • Motor tone may be decreased with hypotonia, or increased with hyper-reflexia and abnormal reflexes. (J98.352.w1)
    • Ataxia and extrapyramidal signs recorded in 17% of patients. (J98.352.w1)
    • Cranial-nerve palsies or seizures recorded in small percentages of patients. (J98.352.w1)
    • Coma resulted in 13% of 352 individuals. (J98.352.w1)
    • Central nervous system involvement in 46% and convulsions in 11%. (J91.61.w1)
    • Signs of meningismus in three individuals, with somnolence in two and dizziness in one.( J102.17.w1)
    • Confusion in 7/7 individuals, with severe somnolence and disorientation in 3/7 individuals, convulsions in 2/7 individuals, dysarthria in 2/7 individuals, urinary incontinence in 1/7 individuals, mild lower paraparesis in 1/7 individuals. Meninigism detected in 6/7 individuals on neurological examination and pyramidal signs in 5/7 patients. (J103.3.w1)
    • Mild encephalitis and severe myelitis, described as resembling the polio syndrome. In one individual, 68 years old. (J105.135.w1)
    • Brainstem and cortical nervous signs including confusion, cranial nerve defects, ataxia and brisk tendon reflexes. Anterior horn cell involvement was indicated by weakness and tongue fasciculations. In one individual, 15 years old. (J106.55.w1)
    • Mild weakness of the left face accompanied by fasciculations, and flaccid paresis of the left lower extremity with loss of deep tendon reflexes but without any sensory changes. In one individual, 22 years old. (J107.36.w1)
    • Guillain-Barr Syndrome (acute inflammatory demyelinating polyradiculoneuritis). Progressive weakness including proximal and distal muscles, bilateral weakness of facial muscles, and reduced respiration such that ventilatory support was required. In one individual 69 years old. (J106.55.w2)
    • Clinical findings included altered mental status (11/19 cases, 58% of cases), abnormal reflexes (four hyporeflexive, two with abnormal plantar responses) (6/19 cases, 32% of cases), stiff neck (6/19 cases, 32% of cases), seizures (3/19 cases, 16% of cases), cerebellar abnormality (ataxia) (2/19 cases, 11% of cases), cranial nerve palsy (2/19 cases, 1% of cases), nystagmus (one case, fatal), depressed gag reflex (one case, fatal), muscle weakness (3/19 cases, 16% of cases) During an outbreak in and near New York, USA 2000. (J84.7.w9)
    • Encephalitis in two individuals, fatal in one case. In one patient confusion, disorientation, somnolence and aphasia, progressing to decreased responsiveness, limb spasticity, bilateral ptosis, facial nerve paralysis, bilateral Babinski response and requirement for mechanical ventilation. In the second individual progression: "became stuporous with severe respiratory acidosis; mechanical ventilation was begun... The patient remained febrile and stuporous and died on day 33 of hospitalization." (J84.7.w10)
    • Patients with encephalitis, some of whom had profound muscle weakness (with axonal neuropathy by electromyelogram and requiring respiratory support). (N7.48.w1)
    • 57.9% of cases presented with encephalitis and 15.9% with meningitis. Neurological signs included a change in level of consciousness (46.8% of cases), confused state (39.5% of cases), nuchal rigidity (28.7% of cases), coma (16.7% of cases) and focal neurological signs (9.4% of cases) during an outbreak in Israel, 2000. (J84.7.w14).
    • Brudzinski's sign indicating meningitis in ten children. (J100.93.w1)
    • In one patient, in addition to signs of meningeal irritation, signs of cortical, brainstem and multiple cranial nerve lesions, including optic neuritis. (J220.162.w1)
    • Complete motor aphagia complicating meningoencephalitis in one four-year-old boy. (J221.86.w1)
    • Confusion (disorientation and difficulty in following commands) in one 89-year-old man with encephalitis, slow recovery over a period of more than one month, with disorientation remaining at one month after onset. In Massachusetts, USA, during 2001. (J221.346.w1)
    • Acute flaccid paralysis syndrome in six individuals. One or more limbs affected with normal sensation but hyporeflexia or areflexia and asymmetrical weakness, sometimes flaccidity. (N7.51.w1)
    • Meningoencephalitis was found in 84.0% of 188 confirmed cases in Mississippi, 2002. Neurological signs included altered mental status (34.6%), stiff neck (29.8%) and seizures (2.1%).(P48.1.w2)
    • In Ontario, Canada in 2002, a decreased level of consciousness was noted in 75% of patients, neuromuscular weakness in 41%, dysphagia in 34%, ataxia in 31%, dysarthria in 17%, vertigo in 14%, intention tremor in 13%, diplopia or ophthalmoplegi in 13%, facial weakness in 11%, blurred vision in 9%, dysdiadokinesis in 8%, seizure in 6%, incontinence in 5%, tongue weakness in 5%, myelopathy in 3%, nystagmus in 3%, Parkinsonism in 3%. (J257.168.w2)
  • Acute flaccid paralysis described in seven patients, three of which did not have other findings suggestive of severe central nervous system involvement. In general, acute, painless asymmetric flaccid paralysis of one or more limbs, sometimes monoplegia, no numbness, paraesthesia or sensory loss, although occasionally myalgia, and often with bowel and/or bladder involvement. (J84.9.w13)
    • Four months after onset at least three individuals remained unable to move the affected limbs. (P48.1.w7)
  • Movement disorders reported include tremor (static/kinetic), sometimes with movement, and occasionally disabling and myoclonus, most frequently involving the upper extremity or face. Movement disorders have generally had onset at more than five days after the initial symptoms. In a prospective series of patients tremor was noted in 15 individuals (94%) and myoclonus in 10 (63%). (P39.4.w3)
  • Parkinsonism was noted in 11 of a prospective series of patients (68%), with cogwheel rigidity, bradykinesia and postural instability, but no tremor at rest. This was seen in individuals with meningitis or encephalitis. (P39.4.w3)
  • Bilateral leg weakness (acute flaccid paralysis) with fever and frontal headache. Marked decreases in motor function of both legs, particularly the right leg, and diminished reflexes in both legs, but intact sensation. (J281.181.w1)

Ocular signs:

  • Conjunctivitis, conjunctival injection or congestion of the eyes sometimes reported. (P31.6.w1, J91.5.w1, J101.59.w1,  J101.64.w1, J123.31.w1, J129.42.w1)
  • Reported in 60% of cases in one outbreak. (P31.6.w1, J101.64.w1)
  • Conjunctivitis rarely noted in the outbreak in the Volgograd region of Russia, 1999 (J84.7.w32)
  • Photophobia in one individual (J102.17.w1); in 6/19 cases (32% of cases). (J84.7.w9)
  • Signs of papillitis (hyperemia and blurring of the disc margins) in one individual. (J102.17.w1)
  • Temporarily decreased visual acuity and development of multiple round, cream-coloured chorioretinal lesions, 300-1000m diameter, scattered in the fundus and persisting for over one year, together with a mild vitritis which cleared after several months, associated with WNV encephalitis (malaise, muscle weakness, dysarthria and gastroenteritis) in an 81-year-old man with long-standing nonproliferative diabetic retinopathy. In a patient in the USA, 2002.(J276.23.w1)
  • Clinical signs of ocular pain and blurred vision affecting one eye, associated with fever, headache, diffuse muscle pain and neck stiffness (WNV meningitis). Ophthalmic examination revealed a swollen slightly pale disc on the clinically affected side and lesser swelling on the other side; optic neuritis was diagnosed. In a young adult in Israel, 2000. (J277.31.w1)
  • Clinical signs of "floaters" in the left eye together with fatigue, left-sided frontal headache and low-grade fever. Anterior uveitis, vitritis and nonnecrotising chorioretinitis were noted in the left eye and milder similar findings in the right eye. Anterior uveitis responded to steroids. Ophthalmological examination showed deep, flat, creamy whitish-yellow outer choroidal lesions, 500-750 um extending superiorly in a linear radial pattern from the optic nerve head in the left eye, and less extensive faint lesions in the right eye. The lesions were actively inflammatory. A moderate vitritis was noted overlying the optic disk and superior retina of the left eye. Small intraretinal haemorrhages, 200um diameter , were present in the right eye and similar haemorrhages were noted associated with some of the lesions in the left eye. Fluorescein angiography revealed blocked fluorescence ad leakage from the lesions. Treatment was initiated with local (ocular) 1% prednisolone acetate QID. The chorioretinitis healed; two weeks after presentation there was significantly less vitritis and a decrease in fluorescein leakage, while the lesions appeared smaller and pigmented. This was accompanied by an improvement in visual acuity (from 20/25 OD and 20/40 OS to20/30 OS.  In a 62 year old woman in Chicago, confirmed positive for WNV IgM antibodies in serum. (J282.121.w1)
Respiratory signs:
  • Respiratory signs (unspecified), without more typical signs, has been noted: in children. (J99.54.w1); in 23% of cases (J91.61.w1).
  • Pharyngitis (sore throat, reddening of the throat, congestion of the throat) has been reported in some cases/outbreaks (P31.6.w1, J91.5.w1, J100.93.w1  J101.59.w1, J101.64.w1, J111.72.w1, J115.13.w4, J129.42.w1, B241.49.w49, B243.31.w1), in 30% of cases in one outbreak and has been described as a characteristic finding. (B242.w1)
    • Dryness of the throat in a small proportion of patients. (J101.59.w1)
  • Slight cough, increased breath sounds in the right axilla. (J91.3.w2)
  • Cough in 8% (P31.6.w1, J101.64.w1); in 3/19, (16% of cases)(J84.7.w9).
  • Shortness of breath in 2/19 (11% of cases). (J84.7.w9)
  • Respiratory signs rarely noted in outbreak in Volgograd region of Russia, 1999. (J84.7.w32)
  • Reduced respiration requiring ventilatory support has been reported associated with central nervous signs. (J106.55.w2)
Miscellaneous signs:
  • Flushed face (J101.59.w1), seen in 55% of cases in one outbreak in Israel, (P31.6.w1, J101.64.w1), may be associated with rash (J115.13.w4)
  • Myocarditis is a rare complication. (J123.31.w1, B243.31.w1, J84.5.w2)
    • In one patient suggested by palpitations, stabbing sensation and pressure in the left chest area, with palpitations and chest discomfort persisting much longer than fever, and ECG changes indicative of myocarditis. (J99.57.w1)
    • Severe angina was present in seven cases. (J100.93.w1)
  • Coating of tongue in 50% of cases. (P31.6.w1, J101.64.w1)
  • Orchitis reported in some cases during an epidemic in South Africa, 1974. (J111.72.w1)
  • Rhabdomyelitis reported in 14 individuals in Chicago in September 2002. (P39.4.w3)

Recovery and Convalescence:

  • Convalescence may take several weeks.
    • Convalescence is generally shorter in children than in adults.
    • Weakness, fatigue and listlessness are characteristic of the convalescent period.

(J91.5.w1, J111.72.w1, J129.42.w1, B241.49.w49)

  • Recovery is generally complete. (J91.5.w1)
  • In WN virus-associated acute flaccid paralysis four months after onset at least three individuals remained unable to move the affected limbs. (P48.1.w7)
  • Long-term disability is occurring in some patients with neurological disease. (J257.168.w3)

LITERATURE REPORTS: 

General reviews: 

  • Usually a febrile, influenza-like illness, commonly with headache and fatigue, sometimes with rash, sometimes with gastro-intestinal signs and occasionally with signs of meningitis and/or encephalitis. (J84.5.w2)
  • "Clinical disease in man produced by WN virus infection is usually mild."  (B241.49.w49)
  • "Characterised by fever, headache, sore throat, muscular pain, rash, lymphadenopathy, and occasionally by meningoencephalitis." (B242.w1)
  • "The signs and symptoms of the disease are not specific, and their percentages seem to differ considerably in the outbreaks reported." (J84.7.w14) "Generally, the signs, symptoms, laboratory findings, and imaging results in WN fever are nonspecific." (J84.7.w14)
  • From endemic disease in Egypt and epidemics in Israel: "a rapid onset of fever, 38-40C, lasting for 5 to 6 days. Malaise, frontal headache, pain associated with eye movement, and muscle pain are common symptoms. Some patients had gastrointestinal disturbances and a sore or congested throat. Prominent signs included enlargement of lymph nodes and a maculopapular rash. Convalescence frequently was prolonged, lasting 1 to 2 weeks." Meningeal involvement or meningoencephalitis were reported less commonly and more frequently in older patients. (B241.49.w49)
  • Signs and symptoms seen vary both within and between outbreaks. (J101.64.w1)
  • "The incubation period is 5 to 15 days. The vast majority of infections are asymptomatic. Mild, nonspecific symptoms include fever, headache, myalgias, rash, conjunctivitis, and lymphadenopathy. In more serious cases, pancreatitis, myocarditis, and hepatitis have been reported. Treatment is currently nonspecific and supportive. Fatalities generally occur in older people, although child fatalities have been documented." (J123.31.w1)
  • "The typical case is quite mild, characterized by fever, headache, backache, generalized myalgia, and anorexia. The course of fever may be biphasic. Rash occurs in approximately half of the cases; onset of rash is either during the febrile phase or at the end of it. The rash is roseolar or maculopapular, is nonirritating, and principally involves the chest, back, and upper extremities. Rash may persist for up to a week and resolves without desquamation. Generalized lymphadenopathy is a common finding. Pharyngitis and gastrointestinal symptoms (nausea, vomiting, diarrhoea, abdominal pain) may occur. (B243.31.w1) Neurological presentations include meningitis or meningoencephalitis in a small proportion of patients (particularly elderly individuals), anterior myelitis and encephalopolyradiculitis. Other, rare, complications include myocarditis, pancreatitis and hepatitis. (B243.31.w1)
  • "West Nile fever in humans usually is a febrile, influenzalike illness, characterised by an abrupt onset (incubation period is 3 to 6 days) of moderate to high fever (3 to 5 days, infrequently biphasic, sometimes with chills), headache (often frontal), sore throat, backache, myalgia, arthralgia, fatigue, conjunctivitis, retrobulbar pain, maculopapular or roseolar rash (in approximately half the cases, spreading from the trunk to the extremities and head), lymphadenopathy, anorexia, nausea, abdominal pain, diarrhoea, and respiratory symptoms. Occasionally (<15% of cases), acute aseptic meningitis or encephalitis (associated with neck stiffness, vomiting, confusion, disturbed consciousness, somnolence, tremor of extremities, abnormal reflexes, convulsions, pareses, and coma), anterior myelitis, hepatosplenomegaly, hepatitis, pancreatitis, and myocarditis occur". (J84.5.w2)
  • Fever, 101 to 105F, usually lasting for two or three days, but ranging from one to 12 days and in about 10% of cases biphasic with one to two days of no fever followed by a second period of fever and other signs. Rash is the second most common signs and is seen most frequently in children. It may appear during or after the fever and lasts usually less than 24 hours but occasionally several days. It is seen mainly on the trunk, less commonly on the face and extremities, is bright pink, discrete, maculo-papular, non-painful, non-itching and not followed by desquamation. In adults severe headache is a common complaint. Other common signs and symptoms include chest and back pain, ocular pain, gastro-intestinal disturbances (anorexia, nausea, vomiting, diarrhoea), lymphadenitis (single node or generalised), sometimes a palpable (enlarged) spleen, injected conjunctiva and pharyngitis (sore throat). Duration of the acute phase is usually three to five days but sometimes up to 12 days. Convalescence in adults may last several weeks (weakness and fatigue) but is shorter in children. CNS involvement may occur more frequently in adults than in children. Encephalitic signs include a depressed sensorium (drowsiness to near coma), involuntary twitching, convulsions, hyperactivity followed by decreased activity of tendon reflexes, cogwheel rigidity, paresis and paralysis. Fatality rate may reach 8%. (J129.42.w1)
  • Symptoms seen may vary between outbreaks. (J98.358.w2)
  • "Clinical features range from fever accompanied by malaise, headache, myalgia, rash, lymphadenopathy, eye pain, anorexia and vomiting lasting for 3 to 6 days, to severe meningoencephalitis. Severe muscular weakness and flaccid paralysis have been experienced in several patients." (J257.168.w3)

Epidemics/Clinical case histories:

  • In an adult technician in Egypt: "Severe headache, primarily in the occipital region, accompanied by muscular fatigue, particularly of the arms and legs, some initial gastric discomfort, anorexia and fever of 38-39C for several days were the outstanding manifestations. Recovery was somewhat retarded but complete." (J91.5.w1)
  • In children in Egypt: "Fever of rapid onset, averaging 38.5-39C, accompanied by gastro-intestinal disturbances, malaise, profuse sweating, a fine papular rash (5 cases), moderate enlargement of the cervical, axillary and inguinal lymph nodes (3 cases), and occasionally congestion of the eyes and throat. The fever remained high for 5-6 days followed by gradual decline and a rather prolonged convalescence. No signs of central nervous system involvement were observed. As far as is known no deaths could be attributed to the infection and frank encephalitis in the highly endemic area was exceedingly rare." (J91.5.w1)
  • In the Middle East: A wide clinical spectrum ranging from inapparent or mild illness to severe encephalitis. "The most prominent features of the disease in clinically typical cases are: fever, severe headache and glandular swelling; following in frequency are a flushed face, injection of the conjunctivae and a skin rash." Meningitis or meningoencephalitis usually occurs at low incidence, "amounting probably to less than 1 in 100 clinical cases." (P31.6.w1) Signs and symptoms may include: fever (100% of cases), headache (80% of cases), backache (40% of cases), chills (35% of cases), muscle pains (25% of cases), ocular pain (45% of cases), lack of appetite (55% of cases), nausea (25% of cases), vomiting (10% of cases), abdominal pain (20% of cases), diarrhoea (30% of cases), sore throat (30% of cases), cough (8% of cases), flushed face (55% of cases), conjunctival injection (60% of cases), coating of tongue (50% of cases), injection of throat (40% of cases), glandular swelling (occipital region 75%, axillary region 90% of cases), inguinal region 85% of cases), rash (50% of cases), spleen enlargement (20% of cases), liver enlargement (10% of cases). (P31.6.w1)
  • In soldiers, fever, lymphadenopathy and rash, with meningoencephalitis in only 1/297 individuals. In other adults "a typical clinical course of varying intensity including abortive, mild and severe cases" and one case complicated by meningo-encephalitis. In children, "the disease ran a typical course, but the symptoms and signs were rather mild. In several children there was involvement of the intestinal or respiratory tracts without the appearance of more typical signs and symptoms of West Nile fever" and one individual with meningo-encephalitis. In elderly individuals, mainly fever of variable degree and duration (33/49 cases), in12 cases "a severe course marked by neurological signs and symptoms of meningo-encephalitis" with prompt recovery and in four cases the development of impaired consciousness, signs and symptoms suggestive of severe brain damage, fulminating course and death. During an outbreak in Israel in 1957. (J99.54.w1).
  • Acute pancreatitis with abdominal pain and high blood and urine amylase for several days together with more usual clinical signs of fever (38C), macular rash and enlarged lymph nodes reported in a 20-year-old woman in Israel, 1969. (J91.23.w1)
  • Acute aseptic meningoencephalitis, meningitis or acute fever. Abrupt onset, fever up to 39-40C, asthenia, headache and vomiting were noted as clinical features but in comparison with most previous outbreaks, the disease seen was generally more severe, with central nervous system involvement frequently observed while rash, conjunctivitis, abdominal pain, diarrhoea, respiratory symptoms and lymphadenopathy were rare. In 183/318 individuals sampled (58% of cases) serum contained anti-WN virus IgM at a level indicative of acute infection, using an IgM-capture ELISA. It was estimated that the epidemic involved 480 overt human cases. During an outbreak in Volgograd region of Russia, 1999. (J84.7.w32)
  • Acute aseptic meningitis and encephalitis in 352 individuals. "The onset of illness was typically abrupt, with fever (91% of patients), acute headache (77% of cases), neck stiffness (57% of cases), vomiting (53% of cases), chills (45% of cases), and confusion (34% of cases). Disorientation, disturbed consciousness, and generalised weakness were the predominant signs in patients with encephalitis; some patients had decreased motor tone with hypotonia, and others had increased tone, hyper-reflexia, and abnormal reflexes. Ataxia and extrapyramidal signs were recorded in 17% of patients, and cranial-nerve palsies or seizures in smaller proportions. The illness progressed to coma in 13% of cases, and among patients with confirmed or probable infection there were 17 deaths (fatality/case ratio 4.3% of cases), all in patients older than 50 years." Also confirmed infection in individuals diagnosed with acute respiratory infection, acute febrile illness, monoparesis, cerebrovascular disease, chronic disease or no diagnosis. During an outbreak in Romania (southeastern Romania including Bucharest) in 1996. (J98.352.w1)
  • "Sudden onset of disease characterised by malaise, general weakness, a chilly sensation with fever, drowsiness, severe frontal headache, aching of the eyes when moved, and pains mostly in the chest and lumbar regions. The fever rose quickly and usually ranged between 38C and 40C. A small number of patients had gastrointestinal disturbances, anorexia, nausea, and dryness in the throat. One of the characteristics was a flushed face and injected conjunctivae." High temperatures usually remained for two to three days before gradually returning to normal over the following three days. General enlargement of one or more lymph nodes was a prominent finding and the spleen was sometimes enlarged. A slight redness of the throat was noted in some individuals and a maculopapular rash of short duration, spreading mostly over the trunk, was present in many patients. "In very few cases light transitory meningeal involvement (a stiff neck and Kernig's sign) was encountered during the acute stage." During an outbreak in Israel, 1952. (J101.59.w1)
  • Typically fever, together with lymphoglandular swelling and/or rash. Sometimes only lymph node enlargement or only fever. Typically (75% of cases) acute onset, almost always with general tiredness and weakness accompanying the initial fever (38-40C). Illness was often moderate but in some individuals there was "great prostration and apathy."  Signs and symptoms included: fever (100% of cases), headache (80% of cases), backache (40% of cases), chills (35% of cases), muscle pains (25% of cases), ocular pain (45% of cases), lack of appetite (55% of cases), nausea (25% of cases), vomiting (10% of cases), abdominal pain (20% of cases), diarrhoea (30% of cases), sore throat (30% of cases), cough (8% of cases), flushed face (55% of cases), conjunctival injection (60% of cases), coating of tongue (50% of cases), injection of throat (40% of cases), glandular swelling (occipital region 75%, axillary region 90% of cases), inguinal region 85% of cases), rash (50% of cases), spleen enlargement (20% of cases), liver enlargement (10% of cases). Rash, when present, appeared at any time from the second to the fifth day of illness and lasted for a period of several hours to days. Forms of rash included discrete pale roseolar spots, diffuse small spotted pale roseolar exanthema, and mottling of the skin - pale roseolar maculae of varying size with an indefinite border. Rash appeared most commonly on the upper chest, back, upper arms, less commonly on the face, flanks and abdomen, and did not appear on the lower extremities. During an outbreak in Israel, 1953. (J101.64.w1)
  • Fever, sore throat, headache, muscle ache, pronounced fatigue, nausea in two children and in one of these also vomiting, flushed face, maculopapular rash and slight enlargement of the inguinal lymph nodes; infection confirmed by a rising titre of virus neutralising antibodies in paired serum samples (at least four-fold increase). Additionally in other individuals with antibodies but without paired samples, in one individual severe headache, muscle ache, pronounced fatigue, nausea, pain on eye movement, maculopapular rash and insomnia and in two others "summer fever" with sore throat, lymphadenitis or headache and pain on eye movement. No clinical signs had been noted in a further eight individuals in which antibodies were detected from serum samples. In the Czech Republic in 1999. (J84.5.w3)
  • Fever (86% of cases), headache (51% of cases), central nervous system involvement (46% of cases), abdominal pain (43% of cases), arthralgia (37% of cases), respiratory signs (23% of cases), convulsions (11% of cases) in individuals 12-40 years old. During an outbreak in the Democratic Republic of Congo in 1998 (J91.61.w1)
  • Fever, headache and signs of meningismus on neurological examination in three individuals. Additionally somnolence, skin rash and signs of papillitis (hyperemia and blurring of the disc margins) on neurological examination in one individual, dizziness and nausea in one individual and ocular pain, photophobia and somnolence in the third individual. In Israel in 1980. (J102.17.w1)
  • "Sudden high fever, disorientation, meningeal and pyramidal signs, and convulsions." High fever, severe headache, and confusion in 7/7 individuals, with severe somnolence and disorientation in 3/7 individuals, convulsions in 2/7 individuals, dysarthria in 2/7 individuals, urinary incontinence in 1/7 individuals, mild lower paraparesis in 1/7 individuals. Meninigism detected in 6/7 individuals on neurological examination and pyramidal signs in 5/7 patients. (J103.3.w1)
  • In one individual, 30 years old: short term fever, headache and anorexia, together with palpitations, stabbing sensation and pressure in the left chest area, the palpitations and chest discomfort persisting much longer than the fever. ECG changes indicative of myocarditis. (J99.57.w1)
  • In one individual, 68 years old: "mild encephalitis and severe myelitis, resembling the "polio syndrome." (J105.135.w1)
  • In one individual, 15 years old. Fever, headache and vomiting, with brainstem and cortical nervous signs including confusion, cranial nerve defects, ataxia and brisk tendon reflexes. Anterior horn cell involvement was indicated by weakness and tongue fasciculations. (J106.55.w1)
  • In one individual, 22 years old. Fever, enlarged lymph nodes, mild splenomegaly, excruciating pain in the neck, back and left lower extremity, mild weakness of the left face accompanied by fasciculations, and flaccid paresis of the left lower extremity with loss of deep tendon reflexes but without any sensory changes. (J107.36.w1)
  • In one individual 69 years old. Guillain-Barr syndrome (acute inflammatory demyelinating polyradiculoneuritis). Progressive weakness including proximal and distal muscles, bilateral weakness of facial muscles, and reduced respiration such that ventilatory support was required. (J106.55.w2)
  • Clinical presentations of diffuse muscle weakness (40%), encephalitis (27%), aseptic meningitis (24%) and fever with headache (9%) during the outbreak in New York, 1999. (P32.1.w2)
  • Encephalitis, meningitis or meningoencephalitis requiring hospitalisation in nineteen individuals. "Of the 19 cases, 16(84) presented with at least one neurological complaint (headache, stiff neck, photophobia, muscle weakness, or change in mental status). Seventeen patients (89) had one or more abnormalities on neurological examination. Motor exams in three patients demonstrated muscle weakness (strength <5/5); of the six with abnormal reflexes, four were hyporeflexive, and two had abnormal plantar responses; the two patients with cerebellar abnormalities were ataxic. Both patients with cranial nerve abnormalities died; one had nystagmus and the other had a depressed gag reflex. Eleven patients (58% of cases) had at least one gastrointestinal symptom or had abnormal abdominal findings. Three patients had rash." Clinical findings included fever (17/19, 90% of cases), fatigue (12/19, 63% of cases), altered mental status (11/19, 58% of cases), headache (11/19, 58% of cases), weakness (8/19, 42% of cases), nausea (8/19, 42% of cases), vomiting (8/19, 42% of cases), myalgia (6/19, 32% of cases), photophobia (6/19, 32% of cases), abnormal reflexes (6/19, 32% of cases), stiff neck (6/19, 32% of cases), abdominal pain (4/19, 21% of cases), cough (3/19, 16% of cases), diarrhoea (3/19, 16% of cases), seizures (3/19, 16% of cases), arthralgia (2/19, 11% of cases), cerebellar abnormality (2/19, 11% of cases), cranial nerve palsy (2/19, 1% of cases), shortness of breath (2/19, 11% of cases). During an outbreak in and near New York, USA 2000. (J84.7.w9)
  • Encephalitis in two individuals, fatal in one case. Fever (to 39.0C) in both individuals, in one individual confusion, disorientation, somnolence and aphasia with progression: "became less responsive, with limb spasticity, bilateral ptosis, facial nerve paralysis, and bilateral Babinski response"..."mechanical ventilation was started." In the second individual fever, chills, dizziness and headache progressed "the patient became stuporous with severe respiratory acidosis; mechanical ventilation was begun"... "the patient remained febrile and stuporous and died on day 33 of hospitalization." (J84.7.w10)
  • Patients with encephalitis, some of whom had profound muscle weakness (with axonal neuropathy by electromyelogram and requiring respiratory support). (N7.48.w1)
  • "The main clinical presentations were encephalitis (57.9% of cases), febrile disease (24.4% of cases), and meningitis (15.9% of cases). Within the study group, 33 (14.1% of cases) hospitalized patients died." Signs and symptoms included: fever of 38C or higher (98.3% of cases), headache (57.9% of cases), change in level of consciousness (46.8% of cases), confused state (39.5% of cases), vomiting (31.3% of cases), nuchal rigidity (28.7% of cases), rash (21.8% of cases), gastro-intestinal symptoms (abdominal pain, diarrhoea) (18.5% of cases), coma (16.7% of cases), myalgia (15.4% of cases), focal neurological signs (9.4% of cases) and lymphadenopathy (4.3% of cases). Outbreak in Israel, 2000. (J84.7.w14)
  • Clinical illness with encephalitis, one individual, USA, July 2001. (N7.50.w2)
  • Fever (39.0-40.0C) in three children aged two, seven and ten years during a short outbreak of disease due to West Nile virus infection in Ibadan, Nigeria in April to June 1973. (J96.72.w1)
  • "The main symptoms of the disease were fever, an examthem, severe headache, sometimes accompanied by pain in back and limbs, anorexia, vomiting and abdominal pain. Enlarged lymph nodes, angina and diarrhoea were less common symptoms."  Fever in all children and 31/37 adults, reaching 39-39.5C, sometimes 40C; sometimes with chills, usually lasting two or three days, sometimes four to five days and in one individual nine days. A second rise in temperature following one to two days of normal temperature was seen in about 10% of cases, and was accompanied by recurrence of other symptoms. Exanthem (bright pinkish, round discrete macules and slightly raised papules, 2-4mm diameter, often on the body and limbs, sometimes on the face, appearing during the fever and sometimes after the fever, often lasting less than 24 hours but sometimes for several days) present most commonly in younger individuals (87% of those less than two years old, 73% of those up to five years old, but reducing to 25% and 20% of older children and 14% of adults. Meningitis in ten children (as indicated by the presence of Brudzinski's sign). Pain in the eyes, particularly on moving the eyeball, was noted by a number of individuals. Severe headache, sometimes accompanied by "malaise and aches in the back and limbs" was noted more frequently in adults (78% of cases) than in children (37% of cases), although it may not have been possible to confirm these symptoms in infants. Abdominal pains, sometimes with diarrhoea, were noted by 19% of patients; anorexia and nausea were common and vomiting occurred in 45% of children and 19% of adults. The throat was often slightly reddened. Severe angina was present in seven cases. Lymph nodes were swollen and tender on pressure more commonly in adults (submaxillary and occipital) than in children. During an outbreak in Israel (Maayan Zvi), 1951. (J100.93.w1)
  • Severe fatigue, malaise, generalized muscular pain with constant moderately severe pain in calves and thighs and tenderness on pressure in the gastrocnemius muscles, slight pain on eye movement, slight cough, increased breath sounds in the right axilla, moderate abdominal tenderness and slight liver enlargement. Temperature 99.8F. In one individual in Egypt, 1952. (J91.3.w2)
  • Fever alone in 89%, and of no more than 1F above baseline in 27% of these individuals. Fever usually occurred first at 24 hours after intramuscular inoculation of virus and persisted during the period of viraemia. A second period of fever in the third week occurred occasionally. Headache was reported only twice but may have been masked by analgesic agents. 11% "showed definite or suggestive clinical signs of diffuse encephalitis" including "depressed sensorium, ranging from drowsiness to near-coma; involuntary twitching of hands, and occasionally of face and legs; and irregular variation of deep tendon reflexes, usually hyperactivity followed by diminished activity. Cogwheel rigidity was usually observed. Paralysis or paresis occurred only once and recovery was complete"... "pyramidal tract signs were observed only in the one patient with paralysis. Cranial nerves and sensory perception were never affected." Experimental infection in patients with terminal neoplasia. (J91.3.w1)
  • Signs and symptoms "frequently seen were fever, rash, muscular pain, backache, joint pain, headache, orbital pain, diarrhoea, nausea, and those less frequently seen were sore throat, enlarged lymph glands, vomiting, insomnia, encephalitis (apparently mild) orchitis, enlarged and tender liver." Recovery was often "slow with continued listlessness and weakness." No deaths were reported associated with infection. During an epidemic in South Africa, 1974. (J111.72.w1)
  • Severe hepatitis associated with WNV infection (confirmed by virus isolation) in four individuals in the Central African Republic. (B241.49.w49)
  • Fever for four days (about 39C), pronounced fatigue, sore throat, headache, myalgia, nausea, with illness lasting seven days and complete recovery after 13 days. In one individual less than sixteen years old, infection confirmed by rising antibody titre, in Czechland (South Moravia) 1997. (J115.13.w4)
  • Fever for three days, 38-39C, pronounced fatigue, maculopapular rash and flushed face, nausea and vomiting, headache, lymphadenitis (slightly enlarged inguinal lymph nodes). In one individual less than sixteen years old, infection confirmed by rising antibody titre, in Czechland (South Moravia) 1997. (J115.13.w4)
  • Severe headache for two weeks, fever (39C), general weakness and myalgia, vomiting, confusion, blurred consciousness, signs of meningeal irritation, photophobia. Later blurred vision, severe vertigo, diplopia and "focal neurological signs including right eyelid ptosis, paralysis of the right lateral rectus muscle, flattening of the right nasolabial fold, multidirectional nystagmus, skew deviation, excessive eye blinking (both eyes), and tongue tremor." Neurological signs worsened, with hyperactive reflexes, particularly on the right side, severe cerebellar ataxia (wide based gait) and unsteadiness, and gradual worsening of visual acuity. There was also "relative afferent pupillary defect on the right eye, swelling of the optic discs (both eyes but more prominent on the right eye), hemorrhages, concentric constriction of the visual fields and a right visual field scotoma." The patient's condition improved gradually with mild improvement first seen after 20 days and discharge from hospital at 30 days. One case during the outbreak of WNV infection in Israel in 2000. (J220.162.w1)
  • Acute fever (38.7C), deterioration of mental status with lethargy, disorientation and repeated generalised seizures, neck rigidity and positive Bruzinski sign, later motor aphasia (completely bedridden, required nasogastric feeding). Slow improvement from the start of the third week of illness, gradual resolution of signs (motor aphasia lasted more than three months). One case in a four-year-old boy undergoing treatment for Hodgkin's lymphoma during the outbreak of WNV infection in Israel in 2000. (J221.86.w1)
  • Fever reaching 39.4C and confusion (disorientation and difficulty in following commands) in one 89-year-old man with encephalitis, slow recovery over a period of more than one month. In Massachusetts, USA, during 2001. (J221.346.w1)
  • Signs in one individual of headache, myalgias, malaise, then chills, sweats, dysesthesias, recurring hot flashes, lymphadenopathy and anorexia, followed after two days by a maculopapular rash and full recovery after one week. Signs in the second individual of initial upper respiratory tract infection, accompanied one day later by malaise, fatigue, chills and low fever (38.3C/ 100.F); In two cases following laboratory accidents in the USA during 2002. (N7.51.w7)
  • Acute flaccid paralysis syndrome in six individuals. One or more limbs affected with normal sensation but hyporeflexia or areflexia and asymmetrical weakness, sometimes flaccidity. Other signs varied (e.g. fever, chills, fatigue, headache, vomiting, confusion, nuchal rigidity etc.). During 2002 in the USA. (N7.51.w1)
  • Natural infection with acute flaccid paralysis in seven patients. At initial presentation fever (at least 38.5C) in 6/7, headache in 6/7, nuchal rigidity in 3/7, altered mental status in 3/7 and tremor in 4/7. One or more limbs, upper and or lower limbs, affected, also bulbar muscles in one individual. Acute flaccid paralysis without sensory loss or paresthesias, marked asymmetric weakness, diminished or absent deep tendon reflexes in affected limb(s). Associated with disease of the anterior horn cells of the spinal cord. (J84.9.w13)
  • Acute flaccid paralysis described in seven patients, three of which did not have other findings suggestive of severe central nervous system involvement. In general, acute, painless asymmetric flaccid paralysis of one or more limbs, sometimes monoplegia, no numbness, paraesthesia or sensory loss, although occasionally myalgia, and often with bowel and/or bladder involvement. (J84.9.w13)
  • Movement disorders reported include tremor (static/kinetic), sometimes with movement, and occasionally disabling and myoclonus, most frequently involving the upper extremity or face. Movement disorders have generally had onset at more than five days after the initial symptoms. In a prospective series of patients tremor was noted in 15 individuals (94%) and myoclonus in 10 (63%). (P39.4.w3)
  • Parkinsonism was noted in 11 of a prospective series of patients (68%), with cogwheel rigidity, bradykinesia and postural instability, but no tremor at rest. This was seen in individuals with meningitis or encephalitis. (P39.4.w3)
  • Reported cases were biased due to monitoring for meningoencephalitis. A total of 158/188 confirmed cases (84.0%)had meningoencephalitis. Clinical signs and symptoms included fever (91.5%), headache (72.3%), muscle weakness (56.9%), nausea (50.8%), vomiting (35.8%), muscle pain (34.6%), altered mental status (34.6%), stiff neck (29.8%), rash (25.0%), joint pain (24.5%), lethargy (24.6%), and occasionally lymphadenopathy (3.7%) and seizures (2.1%). In reported cases in Mississippi, 2002. (P48.1.w2)
  • In Ontario, Canada, 2002. In 57/64 patients there was meningoencephalitis and/or neuromuscular weakness, while 5/64 had uncomplicated aseptic meningitis and two had WNV fever without any neurological manifestations. At the time of presentation 61/64 (95%) had fever, 48/64 (75%) altered mental status, 46/55 (84) anorexia, 40/58 (69%) nausea, 31/58 (53%) vomiting, 17/64(27%) headache and neck stiffness while 13/64 (20%) had neither headache nor neck stiffness, 20/58 (34%) diarrhoea, 26/47 (55%) myalgia, 15/48 (31%) arthralgia, 17/64 (27%) rash and only 2/64 (3%) lymphadenopathy. Nervous signs seen included a decreased level of consciouness  in 75% of patients, neuromuscular weakness in 41%, dysphagia in 34%, ataxia in 31%, dysarthria in 17%, vertigo in 14%, intention tremor in 13%, diplopia or ophthalmoplegia in 13%, facial weakness in 11%, blurred vision in 9%, dysdiadokinesis in 8%, seizure in 6%, incontinence in 5%, tongue weakness in 5%, myelopathy in 3%, nystagmus in 3%, Parkinsonism in 3%. (J257.168.w2)
  • In India, 2002. Mainly (81/88 confirmed cases) classical West Nile fever with fever, headache, general aches, nausea and vomiting, but also seven cases of encephalitis. (J260.33.w1)
  • Temporarily decreased visual acuity and development of multiple round, cream-coloured chorioretinal lesions, 300-1000m diameter, scattered in the fundus and persisting for over one year, together with a mild vitritis which cleared after several months, associated with WNV encephalitis (malaise, muscle weakness, dysarthria and gastroenteritis) in an 81-year-old man with long-standing nonproliferative diabetic retinopathy. In a patient in the USA, 2002. (J276.23.w1)
  • Clinical signs of ocular pain and blurred vision affecting one eye, associated with fever, headache, diffuse muscle pain and neck stiffness (WNV meningitis). Ophthalmic examination revealed a swollen slightly pale disc on the clinically affected side and lesser swelling on the other side; optic neuritis was diagnosed. In a young adult in Israel, 2000. (J277.31.w1)
  • Clinical signs of "floaters" in the left eye together with fatigue, left-sided frontal headache and low-grade fever. Anterior uveitis, vitritis and non-necrotising chorioretinitis were noted in the left eye and milder similar findings in the right eye. Anterior uveitis responded to steroids. Ophthalmological examination showed deep, flat, creamy whitish-yellow outer choroidal lesions, 500-750 um extending superiorly in a linear radial pattern from the optic nerve head in the left eye, and less extensive faint lesions in the right eye. The lesions were actively inflammatory. A moderate vitritis was noted overlying the optic disk and superior retina of the left eye. Small intraretinal haemorrhages, 200um diameter , were present in the right eye and similar haemorrhages were noted associated with some of the lesions in the left eye. Fluorescein angiography revealed blocked fluorescence ad leakage from the lesions. Treatment was initiated with local (ocular) 1% prednisolone acetate QID. The chorioretinitis healed; two weeks after presentation there was significantly less vitritis and a decrease in fluorescein leakage, while the lesions appeared smaller and pigmented. This was accompanied by an improvement in visual acuity (from 20/25 OD and 20/40 OS to20/30 OS.  In a 62 year old woman in Chicago, confirmed positive for WNV IgM antibodies in serum.  (J282.121.w1)
  • Fever (102.9F/39.4C), frontal headache and bilateral leg weakness (acute flaccid paralysis). Marked decreases in motor function of both legs, particularly the right leg, and diminished reflexes in both legs, but intact sensation. (J281.181.w1)

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Domestic horse
General summary:

Infection in horses is commonly asymptomatic. However disease characterised by neurological signs may occur, sometimes with fever reported early in the course of the infection although fever has not been a consistent finding. Onset of nervous signs such as ataxia or paresis may be acute or apparent lameness may progress to obvious ataxia. Ataxia may progress to recumbency with inability to rise. Clinically affected individuals may recover, with or sometimes without supportive treatment, or severe signs may result in death or signs of a severity requiring euthanasia. Full resolution of ataxia in survivors may take weeks to months. (J4.218.w2, J4.222.w1, J64.19.w1, J84.7.w12, J84.7.w17, J84.7.w27, J89.16.w1)

Fever:

  • Low grade fever may be found but is by no means a consistent finding.
    • Low grade fever 38.4-39.4C/101.2-103.0F (4/8 horses). (J4.218.w2); 
    • 7/22 horses (31.8% of cases), 101.4-103F, mean 102.4F (J84.7.w27);
    • Fever over 38.5C in 47/76 horses (62% of cases) (J84.7.w17); 
    • Fever in 23%, USA 2000 (J84.7.w12); 
    • Fever sometimes above 40C (104F), but an inconsistent finding (J89.16.w1). 
    • No fever reported; rectal temperatures normal (J87.32.w1).
    • Pyrexia reported as a typical sign. In horses in Morocco. (J85.108.w1)
    • Fever (and neurological signs) recorded in one of twelve horses following experimental infection in the USA. (J84.8.w4)
    • Fever with no other signs in one horse and in addition to neurological signs in at least three horses in Israel in 2000. (J3.151.w1)
    • Fever was noted in three of five fatal cases during an outbreak in Israel in 2000. (J73.57.w1)
    • USA, equine West Nile encephalitis presentation: increased temperature in 65%. (P39.4.w4)
    • Fever recorded in 13/28 (46%) cases in Ontario, Canada, 2002. (J14.44.w1)
    • Fever was noted in 30/46 horses (65%) admitted in Florida, 2001. The body temperature was considered raised if the rectal temperature reached at least 38.3C. (J4.222.w1)
    • Fever was noted in 21.1% (102/484 horses) in Nebraska and Colorado, USA in 2002. (J4.225.w2)
    • Fever was noted in 7% of horses in the USA (North Dakota) in 2002. (J4.225.w3)
    • Fever was not a common finding in horses in Indiana, USA in 2002. (J4.225.w5)

Neurological-Locomotor:

  • Lameness:
    • Unilateral forelimb lameness progressing to bilateral lameness and ataxia (2/8). (J4.218.w2)
    • Three horses were presented due to lameness in Florida in 2001. (J4.222.w1)
    • Lameness was noted in 20.9% of horses (101/484 horses) in Nebraska and Colorado, USA in 2002. (J4.225.w2)
  • Weakness, paresis, paralysis:
    • Limb weakness 48% of cases. (J84.7.w12)
    • Paresis/paralysis 36/76 (47% of cases). (J84.7.w17)
    • In fatal cases (death or euthanasia required), ascending paresis, tetraplegia and recumbency, or early tetraplegia and recumbency, usually with muscle rigidity and hyperreflexia of the hind limbs (6/14 horses). (J87.32.w1)
    • Weakness considered one of the characteristic signs, Camargue, 1962). (J84.7.w17)
    • Progressive weakness of the hind quarters prior to recumbency in a horse in Egypt. (J86.57.w1)
    • Tetraplegia progressing from ataxia and resulting in recumbency in one horse in Israel in 2000. (J3.151.w1)
    • Paresis in two, hindlimb paraplegia in one and quadriplegia in two, from five fatal cases during an outbreak in Israel in 2000. (J73.57.w1)
    • USA, equine West Nile encephalitis presentation: weakness in 94%. (P39.4.w4)
    • Recorded in 23/28 (82%) cases in Ontario, Canada, 2002.  (J14.44.w1)
    • Weakness was noted in 43/46 horses (94%) admitted in Florida, 2001. (J4.222.w1)
    • Generalised weakness was noted in 53.3% (259/484 horses) in Nebraska and Colorado, USA in 2002. (J4.225.w2)
    • Limb weakness or paralysis was noted in 38% and caudal paresis in 29% of horses in North Dakota, USA in 2002, (J4.225.w3)
    • Hind limb paresis was seen in 60/136 (35.3%) of horses in Indiana, USA in 2002. (J4.225.w5)
    • Weakness was one of the most common signs in horses with WNV lineage 2 neuroinvasive disease in Hungary in 2008.  (J275.25.w1)
  • Ataxia/gait abnormalities:
    • Ataxia (95.7% of cases) (J84.7.w27).; 55/76 horses (72% of cases) (J84.7.w17); 85% of cases. (J84.7.w12)
    • Acute-onset ataxia affecting all four limbs (5/8 cases). (J4.218.w2)
    • Ataxia all four limbs 15/20 horses (75% of cases) (2000). (J84.7.w27)
    • Ataxia rear limbs 19/21 horses (90.5% of cases) (2000). (J84.7.w27)
    • Marked gait abnormalities in all cases; with variable degrees of ataxia and hind limb weakness, sometimes also one or both forelimbs affected. (J87.32.w1)
    • Ataxia considered one of the characteristic signs, Camargue, France, 1962. (J84.7.w17)
    • Ataxia in 95.7% of horses, mainly hind limbs affected (90.5% of cases), usually acute onset (90.5% of cases), USA, 2000. (J84.7.w27)
    • Limb ataxia or paresis, symmetrical or asymmetrical, most commonly involving the hind limbs but occasionally only affecting the front limbs; signs may be exacerbated by moving the animal backwards. (J89.16.w1)
    • Wide-based stance, hypermetric or staggering gait, stumbling, circling. (J89.16.w1)
    • Development of staggering gait following initial signs in a horse in Egypt. (J86.57.w1)
    • Ataxia affecting the hindlimbs or all four limbs. In horses in Israel in 2000. (J3.151.w1)
    • Ataxia was noted in all of five fatal cases during an outbreak in Israel in 2000. (J73.57.w1)
    • USA, equine West Nile encephalitis presentation: ataxia in 72%. (P39.4.w4)
    • Ataxia recorded in 28/28 (100%) cases in Ontario, Canada, 2002. (J14.44.w1)
    • Ataxia was noted in 33/46 horses (72%) admitted in Florida, 2001. (J4.222.w1)
    • Ataxia was noted in 57.4% (278/484 horses) in Nebraska and Colorado, USA in 2002. (J4.225.w2)
    • Incoordination was noted in in 69% of horses in North Dakota, USA in 2002. (J4.225.w3)
    • Ataxia was seen in 75/136 horses (44/1%) in Indiana, USA in 2002. (J4.225.w5)
    • Ataxia was a common finding, seen in 69.1% of horses in a study in Texas, USA, 2002, (J238.118.w1)
    • Abnormal gait was a common finding, seen in 52.2% of horses in a study in Texas, USA, 2002. (J238.118.w1)
    • Ataxia/incoordination was seen in horses with severe clinical signs requiring euthanasia in Kentucky, USA, 2002. (J305.55.w1)
    • Ataxia was one of the most common signs in horses with WNV lineage 2 neuroinvasive disease in Hungary in 2008.  (J275.25.w1)
  • Recumbency:
    • Recumbency (1/8 cases). (J4.218.w2)
    • Recumbency and/or difficulty in rising 45% of cases. (J84.7.w12)
    • Recumbency ( and seizures) (2/8 cases). (J4.218.w2)
    • Sometimes inability to rise. (J84.7.w27)
    • Inability to rise, or able to rise only with assistance: "down" 9/22 horses (40.9% of cases), able to rise with assistance 6/21 horses (28.6% of cases). (J84.7.w27)
    • Recumbency, sometimes scraping of a hole with the fore legs in horses in Morocco. (J85.108.w1)
    • Recumbency prior to death about 60 hours after the onset of illness, in a horse in Egypt. (J86.57.w1)
    • Recumbency prior to death in some horses in Israel in 2000.(J3.151.w1)
    • Recumbency occurred prior to death or euthanasia in all of five fatal cases during an outbreak in Israel in 2000. (J73.57.w1)
    • USA, equine West Nile encephalitis: recumbency in 30% of cases, sometimes intermittent. (P39.4.w4)
    • Recumbency recorded in 10/28 (36%) cases in Ontario, Canada, 2002. (J14.44.w1)
    • Recumbency occurred in 14/46 horses (30%) admitted in Florida, 2001. (J4.222.w1)
    • While 27.5% (133/484 horses) in Nebraska and Colorado, USA, in 2002 were recumbent and unable to rise, a further 24.2% (117/484) were recumbent for long periods but able to rise. (J4.225.w2)
    • Recumbency or difficulty in rising was noted in 23% of horses in North Dakota, USA in 2002. (J4.225.w3)
    • Recumbency was seen in 13/136 (7.6%)of horses in Indiana, USA in 2002. (J4.225.w5)
    • Recumbency was a common finding, seen in 27.7% of horses in a study in Texas, USA, 2002. (J238.118.w1)
  • Other
    • Initial "signs of unilateral radial nerve paralysis" (1/8 cases). (J4.218.w2).
    • Knuckling over at the fetlocks. (J84.7.w27)
    • Marked hypermetria (2/8). (J4.218.w2)
    • Hypermetria 4/16 (25% of cases) (2000). (J84.7.w27)
    • Falling to knees (5/8). (J4.218.w2)
    • Dysmetria was noted in 18/22 horses (82%) admitted in Florida, 2002. (J4.222.w1)
    • Sudden collapse and knuckling were noted to be associated with forelimb weakness in horses admitted in Florida, 2001. (J4.222.w1)
    • Stiffness or reluctance to move was noted in 36.6% (177/484 horses) in Nebraska and Colorado, USA in 2002. (J4.225.w2)
    • Hypermetria was noted in 6.4% of equines (31/484) in Nebraska and Colorado, USA in 2002. (J4.225.w2)
    • It was noted that 10.3% (50/484) used a dog-sitting posture, 3.1% (15/484) used a praying posture and 20.7% (100/484) had abnormal head carriage, in Nebraska and Colorado, USA in 2002. (J4.225.w2)
    • Circling was seen in 6% of horses in North Dakota, USA in 2002. (J4.225.w3)
    • Falling down was noted as one of the less common findings in a study in Texas, USA, 2002. (J238.118.w1)

Neurological-Other:

  • Ocular:
    • Anisocoria and slow pupillary light reflexes (1/8 cases). (J4.218.w2)
    • Central blindness (3/8 cases). (J4.218.w2)
    • Blindness 5% of cases (J84.7.w12)
    • Amaurosis noted as a characteristic sign during the outbreak in the Camargue, 1962. (J84.7.w17)
    • In 3/46 horses (7%) the menace reflex was absent.(J4.222.w1)
    • It was noted that 13 of 484 equines had ocular problems such as blindness, in Nebraska and Colorado, USA, in 2002. (J4.225.w2)
    • Blindness was noted in 3% of horses in North Dakota, USA in 2002. (J4.225.w3). 
  • Tremors/Muscle fasciculations:
    • Tremors in 4/14 horses. (J87.32.w1)
    • Muscle tremors in 7/76 horses (9% of cases). (J84.7.w17)
    • Muscle fasciculation, most pronounced in the neck and triceps region (3/8 horses).(J4.218.w2)
    • Muscle fasciculation in 11/20 (55% of cases). (J84.7.w27)
    • Muscle fasciculation in 40%. (J84.7.w12)
    • Muscle fasciculation and tremors (face, lips, trunk, shoulder) particularly in severe cases. (J89.16.w1)
    • Twitching face or muzzle 13%. (J84.7.w12)
    • Head tremors and lip twitching (3/6).(J4.218.w2)
    • Drooping and twitching lower lip, following experimental infection. (P32.1.w13)
    • USA, equine West Nile encephalitis presentation: fasciculation in 61%. (P39.4.w4)
    • Muscle fasciculation recorded in 14/28 (50%) cases and noted to be associated with a favourable outcome of infection, in Ontario, Canada, 2002. (J14.44.w1)
    • Fasciculations were noted on the face or neck only in 12/46 horses (26%) and on the whole body in 16/46 horses (35%) admitted in Florida, 2001. (J4.222.w1)
    • Muscle fasciculations were noted in 42.6% (206/484) equines in Nebraska and Colorado, USA, 2002. (J4.225.w2)
    • Muscle tremors/twitches were noted in 52% of horses in North Dakota, USA in 2002. (J4.225.w3)
    • Muscle tremors/fasciculations were seen in 60/136 (35.3%) horses in Indiana, USA in 2002. (J4.225.w5)
    • Muscle fasciculations were seen commonly, in 49.4% of horses in a study in Texas, USA, 2002. (J238.118.w1)
    • Face or neck muscle tremors, were seen in horses with severe clinical signs requiring euthanasia in Kentucky, USA, 2002. (J305.55.w1)
  • Proprioceptive defects:
    • Proprioceptive defects seen as toe-dragging. (J89.16.w1).
    • Proprioceptive defects noted in a horse showing clinical signs following experimental infection. (P32.1.w13)
    • Placing deficits were noted in five horses; not all horses were tested. In horses admitted in Florida, 2001. (J4.222.w1)
  • Hypersensitivity to stimuli:
    • Hypersensitivity to touch (6/8). (J4.218.w2)
    • Hypersensitivity to sound (6/8). (J4.218.w2)
    • Hyperaesthesia in 6/76 (8% of cases). (J84.7.w17)
    • Hyperaesthesia recorded in 11/28 (39%) cases in Ontario, Canada, 2002. (J14.44.w1)
    • Hyperaesthesia was noted in 19.0% (92/484) equines in Nebraska and Colorado, USA, 2002. (J4.225.w2)
    • Hyperaesthesia was noted as one of the less common signs in horses in a study in Texas, 2002. (J238.118.w1)
  • Seizures:
    • Seizures in two recumbent horses. (J4.218.w2)
    • USA, equine West Nile encephalitis: seizures in a small number of cases. (P39.4.w4)
    • Seizures occurred in 2/46 horses admitted in Florida, 2002. (J4.222.w1)
    • Seizures were noted in 5.0% (24/484) equines in Nebraska and Colorado, USA, 2002. (J4.225.w2)
    • Seizures were noted as one of the less common signs in horses in a study in Texas, 2002. (J238.118.w1)
    • Seizures were seen in horses with severe clinical signs requiring euthanasia in Kentucky, USA, 2002. (J305.55.w1)
  • Behavioural:
    • Behavioural changes (depression, fearfulness) sometimes observed. (J89.16.w1)
    • Somnolence (5/8 horses). (J4.218.w2)
    • Agitation in 3/19 horses (15.8% of cases) (USA, 2000). (J84.7.w27)
    • Dull and lethargic (3/19 horses, 15.8% of cases) (USA, 2000). (J84.7.w27)
    • Abnormal behaviour 2/76 (3% of cases). (J84.7.w17)
    • Apprehension and reluctance to move, following experimental infection. (P32.1.w13)
    • Hyperexcitability. One horse in Israel in 2000. (J3.151.w1)
    • USA, equine West Nile encephalitis presentation: abnormal mentation in 67%, including nonresponsiveness and somnolence. (P39.4.w4)
    • Depression was recorded in 10/28 (36%) cases in Ontario, Canada, 2002. (J14.44.w1)
    • Abnormal mentation was noted in 31/46 horses (67%) admitted in Florida, 2001. These included four horses which could be roused only with difficulty and four which showed aggression. Four individuals circled or stall-walked compulsively. (J4.222.w1)
    • Lethargy or depression was noted in 43.0% (208/484) equines, altered mentation in 22.1% (107/484), 13/484 were apprehensive and a further eight equines were restless or agitated, in Nebraska and Colorado, USA, 2002. (J4.225.w2)
    • Compulsive behaviour was noted in 6.8% (33/484) of equines in Nebraska and Colorado, USA, 2002. (J4.225.w2)
    • Depression was a common finding, seen in 31.9% of horses in a study in Texas, 2002. (J238.118.w1)
    • Excitability was seen in horses with severe clinical signs requiring euthanasia in Kentucky, USA, 2002. (J305.55.w1)
  • Other:
    • Head tilt. (J89.16.w1)
    • Leaning to one side. (J89.16.w1)
    • Difficulty in swallowing (1/8 horses, during recumbent stage). (J4.218.w2)
    • Teeth grinding 7% of cases (J84.7.w12); 3/76 (4% of cases). (J84.7.w17)
    • Paralysed or drooping lip 18%. (J84.7.w12)
    • Unspecified neurological signs, becoming severe and requiring euthanasia, in one of twelve horses following experimental infection in the USA. (J84.8.w4)
    • Tooth grinding. One horse in Israel in 2000. (J3.151.w1)
    • USA, equine West Nile encephalitis presentation: tooth grinding in 20%. (P39.4.w4)
    • USA, equine West Nile encephalitis presentation: cranial nerve defects in 44%. (P39.4.w4)
    • Cranial nerve deficits were recorded in 3/28 (11%) cases in Ontario, Canada, 2002. (J14.44.w1)
    • Cranial nerve deficits were noted in 20/46 horses (44%) admitted in Florida, 2001. (J4.222.w1)
    • Tooth grinding was noted in 9/46 horses (20%) admitted in Florida, 2001. (J4.222.w1)
    • Ptyalism was noted in 3/46 horses (7%) admitted in Florida, 2001. (J4.222.w1)
    • One horse was dysphagic. (J4.222.w1)
    • Cranial nerve deficits were noted in 19.0% (92/484) of equines in Nebraska and Colorado, USA, 2002. (J4.225.w2)
    • Dysphagia was seen in 8.1% (39/484) of equines in Nebraska and Colorado, USA, 2002. (J4.225.w2)
    • Head-pressing was noted in 2.7% (13/484) of equines in Nebraska and Colorado, USA, 2002. (J4.225.w2)
    • Lip droop was noted in 21% of horses in North Dakota, USA in 2002. (J4.225.w3)
    • Teeth grinding was noted in 8% of horses in North Dakota, USA in 2002. (J4.225.w3)
    • Head-pressing was noted as one of the less common signs in horses in a study in Texas, 2002. (J238.118.w1)
    • Lip droop was noted as one of the less common signs in horses in a study in Texas, 2002. (J238.118.w1)
    • Head pressing was seen in horses with severe clinical signs requiring euthanasia in Kentucky, USA, 2002. (J305.55.w1)
    • Teeth grinding was seen in horses with severe clinical signs requiring euthanasia in Kentucky, USA, 2002. (J305.55.w1)
    • Inability to swallow was seen in horses with severe clinical signs requiring euthanasia in Kentucky, USA, 2002. (J305.55.w1)

Other:

  • Traumatic lesions of the forelimbs and head in recumbent animals, associated with compulsive movements. (J87.32.w1)
  • Lacrimation reported as a typical sign. In horses in Morocco. (J85.108.w1)
  • Colic, haematuria and urine retention reported as initial signs in a horse in Egypt. (J86.57.w1)
  • Hepatitis reported in a donkey. (J84.7.w17)
  • Jaundice. One horse in Israel in 2000. (J3.151.w1)
  • "Mild signs of colic" and reduced appetite. One horse in Israel in 2000; reduced appetite in another. (J3.151.w1)
  • Raised respiratory rate (40-48 per minute), inspiratory dyspnoea and narrowed glottis due to failure to abduct the arytenoids. One horse in Israel in 2000. (J3.151.w1)
  • USA, equine West Nile encephalitis presentation: anorexia in 57%. (P39.4.w4)
  • Anorexia was noted in 24/46 horses (58%) admitted in Florida, 2001. (J4.222.w1)
  • Three horses were presented for colic in Florida in 2001. (J4.222.w1)
  • Poor appetite was noted in 27.9% (135/484) of equines, 13 had ocular problems such as blindness, 7/484 had localised or generalised oedema and 7 had abnormal respiration, in Nebraska and Colorado, USA, 2002. (J4.225.w2)
  • Sweating was noted as one of the less common signs in horses in a study in Texas, 2002 (J238.118.w1)

Recovery and Convalescence:

  • Full eventual recovery of surviving horses. (J84.7.w27)
  • Following discharge from veterinary case, of 19 survivors which could be traced, 3/19 were clinically normal at the time of discharge, a further 5/19 within a month, 5/19 within three months and 4/19 within six months; 2/19 had apparently not returned to normal by six months. (J4.222.w1)
  • A study of 133 horses diagnosed with WNV infection in Minnesota found that of the 125 which survived initial illness, 74 had no residual signs; the duration of clinical abnormalities in these 74 (59.2%) completely recovered horses ranged from one to 180 days (median 21 days, mean 35 days). However, 40% of the horses showed either gait abnormalities, behavioural changes, or both at about six months after the original diagnosis. Additionally, while 92 horses were considered by their owners to be "fully recovered", only 74 had no currently observable behavioural or neurological abnormalities: eight had behavioural changes, two had loss of muscle mass, two showed more frequent stumbling, two had diminished energy level, one had hind limb weakness and one an abnormal gait; eight horses had two abnormalities including four with both behavioural changes and gait abnormalities while one had both loss of muscle mass and vision loss (owner observations). A further 22 horses were owner-classified as having incomplete recovery; 17 of these had gait abnormalities (abnormal gait, hind- and/or fore- limb weakness, or stumbling) (owner-classifications), 15 had behavioural changes, six showed loos of muscle mass and four had decreased energy. Two horses were euthanased at six and seven months post diagnosis because of persistent severe gait defects. Relapses were reported also. Behavioural changes were described as one of three types: change in demeanour, change in mental abilities and abnormal behaviour patterns. The results of the survey "suggest that it will be difficult for veterinarians to give clients a very good prognosis for full recovery from this disease." (P51.49.w1)
  • A study of 482 equids (mostly horses) with clinical WNV infection in Nebraska and Colorado in 2002 found that of 339 individuals which survived infection, 271 (79.9%) recovered fully after a mean disease duration of 22.3 days (+/- 18.8 days, range less than one day to 90 days). However, 20.1% (68 individuals) were reported to be still affected at the time of the survey; in the 67 for which continuing signs were described, they included 14 (21%) with loss of weight or body condition, 13 (19%) with lethargy or decreased stamina, eight (12%) with continuing ataxia, seven (10%) with stumbling, and five (7%) with cranial nerve deficits - droopy ears, lips, muzzle. (J4.225.w2)
  • In 17 horses with WNV lineage 2 neuroinvasive disease in Hungary in 2008,nine horses recovered, five were euthanased or died due to the acute disease and three continued to show clinical signs after six months.  (J275.25.w1)

LITERATURE REPORTS: 

  • "Neurological disease in horses is characterised principally by posterior ataxia, proprioception deficits and altered behaviour. The most severe cases evolve to paralysis of the hind legs, recumbency, terminal convulsion and death." (J64.19.w1)
  • Case fatality rate for horses with clinical disease has been 43-45%. (J64.19.w1)
  • Infection rate in horses residing near to individuals showing clinical signs may be about 20-40%. (J64.19.w1)
  • "WN infection in horses may cause acute, fatal neurological disease, but clinical disease often does not occur. Moderate to severe ataxia, weakness and rear limb incoordination were the most consistent signs; fever was not."(J84.7.w27)
  • In clinical cases, variable from temporary neurological deficits to fulminating fatal encephalitis; infection does not always result in clinical disease. (J89.16.w1)
  • Muscle fasciculation, fever , facial paralysis, facial twitching, grinding of teeth and blindness were all reported more commonly in affected horses in the USA in 2000 than in 1999. (J84.7.w12)

Clinical signs:

  • Characterised by ataxia, weakness and amaurosis. Fatal in about 25-30% of cases. France (Camargue), 1962. (J137.118.w1)
  • Ataxia 85%, limb weakness 48%, recumbency and/or difficulty in rising 45%, muscle fasciculation 40%, fever 23%, paralysed or drooping lip 18%, twitching face or muzzle 13%, grinding teeth 7%, blindness 5%, 38% (23 cases) fatal (died or euthanised); USA 2000, data from 60 horses. Demonstrable WN virus-specific IgM antibodies in acute-phase serum samples from 59/60 horses. (J84.7.w12)
  • Clinical signs included (data for probable and confirmed cases combined): fever >38.5C, (62% of cases), ataxia (72% of cases), paresis/paralysis 47%, tremors 9%, hyperaesthesia (8% of cases), teeth grinding (4% of cases) and abnormal behaviour (3% of cases). One animal (a donkey) had fatal hepatic failure. France, 2000. (J84.7.w17)
  • Clinical WNV infection was characterised by acute onset of rear limb ataxia and included muscle tremors, knuckling over at the fetlocks, and in some instances inability to rise. Death in 4/20 horses, full recovery in the surviving individuals. 
  • No signs in some infected horses (20/69 asymptomatic stable mates of clinically affected horses had positive WN virus titres). In New York State, USA 1999. (J84.7.w27)
  • Ataxia in 95.7% of the 23 confirmed cases, affecting the rear limbs in 90.5% and all four limbs in 75%; acute onset in 90.5% of horses, fever greater than 101F (mean 102.4F, range 101.4-103F) in 31.8%; muscle fasciculation in 55%, almost falling in 47.1%, recumbency in 40.9% of horses while 28.6% were able to rise with assistance; dullness and lethargy in 26.3%; hypermetria in 25% and agitation in 15.8%; 34.8% of ill horses died. Full eventual recovery of surviving individuals. In New York State, USA 2000. (J84.7.w27)
  • Limb ataxia or paresis, symmetrical or asymmetrical, most commonly involving the hind limbs but occasionally only affecting the front limbs; signs may be exacerbated by moving the animal backwards. Wide-based stance, hypermetric or staggering gait, stumbling, circling, leaning to one side, head tilt, proprioceptive deficits (seen as toe-dragging). Behavioural changes (depression, fearfulness) sometimes observed. Ataxia may take weeks to months to fully resolve. (J89.16.w1).
  • Clinical encephalomyelitis in one of 12 horses experimentally infected by mosquitoes. (J133.951.w37)
  • Acute-onset ataxia affecting all four limbs (5/8 cases); marked hypermetria (2/8), recumbency (1/8)(J4.218.w2); unilateral forelimb lameness progressing to bilateral lameness and ataxia (2/8 cases); "signs of unilateral radial nerve paralysis" (1/8 cases), progressing to recumbency and difficulty in swallowing.; anisocoria and slow pupillary light reflexes (1/8); recumbency and seizures (2/8); head tremors and lip twitching (3/6); hypersensitivity to touch (6/8); hypersensitivity to sound (6/8); somnolence (5/8); falling to knees (5/8); central blindness (3/8); muscle fasciculations, most pronounced in the neck and triceps region (3/8 cases). Signs resolved in survivors in 2-7 days after referral. (J4.218.w2)
  • Marked gait abnormalities in all cases; with variable degrees of ataxia and hind limb weakness, sometimes also one or both forelimbs affected. Tremors in 4/14 horses. Recovery in 5-15 days in 8/14 horses. Ascending paresis, tetraplegia and recumbency, or early tetraplegia and recumbency, leading to death or euthanasia; usually with muscle rigidity and hyperreflexia of the hind limbs (6/14 horses). Traumatic lesions of the forelimbs and head in recumbent animals, associated with compulsive movements. Italy, 1998. (J87.32.w1)
  • Pyrexia, lachrymation, asthenia, developing to hindquarter paresis then hind leg paralysis, recumbency, sometimes scraping of a hole with the fore legs, and death in 5-10 days. Morocco. (J85.108.w1)
  • Egypt: Colic, haematuria and urine retention reported, followed by staggering gait, progressive weakness of the hind quarters, recumbency; death in about 60 hours after the onset of illness. (J86.57.w1)
  • Experimental infection with an isolate from a crow (Corvus brachyrhynchos - American Crow). No clinical signs in 3/4 horses. Nervous signs in 1/4, beginning 58 days post-inoculation, including reluctance to move, apprehension, proprioceptive defects and a drooping and twitching lower lip but no fever and no loss of appetite. USA, 1999. (P32.1.w13)
  • Ataxia affecting the hindlimbs or all four limbs, progressing to quadriplegia in one horse and to recumbency in that horse and some other horses. Fever with no other signs was noted in one animal from which virus was isolated and fever was noted in at least three other horses which did have neurological signs. Reduced appetite was noted in two horses, one of which also had "mild signs of colic". Signs noted in single horses included jaundice, hyperexcitability and tooth grinding. One horse had notable respiratory signs, with a raised respiratory rate (40-48 per minute), inspiratory dyspnoea and narrowed glottis due to failure to abduct the arytenoids.  In horses in Israel in 2000. (J3.151.w1)
  • Israel, 2000, data from five fatal cases: ataxia progressing to recumbency in all five horses. Paresis was noted in two animals, paraplegia of the hind legs in two others and quadriplegia in the fifth. Fever was noted in three horses and circling was a feature in one of the horses. Illness lasted 2-7 days, with two animals euthanised when recumbent at two and three days of illness. (J73.57.w1)
  • USA, equine West Nile encephalitis presentation: weakness in 94%, ataxia (72%), abnormal mentation (67%), increased body temperature (65%). fasciculation (61%), anorexia (57%), cranial nerve defects (44%), tooth grinding (20%). (P39.4.w4)
  • Canada, Ontario, 2002, data from 28 cases. Ataxia 28/28 (100%), weakness 23/28 (82%), muscle fasciculation 14/28 (50%), fever 13/28 (46%), hyperaesthesia 11/28 (39%), depression 10/28 (36%), recumbency 10/28 (36%), cranial nerve deficits 3/28 (11%). (J14.44.w1)
  • Canada, Sascatchewan, 2002. A nine-year-old gelding showed acute onset ataxia of all four limbs, with weakness and proprioceptive defects, also muscle fasciculation (particularly the face, upper lip, trunk and limbs, and depression, but with periods of hyperresponsiveness. Appetite remained good and the horse improved after two days. A 16-year-old mare showed acute onset lateral recumbency, initially with normal mental state and appetite, but progressing to reduced responsiveness, thrashing, flaccid tail, tense, firm hind quarters, and reduced anal tone (rectum full of faeces); the mare was euthanized after 24 hours. Treatment was supportive, including provision of a deep bed, and, for treatment of uncontrolled thrashing leading to self-injury, sedation with xylazine, ketamine and acepromazine. (J14.45.w1)
  • Florida, USA, 2001. Data from 46 cases of confirmed WNV infection: fever in 30/46 (65%), anorexia in 26/46 (57%), weakness or ataxia in 46/46 (100%) (including weakness in 43/46 (94%) and ataxia in 33/46 (72%)), recumbency in 14/46% (30%), dysmetria in 18/22 evaluated (82%), abnormal mentation in 31/46 (67%), fasciculations in 28/46 (61%, including face or neck only in 12/46 horses (26%) and the whole body in 16/46 horses (35%), cranial nerve deficits in 20/46 (44%), seizure in 2/46 (4%), teeth grinding in 9/46 (20%) and ptylism in 3/46 (7%). High temperature together with spinal cord deficits was seen in 61%, high temperature and change in mentation in 65% and high temperature together with fasciculation in 54%, but less than 30% showed three of the commonest abnormalities in combination. Abnormalities of mentation included aggression (4/46), periods of sudden cataplexy or narcolepsy (16/46) and compulsive behaviour (circling or stall walking) in 4/46. The overall mortality rate was 30% (including three horses euthanized one to six months later for associated problems). (J4.222.w1)
  • A study of 133 horses diagnosed with WNV infection in Minnesota found that of the 125 which survived initial illness, 74 had no residual signs; the duration of clinical abnormalities in these 74 (59.2%) completely recovered horses ranged from one to 180 days (median 21 days, mean 35 days). Of the 125 horses which had survives the acute illness, 40% of the horses showed either gait abnormalities, behavioural changes, or both at about six months after the original diagnosis. Of the horses in the study group, 92 were considered by their owners to be "fully recovered", but only 74 had no currently observable behavioural or neurological abnormalities: eight had behavioural changes, two had loss of muscle mass, two showed more frequent stumbling, two had diminished energy level, one had hind limb weakness and one an abnormal gait; eight horses had two abnormalities including four with both behavioural changes and gait abnormalities while one had both loss of muscle mass and vision loss (owner observations). A further 22 horses were owner-classified as having incomplete recovery; 17 of these had gait abnormalities (abnormal gait, hind- and/or fore- limb weakness, or stumbling) (owner-classifications), 15 had behavioural changes, six showed loos of muscle mass and four had decreased energy. Two horses were euthanased at six and seven months post diagnosis because of persistent severe gait defects. Relapses were reported also. Behavioural changes were described as one of three types: change in demeanour, change in mental abilities and abnormal behaviour patterns. The results of the survey "suggest that it will be difficult for veterinarians to give clients a very good prognosis for full recovery from this disease." (P51.49.w1)
  • USA (Nebraska and Colorado) in 2002. In a study of 484 affected equids from 57.4% (278/484 ) were ataxic, 53.3% (259/484) had generalised weakness, 43.0% (208/484) were lethargic or depressed, 42.6% (206/484) had muscle fasciculations, 36.6% (177/484) were stiff or reluctant to move, 27.5% (133/484) were recumbent and unable to rise, while a further 24.2% (117/484) were recumbent for long periods but able to rise, 27.9% (135/484) had poor appetite, 22.1% (107/484) showed altered mentation, 21.1% (102/484) fever, 20.9% (101/484) were lame, 20.7% (100/484) had abnormal head carriage, 19.0% (92/484) had cranial nerve deficits, 19.0% (92/484) had hyperaesthesia, 10.3% (50/484) used a dog-sitting posture, 8.1% (39/484) had dysphagia, 6.8% (33/484) compulsive behaviour, 6.4% (31/484) hypermetria, 6.2% (30/484) muscle atrophy, 5.0% (24/484) had seizures, 3.1% (15/484) used a praying posture, 2.7% (13/484) showed head-pressing. 13/484 were apprehensive and a further 8 were restless or agitated, 13 had ocular problems such as blindness, 7/484 had localised or generalised oedema and 7 had abnormal respiration. (J4.225.w2)
  • USA (North Dakota) in 2002. A study of 569 cases found incoordination in 69%, muscle tremors/twitches in 52%, limb weakness or paralysis in 38%, caudal paresis in 29%, recumbency or difficulty in rising in 23%, lip droop in 21%, tooth grinding in 8%, fever in 7%, circling in 6% and blindness in 3%. For the 471 horses in which outcome was known, 27% died or were euthanized. (J4.225.w3)
  • USA (Indiana) 2002. The most common clinical signs were ataxia in 75/136 horses (44/1%), hind limb paresis in 60/136 (35.3%), muscle tremors/fasciculations in 60/136 (35.3%), recumbency in 13/136 (7.6%); fever was not a common finding. (J4.225.w5)
  • USA (Texas) 2002. The most common clinical signs reported were ataxia (69.1%), abnormal gait (52.2%), muscle fasciculations (49.4%), recumbency (27.7%) and depression (31.9%). Other reported signs included excitability, falling down, lip droop, head-pressing, sweating, seizures and hyperaesthesia. (J238.118.w1)
  • USA (Kentucky) 2002. Four horses from one farm developed severe clinical signs and required euthanasia. Signs included ataxia/incoordination, excitability, face or neck muscle tremors, head pressing, teeth grinding, blindness, inability to swallow and seizures. (J305.55.w1)
  • Hungary, 2008. In August to October 2008, neurological disease in 17 horses, with ataxia and weakness the most common signs. Nine horses recovered, five were euthanased or died due to the acute disease and three continued to show clinical signs after six months. (J275.25.w1)

Donkey:

  • USA (Nebraska and Colorado) in 2002. At least one affected donkey became recumbent and was euthanized. (J4.225.w2)

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Rhesus macaque
General summary:
  • Fever and encephalitis with signs such as ataxia and prostration may result following intracranial or intranasal inoculation, but intravenous inoculation has resulted in only fever with asymptomatic infection following subcutaneous inoculation.
  • Asymptomatic following subcutaneous inoculation but intracerebral inoculation may cause encephalitis, sometimes fatal. (J71.75.w1)
  • Fever and encephalitis following intracerebral or intranasal inoculation; only fever following intravenous inoculation, and the development of immunity. (J120.20.w1)
  • "Very susceptible to intracerebral (i.c.) inoculation of the virus." Viraemia, fever, ataxia and prostration following intracerebral inoculation. May be full recovery in one to two months or sometimes prolonged severe flaccid paralysis of the extremities. With intraperitoneal or intramuscular inoculation no clinical disease but sometimes short term viraemia. Egypt strain, 1950. (J122.77.w1)

Fever: 

  • Not seen following subcutaneous inoculation, but recorded developing 7-8 days after intracerebral inoculation, including in individuals with no other clinical signs. (J71.75.w1)
  • Temperature 40.0C or higher on the fifth, sixth and eighth days after intracerebral inoculation in one individual. Subnormal temperature recorded on the tenth day (moribund); in a second individual fever in excess of 40.0C was noted on the 7th and 8th days. (J120.20.w1)
  • Temperature 40.0C or higher on the seventh and eighth days in one individual and on the fifth to eighth days of a second individual (as well as at four and 20 hours post-inoculation in this individual). (J120.20.w1)
  • Fever noted following intracerebral inoculation. Egypt strain, 1950 (J122.77.w1)

Neurological signs:

  • Encephalitis recorded, sometimes fatal, following intracerebral inoculation of virus, starting 3-5 days after the onset of fever in 34/56 individuals inoculated intracerebrally: (J71.75.w1)
    • "ataxia, tonic and clonic convulsions, tremor of the extremities, slight decrease of the muscle power in the upper and lower extremities (usually asymmetrical), decrease or asymmetry or tendon reflexes."  (J71.75.w1)
    • Signs progressed over several days with "the appearance of ptosis, paresis of the extremities and sphincters, adynamia, and marked hypothermia." (J71.75.w1)
    • Death in 2-6 days after the onset of nervous signs or "significant regression of the symptoms" within two weeks. (J71.75.w1)
    • "Reduced muscle power in the extremities" was recorded for up to 35-36 days in some individuals. (J71.75.w1)
  • Obvious signs of encephalitis by the seventh day after intracerebral inoculation of one individual: "tremors, spasticity, nystagmus, excitability and incoordination." By the eighth day marked weakness and convulsions. Weakness progressed to coma; moribund by the tenth day post-inoculation. (J120.20.w1)
  • Illness from the evening of the fourth days, then "rigors and progressive loss of appetite until the 8th day, when coarse tremors, incoordination, and weakness were seen. On the afternoon of the 9th day the animal was very ill; the temperature had fallen and it was sacrificed." (J120.20.w1)
  • One individual "became hyperactive and showed rigors on the 8th day; exhibited marked weakness, loss of appetite, and apathy on the 9th to 11th days; appeared improved on the 12th day; and was apparently recovered by the 14th day." (J120.20.w1)
  • Following intravenous inoculation, no nervous signs seen in two individuals. (J120.20.w1)
  • Ataxia and prostration following intracerebral inoculation of WN virus. Signs may improve to normal by one to two months or a severe flaccid paralysis of the extremities may remain. Egypt strain, 1950. (J122.77.w1)

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Bonnet macaque
General summary:
  • Paralysis and death reported in experimentally infected individuals. (J88.36.w1)

Clinical signs:

  • Nervous: "Symptoms suggestive of viral encephalitis" including paralysis.(J88.36.w1)
  • Death (J88.36.w1)

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Savanna monkey
General summary:
  • Intracerebral inoculation resulted in fever but no other signs of illness; neutralizing antibodies developed. (J120.20.w1)

LITERATURE REPORTS:

  • Temperature exceeding 40.0C on the 7th and 8th days after intracerebral inoculation of one individual and on the 6th and 7th days in a second individual. (J120.20.w1)
  • No other signs of illness. (J120.20.w1)
  • Virus isolated from blood on the first day after inoculation in 1/1 individual tested and possibly at low titre on the 2nd and 3rd days (detection by mouse inoculation test, resulting in the deaths of 1/5 and 1/8 mice (Mus domesticus - Laboratory mouse) respectively). (J120.20.w1)
  • Neutralizing antibodies detected by 19 or 25 days after intracerebral inoculation in two individuals. (J120.20.w1)

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Brown lemur
General summary:
  • Experimental infection resulted in viraemia and seroconversion but no clinical signs. (J91.34.w1)

LITERATURE REPORTS: 

  • No clinical signs recorded following inoculation with either of two strains of WN virus. (J91.34.w1)
    • Viraemia detected at 1-3 days and 3-4 days post infection in two individuals inoculated with Egypt 101 strain and at day 1or 2 to 6, and on day 10, in two lemurs inoculated with MG An 798 stain (originally isolated from a parrot in Madagascar). Viraemia was sufficient to infect mosquitoes (Aedes aegypti), particularly following infection with the Madagascan strain of WN virus. (J91.34.w1)

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Domestic sheep
General summary:
  • Natural infection been reported associated with clinical illness (fever, neurological signs, death) in one individual and with head hanging, lagging behind others, ataxia and teeth grinding, in another individual.
  • With experimental infection, mild biphasic fever has been recorded and in one case congenital deformity associated with infection of a pregnant ewe.

((J3.161.w2, J62.53.w3, W27.16Sept02.wnv1)

Neurological signs:

  • Hind limb paralysis progressing to convulsions and death in one individual. (W27.16Sept02.wnv1)
  • Diffuse muscle fasciculations and inability to stand, progressing to lateral recumbency. Also apparent hyperaesthesia, intermittent rigid extension of the hind limbs, occasional but increasing tonic-clonic convulsions, distended urinary bladder in one individual. (J275.17.w1)
  • Head hanging, lagging behind others, ataxia, teeth grinding, in one ewe. (J3.161.w2)

LITERATURE REPORTS:

  • Fever: Mild biphasic fever following experimental infection of two 7-9 old sheep and moderate increase in body temperature two days after infection in one of two 18 month old pregnant ewes following experimental infection.(J62.53.w3)
  • Reproductive: Of twins born to an experimentally infected ewe in which fever and viraemia were detected, one lamb was clinically normal while the other was weak and “dumb”; this lamb died at two days old and hydroencephaly was observed. (J62.53.w3). 
  • Neurological signs and fever: Fever 104-106C, hind limb paralysis progressing to convulsions and death within two days of the onset of clinical signs in a six-year-old Suffolk ewe in Nebraska, 2002.(W27.16Sept02.wnv1)
  • Neurological signs: Diffuse muscle fasciculations and inability to stand, progressing to lateral recumbency. Also apparent hyperaesthesia, intermittent rigid extension of the hind limbs, occasional but increasing tonic-clonic convulsions, distended urinary bladder and traumatic lesions (abrasions of the facial skin, corneal ulcer) associated with recumbency. Continued to eat and drink, but estimated 6% dehydrated. Appeared depressed but alert and responsive. (J275.17.w1)
  • Neurological signs: in a single ewe in a flock in Hungary, 2005, lagging behind, head hanging, ataxia, grinding of teeth. (J3.161.w2)

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Rocky mountain goats
  • Rocky Mountain Goats
General summary:
  • Natural infection been reported associated with clinical illness (neurological signs and death)

(W27.16Sept02.wnv1)


LITERATURE REPORTS:

  • Neurological signs including nystagmus (horizontal), ataxia, head tilt, lateral recumbency and death in seven goats (males and females, 16 months to two years old). No signs in the remaining five goats of the flock. (W27.16Sept02.wnv1)

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Reindeer
General summary:
  •  Fever, depression, head tilt, flaccid tongue, dysphagia, staggering, tetraplegia and recumbency and death reported. (W27.16Nov02.wnv1, W27.18Nov02.wnv1, W178.29Oct02.WNV1)

  • Fever, lateral recumbency and tetraplegia in two animals. Fever, depression, head tilt, flaccid tongue, dysphagia in another, progressing to tetraplegia within 12 hours. (W27.16Nov02.wnv1, W178.29Oct02.WNV1)

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Domestic pig
General summary:
  • No clinical signs reported following experimental infection. (J88.38.w1)

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Alpaca
General summary:
  • Fatal clinical disease with neurological signs reported. (W27.17Sept02.wnv1)

LITERATURE REPORTS:

  • In one alpaca in 2002, fatal infection with clinical signs of "torticollis, ataxia, recumbency and 'crying like in pain'" in the three and a half days of clinical illness before death. (W27.17Sept02.wnv1)

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Domestic dog
General summary:
  • Fatal clinical illness with fever and nervous signs has been reported in a few animals and fever and paresis have been noted following experimental infection with one strain from an ill dog.
  • In most cases of natural or experimental infection no clinical signs occur. 

(J3.105.w5, J42.100.w2, J84.7.w24, J84.8.w3, J84.9.w17, J84.10.w1, J212.15.w3, P39.4.w16, W27.19Sept02.wnv1, W27.04Oct.wnv2, W27.18Oct.wnv1, W27.24Oct02.wnv1)


LITERATURE REPORTS:

  • In one dog, prostration, severe diarrhoea and frothing at the mouth, progressing to coma with convulsions and death. (J3.105.w5)
  • Experimental infection of three dogs resulted in fever in two individuals together with paresis in one of the individuals. (J3.105.w5, J84.8.w3)
  • No clinical signs observed in natural infection, nor following experimental inoculation.(J42.100.w2, J84.7.w24)
  • No clinical disease following experimental infection via mosquito bite; maintenance of normal activity levels. Mild increase in body temperature in one individual within 12 hours of infection; the individual was in prooestrus at this time. (P39.4.w16, J84.10.w1)
  • Clinical signs of weakness, progressing to neurological and cardiac signs. Euthanised while moribund. The dog had another concurrent immune mediated disease. In Illinois, USA, 2002. (W27.19Sept02.wnv1, J84.9.w17)
  • Fever and sore muscles. In Nebraska, USA, 2002. (W27.04Oct.wnv2)
  • Natural infection reported in four dogs, age five months to six years, with fever and neurological signs; three of the dogs died. WNV infection confirmed by the presence of WN virus neutralising antibodies but the virus was not confirmed to be the cause of the illness. In Louisiana, USA, 2002. (W27.18Oct.wnv1, W27.24Oct02.wnv1)
  • In one individual, inability to bear weight on its limbs even while being supported, conscious deficits in proprioception of the pelvic limbs, altered mentation and pyrexia (40.3C). Infection confirmed serologically in a further four dogs without related clinical signs. (J212.15.w3)

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Wolf
General summary:
  • Neurological and general signs including behavioural and locomotor signs, weakness, ataxia, anorexia and blindness prior to death. (J84.9.w17)

LITERATURE REPORTS:

  • Two day illness; lethargy, depression and irritability progressing to anorexia, weakness, ataxia and blindness. Died after two-day illness. (J84.9.w17)

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Domestic cat
General summary:
  • Lethargy, modest reduction in appetite and mild increase in rectal temperature recorded in some cats following experimental infection by mosquito bite; seizures reported in a single naturally infected individual. (J64.19.w1, P39.4.w16, J84.10.w1)

LITERATURE REPORTS:

  • Seizures reported in a single cat. Euthanised. Infection confirmed by isolation of West Nile virus from the brain. (J64.19.w1)
  • Mild non-specific clinical signs lasting two to three days and increased rectal temperature for days 1-6 after infection in cats experimentally infected via mosquito bite. (P39.4.w16)
  • Flu-like illness for one to two days following experimental infection. (P48.1.w16)
  • Lethargy, modest reduction in appetite and fluctuating febrile response in three of four cats infected by bite of infected mosquitoes but not in any of four cats infected by ingestion of infected mice. (J84.10.w1)

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Polar bear
General summary:
  • Hind limb paresis/paralysis was noted in a male polar bear. He was unable to stand, with a weak left hind leg and inability to move the right hind leg. The bear appeared depressed and also developed more pronounced breathing. (V.w114)

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Laboratory mouse
General summary:
  • Clinical signs in mice include general signs such as hyper- and later hypo-activity, a ruffled/rough coat, weakness, failure to feed and assuming a hunched posture. 
  • Clearly neurological signs which may be seen include hyperirritability, ataxia, paralysis of the limbs/hindquarters, falling on the back and inability to get up, tremors, stupor and coma.
  • (J101.86.w2, J120.20.w1, J133.951.w12)

LITERATURE REPORTS:

  • Adult mice, infection by intracerebral inoculation. Death or illness and sacrifice of 9/10 mice inoculated initially. Subsequently (mouse-to-mouse intracerebral passage of infected mouse brain in saline)100% fatality. Initial inoculation illness by six to eight days post-inoculation. First passage incubation period six days, second and third passages incubation period four days, later three days, sometimes with detectable illness at two days. Longer incubation period if a lower dose of virus was inoculated (incubation period 4-5 days and survival time 5-10 days). (J120.20.w1)
  • Fatal encephalitis following intracerebral, intraperitoneal or subcutaneous inoculation of suckling mice. (J101.86.w2)

Clinical signs:

  • Initial hyperactivity and roughing of the coat. (J120.20.w1)
  • Later hypoactive, weak, hunched. (J120.20.w1)
  • Hind quarter paralysis sometimes seen. (J120.20.w1)
  • Coma prior to death at 12-72 hours after the onset of clinical signs. (J120.20.w1)
  • Infective by intracerebral, intranasal and intraperitoneal inoculation but only slightly if at all by subcutaneous inoculation. (J120.20.w1)
  • Specific signs of disease in most individuals from four days after aerosol exposure. (J127.46.w1)
  • Illness or death by six days after ingestion of virus.(J71.54.w1)
  • "Illness appeared 3 days after inoculation and was manifested by sequential development of the following signs: hyperirritability, failure to feed, falling on back and inability to get up, tremors, stupor, coma and death." In suckling mice inoculated intracerebrally with 100 host LD50 of Egypt 101 strain.(J101.86.w2)
  • Mild clinical signs by day six following intraperitoneal inoculation in one mouse, neurological signs including ataxia, weakness and bilateral limb paralysis days 7-9 in two mice, severe illness by day eight in one mouse (sacrificed on day eight), ruffled fur at day eight and death by day nine in one mouse. Also up to 9% weight loss. (J133.951.w12)

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Laboratory rat
General summary:
  • The results of infection appear to be age dependent, with fatal infection following either intracerebral or intraperitoneal inoculation of newborn rats, encephalitic signs (e.g. sluggishness, hyperirritability) in animals inoculated intracerebrally at 16 days old but no clinical signs following inoculation of animals at even two months old. (J100.93.w1, J101.86.w2, J116.5.w1)

LITERATURE REPORTS:

  • Two months old rats. Intracerebral or intraperitoneal inoculation, no signs. WN virus strain isolated from a rook (Corvus frugilegus - Rook) in the Ukraine, 1980. (J116.5.w1)
  • No clinical signs following intracerebral inoculation. During an outbreak in Israel (Maayan Zvi), 1951. (J100.93.w1)
  • "Encephalitic signs such as sluggishness and hyperirritability on days 4 and 5 after inoculation, but all recovered." In sixteen day old rats following intracerebral inoculation of Egypt 101 strain. (J101.86.w2)
  • "Signs of encephalitis appeared 2 to 8 days after intracerebral inoculation, depending on the virus dose and on the host [age and species i.e. rat or mouse]". (J101.86.w2)
  • Newborn rats (less than six hours old) were highly susceptible to intracerebral or intraperitoneal inoculation with WN virus, with fatal infection. (J101.86.w2)

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"Cotton rat"
General summary:
  • Intracerebral inoculation has resulted variously in either no clinical signs (using Egypt strain) or fatal infection in 2/3 individuals (strain in Israel, 1951). (J100.93.w1, J122.77.w1)

LITERATURE REPORTS:

  • Death in 2/3 individuals following intracerebral inoculation. During an outbreak in Israel (Maayan Zvi), 1951. (J100.93.w1)
  • No clinical signs following intracerebral inoculation but development of high titre antibodies. Egypt strain, 1950 (J122.77.w1)

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Gerbil
General summary:
  • Intracerebral inoculation resulted in death of three of five individuals inoculated. (J100.93.w1)

LITERATURE REPORTS:

Guinea pig
General Summary: 
  • Generally no clinical signs following infection with a variety of WN virus strains, even after intracerebral inoculation. A temperature rise for one day in one animal has been recorded following intracerebral inoculation. Viraemia may be detected and high titres of antibodies develop. (J100.93.w1, J101.59.w1, J116.5.w1, J120.20.w1, J122.77.w1).

LITERATURE REPORTS:

  • Two months old. Intracerebral or intraperitoneal inoculation, no signs. WN virus strain isolated from a rook (Corvus frugilegus - Rook) in the Ukraine, 1980. (J116.5.w1).
  • No clinical signs following very high dose intracerebral inoculation. Seroconversion occurs. (J101.59.w1)
  • No clinical signs following intracerebral, intranasal or intraperitoneal inoculation of adults nor in 150g juveniles. (J120.20.w1)
  • One day rise in body temperature in one individual, otherwise no clinical signs following intracerebral inoculation. Circulating virus demonstrated (by mouse inoculation) on the second day post-inoculation. High level of complement-fixing antibodies developed. During an outbreak in Israel (Maayan Zvi), 1951. (J100.93.w1)
  • No clinical signs following intracerebral inoculation but development of high titre antibodies. Egypt strain, 1950 (J122.77.w1)

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Grey squirrel
General Summary: 
  • Lethargy, walking in circles, ataxia, biting at their own paws and vocalising/crying out as if in pain reported in squirrels in Illinois. (W27.19Sept02.wnv1)

LITERATURE REPORTS:

  • Lethargy, walking in circles, ataxia, biting at their own paws and vocalising/crying out as if in pain reported in squirrels in Illinois. (W27.19Sept02.wnv1)
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Eastern fox squirrel
General Summary: 
  • Various signs of neurological disease. (J26.40.w1)

Neurological signs:

  • Head tilt and torticollis, uncoordinated movements, lateral recumbency, unable to right themselves when pushed over, scratching at the forehead with feet, tremors. (J26.40.w1)

Miscellaneous signs:

  • Weakness and depression, lateral recumbency. (J26.40.w1)

LITERATURE REPORTS:

  • "Various signs of neurological disease including weakness, depression, head tilt, torticollis, lateral recumbency, uncoordinated movements, inability to right themselves when pushed over, and scratching of their foreheads with both feet and tremors." In two juveniles. (J26.40.w1)
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Hamster
General Summary: 
  • Experimental inoculation by a variety of routes commonly produces clinical disease with nervous signs such as hind limb paralysis, tremors, difficulty in walking, tremors, loss of balance prior to death in fatal cases. Residual nervous signs may be seen in survivors. Susceptibility is highest following intracerebral inoculation, lower with intraperitoneal or subcutaneous inoculation. (J84.7.w20, J91.65S3.w2, J100.93.w1 J101.59.w1)

Neurological signs:

  • Signs of encephalitis prior to death. (J101.59.w1)
  • Hind limb paralysis (J84.7.w20); paralysis. (J100.93.w1)
  • Tremors, difficulty in walking, loss of balance.(J84.7.w20)

Miscellaneous signs:

  • Lethargy and huddling together may be seen, e.g. 6-7 days after intraperitoneal inoculation. (J84.7.w20)
  • Reduced feeding, drinking and grooming may be seen, e.g. 6-7 days after intraperitoneal inoculation. (J84.7.w20)

Recovery and Convalescence:

  • .Residual nervous signs including tremors, muscle weakness and difficulty in walking may be seen in animals surviving clinical disease. (J84.7.w20)

LITERATURE REPORTS:

  • One-month-old hamsters. Intracerebral inoculation of strains from humans in Israel resulted in death of all hamsters, frequently with signs of encephalitis prior to death (death within 12-24 hours of clinical symptoms). Lower susceptibility following intraperitoneal or subcutaneous inoculation. (J101.59.w1)
  • Paralysis and death in 3/3 hamsters following intracerebral inoculation and in 2/4 hamsters following intraperitoneal inoculation. During an outbreak in Israel (Maayan Zvi), 1951. (J100.93.w1)
  • Experimental infection by intraperitoneal infection. Illness developed by 6-7 days after inoculation with neurological signs by seven days and death at 7-14 days (in about half the animals) or recovery but with residual neurological signs. (J84.7.w20, J91.65S3.w2)
    • No signs for the first five days after infection. Lethargy and huddling together in corners at six or seven days, with reduced feeding, drinking and grooming. (J84.7.w20)
    • Neurological signs at seven to ten days, such as hind limb paralysis, tremors, difficulty in walking, loss of balance. (J84.7.w20)
    • Death of severely affected animals at seven to fourteen days.(J84.7.w20)
    • Animals which survived sometimes had residual nervous signs: tremors, muscle weakness, difficulty in walking. (J84.7.w20)

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Rabbit
General Summary: 
  • No clinical signs or only a one-day rise in body temperature reported with clinical infection; seroconversion occurs with development of a high titre of antibodies. (J100.93.w1, J101.59.w1, J120.20.w1, J122.77.w1)
  • A rabbit (Oryctolagus cuniculi) has reportedly shown clinical signs and mortality associated with West Nile virus infection. (B519.1.w1)

LITERATURE REPORTS:

  • No clinical signs following very high dose intracerebral inoculation. Seroconversion occurs. (J101.59.w1)
  • No clinical signs following intracerebral inoculation of two adults and only very slight local reaction with intracorneal inoculation. Development of neutralizing antibodies by 19 days after inoculation in 1/1 of each set of rabbits (only one of each set tested). (J120.20.w1)
  • One-day rise in body temperature in some individuals, otherwise no clinical signs following intracerebral inoculation. Circulating virus demonstrated (by mouse inoculation) on the first and second days post-inoculation. During an outbreak in Israel (Maayan Zvi), 1951. (J100.93.w1)
  • No clinical signs following intracerebral inoculation but development of high titre antibodies. No clinical signs in response to inoculation onto scarified cornea. Egypt strain, 1950. (J122.77.w1)
  • A rabbit (Oryctolagus cuniculi) has reportedly shown clinical signs and mortality associated with West Nile virus infection. (B519.1.w1)
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"Hedgehog"
General Summary: 
  • Infection does not appear to result in clinical disease even following intracerebral inoculation. (J120.20.w1)

LITERATURE REPORTS:

Birds: GENERAL
General Summary: 
  • Usually asymptomatic but may result in illness involving non-specific signs such as depression, anorexia, weakness, weight loss and recumbency, or neurological signs which may include abnormal posture of the head or neck, ataxia, tremors, circling, disorientation posterior paresis (unilateral or bilateral) and visual impairment. Sudden death may also occur. 
  • Clinical illness may result in recovery (usually following mild clinical signs) or death after a period of 1-24 days, although clinical illness most commonly has been reported to last less than one week. 
  • Duration and titre of viraemia varies between species, as shown by experimental infection.
  • (J26.37.w1, P30.1.w3, J91.65S3.w1)

LITERATURE REPORTS:

  • "The clinical signs of WNV infection in WCS [Wildlife Conservation Society] collection birds were usually nonspecific. Some were found dead with no premonitory signs. Many exhibited depression, anorexia, weakness, weight loss, and recumbency. However, several birds had neurological abnormalities including abnormal head or neck posture, ataxia, tremors, circling, disorientation, unilateral or bilateral posterior paresis, and impaired vision. The course of clinical illness was usually less than one wk, but ranged from 1-24 days before recovery or death. Hematological and biochemical changes were variable and nonspecific." (P30.1.w3)
  • Pathological examination of 27 birds of 14 species in eight orders that were naturally infected with WN virus in a New York City zoological collection in 1999 revealed a variety of lesions. The most prominent lesions were gross brain haemorrhage, splenomegaly, meningoencephalitis and myocarditis. Virus was isolated from the kidney, (20/20 birds), heart (4/25), intestines, (13/14), brain (23/26), spleen (15/18), pancreas (10/12), adrenal, (10/13), liver (14/20), ovaries (4/8) and lungs (5/12 birds) (J26.37.w1). 
  • Twelve species of wild birds in the United States became viremic following experimental infection with the 1999 New York strain of WN virus, but titers varied greatly among the species. (J91.65S3.w1)

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American crow

Sick crow with WVN infection. Click here for full-page view with caption Sick crow with WVN infection. Click here for full-page view with caption Sick crow with WVN infection. Click here for full-page view with caption

General Summary: 
  • Commonly a fatal infection in crows. Clinical signs which may be seen include general signs of weakness and lethargy, standing with a crouched posture and with difficulty in maintaining balance, inability to walk, perch, stand, fly or to hold the wings in their normal position against the body and lack of a normal response to danger. Prostration and convulsions may be seen prior to death. (V.w42)

LITERATURE REPORTS:

  • General weakness and lethargy. (V.w42)
  • Sedentary. Stand with a crouched, non-erect posture and have difficulty in maintaining balance. (V.w42)
  • Show an inability to walk, perch, stand, fly or to hold the wings in their normal position against the body. (V.w42)
  • Lack of normal response to danger. (V.w42)
  • Prostration and convulsions prior to death. (V.w42)
  • Pathology: commonly myocarditis and calvarial haemorrhage; subtle lesions in the brain. (P30.1.w1)

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Blue Jay
General Summary: 
  • Signs of illness noted included an unusual posture. Following experimental inoculation via mosquito bite. (J84.9.w2)

LITERATURE REPORTS:

  • Signs of illness noted included an unusual posture. Following experimental inoculation via mosquito bite. (J84.9.w2)

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Domestic goose
General Summary: 
  • Severe clinical disease with high morbidity and mortality has been seen in naturally affected young geese (3-8 weeks old) in Israel. In Hungary, fatal infection with neurological signs was seen in 6-10 week old geese. Experimental subcutaneous infection of four two-week-old goslings resulted in decreased activity, depression and weight loss, with death of two birds and nervous signs (intermittent torticollis and opisthotonus, rhythmic side-to-side movement of the head) requiring euthanasia of a third.  (J6.34.w1, J84.7.w29, J133.951.w26)

LITERATURE REPORTS:

  • Experimental subcutaneous inoculation of two-week-old goslings resulted in decreased activity (4/4); depression (4/4), weight loss (4/4), nervous signs in 1/4: intermittent torticollis and opisthotonus, rhythmic side-to-side movement of the head. Of the four geese 2/4 died at five and six days after subcutaneous inoculation while one was euthanised ten days after inoculation due to persistent neurological signs. (J84.7.w29)
  • Natural infection in domestic goose flocks was seen in birds three to eight weeks old. Morbidity and mortality in affected flocks were severe; clinically affected individuals presented with paralytic signs. (J133.951.w26)
  • Fatal infection with neurological signs in a flock of commercially-reared geese. All geese showing clinical signs died, at ages 6 -12 weeks, after 4-5 days of clinical signs including ataxia, incoordination, intermittent torticollis and opisthotonus, abnormal head position, rhythmic side-to-side head movement, neck wriggling, and paralysis. It was considered that the coinfection with circovirus may have made the geese more susceptible to WNV, due to immunosuppression. (J6.34.w1)
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Domestic turkey
General Summary: 
  • Data from experimental inoculation indicates that turkeys become infected, develop low-level viraemia, shed virus in faeces at low level, and seroconvert, but do not develop clinical illness.
    • No clinical signs were seen following experimental subcutaneous inoculation of three-week-old poults.
    • Viraemia was detected at two to ten days post-inoculation, generally at too low a level to infect mosquitoes.
    • Seroconversion occurred at seven days post-inoculation.
    • Cloacal (faecal) shedding of virus occurred but was low-level and insufficient to infect in-contact birds.
    • (J5.44.w2)

LITERATURE REPORTS:

  • Experimental subcutaneous inoculation of three-week-old turkey poults did not cause any clinical signs of disease. One turkey died abruptly at eight days post-inoculation, possibly from peracute bacterial septicaemia; the role of West Nile virus was unclear. Viraemia was detectable at two to ten days post-inoculation but on average at levels too low to infect mosquitoes. Seroconversion occurred at seven days post-inoculation. Low levels of virus shed in faeces were not sufficient to infect in-contact birds. (J5.44.w2)

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Domestic chicken
General Summary: 
  • There are no reports of clinical signs related to natural infection in chickens, nor have such signs been seen in experimentally infected individuals, even in young chicks. However infection of young chicks and sometimes of older birds produces viraemia sufficient to infect mosquitoes, and may also result in cloacal shedding of virus. One case of apparent transmission from an inoculated bird to its uninoculated control cage mate has been recorded. Antibodies may be detected by as soon as five to seven days post-inoculation, depending on the test used. Inoculation of embryonated hens' eggs results in lethal infection. (J5.44.w1, J84.7.w22, J91.5.w1, J100.93.w1, J101.59.w1, J116.5.w1, B241.49.w49)

LITERATURE REPORTS:

  • Experimental infection in young chicks resulted in circulating virus in titres adequate to infect mosquitoes; in older birds titres sufficient to infect mosquitoes developed sometimes. (J91.5.w1)
  • Experimental infection of day-old chicks by intramuscular injection. Day-old chicks were viraemic 24 hours after inoculation at sufficient titre to infect mosquitoes (95 to 100% infection rate of mosquitoes). (J110.11.w1)
  • Experimental subcutaneous inoculation of seven-week-old chickens resulted in no clinical disease, although histopathological lesions could be detected in tissues. Detectable viraemia occurred at 2-8 days post-infection (DPI), peaking at 105/ml at four DPI. Antibodies were first detectable at five DPI (PRNT) or seven DPI (IFA, using IgG conjugate). Virus was isolated from cloacal swabs on days four and five DPI. No transmission to in-contact chickens occurred. (P32.1.w12, J5.44.w1)
  • No clinical signs following subcutaneous inoculation. During an outbreak in Israel (Maayan Zvi), 1951. (J100.93.w1)
  • No clinical signs following experimental subcutaneous or mosquito inoculation with strain WNV-NY99. Development of neutralising antibodies from as early as seven days post-inoculation and detectable viraemia in 20/21. Cloacal shedding of virus at days 2-6 post-inoculation in some birds (5/5 needle-inoculated, 5/5 60-week-old mosquito-inoculated and 2/11 17-week-old mosquito-inoculated birds) and virus detected on throat swabs in 2/6 17-week-old birds. One apparent transmission from a needle-inoculated bird to its cage mate (as shown by a transient low-level viraemia). No development of antibodies or viraemia following oral inoculation. (J84.7.w22)
  • Chick embryo:
    • Yolk sac inoculation resulting in death in 100% of embryos, incubation period 2-3 days. WN virus strain isolated from a rook (Corvus frugilegus - Rook) in the Ukraine, 1980. (J116.5.w1)
    • Yolk sac or chorioallantoic membrane inoculation resulted in the death of 100% of embryos. (J101.59.w1)
    • Lethal infection occurs in embryonated hens' eggs but these are less susceptible than are mice. (B241.49.w49)

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Cooper's hawk Accipiter cooperii - Cooper's hawk
General Summary: 
  • Clinical illness has been reported, with an affected bird having difficulty in standing, spinning in circles, seizures, death. (J22.286.w1)

LITERATURE REPORTS:

Goshawk Accipiter gentilis - Northern goshawk
General Summary: 
  • Affected birds showed neurological signs, varying in severity, including ataxia, depression, head tremors and seizures. Rapid loss of body condition during the illness. In wild birds, neurological signs then death. (J279.7.w2, J238.149.w1)

LITERATURE REPORTS:

  • In a wild-born fledgling Accipiter gentilis - Goshawk being reared at a temporary rehabilitation facility in Hungary in August 2004, sudden onset fatal neurological disease including ataxia and head tremors; terminally, seizures. Milder disease in its nest mate two weeks later, lasting for a week before recovery. In August 2005, two sick free-ranging goshawk fledglings were brought to the same centre and were euthanased with severe neurological signs. Clinical signs also developed in a juvenile and an adult goshawk on the premises, starting after the sick goshawks had been euthanised; these two birds were treated supportively, including force-feeding, and survived; in the adult, the signs lasted only two days. Rapid loss of body condition during the illness. (J279.7.w2)
  • In wild goshawks in Austria, "deviant behaviour caused by neurological symptoms" followed by sudden death. (J238.149.w1)

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Sparrowhawk Accipiter nisus - Eurasian sparrowhawk
General Summary: 
  • Clinical illness has been reported, with an affected bird showing depression, ataxia and mild seizures. Rapid loss of body condition during the illness. Recovery following supportive care including force-feeding. (J279.7.w2)

LITERATURE REPORTS:

  • In a fledgling Accipiter nisus - Eurasian sparrowhawk, in 2005, depression, ataxia and mild seizures. Rapid loss of body condition during the illness. Recovery following supportive care including force-feeding. (J279.7.w2)

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Golden eagle Aquila chrysaetos - Golden eagle
General Summary: 
  • Clinical neurological disease including disorientation, head tilt, visual impairment. Sometimes fatal despite intensive care, or severity of infection may require euthanasia. (J4.224.w1, J84.14.w5)

LITERATURE REPORTS:

  • Spain, 2007. A two-year-old captive bred eagle was found moribund one month after release into the wild; it was debilitated and aggressive, became increasingly disorientated, developed a head tilt and after five days of supportive care, died. An adult male in a captive pair became disorientated with impaired vision and debility; he survived after intensive care. (J84.14.w5)
  • USA, 2002. Natural infection, fatal or requiring euthanasia in four birds. [No further details]. (J4.224.w1)

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Bonelli's eagle Hieraaetus fasciatus - Bonelli's eagle (Accipitridae - Eagles, Hawks, Osprey (Family)):
General Summary: 
  • Clinical neurological disease including disorientation, head tilt, visual impairment; recovery following intensive care. (J84.14.w5)

LITERATURE REPORTS:

  • Spain, 2007. An adult female in a captive pair became disorientated with impaired vision and debility; she survived after intensive care. (J84.14.w5)
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Ring-billed gull Larus delawarensis - Ring-billed gull
General Summary: 
  • Signs of illness noted included an inability to hold the head upright and ataxia. Following experimental inoculation via mosquito bite. (J84.9.w2)

LITERATURE REPORTS:

  • Signs of illness noted included an inability to hold the head upright and ataxia. Following experimental inoculation via mosquito bite. (J84.9.w2)

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Sandhill crane Grus canadensis - Sandhill crane
General Summary: 
  • Usually no clinical signs of illness, but clinical illness (neurological signs) has been reported occasionally crane, in one crane leading to euthanasia, and weight loss in experimentally challenged cranes.  (J2.40.w3, J4.224.w1, P87.10.w3)

LITERATURE REPORTS:

  • Grus canadensis - Sandhill crane:
    • Neurological signs in a naturally infected crane in a zoo. (J4.224.w1)
    • Weight loss following experimental challenge with 5,000 pfu of West Nile virus inoculated subcutaneously. Non-vaccinated birds lost 4.5 - 8.5% of body weight while vaccinated individuals lost 2.2- 5.7% of body weight. (J2.40.w3)
    • Progressive ataxia in one elderly (37 years) Florida sandhill crane which was also quiet and unusually non-aggressive. Developing from difficulty in balancing to a need to use a wall or its wings to support itself, with inability to stand unassisted and several falls, later intention tremor of the head and neck and proprioceptive deficits in the wings. (P87.10.w3)
    • In hatch-year Mississippi sandhill cranes (Grus canadensis pulla), weight loss of up to 100g per day, ataxia and/or weakness for 2-11 days, progressing to recumbency and death. (P87.10.w3)
    • In adult greater sandhill cranes following experimental inoculation with 5,000 pfu WNV (equivalent to one mosquito dose), mild weight loss of 4-8% of body weight. (P87.10.w3)

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Owls "Owls" (Asio flammeus - Short-eared owl, Bubo virginianus - Great horned owl, Nyctea scandiaca - Snowy owl and Strix varia - Barred owl (Strix (Genus)))
General Summary: 
  • General signs of weakness, depression and recumbency and various neurological signs including incoordination, torticollis and seizures. (J5.47.w2)

LITERATURE REPORTS:

  • Observed clinical signs included "weakness, uncoordinated flight, inability to fly, depression, recumbency, head tilt, torticollis, tremors, and seizures; three owls were found dead with no observed signs" (J5.47.w2)

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Alligator Florida Alligators (Alligator mississippiensis - American alligator (Alligatoridae - Alligators & Caimans (Family)))
General Summary: 
  • Neurological signs, deaths. (P39.4.w16)

LITERATURE REPORTS:

Crocodile monitor Crocodile monitor (Varana salvidorii) (Varanidae - Monitors (Family)))
General Summary: 
  • Natural infection with neurological clinical signs. (P39.3.w8)

LITERATURE REPORTS: