West Nile Virus

Oregon State and Ohio State Universities
Working Together to Investigate West Nile Virus in Llamas and Alpacas

Michelle Kutzler DVM, PhD
College of Veterinary Medicine
Oregon State University
Corvallis, Oregon 97331
Phone: 541-737-2858
Facsimile: 541-737-8651
E-mail: michelle.kutzler@oregonstate.edu
David E Anderson, DVM, MS
College of Veterinary Medicine
The Ohio State University
Columbus, Ohio 43210
Phone: 614-292-6661
Facsimile: 614-292-3530
E-mail: Anderson.670@osu.edu
In recent years, West Nile Virus infection has been spreading westward from the eastern USA. The WNV was introduced into the USA in the late 1990's and has become a vital concern to the avian and equine industries. Although rare, WNV may infected humans and can cause fatal encephalomyelitis. The case fatality rate in humans infected with WNV is less than 5%. Many species of mammals have been infected with WNV including cattle, sheep, goats, llamas, alpacas, and camels but clinical disease is rare. In endemic WNV countries, seropositive rates vary widely among ruminant species (e.g. cattle, sheep, goats, camels, and water buffalo). Although seropositive rates may approach 75 %, clinical WNV infection in ruminating species appears infrequent. Llamas and alpacas are considered to be a low-risk species. This assertion was based on preliminary data from the USA in which approximately 1 clinically infected llama or alpaca has been documented for each 1500 horses documented. However, several cases of fatal WNV have been diagnosed in llamas and alpacas.

What is WNV?
West Nile Virus is a type of virus termed "Flavivirus".
Where does it come from?
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.
How is it spread?
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.
What species can become infected?
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.
What are the clinical signs of the disease?
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.
How is WNV infection diagnosed?
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.).
What is the treatment for affected animals?
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.
How can the disease be prevented?
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).
Is there a safe vaccine against WNV?
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.
Is there an effective vaccine against WNV?
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.
What about the Epidemiology of WNV?
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.
Summary:
West Nile Virus is a new disease in North America and can be rapidly spread by mosquitoes. Although extremely unlikely, WNV may infect llamas or alpacas. No information is currently available regarding efficacy of vaccination against natural infection with WNV in llamas or alpacas. Preliminary vaccination results warrant further investigation. Prevention of WNV infection should center on elimination of risk factors such as mosquitoes and environments conducive to mosquitoes. The issues surrounding vaccination against WNV must be made on a farm-specific and geographical basis. Discuss the risks and benefits of vaccination with your veterinarian to determine if this is right for your herd.

Latest Update on West Nile Virus 
 
August 2003

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