West Nile Virus
History
West Nile Virus (WNV) is an arbovirus (a mosquito-borne virus) found worldwide. This virus belongs to the genus Flavivirus, and infects over 300 species of birds. WNV was first isolated in Uganda in 1937 but has expanded its range to southern and northern Africa, Middle East, Europe, United States, southern Canada, Mexico, and portions of Central and South America. Most mammals can become infected but usually will not develop clinical disease. Besides humans, the main exception is the horse, which represents 97% of reported non-human mammalian cases. WNV has been documented in squirrels, chipmunks, mice, rats and other rodents, skunks, canids, white-tailed deer, raccoons, bears, opossums, bats and non-human primates. WNV infections became evident in migrating storks and domestic geese in the Middle East in the late 1990s and made the jump to the United States in 1999. WNV is now considered an important pathogen of wild and captive birds in the United States and Canada, and one of concern for humans and horses.
Transmission
Although over 300 species of birds have been affected by WNV, birds belonging to the Corvidae family (crows, ravens, jays, magpies, rooks, jackdaws, treepies, etc) have been severely affected, leading to conservation concerns. Birds are considered the primary host for WNV and transmission of this virus is propagated between the bird and mosquito vectors, especially Culex spp. There has been the suggestion that non-mosquito arthropods (louse, flies, ticks, swallow bugs) may also be a source of WNV transmission, but more field research is needed to confirm this hypothesis. While most infections of WNV occur through mosquitoes taking a blood meal, some infections may occur from the ingestion of an infectious prey. This is very significant in the raptor species.
WNV transmission may occur year-round in tropical and subtropical climates, while temperate regions see WNV infections from June through October. The rate and severity of infections will vary considerably from year to year and region to region, influenced by the hosts, environmental factors such as rainfall and temperature, and of course the prevalence of mosquito vectors.
Development of Disease
A raptor infected with WNV will have a period of time that the virus replicates in the blood and other tissues. This will be followed with a humoral immune response. To fully understand how the virus affects raptors, controlled studies of experimental infections in raptors and other birds were performed. Two situations occur when a raptor becomes infected with WNV. Viremia refers to the initial spread of the virus in the blood from the first site of infection, with the potential to spread to the rest of the body. Viral shedding occurs with the release of virus progeny following replication and reproduction of the virus. Viral shedding may occur from one part of the body to another, or be released into the environment to potentially infect other animals. It was determined that a raptor infected with WNV would become viremic and shed the virus through oral and cloacal secretions 1-3 days post infection and continue shedding intermittently through 14 days post infection. Post infection is defined as “relating to or occurring in the period after infection.” It is possible for the raptor to shed this virus prior to or in the absence of clinical signs. For raptors that survive the acute infection, their viremia is cleared by 6-8 days post infection.
It is a known fact that WNV will infiltrate many organ systems. While most raptors that survive the disease will clear the virus from their tissues within 1-2 weeks, research has shown that some raptors, clinically normal following disease, have had WNV particles detected in their tissues for up to 27-30 days post infection. The raptor’s ability to mount a humoral immune response is critical to survival. The humoral immune response is determined by the bird’s ability to produce antibodies that will bind to the pathogen (virus) and neutralize the pathogen. Raptors with WNV infections may develop detectable serum antibodies to WNV in 5-7 days post infection, however this antibody titer usually increases fourfold or more within the first month after infection. The antibodies produced may persist and continue to protect the raptor for four years or longer.
The development of disease will be influenced by the species of raptor affected, genetic factors influencing their susceptibility, age of the raptor and the maturity of their immune system, concurrent disease, and stress factors. Raptors that die from WNV infections will show changes in the tissues of the brain (encephalitis), liver, spleen, kidney, heart (myocarditis), eye, and skin. Many of the pathological changes are the result of the direct effect of the virus or secondary to the marked inflammatory response caused by the virus resulting in tissue necrosis and degeneration. Raptors that survive the infection may suffer from relapses of the neurologic signs and have feather pulp abnormalities affecting the molt for up to 4 years.
Clinical Signs
The clinical signs of WNV infections are highly variable and may be affected by species of raptor and age. This virus is inflammatory in nature and causes encephalitis (inflammation of the brain and spinal cord). In addition to encephalitis, other organs such as the kidney, liver, spleen, heart and eyes can also be affected. Mild forms of this virus can cause abnormal feather growth and development. Death or permanent disabilities are possible with infection. Three phases of infection have been classified and are as follows:
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Phase one: depression, anorexia, regurgitation, and lethargy. Abnormal blood feathers may become evident also. A complete blood count will show an elevated white blood cell count, with reactive lymphocytes
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Phase two: the above mentioned; green urates, mental dullness/vision issues, weakness in the legs and ataxia
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Phase three: severe tremors and seizures
Clinical signs can progress rapidly over 7 days. Not so obvious are the effects of this virus on the eyes, heart, and kidney. Anterior uveitis and fundic changes of the eyes such as fibrin adhesions, chorioretinal lesions and retinal atrophy are possible. These changes will need the evaluation by a veterinarian or veterinary ophthalmologist. Some of these changes will be permanent and affect the raptor’s vision for the rest of its life. Heart or myocardial lesions are varied and may include myocardial necrosis, degeneration, mineralization, fibrosis and hemorrhage. Certainly, this will affect the raptor’s stamina and ability to fly. Most raptors affected with WNV will have kidney tubular epithelial and glomerular cell degeneration and necrosis. These changes can be permanent.
Diagnosis
The clinical signs can suggest any number of diseases, including inflammatory, head trauma, metabolic, nutritional and toxic etiologies. The geographical location of the raptor, time of year and reports of WNV infections in your area will be important history information. Confirmation of WNV in the live patient is usually determined with detection of circulating antibodies against WNV or antigen (viral particle) assay testing. Examination of the eyes showing optic neuritis, anterior uveitis, vitritis and chorioretinits can be suggestive of a WNV infection. The complete blood count usually reveals extremely elevated white blood cell numbers with reactive changes of the lymphocytes. Blood chemistries will evaluate internal organ function.
Treatment
Aggressive supportive care is recommended for raptors suffering from WNV infections. The best success for treatment is in the beginning stages of infection. Here are the recommendations:
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Warmth
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Fluids
Fluid therapy is a must for 1-5 days depending on the severity of the case. This will help to stabilize the patient and protect the kidneys. Lactated Ringers Solution is a common balanced replacement fluid used. This is given intravenously or subcutaneously. Orals are not used if the bird is neurologic or not standing. The average dose is 40-60 ml/Kg/day. Certainly the dehydration deficit must be added in to the maintenance dose and administered over 24 hours if the patient is dehydrated.
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Nutrition
Nutritional support may be in the form of hand feeding or syringe feeding with Emeraid Intensive Care Carnivore and a gavage tube.
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Vitamin B
Vitamin B complex is given at 1-3 mg/Kg (dose is based on the thiamine fraction) intramuscularly every 7 days for 1-3 weeks (this may help with the neurologic signs)
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Antibiotics:
minocycline @ 15 mg/Kg PO BID or doxycycline @ 25 mg/Kg PO BID
These antibiotics have anti-inflammatory effects and will cross the blood brain barrier.
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Anti-parasitic
Ivermectin may have the ability to help prevent the virus from replicating. Use only the cattle product, which is pure ivermectin. This is an injectable, but can be used orally at 0.2 mg/Kg once every 3-4 days for 3 treatments. Overdosing will cause seizures and possibly death. The volume is extremely small and is placed under the tongue on the mucus membranes.
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Anti-fungal medication for sensitive species
This will be a preventative program for secondary aspergillosis
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Anti-inflammatory
