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Leishmania Infection, Lymphatic Filariasis, Chagas Disease, East African Trypanosomiasis, West African Trypanosomiasis, West Nile Virus, Plague, Rocky Mountain spotted fever, Ehrlichiosis, Babesiosis, Arboviral Encephalitides
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What is leishmaniasis?

Leishmaniasis is a parasitic disease spread by the bite of infected sand flies. There are several different forms of leishmaniasis. The most common forms are cutaneous leishmaniasis, which causes skin sores, and visceral leishmaniasis, which affects some of the internal organs of the body (for example, spleen, liver, bone marrow).

What are the signs and symptoms of cutaneous leishmaniasis?

People who have cutaneous leishmaniasis have one or more sores on their skin. The sores can change in size and appearance over time. They often end up looking somewhat like a volcano, with a raised edge and central crater. Some sores are covered by a scab. The sores can be painless or painful. Some people have swollen glands near the sores (for example, under the arm if the sores are on the arm or hand).

What are the signs and symptoms of visceral leishmaniasis?

People who have visceral leishmaniasis usually have fever, weight loss, and an enlarged spleen and liver (usually the spleen is bigger than the liver). Some patients have swollen glands. Certain blood tests are abnormal. For example, patients usually have low blood counts, including a low red blood cell count (anemia), low white blood cell count, and low platelet count.

How common is leishmaniasis?

The number of new cases of cutaneous leishmaniasis each year in the world is thought to be about 1.5 million. The number of new cases of visceral leishmaniasis is thought to be about 500,000.

In what parts of the world is leishmaniasis found?

Leishmaniasis is found in parts of about 88 countries. Approximately 350 million people live in these areas. Most of the affected countries are in the tropics and subtropics. The settings in which leishmaniasis is found range from rain forests in Central and South America to deserts in West Asia. More than 90 percent of the world's cases of visceral leishmaniasis are in India, Bangladesh, Nepal, Sudan, and Brazil.

Leishmaniasis is found in some parts of the following areas:

  • in Mexico, Central America, and South America -- from northern Argentina to southern Texas (not in Uruguay, Chile, or Canada)
  • southern Europe (leishmaniasis is not common in travelers to southern Europe)
  • Asia (not Southeast Asia)
  • the Middle East
  • Africa (particularly East and North Africa, with some cases elsewhere)

Leishmaniasis is not found in Australia or Oceania (that is, islands in the Pacific, including Melanesia, Micronesia, and Polynesia).

Could I get leishmaniasis in the United States?

Probably not. It is possible but very unlikely that you would get leishmaniasis in the United States. Very rarely, people living in rural southern Texas have developed skin sores from cutaneous leishmaniasis.

No cases of visceral leishmaniasis are known to have been acquired in the United States.

How is leishmaniasis spread?

Leishmaniasis is spread by the bite of some types of phlebotomine sand flies. Sand flies become infected by biting an infected animal (for example, a rodent or dog) or person. Since sand flies do not make noise when they fly, people may not realize they are present. Sand flies are very small and may be hard to see; they are only about one-third the size of typical mosquitoes. Sand flies usually are most active in twilight, evening, and night-time hours (from dusk to dawn). Sand flies are less active during the hottest time of the day. However, they will bite if they are disturbed, such as when a person brushes up against the trunk of a tree where sand flies are resting. Rarely, leishmaniasis is spread from a pregnant woman to her baby. Leishmaniasis also can be spread by blood transfusions or contaminated needles.

Who is at risk for leishmaniasis?

People of all ages are at risk for leishmaniasis if they live or travel where leishmaniasis is found. Leishmaniasis usually is more common in rural than urban areas; but it is found in the outskirts of some cities. The risk for leishmaniasis is highest from dusk to dawn because this is when sand flies are the most active. All it takes to get infected is to be bitten by one infected sand fly. This is more likely to happen the more people are bitten, that is, the more time they spend outside in rural areas from dusk to dawn. Adventure travelers, Peace Corps volunteers, missionaries, ornithologists (people who study birds), other people who do research outdoors at night, and soldiers are examples of people who may have an increased risk for leishmaniasis (especially cutaneous leishmaniasis).

If I were bitten by an infected sand fly, how quickly would I become sick?

People with cutaneous leishmaniasis usually develop skin sores within a few weeks (sometimes as long as months) of when they were bitten.

People with visceral leishmaniasis usually become sick within several months (rarely as long as years) of when they were bitten.

Can leishmaniasis be a serious disease if not treated?

Yes, it can be. The skin sores of cutaneous leishmaniasis will heal on their own, but this can take months or even years. The sores can leave ugly scars. If not treated, infection that started in the skin rarely spreads to the nose or mouth and causes sores there (mucosal leishmaniasis). This can happen with some of the types of the parasite found in Central and South America. Mucosal leishmaniasis might not be noticed until years after the original skin sores healed. The best way to prevent mucosal leishmaniasis is to treat the cutaneous infection before it spreads.

If not treated, visceral leishmaniasis can cause death.

What should I do if I think I might have leishmaniasis?

See your health care provider, particularly if you have traveled to an area where leishmaniasis is found and you have developed skin sores that aren't healing. Be sure to tell your health care provider where you have traveled and that you might be at risk for leishmaniasis.

It is very rare for travelers to get visceral leishmaniasis.

How will my health care provider know if I have leishmaniasis?

The first step is to find out if you have traveled to a part of the world where leishmaniasis is found. Your health care provider will ask you about any signs or symptoms of leishmaniasis you may have, such as skin sores that have not healed. If you have skin sores, your health care provider will likely want to take some samples directly from the sores. These samples can be examined for the parasite under a microscope, in cultures, and through other means. A blood test for detecting antibody (immune response) to the parasite can be helpful, particularly for cases of visceral leishmaniasis. However, tests to look for the parasite itself should also be done. CDC staff can help with the laboratory testing. Diagnosing leishmaniasis can be difficult. Sometimes the laboratory tests are negative even if a person has leishmaniasis.

How is leishmaniasis treated?

Your health care provider can talk with CDC staff about whether your case of leishmaniasis should be treated, and, if so, how. Most people who have cutaneous leishmaniasis do not need to be hospitalized during their treatment.

How is leishmaniasis prevented?

The best way for travelers to prevent leishmaniasis is by protecting themselves from sand fly bites. Vaccines and drugs for preventing infection are not yet available. To decrease their risk of being bitten, travelers should:

  • Stay in well-screened or air-conditioned areas as much as possible. Avoid outdoor activities, especially from dusk to dawn, when sand flies are the most active.
  • When outside, wear long-sleeved shirts, long pants, and socks. Tuck your shirt into your pants.

  • Apply insect repellent on uncovered skin and under the ends of sleeves and pant legs. Follow the instructions on the label of the repellent. The most effective repellents are those that contain the chemical DEET (N,N-diethylmetatoluamide). The concentration of DEET varies among repellents. Repellents with DEET concentrations of 30-35% are quite effective, and the effect should last about 4 hours. Lower concentrations should be used for children (no more than 10% DEET). Repellents with DEET should be used sparingly on children from 2 to 6 years old and not at all on children less than 2 years old.

  • Spray clothing with permethrin-containing insecticides. The insecticide should be reapplied after every five washings.

  • Spray living and sleeping areas with an insecticide to kill insects.

  • If you are not sleeping in an area that is well screened or air-conditioned, use a bed net and tuck it under your mattress. If possible, use a bed net that has been soaked in or sprayed with permethrin. The permethrin will be effective for several months if the bed net is not washed. Keep in mind that sand flies are much smaller than mosquitoes and therefore can get through smaller holes. Fine-mesh netting (at least 18 holes to the inch; some sources say even finer) is needed for an effective barrier against sand flies. This is particularly important if the bed net has not been treated with permethrin. However, it may be uncomfortable to sleep under such a closely woven bed net when it is hot.

NOTE: Bed nets, repellents containing DEET, and permethrin should be purchased before traveling and can be found in hardware, camping, and military surplus stores.

If I have already had leishmaniasis, could I get it again?

Yes. Some people have had cutaneous leishmaniasis more than once. Therefore, you should follow the preventive measures listed above whenever you are in an area where leishmaniasis is found.

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What is lymphatic filariasis?

Lymphatic filariasis is a parasitic disease caused by microscopic, thread-like worms. The adult worms only live in the human lymph system. The lymph system maintains your body's fluid balance and fights infections.

Lymphatic filariasis affects over 120 million people in 80 countries throughout the tropics and sub-tropics of Asia, Africa, the Western Pacific, and parts of the Caribbean and South America. You cannot get the worms in the United States.

How does infection occur?

The disease spreads from person to person by mosquito bites. When a mosquito bites a person who has lymphatic filariasis, microscopic worms circulating in the person's blood enter and infect the mosquito. If the infected mosquito bites you, you can get lymphatic filariasis. The microscopic worms pass from the mosquito through your skin, and travel to your lymph vessels. In your lymph vessels they grow into adults. An adult worm lives for about 7 years. The adult worms mate and release millions of microscopic worms into your blood. Once you have the worms in your blood when a mosquito bites you, you can give the infection to others through mosquitoes.

Who is at risk for infection?

You need many mosquito bites over several months to years to get lymphatic filariasis. People living or staying for a long time in tropical or sub-tropical areas where the disease is common are at the greatest risk for infection. Short-term tourists have a very low risk. An infection will show up on a blood test.

What are the symptoms of lymphatic filariasis?

At first, most people don't know they have lymphatic filariasis. They usually don't feel any symptoms until after the adult worms die. The disease usually is not life threatening, but it can permanently damage your lymph system and kidneys. Because your lymph system does not work right, fluid collects and causes swelling in the arms, breasts legs, and, for men, the genital area. The name for this swelling is lymphedema (limf-ah-DE-ma). The entire leg, arm, or genital area may swell to several times its normal size. Also, the swelling and the decreased function of the lymph system make it difficult for your body to fight germs and infections. You will have more bacterial infections in your skin and lymph system. This causes hardening and thickening of the skin, which is called elephantiasis (el-ah-fan-TIE-ah-sis).

What is the impact of this disease?

Lymphatic filariasis is a leading cause of permanent and long-term disability worldwide. People with the disease can suffer pain, disfigurement, and sexual disability. Communities frequently shun women and men disfigured by the disease. Many women with visible signs of the disease will never marry, or their spouses and families will reject them. Affected people frequently are unable to work because of their disability. This hurts their families and their communities. Poor sanitation and rapid population growth in tropical and subtropical areas of the world, where the disease is common, has created more places for mosquitoes to breed and has led to more people becoming infected.

How can I prevent infection?

Prevention includes giving entire communities medicine that kills the microscopic worms and controlling mosquitoes. Avoiding mosquito bites is another form of prevention. The mosquitoes that carry the microscopic worms usually bite between the hours of dusk and dawn. If you live in an area with lymphatic filariasis:

  • Sleep under a mosquito net.
  • Use mosquito repellant on your exposed skin between dusk and dawn.
  • Take a yearly dose of medicine that kills the worms circulating in the blood. The medicine will kill all of the microscopic worms in the blood and some of the adult worms. It does not kill all of them.
What is the treatment for lymphatic filariasis?

If you have adult worms, you should take a yearly dose of medicine that kills the microscopic worms circulating in your blood. While this does not kill the adult worms, it does prevent you from giving the disease to someone else. Even after the adult worms die, you can have swelling of your arms, legs, breasts, or genitals. You can keep the swelling from getting worse.

  • Carefully wash the swollen area with soap and water every day.
  • Use anti-bacterial cream on any wounds. This stops bacterial infections and keeps the swelling from worsening.
  • Elevate and exercise the swollen arm or leg to move the fluid and improve the lymph flow.

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What is Chagas disease?

Also called American trypanosomiasis , Chagas disease is an infection caused by the parasite Trypanosoma cruzi. It is estimated that 16-18 million people are infected with Chagas disease; of those infected, 50,000 will die each year.

How is Chagas disease spread?

Reduviid bugs, or "kissing bugs" live in cracks and holes of substandard housing primarily found in South and Central America. Insects become infected after biting an animal or person who already has Chagas disease. Infection is spread to humans when an infected bug deposits feces on a person's skin, usually while the person is sleeping at night. The person often accidently rubs the feces into the bite wound, an open cut, the eyes, or mouth. Animals can become infected the same way, and they can also contract the disease by eating an infected bug.

How can I become infected?
  • By infective feces contacting your eyes, mouth, or open cuts.
  • By infected mothers passing infection to their baby during pregnancy, at delivery, or while breastfeeding.
  • By blood transfusion or organ transplant.
  • By eating uncooked food contaminated with infective feces of "kissing bugs."
Is Chagas disease a serious illness?

Yes. Chagas disease primarily affects low income people living in rural areas. Many people get the infection during childhood. The early stage of infection (acute Chagas disease) usually is not severe, but sometimes it can cause death, particularly in infants. However, in about one-third of those who get the infection, chronic symptoms develop after 10-20 years. For these persons who develop chronic symptoms, the average life expectancy decreases by an average of 9 years.

What are the symptoms of Chagas disease?

There are three stages of infection with Chagas disease; each stage has different symptoms. Some persons may be infected and never develop symptoms.

Acute:

Acute symptoms only occur in about 1% of cases. Most people infected do not seek medical attention. The most recognized symptom of acute Chagas infection is the Romaña's sign, or swelling of the eye on one side of the face, usually at the bite wound or where feces were rubbed into the eye. Other symptoms are usually not specific for Chagas infection. These symptoms may include fatigue, fever, enlarged liver or spleen, and swollen lymph glands. Sometimes, a rash, loss of appetite, diarrhea, and vomiting occur. In infants and in very young children with acute Chagas disease, swelling of the brain can develop in acute Chagas disease, and this can cause death. In general, symptoms last for 4-8 weeks and then they go away, even without treatment.

Indeterminate:

Eight to 10 weeks after infection, the indeterminate stage begins. During this stage, people do not have symptoms.

Chronic:

Ten to 20 years after infection, people may develop the most serious symptoms of Chagas disease. Cardiac problems, including an enlarged heart, altered heart rate or rhythm, heart failure, or cardiac arrest are symptoms of chronic disease. Chagas disease can also lead to enlargement of parts of the digestive tract, which result in severe constipation or problems with swallowing. In persons who are immune compromised, including persons with HIV/AIDS, Chagas disease can be severe. Not everyone will develop the chronic symptoms of Chagas disease.

How soon after infection will I have symptoms of Chagas disease?

Symptoms may occur within a few days to weeks. Most people do not have symptoms until the chronic stage of infection, 10-20 years after first being infected.

Can I take medication to prevent Chagas disease?

No. There is neither a vaccine nor recommended drug available to prevent Chagas disease.

What should I do if I think I have Chagas disease?

See your health care provider who will order blood tests to look for the parasite or for antibodies in your blood.

What is the treatment for Chagas disease?

Medication for Chagas disease is usually effective when given during the acute stage of infection. Once the disease has progressed to later stages, medication may be less effective. In the chronic stage, treatment involves managing symptoms associated with the disease.

Where can I contract Chagas disease?

Chagas disease is locally transmitted in Argentina, Belize, Bolivia, Brazil, Chile, Colombia, Costa Rica, Ecuador, El Salvador, French Guiana, Guatemala, Guyana, Honduras, Mexico, Nicaragua, Panama, Paraguay, Peru, Suriname, Uruguay, and Venezuela.

Who is at risk for Chagas disease?

Those people who sleep in poorly constructed houses found in the rural areas of the above-mentioned countries are at elevated risk of infection. Houses constructed from mud, adobe, or thatch present the greatest risk.

Travelers planning to stay in hotels, resorts, or other well-constructed housing facilities are NOT at high risk for contracting Chagas disease from reduviid bugs.

How can I prevent Chagas disease?
  • Avoid sleeping in thatch, mud, or adobe houses.
  • Use insecticides to kill insects and reduce the risk of transmission.
  • Be aware that, in some countries, the blood supply may not always be screened for Chagas disease, and blood transfusions may carry a risk of infection.

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What is East African trypanosomiasis?

There are two types of African trypanosomiasis (also called sleeping sickness); each is named for the region of Africa in which they are found. The disease is caused by a parasite named Trypanosoma brucei rhodesiense (tri-PAN-o-SO-ma BREW-see-eye rho-DEE-see-ense), carried by the tsetse fly. Worldwide, approximately 40,000 new cases of both East and West African trypanosomiasis are reported to the World Health Organization each year. However, the majority of cases are not reported due to a lack of infrastructure and it is likely that there are more than 100,000 new cases annually. Since 1967, twenty-one cases of East African trypanosomiasis have been reported within the United States, all among individuals who had traveled to Africa. (See also West African trypanosomiasis.)

How is East African trypanosomiasis spread?

An individual will get East African trypanosomiasis if they are bitten by a tsetse fly infected with the Trypanosoma brucei rhodesiense parasite. The tsetse fly is common only to Africa.

Is East African trypanosomiasis a serious illness?

Yes. If a person fails to receive medical treatment for East African trypanosomiasis, death will occur within several weeks to months.

Where can you become infected with East African trypanosomiasis?

East African trypanosomiasis is found in parts of Eastern and Central Africa, including Uganda, Kenya, Tanzania, Malawi, Ethiopia, Zaire, Zimbabwe, and Botswana. Areas where infection is spread are largely determined by the location of the infected tsetse fly and wild animal population.

What are the symptoms of East African trypanosomiasis?

A bite by the tsetse fly is often painful and can develop into a red sore, also called a chancre (SHAN-ker). Fever, severe headaches, irritability, extreme fatigue, swollen lymph nodes, and aching muscles and joints are common symptoms of sleeping sickness. Some people develop a skin rash. Progressive confusion, personality changes, slurred speech, seizures, and difficulty in walking and talking occur when infection has invaded the central nervous system. If left untreated, infection becomes worse and death will occur within several weeks or months.

How soon after infection will I have symptoms of East African trypanosomiasis?

Symptoms begin within 1 to 4 weeks of getting an infected tsetse fly bite.

What should I do if I think I may have African trypanosomiasis?

If you suspect that you may have East African trypanosomiasis, immediately consult with your health care provider who will order several tests to look for the parasite. Common tests include blood samples, a spinal tap, and skin biopsies, especially if you have a chancre.

What is the treatment for East African trypanosomiasis?

Medical treatment of East African trypanosomiasis should begin as soon as possible and is based on the infected person’s symptoms and laboratory results. Medication for the treatment of East African trypanosomiasis is available through the CDC. Hospitalization for treatment is necessary. Periodic follow-up exams that include a spinal tap are required for 2 years.

Once infected, am I immune to East African trypanosomiasis?

No one is immune from East African trypanosomiasis. Even if you had the disease once, you can get re-infected.

Who is at risk for contracting East African trypanosomiasis?

East African trypanosomiasis is usually found in woodland and savannah areas away from human habitation. Tourists, hunters, game wardens, and other persons working or visiting game parks in East and Central Africa are at greatest risk for illness.

Can I take a medication to prevent East African trypanosomiasis?

There is neither a vaccine nor recommended drug available to prevent East African trypanosomiasis.

How can I prevent African trypanosomiasis and prevent other insect bites?

  1. Wear protective clothing, including long-sleeved shirts and pants. The tsetse fly can bite through thin fabrics, so clothing should be made of thick material.

  2. Wear khaki or olive colored clothing. The tsetse fly is attracted to bright colors and very dark colors.

  3. Use insect repellant. Though insect repellants have not proven effective in preventing tsetse fly bites, they are effective in preventing other insects from biting and causing illness.

  4. Use bed netting when sleeping.

  5. Inspect vehicles for tsetse flies before entering.

  6. Do not ride in the back of jeeps, pickup trucks or other open vehicles. The tsetse fly is attracted to the dust that moving vehicles and wild animals create.

  7. Avoid bushes. The tsetse fly is less active during the hottest period of the day. It rests in bushes but will bite if disturbed.

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What is West African trypanosomiasis?

There are two types of African trypanosomiasis (also called sleeping sickness); each named for the region of Africa in which it is found. Individuals can become infected with West African trypanosomiasis if they receive a bite from an infected tsetse fly, found only in Africa.West African trypanosomiasis, also called Gambian sleeping sickness, is caused by a parasite called Trypanosoma brucei gambiense (tri-PAN-o-SO-ma BREW-see-eye GAM-be-ense) carried by the tsetse fly. Worldwide, approximately 40,000 new cases of both East and West African trypanosomiasis are reported to the World Health Organization each year. However, the majority of cases are not reported due to a lack of infrastructure and it is likely that there are more than 100,000 new cases annually. Few cases of West African trypanosomiasis have been reported in the United States.

How can I get West African trypanosomiasis?

An individual gets West African trypanosomiasis through the bite of an infected tsetse fly, found only in Africa.  On rare occasions, a pregnant woman may pass the infection to her baby, or an individual may become infected through a blood transfusion or organ transplant.

Is West African trypanosomiasis a serious illness?

Yes.  West African trypanosomiasis is fatal if it is not treated.

Where can I contract West African trypanosomiasis?

West African trypanosomiasis can be contracted in parts of Western and Central Africa. The tsetse fly lives only in Africa; areas where infection is spread are largely determined by where the infected tsetse fly is found.

What are the symptoms of West African trypanosomiasis?

A bite by the tsetse fly is often painful.  Occasionally, within 1 to 2 weeks, the infective bite develops into a red sore, also called a chancre (SHAN-ker). Several weeks to months later, other symptoms of sleeping sickness occur. These include fever, rash, swelling around the eye and hands, severe headaches, extreme fatigue, aching muscles and joints. You may develop swollen lymph nodes on the back of your neck called Winterbottom's sign. Weight loss occurs as the illness progresses. Progressive confusion, personality changes, slurred speech, irritability, loss of concentration, seizures, and difficulty in walking and talking occurs when infection has invaded the central nervous system. These symptoms become worse as the illness progresses. Sleeping for long periods of the day and having insomnia at night is a common symptom. If left untreated, infection becomes worse and death will occur within several months to years after infection.

How soon after infection will I have symptoms of West African trypanosomiasis?

Symptoms occur within months to years after getting an infected tsetse fly bite.

What should I do if I think I have African trypanosomiasis?

If you suspect that you may have West African trypanosomiasis, see your health care provider who will order several tests to look for the parasite. Common tests include blood samples and a spinal tap. Your physician may also take a sample of fluid from swollen lymph nodes.

Is treatment available for West African trypanosomiasis?

Medication for the treatment of West African trypanosomiasis is available. Hospitalized treatment of West African trypanosomiasis should begin as soon as possible and is based on the infected person’s symptoms and laboratory results. Hospitalization for treatment is necessary.  Periodic follow-up exams that include a spinal tap are required for 2 years.

Who is at risk for contracting West African trypanosomiasis?

Tsetse flies can be found in Western and Central African forests, in areas of thick shrubbery and trees by rivers and waterholes. Risk of infection increases with the number of times a person is bitten by the tsetse fly. Therefore, tourists are not at great risk for contracting West African trypanosomiasis unless they are traveling and spending long periods of time in rural areas of Western and Central Africa.

Can I take medication to prevent West African trypanosomiasis?

There is neither a vaccine nor recommended drug available to prevent West African trypanosomiasis.

How can I prevent African trypanosomiasis and other insect bites?

  1. Wear protective clothing, including long-sleeved shirts and pants. The tsetse fly can bite through thin fabrics, so clothing should be made of thick material.

  2. Wear khaki or olive colored clothing. The tsetse fly is attracted to bright colors and very dark colors.

  3. Use insect repellant. Though insect repellants have not proven effective in preventing tsetse fly bites, they are effective in preventing other insects from biting and causing illness.

  4. Use bed netting when sleeping.

  5. Inspect vehicles for tsetse flies before entering.

  6. Do not ride in the back of jeeps, pickup trucks or other open vehicles. The tsetse fly is attracted to the dust that moving vehicles and wild animals create.

  7. Avoid bushes. The tsetse fly is less active during the hottest period of the day. It rests in bushes but will bite if disturbed.

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Introduction To West Nile Virus Exposure

Disease:

The West Nile virus (WNV) is spread by mosquitoes to birds and other animals through a mosquito bite. The virus normally passes between mosquitoes and birds. However, people may also be infected if they are bitten by a WNV-infected mosquito.

The most likely route of WNV infection to humans is through the bite of an infected mosquito. In addition, WNV may be spread through organ transplantation, blood transfusion, or possibly breast milk. Transplacental (mother-to-fetus) infection has occurred. Workers are at risk of WNV infection if their skin is penetrated or cut while handling WNV-infected tissues. Turkey breeder farm workers have been infected with WNV. The mode of transmission to these farm workers is uncertain.

Most human infections cause either mild flu-like symptoms or no symptoms at all. Mild symptoms may include fever, fatigue, headache, and muscle or joint pain. Although rare, some people may become severely ill. Severe symptoms may include high fever, stiff neck, disorientation, tremors, muscle weakness, and paralysis. Severely affected persons may develop encephalitis, meningitis, or meningoencephalitis—inflammation of the brain, membranes of the brain or spinal cord, or both, respectively. Severe cases of WNV may be fatal. Persons over the age of 50 are at higher risk of severe illness.

History: From 1999 to 2001 in the United States, 149 cases of illness and 18 deaths due to WNV were reported in humans. In 2002, more than 4,100 cases of WNV in humans and 280 deaths due to WNV were reported by State health departments to the Centers for Disease Control and Prevention (CDC). In 2003, more than 9800 cases and 264 deaths were reported.

Location: WNV is commonly found in Africa, West Asia, and the Middle East. It was first reported in the Uited States in New York State in 1999. The geographic range of WNV has expanded annually. In 2003 it was reported in most of the continental United States.

Occupational Risk Occupational exposure to WNV is possible. Workers at risk of WNV exposure include those working outdoors when mosquitoes are actively biting—farmers, foresters, landscapers, groundskeepers and gardeners, painters, roofers, pavers, construction workers, laborers, mechanics, and other outdoor workers. Turkey breeder farm workers have been infected with WNV. The mode of transmission to these farm workers is uncertain. Laboratory workers who handle WNV-infected tissue and fluids are also at risk of WNV infection if skin penetration or laceration occurs.

Occupational groups at risk should receive training that describes and reinforces the potential occupational hazards and risks of WNV exposure and infection. The importance of timely reporting of all injuries and illnesses of suspected occupational origin should be emphasized. A medical surveillance system should be in place which includes the reporting of symptoms consistent with WNV infection and employee absenteeism.

Frequently Asked Questions

Who Is At Risk Of WNV Exposure?

Anyone who lives or works in an area where there are WNV-infected mosquitoes is at risk of WNV infection. Persons over 50 years of age have the highest risk of severe disease due to WNV infection. Even though older workers may be at higher risk, all workers should be careful to follow the recommendations listed below.

Which Outdoor Workers Are At Risk Of WNV Exposure?

Workers at risk of WNV exposure include those working outdoors when mosquitoes are actively biting—farmers, foresters, landscapers, groundskeepers and gardeners, painters, roofers, pavers, construction workers, laborers, mechanics, and other outdoor workers. Many mosquitoes are most active from dusk to dawn. However, some mosquitoes are active during the day. When possible, avoid working outdoors during mosquitoes’ peak activity times.

Is a Woman's Pregnancy at Risk if She is Infected With WNV?

There is one documented case of transplacental (mother-to-fetus) transmission of WNV in humans. The newborn in this case was infected with WNV at birth and had severe medical problems. It is unknown whether the WNV infection itself caused these problems. More research is needed to understand the possible effects of WNV on pregnancy.

Pregnant women should take precautions to reduce their risk for WNV infection by avoiding mosquitoes, wearing protective clothing and using repellents containing DEET according to manufacturers' directions. Pregnant women who become ill should see their health care provider.

Where Are Mosquitoes Most Commonly Found?

Mosquitoes develop in any standing body of water that persists for more than four days. Stagnant pools, ponds, watering troughs, irrigation ditches, rain barrels, manure lagoons, and other stagnant bodies of water increase mosquito populations. Weedy, bushy, and wooded work environments may also have large mosquito populations. Workers in these environments should protect themselves from mosquito bites.

When Are Mosquitoes Most Active?

Many mosquitoes are most active from dusk to dawn. However, some mosquitoes are also active during the day. When possible, avoid working outdoors during mosquitoes’ peak activity times. When this is unavoidable, use personal protection such as protective clothing and insect repellent to reduce the potential for exposure.

How Can I Be Protected From WNV Exposure?

Recommendations for Employers

Whether controls such as local mosquito control programs are in place, employers should protect their workers by implementing the following controls:

  • Avoid having workers outdoors when mosquitoes are most active and biting, most often from dusk to dawn.

  • Make insect repellents available to workers.

  • Recommend that outdoor workers wear long-sleeved shirts, long pants, and socks when possible.
    • If employee uniforms are provided include long-sleeved shirts and long pants among uniform options.
  • Eliminate as many sources of standing water as possible to decrease mosquito populations. Water that persists for more than four days provides a site for mosquitoes to develop.
    • Change the water twice a week in animal drinking troughs, birdbaths, and other water containers.
    • Add an aerator to ponds and water gardens to keep the water circulating or add fish that will eat the mosquito larvae or adults.
    • Remove discarded tires from the worksite.
    • Turn over, cover, or remove equipment such as tarps, buckets, barrels, wheel barrows, and containers to avoid water accumulation.
    • Place drain holes in containers that collect water and cannot be discarded.
    • Clean out rain gutters.
    • Remove debris—leaves, twigs, trash—from ditches frequently.
    • Fill in or drain ruts and other areas that accumulate water.

Recommendations for Workers

Outdoor workers can reduce their risk of WNV exposure by taking the following action steps:

  • Insect Repellent
    • Apply insect repellent to exposed skin.
    • Carefully follow label directions for repellent use.
    • Do not apply pump or aerosol products directly to the face. These products should be sprayed onto the hands and then carefully rubbed over the face, avoiding the eyes and mouth.
    • Use repellents at the lowest effective concentrations.
    • The most effective insect repellents contain DEET (N,N-diethyl-m-toluamide or N,N-diethyl-3-methylbenzamide).
      • The more DEET a repellent contains the longer it will protect against mosquito bites.
      • DEET concentrations higher than 50% do not increase its length of protection.
    • Wash skin treated with insect repellent with soap and water after returning indoors.
  • Clothing
    • Wear long-sleeved shirts, long pants, and socks when working outdoors.
    • Spray clothing with products containing DEET or permethrin, as mosquitoes may penetrate thin clothing.
      • Permethrin should only be used on clothing; do not apply it directly to skin.
    • Wash clothing treated with insect repellent before wearing it again.
    • Do not apply repellent to skin that is under clothing.


What Should I Do If I Have To Handle Dead Animals?

Anyone handling dead animals should wear gloves. Appropriate gloves provide a protective barrier that prevents blood and other body fluids from passing through them. Medical examination gloves are recommended. Cotton, leather, and other absorbent glove materials are not protective. If latex gloves are used they should be reduced protein, powder-free gloves to reduce workers' exposure to allergy-causing proteins.

What Should I Do If I Develop Symptoms Of WNV?

Any worker who develops mild symptoms of WNV such as fever, fatigue, headache, and muscle or joint pain or severe symptoms such as high fever, stiff neck, disorientation, tremors, muscle weakness, and paralysis should contact their health care provider immediately. If the worker is at risk of WNV infection, a biological sample may be tested for infection. The period from the infected bite to developing symptoms is reported to be 3 to 14 days.

Is There Treatment Available If I Am Infected With WNV?

No specific treatment exists for WNV infection. Treatment consists of supportive care to treat the symptoms. Currently, no approved vaccine exists to prevent WNV infection in humans.

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What is Plague

Plague, caused by a bacterium called Yersinia pestis, is transmitted from rodent to rodent by infected fleas.

Plague is characterized by periodic disease outbreaks in rodent populations, some of which have a high death rate. During these outbreaks, hungry infected fleas that have lost their normal hosts seek other sources of blood, thus increasing the increased risk to humans and other animals frequenting the area.

Epidemics of plague in humans usually involve house rats and their fleas. Rat-borne epidemics continue to occur in some developing countries, particularly in rural areas. The last rat-borne epidemic in the United States occurred in Los Angeles in 1924-25. Since then, all human plague cases in the U.S. have been sporadic cases acquired from wild rodents or their fleas or from direct contact with plague-infected animals.

Rock squirrels and their fleas are the most frequent sources of human infection in the southwestern states. For the Pacific states, the California ground squirrel and its fleas are the most common source. Many other rodent species, for instance, prairie dogs, wood rats, chipmunks, and other ground squirrels and their fleas, suffer plague outbreaks and some of these occasionally serve as sources of human infection. Deer mice and voles are thought to maintain the disease in animal populations but are less important as sources of human infection. Other less frequent sources of infection include wild rabbits, and wild carnivores that pick up their infections from wild rodent outbreaks. Domestic cats (and sometimes dogs) are readily infected by fleas or from eating infected wild rodents. Cats may serve as a source of infection to persons exposed to them. Pets may also bring plague-infected fleas into the home.

Between outbreaks, the plague bacterium is believed to circulate within populations of certain species of rodents without causing excessive mortality. Such groups of infected animals serve as silent, long-term reservoirs of infection.

Geographic Distribution of Plague

In the United States during the 1980s plague cases averaged about 18 per year. Most of the cases occurred in persons under 20 years of age. About 1 in 7 persons with plague died.

Worldwide, there are 1,000 to 2,000 cases each year. During the 1980s epidemic plague occurred each year in Africa, Asia, or South America. Epidemic plague is generally associated with domestic rats. Almost all of the cases reported during the decade were rural and occurred among people living in small towns and villages or agricultural areas rather than in larger, more developed, towns and cities.

The following information provides a worldwide distribution pattern:

  • There is no plague in Australia.

  • There is no plague in Europe; the last reported cases occurred after World War II.

  • In Asia and extreme southeastern Europe, plague is distributed from the Caucasus Mountains in Russia, through much of the Middle East, eastward through China, and then southward to Southwest and Southeast Asia, where it occurs in scattered, localized foci. Within these plague foci, there are isolated human cases and occasional outbreaks. Plague regularly occurs in Madagascar, off the southeastern coast of Africa.

  • In Africa, plague foci are distributed from Uganda south on the eastern side of the continent, and in southern Africa. Severe outbreaks have occurred in recent years in Kenya, Tanzania, Zaire, Mozambique, and Botswana, with smaller outbreaks in other East African countries. Plague also has been reported in scattered foci in western and northern Africa.

  • In North America, plague is found from the Pacific Coast eastward to the western Great Plains and from British Columbia and Alberta, Canada southward to Mexico. Most of the human cases occur in two regions; one in northern New Mexico, northern Arizona, and southern Colorado, another in California, southern Oregon, and far western Nevada.

  • In South America, active plague foci exist in two regions; the Andean mountain region (including parts of Bolivia, Peru, and Ecuador) and in Brazil.

How Is Plague Transmitted?

Plague is transmitted from animal to animal and from animal to human by the bites of infective fleas. Less frequently, the organism enters through a break in the skin by direct contact with tissue or body fluids of a plague-infected animal, for instance, in the process of skinning a rabbit or other animal. Plague is also transmitted by inhaling infected droplets expelled by coughing, by a person or animal, especially domestic cats, with pneumonic plague. Transmission of plague from person to person is uncommon and has not been observed in the United States since 1924 but does occur as an important factor in plague epidemics in some developing countries.

Diagnosis

The pathognomic sign of plague is a very painful, usually swollen, and often hot-to-the touch lymph node, called a bubo. This finding, accompanied with fever, extreme exhaustion, and a history of possible exposure to rodents, rodent fleas, wild rabbits, or sick or dead carnivores should lead to suspicion of plague.

Onset of bubonic plague is usually 2 to 6 days after a person is exposed. Initial manifestations include fever, headache, and general illness, followed by the development of painful, swollen regional lymph nodes. Occasionally, buboes cannot be detected for a day or so after the onset of other symptoms. The disease progresses rapidly and the bacteria can invade the bloodstream, producing severe illness, called plague septicemia.

Once a human is infected, a progressive and potentially fatal illness generally results unless specific antibiotic therapy is given. Progression leads to blood infection and, finally, to lung infection. The infection of the lung is termed plague pneumonia, and it can be transmitted to others through the expulsion of infective respiratory droplets by coughing.

The incubation period of primary pneumonic plague is 1 to 3 days and is characterized by development of an overwhelming pneumonia with high fever, cough, bloody sputum, and chills. For plague pneumonia patients, the death rate is over 50%.

Treatment Information

As soon as a diagnosis of suspected plague is made, the patient should be isolated, and local and state health departments should be notified. Confirmatory laboratory work should be initiated, including blood cultures and examination of lymph node specimens if possible. Drug therapy should begin as soon as possible after the laboratory specimens are taken. The drugs of choice are streptomycin or gentamycin, but a number of other antibiotics are also effective.

Those individuals closely associated with the patient, particularly in cases with pneumonia, should be traced, identified, and evaluated. Contacts of pneumonic plague patients should be placed under observation or given preventive antibiotic therapy, depending on the degree and timing of contact.

It is a U.S. Public Health Service requirement that all suspected plague cases be reported to local and state health departments and the diagnosis confirmed by the CDC. As required by the International Health Regulations, CDC reports all U.S. plague cases to the World Health Organization.

Prevention

Plague will probably continue to exist in its many localized geographic areas around the world, and plague outbreaks in wild rodent hosts will continue to occur. Attempts to eliminate wild rodent plague are costly and futile. Therefore, primary preventive measures are directed toward reducing the threat of infection in humans in high risk areas through three techniques -- environmental management, public health education, and preventive drug therapy.

Environmental Management

Epidemic plague is best prevented by controlling rat populations in both urban and rural areas. This goal has been reached in the cities, towns, and villages of most developed countries. It has not been achieved in either the rural or urban areas of many developing countries where the threat of epidemic plague continues to exist. Control of plague in such situations requires two things: 1) close surveillance for human plague cases, and for plague in rodents, and 2) the use of an effective insecticide to control rodent fleas when human plague cases and rodent outbreaks occur.

Public Health Education

In regions such as the American West where plague is widespread in wild rodents, the greatest threat is to people living, working, or playing in areas where the infection is active. Public health education of citizens and the medical community should include information on the following plague prevention measures:

  • Eliminating food and shelter for rodents in and around homes, work places, and recreation areas by making buildings rodent-proof, and by removing brush, rock piles, junk, and food sources (such as pet food), from properties.

  • Surveillance for plague activity in rodent populations by public health workers or by citizens reporting rodents found sick or dead to local health departments.

  • Use of appropriate and licensed insecticides to kill fleas during wild animal plague outbreaks to reduce the risk to humans.

  • Treatment of pets (dogs and cats) for flea control once each week.

Preventive Drug Therapy

Antibiotics may be taken in the event of exposure to the bites of wild rodent fleas during an outbreak or to the tissues or fluids of a plague-infected animal. Preventive therapy is also recommended in the event of close exposure to another person or to a pet animal with suspected plague pneumonia. For preventive drug therapy, the preferred antibiotics are the tetracyclines, chloramphenicol, or one of the effective sulfonamides.

Vaccines

The plague vaccine is no longer commercially available in the United States.

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What is Rocky Mountain spotted fever?

Rocky Mountain spotted fever (RMSF) is the most severe tick-borne rickettsial illness in the United States. This disease is caused by infection with the bacterial organism Rickettsia rickettsii.

How do people get Rocky Mountain spotted fever?

The organism that causes Rocky Mountain spotted fever is transmitted by the bite of an infected tick. The American dog tick (Dermacentor variabilis) and Rocky Mountain wood tick (Dermacentor andersoni) are the primary vectors of Rocky Mountain spotted fever bacteria in the United States.

What are the symptoms of Rocky Mountain spotted fever?

Patients infected with R. rickettsii usually visit a physician in their first week of illness, following an incubation period of about 5-10 days after a tick bite. The early clinical presentation of Rocky Mountain spotted fever is often nonspecific and may resemble many other infectious and non-infectious diseases. Initial symptoms may include fever, nausea, vomiting, muscle pain, lack of appetite and severe headache.  Later signs and symptoms include rash, abdominal pain, joint pain, and diarrhea. Three important components of the clinical presentation are fever, rash, and a previous tick bite, although one or more of these components may not be present when the patient is first seen for medical care. Rocky Mountain spotted fever can be a severe illness, and the majority of patients are hospitalized.

In the United States, where do most cases of Rocky Mountain spotted fever occur?

Rocky Mountain spotted fever is a seasonal disease and occurs throughout the United States during the months of April through September. Over half of the cases occur in the south-Atlantic region of the United States (Delaware, Maryland, Washington D.C., Virginia, West Virginia, North Carolina, South Carolina, Georgia, and Florida). The highest incidence rates have been found in North Carolina and Oklahoma. Although this disease was reported most frequently in the Rocky Mountain area early after its discovery, relatively few cases are reported from that area today.

How is Rocky Mountain spotted fever diagnosed?

A diagnosis of Rocky Mountain spotted fever is based on a combination of clinical signs and symptoms and specialized confirmatory laboratory tests.  Other common laboratory findings suggestive of Rocky Mountain spotted fever include thrombocytopenia, hyponatremia, and elevated liver enzyme levels.

How is Rocky Mountain spotted fever treated?

Rocky Mountain spotted fever is best treated by using a tetracycline antibiotic, usually doxycycline. This medication should be given in doses of 100 mg every 12 hours for adults or 4 mg/kg body weight  per day in two divided doses for children under 45 kg (100 lbs). Patients are treated for at least 3 days after the fever subsides and until there is unequivocal evidence of clinical improvement.  Standard duration of treatment is 5 to 10 days.

Can a person get Rocky Mountain spotted fever more than once?

Infection with R. rickettsii is thought to provide long lasting immunity against re-infection.  However, prior illness with Rocky Mountain spotted fever should not deter persons from practicing good tick-preventive measures or visiting a physician if signs and symptoms consistent with Rocky Mountain spotted fever occur, especially following a tick bite.

How can Rocky Mountain spotted fever be prevented?

Limiting exposure to ticks reduces the likelihood of Rocky Mountain spotted fever infection. In persons exposed to tick-infested habitats, prompt careful inspection and removal of crawling or attached ticks is an important method of preventing disease. It may take several hours of attachment before organisms are transmitted from the tick to the host.

It is unreasonable to assume that a person can completely eliminate activities that may result in tick exposure. Therefore, prevention measures should be aimed at personal protection:

  • Wear light-colored clothing to allow you to see ticks that are crawling on your clothing.

  • Tuck your pants legs into your socks so that ticks cannot crawl up the inside of your pants legs.

  • Apply repellants to discourage tick attachment. Repellents containing permethrin can be sprayed on boots and clothing, and will last for several days. Repellents containing DEET (n, n-diethyl-m-toluamide) can be applied to the skin, but will last only a few hours before reapplication is necessary. Use DEET with caution on children.  Application of large amounts of DEET on children has been associated with adverse reactions.

  • Conduct a body check upon return from potentially tick-infested areas by searching your entire body for ticks. Use a hand-held or full-length mirror to view all parts of your body. Remove any tick you find on your body.

  • Parents should check their children for ticks, especially in the hair, when returning from potentially tick-infested areas.  Additionally, ticks may be carried into the household on clothing and pets.  Both should be examined carefully.

What is the best way to remove a tick?

To remove attached ticks, use the following procedure:

  1. Use fine-tipped tweezers or shield your fingers with a tissue, paper towel, or rubber gloves .  When possible, persons should avoid removing ticks with bare hands. 
  2. Grasp the tick as close to the skin surface as possible and pull upward with steady, even pressure . Do not twist or jerk the tick; this may cause the mouthparts to break off and remain in the skin. (If this happens, remove mouthparts with tweezers.  Consult your health care provider if infection occurs.)
  3. Do not squeeze, crush, or puncture the body of the tick because its fluids (saliva, body fluids, gut contents) may contain infectious organisms.
  4. After removing the tick, thoroughly disinfect the bite site and wash your hands with soap and water.
  5. Save the tick for identification in case you become ill. This may help your doctor make an accurate diagnosis. Place the tick in a plastic bag and put it in your freezer. Write the date of the bite on a piece of paper with a pencil and place it in the bag.

Folklore Remedies Don't Work!

Folklore remedies, such as the use of petroleum jelly or hot matches, do little to encourage a tick to detach from skin. In fact, they may make matters worse by irritating the tick and stimulating it to release additional saliva or regurgitate gut contents, increasing the chances of transmitting the pathogen. These methods of tick removal should be avoided.  A number of tick removal devices have been marketed, but none are better than a plain set of fine tipped tweezers.

How can ticks be controlled?

Strategies to reduce vector tick densities through area-wide application of acaricides (chemicals that will kill ticks and mites) and control of tick habitats (e.g., leaf litter and brush) have been effective in small-scale trials. New methods being developed include applying acaricides to rodents by using baited tubes, boxes, and feeding stations in areas where these pathogens are endemic. Biological control with fungi, parasitic nematodes, and parasitic wasps may play alternate roles in integrated tick control efforts. Community-based integrated tick management strategies may prove to be an effective public health response to reduce the incidence of tick-borne infections. However, limiting exposure to ticks is presently the most effective method of prevention.

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What is ehrlichiosis?


Ehrlichiosis is the general name used to describe several bacterial diseases that affect animals and humans. These diseases are caused by the organisms in the genus Ehrlichia. Worldwide, there are currently four ehrlichial species that are known to cause disease in humans.

How do people get ehrlichiosis?
In the United States, ehrlichiae are transmitted by the bite of an infected tick. The lone star tick (Amblyomma americanum), the blacklegged tick (Ixodes scapularis), and the western blacklegged tick (Ixodes pacificus) are known vectors of ehrlichiosis in the United States. Ixodes ricinus is the primary vector in Europe.

What are the symptoms of ehrlichiosis?
The symptoms of ehrlichiosis may resemble symptoms of various other infectious and non-infectious diseases. These clinical features generally include fever, headache, fatigue, and muscle aches. Other signs and symptoms may include nausea, vomiting, diarrhea, cough, joint pains, confusion, and occasionally rash. Symptoms typically appear after an incubation period of 5-10 days following the tick bite. It is possible that many individuals who become infected with ehrlichiae do not become ill or  they develop only very mild symptoms.

In the United States, where do most cases of ehrlichiosis occur?
Most cases of ehrlichiosis are reported within the geographic distribution of the vector ticks. Occasionally, cases are reported from areas outside the distribution of the tick vector. In most instances, these cases have involved persons who traveled to areas where the diseases are endemic, and who had been bitten by an infected tick and developed symptoms after returning home. Therefore, if you traveled to an ehrlichiosis-endemic area 2 weeks prior to becoming ill, you should tell your doctor where you traveled.

How is ehrlichiosis diagnosed?
A diagnosis of ehrlichiosis is based on a combination of clinical signs and symptoms and confirmatory laboratory tests. Your doctor can send your blood sample to a reference laboratory for testing. However, the availability of the different types of laboratory tests varies considerably. Other laboratory findings indicative of ehrlichiosis include low white blood cell count, low platelet count, and elevated liver enzymes.

How is ehrlichiosis treated?
Ehrlichiosis is treated with a tetracycline antibiotic, usually doxycycline.

Can a person get ehrlichiosis more than once?
Very little is known about immunity to ehrlichial infections. Although it has been proposed that infection with ehrlichiae confers long-term protection against reinfection, there have been occassional reports of laboratory-confirmed reinfection. Short-term protection has been described in animals infected with some Ehrlichia species and this protection wanes after about 1 year. Clearly, more studies are needed to determine the extent and duration of protection against reinfection in humans.

How can ehrlichiosis be prevented?
Limiting exposure to ticks reduces the likelihood of infection in persons exposed to tick-infested habitats.  Prompt careful inspection of your body and removal of crawling or attached ticks is an important method of preventing disease. It may take 24–48 hours of attachment before microorganisms are transmitted from the tick to you.

It is unreasonable to assume that a person can completely eliminate activities that may result in tick exposure. Therefore, prevention measures should be aimed at personal protection:

  • Wear light-colored clothing-- this will allow you to see ticks that are crawling on your clothing.

  • Tuck your pants legs into your socks so that ticks cannot crawl up the inside of your pants legs.

  • Apply repellants to discourage tick attachment. Repellents containing permethrin can be sprayed on boots and clothing, and will last for several days. Repellents containing DEET (n, n-diethyl-m-toluamide) can be applied to the skin, but will last only a few hours before reapplication is necessary. Use DEET with caution on children because adverse reactions have been reported.

  • Conduct a body check upon return from potentially tick-infested areas by searching your entire body for ticks. Use a hand-held or full-length mirror to view all parts of your body. Promptly, remove any tick you find on your body.

What is the best way to remove a tick?
To remove attached ticks, use the following procedure:

  1. Use fine-tipped tweezers or shield your fingers with a tissue, paper towel, or rubber gloves.
  2. Grasp the tick as close to the skin surface as possible and pull upward with steady, even pressure. Do not twist or jerk the tick; this may cause the mouthparts to break off and remain in the skin.  (If this happens, remove mouthparts with tweezers.  Consult your healthcare provider if infection occurs.)
  3. Do not squeeze, crush, or puncture the body of the tick because its fluids (saliva, hemolymph, gut contents) may contain infectious organisms.
  4. Do not handle the tick with bare hands because infectious agents may enter through mucous membranes or breaks in the skin. This precaution is particularly directed to individuals who remove ticks from domestic animals with unprotected fingers. Children, the elderly, and immunocompromised persons may be at greater risk of infection and should avoid this procedure. 
  5. After removing the tick, thoroughly disinfect the bite site and wash your hands with soap and water.
  6. You may wish to save the tick for identification in case you become ill within 2 to 3 weeks. Your doctor can use the information to assist in making an accurate diagnosis. Place the tick in a plastic bag and put it in your freezer. Write the date of the bite on on a piece of paper with a pencil and place it in the bag.

Note:  Folklore remedies such as petroleum jelly or hot matches do little to encourage a tick to detach from skin. In fact, they may make matters worse by irritating the tick and stimulating it to release additional saliva, increasing the chances of transmitting the pathogen. These methods of tick removal should be avoided. In addition, a number of tick removal devices have been marketed, but none are better than a plain set of fine tipped tweezers.

How can ticks be controlled?
Strategies to reduce vector tick densities through area-wide application of acaricides (chemicals that will kill ticks and mites) and control of tick habitats (e.g., leaf litter and brush) have been effective in small-scale trials. New methods under development include applying acaricides to rodents and deer by using baited tubes, boxes, and deer feeding stations in areas where these pathogens are endemic. Biological control with fungi, parasitic nematodes, and parasitic wasps may play important roles in integrated tick control efforts.  Community-based integrated tick management strategies may prove to be an effective public health response to reduce the incidence of tick-borne infections. However, limiting exposure to ticks is presently the most effective method of prevention.

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What is Babesiosis:

Babesiosis is caused by hemoprotozoan parasites of the genus Babesia.  While more than 100 species have been reported, only a few have been identified as causing human infections.  Babesia microti and Babesia divergens have been identified in most human cases, but variants (considered different species) have been recently identified.  Little is known about the occurrence of Babesia species in malaria-endemic areas where Babesia can easily be misdiagnosed as Plasmodium.

Life Cycle:

Life cycle of Babesia microti

The Babesia microti life cycle involves two hosts, which includes a rodent, primarily the white-footed mouse, Peromyscus leucopus.  During a blood meal, a Babesia-infected tick introduces sporozoites into the mouse host (1).  Sporozoites enter erythrocytes and undergo asexual reproduction (budding) (2).  In the blood, some parasites differentiate into male and female gametes although these cannot be distinguished at the light microscope level (3).  The definitive host is a tick, in this case the deer tick, Ixodes dammini (I. scapularis).  Once ingested by an appropriate tick (4), gametes unite and undergo a sporogonic cycle resulting in sporozoites (5).  Transovarial transmission (also known as vertical, or hereditary, transmission) has been documented for “large” Babesia spp. but not for the “small” babesiae, such as B. microti (A).

Note: Deer are the hosts upon which the adult ticks feed and are indirectly part of the Babesia cycle as they influence the tick population.  When deer populations increase, the tick population also increases, thus heightening the potential for transmission.

Geographic Distribution:
Worldwide, but little is known about the prevalence of Babesia in malaria-endemic countries, where misidentification as Plasmodium probably occurs.  In Europe, most reported cases are due to B. divergens and occur in splenectomized patients.  In the United States, B. microti is the agent most frequently identified (Northeast and Midwest), and can occur in non-splenectomized individuals.  Two variants, arguably different species, have been reported in the U.S. states of Washington and California (WA1- type and related parasites) and Missouri (MO1).

Clinical Features:
Most infections are probably asymptomatic, as indicated by serologic surveys.  Manifestations of disease include fever, chills, sweating, myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia.  Symptoms typically occur after an incubation period of 1 to 4 weeks, and can last several weeks.  The disease is more severe in patients who are immunosuppressed, splenectomized, and/or elderly.  Infections caused by B. divergens tend to be more severe (frequently fatal if not appropriately treated) than those due to B. microti, where clinical recovery usually occurs.

Laboratory Diagnosis:
Diagnosis can be made by microscopic examination of thick and thin blood smears stained with Giemsa.  Repeated smears may be needed.

Diagnostic findings

  • Microscopy
  • Antibody detection by indirect fluorescent antibody (IFA) test is a complementary diagnostic test.
  • Molecular methods

Isolation of the organisms by inoculation of patient blood into hamsters or gerbils may also assist in diagnosis.  Animals inoculated with infective blood typically develop parasitemia within 1 to 4 weeks.

Treatment:
Treatment with clindamycin* plus quinine or atovaquone* plus azithromycin* are the options.  The Medical Letter notes that exchange transfusion has been used in severely ill patients with high parasitemias. 

* These drugs are approved by the FDA, but considered investigational for this purpose.

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Arboviral Encephalitides

Perspectives

Arthropod-borne viruses, i.e., arboviruses, are viruses that are maintained in nature through biological transmission between susceptible vertebrate hosts by blood feeding arthropods (mosquitoes, psychodids, ceratopogonids, and ticks). Vertebrate infection occurs when the infected arthropod takes a blood meal. The term 'arbovirus' has no taxonomic significance. Arboviruses that cause human encephalitis are members of three virus families: the Togaviridae (genus Alphavirus), Flaviviridae, and Bunyaviridae.

All arboviral encephalitides are zoonotic, being maintained in complex life cycles involving a nonhuman primary vertebrate host and a primary arthropod vector. These cycles usually remain undetected until humans encroach on a natural focus, or the virus escapes this focus via a secondary vector or vertebrate host as the result of some ecologic change. Humans and domestic animals can develop clinical illness but usually are "dead-end" hosts because they do not produce significant viremia, and do not contribute to the transmission cycle. Many arboviruses that cause encephalitis have a variety of different vertebrate hosts and some are transmitted by more than one vector. Maintenance of the viruses in nature may be facilitated by vertical transmission (e.g., the virus is transmitted from the female through the eggs to the offspring).

Arboviral encephalitides have a global distribution, but there are four main virus agents of encephalitis in the United States: eastern equine encephalitis (EEE), western equine encephalitis (WEE), St. Louis encephalitis (SLE) and La Crosse (LAC) encephalitis, all of which are transmitted by mosquitoes. Another virus, Powassan, is a minor cause of encephalitis in the northern United States, and is transmitted by ticks. A new Powassan-like virus has recently been isolated from deer ticks. Its relatedness to Powassan virus and its ability to cause disease has not been well documented. Most cases of arboviral encephalitis occur from June through September, when arthropods are most active. In milder (i.e., warmer) parts of the country, where arthropods are active late into the year, cases can occur into the winter months.

The majority of human infections are asymptomatic or may result in a nonspecific flu-like syndrome. Onset may be insidious or sudden with fever, headache, myalgias, malaise and occasionally prostration. Infection may, however, lead to encephalitis, with a fatal outcome or permanent neurologic sequelae. Fortunately, only a small proportion of infected persons progress to frank encephalitis.

Experimental studies have shown that invasion of the central nervous system (CNS), generally follows initial virus replication in various peripheral sites and a period of viremia. Viral transfer from the blood to the CNS through the olfactory tract has been suggested. Because the arboviral encephalitides are viral diseases, antibiotics are not effective for treatment and no effective antiviral drugs have yet been discovered. Treatment is supportive, attempting to deal with problems such as swelling of the brain, loss of the automatic breathing activity of the brain and other treatable complications like bacterial pneumonia.

There are no commercially available human vaccines for these U.S. diseases. There is a Japanese encephalitis vaccine available in the U.S. A tick-borne encephalitis vaccine is available in Europe. An equine vaccine is available for EEE, WEE and Venezuelan equine encephalitis (VEE). Arboviral encephalitis can be prevented in two major ways: personal protective measures and public health measures to reduce the population of infected mosquitoes. Personal measures include reducing time outdoors particularly in early evening hours, wearing long pants and long sleeved shirts and applying mosquito repellent to exposed skin areas. Public health measures often require spraying of insecticides to kill juvenile (larvae) and adult mosquitoes.

Selection of mosquito control methods depends on what needs to be achieved; but, in most emergency situations, the preferred method to achieve maximum results over a wide area is aerial spraying. In many states aerial spraying may be available in certain locations as a means to control nuisance mosquitoes. Such resources can be redirected to areas of virus activity. When aerial spraying is not routinely used, such services are usually contracted for a given time period.

Financing of aerial spraying costs during large outbreaks is usually provided by state emergency contingency funds. Federal funding of emergency spraying is rare and almost always requires a federal disaster declaration. Such disaster declarations usually occur when the vector-borne disease has the potential to infect large numbers of people, when a large population is at risk and when the area requiring treatment is extensive. Special large planes maintained by the United States Air Force can be called upon to deliver the insecticide(s) chosen for such emergencies. Federal disaster declarations have relied heavily on risk assessment by the CDC.

Laboratory diagnosis of human arboviral encephalitis has changed greatly over the last few years. In the past, identification of antibody relied on four tests: hemagglutination-inhibition, complement fixation, plaque reduction neutralization test, and the indirect fluorescent antibody (IFA) test. Positive identification using these immunoglobulin M (IgM) - and IgG-based assays requires a four-fold increase in titer between acute and convalescent serum samples. With the advent of solid-phase antibody-binding assays, such as enzyme-linked immunosorbent assay (ELISA), the diagnostic algorithm for identification of viral activity has changed. Rapid serologic assays such as IgM-capture ELISA (MAC-ELISA) and IgG ELISA may now be employed soon after infection. Early in infection, IgM antibody is more specific, while later in infection, IgG antibody is more reactive. Inclusion of monoclonal antibodies (MAbs) with defined virus specificities in these solid phase assays has allowed for a level of standardization that was not previously possible.

Virus isolation and identification have also been useful in defining viral agents in serum, cerebrospinal fluid and mosquito vectors. While virus isolation still depends upon growth of an unknown virus in cell culture or neonatal mice, virus identification has also been greatly facilitated by the availability of virus-specific MAbs for use in IFA assays. Similarly, MAbs with avidities sufficiently high to allow for specific binding to virus antigens in a complex protein mixture (e.g., mosquito pool suspensions) have enhanced our ability to rapidly identify virus agents in situ. While polymerase chain reaction (PCR) has been developed to identify a number of viral agents, such tests have not yet been validated for routine rapid identification in the clinical setting.

Mosquito-borne encephalitis offers a rare opportunity in public health to detect the risk of a disease before it occurs and to intervene to reduce that risk substantially. The surveillance required to detect risk is being increasingly refined by the potential utilization of these new technologies which allows for rapid identification of dangerous viruses in mosquito populations. These rapid diagnostic techniques used in threat recognition can shorten public health response time and reduce the geographic spread of infected vectors and thereby the cost of containing them. The Arbovirus Diseases Branch of NCID's Division of Vector-Borne Infectious Diseases has responsibility for CDC's programs in surveillance, diagnosis, research and control of arboviral encephalitides.

La Crosse Encephalitis

La Crosse (LAC) encephalitis was discovered in La Crosse, Wisconsin in 1963. Since then, the virus has been identified in several Midwestern and Mid-Atlantic states. During an average year, about 75 cases of LAC encephalitis are reported to the CDC. Most cases of LAC encephalitis occur in children under 16 years of age. LAC virus is a Bunyavirus and is a zoonotic pathogen cycled between the daytime-biting treehole mosquito, Aedes triseriatus, and vertebrate amplifier hosts (chipmunks, tree squirrels) in deciduous forest habitats. The virus is maintained over the winter by transovarial transmission in mosquito eggs. If the female mosquito is infected, she may lay eggs that carry the virus, and the adults coming from those eggs may be able to transmit the virus to chipmunks and to humans.

Historically, most cases of LAC encephalitis occur in the upper Midwestern states (Minnesota, Wisconsin, Iowa, Illinois, Indiana, and Ohio). Recently, more cases are being reported from states in the mid-Atlantic (West Virginia, Virginia and North Carolina) and southeastern (Alabama and Mississippi) regions of the country. It has long been suspected that LAC encephalitis has a broader distribution and a higher incidence in the eastern United States, but is under-reported because the etiologic agent is often not specifically identified.

LAC encephalitis initially presents as a nonspecific summertime illness with fever, headache, nausea, vomiting and lethargy. Severe disease occurs most commonly in children under the age of 16 and is characterized by seizures, coma, paralysis, and a variety of neurological sequelae after recovery. Death from LAC encephalitis occurs in less than 1% of clinical cases. In many clinical settings, pediatric cases presenting with CNS involvement are routinely screened for herpes or enteroviral etiologies. Since there is no specific treatment for LAC encephalitis, physicians often do not request the tests required to specifically identify LAC virus, and the cases are reported as aseptic meningitis or viral encephalitis of unknown etiology.

Also found in the United States, Jamestown Canyon and Cache Valley viruses are related to LAC, but rarely cause encephalitis.

Eastern Equine Encephalitis

Eastern equine encephalitis (EEE) is also caused by a virus transmitted to humans and equines by the bite of an infected mosquito. EEE virus is an alphavirus that was first identified in the 1930's and currently occurs in focal locations along the eastern seaboard, the Gulf Coast and some inland Midwestern locations of the United States. While small outbreaks of human disease have occurred in the United States, equine epizootics can be a common occurrence during the summer and fall.

It takes from 4-10 days after the bite of an infected mosquito for an individual to develop symptoms of EEE. These symptoms begin with a sudden onset of fever, general muscle pains, and a headache of increasing severity. Many individuals will progress to more severe symptoms such as seizures and coma. Approximately one-third of all people with clinical encephalitis caused by EEE will die from the disease and of those who recover, many will suffer permanent brain damage with many of those requiring permanent institutional care.

In addition to humans, EEE virus can produce severe disease in: horses, some birds such as pheasants, quail, ostriches and emus, and even puppies. Because horses are outdoors and attract hordes of biting mosquitoes, they are at high risk of contracting EEE when the virus is present in mosquitoes. Human cases are usually preceded by those in horses and exceeded in numbers by horse cases which may be used as a surveillance tool.

EEE virus occurs in natural cycles involving birds and Culiseta melanura, in some swampy areas nearly every year during the warm months. Where the virus resides or how it survives in the winter is unknown. It may be introduced by migratory birds in the spring or it may remain dormant in some yet undiscovered part of its life cycle. With the onset of spring, the virus reappears in the birds (native bird species do not seem to be affected by the virus) and mosquitoes of the swamp. In this usual cycle of transmission, virus does not escape from these areas because the mosquito involved prefers to feed upon birds and does not usually bite humans or other mammals.

For reasons not fully understood, the virus may escape from enzootic foci in swamp areas in birds or bridge vectors such as Coquilletidia perturbans and Aedes sollicitans. These species feed on both birds and mammals and can transmit the virus to humans, horses, and other hosts. Other mosquito species such as Ae. vexans and Culex nigripalpus can also transmit EEE virus. When health officials maintain surveillance for EEE virus activity, this movement out of the swamp can be detected, and if the level of activity is sufficiently high, can recommend and undertake measures to reduce the risk to humans.

Western Equine Encephalitis

The alphavirus western equine encephalitis (WEE) was first isolated in California in 1930 from the brain of a horse with encephalitis, and remains an important cause of encephalitis in horses and humans in North America, mainly in western parts of the USA and Canada. In the western United States, the enzootic cycle of WEE involves passerine birds, in which the infection is inapparent, and culicine mosquitoes, principally Cx. tarsalis, a species that is associated with irrigated agriculture and stream drainages. The virus has also been isolated from a variety of mammal species. Other important mosquito vector species include Aedes melanimon in California, Ae. dorsalis in Utah and New Mexico and Ae. campestris in New Mexico. WEE virus was isolated from field collected larvae of Ae. dorsalis, providing evidence that vertical transmission may play an important role in the maintenance cycle of an alphavirus.

Expansion of irrigated agriculture in the North Platte River Valley during the past several decades has created habitats and conditions favorable for increases in populations of granivorous birds such as the house sparrow, Passer domesticus, and mosquitoes such as Cx. tarsalis, Aedes dorsalis and Aedes melanimon. All of these species may play a role in WEE virus transmission in irrigated areas. In addition to Cx. tarsalis, Ae. dorsalis and Ae. melanimon, WEE virus also has been isolated occasionally from some other mosquito species present in the area. Two confirmed and several suspect cases of WEE were reported from Wyoming in 1994. In 1995, two strains of WEE virus were isolated from Culex tarsalis and neutralizing antibody to WEE virus was demonstrated in sera from pheasants and house sparrows. During 1997, 35 strains of WEE virus were isolated from mosquitoes collected in Scotts Bluff County, Nebraska.

Human WEE cases are usually first seen in June or July. Most WEE infections are asymptomatic or present as mild, nonspecific illness. Patients with clinically apparent illness usually have a sudden onset with fever, headache, nausea, vomiting, anorexia and malaise, followed by altered mental status, weakness and signs of meningeal irritation. Children, especially those under 1 year old, are affected more severely than adults and may be left with permanent sequelae, which is seen in 5 to 30% of young patients. The mortality rate is about 3%.

St. Louis Encephalitis

In the United States, the leading cause of epidemic flaviviral encephalitis is St. Louis encephalitis (SLE) virus. SLE is the most common mosquito-transmitted human pathogen in the U.S. While periodic SLE epidemics have occurred only in the Midwest and southeast, SLE virus is distributed throughout the lower 48 states. Since 1964, there have been 4,437 confirmed cases of SLE with an average of 193 cases per year (range 4 - 1,967). However, less than 1% of SLE viral infections are clinically apparent and the vast majority of infections remain undiagnosed. Illness ranges in severity from a simple febrile headache to meningoencephalitis, with an overall case-fatality ratio of 5-15 %. The disease is generally milder in children than in adults, but in those children who do have disease, there is a high rate of encephalitis. The elderly are at highest risk for severe disease and death. During the summer season, SLE virus is maintained in a mosquito-bird-mosquito cycle, with periodic amplification by peridomestic birds and Culex mosquitoes. In Florida, the principal vector is Cx. nigripalpus, in the Midwest, Cx. pipiens pipiens and Cx. p. quinquefasciatus and in the western United States, Cx. tarsalis and members of the Cx. pipiens complex.

Powassan Encephalitis

Powassan (POW) virus is a flavivirus and currently the only well documented tick-borne transmitted arbovirus occurring in the United States and Canada. Recently a Powassan-like virus was isolated from the deer tick, Ixodes scapularis. Its relationship to POW and its ability to cause human disease has not been fully elucidated. POW's range in the United States is primarily in the upper tier States. In addition to isolations from man, the virus has been recovered from ticks (Ixodes marxi, I. cookei and Dermacentor andersoni) and from the tissues of a skunk (Spiligale putorius). It is a rare cause of acute viral encephalitis. POW virus was first isolated from the brain of a 5-year-old child who died in Ontario in 1958. Patients who recover may have residual neurological problems.

Venezuelan Equine Encephalitis

Like EEE and WEE viruses, Venezuelan equine encephalitis (VEE) is an alphavirus and causes encephalitis in horses and humans and is an important veterinary and public health problem in Central and South America. Occasionally, large regional epizootics and epidemics can occur resulting in thousands of equine and human infections. Epizootic strains of VEE virus can infect and be transmitted by a large number of mosquito species. The natural reservoir host for the epizootic strains is not known. A large epizootic that began in South America in 1969 reached Texas in 1971. It was estimated that over 200,000 horses died in that outbreak, which was controlled by a massive equine vaccination program using an experimental live attenuated VEE vaccine. There were several thousand human infections. A more recent VEE epidemic occurred in the fall of 1995 in Venezuela and Colombia with an estimated 90,000 human infections. Infection of man with VEE virus is less severe than with EEE and WEE viruses, and fatalities are rare. Adults usually develop only an influenza-like illness, and overt encephalitis is usually confined to children. Effective VEE virus vaccines are available for equines.

Enzootic strains of VEE virus have a wide geographic distribution in the Americas. These viruses are maintained in cycles involving forest dwelling rodents and mosquito vectors, mainly Culex (Melanoconion) species. Occasional cases or small outbreaks of human disease are associated with there viruses, the most recent outbreaks were in Venezuela in 1992, Peru in 1994 and Mexico in 1995-96.

Other Arboviral Encephalitides

Many other arboviral encephalitides occur throughout the world. Most of these diseases are problems only for those individuals traveling to countries where the viruses are endemic.

Japanese Encephalitis

Japanese encephalitis (JE) virus is a flavivirus, related to SLE, and is widespread throughout Asia. Worldwide, it is the most important cause of arboviral encephalitis with over 45,000 cases reported annually. In recent years, JE virus has expanded its geographic distribution with outbreaks in the Pacific. Epidemics occur in late summer in temperate regions, but the infection is enzootic and occurs throughout the year in many tropical areas of Asia. The virus is maintained in a cycle involving culicine mosquitoes and waterbirds. The virus is transmitted to man by Culex mosquitoes, primarily Cx. tritaeniorhynchus, which breed in rice fields. Pigs are the main amplifying hosts of JE virus in peridomestic environments.

The incubation period of JE is 5 to 14 days. Onset of symptoms is usually sudden, with fever, headache and vomiting. The illness resolves in 5 to 7 days if there is no CNS involvement. The mortality in most outbreaks is less than 10%, but is higher in children and can exceed 30%. Neurologic sequelae in patients who recover are reported in up to 30% of cases. A formalin-inactivated vaccine prepared in mice is used widely in Japan, China, India, Korea, Taiwan and Thailand. This vaccine is currently available for human use in the United States, for individuals who might be traveling to endemic countries.

Tick-Borne Encephalitis

Tick-borne encephalitis (TBE) is caused by two closely related flaviviruses which are distinct biologically. The eastern subtype causes Russian spring-summer encephalitis (RSSE) and is transmitted by Ixodes persulcatus, whereas the western subtype is transmitted by Ixodes ricinus and causes Central European encephalitis (CEE). The name CEE is somewhat misleading, since the condition can occur throughout much of Europe. Of the two subtypes, RSSE is the more severe infection, having a mortality of up to 25% in some outbreaks, whereas mortality in CEE seldom exceeds 5%.

The incubation period is 7 to 14 days. Infection usually presents as a mild, influenza-type illness or as benign, aseptic meningitis, but may result in fatal meningoencephalitis. Fever is often biphasic, and there may be severe headache and neck rigidity, with transient paralysis of the limbs, shoulders or less commonly the respiratory musculature. A few patients are left with residual paralysis. Although the great majority of TBE infections follow exposure to ticks, infection has occurred through the ingestion of infected cows' or goats' milk. An inactivated TBE vaccine is currently available in Europe and Russia.

West Nile Encephalitis

WNV is a flavivirus belonging taxonomically to the Japanese encephalitis serocomplex that includes the closely related St. Louis encephalitis (SLE) virus, Kunjin and Murray Valley encephalitis viruses, as well as others. WNV was first isolated in the West Nile Province of Uganda in 1937 (2). The first recorded epidemics occurred in Israel during 1951-1954 and in 1957. Epidemics have been reported in Europe in the Rhone delta of France in 1962 and in Romania in 1996 (3-5). The largest recorded epidemic occurred in South Africa in 1974 (6).

An outbreak of arboviral encephalitis in New York City and neighboring counties in New York state in late August and September 1999, was initially attributed to St. Louis encephalitis virus based on positive serologic findings in cerebrospinal fluid (CSF) and serum samples using a virus-specific IgM-capture enzyme-linked immunosorbent assay (ELISA). The outbreak has been subsequently confirmed as caused by West Nile virus based on the identification of virus in human, avian, and mosquito samples. See also these MMWR articles Outbreak of West Nile-Like Viral Encephalitis -- New York, 1999. MMWR, 1999:48(38);845-9 and Update: West Nile-Like Viral Encephalitis -- New York, 1999. MMWR, 1999:48(39);890-2. A recent outbreak WN encephalitis occurred in Bucharest, Romania in 1996.

The virus that caused the New York area outbreak has been definitively identified as a strain of WNV. The genomic sequences identified to date from human brain, virus isolates from zoo birds, dead crows, and mosquito pools are identical. SLE and West Nile viruses are antigenically related, and cross reactions are observed in most serologic tests. The isolation of viruses and genomic sequences from birds, mosquitoes, and human brain tissue permitted the discovery of West Nile virus in North America and prompted more specific testing. The limitations of serologic assays emphasize the importance of isolating the virus from entomologic, clinical, or veterinary material.

Although it is not known when and how West Nile virus was introduced into North America, international travel of infected persons to New York or transport by imported infected birds may have played a role. WNV can infect a wide range of vertebrates; in humans it usually produces either asymptomatic infection or mild febrile disease, but can cause severe and fatal infection in a small percentage of patients. Within its normal geographic distribution of Africa, the Middle East, western Asia, and Europe, WNV has not been documented to cause epizootics in birds; crows and other birds with antibodies to WNV are common, suggesting that asymptomatic or mild infection usually occurs among birds in those regions. Similarly, substantial bird virulence of SLE virus has not been reported. Therefore, an epizootic producing high mortality in crows and other bird species is unusual for either WNV or SLE virus. For both viruses, migratory birds may play an important role in the natural transmission cycles and spread. Like SLE virus, WNV is transmitted principally by Culex species mosquitoes, but also can be transmitted by Aedes, Anopheles, and other species. The predominance of urban Culex pipiens mosquitoes trapped during this outbreak suggests an important role for this species. Enhanced surveillance for early detection of virus activity in birds and mosquitoes will be crucial to guide control measures.

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