What is West Nile virus?

West Nile virus is a mosquito-borne disease that can cause encephalitis, or a brain infection. Mosquitoes acquire the virus from birds and pass it on to other birds, animals and people.

In 1999, West Nile virus first appeared in New York. For the first time, in the summer of 2000, Pennsylvania found the virus in mosquitoes, birds and a horse.

Mosquitoes spread this virus after they feed on infected birds and then bite people, other birds and animals. It is not spread by person-to-person contact and there is no evidence that people can get the virus by handling infected animals.

West Nile virus cases occur primarily in the late summer or early Fall, although the mosquito season is April through October.

West Nile encephalitis (WNE) is caused by West Nile virus (WNV), a flavivirus previously only found in Africa, Eastern Europe, and West Asia. WNV is closely related to St. Louis encephalitis virus (SLEV) which is found in the United States and to Kunjin virus (KV) which is found in Australia, some Western Pacific islands and parts of South East Asia.

People can only become infected with West Nile virus after being bitten by an infected mosquito. There is no evidence that people can get West Nile virus from infected animals or people, or that people can transmit the West Nile virus to other animals, birds, or people.

People over 50 years of age have the highest risk of developing a severe illness because as we age, our bodies have a harder time fighting off disease. People with compromised immune systems are also at increased risk, however, anyone can get the virus.

What are the symptoms?

People with mild infections may experience fever, headache, body aches, skin rash and swollen lymph glands. People with more severe infections may experience high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions and paralysis. If you have any of these symptoms, contact your doctor.

There is no specific treatment for West Nile virus infection, or a vaccine. While most people fully recover from the virus, in some severe cases hospitalization may be needed.

There are about 60 different species of mosquitoes in Pennsylvania. While most do not transmit West Nile virus, several mosquito species have been found to transmit the virus.

Mosquitoes lay their eggs in stagnant water around the home. Weeds, tall grass, shrubbery and discarded tires also provide an outdoor home for adult mosquitoes. By eliminating places for mosquitoes to breed, we can go a long way to prevent West Nile virus.

Mosquitoes breed in standing water. Even a small bucket that has stagnant water in it for seven days can become home to up to 1,000 mosquitoes. Here are some easy tips to eliminate standing water:

1. Dispose of tin cans, plastic containers, ceramic pots or similar water holding containers that have accumulated on your property. Do not overlook containers that have become overgrown by aquatic vegetation.
2. Pay special attention to discarded tires that may have accumulated on your property.
3. Drill holes in the bottom of recycling containers that are left out of doors. Drainage holes that are located on the container sides collect enough water for mosquitoes to breed in.
4. Clean clogged roof gutters on an annual basis, particularly if the leaves from surrounding trees have a tendency to plug up the drains. Roof gutters are easily overlooked but can produce millions of mosquitoes each season.
5. Turn over plastic wading pools when not in use. A wading pool becomes a mosquito producer if it is not used on a regular basis.
6. Turn over wheelbarrows and do not allow water to stagnate in birdbaths. Both provide breeding habitat for domestic mosquitoes.
7. Aerate ornamental pools or stock them with fish. Water gardens are fashionable but become major mosquito producers if they are allowed to stagnate. Clean and chlorinate swimming pools that are not being used. A swimming pool that is left untended by a family that goes on vacation for a month can produce enough mosquitoes to result in neighborhood-wide complaints. Be aware that mosquitoes may even breed in the water that collects on swimming pool covers.
8. Use landscaping to eliminate standing water that collects on your property. Mosquitoes will develop in any puddle that lasts for more than four days.

It is not necessary to limit any outdoor activities, unless local officials advise you otherwise.

However, you can and should try to reduce your risk of being bitten by mosquitoes. In addition to reducing stagnant water in your yard, make sure all windows and doors have screens, and that all screens are in good repair.

If West Nile virus is found in your area:

• Take normal steps to prevent insect bites.
• Wear shoes, socks, long pants and a long-sleeved shirt when outdoors for long periods of time, or when mosquitoes are most active.
• Consider the use of mosquito repellent, according to directions, when it is necessary to be outdoors. Wash all treated skin and clothing when returning indoors.

Remember, electromagnetic and ultrasound devices and Vitamin B are not effective in preventing mosquito bites.

Prior to 1999, no West Nile virus cases had been reported in the United States. During the 1999 encephalitis outbreak, there were 62 human cases and seven deaths. In 2000, there were 21 diagnosed cases and two deaths. However many infected people showed mild flu-like symptoms or no symptoms at all.

In 2000, West Nile virus had been found in New York, New Jersey, Connecticut, Rhode Island, Massachusetts, Vermont, Virginia, Maryland, Pennsylvania, North Carolina, and New Hampshire. Positive horses have been found in New York, New Jersey, Connecticut, Rhode Island, Pennsylvania, and Massachusetts.

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Prevention and Control of West Nile Virus Infection in Equine and Other Livestock or Poultry
August 2001

 West Nile virus (WNV) is a vector-borne virus that was recognized in the Western Hemisphere for the first time in 1999. Invertebrate vectors, such as mosquitoes, circulate the virus among wild birds. Occasionally the virus is introduced into other vertebrate populations, such as humans or horses, that serve as incidental hosts. Incidental hosts are infected animals that do not pass the virus on to vectors or other animals.

The only vectors found to be associated with outbreaks of WNV in 1999 and 2000 in the northeast United States were mosquitoes. At least 14 species of mosquitoes were found positive for WNV. No evidence has been found to suggest that any invertebrate vectors other than mosquitoes were involved in WNV transmission in either year.

Horses are affected by WNV more often than other domestic animals. Many horses infected with WNV do not develop any illness, but of the 85 that did become ill in the 1999 or 2000 outbreak, 32 (38 percent) died or were euthanatized. Other livestock and poultry do not commonly show illness if infected with WNV.

Given that mosquitoes are associated with WNV transmission, the key to preventing or controlling future outbreaks of WNV among horses is to control mosquito populations and to prevent horses from being exposed to any adult mosquitoes that may be present. The following recommendations are based on our current knowledge of WNV and of the 1999 and 2000 U.S. outbreaks. Similar recommendations would apply for other livestock or poultry should illness due to WNV in those types of animals come to be commonly recognized.

Reduction of Mosquito Breeding Sites

Reducing the population of mosquitoes, especially species that are apparently involved with bird-to-bird transmission of WNV, such as some Culex species, can help to reduce or eliminate the presence of virus in a given geographical area. The most important step any property owner can take to control such mosquito populations is to remove all man-made potential sources of stagnant water in which mosquitoes might breed. Dispose of any water-holding containers, including discarded tires. Drill holes in the bottom of containers that are left outdoors. Clean clogged roof gutters annually. Turn over plastic wading pools or wheelbarrows when not in use and do not allow water to stagnate in bird baths. Aerate ornamental pools or stock them with fish, such as Gambusia, that eat mosquito larvae. Clean and chlorinate swimming pools that are not in use and be aware that mosquitoes can breed in the water that collects on swimming pool covers. Use landscaping to eliminate standing water that collects on your property; mosquitoes can breed in any puddle that lasts more than 4 days. Thoroughly clean livestock watering troughs monthly. Local mosquito control authorities may be able to help in assessing the mosquito breeding risks associated with a specific property.

Decreasing Exposure to Adult Mosquitoes

It is also important to prevent horses from being exposed to adult mosquitoes.   Several actions may help in that effort.

• Screened housing

Housing animals in structures with well-maintained insect screening can be useful to reduce exposure to adult mosquitoes. Use of such mosquito-resistant structures may actually lead to mosquito exposure unless precautions are first taken to eliminate mosquitoes from inside the structure. This may be accomplished through a number of means including the use of mosquito adulticides. In addition, use of fans may reduce the potential ability of mosquitoes to feed on horses.

• Insect repellents

Use of insect repellents may be of some value in decreasing exposure of horses to adult mosquitoes. Due to practical limitations in the coverage area that may be achieved on any given horse with a particular product formulation, and due to limited duration of effectiveness of some formulations under certain conditions (e.g., perspiration), repellents should not be solely relied upon to prevent mosquito exposure. Repellents should be used according to their label instructions regarding appropriate species, method of application, and other precautions. Topical application of a product containing a synthetic pyrethroid compound (e.g., permethrin) as the active ingredient may offer the best combination of safety and efficacy.

• Outdoor exposure

Although some species of mosquitoes feed at dusk or dawn, others are daytime feeders or feed at any time of the day or night. As it is not yet clear which mosquitoes are responsible for the transmission of WNV to horses and other mammalian species, making recommendations as to when certain animals should avoid outdoor exposure may not be particularly useful at this time. However, a recently completed epidemiological study of WNV suggests that keeping horses in stalls at night may be helpful in reducing their risk of infection.

Vaccination

Vaccine hope for West Nile virus
Courtesy: BBC News

Scientists have developed a vaccine against the deadly West Nile virus. At present the vaccine is only effective in horses, but researchers hope it will pave the way for a human version.  West Nile virus was first identified in Uganda in 1937. It can cause fever, skin rashes, severe aches and meningitis. Until 1999 it had only ever been recorded in Africa, Asia and some Middle Eastern countries. But two years ago a wave of infection took New York by surprise, killing seven people and making dozens of others sick. Many wild birds succumbed to the virus, as did dozens of horses. Last year an outbreak in southern France killed about 20 horses.

Virus family

Because there has been no vaccine against the virus, public health efforts have focused on controlling mosquitoes, which spread the disease. But New Scientist magazine reports that Dr Jeffrey Chang of the Centers for Disease Control and Prevention in Fort Collins, Colorado, has now successfully developed a vaccine. West Nile virus is part of a family that includes Japanese encephalitis, and Dr Chang's team was already designing vaccines against that virus. They were able to modify that vaccine to target West Nile virus.

Genetic material

The vaccine contains genetic material from the West Nile virus. When injected into animals it triggers an immune response. Dr Chang said: "It looks like the virus to the immune system. But it is completely harmless." Within three months, the researchers had showed the vaccine could protect mice from infection, so they moved on to a more relevant species.  Four horses were given a single injection of the DNA. Thirty-nine days later, mosquitoes carrying West Nile virus were allowed to bite them. None of the horses developed any signs of viral replication, fever, infection or sickness.

Funding search

In contrast the virus replicated rapidly in seven out of eight unvaccinated horses.   Dr Chang thinks his vaccine might also protect people and is looking for funding to test it on monkeys. He also plans to test his vaccine on American crows to see if it is versatile enough to protect birds as well. Tom Monath, of Acambis, a vaccine company based in Massachusetts, said: "Anyone can protect a mouse, but the horse result is quite promising.  "Many vaccine approaches don't work in animals of that scale." Dr Monath's company is also developing a human vaccine based on weakened yellow fever virus containing West Nile genes. But it is yet to report results.

• Life Cycle
  
• The organism that causes EPM was tentatively named Sarcocystis neurona in 1990, because we did not have a positive identification of the species. However, since the opossum has been identified as the definitive host, DNA testing (Fenger et al., 1995) and infection studies (Fenger et al., 1997) have shown that the organism is closely related to the protozoan Sarcocystis falcatula, a species that cycles in nature between two host species, birds and opossums. This protozoan can cause a severe life-threatening disease in some of its natural intermediate hosts, such as budgerigars, but may cause few clinical signs in others, such as pigeons. Subsequent research performed at the University of Florida and Cornell University has demonstrated that S. falcatula and S. neurona are not the same species. In the normal life cycle, the parasite is ingested (fecal-oral transmission) in the form of a sporocyst by the intermediate host, undergoes asexual reproduction in the blood vessels of the liver, lungs and muscles and then encysts in the intermediate host's muscle tissue, without traveling to the central nervous system. When this tissue is eaten by the opossum, the organism undergoes sexual reproduction in the intestinal cells, and forms the infective sporocysts, which are passed in the feces. The opossum does not become sick, but may shed the parasites for months.

Horses represent an aberrant host of S. neurona. Sporocysts are ingested, but never encyst in the tissues of the horse. Instead, they migrate to the central nervous system, where they continue to undergo asexual reproduction intracellularly in neurons, without forming tissue cysts. Horses cannot transmit the organism to other horses, or even to opossums. Horses probably eat the opossum sporocysts inadvertently while eating grass, hay or grain.

In a recent research study (Fenger et al., 1997), we were able to reproduce the disease by feeding opossum-derived sporocysts to horses. The horses had detectable serum antibodies at about 3 weeks after infection, and all of the horses that ultimately developed EPM had spinal fluid antibodies about a week later. Those that did not develop EPM never had antibodies in the spinal fluid, even as long as 4 months later.

Antiinflammatory therapy is indicated in acute EPM cases. This may include treatment with phenylbutazone or banamine (1.1 mg/kg 1-2 times daily for 3-7 days), as well as the addition of DMSO (1 g/kg in a 10% solution) administered either intravenously or by nasogastric tube. Corticosteroids may be used if necessary. Antiinflammatory drugs are occasionally necessary at other times during the first six weeks of treatment. Some horses actually get worse during treatment, presumably because of a reaction to the dying parasites (Fenger et al., 1997, b). Supplementation with vitamin E, folic acid and thiamine may be helpful adjunct treatment (Fenger et al., 1997, b). Some recent evidence has put the use of folic acid supplementation into question. However, it is probably safe and recommended for most performance horses, but not recommended for use in pregnant animals.

FDA has approved Marquis (ponazuril) the first drug to treat equine protozoal myeloencephalities (EPM) in horses. EPM is caused by a parasite (Sarcocystis neurona) and is the most commonly diagnosed neurological condition in horses in America. EPM is widespread in North America, South America, and in Canada. In some areas of the United States, as much as 80-90% of the horse population may have been exposed to EPM. An estimated one percent of the horses exposed to the disease will develop clinical signs of EPM and require treatment.

The Clinical signs of EPM may vary, and they may include weakness (particularly on one side), serious lack of coordination, and muscle wasting involving all four limbs. EPM is more prevalent in young (less than 5 years ago) and older horses (more than 13 years old). Diagnosis of EPM is difficult since there are at least four other central nervous system diseases that can closely resemble the disease.

FDA expedited the approval process for ponazuril because it may help reduce the suffering and death associated with EPM, and because there is no other approved therapeutic for treating this devastating disease.

Ponazuril is supplied as an oral paste to be given once a day at the dose of 5mg/kg for 28 days in adult horses. Beyer Animal Health, Shawnee Mission, Kansas, is the sponsor of the drug that will be available by prescription only from a licensed veterinarian.

FDA Talk Paper 7/19/2001

What is Equine Protozoal Myeloencephalitis (EPM)?
EPM is a devastating disease that attacks the central nervous system (CNS) of the horse creating inflammation to the brain and spinal cord. The organism that causes EPM is the protozoan Sarcocystis neurona.

What are the clinical signs?
Clinical signs of EPM may include seizures, depression, muscle atrophy, the inability to coordinate voluntary muscle activity and paralysis. Many of these symptoms are similar to other equine diseases that affect the CNS, thus making EPM difficult to diagnose. In addition, the clinical signs of EPM can be subtle or severe. Clinical signs may progress rapidly, or in other cases progression may be slow and signs may even diminish.

How prevalent is EPM?
Studies indicate the prevalence of exposure to S. neurona in some areas to be as high as 50% for all horses, with the percentage increasing to 80% for older, adult horses in some parts of the United States. Although the chances of being seropositive increase with age, the incidence of clinical disease peaks between 15 months and five years. Stress appears to play an important role in clinical cases and the incubation period is variable. If left untreated, an infection by S. neurona may remain in the horse's system indefinitely. Which horses will display clinical signs and which horses won't is yet unexplained.

How is transmitted?
The organism that causes EPM is mainly transmitted to horses by the opossum. The opossum releases infective sporocysts into the environment through its feces. The horse ingests the sporocysts via contaminated feed or water. How the sporocysts migrate to the CNS to cause disease isn't completely clear. However, a reasonable assumption is that after the sporocysts are ingested, they invade the CNS via the circulatory system. Once the infective organisms reach the CNS, they may proliferate by asexual reproduction and cause disease by their presence and the associated inflammatory response. Insects, birds or small mammals may also transport or ingest the sporocysts, contributing to the cycle of EPM transmission. The horse, however, is considered to be a "dead-end" host, and therefore not infectious to other animals.

Which horses are at greatest risk?
Infection is believed to occur along the western coast and from the central states eastward in the United States, most of Mexico, Central America, and South America. Virtually all equine breeds have tested positive in seroprevalence studies. The disease is most common in young (three-year-old) horses, with racehorses (especially standardbreds) and show horses at higher risk than breeding and pleasure horses.

How is EPM diagnosed?
Diagnosis of EPM infection is difficult to pinpoint. One notable clue of the disease is that it tends to affect one side or part of the horse more than another. If your veterinarian suspects EPM, a blood and cerebrospinal fluid (CSF) analysis may be conducted. This procedure requires a spinal tap be performed on the horse. If the blood test is positive, this indicates the horse has been exposed to the organism, not that it has attacked the CNS or that it will develop clinical signs. Another test called the Western blot analysis can also be conducted on the CSF and serum. The greatest value of the Western blot test on CSF is when the result is negative. A negative Western blot result on CSF generally rules out EPM.

Can EPM infection be treated?
Several treatment regimens have been developed. They are expensive and can last several months. Treatment consists of antiprotozoal, anti-inflammatory, antiedema and antioxidant therapy. Immunomodulator treatment and physical therapy may also be attempted. The antiprotozoal treatment is the cornerstone of the treatment programs. The oldest and most commonly used antiprotozoal treatment is a combination of the folate synthesis inhibitors pyrimethamine and a sulfonamide. This combination of drugs is administered orally. Relapses, particularly following stressful situations, are common.

Can EPM infection be prevented?
Only now has a vaccine been developed which may aid in the prevention of EPM. The Sarcocystis neurona vaccine stimulates the development of neutralizing antibodies to S. neurona which may aid in the prevention of disease due to new infections, but efficacy and potency tests are still in progress. The USDA license is conditional. Considering the prevalence of exposure to S. neurona, the difficulty in diagnosing the disease as well as the expense and timeinvolved in treatment programs, use of the vaccine for its potential to aid in the prevention of new infection may be of utmost importance to some horse owners. Practical management tools also include proper maintenance of the horses' living and feeding areas. Limiting exposure to opossums, as well as controlling exposure to contaminated feed, will aid in breaking the cycle of transmission.

Vaccination schedule
Because the efficacy studies are still underway, the optimal vaccination schedule has not yet been determined. For now however, Fort Dodge is recommending a similar program as is used for many other killed vaccines. The initial vaccination consists of two injections. The second injection is given 3 to 6 weeks after the first injection, followed by an annual booster.