West Nile Virus is a type of virus termed "Flavivirus".

West Nile Virus is endemic to North Africa. The virus is ubiquitous in the Nile River Valley and epidemiological studies have shown seroconversion in a large range of native species.

Birds serve as the natural reservoir for WNV. Mosquitoes are the most importrant vector for transmission of the virus. Horses are viremic for a relatively short period of time but may remain viremic for a long enough period to allow infection of the insect vectors. This does not seem to occur in the ruminant species. The physiology of South American Camelids (SAC's: llama, alpaca, vicuna, guanacoe) most closely resembles that of ruminants. Thus, we anticipate that llamas and alpacas will not serve as a reservoir for infection of herdmates and the insect vectors.

WNV is most pathogenic in avian species and horses. Humans and other mammals can become infected but usually remain assymptomatic. Serological surveys of sheep, goats, cattle, and camels indicate that up to 75 % of the population may have circulating antibodies to WNV and these antibodies may remain detectable for at least 12 months after exposure. However, clinical disease in these species is rare.

Clinical signs are variable in horses, but neurological signs are most common. These signs include ataxia, recumbency, tachycardia, tachypnea, seizures and death. At Ohio State University's Veterinary Teaching Hospital, two cases of WNV infection in alpacas were diagnosed in the fall of 2002. The infection progressed from head tilt and ataxia to recumbency and seizures over a period of 72 hours. Death occurred within 96 hours despite intensive medical therapy.

A number of diagnostic tests have been developed. In living animals, the virus neutralization (VN) test is used to detect antibodies in the bloodstream and is not species specific. In horses, an ELISA test for the immunoglobulin type IgM specific to WNV has been developed. This test is specific to horses and can not be applied to ruminants or SAC's. In animals that have died, immunohistochemistry tests can be performed on frozen tissues (e.g. brain, heart muscle, etc.).

No specific anti-viral treatments are available for WNV. Clinical management of infected animals is achieved through symptomatic treatment. These may include anti-inflammatory drugs or steroids, IV fluids and electrolyte therapy, physical therapy, and nutritional and environmental management.

The single most important tool in WNV prevention is elimination of insect vectors. Since mosquitoes are the most prevalent vector, control measures should include management practices to eliminate mosquitoes. Mosquito control includes drainage of standing water sources, mowing vegetation around ponds and lakes, and aerating water sources to decrease mosquito larvae survival (e.g. mosquito larval survival is significantly reduced if oxygen dissolved in water can be maintained above 400 ppm).

A killed virus vaccine has been developed for use in horses (Fort Dodge Animal Health). The manufacturer's recommendation includes an initial vaccination followed 3 to 6 weeks later by a booster vaccination. This vaccine was recently tested for safety by Oregon State University where 70 male llamas and alpacas were innoculated and at The Ohio State University where 14 female llamas and alpacas, including pregnant females, were inncoluated. These studies found no adverse reactions or abnormal health events after the initial dose of the vaccine in adult llamas and alpacas. The initial vaccine dose was not inflammatory and no adverse tissue reactions could be found. In the Ohio State study, the booster dose 3 weeks later stimulated a mild injection site swelling. The reaction was milder and resolved faster than that typically seen after Clostridial vaccination. No other adverse effects occurred.

The efficacy of the vaccine to stimulate antibody production is variable. In studies at Ohio State University, no antibody response was observed after a single dose of the WNV vaccine. After a booster dose, given 3 weeks after the initial vaccination, serum titer rose dramatically during the three weeks following the booster. However, serum titers had decreased dramatically by week 10 (7 weeks after the booster). The results of this study suggest that the WNV vaccine may stimulate immunity but that this immunity may be short-lived. The efficacy of the vaccine against actual infection with WNV has not been investigated and no data exists to determine if these antibody concentrations will prevent or lessen the severity of infection. However, the antibody response is appropriate for this vaccine. Thus, the WNV vaccine likely can be administered safely to llamas and alpacas, but no information is available regarding its efficacy against natural infection or the frequency of vaccination required to maintain protective immunity. Oregon State University is currently studying a 3 dose protocol to attempt to gain greater and longer lived antibody concentration in the blood stream.

The true risk factors for WNV in llamas and alpacas remain unknown. Both Oregon State University and Ohio State Univerity are gathering epidemiological data at this time. Oregon State University will closely track the disease as it moves to the western USA. Ohio State University will evaluate the effect of established WNV infection in the environment on resident camelid populations. This data will reflect events that occurred in 2002 as well as the progression of the disease throughout 2003.