Humoral response to an equine encephalitis vaccine in healthy alpacas.

OBJECTIVE: To determine humoral responses to an equine encephalitis vaccine in healthy alpacas. DESIGN: Clinical trial. ANIMALS: 39 healthy alpacas on 1 farm and 86 healthy alpacas on a second farm. PROCEDURES: All alpacas were given 3 doses IM of a bivalent, killed-virus equine encephalitis vaccine, with 4 weeks between doses. Eastern equine encephalitis (EEE) virus neutralizing antibody responses were determined with a plaque reduction neutralization assay every 14 days in alpacas on the first farm and 70 days after the first dose of vaccine on the second farm. RESULTS: For alpacas on the first farm, geometric mean virus neutralizing antibody titer peaked 2 weeks after the third vaccine dose was given (ie, day 70). At this time, 29 of 38 (76%) animals were seropositive for antibodies against EEE virus, and percentage of animals 6 years old that were seropositive (1/5). For alpacas on the second farm, 76 (88%) were seropositive on day 70, and percentage of animals 6 years old that were seropositive (27/33). For both farms, geometric mean titer on day 70 was significantly higher in animals < 2 years old than in animals > 6 years old. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that inoculation of alpacas with 3 doses of a bivalent, killed-virus equine encephalitis vaccine induced a humoral antibody response against EEE virus.

Immunologic responses to West Nile virus in vaccinated and clinically affected horses.

OBJECTIVE: To compare neutralizing antibody response between horses vaccinated against West Nile virus (WNV) and horses that survived naturally occurring infection. DESIGN: Cross-sectional observational study. ANIMALS: 187 horses vaccinated with a killed WNV vaccine and 37 horses with confirmed clinical WNV infection. PROCEDURE: Serum was collected from vaccinated horses prior to and 4 to 6 weeks after completion of an initial vaccination series (2 doses) and 5 to 7 months later. Serum was collected from affected horses 4 to 6 weeks after laboratory diagnosis of infection and 5 to 7 months after the first sample was obtained. The IgM capture ELISA, plaque reduction neutralization test (PRNT), and microtiter virus neutralization test were used. RESULTS: All affected horses had PRNT titers > or = 1:100 at 4 to 6 weeks after onset of disease, and 90% (18/20) maintained this titer for 5 to 7 months. After the second vaccination, 67% of vaccinated horses had PRNT titers > or = 1:100 and 14% had titers < 1:10. Five to 7 months later, 33% (28/84) of vaccinated horses had PRNT titers > or = 1:100, whereas 29% (24/84) had titers < 1:10. Vaccinated and clinically affected horses' end point titers had decreased by 5 to 7 months after vaccination. CONCLUSIONS AND CLINICAL RELEVANCE: A portion of horses vaccinated against WNV may respond poorly. Vaccination every 6 months may be indicated in certain horses and in areas of high vector activity. Other preventative methods such as mosquito control are warranted to prevent WNV infection in horses.

West Nile virus infection in reindeer (Rangifer tarandus).

West Nile virus (WNV) infection in 4 reindeer (Rangifer tarandus) resulted in lymphohistiocytic encephalomyelitis within the medulla oblongata and cervical spinal cord. Immunohistochemistry revealed WNV antigen within neurons and among mononuclear cell infiltrates. These represent the first known cases of clinical WNV infection in Cervidae. Clinical signs and lesions were similar to those described in horses. Nucleotide sequence of a 768-bp region of the WNV E-glycoprotein gene revealed 1 nucleotide mutation, which resulted in a single amino acid substitution from a serine to a glycine (position 227 of E-glycoprotein) when compared with the prototype WNV-NY99 strain (isolated from Bronx zoo flamingo 382-99).

Induction of neutralizing antibodies in reindeer (Rangifer tarandus) after administration of a killed West Nile virus vaccine.

In 2002, West Nile virus (WNV) infection with clinical neurologic disease and encephalomyelitis was described in reindeer (Rangifer tarandus). The susceptibility of reindeer to WNV prompted questions concerning vaccination of reindeer to prevent WNV infection. Between January and April 2003, eleven 2-4-yr-old, castrated male reindeer, some of which had antibody titers suggestive of prior exposure to WNV, were vaccinated three times at 4-wk intervals with a commercially available vaccine approved for use in horses. No adverse reactions to vaccination were noted. All vaccinated reindeer developed high neutralizing antibody titers to WNV, as determined by the plaque reduction neutralization test. Reindeer without antibody titers from previous natural exposure to WNV required a primary vaccination and one or two booster vaccinations for development of neutralizing antibody to WNV. Protective efficacy of vaccination was not evaluated. Vaccination of reindeer for WNV may be warranted in certain circumstances combined with management practices to limit exposure to potential vectors.

Pathogenicity of a Venezuelan equine encephalomyelitis serotype IE virus isolate for ponies.

The enzootic or endemic strains of Venezuelan equine encephalomyelitis (VEE) virus (ID, IE, IF, and II-VI) are considered avirulent. In 1993 and 1996, outbreaks of encephalitis occurred in the horse populations in the Chiapas and Oaxaca provinces of Mexico, respectively. In both instances, enzootic VEE virus subserotype IE was isolated from brain tissues of dead horses. The present study investigated the pathogenicity of the Chiapas viral isolate (NVSL VEE IE 93-42124) in ponies. Three ponies were inoculated intradermally with 4, 5, and 6 logs, respectively, of the NVSL VEE IE 93-42124 viral isolate. All ponies showed fluctuations in body temperature, encephalitis, and other signs of infection with VEE virus. Virus was isolated only from the blood of ponies from day 1 to day 3 postinfection. Microscopic examination of hematoxylin and eosin-stained tissue sections showed mild to moderate nonsuppurative encephalitis, perivascular cuffing by mononuclear cells, gliosis, and meningoencephalitis. Antibody (IgM) to VEE virus IE was unable to differentiate between various subserotypes of VEE I viruses (serotypes IAB, IC, ID, and IF). Virus neutralizing antibody titers to heterologous VEE I viruses were 10-100-fold less than those for NVSL VEE IE 93-42124 virus and Mena II, a human isolate of VEE IE virus. The study confirmed that NVSL VEE IE 93-42124 virus, which was isolated from a brain of a horse during an outbreak of VEE in Chiapas, Mexico, was pathogenic for ponies.

Serologic survey of cattle in the northeastern and north central United States, Virginia, Alaska, and Hawaii for antibodies to Cache Valley and antigenically related viruses (Bunyamwera serogroup virus).

Bovine sera from northeastern states (Connecticut, Delaware, Maine, Maryland, Massachusetts, New York, Pennsylvania, Vermont, and West Virginia), north central states (Indiana, Illinois, Iowa, Kentucky, Michigan, Minnesota, North Dakota, Ohio, South Dakota, and Wisconsin), Virginia, Alaska, and Hawaii were examined for the presence of neutralizing antibodies to Cache Valley (CV), Lokern (LK), Main Drain (MD), Northway (NW), and Tensaw (TS) viruses. Microneutralization tests were performed using Vero cells. Ninety percent inhibition of the virus at a 1:10 serum dilution was considered positive for the presence of specific antibody. Sera having antibody to more than one virus were titrated from 1:10 to 1:640. The results indicated that 4-28% of the cattle per region had specific antibodies to CV virus. Neutralizing antibodies to NW, LK, and TS viruses were also detected, indicating possible exposure to these Bunyamwera serogroup viruses along with CV virus. Antibody titers measured against NW virus were very similar to those against CV virus. Antibodies to MD virus were present in low levels in bovine sera from Illinois, Maryland, and Ohio. Cattle from Alaska had only antibodies to NW virus. Antibodies to Bunyamwera serogroup viruses were not observed in sera from Hawaii.