Virus / Flaviviridae / West Nile Virus / Detailed Viral Descriptions:
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Ý ß  DEFINITIVE MAMMAL HOST SPECIES with literature reports for West Nile Virus:

Species/Taxa Recorded and Diagnostic Method used for Confirmation

Editorial Summary (Editorial Overview Text Replicated on Overall Virus page - West Nile virus)

A wide variety of mammals have been recorded to be infected with West Nile virus, either by virus isolation or more frequently by detection of antibodies. With the exceptions of equines (Equidae - Horses (Family)) and humans (Homo sapiens - Human), natural infection appears to be associated with clinical disease only rarely. Levels of viraemia in mammals are generally low and in most species probably are only rarely sufficient to infect mosquitoes.

(References available in detailed literature reports below)

Data Source Information Orders affected (detailed information available below):

The following list indicates the species which West Nile virus has been reported to infect, and indicates whether the infection was natural or experimental, and the level of diagnosis:

Perissodactyla - Odd-toed ungulates (Order)

Equus caballus - Domestic horse:

  • Argentina, 2006. Natural infection with encephalitis in three horses, fatal; virus detected by culture and IFA. (J84.12.w3)
  • Australia (In Quarantine), 2002. Natural infection detected in a horse from Canada showing signs of encephalitis five days into a 14-day quarantine period after arriving in Australia. Infection confirmed by PRNT. (W27.04Oct02.wnv2)
  • Canada (Manitoba), 2002.  Natural infection confirmed in ten horses. (W27.21Aug02.wnv1)
  • Canada (Saskatchewan), 2002.  Natural infection confirmed in six horses. (W27.10Sept02.wnv1)
  • Canada (Ontario), 2002.  Natural infection diagnosed in five horses by immunohistochemistry with at least one confirmed by PCR, also two further cases suspected (diagnosed by IgM capture ELISA). (W27.12Sept02.wnv1)
  • Canada (Ontario, Manitoba), 2002.  Natural infection confirmed in five horses with presumptive diagnosis in a further 31 individuals in Ontario, and a total of 99 horses confirmed positive in Manitoba. (W27.27Sept02.wnv1)
  • Canada (Manitoba, Quebec, Ontario, Saskatchewan), 2002. Natural infection in 336 equines [data to 04 December 2002]. (P39.4.w1)
  • Canada (Ontario) 2002. Natural infection in 28 horses, fatal or requiring euthanasia in 12 cases (43%). Infection confirmed by serology (25/28, 89%) and/or IHC (positive for 11 seropositive horses and one seronegative horse) or RT-PCR (one horse) or the presence of antibodies in CSF (one horse). (J14.44.w1)
  • Canada (Saskatchewan) 2002. Two cases reported, confirmed by IgM capture ELISA (one horse) and PCR from brain tissue (one horse). (J14.45.w1)
  • Canada, 2003. WN virus seropositive horses (presumed plus confirmed cases) were recorded in Nova Scotia (1), Quebec (8), Ontario (41), Manitoba (53), Saskatchewan (162) and Alberta (180). It was noted that some IgG-positive results reported to CFIA could be due to previous exposure or to vaccination. [Data updated 12 January 2004](W181.19Jan04.WNV3)
  • Chad (N'Djamena), 2003-2004. Natural infection without clinical illness. Antibodies detected by IgG ELISA and confirmed by Western blot or PRNT90 in 29/30 horses (97%) from two riding stables. Two horses seroconverted between 2003 and 2004.  (J84.12.w5)
  • Colombia (Cordoba and Sucre), 2004. Natural infection without clinical signs. WN virus antibodies were confirmed in 12 horses (12% of those sampled) by PRNT (90% neutralisation) titles of 1:40 or higher (titres for other flaviviruses at least four-fold lower in each positive horse). (J84.11.w2)
  • Cote d'Ivoire (Abidjan) 2003-2005. Natural infection without clinical illness. Antibodies detected by IgG ELISA and confirmed by Western blot or PRNT90 27/95 horses (28%) from three riding stables. (J84.12.w5)
  • Croatia, 2001-2002. Natural infection without clinical signs. Antibodies were detected (initially by IgG ELISA, confirmation by PRNT) in four of 81 horses from a stud farm in the Dakova region; 899 sera from other horses in Croatia were negative. (J3.160.w)
  • Djibouti (Djibouti), 2004-2005. Natural infection without clinical illness. Antibodies detected by IgG ELISA and confirmed by Western blot in 1/11 horses (9%) from two riding stables. (J84.12.w5)
  • DRC (Kinshasa) 2004. Natural infection without clinical illness. Antibodies detected by IgG ELISA and confirmed by Western blot in 6/20 (30%) horses from one riding stables. (J84.12.w5)
  • Cuba, 2003-2004. Natural infection, antibodies detected in four horses (of 210 sampled) (flavivirus antibodies detected by ELISA, WN virus confirmed by PRNT 90% neutralisation titre. (J84.12.w4)
  • Egypt 1950's. Natural infection not associated with clinical illness. Neutralizing antibodies detected in sera. (J91.5.w1)
  • Egypt, 1959. Natural infection resulting in encephalitis and nervous signs in one horse, experimental infection by inoculation in three horses (and several donkeys) resulting in no clinical signs, and serological evidence of infection (presence of West Nile virus neutralising antibodies in horses, also in mules and donkeys). Confirmation of infection by recovery of virus from the brain of the naturally infected horse. (J86.57.w1)
  • Egypt 1996, 1999. Natural infection, IgG antibodies detected by ELISA in 24/490 horses (4.9%) in samples from 1996 and in 21/205 horses (10.2%) in samples from 1999. (J91.65S3.w1)
  • El Salvador (2003) Natural fatal infection, WNV positive in three horses. (W27.04May03.wnv2)
  • El Salvador, 2001-2003. Natural infection, fatal in 203 equines, November 2001 - April 2003; antibodies detected by ELISA  in 18/73 stablemates (25%) tested in 2003, with confirmation by PRNT in 10 individuals. (J91.72.w1)  
  • France, Camargue, 1962. Natural infection resulting in encephalitis and nervous signs in about 50 domestic horses and an unknown number of feral horses. Antibodies detected by serum neutralisation tests and IHA (J137.118.w1, J84.7.w17)
  • France, Camargue, 1965. Natural infection resulting in encephalitis and nervous signs in at least three horses. Infection confirmed by detection of antibodies and changes in antibody titres in two cases and by isolation of virus from the spinal cord in a fatal case. (J137.118.w1, J84.7.w17)
  • France, "Little Camargue" (Herault Province, southern France), September to November 2000. Natural infection resulting in encephalitis and nervous signs and sometimes fever in 76 horses, diagnosis by serology (case considered confirmed if positive on IgM- capture ELISA (MAC-ELISA) or probable if IgM negative but positive with indirect IgG ELISA) and by virus isolation from the brains of dead horses (J84.7.w17). Natural infection resulting in encephalitis and nervous signs and sometimes fever in 76 horses, diagnosis by serology (case considered confirmed if positive on IgM- capture ELISA (MAC-ELISA) or probable if IgM negative but positive with indirect IgG ELISA) and by virus isolation from the brains of dead horses. (J84.7.w17)  
  • France, 2000. A large-scale serological survey conducted during 2000, involving all horses and donkeys (not including half-wild horses which could not be sampled) within 10km of a laboratory-confirmed case of WNV infection in southern France during 2000, found IgG antibodies to WN virus in 432/5,107 animals (8.5%). Of the IgG-positive animals 182 (42.1%) were also IgM positive. Seroprevalence was highest in one central region of the study area. This area, considered to be the "epidemic hot spot" was described as a rather dry area. Prevalence was highest in native breed Camargue horses which are maintained outside at all times. (J84.8.w8)
  • France, the Var, September to October 2003. One confirmed (positive IgG and IgM by ELISA and PRNT) and two probable cases (also one confirmed and one probable human cases). (J486.7.w1)
  • France, southern, September 2004. 37 suspected cases over a period of six weeks, four being fatal or requiring euthanasia. Of 18 tested, 14 were confirmed by detection of WNV IgM or by PCR). (J486.8.w1)
  • France (near Perpignan), 2006. Natural infection. [No further details provided](J279.8.w1)
  • Gabon (Libreville, Port Gentil, Moanda) 2004. Natural infection without clinical illness. Antibodies detected by IgG ELISA and confirmed by Western blot or in 2/54 horses (3%) from four riding stables. (J84.12.w5)
  • Guadeloupe 2002-3. Natural infection reported. No details provided. (W27.11Oct03.wnv1)
  • Guadeloupe 2002-3. Natural infection, Ig G antibodies detected in 10 of 113 horses tested July 2002, increasing to 50% of horses tested January 2003, with seroconversion detected in paired samples of 54/114 horses which had been negative in July 2002; IgM antibodies were not detected in January 2003. (J84.10.w4)
  • Guadeloupe, 2003-2004. Natural infection detected by surveillance in clinically normal equines. In July 2003, 19.3% of sampled equines (94/453 horses, 37 donkeys) were confirmed with WNV antibodies (PRNT90). In August 2004, 16.2% of tested equines (404 horses, 27 donkeys) were seropositive; no equines were confirmed to seroconvert during this period, suggesting a large reduction in virus circulation in 2004 (possibly related to a seven-month drought, November 2002 to May 2003, which may have decreased mosquito populations). Seropositive horses were mainly from near mangroves, swamps and humid plains, not from dry areas. (J84.11.w3)
  • Guatemala, 2003-4. Natural infection (no clinical disease) detected by epitope-blocking ELISA on samples collected September 2003 - March 2004, and further confirmed by PRNT. (J84.12.w2)
  • Israel 1959-60.  Natural infection. Haemagglutination-inhibition antibodies to WNV detected in 28/81horses (35%). (J109.34.w1)
  • Israel, 1998. Natural infection. Neutralizing antibodies detected in 18/24 serum samples from horses suffering from neurological disease. (P34.2.w1)
  • Israel, 2000. Natural infection. Neurological signs in 76 horses, 15/76 died or euthanised. WN virus detected from the brains of three horses with encephalomyelitis and the buffy coat layer of a blood sample from one horse with fever. Seroconversion proved in five other animals. (J3.151.w1, J73.57.w1)
  • Italy (Tuscany), August to October 1998. Natural infection resulting in nervous signs in 14 horses, diagnosis by "appropriate serological, virological and biomolecular tests", including virus isolation from the central nervous system of one dead horse. (J87.32.w1)
  • Italy (Tuscany), August to October 1998. Natural infection resulting in nervous signs in 14 horses in a wetland area (Padule del Fucecchio). Six cases were fatal including three in horses less than six years old; there was no difference in age between horses that died and those that recovered. Sera was available from 12 of the horses; all were positive for WN virus by the complement fixation (CF) test (titres 1:4 to 1:128). Seroprevalence in the stables from which these horses had been notified ranged from 10.2% to 75% (total 63/159, 39.6%) when blood samples were taken in October. Samples were taken from many of the same horses in November; CF titres fell from October to November. Samples from a further 161 horses collected in November from stables within a 3.0 km radius of the clinical cases gave 30/151 (19%) positive with CF test and 63/155 (41%) positive with an IgG ELISA (six horses tested inconclusive). In a further zone around the central area 43/120 (36%) of horses were seropositive by IgG ELISA (plus three inconclusives) while 19/123 (15%) were positive by CF test. There was no age-related pattern to seroprevalence; it was considered that the data indicated introduction of the virus into the area in 1998. (J84.8.w11)
  • Hungary, 2000-2001. Natural infection. Sera from four horses, passing through Austria in 2000-2001, originating in Hungary, were positive for WNV antibodies by PRNT; none showed any clinical signs at the time of sampling. (J19.131.w1)
  • Mexico (Coahuila State), 2002.  Natural infection confirmed with and without neurological signs. A serological survey carried out in Coahuila State, Mexico, December 2002 found 15/24 horses (62.5%) to be seropositive for WNV neutralising antibodies in a PRNT. Eleven of 14 horses were seropositive from one site at which one horse had died following neurological signs in October 2002 and a further five horses had shown neurological signs during mid-to late October 2002; all five of the horses which had shown neurological signs and survived were seropositive for WNV. Additionally 11/19 horses which had not shown any clinical signs were seropositive. (J84.9.w10)
  • Mexico (Yucatan State), 2002. Natural infection detected on the basis of the presence of neutralising antibodies. A serological survey carried out in Yucatan State, Mexico, July to October 2002 found 3/252 horses to be seropositive for WNV neutralising antibodies in a PRNT. (J84.9.w11)
  • Mexico (Tamaulipas State), 2002.  Natural fatal infection confirmed in a horse which died in August 2002, 15 days after being transported from near the frontier with Texas, USA. (W27.25Mar03.wnv1)
  • Mexico ((Veracruz, Yucatan, Chihuahua, Coahuila and Tamaulipas) 2002. Natural infection detected by IgG ELISA and confirmed by 90% PRNT against WN virus, and cross-checked for reaction with other arboviruses including St. Louis encephalitis virus (SELV). Of 441 serum samples analysed from populations with a history of clinical cases of encephalitis, WN virus antibodies were detected in 97 (22%)(J84.9.w23)
  • Mexico (Chihuahua, Tamaulipas, Coahuila, Veracruz, Tabasco, Quintana Roo, and Yucatan States), 2003. Natural infection in horses. [Data to 14th July] (W27.15Jul03.wnv1)
  • Morocco, 1996. Natural infection resulting in influenza-like and nervous signs in 94 equids (horses, mules and donkeys). Diagnosis by serology and by isolation of WN virus in cell culture with characterisation using physicochemical and biological tests. (J85.108.w1)
  • Morocco, 2003. Natural infection in eight adult horses (seven to eight years old) with five fatal cases. Diagnosis by ELISA and virus neutralisation. (J90.16.w5)
  • Oman, 2003. Natural infection in 19 of 240 individuals in the town of Sib, govenorate of Muscat, with four cases euthanised. Infection confirmed by virus isolation from brain. (J90.16.w4)
  • Portugal, 1973 (approx.). Natural infection associated with an outbreak of encephalomyelitis. WNV infection confirmed by the presence of virus neutralising antibodies in 29% of surviving horses. (J88.34.w1)
  • Senegal (Dakar), 2002-2003. Natural infection without clinical illness. Antibodies detected by IgG ELISA and confirmed by Western blot or PRNT90 in 23/25 horses (92%) at one riding stables. (J84.12.w5)
  • South Africa (2000-2001). Natural infection without any reported clinical disease shown by seroconversion of 11% of 488 yearling thoroughbreds over a period of about 12 months; approximately 75% of the dams (mothers, i.e. adult horses) of the yearlings were seropositive. No clinical disease occurred following inoculation of two individuals with a recent lineage 2 isolate of WN virus. (J87.35.w1)
  • USA (New York City) 1999. Clinical disease with nervous signs in at least 20 (confirmed) and probably a further five horses (J84.7.w27); serological evidence of infection in 20/69 asymptomatic stable mates (J84.7.w27) and in 2/73 other healthy horses tested in New York City (J84.7.w24). Diagnosis by clinical signs, post mortem examination and laboratory tests including the presence of virus-neutralising antibodies (plaque reduction virus-neutralising antibody test) and virus isolation. (J90.1999.w1, J84.7.w24, J84.7.w27, J4.218.w2, J64.19.w1)
  • USA (1999). Experimental infection by intravenous and subcutaneous inoculation. Mild nervous signs in 1/4 individuals beginning 58 days after infection.(P32.1.w13)
  • USA (New York City) 1999. Natural infection, 6% of horses birds tested were positive for neutralising antibodies in North-east Queens in 1999 . (P39.2.w2)
  • USA (New York State) 2000. Clinical disease (neurological signs, sometimes with fever) in 23 horses and serological evidence of infection in a further 7/91 clinically normal horses, including 5/6 horses at one premises. Diagnosis of clinical cases by clinical signs plus confirmation by laboratory testing: IgM antibody and positive WNV neutralisation, a fourfold rise in virus neutralisation titre from paired serum samples, or detection of viral sequence by reverse transcription-polymerase chain reaction (RT-PCR). (J84.7.w27)
  • USA (Connecticut, Delaware, Massachusetts, New Jersey, New York, Pennsylvania and Rhode Island) 2000. Clinical disease with nervous signs, death or euthanasia in 23/60 individuals. Diagnosis by clinical signs plus laboratory testing, including virus isolation from the brain of 7 horses, positive reverse transcriptase-nested polymerase chain reaction (RT-nPCR) in the brains of 10 horses (including the seven from which virus was isolated), positive IgM in serum using IgM-capture ELISA in 59 horses, and positive titres of serum by plaque-reduction neutralisation test (PRNT) in 55 horses, including a four-fold increase in PRNT between acute phase and convalescent phase serum samples in one horse. (J90.2000.w1, J90.2000.w2, J90.2001.w1).
  • USA Connecticut, Delaware, Massachusetts, New Jersey, New Yourk, Pennsylvania and Rhode Island (2000). 60 equine cases confirmed by USDA - APHIS-VS; Of these, 37 survived and 23 died or were euthanatized ( case-fatality rate 38%). Affected equids were five months to 38 years old, average 14 years old; 36 were males and 24 were females. (D341.IIB.w3 - full text included, D345 - full text included)
  • USA (2000). Natural infection with neurological disease. Infection identified in 63 horses from 26 counties in seven states, including New Jersey (28 horses), New York (21), Connecticut (7), Delaware (4), Massachusetts (1), Pennsylvania (1) and Rhode Island (1). (J84.7.w23)
  • USA 2000. Experimental infection of 12 horses via bites of infected mosquitoes. Clinical encephalitis in 1/12 individuals. Development of neutralizing antibody in all surviving horses. Highest viraemia titre approximately 460 Vero cell plaque forming units (PFUs) per ml. Viraemias were not sufficient to infect Aedes albopictus mosquitoes fed on eight of the horses on days 3,4  and 5 post-infection. (J133.951.w37)
  • USA, 2001. "Equine surveillance identified three horses with neurologic disease attributed to WNV infection in Jefferson County, Florida, with illness onsets beginning on June 24". (N7.50.w2)
  • USA  (Jefferson County, Florida) 2001. Clinical disease in four horses including one death. Diagnosis from central nervous system clinical signs in conjunction with results of laboratory testing (serological and testing of nervous tissue). (J90.2001.w2)
  • USA, 2001. Natural infection confirmed in 413 horses and probable in three horses, 1st January to 20th November 2001, in 19 states. Fatal infection (died or euthanased in at least 70/294 individuals (outcome not reported for all cases). (W27.27Nov01.wnv1) 
  • USA, 2001. Natural infection with clinical signs in 652 horses. Individuals of more than 30 breeds were affected and there was no breed predilection. Slightly more males were affected than females (males 350/652, 53.7%). The case fatality rate for those with a known outcome was 156/470 (33.2%). On average horses that died were older than those that recovered. (P39.3.w2)
  • USA (1999-2001) Natural infection confirmed in 25 individuals in 1999, 63 in 2000 and 733 in 2001 [ArboNET data as of 21 Jan 2003]. (P39.4.w1)
  • USA, 2001. Natural infection, 738 equine cases. (D341.IIB.w3, W30.May08.w3)
  • USA, 2002. Natural infection, 9,144 cases of infection in horses reported 01 January 2002 to 30 November 2002. (N7.51.w6)
  • USA, 2002. Natural infection reported in 14,901 cases [reported to 26 January 2003]. States with 800 or more cases included Illinois, Iowa, Minnesota, Missouri, Nebraska, Oklahoma and Texas, with 400-799 cases in each of Florida, Indiana, Kansas, Kentucky, North Dakota, Ohio and South Dakota. (P39.4.w4)
  • USA (1,678 counties in 39 states) 2002. Natural infection confirmed in 12,038 horses [ArboNET data as of 21 Jan 2003]. (P39.4.w1)
  • USA, 2002. Natural infection, 15,257 equine cases, including four states with more than 1,000 cases and a further six states with 500 - 1,000 cases. (D341.IIB.w3, W30.May08.w3)
  • USA (Florida) 2002. Natural infection in 499 horses. (P48.1.w4)
  • USA. Experimental infection of twelve horses by bite of infected mosquitoes. Development of a low viraemia (e.g. 101.0-102.2 PFU/mL blood) of short duration (one to five days). Horses did not transmit infection to Aedes albopictus mosquitoes allowed to feed on the horses during the period of viraemia. NT (PRNT) antibodies greater than or equal to 1:10 developed by day 7-11 post infection. NT titres reached 1:20 to greater than 1:320 and in one horse greater than 1:1,280. Clinical signs (fever, progressive neurological signs requiring euthanasia) were seen in only one horse, with severe encephalomyelitis and relatively high titres of virus (by plaque assay) isolated from the brain and spinal cord. (J84.8.w4)
  • USA (Minnesota), 2003. Natural fatal infection, first case in a horse in 2003, in April. (W27.02May03.wnv1)
  • USA, 2003. Natural infection. Infection reported in 4,146 horses during 2003; infection was reported in 61 sentinel horses [Data to 25 November 2003]. (N7.52.w6)
  • USA, 2003. Natural infection, 5,181 equine cases reported. (D341.IIB.w3, W30.May08.w3)
  • USA, 2004. Natural infection, 1,406 equine cases reported. (D341.IIB.w3, W30.May08.w3)
  • USA, 2005. Natural infection, 1,088 equine cases reported. (D341.IIB.w3, W30.May08.w3)
  • USA, 2006. Natural infection. Infection reported in 1,086 equines from 414 counties of 34 states; 31% of cases were reported from Idaho and infection peaked in August. (D342, N7.56.w1, W30.May08.w4)
  • USA, 2007. Natural infection. Infection reported (from state veterinarians and the ArboNET reporting system) in 468 equines. (D343, W30.May08.w5)
  • USA (Nebraska and Colorado), 2002. Natural infection with clinical signs. About 1,500 horses affected. (J4.225.w2)
  • USA (Texas), 2002-2004. Natural infection with clinical signs in 1,377 horses in 2002, 396 horses in 2003 and 134 in 2004. Hyperendemic foci ("hot spots") were detected in southeastern Texas and (although shifting away in 2003-4) in northwestern Texas. (J13.69.w1)
  • Venezuela, 2004-2006. Natural infection, flavivirus antibodies detected by ELISA in 141/791 horses and WNV infection confirmed by PRNT in 34 horses; samples from WNV-positive horses were collected between February 2004 and May 2006. (J84.13.w1)

Donkey (Equidae - Horses (Family)):

  • Guadeloupe, 2003-2004. Natural infection detected by surveillance in clinically normal equines. In July 2003, 19.3% of sampled equines (94/453 horses, 37 donkeys) were confirmed with WNV antibodies (PRNT90). In August 2004, 16.2% of tested equines (404 horses, 27 donkeys) were seropositive; no equines were confirmed to seroconvert during this period, suggesting a large reduction in virus circulation in 2004 (possibly related to a seven-month drought, November 2002 to May 2003, which may have decreased mosquito populations). Seropositive horses were mainly from near mangroves, swamps and humid plains, not from dry areas. (J84.11.w3)
  • Egypt 1950's. Natural infection not associated with clinical illness. Neutralizing antibodies detected in sera. (J91.5.w1)
  • Israel 1959-60.  Natural infection. Haemagglutination-inhibition antibodies to WN virus detected in 4/9 individuals (44%). (J109.34.w1)
  • USA/Canada, 1999-2003. Natural infection in domestic individual(s). Reported positive in surveillance efforts. Virus or viral DNA detected. [Data to 15th April 2003](W8.Nov01.WNV2)
  • USA ( Nebraska and Colorado), 2002. Natural infection with clinical signs. Two donkeys affected (at least). (J4.225.w2)

Mule (Equidae - Horses (Family)):

  • Egypt 1950's. Experimental infection resulting in low level circulating virus in one of two mules; both developed neutralizing antibodies by one month after infection. (J91.5.w1)
  • Israel 1959-60.  Natural infection. Haemagglutination-inhibition antibodies to WN virus detected in 25/38 individuals (66%). (J109.34.w1)
  • USA/Canada, 1999-2003. Natural infection in domestic individual(s). Reported positive in surveillance efforts. Virus or viral DNA detected. [Data to 15th April 2003] (W8.Nov01.WNV2)
  • USA ( Nebraska and Colorado), 2002. Natural infection with clinical signs. Three mules affected (at least). (J4.225.w2)

Rhinoceros unicornis - Greater Indian rhinoceros (Rhinocerotidae - Rhinoceroses (Family)):

  • USA (New York City, Wildlife Conservation Society collections) June 1999-February 2000. Natural infection,  history of illness with depression, anorexia and a lip droop; spontaneous recovery. Found positive for WN virus specific antibodies on plaque reduction neutralization assay. (P30.1.w3)

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Proboscidea - Elephants (Order)

Elephas maximus - Asian Elephant:

  • USA (New York City, Wildlife Conservation Society collections) June 1999-February 2000. Natural infection in two individuals, no history of clinical illness. Found positive for WNV specific antibodies on plaque reduction neutralization assay. (P30.1.w3)

Elephants (Elephantidae - Elephants (Family)):

  • USA to June 2004. High WNV antibody titres, including titres of 1:4,000 have been reported in a number of elephants without any associated clinical signs. There has been no confirmed clinical illness associated with WN virus infection in elephants, although two WN virus antibody positive bulls at Kansas City Zoo died in fall 2003. (D309, W580.Sept2005.w5)

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Carnivora - Carnivores (Order)

Canis familiaris - Domestic dog:

  • Botswana (1965-1980). Natural infection. West Nile virus isolated once. No further details. (P33.3.w1)
  • Botswana (1977). Natural infection resulting in nervous signs and death in one dog. N.B. misdiagnosed and reported as Wesselsbron virus. (J3.105.w5, J84.8.w3) 
  • Botswana (1977). 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) 
  • South Africa (Orange Free State, highveld area, and Onderstepoort) Natural infection and experimental infection by subcutaneous and intravenous inoculation. Natural infection in dogs detected by serology; 174/377 individuals (46%) positive for arbovirus antibodies at 1 in 20 or higher in the haemagglutination-inhibition (HI) test, with 25 of these having titres in excess of 1 in 640. 138/162 dogs tested had WN neutralising test antibodies at 1 in 8 or greater titres. Virus was detected in serum from one seronegative individual. Seroconversion in experimentally infected dogs  shown by development of haemagglutination inhibition (HI) and neutralisation test (NT) antibodies. Low level viraemia recorded in 1/3 dogs infected experimentally (later found to be suffering from Cushing's disease). (J42.100.w2)
  • USA (New York City) 1999. Natural infection. Infection confirmed by the presence of neutralising antibodies with titres at least fourfold higher than titres to St Louis encephalitis virus (SLE) in 10/198 clinically normal dogs. (J84.7.w24)
  • USA (New York City) 1999. Natural infection, 111% of individuals tested were positive for neutralising antibodies in North-east Queens in 1999 . (P39.2.w2)
  • USA (Illinois), 2002. Natural infection with clinical signs (weakness, progressing to neurological and cardiac signs), euthanased when moribund in an eight-year-old dog with a concurrent immune-mediated disease. Histological lesions of viral encephalitis and myocarditis. WNV infection confirmed by immunohistochemistry and PCR, from three laboratories. (W27.19Sept02.wnv1, , J84.9.w17) 
  • USA, 2002. Natural infection, three cases of infection in dogs reported 01 January 2002 to 30 November 2002. (N7.51.w6)
  • USA (Nebraska) 2002. Natural infection with fever and sore muscles. WNV infection laboratory confirmed. (W27.04Oct.wnv2)
  • USA (Louisiana) 2002. 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. (W27.18Oct.wnv1, W27.24Oct02.wnv1)
  • USA (Louisiana) 2002. Natural infection, 85/300 dogs sampled during a three-month period in Slidell, Louisiana were WN virus-seropositive. (P48.1.w16)
  • USA, 2003. Natural infection. Infection reported in 30 dogs during 2003 [Data to 25 November 2003]. (N7.52.w6)
  • USA (Missouri) 2002.  Natural infection with clinical and possibly fatal disease in one individual (euthanased due to clinical signs), also detection of  antibodies to WN virus by IgM-capture ELISA in an additional four dogs. (J212.15.w3)
  • Experimental infection by bite of infected mosquitoes. No clinical disease, viraemia but no isolation of virus from saliva. (P39.4.w16)

Canis lupus - Wolf ((Canidae - Dogs, foxes (Family)):

  • USA (Illinois), 2002. Natural infection with signs of CNS disease in a three-month-old animal from a small zoological collection. WNV infection confirmed by immunohistochemistry and PCR, from three laboratories. (W27.19Sept02.wnv1) 

Felis catus - Domestic cat:

  • USA (New York City) 1999. Nervous signs (seizures), euthanased. Diagnosis by isolation of WN virus from the brain (J64.19.w1, W8.Nov01.WNV2)
  • USA, 2003. Natural infection. Infection reported in one cat during 2003 [Data to 25 November 2003]. (N7.52.w6)
  • Experimental infection by bite of infected mosquitoes. Viraemia developed in 12-36 hours, peak titre 103.0 to 104.0 pfu/ml ( a level that may be sufficient to detect mosquitoes). No viraemia after 4.5 days. Mild non-specific clinical signs lasting two to three days, increased rectal temperature for days 1-6 after infection, no virus isolated from saliva. (P39.4.w16)
  • Experimental infection by consumption of infected mice. Viraemia developed, within 24 hours for cats eating three infected mice and at 2.5 and 4.0 days for cats ingesting a single mouse with lower virus content, reaching peak titres of 102.0, 102.2,103.7 to 103.9 pfu/ml, but no clinical signs or elevated temperature. Seroconversion occurred by day 14 post exposure in 3/4 cats fed infected mice and by day 21 in the fourth individual. (P39.4.w16)

Panthera uncia - Snow leopard (Felidae - Cats (Family)):

  • USA (New York City, Wildlife Conservation Society collections) June 1999-February 2000. Natural infection, no history of clinical illness. Found positive for WN virus specific antibodies on plaque reduction neutralization assay. (P30.1.w3)

Ailurus fulgens - Lesser (Red) Panda (Ursidae - Bears (Family)):

  • USA (New York City, Wildlife Conservation Society collections) June 1999-February 2000. Natural infection, no history of clinical illness. Found positive for WN virus specific antibodies on plaque reduction neutralization assay. (P30.1.w3)

Procyon lotor - Common Raccoon:

  • USA 1999-2001. Natural infection. Found positive for WN virus in surveillance efforts. (W8.Nov01.WNV2)

Mephitis mephitis - Striped skunk (Mustelidae - Weasels (Family)):

  • USA 1999-2001. Natural infection. Found positive for WN virus in surveillance efforts. (W8.Nov01.WNV2)
  • USA (Connecticut) 2000. Natural infection with illness, WNV infection confirmed (J84.7.w23)
  • USA/Canada, 1999-2003. Natural infection in wild individual(s). Reported positive in surveillance efforts. Virus or viral DNA detected. [Data to 15th April 2003](W8.Nov01.WNV2)

Ursus americanus - American black bear:

  • USA (New Jersey), 2002. Natural infection, no clinical signs reported. WN virus neutralising antibodies detected in 3/51 samples (6% of individuals) from bears, mainly adult females. Reciprocal 90% neutralizing antibody positive, 160 to > 320 and always at least fourfold higher than SLEV-neutralising antibody titres. (W27.24Jul02.wnv1, J1.39.w2)

Ursus arctos - Brown bear:

  • Natural infection, antibodies detected by haemagglutination-inhibition (HI) test in 4/15 sera from Ursus arctos - Brown bear from Croatia (all seropositive bears were free-living). [1993](J1.29.w15)

Ursus maritimus - Polar bear:

  • Natural infection, euthanasia due to severe illness in a bear in a zoo in Canada, 2006. Infection confirmed. (V.w112, V.w114)

Phoca vitulina - Common seal (Harbor seal):

  • USA (New Jersey) 2002. Natural infection, fatal following ten day illness in a 12-year-old male seal. Infection confirmed. (W27.31Oct02.wnv1)
  • USA/Canada, 1999-2003. Natural infection in wild individual(s). Reported positive in surveillance efforts. Virus or viral DNA detected. [Data to 15th April 2003](W8.Nov01.WNV2)

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Primates - Primates (Order)

Homo sapiens - Human

  • Albania, 1958. Natural infection with West Nile virus specific antibodies detected in two individuals. (J84.5.w2)
  • Algeria, 1994. Natural infection with clinical signs affecting about 50 individuals and fatal in eight individuals. (J84.5.w2)
  • Canada (Ontario), 2002.  Natural infection, confirmed; first human case in Ontario. (W27.09Sept02.wnv2)
  • Canada (Quebec), 2002.  Natural infection, confirmed; first human case in Quebec, with a further three probable cases. (W27.27Sept02.wnv1)
  • Canada (Alberta), 2002.  Natural infection, confirmed; first human case in Alberta but infection probably acquired in USA. (W27.23Oct02.wnv1)
  • Canada (Alberta, Quebec, Ontario), 2002.  Natural infection, 84 suspected and 57 confirmed cases including two deaths, with investigation continuing to determine cause of death (i.e. whether or not death was attributable to WNV infection) in another confirmed case and five suspect cases. (W27.13Nov02.wnv1)
  • Canada (Alberta, Quebec, Ontario), 2002. Natural infection with 198 cases, two fatal. (P39.4.w1)
  • In Canada in 2003 WN virus cases had been recorded in humans in Nova Scotia (two cases confirmed), New Brunswick (one case confirmed), Quebec (16 cases confirmed, one probable), Ontario (89 cases confirmed), Manitoba (35 cases confirmed, 106 probable), Saskatchewan (792 cases confirmed), Alberta (272 cases confirmed), British Columbia (12 cases confirmed, eight probable) and Yukon Territory (one confirmed case). However, cases in humans in Nova Scotia, New Brunswick, British Columbia and Yukon Territory were considered likely to be related to travel outside the Province or Territory. [Data updated 12 January 2004](W181.19Jan04.WNV1)
  • Central African Republic, 1985. Natural infection, associated with severe hepatitis. Infection confirmed by virus isolation in four individuals. (B241.49.w49)
  • Cuba, 2003-2004. Natural infection with encephalitis, IgM and IgG antibodies detected by ELISA; WNV antibodies confirmed by PRNT 90% neutralisation titre. (J84.12.w4)
  • Czechland (South Moravia) 1997. Neutralising antibodies detected in 13 of 619 humans (hospitalised or attending outpatient clinics). Symptoms compatible with West Nile fever were seen in five individuals and a rising antibody titre confirmed in two of these.(J115.13.w4)
  • Czech Republic, 1999. Natural infection, with clinical disease in some individuals and apparent asymptomatic infection in others. Infection detected by presence of virus neutralising antibodies in 13/619 individuals and acute infection confirmed by a significant increase (> 4 times) in titre in paired serum samples from four individuals. Associated with heavy rains, extensive flooding and rapid increases in Aedes mosquito populations in the summer. (J84.5.w3)
  • Democratic Republic of Congo, 1998. Natural infection with clinical illness including fever and sometimes central nervous system signs. Infection confirmed by the presence of IgM antibodies at high titre to West Nile virus in 66% of febrile individuals. (J91.61.w1)
  • Egypt, 1950. Natural infection . Virus isolated from three individuals (children) without apparent clinical disease (2/3) or with fever (1/3). High percentage of the population seropositive (70-80% seropositive with both neutralizing and complement fixing antibodies by age of four years and continuing at this level or higher to and past 40 years old). (J122.77.w1)
  • Egypt, 1952.  Natural infection of a technician working with WN virus in a laboratory (laboratory acquisition of infection probably but not confirmed). (J91.3.w2) 
  • Egypt (Alexandria), 1968. Natural infection in children with fever. Haemagglutination-inhibiting antigens in 4% of acute sera, and in 15% (7/48) convalescent sera (1.5 months later), with seroconversion from negative in acute sera. (J19.68.w6)
  • Egypt, 1966 to 1986. Natural infection with aseptic meningitis or encephalitis. WNV infection confirmed in four individuals. (B240.14.w14)
  • France (Camargue region), 1962-1964. Natural infection with clinical signs in thirteen individuals, some with encephalitis. (B240.14.w14)
  • France (following visit to Israel) 1982. Natural infection with mild encephalitis and severe myelitis. Infection confirmed by increasing antibody levels in serum. (J105.135.w1)
  • France (recently arrived from USA) 2002. Natural infection with encephalitis including chills, fever (40C), weakness, malaise, diarrhoea and headache progressing to hyporeflexia and mild changes in mental status. IgM antibodies detected by ELISA. (J84.9.w7)
  • France, the Var, 2003. One confirmed and one probable human cases in late August. One confirmed by IgM ELISA of blood and CSF initially and detection of IgM and IgG three weeks in serum later, the second positive for IgM and IgG antibodies. Also one confirmed and two probable equine cases. (J486.7.w1)
  • India, 2002. Natural infection detected in 88 individuals with suspected viral fevers, including 81 (92%) with classical WN fever and seven (8%) with encephalitis. Neutralising antibodies, predominantly to WNV, detected in CSF at titres of 1:5 - 1:375. (J260.33.w1)
  • Israel, 1951-1952. Natural infection with clinical illness in children and adults. Virus isolated from the blood of one individual. (J100.93.w1)
  • Israel, 1952. Natural infection with clinical illness including fever, malaise and general weakness; rarely signs of mild meningeal involvement. Virus isolated from some individuals and complement fixing antibodies demonstrated with a rise in titre. (J101.59.w1)
  • Israel, 1953. Natural infection with clinical illness typically involving fever together with enlarged lymph nodes and/or rash. Cases confirmed by virus isolation and/or development of complement-fixing and virus neutralising antibodies. (J101.64.w1)
  • Israel, 1957. Natural infection with clinical illness. Confirmation by virus isolation from acute-phase blood sample or by complement fixation and neutralization tests on paired sera. (J99.54.w1)
  • Israel, 1959.  Infection of one laboratory worker by aerosol. (J127.46.w1)
  • Israel, (August and September, published 1962). Natural infection with encephalitis. Diagnosis confirmed by complement fixation test, with significant titres confirmed in four cases, although performed late and therefore inconclusive in the other three  individuals. (J103.3.w1)
  • Israel, 1969. Natural infection with pancreatitis in one individual. Fever (38°C), rash, lymphadenopathy, severe abdominal pain, leucopaenia, low platelet count, raised blood and urine amylase. Diagnosis by gradually increasing WN virus complement fixation test titre. (J91.23.w1)
  • Israel, 1980. Natural infection with clinical disease including fever and signs of meningeal irritation in three patients. Diagnosis  by detection of complement fixing antibodies with a clear rise in titre in the two patients from whom more than one sample was taken. (J102.17.w1)
  • Israel. Natural infection; clinical illness with myocarditis. Diagnosis by seroconversion (complement fixation test). (J99.57.w1)
  • Israel, 1977. Natural infection with high fever, enlarged lymph nodes and acute anterior myelitis. Infection confirmed by rising complement fixing antibody titre. (J107.36.w1)
  • Israel, 1999. Natural infection with encephalitis in two individuals, fatal in one case. Infection confirmed by detection of IgM to WN virus in serum and cerebrospinal fluid using IgM-capture ELISA , and by serum-dilution plaque reduction neutralisation test (PRNT). In one individual WN viral RNA detected in brain biopsy by TaqMan reverse-transcriptase-polymerase chain reaction (RT-PCR) assay. (J84.7.w10)
  • Israel, 2000. Natural infection; epidemic with 417 serologically confirmed cases, 326 hospitalised and 33 deaths. Diagnosis on the basis of IgM-capture ELISA on serum or CSF. (J84.7.w16); "A case of WN fever was defined as illness in a patient with a clinical picture consistent with WN fever and with anti-WN virus immunoglobulin (Ig) M antibodies detected in either a serum or cerebrospinal fluid (CSF) specimen." (J84.7.w14); 452 cases, 326 hospitalised and 29 fatalities. (W27.01Aug02.wnv2)
  • Israel, 2000. Natural infection with meningoencephalitis and unusual neurological signs including optic neuritis in a 55-year-old woman. Infection confirmed by positive IgM antibody titre for WN virus. (J220.162.w1)
  • Israel, 2000. Natural infection with meningoencephalitis and motor aphasia in a four-year-old immunocompromised boy being treated for Hodgkin's lymphoma. Infection confirmed by positive serum IgM antibody titre for WN virus. One of 24 children confirmed to have WNV infection during the epidemic. (J221.86.w1)
  • Israel, 2002. Natural infection in 44 people; three cases fatal. (W27.01Aug02.wnv2)
  • Israel, 2002. Natural infection in 26 people; two cases fatal. (W27.21Oct02.wnv1)
  • Israel, 2003. Natural infection in two people. [Data to 12th July 2003]. (W27.12Jul03.wnv1)
  • Jordan (Hashimiah), 1998. Natural infection, not obviously associated with clinical disease. Presence of IgG antibodies in 21/261 (8.0%) individuals five years old or older, during a serological survey using an ELISA; no evidence of acute infection (no samples positive for IgM by ELISA). (J84.6.w2)
  • Madagascar (near Antananarivo), 1988-89. Natural infection. IgG antibodies detected by ELISA in 13.4% of inhabitants in December and in 21.8% in July, with 14.7% seroconversion (seronegative to seropositive) in 354 paired samples taken at the start and the end of the rainy season, as well as 10 samples converting from seropositive to seronegative in the same time.  (J95.70.w1)
  • Nigeria (Ibadan), 1973. Natural infection, outbreak of clinical disease reported. West Nile virus isolated from three individuals two to ten years old, at two, three and six days after the onset of clinical disease (fever 39.0-40.0°C). (J96.72.w1)
  • Nigeria, 1989 (approx.) Natural infection. Antibodies detected by haemagglutination-inhibition test in 123/304 sera (40%), with higher prevalence in adults than in children but no significant difference between males and females. (J112.13.w1)
  • Nigeria (Ibadan and Ogbomoso), 1990 (approx.) Natural infection. Complement fixing antibodies detected in 65% of individuals tested (53% of individuals from Ibadan and 75% of individuals from Ogbomoso). Antibody prevalence increased with age at both locations; 49/82 females (60%) and 62/88 males (75%) were seropositive. (J108.34.w1)
  • Pakistan (Punjab Province) 1968, 1978-79. Natural infection. Antibodies detected by plaque reduction neutralization test (PRNT) and/or haemagglutination inhibition test. (J96.76.w2)
  • Pakistan (Karachi), 1983, 1985. Natural infection without apparent clinical disease. Haemagglutination inhibition and/or neutralising antibodies detected. Seroprevalence about 50-65%. 13% seroconversion to seropositive between July and October in one year. Also loss of detectable antibodies in 8% of individuals over the same time period. (J117.26.w1)
  • Romania (south-eastern, Bucharest) 1996. Natural infection with acute aseptic meningitis and encephalitis in 352 individuals; total 393 patients with "serologically confirmed or probable WNF infections.". Infections confirmed using IgM capture and indirect IgG ELISAs.  (J98.352.w1)
  • Romania (south-eastern, Bucharest) 1996. WNV infection was diagnosed serologically in 236/290 patients from whom acute serum or CSF samples were available: 216/257 (84%) of those with meningoencephalitis, 101/115 (89%) of those with encephalitis and 74/93 (80%) of those with meningitis, also in 8/10 (80%) individuals tested with fever and headache, 5/5 (100%) individuals tested with respiratory tract infections and 7/18 (39%) individuals hospitalised with nonspecific febrile illness. (J93.38.w5)
  • Romania (south-eastern), 1997-1998. Natural infection with clinical illness in 12 individuals, fatal in one individual in 1997, and in one individual in 1998. Clinical meningoencephalitis and IgM (IgM-capture ELISA) detected in serum or CSF samples; also IgG conversion (indirect ELISA) between acute-phase and convalescent-phase sera in non-fatal cases. Infection also diagnosed by detection of IgM in serum of two individuals during a measles epidemic in 1998, with fever and exanthema in both individuals and hepatitis in one individual. (J100.181.w1)
  • Russia (Volgograd region) 1999. Natural infection, with acute aseptic meningoencephalitis, meningitis or acute  fever; 183 confirmed cases and a total of 480 cases (estimated). Serum samples from 138/318 patients sampled using IgM-capture ELISA contained anti-WN virus IgM at a level indicative of acute infection. (J84.7.w32) West Nile virus RNA detected in 5/5 brain samples from individuals following death from meningoencephalitis. Two strains of virus isolated, from the serum of one individual with West Nile virus infection and from the brain of one individual with meningoencephalitis. (J84.6.w3)
  • Senegal (Barkedji area), 1990. Natural infection with clinical disease (fever). Virus isolated from serum in one individual and antibodies to WN virus detected in another individual. (J110.31.w1, J110.38.w1)
  • South Africa (northern Natal), 1958. Natural infection. Virus isolated. (J125.33.w1)
  • South Africa (Cape Province), 1962, 1964. Natural infection. Serological survey, presence of haemagglutination-inhibition and/or neutralising antibodies. (J94.30.w1)
  • South Africa (Upington and surrounding area), 1974. Natural infection, extensive epidemic characterised by fever, rash, myalgia and arthralgia. An estimated 18,000 people infected during the epidemic, with 1,700 individuals with clinical disease seen by medical practitioners in Upington. Haemagglutination-inhibition and neutralising antibodies detected, with documented seroconversion and rises in antibody levels during convalescence. (J111.72.w1)
  • South Africa (Witwatersrand-Pretoria region), 1983-84. Natural infection with clinical illness. Infection serologically confirmed.  (J125.70.w1)
  • Southern Africa. (1965-1980). Natural infection. West Nile virus isolated fourteen times. No further details. (P33.3.w1)
  • Southern Africa (South Africa, Mozambique, northern borders of Namibia and Botswana) (1965-1980). Natural infection. Neutralising antibodies detected. No further details. (P33.3.w1)
  • Thailand (1999-2000). Natural infection with clinical illness (e.g. fever, malaise, headache, myalgia) in some cases. 53/369 villagers (14%) had very high titres to WN virus by haemagglutination inhibition test and much lower titres to Japanese encephalitis virus. (J91.67S2.w1)
  • Tunisia , 1997. Natural infection with meningitis or meningoencephalitis in 173 individuals, eight fatal. Peak of epidemic late October to mid November. WNV IgM positive in 86% of patients from whom samples were available (111/129 patients were WNV-positive; only CSF was tested for four of the "negatives" and it was noted that only 9/23 cases with IgM confirmed had positive CSF). (J214.267.w10, J246.24.w1)
  • Uganda (Omogo, West Nile district), 1937. Natural infection with fever (oral temperature 100.6°F); no other signs and no symptoms reported, although the patient "was not altogether co-operative and it is possible that she withheld pertinent facts." First isolation of WN virus. (J120.20.w1)
  • Ukraine, 1980 (approx.) Natural infection, sometimes with clinical disease. Antibodies detected by complement fixation test and IHAT in 4.3% of patients with fever and in 3.9% of apparently healthy individuals. (J116.5.w1)
  • USA (New York) 1999. Natural infection with clinical illness notably encephalitis, sometimes fatal, mainly in elderly individuals. "As of October 19, 56 (31 confirmed and 25 probable) cases of WNV infection have been identified, including seven deaths". (N7.48.w3) Confirmed by laboratory investigations. Initially "the cause of the outbreak has been confirmed as a West Nile-like virus based on the identification of virus in human, avian, and mosquito samples" (N7.48.w1); cases in individuals confirmed by the presence of WN virus antibodies using an IgM ELISA. (N7.48.w1, N7.48.w2, N7.48.w3). "62 persons with WNV illness, including seven deaths, were detected in New York City (NYC) and nearby New York counties" (N7.50.w1).
  • USA (New York), 1999.  Natural infection with clinical illness. Initial case cluster of eight cases in individuals over 58 years of age with fever, altered mental status, muscle weakness in 7/8 individuals (including flaccid paralysis) and abnormal CSF (elevated protein and/or mild to moderate pleocytosis). (P32.1.w2)
  • USA (New York), 1999. Natural infection with clinical illness including fever, headache, vomiting and neurological signs. Infection confirmed by the presence of high levels of IgM in the blood and cerebrospinal fluid. (J106.55.w1)
  • USA (New York), 1999. Natural infection without fever but with neurological signs diagnosed as Guillain-Barré Syndrome. (J106.55.w2)
  • USA (New York), 1999. Natural infection, fatal. (J84.6.w4)
  • USA (New York), 1999. Natural infection with no clinical signs or mild non-specific febrile illness in an estimated 8,200 (range 3500-13,000) individuals. Infection confirmed by the use of IgM capture (MAC) ELISA, indirect IgG ELISA and further identification using plaque reduction neutralisation test (PRNT) in Vero cells. (J98.358.w1)
  • USA (New York City) 1999-2000. Natural infection, 2.6% of individuals tested were positive for neutralising antibodies in North-east Queens in 1999 and 0.5% were positive in Staten Island in 2000. (P39.2.w2)
  • USA (New York and New Jersey) 2000. Natural infection with clinical illness including meningitis and/or encephalitis requiring hospitalization in 19 individuals. Infection confirmed by laboratory testing: positive IgM-capture EIA for cerebrospinal fluid (CSF) or positive serum Ig-M capture ELISA and PRNT with (in nine cases) fourfold rise in antibodies between acute and convalescent samples. (J84.7.w9)
  • USA (New York, New Jersey and Connecticut) 2000. Natural infection with clinical illness. West Nile virus infection laboratory confirmed: "21 persons were identified with acute WNV infection (14 in New York, six in New Jersey, and one in Connecticut), including two deaths (one each in New York and New Jersey)." (N7.50.w1)
  • USA 2001. Natural infection with clinical illness: "The first human infection in 2001 was identified in a 73-year-old man from Madison County, Florida, with illness onset on approximately July 15. He remains hospitalized with encephalitis." (N7.50.w2)
  • USA (New York) 2001. Natural infection in a patient undergoing chemotherapy, with fever, cough, chills, rhinorrhoea, joint aches, decreased appetite, lethargy, lightheadedness, later mild headache, dizziness, progression to confusion and encephalitis. Virus isolated from a blood sample and viral genome detected in a sample of cerebrospinal fluid. (J84.8.w10)
  • USA (Massachusetts) 2001. Natural infection with fever and encephalitis in a 89-year-old man, with slow recovery over a period of more than one month. WNV infection confirmed by serum IgM titre and positive PRNT. (J221.346.w1)
  • USA, 2001. A total of 66 cases of human illness were attributed to WNV infection and reported to ArboNET from 39 counties in 10 states. Two cases involved West Nile fever; the other 64 individuals had severe neurological illness. (P39.3.w1)
  • USA (Georgia and Florida), 2002. Natural infection following transplantation of solid organs into four recipients. Clinical illness compatible with WNV infection occurred in all four recipients and fatal encephalitis developed in one of the recipients. Infection was confirmed in the fatal case by strong positive quantitative PCR on brain tissue and flavivirus-specific immunohistochemical staining of brain tissue; fever had developed 17 days after kidney transplant and progressed to encephalitis. In another recipient who developed fever 13 days after transplant of a kidney and progressed to encephalitis (with transient requirement for mechanical ventilation) the CSF was positive for WN virus antibodies. In the third patient neurological disease was seen initially as ataxia eight days following a heart transplant, progressing to unresponsiveness and requirement for mechanical ventilation; CSF and serum were strongly positive for WNV IgM. The fourth patient developed only fever, cough and malaise seven days after a liver transplant; WNV infection was confirmed. The donor, who had been healthy prior to a fatal car crash, had received multiple blood donations prior to her death, raising the possibility that the infection in the donor had been received from one of the blood transfusions. (W27.04Sept02.wnv1, W27.09Sept02.wnv1)
  • USA (Mississippi, Louisiana) 2002. Natural infection with 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.). WNV infection confirmed by IgM and neutralising antibodies. (N7.51.w1)
  • USA, 2002. WN virus has been detected in human breast milk, by TaqMan PCR, from a woman who developed febrile illness with headache progressing to meningoencephalitis, onset eight days following receipt of WN virus-contaminated blood after delivery of her baby. The milk was positive also for WN virus-specific IgM and IgG. The woman's infant, who was breast fed, tested positive for WN virus IgM antibodies at 25 days old (the youngest person to be confirmed IgM positive in the USA to that date). The infant showed no clinical signs of illness. It was considered that the IgM antibodies in the infant indicated WNV infection in the infant, since transmission of IgM antibodies through milk is inefficient, and that the most likely source of the virus in the infant was from the mother's breast milk. (W27.29Sept02.wnv1, W27.04Oct02.wnv1, N7.51.w4)
  • USA, 2002. Infections from laboratory accidents (laceration from a contaminated scalpel and puncture by a contaminated needle). Infection occurred despite cleansing of the wounds, with onset at four and three days after exposure respectively . 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; diagnosis confirmed by serology (negative for IgM antibodies three days after illness onset, positive for WN virus IgM at 13 days and for IgM and neutralising antibodies at 15 days. Signs in the second individual of initial upper respiratory tract infection,  accompanied one day later by malaise, fatigue, chills and low fever (38.3°C/ 100.°F); WNV infection confirmed by serology, with negative IgM at one day after injury and two days after onset of fever, but positive for WNV-specific IgM at ten days after onset of illness. (N7.51.w7)
  • USA (New York) 2002. Intrauterine infection in an infant born with severe cerebral abnormalities following maternal infection in about the 27th week of pregnancy.  Infection confirmed by the presence of WNV-specific IgM antibodies in serum and cerebrospinal fluid of the infant. (W27.19Dec02.wnv1, N7.51.w8)
  • USA, 2002. Natural infection, 3,389 reported cases of human infection 01 January 2002 to 30 November 2002. 2,354/3,389 (69%) cases West Nile virus meningoencephalitis with 199 fatalities (9%), 704/3,389 (21%) classical West Nile Fever with two fatalities (0.3%)and 331/3,389 (10%) unspecified illness. Cases were reported from 619 counties in 37 states plus the District of Colombia. Cases reported with onset dates 10th June to 4th November, peaking in the week ending 24th August (10th June to 4th November in southerly states, compared with 10th July to 28th October in northerly states, and with an earlier (by one week, in week ending 17th August) peak in the southerly states. Age range of individuals with meningoencephalitis one month to 99 years, median 55 years old, and for West Nile Fever 1-93 years, median 48 years old. Deaths occurred in persons 24-99 years old, median 78 years old. N.B. this is both the largest reported WNV meningoencephalitis epidemic worldwide and the largest documented arbovirus epidemic in the western hemisphere. Cases occurred in states on the west coast of the USA (California and Washington State) although activity was most intense in the central USA (particularly the Great Lakes region). (N7.51.w6)
  • USA, 2002. Confirmed infections totalling 3,862 cases, including 2,741 meningoencephalitis cases and 1,267 cases of West Nile fever or unknown clinical signs, with 263 deaths, in 708 counties within 39 states plus D.C. [ArboNET verified data as of 21 Jan 2003]. (P39.4.w1)
  • USA (Louisiana, Mississippi) 2002. Natural infection with acute flaccid paralysis in seven patients. At initial presentation fever (at least 38.5°C) 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 paraesthesias, 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. Infection confirmed by IgM antibody-capture enzyme immunoassay and in several patients by PRNT. (J84.9.w13)
  • USA (Georgia) 2002. Natural infection in 43 individuals, CDC confirmed in 24 cases, with five fatal cases. Age range 12-82 years, mean 52 years. (P48.1.w5)
  • USA (Florida) 2002. Natural or iatrogenic infection in 28 people. (P48.1.w4)
  • USA (Michigan) 2002. Natural infection with encephalitis in an individual with common variable immunodeficiency. (J84.9.w19)
  • USA (Wisconsin) 2002. Natural infection in workers on a turkey breeder farm, with fever, headache and rash in all cases and meningoencephalitis requiring hospitalisation in one case; infection confirmed by presence of WN virus-specific IgM antibodies. Infection also confirmed in the turkeys; route of transmission was not determined. (N7.52.w5)
  • USA (South Carolina) 2003. Natural infection, first confirmed human case for 2003. (W170.07Jul03.WNV1)
  • USA 2003. Infection recorded in 8,567 individuals by 25 November 2003. Among blood donors, presumptive WN viraemia was reported in 737 individuals; 98 (16) of the 605 for whom full data were reported subsequently had West Nile fever and six (1%) developed neuroinvasive disease. [Data to 25 November 2003](N7.52.w6)
  • USA, 2003. Infection recorded in 9,006 individuals, including 220 fatal cases; 6,140 cases (68%) were reported as West Nile fever (milder disease), 2,587 cases were reported as WNV meningitis or encephalitis and 167 (2%) were not specified clinically [data to 14 January 2004]. (W170.19Jan04.WNV1)
  • USA, 2003. Infection reported in 9,862 individuals, including 2,866 cases of encephalitis/meningitis, 6,830 cases of West Nile fever, and 166 cases of unspecified clinical signs; there were 264 fatal cases. (W170.12May08.wnv1)
  • USA, 2004. Infection reported in 2,539 individuals, including 1,142 cases of encephalitis/meningitis, 1,269 cases of West Nile fever, and 128 cases of unspecified clinical signs; there were 100 fatal cases. (W170.12May08.wnv2)
  • USA, 2005. Infection reported in 3,000 individuals, including 1,294 cases of encephalitis/meningitis, 1,607 cases of West Nile fever, and 99 cases of "other" or unspecified clinical signs. (W170.12May08.wnv3)
  • USA, 2006. Infection reported in 4,269 individuals, including 1,459 cases of encephalitis/meningitis, 2,616 cases of West Nile fever, and 194 cases of "other" or unspecified clinical signs; there were 177 fatal cases. (W170.12May08.wnv4)
  • USA, 2007. Infection reported in 3,623 individuals, including 1,213 cases of encephalitis/meningitis, 2,347 cases of West Nile fever, and 63 cases of unspecified clinical signs; there were 264 fatal cases. Reported to CDC as of 1st April 2008. (W170.12May08.wnv5)
  • Algeria, Azerbaijan, Belarus, Central African Republic, Czechland, Democratic Republic of Congo (former Zaire), Egypt, Ethiopia, France, India, Israel, Madagascar, Nigeria, Pakistan, Romania, Russia, Senegal, Spain, South Africa, Sudan, Ukraine. Natural infection with clinical cases or outbreaks recorded. (J84.5.w2)
  • Natural infection with hepatitis, sometimes fatal. Virus isolated from liver biopsies. (B244.w1)
  • Experimental infection in patients with advanced cancer. (J91.3.w1, J104.7.w1)

Pan troglodytes - Chimpanzee:

  • Congo (Stanleyville) 1960 (approx.), Natural infection. Antibodies detected in recently captured individuals from savannah areas but not in individuals from the forest. (J95.1.w1)
  • Egypt, 1950. Experimental infection. No clinical signs following intracutaneous inoculation. Three days of viraemia followed by the development of neutralizing antibodies, at "significant titre" by six days and maximum by 2-3 weeks. Development of complement fixing antibodies "a few days after neutralizing antibodies appear". No isolation of virus from throat or faeces. No development of antibodies and no virus in throat or faeces following feeding of virus. (J122.77.w1)

Chlorocebus aethiops - Savanna monkey (Synonym: Cercopithecus ethiops centralis):

  • Uganda, 1937-39. Experimental infection. Fever but no other signs, and development of neutralizing antibodies, following intracerebral inoculation of two individuals. (J120.20.w1)

Macaca mulatta (Macaca rhesus) - Rhesus macaque (Rhesus monkey) (Cercopithecidae - Old-world monkeys (Family)):

  • Russia/USSR (Moscow) 1982 (approx.). Experimental intracerebral infection resulted in illness varying from no clinical signs or short duration fever to encephalitis, sometimes fatal; subcutaneous inoculation resulted in asymptomatic infection. Viraemia detected mainly at 4-7 days post infection and virus was isolated from the central nervous system or other organs for fatally infected animals and also detected in individuals surviving infection for as long as 5.5 months after infection. (J71.75.w1)
  • Uganda, 1937-39. Experimental infection. Fever and encephalitis, fatal in 2/3 individuals inoculated intracerebrally, fever and nervous signs in one individual inoculated intranasally, fever in two individuals inoculated intravenously. (J120.20.w1)
  • USA (Louisiana), 2002. Natural infection in a laboratory colony housed outdoors. Seroconversion detected by HI and confirmed by PRNT and CF. Of 726 individuals bled August to November 2002, 286 (39.3%) were HI positive including 42.2% of 462 females and 34.5% of 264 males. Cross-reactions with other flavivirus antigens was detected by HI but titres were always highest for WN virus;  WNV infection was confirmed by PRNT and CF of a subsection of samples. No associated clinical signs were noted in any individuals. (J84.9.w20)

Macaca nemestrina - Pigtail macaques (Cercopithecidae - Old-world monkeys (Family)):

  • USA (Louisiana), 2002. Natural infection in a laboratory colony housed outdoors. Seroconversion detected by HI in 114 of 563 individuals (20.25%). No associated clinical signs were noted in any individuals. (J84.9.w20)

Macaca radiata - Bonnet macaque (Cercopithecidae - Old-world monkeys (Family)):

  • India, 1990 (approx.) Experimental infection resulting in paralysis and death in 2/3 individuals. Viraemia detected following infection and WN virus isolated from the central nervous system. (J88.36.w1)

Macaca sylvanus - Barbary macaque (Cercopithecidae - Old-world monkeys (Family)):

  • Canada (Toronto), 2002. Natural infection with severe clinical illness necessitating euthanasia in a 25-year-old captive male. (W27.24Nov02.wnv1)
  • USA/Canada, 1999-2003. Natural infection in captive individual(s). Reported positive in surveillance efforts. Virus or viral DNA detected. [Data to 15th April 2003](W8.Nov01.WNV2)

Papio spp. - (Savanna) baboons (Cercopithecidae - Old-world monkeys (Family)):

  • USA (Louisiana), 2002. Natural infection in a laboratory colony housed outdoors. Seroconversion detected by HI in 207 of 403 individuals tested (51.36%). No associated clinical signs were noted in any individuals. (J84.9.w20)

Eulemur (Lemur) fulvus - Brown lemur (Lemuridae - Large lemurs (Family)):

  • France, 1984 (approx.). Experimental infection with two different strains of West Nile virus; no clinical illness. Viraemia detected and antibody development detected. (J91.34.w1)

Lemur catta - Ring-tailed lemur (Lemuridae - Large lemurs (Family)):

  • Madagascar (Berenty) 1978. Natural infection. Found positive for flavivirus (probably WN virus) in surveillance efforts (9/22 animals). (J96.76.w1)
  • USA/Canada, 1999-2003. Natural infection in captive individual(s). Reported positive in surveillance efforts. Antibodies detected. [Data to 15th April 2003](W8.Nov01.WNV2)

Lemur macaco (Lemuridae - Large lemurs (Family)):

  • Madagascar (Nosy-Komba) 1978. Natural infection. Found positive for flavivirus (probably WN virus) in surveillance efforts (3/28 animals). (J96.76.w1)

Lepilemur dorsalis (Lemuridae - Large lemurs (Family)):

  • Madagascar (Nosy-Bé) 1978. Natural infection. Found positive for flavivirus (probably WN virus) in surveillance efforts (12/44 animals). (J96.76.w1)

Lepilemur mustelinus (Lemuridae - Large lemurs (Family)):

  • Madagascar (Berenty) 1978. Natural infection. Found positive for flavivirus (probably WN virus) in surveillance efforts (2/12 animals). (J96.76.w1)

Lepilemur edwardsi (Lemuridae - Large lemurs (Family)):

  • Madagascar (Ampijoroa) 1979-1980. Natural infection. Found positive for flavivirus (probably WN virus) in surveillance efforts (6/28 animals, including one individual seronegative in 1979 and seropositive one year later). (J96.76.w1)

Propithecus verreauxi (Lemuridae - Large lemurs (Family)):

  • Madagascar (Ampijoroa and Marohogo) 1979-1980. Natural infection. Found positive for flavivirus (probably WN virus) in surveillance efforts (6/24 animals from Ampijoroa, 1/1 animal from Marohogo). (J96.76.w1)

Lemur species (Lemuridae - Large lemurs (Family)):

  • Madagascar (Tsimbazaza Zoological Park) 1978-1980. Natural infection. Found positive for flavivirus (probably WN virus) in surveillance efforts (11/37 individuals of six species). (J96.76.w1)

Galago senegalensis (Galagonidae - Bush-babys and Galagos (Family)):

  • Natural infection. Virus isolated. (J84.5.w2)

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Chiroptera - Bats (Order)

Eptesicus fuscus - Big brown bat:

  • USA 1999-2001. Natural infection. Found positive for WN virus in surveillance efforts. (W8.Nov01.WNV2)
  • USA (New York State) 2000. Natural infection with illness, WN infection confirmed. (J84.7.w23, J133.951.w12)

Myotis lucifugus - Little brown myotis:

  • USA 1999-2001. Natural infection. Found positive for WN virus in surveillance efforts. (W8.Nov01.WNV2)
  • USA (New York State) 2000. Natural infection with illness, WN infection confirmed. (J84.7.w23, J133.951.w12)

Rousettus leschenaulti - Frugivorous Bat: (Pteropodidae - Old-world fruit bats (Family)):

  • India (Sagar Taluk, Shimoga District, Mysore State) 1968. Natural infection. Virus isolated from the spleen by mouse inoculation and the identity of the virus confirmed by neutralisation test, cross-neutralisation test and complement fixation test. (J92.58.w1)

Rousettus aegypticus - Fruit bat: (Pteropodidae - Old-world fruit bats (Family)):

  • Israel 1959-60.  Natural infection. Haemagglutination-inhibition antibodies to WN virus detected in 3/37 individuals (8%). (J109.34.w1)

Pteropus rufus - Fruit bat (Pteropodidae - Old-world fruit bats (Family)):

  • Madagascar (1975-88). Natural infection. Antibodies detected. (J95.69.w1)

"Bats" (Chiroptera - Bats (Order)):

  • Egypt 1950's. Natural infection not associated with clinical illness. Neutralizing antibodies detected in sera. (J91.5.w1)

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Artiodactyla - Even toed ungulates (Order)

Capreolus capreolus - Western roe deer:

  • Czechoslovakia (Moravia), 1990. Natural infection, no apparent clinical illness. Haemagglutination-inhibition antibodies detected in 7/33 individuals. (J113.37.w1)
  • Czech Republic (Moravia) 1993-1998. Natural infection, no apparent clinical illness. Haemagglutination-inhibition antibodies detected in 12.7% of 55 individuals. (J131.48.w1)

Cervus elaphus - Red Deer:

  • Czech Republic (Moravia) 1993-1998. Natural infection, no apparent clinical illness. Haemagglutination-inhibition antibodies detected in 14.3% of 56  individuals. (J131.48.w1)

Dama dama - Fallow Deer:

  • Czechoslovakia (Moravia), 1990. Natural infection, no apparent clinical illness. Haemagglutination-inhibition antibodies detected in 1/4 individuals. (J113.37.w1)
  • Czech Republic (Moravia) 1993-1998. Natural infection, no apparent clinical illness. Haemagglutination-inhibition antibodies detected in 15.3% of 209 individuals. (J131.48.w1)

Odocoileus virginianus - White-tailed deer:

  • USA (New Jersey) 2002. Natural infection, serological evidence of exposure to WN virus in seven of 689 samples. (W27.14Sept02.wnv1)

Rangifer tarandus - Reindeer:

  • USA (Minnesota), 2002. Natural infection with clinical illness and mortality. Seropositive and PCR positive brain stem and spinal cord (W27.16Nov02.wnv1, W27.18Nov02.wnv1)

Babyrousa babyrussa - Babirusa:

  • USA (New York City, Wildlife Conservation Society collections) June 1999-February 2000. Natural infection, no history of clinical illness. Found positive for WN virus specific antibodies on plaque reduction neutralization assay. (P30.1.w3)

Sus domesticus - Domestic pig:

  • India, before 1994. Experimental infection by intramuscular inoculation, and experimental infection by mosquito bite. (J88.38.w1)
  • Thailand (1999-2000). Natural infection with seroconversion in sentinel pigs; higher titres to WN virus than to Japanese encephalitis virus in 30/77 pigs. (J91.67S2.w1)
  • Experimental infection, USA, 2002. No clinical illness, development of low level viraemia. (P48.1.w16)

Sus scrofa - Wild boar:

  • Czechoslovakia (Moravia), 1990. Natural infection, no apparent clinical illness. Haemagglutination-inhibition antibodies detected in 4/24 individuals. (J113.37.w1)
  • Czech Republic (Moravia) 1993-1998. Natural infection, no apparent clinical illness. Haemagglutination-inhibition antibodies detected in 13.3% of 150 individuals. (J131.48.w1)

Ovis aries - Domestic sheep:

  • Egypt 1950's. Natural infection not associated with clinical illness. Neutralizing antibodies detected in sera. (J91.5.w1)
  • Egypt 1950's. Experimental infection not resulting in circulating virus, but with neutralizing antibodies detected  in one of two animals following infection. (J91.5.w1)
  • Nigeria, 1989 (approx.) Natural infection. Antibodies detected by haemagglutination-inhibition test in 10/51 sera (20%). (J112.13.w1)
  • Portugal, 1966-1967. Natural infection, haemagglutination-inhibition antibodies detected in 190/1,165 cattle (16%). (J91.18.w2)
  • Slovakia (Eastern area), 1983. Natural infection. West Nile virus haemagglutination-inhibition antibodies detected in 1% of sheep tested. (J119.33.w1)
  • South Africa (Cape Province), 1962, 1964. Natural infection. Serological survey, presence of neutralising antibodies. (J94.30.w1)
  • South Africa, before 1986. Experimental infection by intravenous inoculation.(J62.53.w3)
  • USA (Nebraska), 2002. Natural infection with clinical signs and death in one ewe. WNV infection confirmed by immunohistochemistry on the brain, PCR on the brain and virus isolation from brain tissue, also serum neutralisation titre greater than 1:100. (W27.16Sept02.wnv1,  W27.20Sept02.wnv1)
  • USA (Colorado) 2002. Natural infection with clinical illness. (P48.1.w16)
  • USA (Missouri) 2002. Natural infection with neurological signs requiring euthanasia in a two-year-old ram. Infection confirmed by detection of WNV in brain tissue using RT-PCR. (J275.17.w1)

Ovis orientalis - Mouflon (Ovis musimon):

  • Czech Republic (Moravia) 1993-1998. Natural infection, no apparent clinical illness. Haemagglutination-inhibition antibodies detected in 15.0% of 80 individuals. (J131.48.w1)

Capra hircus - Domestic goat:

  • Nigeria, 1989 (approx.) Natural infection. Antibodies detected by haemagglutination-inhibition test in 9/50 sera (18%). (J112.13.w1)

Oreamnos americanus - Mountain goat:

  • USA (Nebraska), 2002. Natural infection with clinical (neurological) signs and fatalities in a herd of Rocky Mountain goats WNV infection confirmed by immunohistochemistry on the brain, PCR on the brain and virus isolation from brain tissue, also serum neutralisation titre greater than 1:100. (W27.14Sept02.wnv1, W27. 20Sept02.wnv1)
  • USA (Wyoming), 2002. Natural infection with clinical signs in Rocky Mountain goats. Confirmed by histopathological lesions in the brain, positive immunohistochemistry, TaqMan RT-PCR and virus isolation from the brain. (W27.14Sept02.wnv1, W27. 20Sept02.wnv1)

Camelus dromedarius - Dromedary:

  • Egypt 1950's. Natural infection not associated with clinical illness. Neutralizing antibodies detected in sera. (J91.5.w1)
  • Nigeria (Kano, Northern Nigeria) 1969. Natural infection. Virus isolated from a blood sample (taken at the time of slaughter) by mouse inoculation and identified by complement fixation and neutralisation tests using known hyperimmune mouse ascitic fluids. (J13.34.w2)
  • Nigeria (Kano), 1966-72. Natural infection. Virus isolated on two occasions. (J96.72.w1, J88.19.w3)
  • Nigeria, 1989 (approx.) Natural infection. Antibodies detected by haemagglutination-inhibition test in 13/50 sera (26%). (J112.13.w1)
  • Nigeria (Ibadan and Maiduguri), 1990 (approx.) Natural infection. Complement fixing antibodies detected in 62% of individuals tested. (J108.34.w1)

Lama glama - Llama:

  • USA (Connecticut), 2000. Two llamas reported to be WN virus-positive; clinical status unknown. (W27.17Sept02.wnv1)
  • USA (Massachusetts), 2001. One llama reported to be WN virus-positive; clinical status unknown. (W27.17Sept02.wnv1)
  • USA (Massachusetts), 2002. One llama reported to be WN virus-positive; clinical status unknown. (W27.01Sept02.wnv1)
  • USA/Canada, 1999-2003. Natural infection in domestic individual(s). Reported positive in surveillance efforts. Virus or viral DNA detected. [Data to 15th April 2003](W8.Nov01.WNV2)

Lama pacos - Alpaca:

  • USA (IOWA), 2002. Natural infection with neurological signs, mild to moderate diffuse non-suppurative meningoencephalitis and detection of WNV by RT-PCR.  (W27.17Sept02.wnv1)

Bos taurus - Domestic cattle:

  • Egypt 1950's. Natural infection not associated with clinical illness. Neutralizing antibodies detected in sera. (J91.5.w1)
  • Israel 1959-60.  Natural infection. Haemagglutination-inhibition antibodies to WN virus detected in 12/51 (24%). (J109.34.w1)
  • Madagascar (1975-88). Natural infection. Antibodies detected. (J95.69.w1)
  • Nigeria, 1989 (approx.) Natural infection. Antibodies detected by haemagglutination-inhibition test in 3/49 sera (6%). (J112.13.w1)
  • Nigeria (Ibadan and Maiduguri), 1990 (approx.) Natural infection. Complement fixing antibodies detected in 4% of individuals tested. (J108.34.w1)
  • Pakistan (Punjab Province), 1978-79. Natural infection in Bos taurus indicus - Zebu cattle (Domestic Variety - Species Summary). Antibodies detected by plaque reduction neutralization test (PRNT) in 6/19 (31.6%) of individuals up to one year old and 15/39 (38.5%) more than one year old (J96.76.w2)
  • Portugal, 1966-1967. Natural infection, haemagglutination-inhibition antibodies detected in 4/129 sheep (3%). (J91.18.w2)
  • South Africa (Cape Province), 1962, 1964. Natural infection. Serological survey, presence of neutralising antibodies. (J94.30.w1)
  • USA (Nebraska), 2002. Natural infection in two animals, from different properties, with hind limb ataxia progressing to recumbency. WNV infection was confirmed by the presence of WN virus neutralising antibodies in serum but further samples were not available and WN virus was not confirmed (nor disproved) to be the cause of the clinical signs in either case. (W27.16Oct02.wnv1)
  • Experimental infection of calves failed to produce viraemia. (B242.w1)
  • USA (Wisconsin) 2002. Natural infection with clinical illness confirmed in a cow. (P48.1.w16)
  • USA/Canada, 1999-2003. Natural infection in domestic individual(s). Reported positive in surveillance efforts. Virus or viral DNA detected. [Data to 15th April 2003](W8.Nov01.WNV2)

Bubalus bubalis - Domestic water buffalo (Domestic Variety - Species Summary)(Gamoose):

  • Egypt 1950's. Natural infection not associated with clinical illness. Neutralizing antibodies detected in sera. (J91.5.w1)
  • Egypt 1950's. Experimental infection not resulting in circulating virus in one individual; no serological data. (J91.5.w1)

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Rodentia - Rodents (Order)

Aethomys chrysophilus - African rat. (Muridae - Rats, mice, voles, gerbils etc. (Family)):

  • Experimental infection resulting in low-level detectable viraemia for two days. (B241.49.w49, B244.w1) 

Apodemus flavicollis - Yellow-necked mouse:

  • Natural infection. Virus isolated. (J84.5.w2)

Apodemus sp. (Apodemus - (Genus)):

  • Austria 1976-1986. Natural infection. Antibodies detected in 1/126 individuals. (J132.S2.w1)

Arvicanthis niloticus (Arvicanthis - (Genus)):

  • Natural infection. Virus isolated. (J84.5.w2)

Clethrionomys glareolus - Bank vole:

  • Austria 1976-1986. Natural infection. Antibodies detected in 3/84 individuals. (J132.S2.w1)
  • Natural infection. Virus isolated. (J84.5.w2)

Mus domesticus - Laboratory mouse:

  • Israel 1952. Experimental infection. Adult mice highly susceptible to infection by intracerebral inoculation and less susceptible by intraperitoneal or subcutaneous inoculation. Signs and histopathological lesions "typical of the viral encephalitides"; death in 12-48 hours after the onset of clinical signs (J101.59.w1)
  • Nigeria 1965, 1967, 1969. Natural infection in sentinel mice, virus isolated. (J1.10.w3)
  • Nigeria, 1966-1972. Natural infection in sentinel mice. Virus detected on twelve occasions. (J96.72.w1)
  • Nigeria, 1965, 67, 69. Natural infection in sentinel mice; virus isolated on three occasions. (J88.19.w3)
  • Uganda, 1937-39. Experimental infection. Adults highly susceptible to intracerebral or intraperitoneal inoculation  (fatal infections) but not subcutaneous inoculation. (J120.20.w1)
  • Experimental infection by aerosol. (J127.46.w1)
  • Experimental infection by intracerebral, intraperitoneal and subcutaneous inoculation. Greater susceptibility in very young (less than three days old) mice than in older mice. (J101.86.w2)
  • Experimental infection by intraperitoneal or intramuscular infection, resulting in lethal or sublethal infection. (J19.68.w7)
  • Experimental infection by intraperitoneal inoculation resulting in clinical, mainly neurological signs, in several mice, fatal infection in one mouse with gross necropsy lesions and detection of virus in various organs. (J133.951.w12)

Mus musculus - House mouse:

  • Egypt (Nile Delta), 1990. Natural infection. Antibodies detected by ELISA in 26% of individuals tested. (J91.45.w1)
  • Israel, 1965-1966. Natural infection. Group B arbovirus (probably WN virus) haemagglutination inhibition antibodies, detected in 1/19 individuals (5%). (J91.18.w1)

Rattus norvegicus - Brown rat:

  • Austria 1976-1986. Natural infection. Antibodies detected in 15/280 individuals. (J132.S2.w1)
  • Israel 1959-60.  Natural infection. Haemagglutination-inhibition antibodies to WN virus detected in 22/219 individuals (10%). (J109.34.w1)

Laboratory rat (Rattus