West Nile virus in livestock and wildlife.

WN virus is one of the most ubiquitous arboviruses occurring over a broad geographical range and in a wide diversity of vertebrate host and vector species. The virus appears to be maintained in endemic foci on the African continent and is transported annually to temperate climates to the north in Europe and to the south in South Africa. Reports of clinical disease due to natural WN virus infection in wild or domestic animals were much less common than reports of infection (virus isolation or antibody detection). Until recently, records of morbidity and mortality in wild birds were confined to a small number of cases and infections causing encephalitis, sometimes fatal, in horses were reported infrequently. In the period 1996-2001, there was an increase in outbreaks of illness due to WN virus in animals as well as humans. Within the traditional range of WN virus, encephalitis was reported in horses in Italy in 1998 and in France in 2000. The first report of disease and deaths caused by WN virus infection in domestic birds was reported in Israel in 1997-1999, involving hundreds of young geese. In 1999 WN virus reached North America and caused an outbreak of encephalitis in humans in the New York area at the same time as a number of cases of equine encephalitis and deaths in American crows and a variety of other bird species, both North American natives and exotics. Multi-state surveillance for WN virus has been in place since April 2000 and has resulted in the detection of WN virus in thousands of dead birds from an increasing number of species in North America, and also in several species of mammals. The surveillance system that has developed in North America because of the utility of testing dead birds for the rapid detection of WN virus presence has been a unique integration of public health and wildlife health agencies. It has been suggested that the recent upsurge in clinical WN virus infection in wild and domestic animals as well as in humans may be related to the emergence of one or more new strains of WN virus. Virus isolated in New York in 1999 was found to be identical to that from Israel. It was alarming for WN virus to so easily invade the United States and surprising that it became established so quickly in the temperature climate of New York. Its persistence and rapid expansion in the United States leave a number of unanswered questions. New disease characteristics and patterns have occurred and more are evolving as WN virus further invades the western hemisphere. Additional animal research is needed to answer these questions. Some of the research needs include bird migration as a mechanism of virus dispersal, vector and vertebrate host relationships, virus persistence mechanisms, laboratory diagnosis, viral pathogenesis, risk factor studies, vaccine development, and WN virus impact on wildlife (CDC 2001a). Determination of the primary reservoir host species that are involved in the epidemiology of WN virus and the suitable sentinel species for active surveillance are also important research areas.

West Nile virus transmission and ecology in birds.

The ecology of the strain of West Nile virus (WNV) introduced into the United States in 1999 has similarities to the native flavivirus, St. Louis encephalitis (SLE) virus, but has unique features not observed with SLE virus or with WNV in the old world. The primary route of transmission for most of the arboviruses in North America is by mosquito, and infected native birds usually do not suffer morbidity or mortality. An exception to this pattern is eastern equine encephalitis virus, which has an alternate direct route of transmission among nonnative birds, and some mortality of native bird species occurs. The strain of WNV circulating in the northeastern United States is unique in that it causes significant mortality in exotic and native bird species, especially in the American crow (Corvus brachyrhynchos). Because of the lack of information on the susceptibility and pathogenesis of WNV for this species, experimental studies were conducted at the USGS National Wildlife Health Center. In two separate studies, crows were inoculated with a 1999 New York strain of WNV, and all experimentally infected crows died. In one of the studies, control crows in regular contact with experimentally inoculated crows in the same room but not inoculated with WNV succumbed to infection. The direct transmission between crows was most likely by the oral route. Inoculated crows were viremic before death, and high titers of virus were isolated from a variety of tissues. The significance of the experimental direct transmission among captive crows is unknown.

Ticks, Lyme disease spirochetes, trypanosomes, and antibody to encephalitis viruses in wild birds from coastal Georgia and South Carolina.

Ticks and blood samples were collected from wild birds mist-netted on St. Catherine's Island, Georgia, and at the Wedge Plantation in coastal South Carolina in 1994 and 1995. Immature stages of 5 species of ixodid ticks were recovered from 10 of 148 (7%) birds belonging to 6 species in Georgia, whereas 6 ixodid species were recovered from 45 of 259 (17%) birds representing 10 avian species in South Carolina. Borrelia burgdorferi sensu lato was isolated from 27 of 120 (23%) screened ticks (Ixodes scapularis and Ixodes minor) recovered from South Carolina birds, but from none of 16 screened ticks removed from Georgia birds. This spirochete was also isolated from 1 of 97 (1%) birds in South Carolina. In 1995, neither eastern equine encephalitis (EEE) virus nor St. Louis encephalitis (SLE) virus was isolated from any of 218 bird sera screened, but serum neutralizing antibodies were found to EEE virus in 4 of 121 (3%) sera and to SLE virus in 2 of 121 (2%) sera from South Carolina. No antibody to either virus was detected in 51 avian sera screened from Georgia. Trypanosomes (probably Trypanosoma avium) were isolated from 1 of 51 (2%) birds from Georgia and from 13 of 97 (13%) birds from South Carolina. Our data suggest that some wild birds may be reservoir hosts for the Lyme disease spirochete and for encephalitis viruses in coastal Georgia and South Carolina and that migrating birds can disperse immature ticks infected with B. burgdorferi.

Susceptibility of selected rodent species from Colorado to Borrelia burgdorferi.

To determine the susceptibility of some common Colorado (USA) rodent species to Borrelia burgdorferi, pregnant Peromyscus maniculatus, Tamias minimus, and Spermophilus lateralis were trapped in May 1990 and kept in quarantine until their young were old enough to be used in the experiment. Six to eight 8-wk-old individuals of each of the Colorado species and, for comparison, eight laboratory raised P. leucopus were subcutaneously inoculated with > or = 10(5) spirochetes in 0.1 ml in July 1990. Tissue specimens were collected for isolation from these animals through April 1991. Spirochetes were isolated from blood, ear, bladder, kidney, spleen, liver, and eye in Barbour-Stoener-Kelly (BSK) medium from P. maniculatus, P. leucopus and T. minimus. Spirochetes were isolated from at least one tissue from all of these animals and no isolations were obtained from any of the S. lateralis. Thus, three of the four rodent species tested are susceptible to, and could harbor, B. burgdorferi.

Serologic survey of neotropical bats in Guatemala for virus antibodies.

Neotropical bats were collected from different life zones in Guatemala in 1983 and 1984 to determine the presence and distribution of antibody against 10 viruses. Bats were collected with mist nets at 13 sites in eight departments and 332 serum specimens were obtained for testing for neutralizing (N) antibody by the plaque-reduction neutralization test. Eighty-seven (26%) of the 332 bats from 16 (38%) of 42 bat species sampled were serologically positive for five of six arboviruses and for two other viruses tested. Antibodies against Venezuelan equine encephalitis (VEE) variant I-A/B, eastern equine encephalitis, western equine encephalitis, St. Louis encephalitis, vesicular stomatitis, Tacaribe, and Rio Bravo viruses were detected in resident species of bats. However, N antibodies against the enzootic strain of VEE (Mena II, variant I-E) or Nepuyo viruses were not detected.

Experimental infection of the eastern chipmunk (Tamias striatus) with the Lyme disease spirochete (Borrelia burgdorferi).

Lyme disease, caused by the spirochete Borrelia burgdorferi, is endemic in the northeast, north-central, and Pacific coastal states of the United States. The eastern chipmunk (Tamias striatus) is found throughout the disease-enzootic regions except along the Pacific coast, and may serve as an important reservoir host in some locations. To characterize their potential as a host, 11 adult chipmunks were inoculated with 10(5) spirochetes from strains of B. burgdorferi isolated from Peromyscus leucopus and Ixodes scapularis in a hyperendemic area of Westchester County, New York (USA). All inoculated chipmunks became infected. Spirochetemias were detected by isolating spirochetes in Barbour-Stoenner-Kelly media in eight of eight chipmunks, and lasted for 2 to 5 days. Spirochetes were isolated from the ears of all animals, starting at 1 wk and for < or = 4 mo, and from various internal organs at 133 days post-inoculation. Laboratory-reared larval I. scapularis ticks became infected with spirochetes after feeding on two of the inoculated chipmunks.

Isolation and characterization of Borrelia burgdorferi from blood of a bird captured in the Saint Croix River Valley.

Field investigations were conducted to further evaluate the role of birds in the maintenance and dissemination of Borrelia burgdorferi. Blood specimens were taken from 39 passerine birds of 17 species captured during June 1991 at the Saint Croix National Riverway in Wisconsin, and one isolate, WI91-23, was cultured from an adult song sparrow (Melospiza melodia). This isolate was shown to be infectious for Peromyscus leucopus and Mesocricetus auratus (golden hamster). Isolate WI91-23 was confirmed as B. burgdorferi by immunofluorescence assay by using species-specific anti-OspA monoclonal antibodies H3TS and H5332 and anti-OspB antibody H5TS. Isolate WI91-23 was compared with Borrelia anserina Es, Borrelia hermsii MAN-1, and other B. burgdorferi strains (ATCC 53210, CT-1, and Catharus fuscescens [veery] liver 10293). Pulsed-field gel electrophoresis of in situ-lysed spirochetes revealed that the DNA plasmid profile of WI91-23 was most similar to those of plasmids from B. burgdorferi and most different from those of plasmids from B. anserina and B. hermsii. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis indicated that the protein profile of WI91-23 was like that of other B. burgdorferi strains studied, with dominant proteins corresponding to OspA and OspB, and that it differed from the protein profiles of B. anserina and B. hermsii. These findings indicate that passerine birds may serve as reservoirs for B. burgdorferi.

A plague epizootic in the white-tailed prairie dogs (Cynomys leucurus) of Meeteetse, Wyoming.

Surveillance for sylvatic plague (Yersinia pestis) was conducted near Meeteetse, Wyoming (USA) from 24 May to 14 June 1985. Ten species of fleas were collected from white-tailed prairie dogs (Cynomys leucurus), and from their burrows and associated rodents. Five of these flea species and two adult prairie dogs were positive for plague. The progression of this plague epizootic appeared to be slower and the intensity was less than in previous epizootics in other prairie dog colonies. The plague epizootic occurred within the only known colony of black-footed ferrets (Mustela nigripes) and was a potential threat to the food source of this endangered species.