Preventive measures against Marburg virus infection are not well defined, as transmission from wildlife to humans remains an area of ongoing research. However, avoiding fruit bats, and sick non-human primates in central Africa, is one way to protect against infection.

Measures for prevention of secondary, or person-to-person, transmission are similar to those used for other hemorrhagic fevers. If a patient is either suspected or confirmed to have Marburg hemorrhagic fever, barrier nursing techniques should be used to prevent direct physical contact with the patient. These precautions include wearing of protective gowns, gloves, and masks; placing the infected individual in strict isolation; and sterilization or proper disposal of needles, equipment, and patient excretions.

In conjunction with the World Health Organization, CDC has developed practical, hospital-based guidelines, titled: Infection Control for Viral Haemorrhagic Fevers In the African Health Care Setting. The manual can help health-care facilities recognize cases and prevent further hospital-based disease transmission using locally available materials and few financial resources.

Marburg hemorrhagic fever is a very rare human disease. However, when it occurs, it has the potential to spread to other people, especially health care staff and family members who care for the patient. Therefore, increasing awareness in communities and among health-care providers of the clinical symptoms of patients with Marburg hemorrhagic fever is critical. Better awareness can lead to earlier and stronger precautions against the spread of Marburg virus in both family members and health-care providers. Improving the use of diagnostic tools is another priority. With modern means of transportation that give access even to remote areas, it is possible to obtain rapid testing of samples in disease control centers equipped with Biosafety Level 4 laboratories in order to confirm or rule out Marburg virus infection.


Leishmaniasis is a parasitic disease that is found in parts of the tropics, subtropics, and southern Europe. Leishmaniasis is caused by infection with Leishmania parasites, which are spread by the bite of infected sand flies. There are several different forms of leishmaniasis in people. The most common forms are cutaneous leishmaniasis, which causes skin sores, and visceral leishmaniasis, which affects several internal organs (usually spleen, liver, and bone marrow).


Leishmaniasis is found in people in focal areas of more than 90 countries in the tropics, subtropics, and southern Europe. The ecologic settings range from rain forests to deserts. Leishmaniasis usually is more common in rural than in urban areas, but it is found in the outskirts of some cities. Climate and other environmental changes have the potential to expand the geographic range of the sand fly vectors and the areas in the world where leishmaniasis is found.

Leishmaniasis is found on every continent except Australia and Antarctica.

     - In the Old World (the Eastern Hemisphere), leishmaniasis is found in some parts of Asia, the Middle East, Africa (particularly in the tropical region and North Africa, with some cases elsewhere), and southern Europe. It is not found in Australia or the Pacific islands.
     - In the New World (the Western Hemisphere), it is found in some parts of Mexico, Central America, and South America. It is not found in Chile or Uruguay. Occasional cases of cutaneous leishmaniasis have been acquired in Texas and Oklahoma.

The number of new cases per year is not known with certainty. For cutaneous leishmaniasis, estimates of the number of cases range from approximately 0.7 million (700,000) to 1.2 million (1,200,000). For visceral leishmaniasis, estimates of the number of cases range from approximately 0.2 million (200,000) to 0.4 million (400,000). The cases of leishmaniasis evaluated in the United States reflect travel and immigration patterns. For example, many of the cases of cutaneous leishmaniasis in U.S. civilian travelers have been acquired in common tourist destinations in Latin America, such as in Costa Rica.

Overall, infection in people is caused by more than 20 species (types) of Leishmania parasites, which are spread by about 30 species of phlebotomine sand flies; particular species of the parasite are spread by particular sand flies. The sand fly vectors generally are the most active during twilight, evening, and night-time hours (from dusk to dawn).

In many geographic areas where leishmaniasis is found in people, infected people are not needed to maintain the transmission cycle of the parasite in nature; infected animals (such as rodents or dogs), along with sand flies, maintain the cycle. However, in some parts of the world, infected people are needed to maintain the cycle; this type of transmission (human—sand fly—human) is called anthroponotic. In areas with anthroponotic transmission, effective treatment of individual patients can help control the spread of the parasite.


Various laboratory methods can be used to diagnose leishmaniasis—to detect the parasite as well as to identify the Leishmania species (type). Some of the methods are available only in reference laboratories. In the United States, CDC staff can assist with the testing for leishmaniasis.

Tissue specimens—such as from skin sores (for cutaneous leishmaniasis) or from bone marrow (for visceral leishmaniasis)—can be examined for the parasite under a microscope, in special cultures, and in other ways. Blood tests that detect antibody (an immune response) to the parasite can be helpful for cases of visceral leishmaniasis; tests to look for the parasite itself usually also are done.

More on: Resources for Health Professionals: Diagnosis


Before considering treatment, the first step is to make sure the diagnosis is correct.

Treatment decisions should be individualized. Health care providers may consult CDC staff about the relative merits of various approaches. Examples of factors to consider include the form of leishmaniasis, the Leishmania species that caused it, the potential severity of the case, and the patient's underlying health.

The skin sores of cutaneous leishmaniasis usually heal on their own, even without treatment. But this can take months or even years, and the sores can leave ugly scars. Another potential concern applies to some (not all) types of the parasite found in parts of Latin America: certain types might spread from the skin and cause sores in the mucous membranes of the nose (most common location), mouth, or throat (mucosal leishmaniasis). Mucosal leishmaniasis might not be noticed until years after the original sores healed. The best way to prevent mucosal leishmaniasis is to ensure adequate treatment of the cutaneous infection.

If not treated, severe (advanced) cases of visceral leishmaniasis typically are fatal.

More on: Resources for Health Professionals: Treatment


No vaccines or drugs to prevent infection are available. The best way for travelers to prevent infection is to protect themselves from sand fly bites. To decrease the risk of being bitten, follow these preventive measures:

Avoid outdoor activities, especially from dusk to dawn, when sand flies generally are the most active.

When outdoors (or in unprotected quarters):

     - Minimize the amount of exposed (uncovered) skin. To the extent that is tolerable in the climate, wear long-sleeved shirts, long pants, and socks; and tuck your shirt into your pants. (See below about wearing insecticide-treated clothing.)
     - Apply insect repellent to exposed skin and under the ends of sleeves and pant legs. Follow the instructions on the label of the repellent. The most effective repellents generally are those that contain the chemical DEET (N,N-diethylmetatoluamide).

When indoors:

     - Stay in well-screened or air-conditioned areas.
     - Keep in mind that sand flies are much smaller than mosquitoes and therefore can get through smaller holes.
     - Spray living/sleeping areas with an insecticide to kill insects.
     - If you are not sleeping in a well-screened or air-conditioned area, use a bed net and tuck it under your mattress. If possible, use a bed net that has been soaked in or sprayed with a pyrethroid-containing insecticide. The same treatment can be applied to screens, curtains, sheets, and clothing (clothing should be retreated after five washings).

More on: Insect Bite Prevention


A single-celled parasite called Toxoplasma gondii causes a disease known as toxoplasmosis. While the parasite is found throughout the world, more than 60 million people in the United States may be infected with the Toxoplasma parasite. Of those who are infected, very few have symptoms because a healthy person’s immune system usually keeps the parasite from causing illness. However, pregnant women and individuals who have compromised immune systems should be cautious; for them, a Toxoplasma infection could cause serious health problems.


Toxoplasmosis is caused by the protozoan parasite Toxoplasma gondii. In the United States it is estimated that 22.5% of the population 12 years and older have been infected with Toxoplasma. In various places throughout the world, it has been shown that up to 95% of some populations have been infected with Toxoplasma. Infection is often highest in areas of the world that have hot, humid climates and lower altitudes.

Toxoplasmosis is not passed from person-to-person, except in instances of mother-to-child (congenital) transmission and blood transfusion or organ transplantation. People typically become infected by three principal routes of transmission.

    Foodborne transmission

The tissue form of the parasite (a microscopic cyst consisting of bradyzoites) can be transmitted to humans by food. People become infected by:

     - Eating undercooked, contaminated meat (especially pork, lamb, and venison)
     - Accidental ingestion of undercooked, contaminated meat after handling it and not washing hands thoroughly (Toxoplasma cannot be absorbed through intact skin)
     - Eating food that was contaminated by knives, utensils, cutting boards, or other foods that had contact with raw, contaminated meat

    Animal-to-human (zoonotic) transmission

Cats play an important role in the spread of toxoplasmosis. They become infected by eating infected rodents, birds, or other small animals. The parasite is then passed in the cat's feces in an oocyst form, which is microscopic.

Kittens and cats can shed millions of oocysts in their feces for as long as 3 weeks after infection. Mature cats are less likely to shed Toxoplasma if they have been previously infected. A Toxoplasma-infected cat that is shedding the parasite in its feces contaminates the litter box. If the cat is allowed outside, it can contaminate the soil or water in the environment as well.

People can accidentally swallow the oocyst form of the parasite. People can be infected by:

     - Accidental ingestion of oocysts after cleaning a cat's litter box when the cat has shed Toxoplasma in its feces
     - Accidental ingestion of oocysts after touching or ingesting anything that has come into contact with a cat's feces that contain Toxoplasma
     - Accidental ingestion of oocysts in contaminated soil (e.g., not washing hands after gardening or eating unwashed fruits or vegetables from a garden)
     - Drinking water contaminated with the Toxoplasma parasite

    Mother-to-child (congenital) transmission

A woman who is newly infected with Toxoplasma during pregnancy can pass the infection to her unborn child (congenital infection). The woman may not have symptoms, but there can be severe consequences for the unborn child, such as diseases of the nervous system and eyes.

    Rare instances of transmission

Organ transplant recipients can become infected by receiving an organ from a Toxoplasma-positive donor. Rarely, people can also become infected by receiving infected blood via transfusion. Laboratory workers who handle infected blood can also acquire infection through accidental inoculation.


The diagnosis of toxoplasmosis is typically made by serologic testing. A test that measures immunoglobulin G (IgG) is used to determine if a person has been infected. If it is necessary to try to estimate the time of infection, which is of particular importance for pregnant women, a test which measures immunoglobulin M (IgM) is also used along with other tests such as an avidity test.

Diagnosis can be made by direct observation of the parasite in stained tissue sections, cerebrospinal fluid (CSF), or other biopsy material. These techniques are used less frequently because of the difficulty of obtaining these specimens.

Parasites can also be isolated from blood or other body fluids (for example, CSF) but this process can be difficult and requires considerable time.

Molecular techniques that can detect the parasite's DNA in the amniotic fluid can be useful in cases of possible mother-to-child (congenital) transmission.

Ocular disease is diagnosed based on the appearance of the lesions in the eye, symptoms, course of disease, and often serologic testing.


Healthy people (nonpregnant)

Most healthy people recover from toxoplasmosis without treatment. Persons who are ill can be treated with a combination of drugs such as pyrimethamine and sulfadiazine, plus folinic acid.

    Pregnant women, newborns, and infants

Pregnant women, newborns, and infants can be treated, although the parasite is not eliminated completely. The parasites can remain within tissue cells in a less active phase; their location makes it difficult for the medication to completely eliminate them.

    Persons with ocular disease

Persons with ocular toxoplasmosis are sometimes prescribed medicine to treat active disease by their ophthalmologist. Whether or not medication is recommended depends on the size of the eye lesion, the location, and the characteristics of the lesion (acute active, versus chronic not progressing).

    Persons with compromised immune systems

Persons with compromised immune systems need to be treated until they have improvement in their condition. For AIDS patients, continuation of medication for the rest of their lives may be necessary, or for as long as they are immunosuppressed.

More on: Resources for Health Professionals: Treatment


People who are healthy should follow the guidelines below to reduce risk of toxoplasmosis. If you have a weakened immune system, please see guidelines for Immunocompromised Persons.
   Reduce Risk from Food

To prevent risk of toxoplasmosis and other infections from food:

    - Freeze meat for several days at sub-zero (0° F) temperatures before cooking to greatly reduce chance of infection.
    - Peel or wash fruits and vegetables thoroughly before eating.

    - Wash cutting boards, dishes, counters, utensils, and hands with hot soapy water after contact with raw meat, poultry, seafood, or unwashed fruits or vegetables.

More on: Handwashing

The U.S. Government and the meat industry continue their efforts to reduce T. gondii in meat.
   Reduce Risk from the Environment

To prevent risk of toxoplasmosis from the environment:

    - Avoid drinking untreated drinking water.
    - Wear gloves when gardening and during any contact with soil or sand because it might be contaminated with cat feces that contain Toxoplasma. Wash hands with soap and warm water after gardening or contact with soil or sand.
    - Teach children the importance of washing hands to prevent infection.
    - Keep outdoor sandboxes covered.

    - Feed cats only canned or dried commercial food or well-cooked table food, not raw or undercooked meats.
    - Change the litter box daily if you own a cat. The Toxoplasma parasite does not become infectious until 1 to 5 days after it is shed in a cat's feces. If you are pregnant or immunocompromised:

      - Avoid changing cat litter if possible. If no one else can perform the task, wear disposable gloves and wash your hands with soap and warm water afterwards.
      - Keep cats indoors.
      - Do not adopt or handle stray cats, especially kittens. Do not get a new cat while you are pregnant.


Hookworm is an intestinal parasite of humans. The larvae and adult worms live in the small intestine can cause intestinal disease. The two main species of hookworm infecting humans are Ancylostoma duodenale and Necator americanus.


Hookworm is a soil-transmitted helminth (STH) and is one of the most common roundworm of humans. Infection is caused by the nematode parasites Necator americanus and Ancylostoma duodenale. Hookworm infections often occur in areas where human feces are used as fertilizer or where defecation onto soil happens.
    Geographic Distribution

The geographic distributions of the hookworm species that are intestinal parasites in human, Ancylostoma duodenale and Necator americanus, are worldwide in areas with warm, moist climates and are widely overlapping. Necator americanus was widespread in the Southeastern United States until the early 20th century.


The standard method for diagnosing the presence of hookworm is by identifying hookworm eggs in a stool sample using a microscope. Because eggs may be difficult to find in light infections, a concentration procedure is recommended.


Anthelminthic medications (drugs that rid the body of parasitic worms), such as albendazole and mebendazole, are the drugs of choice for treatment of hookworm infections. Infections are generally treated for 1-3 days. The recommended medications are effective and appear to have few side effects. Iron supplements may also be prescribed if the infected person has anemia.

More on: Resources for Health Professionals: Treatment


The best way to avoid hookworm infection is not to walk barefoot in areas where hookworm is common and where there may be human fecal contamination of the soil. Also, avoid other skin contact with such soil and avoid ingesting it.

Infection can also be prevented by not defecating outdoors and by effective sewage disposal systems.


Chagas disease is caused by the parasite Trypanosoma cruzi, which is transmitted to animals and people by insect vectors that are found only in the Americas (mainly, in rural areas of Latin America where poverty is widespread). Chagas disease (T. cruzi infection) is also referred to as American trypanosomiasis.
It is estimated that as many as 8 million people in Mexico, Central America, and South America have Chagas disease, most of whom do not know they are infected. If untreated, infection is lifelong and can be life threatening.
The impact of Chagas disease is not limited to the rural areas in Latin America in which vectorborne transmission occurs. Large-scale population movements from rural to urban areas of Latin America and to other regions of the world have increased the geographic distribution and changed the epidemiology of Chagas disease. In the United States and in other regions where Chagas disease is now found but is not endemic, control strategies should focus on preventing transmission from blood transfusion, organ transplantation, and mother-to-baby (congenital transmission).


Chagas disease, or American trypanosomiasis, is caused by the parasite Trypanosoma cruzi. Infection is most commonly acquired through contact with the feces of an infected triatomine bug (or "kissing bug"), a blood-sucking insect that feeds on humans and animals.

Infection can also occur from:

     - mother-to-baby (congenital),
     - contaminated blood products (transfusions),
     - an organ transplanted from an infected donor,
     - laboratory accident, or
     - contaminated food or drink (rare)

Chagas disease is endemic throughout much of Mexico, Central America, and South America where an estimated 8 million people are infected. The triatomine bug thrives under poor housing conditions (for example, mud walls, thatched roofs), so in endemic countries, people living in rural areas are at greatest risk for acquiring infection. Public health efforts aimed at preventing transmission have decreased the number of newly infected people and completely halted vectorborne transmission in some areas. Infection acquired from blood products, organ transplantation, or congenital transmission continues to pose a threat.

By applying published seroprevalence figures to immigrant populations, CDC estimates that more than 300,000 persons with Trypanosoma cruzi infection live in the United States. Most people with Chagas disease in the United States acquired their infections in endemic countries. Although there are triatomine bugs in the U.S. , only rare vectorborne cases of Chagas disease have been documented.

More on: Triatomine Bugs


The diagnosis of Chagas disease can be made by observation of the parasite in a blood smear by microscopic examination. A thick and thin blood smear are made and stained for visualization of parasites. However, a blood smear works well only in the acute phase of infection when parasites are seen circulating in blood.

Diagnosis of chronic Chagas disease is made after consideration of the patient's clinical findings, as well as by the likelihood of being infected, such as having lived in an endemic country. Diagnosis is generally made by testing with at least two different serologic tests.


Treatment for Chagas disease is recommended for all people diagnosed with an acute infection, congenital infection, and for those with suppressed immune systems, and for all children with chronic infection. Adults with chronic infection may also benefit from treatment.

For cardiac or gastrointestinal problems resulting from Chagas disease, symptomatic treatment may be helpful. Patients should consult with their primary health care provider. Some patients may be referred to a specialist, such as a cardiologist, gastroenterologist, or infectious disease specialist.

In the U.S., medication for Chagas is available only through CDC. Your health care provider can talk with CDC staff about whether and how you should be treated.

More on: Resources for Health Professionals: Antiparasitic Treatment


In endemic areas of Mexico, Central America, and South America improved housing and spraying insecticide inside housing to eliminate triatomine bugs has significantly decreased the spread of Chagas disease. Further, screening of blood donations for Chagas is another important public health tool in helping to prevent transfusion-acquired disease. Early detection and treatment of new cases, including mother-to-baby (congenital) cases, will also help reduce the burden of disease.

In the United States and in other regions where Chagas disease is now found but is not endemic, control strategies are focused on preventing transmission from blood transfusion, organ transplantation, and mother-to-baby.


The bacteria that cause nocardiosis are commonly found in soil and water.

You could become sick with nocardiosis if:

     - You inhale (breathe in) the bacteria
     - Bacteria gets into an open wound or cut

In rare cases, infection can occur during surgical procedures.

Fortunately, nocardiosis is not spread person to person, so being around someone who has the disease will not make you sick.


People with very weak immune (body defense) systems are at risk for getting nocardiosis.

Several diseases and circumstances can cause the immune system to be weak. These include:

     - Diabetes
     - Cancer
     - HIV/AIDS
     - Pulmonary alveolar proteinosis (an illness that causes the air sacs of the lungs to become plugged)
     - Connective tissue disorder (a disease that affects the tissue that connects and supports different parts of the body)
     - Alcoholism
     - Having a bone marrow or solid organ transplant
     - Taking high doses of drugs called corticosteroids

In the United States, it has been estimated that 500-1,000 new cases of nocardiosis infection occur every year. Approximately 60% of nocardiosis cases are associated with pre-existing immune compromise.

In addition, men have a greater risk of getting the infection than women; for every female who gets sick with nocardiosis, there are about 3 males who get the disease.


The symptoms of nocardiosis vary depending on which part of your body is affected.

Nocardiosis infection most commonly occurs in the lung. If your lungs are infected, you can experience:

     - Fever
     - Weight loss
     - Night sweats
     - Cough
     - Chest pain
     - Pneumonia

When lung infections occur, the infection commonly spreads to the brain. If your central nervous system (brain and spinal cord) is infected, you can experience:

     - Headache
     - Weakness
     - Confusion
     - Seizures (sudden, abnormal electrical activity in the brain)

Skin infections can occur when open wounds or cuts come into contact with contaminated soil. If your skin is affected, you can experience:

     - Ulcers
     - Nodules sometimes draining and spreading along lymph nodes


If you think you might be sick with nocardiosis, talk to your doctor.

He or she can help find out if you have the disease by performing tests that can identify the bacteria that causes nocardiosis.

Testing may involve taking tissue samples from the part of the body that is infected. Tissue samples may include the:

     - Brain
     - Skin
     - Lungs (or other parts of the lower airways)
     - Mucus from the lower airways


Like all arenaviruses, Chapare virus has a rodent host as its reservoir. Humans can contract CHHF through contact with an infected rodent. Contact can be direct or through inhalation of aerosolized Chapare virus from the urine or feces of infected rodents.

Although arenaviruses have been isolated from insects, neither they nor any other intermediary host appear to spread CHHF.

Person-to-person transmission of arenaviruses through aerosolization, although possible, is rare. From the only observed cluster of cases of CHHF, there was no evidence of person-to-person transmission.

Transmission, if it can occur with CHHF, is most likely the result of direct contact with an infected person.


The symptoms of CHHF, as reported in the only described patient, resemble those of other South American hemorrhagic fevers, such as Argentine HF or Bolivian HF. The incubation period is unknown, but for Argentine hemorrhagic fever (AHF) is 6 to 16 days.

The CHHF clinical course included:

    - fever
    - headache
    - articulation and muscle pain
    - vomiting

These symptoms were followed by deterioration with multiple hemorrhagic signs. The only described CHHF patient died 14 days after onset of symptoms.

Since Arenaviruses may enter the fetus through infection of the mother, and anecdotal evidence suggests that infected pregnant women may suffer miscarriages, it is reasonable to assume that both infection of the fetus and miscarriage may be associated with CHHF infection in the mother.


CHHF occurs in the Cochabamba region of Bolivia.
Field workers

Field workers are at greatest risk because of increased human contact with the reservoir rodent population. Sexual partners of field workers may be at greater risk as well. Laboratory infections have been frequently described with Arenaviruses and Chapare virus can certainly be transmitted to laboratory workers during manipulation of the virus especially during experimental infections of rodents.


CHHF virus has been successfully isolated from both blood and serum during the acute febrile phase of illness. Although not undertaken at the time of the initial cluster, virus can certainly be isolated from tissue obtained post-mortem if available. A subsequent complete genomic analysis of Chapare virus facilitated the development of specific molecular detection (RT-PCR) assays.

Serologic diagnosis of CHHF can be made by indirect immunofluorescent assay and ELISA. However, individuals from endemic areas who show fever, dizziness, and myalgia, accompanied by laboratory findings of low white blood cell and platelet counts and excess protein in the urine, should be suspected of having one of the South American hemorrhagic fever viruses. Clinical specimens should be tested using specific assays.


Supportive therapy is important in CHHF. This includes:

    - maintenance of hydration
    - management of shock
    - sedation
    - pain relief
    - usual precautions for patients with bleeding disorders
    - transfusions (when necessary)

Use of convalescent plasma therapy for treatment of AHF reduces mortality significantly and anecdotal evidence shows that the antiviral drug ribavirin may also hold promise for treating AHF. Ribavirin has also been considered for preventing development of disease in people exposed to other arenaviruses.
   Recovery

The precise mortality of CHHF is unknown and the only described case was fatal.

Patients who have suffered from other arenaviruses may continue to excrete virus in urine or semen for weeks after recovery. For this reason, these fluids should be monitored for infectivity, since convalescent patients have the potential to infect others (particularly sexual partners) via these fluids.


Although rodent control would be desirable, it will not be a successful strategy for preventing Chapare hemorrhagic fever cases caused by exposures outdoors.

As for other hemorrhagic fevers, full barrier nursing procedures should be implemented during management of suspected or confirmed CHHF cases.


Yersiniosis is an infectious disease caused by a bacterium of the genus Yersinia. In the United States, most human illness is caused by one species, Y. enterocolitica. Infection with Y. enterocolitica can cause a variety of symptoms depending on the age of the person infected. Infection with Y. enterocolitica occurs most often in young children. Common symptoms in children are fever, abdominal pain, and diarrhea, which is often bloody. Symptoms typically develop 4 to 7 days after exposure and may last 1 to 3 weeks or longer. In older children and adults, right-sided abdominal pain and fever may be the predominant symptoms, and may be confused with appendicitis. In a small proportion of cases, complications such as skin rash, joint pains, or spread of bacteria to the bloodstream can occur.


Y. enterocolitica is a relatively infrequent cause of diarrhea and abdominal pain. Based on data from the Foodborne Diseases Active Surveillance Network (FoodNet), which measures the burden and sources of specific diseases over time, approximately one culture-confirmed Y. enterocolitica infection per 100,000 persons occurs each year. Children are infected more often than adults, and the infection is more common in the winter.


Y. enterocolitica infections are generally diagnosed by detecting the organism in the stools. Many laboratories do not routinely test for Y. enterocolitica,so it is important to notify laboratory personnel when infection with this bacterium is suspected so that special tests can be done. The organism can also be recovered from other sites, including the throat, lymph nodes, joint fluid, urine, bile, and blood.


Uncomplicated cases of diarrhea due to Y. enterocolitica usually resolve on their own without antibiotic treatment. However, in more severe or complicated infections, antibiotics such as aminoglycosides, doxycycline, trimethoprim-sulfamethoxazole, or fluoroquinolones may be useful.


The Centers for Disease Control and Prevention (CDC) monitors the frequency of Y. enterocolitica infections through the foodborne disease active surveillance network (FoodNet). In addition, CDC conducts investigations of outbreaks of yersiniosis to control them and to learn more about how to prevent these infections. CDC has collaborated in an educational campaign to increase public awareness about prevention of Y. enterocolitica infections. The U.S. Food and Drug Administration inspects imported foods and milk pasteurization plants and promotes better food preparation techniques in restaurants and food processing plants. The U.S. Department of Agriculture monitors the health of food animals and is responsible for the quality of slaughtered and processed meat. The U.S. Environmental Protection Agency regulates and monitors the safety of our drinking water supplies.


Frequently Asked Questions (FAQs)

    Vector Information


There are three different filarial species that can cause lymphatic filariasis in humans. Most of the infections worldwide are caused by Wuchereria bancrofti. In Asia, the disease can also be caused by Brugia malayi and Brugia timori.

The infection spreads from person to person by mosquito bites. The adult worm lives in the human lymph vessels, mates, and produces millions of microscopic worms, also known as microfilariae. Microfilariae circulate in the person's blood and infect the mosquito when it bites a person who is infected. Microfilariae grow and develop in the mosquito. When the mosquito bites another person, the larval worms pass from the mosquito into the human skin, and travel to the lymph vessels. They grow into adult worms, a process that takes 6 months or more. An adult worm lives for about 5–7 years. The adult worms mate and release millions of microfilariae into the blood. People with microfilariae in their blood can serve as a source of infection to others.

A wide range of mosquitoes can transmit the parasite, depending on the geographic area. In Africa, the most common vector is Anopheles and in the Americas, it is Culex quinquefasciatus. Aedes and Mansonia can transmit the infection in the Pacific and in Asia.

Many mosquito bites over several months to years are needed to get lymphatic filariasis. People living 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.

Programs to eliminate lymphatic filariasis are under way in more than 50 countries. These programs are reducing transmission of the filarial parasites and decreasing the risk of infection for people living in or visiting these communities.
    Geographic distribution

Lymphatic filariasis affects over 120 million people in 73 countries throughout the tropics and sub-tropics of Asia, Africa, the Western Pacific, and parts of the Caribbean and South America.

In the Americas, only four countries are currently known to be endemic: Haiti, the Dominican Republic, Guyana and Brazil.

In the United States, Charleston, South Carolina, was the last known place with lymphatic filariasis. The infection disappeared early in the 20th century. Currently, you cannot get infected in the U.S.


The standard method for diagnosing active infection is the identification of microfilariae in a blood smear by microscopic examination. The microfilariae that cause lymphatic filariasis circulate in the blood at night (called nocturnal periodicity). Blood collection should be done at night to coincide with the appearance of the microfilariae, and a thick smear should be made and stained with Giemsa or hematoxylin and eosin. For increased sensitivity, concentration techniques can be used.

Serologic techniques provide an alternative to microscopic detection of microfilariae for the diagnosis of lymphatic filariasis. Patients with active filarial infection typically have elevated levels of antifilarial IgG4 in the blood and these can be detected using routine assays.

Because lymphedema may develop many years after infection, lab tests are most likely to be negative with these patients.


Patients currently infected with the parasite

Diethylcarbamazine (DEC) is the drug of choice in the United States. The drug kills the microfilaria and some of the adult worms. DEC has been used world-wide for more than 50 years. Because this infection is rare in the U.S., the drug is no longer approved by the Food and Drug Administration (FDA) and cannot be sold in the U.S. Physicians can obtain the medication from CDC after confirmed positive lab results. CDC gives the physicians the choice between 1 or 12-day treatment of DEC (6 mg/kg/day). One day treatment is generally as effective as the 12-day regimen. DEC is generally well tolerated. Side effects are in general limited and depend on the number of microfilariae in the blood. The most common side effects are dizziness, nausea, fever, headache, or pain in muscles or joints.

DEC should not be administered to patients who may also have onchocerciasis as  DEC can worsen onchocercal eye disease.  In patients with loiasis, DEC can cause serious adverse reactions, including encephalopathy and death. The risk and severity of the adverse reactions are related to Loa loa microfilarial density.
The drug ivermectin kills only the microfilariae, but not the adult worm; the adult worm is responsible for the pathology of lymphedema and hydrocele.

Some studies have shown adult worm killing with treatment with doxycycline (200mg/day for 4–6 weeks).
    Patients with clinical symptoms

Lymphedema and elephantiasis are not indications for DEC treatment because most people with lymphedema are not actively infected with the filarial parasite.

To prevent the lymphedema from getting worse, patients should ask their physician for a referral to a lymphedema therapist so they can be informed about some basic principles of care such as hygiene, exercise and treatment of wounds.

Patients with hydrocele may have evidence of active infection, but typically do not improve clinically following treatment with DEC. The treatment for hydrocele is surgery.

More on: Resources for Health Professionals: Treatment


The best way to prevent lymphatic filariasis is to avoid mosquito bites. 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:

    - at night

      - sleep in an air-conditioned room or
      - sleep under a mosquito net

    - between dusk and dawn

      - wear long sleeves and trousers and
      - use mosquito repellent on exposed skin.

Another approach to prevention includes giving entire communities medicine that kills the microscopic worms -- and controlling mosquitoes. Annual mass treatment reduces the level of microfilariae in the blood and thus, diminishes transmission of infection. This is the basis of the global campaign to eliminate lymphatic filariasis.

Experts consider that lymphatic filariasis, a neglected tropical disease (NTD), can be eradicated and a global campaign to eliminate lymphatic filariasis as a public health problem is under way. The elimination strategy is based on annual treatment of whole communities with combinations of drugs that kill the microfilariae. As a result of the generous contributions of these drugs by the companies that make them, tens of millions of people are being treated each year. Since these drugs also reduce levels of infection with intestinal worms, benefits of treatment extend beyond lymphatic filariasis. Successful campaigns to eliminate lymphatic filariasis have taken place in China and other countries.

More on: Insect Bite Prevention


Loiasis is an infection caused by the parasitic worm Loa loa.


Loa loa parasites are found in West and Central Africa. Ten countries have areas where there are high rates of infection (i.e., where more than 40% of the people who live in that area report that they have had eye worm in the past). An estimated 14.4 million people live in these areas of high rates of infection. Another 15.2 live in areas where 20–40% of people report that they have had eye worm in the past.

More on: Where Loa Loa is Prevelant [WHO Map]

The people most at risk for loiasis are those who live in the certain rain forests in West and Central Africa. The deerflies that pass the parasite to humans usually bite during the day and are more common during the rainy season. They are attracted by the movement of people and by smoke from wood fires. Rubber plantations are areas where more deerflies may be found. The flies do not typically enter homes, but they might be attracted to homes that are well lit.

Travelers are more likely to become infected if they are in areas where they are bitten by deerflies for many months, though occasionally they get infected even if they are in an affected area for less than 30 days.

Your risk of infection depends on the number of bites received, the number of infected deerflies in the area you visit, and the length of your stay in the area.


In people who have been bitten by the flies that carry Loa loa in areas where Loa loa is known to exist, the diagnosis can be made in the following ways:

   - Identification of the adult worm by a microbiologist or pathologist after its removal from under the skin or eye
   - Identification of an adult worm in the eye by a health care provider
   - Identification of the microfilariae on a blood smear made from blood taken from the patient between 10AM and 2PM
   - Identification of antibodies against L. loa on specialized blood test

Diagnosis of loiasis can be difficult, especially in light infections where there are very few microfilariae in the blood. The specialized blood test is not widely available in the United States. A positive antibody blood test in someone with no symptoms means only that the person was infected sometime in his/her life. It does not mean that the person still has living parasites in his/her body.


Decisions about treatment of loiasis can be difficult and often require advice from an expert in infectious diseases or tropical medicine. Although surgical removal of adult worms moving under the skin or across the eye can be done to relieve anxiety, loiasis is not cured by surgery alone. There are two medications that can be used to treat the infection and manage the symptoms. The treatment of choice is diethylcarbamazine (DEC), which kills the microfilariae and adult worms. Albendazole is sometimes used in patients who are not cured with multiple DEC treatments. It is thought to kill adult worms. Certain people with heavy infections are at risk of brain inflammation when treated with DEC. This can cause coma or sometimes death. People with heavy infections need to be treated by experienced specialists.  Sometimes, other medical conditions need to be addressed first in order to make it safer to use DEC. Sometimes treatment is not recommended.

More on: Resources for Health Professionals: Treatment


There are no programs to control or eliminate loiasis in affected areas. Your risk of infection may be less in areas where communities receive regular treatment for onchocerciasis or lymphatic filariasis.

There are no vaccines that protect you from loiasis. If you are going to be in an area with loiasis for a long period of time, diethylcarbamazine (DEC)—300mg taken once a week—can reduce your risk of infection. Avoiding areas where the deerflies are found, such as muddy, shaded areas along rivers or around wood fires, may also reduce your risk of infection. You may reduce your risk of bites by using insect repellants that contain DEET (N,N-Diethyl-meta-toluamide) and wearing long sleeves and long pants during the day, which is when deerflies bite. Treating your clothes with permethrin may also help. For a description of CDC's information for preventing insect bites, see CDC's Yellow Book.

More on: Insect Bite Prevention


Humans can become infected through tick bites or through contact with the blood, feces, or urine of an infected, sick, or dead animal – most commonly, rodents. Occupational and recreational activities such as hunting or trapping may increase human risk of infection.

Transmission may also occur with no direct tick or rodent exposure as OHFV appears to be extremely stable in different environments. It has been isolated from aquatic animals and water and there is even evidence that OHFV can be transmitted through the milk of infected goats or sheep to humans.

No human-to-human transmission of OHFV has been documented but infections due to lab contamination have been described.


After an incubation period of 3-8 days, the symptoms of OHF begin suddenly with chills, fever, headache, and severe muscle pain with vomiting, gastrointestinal symptoms and bleeding problems occurring 3-4 days after initial symptom onset. Patients may experience abnormally low blood pressure and low platelet, red blood cell, and white blood cell counts.

After 1-2 weeks of symptoms, some patients recover without complication. However, the illness is biphasic for a subset of patients who experience a second wave of symptoms at the beginning of the third week. These symptoms include fever and encephalitis (inflammation of the brain).

The case fatality rate of OHF is low (0.5% to 3%).


In areas where rodent reservoirs and tick species are prevalent, people with recreational or occupational exposure to rural or outdoor settings (e.g., hunters, campers, forest workers, farmers) are potentially at increased risk for OHF by contact with infected ticks and animals. Furthermore, those in Siberia who hunt and trap muskrats specifically are at higher risk for OHF.

Exposure may also occur in the laboratory environment.


OHF virus may be detected in blood samples by virus isolation in cell culture or using molecular techniques such as PCR. Blood samples can also be tested for antibody presence using enzyme-linked immunosorbent seologic assay (ELISA).


There is no specific treatment for OHF, but supportive therapy is important. Supportive therapy includes the maintenance of hydration and the usual precautions for patients with bleeding disorders.

Though rare, OHF can cause hearing loss, hair loss, and behavioral or psychological difficulties associated with neurological conditions and long term supportive case may be needed.


There is no vaccine currently available for OHF, but vaccines for tick-borne encephalitis disease (TBE) have been shown to confer some immunity and may be used for high-risk groups.

Additionally, utilizing insect repellents and wearing protective clothing in areas where ticks are endemic is recommended.


A pinworm ("threadworm") is a small, thin, white roundworm (nematode) called Enterobius vermicularis that sometimes lives in the colon and rectum of humans. Pinworms are about the length of a staple. While an infected person sleeps, female pinworms leave the intestine through the anus and deposit their eggs on the surrounding skin.


Risk Factors

The people most likely to be infected with pinworm are children under 18, people who take care of infected children and people who are institutionalized. In these groups, the prevalence can reach 50%.

Pinworm is the most common worm infection in the United States. Humans are the only species that can transfer this parasite. Household pets like dogs and cats cannot become infected with human pinworms. Pinworm eggs can survive in the indoor environment for 2 to 3 weeks.
    Epidemiology

Pinworm infections are more common within families with school-aged children, in primary caregivers of infected children, and in institutionalized children.

A person is infected with pinworms by ingesting pinworm eggs either directly or indirectly. These eggs are deposited around the anus by the worm and can be carried to common surfaces such as hands, toys, bedding, clothing, and toilet seats. By putting anyone’s contaminated hands (including one’s own) around the mouth area or putting one’s mouth on common contaminated surfaces, a person can ingest pinworm eggs and become infected with the pinworm parasite. Since pinworm eggs are so small, it is possible to ingest them while breathing.

Once someone has ingested pinworm eggs, there is an incubation period of 1 to 2 months or longer for the adult gravid female to mature in the small intestine. Once mature, the adult female worm migrates to the colon and lays eggs around the anus at night, when many of their hosts are asleep. People who are infected with pinworm can transfer the parasite to others for as long as there is a female pinworm depositing eggs on the perianal skin. A person can also re-infect themselves, or be re-infected by eggs from another person.


A person infected with pinworm is often asymptomatic, but itching around the anus is a common symptom. Diagnosis of pinworm can be reached from three simple techniques. The first option is to look for the worms in the perianal reqion 2 to 3 hours after the infected person is asleep. The second option is to touch the perianal skin with transparent tape to collect possible pinworm eggs around the anus first thing in the morning. If a person is infected, the eggs on the tape will be visible under a microscope. The tape method should be conducted on 3 consecutive mornings right after the infected person wakes up and before he/she does any washing. Since anal itching is a common symptom of pinworm, the third option for diagnosis is analyzing samples from under fingernails under a microscope. An infected person who has scratched the anal area may have picked up some pinworm eggs under the nails that could be used for diagnosis.

Since pinworm eggs and worms are often sparse in stool, examining stool samples is not recommended. Serologic tests are not available for diagnosing pinworm infections.


The medications used for the treatment of pinworm are mebendazole, pyrantel pamoate, and albendazole. All three of these drugs are to be given in 1 dose at first and then another single dose 2 weeks later. Pyrantel pamoate is available without prescription. The medication does not reliably kill pinworm eggs. Therefore, the second dose is to prevent re-infection by adult worms that hatch from any eggs not killed by the first treatment.Health practitioners and parents should weigh the health risks and benefits of these drugs for patients under 2 years of age.

Repeated infections should be treated by the same method as the first infection. In households where more than one member is infected or where repeated, symptomatic infections occur, it is recommended that all household members be treated at the same time. In institutions, mass and simultaneous treatment, repeated in 2 weeks, can be effective.


Washing your hands with soap and warm water after using the toilet, changing diapers, and before handling food is the most successful way to prevent pinworm infection. In order to stop the spread of pinworm and possible re-infection, people who are infected should bathe every morning to help remove a large amount of the eggs on the skin. Showering is a better method than taking a bath, because showering avoids potentially contaminating the bath water with pinworm eggs. Infected people should not co-bathe with others during their time of infection.

Also, infected people should comply with good hygiene practices such as washing their hands with soap and warm water after using the toilet, changing diapers, and before handling food. They should also cut fingernails regularly, and avoid biting the nails and scratching around the anus. Frequent changing of underclothes and bed linens first thing in the morning is a great way to prevent possible transmission of eggs in the environment and risk of reinfection. These items should not be shaken and carefully placed into a washer and laundered in hot water followed by a hot dryer to kill any eggs that may be there.

In institutions, day care centers, and schools, control of pinworm can be difficult, but mass drug administration during an outbreak can be successful. Teach children the importance of washing hands to prevent infection.

More on: Handwashing


Diagnosing HPS

Diagnosing HPS in an individual who has only been infected a few days is difficult, because early symptoms such as fever, muscle aches, and fatigue are easily confused with influenza. However, if the individual is experiencing fever and fatigue and has a history of potential rural rodent exposure, together with shortness of breath, would be strongly suggestive of HPS. If the individual is experiencing these symptoms they should see their physician immediately and mention their potential rodent exposure.
  Treating HPS

There is no specific treatment, cure, or vaccine for hantavirus infection. However, we do know that if infected individuals are recognized early and receive medical care in an intensive care unit, they may do better. In intensive care, patients are intubated and given oxygen therapy to help them through the period of severe respiratory distress.

The earlier the patient is brought in to intensive care, the better. If a patient is experiencing full distress, it is less likely the treatment will be effective.

Therefore, if you have been around rodents and have symptoms of fever, deep muscle aches, and severe shortness of breath, see your doctor immediately. Be sure to tell your doctor that you have been around rodents—this will alert your physician to look closely for any rodent-carried disease, such as HPS.


Due to the small number of HPS cases, the "incubation time" is not positively known. However, on the basis of limited information, it appears that symptoms may develop between 1 and 5 weeks after exposure to fresh urine, droppings, or saliva of infected rodents.
  Early Symptoms

Early symptoms include fatigue, fever and muscle aches, especially in the large muscle groups—thighs, hips, back, and sometimes shoulders. These symptoms are universal.

There may also be headaches, dizziness, chills, and abdominal problems, such as nausea, vomiting, diarrhea, and abdominal pain. About half of all HPS patients experience these symptoms.

  Late Symptoms

Four to 10 days after the initial phase of illness, the late symptoms of HPS appear. These include coughing and shortness of breath, with the sensation of, as one survivor put it, a "...tight band around my chest and a pillow over my face" as the lungs fill with fluid.

  Is the Disease Fatal?

Yes. HPS can be fatal. It has a mortality rate of 38%.


Eliminate or minimize contact with rodents in your home, workplace, or campsite. If rodents don't find that where you are is a good place for them to be, then you're less likely to come into contact with them. Seal up holes and gaps in your home or garage. Place traps in and around your home to decrease rodent infestation. Clean up any easy-to-get food.

Recent research results show that many people who became ill with HPS developed the disease after having been in frequent contact with rodents and/or their droppings around a home or a workplace. On the other hand, many people who became ill reported that they had not seen rodents or rodent droppings at all. Therefore, if you live in an area where the carrier rodents are known to live, try to keep your home, vacation place, workplace, or campsite clean.

For more information on how you can prevent rodent infestations, the following information is available on the CDC Rodents site:


The "First"Outbreak

In May 1993, an outbreak of an unexplained pulmonary illness occurred in the southwestern United States, in an area shared by Arizona, New Mexico, Colorado and Utah known as "The Four Corners". A young, physically fit Navajo man suffering from shortness of breath was rushed to a hospital in New Mexico and died very rapidly.

While reviewing the results of the case, medical personnel discovered that the young man's fiancée had died a few days before after showing similar symptoms, a piece of information that proved key to discovering the disease. As Dr. James Cheek of the Indian Health Service (IHS) noted, "I think if it hadn't been for that initial pair of people that became sick within a week of each other, we never would have discovered the illness at all".

An investigation combing the entire Four Corners region was launched by the New Mexico Office of Medical Investigations (OMI) to find any other people who had a similar case history. Within a few hours, Dr. Bruce Tempest of IHS, working with OMI, had located five young, healthy people who had all died after acute respiratory failure.

A series of laboratory tests had failed to identify any of the deaths as caused by a known disease, such as bubonic plague. At this point, the CDC Special Pathogens Branch was notified. CDC, the state health departments of New Mexico, Colorado and Utah, the Indian Health Service, the Navajo Nation, and the University of New Mexico all joined together to confront the outbreak.

During the next few weeks, as additional cases of the disease were reported in the Four Corners area, physicians and other scientific experts worked intensively to narrow down the list of possible causes. The particular mixture of symptoms and clinical findings pointed researchers away from possible causes, such as exposure to a herbicide or a new type of influenza, and toward some type of virus. Samples of tissue from patients who had gotten the disease were sent to CDC for exhaustive analysis. Virologists at CDC used several tests, including new methods to pinpoint virus genes at the molecular level, and were able to link the pulmonary syndrome with a virus, in particular a previously unknown type of hantavirus.
  Researchers Launch Investigations to Pin Down the Carrier of the New Virus

Researchers knew that all other known hantaviruses were transmitted to people by rodents, such as mice and rats. Therefore, an important part of their mission was to trap as many different species of rodents living in the Four Corners region as possible to find the particular type of rodent that carried the virus. From June through mid-August of 1993, all types of rodents were trapped inside and outside homes where people who had hantavirus pulmonary syndrome had lived, as well as in piñon groves and summer sheep camps where they had worked. Additional rodents were trapped for comparison in and around nearby households as well. Taking a calculated risk, researchers decided not to wear protective clothing or masks during the trapping process. "We didn't want to go in wearing respirators, scaring...everybody", John Sarisky, an Indian Health Service environmental disease specialist said. However, when the almost 1,700 rodents trapped were dissected to prepare samples for analysis at CDC, protective clothing and respirators were worn.

Among rodents trapped, the deer mouse (Peromyscus maniculatus) was found to be the main host to a previously unknown type of hantavirus. Since the deer mouse often lives near people in rural and semi-rural areas—in barns and outbuildings, woodpiles, and inside people's homes—researchers suspected that the deer mouse might be transmitting the virus to humans. About 30% of the deer mice tested showed evidence of infection with hantavirus. Tests also showed that several other types of rodents were infected, although in lesser numbers.

The next step was to pin down the connection between the infected deer mice and households where people who had gotten the disease lived. Therefore, investigators launched a case-control investigation. They compared "case" households, where people who had gotten the disease lived, with nearby "control" households. Control households were similar to those where the case-patients lived, except for one factor: no one in the control households had gotten the disease.

The results? First, investigators trapped more rodents in case households than in control households, so more rodents may have been living in close contact with people in case households. Second, people in case households were more likely than those in control households to do cleaning around the house or to plant in or hand-plow soil outdoors in fields or gardens. However, it was unclear if the risk for contracting HPS was due to performing these tasks, or with entering closed-up rooms or closets to get tools needed for these tasks.

In November 1993, the specific hantavirus that caused the Four Corners outbreak was isolated. The Special Pathogens Branch at CDC used tissue from a deer mouse that had been trapped near the New Mexico home of a person who had gotten the disease and grew the virus from it in the laboratory. Shortly afterwards and independently, the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) also grew the virus, from a person in New Mexico who had gotten the disease as well as from a mouse trapped in California.

The new virus was called Muerto Canyon virus — later changed to Sin Nombre virus (SNV) — and the new disease caused by the virus was named hantavirus pulmonary syndrome, or HPS.

The isolation of the virus in a matter of months was remarkable. This success was based on close cooperation of all the agencies and individuals involved in investigating the outbreak, years of basic research on other hantaviruses that had been conducted at CDC and USAMRIID, and on the continuing development of modern molecular virologic tests. To put the rapid isolation of the Sin Nombre virus in perspective, it took several decades for the first hantavirus discovered, the Hantaan virus, to be isolated.

  HPS Not Really a New Disease

As part of the effort to locate the source of the virus, researchers located and examined stored samples of lung tissue from people who had died of unexplained lung disease. Some of these samples showed evidence of previous infection with Sin Nombre virus—indicating that the disease had existed before the "first" known outbreak—it simply had not been recognized!

Other early cases of HPS have been discovered by examining samples of tissue belonging to people who had died of unexplained adult respiratory distress syndrome. By this method, the earliest known case of HPS that has been confirmed has been the case of a 38-year-old Utah man in 1959.

Interestingly, while HPS was not known to the epidemiologic and medical communities, there is evidence that it was recognized elsewhere. The Navajo Indians, a number of whom contracted HPS during the 1993 outbreak, recognize a similar disease in their medical traditions, and actually associate its occurrence with mice. As strikingly, Navajo medical beliefs concur with public health recommendations for preventing the disease.

  Why Did the Outbreak Occur in the Four Corners Area?

But why this sudden cluster of cases? The key answer to this question is that, during this period, there were suddenly many more mice than usual. The Four Corners area had been in a drought for several years. Then, in early 1993, heavy snows and rainfall helped drought-stricken plants and animals to revive and grow in larger-than-usual numbers. The area's deer mice had plenty to eat, and as a result they reproduced so rapidly that there were ten times more mice in May 1993 than there had been in May of 1992. With so many mice, it was more likely that mice and humans would come into contact with one another, and thus more likely that the hantavirus carried by the mice would be transmitted to humans.

  Person-to-Person Spread of HPS Decided Unlikely

"Although person-to-person spread [of HPS] has not been documented with any of the other known hantaviruses, we were concerned [during this outbreak] because we were dealing with a new agent", said Charles Vitek, a CDC medical investigator.

Researchers and clinicians investigating the ongoing outbreak were not the only groups concerned about the disease. Shortly after the first few HPS patients died and it became clear that a new disease was affecting people in the area, and that no one knew how it was transmitted, the news media began extensive reporting on the outbreak. Widespread concern among the public ensued.

Unfortunately, the first victims of the outbreak were Navajo. News reports focused on this fact, and the misperception grew that the unknown disease was somehow linked to Navajos. As a consequence, Navajos found themselves at the center of intense media attention and the objects of the some people's fears.

By later in the summer of 1993, the media frenzy had quieted somewhat, and the source of the disease was pinpointed. Researchers determined that, like other hantaviruses, the virus that causes HPS is not transmitted from person to person the way other infections, such as the common cold, may be. The exception to this is an outbreak of HPS in Argentina in 1996. Evidence from this outbreak suggests that strains of hantaviruses in South America may be transmissable from person to person.

To date, no cases of HPS have been reported in the United States in which the virus was transmitted from one person to another. In fact, in a study of health care workers who were exposed to either patients or specimens infected with related types of hantaviruses (which cause a different disease in humans), none of the workers showed evidence of infection or illness.

  HPS Since the First Outbreak

After the initial outbreak, the medical community nationwide was asked to report any cases of illness with symptoms similar to those of HPS that could not be explained by any other cause. As a result, additional cases have been reported.

Since 1993, researchers have discovered that there is not just one hantavirus that causes HPS, but several. In June 1993, a Louisiana bridge inspector who had not traveled to the Four Corners area developed HPS. An investigation was begun. The patient's tissues were tested for the presence of antibodies to hantavirus. The results led to the discovery of another hantavirus, named Bayou virus, which was linked to a carrier, the rice rat (Oryzomys palustris). In late 1993, a 33-year-old Florida man came down with HPS symptoms; he later recovered. This person also had not traveled to the Four Corners area. A similar investigation revealed yet another hantavirus, named the Black Creek Canal virus, and its carrier, the cotton rat (Sigmodon hispidus). Another case occurred in New York. This time, the Sin Nombre-like virus was named New York-1, and the white-footed mouse (Peromyscus leucopus), was implicated as the carrier.

More recently, cases of HPS stemming from related hantaviruses have been documented in Argentina, Brazil, Canada, Chile, Paraguay, and Uruguay, making HPS a pan-hemispheric disease.

  References

Information for this page was developed using the CDC video Preventing Hantavirus Disease and resource articles listed in the bibliography.


Q fever can cause acute or chronic illness in humans, who usually acquire infection after contact with infected animals or exposure to contaminated environments. The acute symptoms caused by infection with Coxiella burnetii usually develop within 2-3 weeks of exposure, although as many as half of humans infected withC. burnetii do not show symptoms.

The following is a list of symptoms commonly seen with acute Q fever. However, it is important to note that the combination of symptoms varies greatly from person to person.

  - high fevers (up to 104-105°F)
  - severe headache
  - general malaise
  - myalgia
  - chills and/or sweats
  - non-productive cough
  - nausea
  - vomiting
  - diarrhea
  - abdominal pain
  - chest pain

Although most persons with acute Q fever infection recover, others may experience serious illness with complications that may include pneumonia, granulomatous hepatitis (inflammation of the liver), myocarditis (inflammation of the heart tissue) and central nervous system complications. Pregnant women who are infected may be at risk for pre-term delivery or miscarriage. The estimated case fatality rate (i.e. the proportion of persons who die as a result of their infection) is low,  at < 2% of hospitalized patients. Treatment with the correct antibiotic may shorten the course of illness for acute Q fever.

Chronic Q fever is a severe disease occurring in <5% of acutely infected patients. It may present soon (within 6 weeks) after an acute infection, or may manifest years later.  The three groups at highest risk for chronic Q fever are pregnant women, immunosuppressed persons and patients with a pre-existing heart valve defects. Endocarditis is the major form of chronic disease, comprising 60-70% of all reported cases. The estimated case fatality rate in untreated patients with endocarditis is 25-60%. Patients with endocarditis require early diagnosis and long-term antibiotic treatment (at least 18 months) for a successful outcome.   Other forms of chronic Q fever include aortic aneurysms and infections of the bone, liver or reproductive organs, such as the testes in males.

Coxiella burnetii has the ability to persist for long periods of time in the host after infection. Although the majority of people with acute Q fever recover completely, a post-Q fever fatigue syndrome has been reported to occur in 10-25% of some acute patients. This syndrome is characterized by constant or recurring fatigue, night sweats, severe headaches, photophobia (eye sensitivity to light), pain in muscles and joints, mood changes, and difficulty sleeping.

 Physician Diagnosis

There are several aspects of Q fever that make it challenging for healthcare providers to diagnose and treat.  The symptoms vary from patient to patient and can be difficult to distinguish from other diseases.  Treatment is more likely to be effective if started in the first three days of symptoms. Diagnostic tests based on the detection of antibodies will frequently appear negative in the first 7-10 days of illness.  For this reason, healthcare providers must use their judgment to treat patients based on clinical suspicion alone. Healthcare providers may find important information in the patient’s history and physical examination that may aid clinical diagnosis. Information such as recent travel to rural or agricultural communities where infected livestock may be present, or employment in high risk occupations such as veterinarians or farmers can be helpful in making the diagnosis.  Chronic Q fever is a risk for anyone with a history of acute Q fever illness, particularly those persons with valvular disease, blood vessel abnormalities, immunosuppressed persons, and women who were pregnant when they became infected.

The healthcare provider should also look at routine blood tests, such as a complete blood cell count or a chemistry panel. Clues such as a prolonged fever with low platelet count, normal leukocyte count, and elevated liver enzymes are suggestive of acute Q fever infection, but may not be present in all patients.  After a suspect diagnosis is made based on clinical suspicion and treatment has begun, specialized laboratory testing should be used to confirm the diagnosis of Q fever.

Suspect diagnosis of Q fever is made based on signs and symptoms and a high index of clinical suspicion.  Diagnosis can later be confirmed using specialized confirmatory laboratory tests. Treatment should never be delayed pending the receipt of laboratory test results, or be withheld on the basis of an initial negative laboratory result.

 Laboratory Confirmation

During the acute phase of illness, a sample of whole blood can be tested by polymerase chain reaction (PCR) assay to determine if a patient has Q fever. This method is most sensitive in the first week of illness, and rapidly decreases in sensitivity following the administration of appropriate antibiotics. PCR or immunohistochemistry of biopsy specimens has also been used to diagnose Q fever. These tests may be appropriate for endocarditis patients undergoing valve replacement surgery or patients with hepatitis. Although a positive PCR result is helpful, a negative result does not rule out the diagnosis, and treatment should not be withheld due to a negative result. Culture isolation of C. burnetii is only available at specialized laboratories; routine hospital blood cultures cannot detect the organism.

When a person develops Q fever, their immune system produces antibodies to C. burnetii, with detectable antibody titers usually observed by 7-10 days after illness onset.  It is important to note that a negative test during the first week of illness does not rule out Q fever as a cause of illness. There are two distinct antigenic phases to which humans develop antibody responses. In acute infection, an antibody response to C. burnetii Phase II antigen is predominant and is higher than Phase I antibody response; the reverse is true in chronic infection which is associated with a rising Phase I IgG titer (according to current U.S. case definitions >1:800) that is often much higher than Phase II IgG.  The gold standard serologic test for diagnosis of acute Q fever is the indirect immunofluorescence assay (IFA) using C. burnetii antigen, performed on paired serum samples to demonstrate a significant (four-fold) rise in antibody titers. The first sample should be taken as early in the disease as possible, preferably in the first week of symptoms, and the second sample should be taken 2 to 4 weeks later. In most cases of Q fever, the first IgG IFA titer is typically low, or “negative,” and the second typically shows a significant (four-fold) increase in IgG antibody levels. IgM antibodies usually rise at the same time as IgG near the end of the first week of illness and remain elevated for months or longer.  Also, IgM antibodies are less specific than IgG antibodies and more likely to result in a false positive.  For these reasons, physicians should request both Phase I and Phase II IgG and IgM serologic titers for diagnostic confirmation of acute and chronic Q fever.  Antibodies to C. burnetii may remain elevated for months or longer after the disease has resolved, or may be detected in persons who were previously exposed to antigenically related organisms.  Approximately 3% of currently healthy people in the U.S. general population and up to 20% of people in high-risk professions (veterinarians, ranchers, etc.) have elevated antibody titers due to past exposure to C. burnetii. Therefore, if only one sample is tested it can be difficult to interpret the findings.

Paired samples taken 2-3 weeks apart demonstrating a significant (four-fold) rise in antibody titer provides the best evidence for a correct diagnosis of acute Q fever. Diagnosis of chronic Q fever is confirmed by elevated Phase I IgG antibody (according to current U.S. case definitions >1:800 and higher than Phase II IgG) and an identifiable persistent focus of infection (e.g. endocarditis).  Elevated Phase I titers alone do not confirm a chronic Q fever diagnosis and would not warrant treatment in a clinically normal patient. Because chronic Q fever involves lengthy persistence of the organism in the body, the antibody levels are often quite high and you will not see a rising titer between paired serum specimens.

For more in-depth information about the diagnosis of Q fever, please visit http://www.bt.cdc.gov/agent/qfever/clinicians/diagnosis.asp

 Treatment

Doxycycline is the first line treatment for all adults, and for children with severe illness. Treatment should be initiated immediately whenever Q fever is suspected.

Use of antibiotics other than doxycycline or other tetracyclines is associated with a higher risk of severe illness. Doxycycline is most effective at preventing severe complications from developing if it is started early in the course of disease. Therefore, treatment must be based on clinical suspicion alone and should always begin before laboratory results return.

If the patient is treated within the first 3 days of the disease, fever generally subsides within 72 hours.  In fact, failure to respond to doxycycline suggests that the patient’s condition might not be due to Q fever. Severely ill patients may require longer periods before their fever resolves. Resistance to doxcycline has not been documented.

There is no role for prophylactic antimicrobial agents in preventing Q fever after a known exposure and prior to symptom onset; attempts at prophylaxis will likely extend the incubation period by several days but will not prevent infection from occurring.

Recommended Dosage for Acute Q fever
 Doxycycline is the first line treatment for children with severe illness of all ages and adults:

  - Adults: 100 mg every 12 hours
  - Children under 45 kg (100 lbs): 2.2 mg/kg body weight given twice a day

Patients should be treated for at least 3 days after the fever subsides and until there is evidence of clinical improvement. Standard duration of treatment is 2-3 weeks.

Recommended Dosage for Chronic Q fever

  - Adults: Doxycycline 100 mg every 12 hours and hydroxychloroquine 200 mg every 8 hours.

Standard duration of treatment is 18 months.

 Treating children

The use of doxycycline is recommended to treat Q fever in children of all ages who are hospitalized or are severely ill. Unlike older generations of tetracyclines, doxycycline has not been shown to cause staining of permanent teeth, and most experts consider the benefit of doxycycline in treating Q fever in children younger than 8 years of age with severe illness or who are hospitalized greater than the potential risk of dental staining.  Children with mild illness who are less than 8 years of age may be treated with co-trimoxazole, but therapy should be switched to doxycycline if their course of illness worsens.

 Other Treatments

In cases of life threatening allergies to doxycycline and in pregnant patients, physicians may need to consider alternate antibiotics. Treatment of pregnant women diagnosed with acute Q fever with once daily co-trimoxazole throughout pregnancy has been shown to significantly decrease the risk of adverse consequences for the fetus.


More detailed information on the diagnosis, management, and treatment of Q fever is available in other sections of this web site and in the materials referenced in the section titled “Further Reading”.
 How to Contact the Rickettsial Zoonoses Branch at CDC

The general public and healthcare providers should first call 1-800-CDC-INFO (1-800-232-4636) for questions regarding Q fever. If a consultation with a CDC scientist specializing in Q fever is advised, your call will be appropriately forwarded.
 Case Definitions

As of January 1, 2009, Q fever infections are reported under distinct reporting categories described in the 2009 Q fever surveillance case definition.
2009 Q Fever Case Definition
 Case Report Forms

For confirmed and probable cases of Q fever that have been identified and reported through the National Notifiable Disease Surveillance System, states are also encouraged to submit additional information using the CDC Case Report Form (CRF). This form collects additional important information that routine electronic reporting does not, such as information on how the diagnosis was made, and whether the patient was hospitalized or died. If a different state-specific form is already used to collect this information, this information may be submitted to CDC in lieu of a CRF.

 How to Submit Specimens to CDC for Q FeverTesting

Private citizens may not directly submit specimens to CDC for testing. If you feel that diagnostic testing is necessary, consult your healthcare provider or state health department. Laboratory testing is available at many commercial laboratories.
 State Health Departments

Specimens may be submitted to CDC for reference testing for Q fever. To coordinate specimen submission, please call 404-639-1075 during business hours (8:00 - 4:30 ET).
 U.S. Healthcare Providers

Q fever laboratory testing is available at many commercial laboratories. U.S. healthcare providers should not submit specimens for testing directly to CDC. CDC policy requires that specimens for testing be submitted through or with the approval of the state health department. Please contact your state health department and request assistance with specimen submission and reporting of infection. For general questions about Q fever, please call 1-800-CDC-INFO (1-800-232-4636). If you have questions about a suspect Q fever case, please first consult your state health department. Healthcare providers requiring an epidemiologic or laboratory consultation on Q fever may also call 404-639-1075 during business hours (8:00 - 4:30 ET). Or 770-488-7100 after hours.
 Non-U.S. Healthcare Providers

Non-U.S. healthcare providers should consult CDC prior to submitting specimens for testing. For general questions about Q fever, please call 1-800-CDC-INFO (1-800-232-4636). If you would like to discuss a suspect Q fever case with CDC, please call 404-639-1075 during business hours (8:00 - 4:30 ET), or 770-488-7100 after hours.


In the United States, Q fever outbreaks have resulted mainly from occupational exposure involving veterinarians, meat processing plant workers, sheep and dairy workers, livestock farmers, and researchers at facilities housing sheep. Prevention and control efforts should be directed primarily toward these groups and environments.

The following measures should be used in the prevention and control of Q fever:

  - Educate the public on sources of infection.
  - Appropriately dispose of placenta, birth products, fetal membranes, and aborted fetuses at facilities housing sheep and goats.
  - Restrict access to barns and laboratories used in housing potentially infected animals.
  - Use appropriate procedures for bagging, autoclaving, and washing of laboratory clothing.
  - Vaccinate (where possible) individuals engaged in research with pregnant sheep or live C. burnetii.
  - Quarantine imported animals.
  - Ensure that holding facilities for sheep should be located away from populated areas. Animals should be routinely tested for antibodies to C. burnetii, and measures should be implemented to prevent airflow to other occupied areas.
  - Counsel persons at highest risk for developing chronic Q fever, especially persons with pre-existing cardiac valvular disease or individuals with vascular grafts.

A vaccine for Q fever has been developed and has successfully protected humans in occupational settings in Australia. However, this vaccine is not commercially available in the United States. Persons wishing to be vaccinated should first have a skin test to determine a history of previous exposure. Individuals who have previously been exposed to C. burnetii should not receive the vaccine because severe reactions, localized to the area of the injected vaccine, may occur. A vaccine for use in animals has also been developed, but it is not available in the United States.
 Significance for Bioterrorism

Coxiella burnetii is a highly infectious agent that is rather resistant to heat and drying. It can become airborne and inhaled by humans. A single C. burnetii organism may cause disease in a susceptible person. This agent has a past history of being developed for use in biological warfare and is considered a potential terrorist threat.


Transmission of Hendra virus to humans can occur after exposure to body fluids and tissues or excretions of horses infected with Hendra virus.

Horses may be infected after exposure to virus in the urine of infected flying foxes.

To date, no human-to-human transmission has been documented.


After an incubation of 9-16 days, infection with Hendra virus can lead to respiratory illness with severe flu-like signs and symptoms. In some cases, illness may progress to encephalitis.

Although infection with Hendra virus is rare, the case fatality is high: 4/7 (57%).


Australia’s “Flying fox” bats (genus Pteropus) are the natural reservoir of Hendra virus. Serologic evidence for HeV infection have been found in all fours species of Australian flying foxes, but spillover of the virus in horses is limited to coastal and forested regions in Australia (Queensland and New South Wales states)  (see Henipavirus Distribution Map).

People at highest risk are those living within the distribution of the flying foxes and with occupational or recreational exposure to horses that have had potential contact with flying foxes in Australia.


Laboratory tests that are used to diagnose Hendra virus (HV) and Nipah virus (NV) include detection of antibody by ELISA (IgG and IgM), real time polymerase chain reaction (RT-PCR), and virus isolation attempts.  In most countries, handling Hendra virus needs to be done in high containment laboratories. Laboratory diagnosis of a patient with a clinical history of HV or NV can be made during the acute and convalescent phase of the disease by using a combination of tests including detection of antibody in the serum or the cerebrospinal fluid (CSF), viral RNA detection (RT-PCR) in the serum, CSF, or throat swabs, and virus isolation from the CSF or throat swabs.


The drug ribavirin has been shown to be effective against the viruses in vitro, but the clinical usefulness of this drug is uncertain.

A post-exposure therapy with a Nipah/Hendra neutralizing antibody, efficacious in animal models is in human preclinical development stages in Australia.


The occurrence of the disease in humans has been associated only with infection of an intermediate species such as horses.  Early recognition of the disease in the intermediate animal host is probably the most crucial means of limiting future human cases.

Hendra virus infection can be prevented by avoiding horses that are ill or may be infected with HeV and using appropriate personal protective equipment when contact is necessary, as in veterinary procedures.

A commercial vaccine has been recently licensed in Australia for horses and could be beneficial for other animal species and eventually humans.


There are many different species of hookworms, some are human parasites and some are animal parasites. People can be infected by larvae of animal hookworms, usually dog and cat hookworms. The most common result of animal hookworm infection is a skin condition called cutaneous larva migrans.


Dog and cat hookworms are found throughout the world, especially in warmer climates. In the United States, zoonotic hookworms are found everywhere but more commonly along the East Coast than the West Coast. Worldwide, zoonotic hookworms are found in tropical and subtropical regions where the parasite is better able to survive because of environmental conditions. However, there is one type of dog and cat hookworm that is more commonly found in cooler climates.

The global burden of zoonotic hookworm in dogs and cats is not known; also, the amount of disease in people caused by these parasites is also unknown. Cutaneous larva migrans (CLM) is most often reported by returning travelers to tropical regions who have had soil and/or sand exposures in places where dogs and cats are likely to have hookworms. However, CLM is likely causing significant problems for the people who live in less developed parts of the world, even though the disease is not reported regularly. In less developed areas of the world, dogs and cats are often free-ranging and have high rates of infection with hookworm which leads to widespread contamination of sand and soil. In a survey of a rural population in Brazil, the prevalence of CLM during the rainy season was 14.9% among children less than 5 years old and 0.7% among adults aged 20 years and older.


Cutaneous larva migrans (CLM) is a clinical diagnosis based on the presence of the characteristic signs and symptoms, and exposure history to zoonotic hookworm. For example, the diagnosis can be made based on finding red, raised tracks in the skin that are very itchy. This is usually found on the feet or lower part of the legs on persons who have recently traveled to tropical areas and spent time at the beach. There is no blood test for zoonotic hookworm infection. Persons who think they have CLM should consult their health care provider for accurate diagnosis.


The zoonotic hookworm larvae that cause cutaneous larva migrans (CLM) usually do not survive more than 5 – 6 weeks in the human host. In most patients with CLM, the signs and symptoms resolve without medical treatment. However, treatment may help control symptoms and help prevent secondary bacterial infections. Antiparasitic treatments may be prescribed by your health care provider.

More on: Resources For Health Professionals: Treatment


Wearing shoes and taking other protective measures to avoid skin contact with sand or soil will prevent infection with zoonotic hookworms. Travelers to tropical and subtropical climates, especially where beach exposures are likely, should be advised to wear shoes and use protective mats or other coverings to prevent direct skin contact with sand or soil. Routine veterinary care of dogs and cats, including regular deworming, will reduce environmental contamination with zoonotic hookworm eggs and larvae. Prompt disposal of animal feces prevents eggs from hatching and contaminating soil -- which makes it important for control of this parasitic infection.


Chronic fatigue syndrome, or CFS, is a devastating and complex disorder. People with CFS have overwhelming fatigue and a host of other symptoms that are not improved by bed rest and that can get worse after physical activity or mental exertion. They often function at a substantially lower level of activity than they were capable of before they became ill.

Besides severe fatigue, other symptoms include muscle pain, impaired memory or mental concentration, insomnia, and post-exertion malaise lasting more than 24 hours. In some cases, CFS can persist for years.

Researchers have not yet identified what causes CFS, and there are no tests to diagnose CFS. Moreover, because many illnesses have fatigue as a symptom, doctors need to take care to rule out other conditions, which may be treatable.


Despite a vigorous search, scientists have not yet identified what causes CFS. While a single cause for CFS may yet be identified, another possibility is that CFS has multiple causes. Conditions that have been studied to determine if they cause or trigger the development of CFS include infections, immune disorders, stress, trauma, and toxins.
  Infection

Various types of infections have been studied to determine if they might cause or trigger CFS:

   - Candida albicans, a fungus that causes yeast infections
   - Mycoplasma, a cause of atypical pneumonia
   - Ross River virus, which causes Ross River Fever, a mosquito-borne tropical disease

  Could One Type of Infection Lead to CFS?

Researchers from around the world have studied if a single type of infection might be the cause of CFS, analyzed the data, and not yet found any association between CFS and infection. Researchers are still analyzing samples from CFS patients using the latest molecular methods to search for previously unknown infections (pathogen discovery). To date, these studies suggest that no one infection or pathogen causes CFS and that the illness may be triggered by a variety of illnesses or conditions. In fact, infection with Epstein-Barr virus, Ross River virus, and Coxiella burnetti will lead to a post-infective condition that meets the criteria for CFS in approximately 10-12% of cases. People who had severe symptoms when they became infected were more likely than those with mild symptoms to later develop CFS symptoms. The possibility remains that there may be a variety of different ways in which patients can develop CFS.
  Immune System and Allergies

Studies have looked to see if changes in a person's immune system might lead to CFS. The findings have been mixed. Similarities in symptoms from immune responses to infection and CFS lead to hypotheses that CFS may be caused by stress or a viral infection, which may lead to the chronic production of cytokines and then to CFS.

Antibodies against normal parts of the body (auto-antibodies) and immune complexes have been seen in some CFS patients. However, no associated tissue damage typical of autoimmune disease has been described in CFS patients. The opportunistic infections or increased risk for cancer observed in persons with immunodeficiency diseases or in immunosuppressed individuals is also not observed in CFS.

T-cell activation markers have been reported to be different between groups of CFS patients and healthy persons, but not all investigators have consistently observed these differences.

Allergic diseases and secondary illnesses such as sinusitis could be one predisposing factor for CFS, but not all CFS patients have allergies. Many patients do, however, report intolerances for certain substances that may be found in foods or over-the-counter medications, such as alcohol.

  Hypothalamic-Pituitary Adrenal (HPA) Axis

The central nervous system plays an important role in CFS. Physical or emotional stress, which is commonly reported as a pre-onset condition in CFS patients, alters the activity of the hypothalamic-pituitary-adrenal axis, or HPA axis, leading to altered release of corticotrophin-releasing hormone (CRH), cortisol, and other hormones. These hormones can influence the immune system and many other body systems.

Some CFS patients produce lower levels of cortisol than do healthy people. Similar hormonal abnormalities have also been observed among CFS patients and in persons with related disorders like fibromyalgia. Cortisol suppresses inflammation and cellular immune activation, and reduced levels might relax constraints on inflammatory processes and immune cell activation. Even though CFS patients had lower levels of cortisol than healthy individuals, their cortisol levels were still within the acceptable range of what is considered normal. Therefore, doctors cannot use cortisol levels as a way to diagnose CFS.

  Abnormally Low Blood Pressure and Lightheadedness (Neurally Mediated Hypotension)

Disturbances in the autonomic regulation of blood pressure and pulse have been found in CFS patients. This problem with maintaining blood pressure can be diagnosed by using tilt table testing, which involves laying the patient horizontally on a table and then tilting the table upright to 70 degrees for 45 minutes while monitoring blood pressure and heart rate. Persons with neurally mediated hypotension (NMH) or postural orthostatic tachycardia (POTS) will develop lower blood pressure under these conditions, as well as other characteristic symptoms, such as lightheadedness, visual dimming, or a slow response to verbal stimuli. Others may develop an unusually rapid heart rate also associated with the symptoms of the syndrome. Many CFS patients experience lightheadedness or worsened fatigue when they stand for prolonged periods or when in warm places, such as in a hot shower -- all circumstances that are known to trigger NMH or POTS.

NMH and/or POTS share some of the symptoms of CFS. They should be considered in a CFS patients whose symptoms are worsened with changes in position, after eating, following unusual amounts of or inadequate fluid intake, or increases in activity. Not all patients with CFS will have these conditions, however.

  Nutritional Deficiency

There is no published scientific evidence that CFS is caused by a nutritional deficiency. While evidence is currently lacking for nutritional defects in CFS patients, it should also be added that a balanced diet can be favorable to better health in general and would be expected to benefit a person with any chronic illness.


Diagnostic Challenges

For doctors, diagnosing chronic fatigue syndrome (CFS) can be complicated by a number of factors:

   - There's no lab test or biomarker for CFS.
   - Fatigue and other symptoms of CFS are common to many illnesses.
   - For some CFS patients, it may not be obvious to doctors that they are ill.
   - The illness has a pattern of remission and relapse.
   - Symptoms vary from person to person in type, number, and severity.

These factors have contributed to a low diagnosis rate. Of the one to four million Americans who have CFS, less than 20% have been diagnosed.
  Exams and Screening Tests for CFS

Because there is no blood test, brain scan, or other lab test to diagnose CFS, the doctor should first rule out other possible causes.

If a patient has had 6 or more consecutive months of severe fatigue that is reported to be unrelieved by sufficient bed rest and that is accompanied by nonspecific symptoms, including flu-like symptoms, generalized pain, and memory problems, the doctor should consider the possibility that the patient may have CFS. Further exams and tests are needed before a diagnosis can be made:

   - A detailed medical history will be needed and should include a review of medications that could be causing the fatigue and symptoms
   - A thorough physical and mental status examination will also be needed
   - A battery of laboratory screening tests will be needed to help identify or rule out other possible causes of the symptoms that could be treated
   - The doctor may also order additional tests to follow up on results of the initial screening tests

A CFS diagnosis requires that the patient has been fatigued for 6 months or more and has 4 of the 8 symptoms for CFS for 6 months or more. If, however, the patient has been fatigued for 6 months or more but does not have four of the eight symptoms, the diagnosis may be idiopathic fatigue.

The complete process for diagnosing CFS can be found here.

Additional information for healthcare professionals on use of tests can be found here.