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H1N1 virus

https://en.wikipedia.org/wiki/Influenza_A_virus_subtype_H1N1

Influenza A virus subtype H1N1

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'Influenza' A (H1N1) virus is a subtype of influenza A virus and was the most common cause of human influenza (flu) in 2009. Some strains of H1N1 are endemic in humans and cause a small fraction of all influenza-like illness and a small fraction of all seasonal influenza. H1N1 (pronounced "HEE-NEE" by healthcare professionals) strains caused a small percentage of all human flu infections in 2004–2005.[1] Other strains of H1N1 are endemic in pigs (swine influenza) and in birds (avian influenza).

In June 2009, the World Health Organization declared the new strain of swine-origin H1N1 as a pandemic. This strain is often called swine flu by the public media. This novel virus spread worldwide and had caused about 17,000 deaths by the start of 2010. On August 10, 2010, the World Health Organization declared the H1N1 influenza pandemic over, saying worldwide flu activity had returned to typical seasonal patterns.[2]

As of 26 April 2011, an H1N1 pandemic preparedness alert has been issued by the World Health Organisation (WHO) for the Americas.[3] The affected areas have included the Chihuahua region of Mexico where its severity and work load have been high. It is reported by the aforementioned Recombinomics source that the current vaccine (California/7/2009) for H1N1 influenza might be losing its effectiveness in 2011. This point is all the more significant since it is the current virus target for the northern hemisphere's flu vaccine, and is the intended choice for the southern hemisphere.

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[edit] Swine influenza

Swine influenza (also called swine flu, or pig flu) is an infection by any one of several types of swine influenza virus. Swine influenza virus (SIV) is any strain of the influenza family of viruses that is endemic in pigs. As of 2009, the known SIV strains include influenza C and the subtypes of influenza A known as H1N1, H1N2, H3N1, H3N2, and H2N3.

Swine influenza virus is common throughout pig populations worldwide. Transmission of the virus from pigs to humans is not common and does not always lead to human influenza, often resulting only in the production of antibodies in the blood. If transmission does cause human influenza, it is called zoonotic swine flu. People with regular exposure to pigs are at increased risk of swine flu infection. The meat of an infected animal poses no risk of infection when properly cooked.

Pigs experimentally infected with the strain of swine flu that is causing the current human pandemic showed clinical signs of flu within four days, and the virus spread to other uninfected pigs housed with the infected ones.[4]

During the mid-20th century, identification of influenza subtypes became possible, allowing accurate diagnosis of transmission to humans. Since then, only 50 such transmissions have been confirmed. These strains of swine flu rarely pass from human to human. Symptoms of zoonotic swine flu in humans are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness, and general discomfort. The recommended time of isolation is about five days.

[edit] Notable incidents

[edit] Spanish flu

The Spanish flu, also known as la grippe, La Gripe Española, or La Pesadilla, was an unusually severe and deadly strain of avian influenza, a viral infectious disease, that killed some 50 to 100 million people worldwide over about a year in 1918 and 1919. It is thought to be one of the most deadly pandemics in human history.

The 1918 flu caused an unusual number of deaths, possibly due to it causing a cytokine storm in the body.[5][6] (The current H5N1 bird flu, also an Influenza A virus, has a similar effect.)[7] The Spanish flu virus infected lung cells, leading to overstimulation of the immune system via release of cytokines into the lung tissue. This leads to extensive leukocyte migration towards the lungs, causing destruction of lung tissue and secretion of liquid into the organ. This makes it difficult for the patient to breathe. In contrast to other pandemics, which mostly kill the old and the very young, the 1918 pandemic killed unusual numbers of young adults, which may have been due to their healthy immune systems mounting a too-strong and damaging response to the infection.[8]

The term "Spanish" flu was coined because Spain was at the time the only European country where the press were printing reports of the outbreak, which had killed thousands in the armies fighting World War I. Other countries suppressed the news in order to protect morale.[9]

[edit] Fort Dix outbreak

In 1976, a novel swine influenza A (H1N1) caused severe respiratory illness in 13 soldiers with 1 death at Fort Dix, New Jersey. The virus was detected only from January 19 to February 9 and did not spread beyond Fort Dix.[10] Retrospective serologic testing subsequently demonstrated that up to 230 soldiers had been infected with the novel virus, which was a H1N1 strain. The cause of the outbreak is still unknown and no exposure to pigs was identified. [11]

[edit] Russian flu

The 1977–1978 Russian flu epidemic was caused by strain Influenza A/USSR/90/77 (H1N1). It infected mostly children and young adults under 23 because a similar strain was prevalent in 1947–57, causing most adults to have substantial immunity. Because of a striking similarity in the viral RNA of both strains – one which is unlikely to appear in nature due to antigenic drift – it is being speculated that the later outbreak was due to a laboratory incident in Russia or Northern China, though this is being denied by scientists in those countries.[12][13][14] The virus was included in the 1978–1979 influenza vaccine.[15][16][17][18]

See also Influenza A virus subtype H2N2#Russian flu for the 1889–1890 Russian flu

[edit] 2009 A(H1N1) pandemic

Illustration of influenza antigenic shift.

In the 2009 flu pandemic, the virus isolated from patients in the United States was found to be made up of genetic elements from four different flu viruses – North American swine influenza, North American avian influenza, human influenza, and swine influenza virus typically found in Asia and Europe – "an unusually mongrelised mix of genetic sequences."[19] This new strain appears to be a result of reassortment of human influenza and swine influenza viruses, in all four different strains of subtype H1N1.

Preliminary genetic characterization found that the hemagglutinin (HA) gene was similar to that of swine flu viruses present in U.S. pigs since 1999, but the neuraminidase (NA) and matrix protein (M) genes resembled versions present in European swine flu isolates. The six genes from American swine flu are themselves mixtures of swine flu, bird flu, and human flu viruses.[20] While viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, there is no formal national surveillance system to determine what viruses are circulating in pigs in the U.S.[21]

In April 2009, an outbreak of Influenza-like illness occurred in Mexico and the USA; the CDC reported seven cases of novel A/H1N1 influenza. By April 24 it became clear that the outbreak of ILI in Mexico and the confirmed cases of novel influenza A in the southwest US were related and WHO issued a health advisory on the outbreak of "influenza like illness in the United States and Mexico". [22] The disease then spread very rapidly, with the number of confirmed cases rising to 2,099 by May 7, despite aggressive measures taken by the Mexican government to curb the spread of the disease.[23]

On June 11, 2009, the WHO declared an H1N1 pandemic, moving the alert level to phase 6, marking the first global pandemic since the 1968 Hong Kong flu.[24]

On October 25, 2009 U.S. President Barack Obama officially declared H1N1 a national emergency[25] Despite President Obama's concern, a Fairleigh Dickinson University PublicMind poll found in October 2009 that an overwhelming majority of New Jerseyans (74%) were not very worried or not at all worried about contracting the H1N1 flu virus.[26] Though the President’s declaration caused many U.S. employers to take actions to help stem the spread of the swine flu and to accommodate employees and / or workflow which may be impacted by an outbreak. [27]

A study conducted in coordination with the University of Michigan Health Service is scheduled for publication in the December 2009 American Journal of Roentgenology warning that H1N1 flu can cause pulmonary embolism, surmised as a leading cause of death in this current pandemic. The study authors suggest physician evaluation via contrast enhanced CT scans for the presence of pulmonary emboli when caring for patients diagnosed with respiratory complications from a "severe" case of the H1N1 flu.[28]

March 21, 2010 worldwide update by the U.N.'s World Health Organization (WHO) states that "213 countries and overseas territories/communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including at least 16,931 deaths." [29]

As of May 30, 2010 worldwide update by World Health Organization(WHO) more than 214 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including over 18,138 deaths. [30]

The research team of Andrew Miller MD showed pregnant patients are at increased risk.[31] It has been suggested that pregnant women and certain populations such as native North Americans have a greater likelihood of developing a T helper type 2 response to H1N1 influenza which may be responsible for the systemic inflammatory response syndrome that causes pulmonary edema and death. [32

https://en.wikipedia.org/wiki/Influenza_A_virus_subtype_H1N1

Swine Flu
(Swine Influenza A [H1N1] Virus)

What to Do if You Think You Have H1N1 Swine Flu Virus

Medical Author: Melissa Conrad Stöppler, MD
Medical Editor: William C. Shiel Jr., MD, FACP, FACR

What should you do if you think you have H1N1 swine flu?If you've got fever, cough, or one of the other symptoms of the flu, you may be wondering if you have contracted the H1N1 swine flu virus. The reality is that it isn't possible to know unless specialized testing is ordered, and for uncomplicated cases of the flu in non-hospitalized patients, routine testing for the H1N1 virus is not being carried out.

Experts recommend that people who suspect that they have H1N1 infection stay home and avoid contact with other people. The only time you should leave home is to access medical care if needed. That said, it is important to remember that the vast majority of flu cases (even H1N1 cases) produce only a mild illness for which doctor's visits and/or antiviral drugs are not necessary. So, the presence of cough and fever in an individual who is not at high risk for complications (see below) and who does not have warning signs of a medical emergency should not be a reason to visit an ER. The emergency department should be used for the treatment of people who are very sick or who have life-threatening emergencies (listed below). If you're in doubt, a call to your health-care practitioner can help you decide whether or not you need to access medical care.

What is swine flu (novel H1N1 influenza A swine flu)?

Swine flu (swine influenza) is a respiratory disease caused by viruses (influenza viruses) that infect the respiratory tract of pigs and result in nasal secretions, a barking-like cough, decreased appetite, and listless behavior. Swine flu produces most of the same symptoms in pigs as human flu produces in people. Swine flu can last about one to two weeks in pigs that survive. Swine influenza virus was first isolated from pigs in 1930 in the U.S. and has been recognized by pork producers and veterinarians to cause infections in pigs worldwide. In a number of instances, people have developed the swine flu infection when they are closely associated with pigs (for example, farmers, pork processors), and likewise, pig populations have occasionally been infected with the human flu infection. In most instances, the cross-species infections (swine virus to man; human flu virus to pigs) have remained in local areas and have not caused national or worldwide infections in either pigs or humans. Unfortunately, this cross-species situation with influenza viruses has had the potential to change. Investigators think the 2009 swine flu strain, first seen in Mexico, should be termed novel H1N1 flu since it is mainly found infecting people and exhibits two main surface antigens, H1 (hemagglutinin type 1) and N1 (neuraminidase type1). Recent investigations show the eight RNA strands from novel H1N1 flu have one strand derived from human flu strains, two from avian (bird) strains, and five from swine strains.

Why is swine flu (H1N1) now infecting humans?

Many researchers now consider that two main series of events can lead to swine flu (and also avian or bird flu) becoming a major cause for influenza illness in humans.

First, the influenza viruses (types A, B, C) are enveloped RNA viruses with a segmented genome; this means the viral RNA genetic code is not a single strand of RNA but exists as eight different RNA segments in the influenza viruses. A human (or bird) influenza virus can infect a pig respiratory cell at the same time as a swine influenza virus; some of the replicating RNA strands from the human virus can get mistakenly enclosed inside the enveloped swine influenza virus. For example, one cell could contain eight swine flu and eight human flu RNA segments. The total number of RNA types in one cell would be 16; four swine and four human flu RNA segments could be incorporated into one particle, making a viable eight RNA segmented flu virus from the 16 available segment types. Various combinations of RNA segments can result in a new subtype of virus (known as antigenic shift) that may have the ability to preferentially infect humans but still show characteristics unique to the swine influenza virus (see Figure 1). It is even possible to include RNA strands from birds, swine, and human influenza viruses into one virus if a cell becomes infected with all three types of influenza (for example, two bird flu, three swine flu, and three human flu RNA segments to produce a viable eight-segment new type of flu viral genome). Formation of a new viral type is considered to be antigenic shift; small changes in an individual RNA segment in flu viruses are termed antigenic drift and result in minor changes in the virus. However, these can accumulate over time to produce enough minor changes that cumulatively change the virus' antigenic makeup over time (usually years).

Second, pigs can play a unique role as an intermediary host to new flu types because pig respiratory cells can be infected directly with bird, human, and other mammalian flu viruses. Consequently, pig respiratory cells are able to be infected with many types of flu and can function as a "mixing pot" for flu RNA segments (see Figure 1). Bird flu viruses, which usually infect the gastrointestinal cells of many bird species, are shed in bird feces. Pigs can pick these viruses up from the environment and seem to be the major way that bird flu virus RNA segments enter the mammalian flu virus population.

Picture of antigenic shift and antigenic drift in swine flu (H1N1).
Figure 1.

What are the symptoms of swine flu (H1N1)?

Symptoms of swine flu are similar to most influenza infections: fever (100F or greater), cough, nasal secretions, fatigue, and headache, with fatigue being reported in most infected individuals. Some patients also get nausea, vomiting, and diarrhea. In Mexico, many of the patients are young adults, which made some investigators speculate that a strong immune response may cause some collateral tissue damage. Some patients develop severe respiratory symptoms and need respiratory support (such as a ventilator to breathe for the patient). Patients can get pneumonia (bacterial secondary infection) if the viral infection persists, and some can develop seizures. Death often occurs from secondary bacterial infection of the lungs; appropriate antibiotics need to be used in these patients. The usual mortality (death) rate for typical influenza A is about 0.1%, while the 1918 "Spanish flu" epidemic had an estimated mortality rate ranging from 2%-20%. Swine flu in Mexico (as of April 2009) has had about 160 deaths and about 2,500 confirmed cases, which would correspond to a mortality rate of about 6%, but these initial data have been revised and the mortality rate currently in Mexico is estimated to be much lower. By June 2009, the virus had reached 74 different countries on every continent except Antarctica, and by September 2009, the virus had been reported in most countries in the world. Fortunately, the mortality rate as of October 2009 has been low but higher than for the conventional flu (average conventional flu mortality rate is about 36,000 per year; projected novel H1N1 flu mortality rate is 90,000 per year in the U.S. as determined by the president's advisory committee).

How is swine flu (H1N1) diagnosed?

Swine flu is presumptively diagnosed clinically by the patient's history of association with people known to have the disease and their symptoms listed above. Usually, a quick test (for example, nasopharyngeal swab sample) is done to see if the patient is infected with influenza A or B virus. Most of the tests can distinguish between A and B types. The test can be negative (no flu infection) or positive for type A and B. If the test is positive for type B, the flu is not likely to be swine flu (H1N1). If it is positive for type A, the person could have a conventional flu strain or swine flu (H1N1). However, the accuracy of these tests has been challenged, and the U.S. Centers for Disease Control and Prevention (CDC) has not completed their comparative studies of these tests. However, a new test developed by the CDC and a commercial company reportedly can detect H1N1 reliably in about one hour; as of October 2009, the test is only available to the military.

Swine flu (H1N1) is definitively diagnosed by identifying the particular antigens associated with the virus type. In general, this test is done in a specialized laboratory and is not done by many doctors' offices or hospital laboratories. However, doctors' offices are able to send specimens to specialized laboratories if necessary. Because of the large number of novel H1N1 swine flu cases (as of October 2009, the vast majority of flu cases [about 99%] are due to novel H1N1 flu viruses), the CDC recommends only hospitalized patients' flu virus strains be sent to reference labs to be identified.

CDC developed PCR diagnostic test to detect novel H1N1 virus.
The CDC developed a PCR diagnostic test to detect novel H1N1 virus. Photo courtesy of the CDC


What are the symptoms of swine flu (H1N1)?

Symptoms of swine flu are similar to most influenza infections: fever (100F or greater), cough, nasal secretions, fatigue, and headache, with fatigue being reported in most infected individuals. Some patients also get nausea, vomiting, and diarrhea. In Mexico, many of the patients are young adults, which made some investigators speculate that a strong immune response may cause some collateral tissue damage. Some patients develop severe respiratory symptoms and need respiratory support (such as a ventilator to breathe for the patient). Patients can get pneumonia (bacterial secondary infection) if the viral infection persists, and some can develop seizures. Death often occurs from secondary bacterial infection of the lungs; appropriate antibiotics need to be used in these patients. The usual mortality (death) rate for typical influenza A is about 0.1%, while the 1918 "Spanish flu" epidemic had an estimated mortality rate ranging from 2%-20%. Swine flu in Mexico (as of April 2009) has had about 160 deaths and about 2,500 confirmed cases, which would correspond to a mortality rate of about 6%, but these initial data have been revised and the mortality rate currently in Mexico is estimated to be much lower. By June 2009, the virus had reached 74 different countries on every continent except Antarctica, and by September 2009, the virus had been reported in most countries in the world. Fortunately, the mortality rate as of October 2009 has been low but higher than for the conventional flu (average conventional flu mortality rate is about 36,000 per year; projected novel H1N1 flu mortality rate is 90,000 per year in the U.S. as determined by the president's advisory committee).

How is swine flu (H1N1) diagnosed?

Swine flu is presumptively diagnosed clinically by the patient's history of association with people known to have the disease and their symptoms listed above. Usually, a quick test (for example, nasopharyngeal swab sample) is done to see if the patient is infected with influenza A or B virus. Most of the tests can distinguish between A and B types. The test can be negative (no flu infection) or positive for type A and B. If the test is positive for type B, the flu is not likely to be swine flu (H1N1). If it is positive for type A, the person could have a conventional flu strain or swine flu (H1N1). However, the accuracy of these tests has been challenged, and the U.S. Centers for Disease Control and Prevention (CDC) has not completed their comparative studies of these tests. However, a new test developed by the CDC and a commercial company reportedly can detect H1N1 reliably in about one hour; as of October 2009, the test is only available to the military.

Swine flu (H1N1) is definitively diagnosed by identifying the particular antigens associated with the virus type. In general, this test is done in a specialized laboratory and is not done by many doctors' offices or hospital laboratories. However, doctors' offices are able to send specimens to specialized laboratories if necessary. Because of the large number of novel H1N1 swine flu cases (as of October 2009, the vast majority of flu cases [about 99%] are due to novel H1N1 flu viruses), the CDC recommends only hospitalized patients' flu virus strains be sent to reference labs to be identified.

CDC developed PCR diagnostic test to detect novel H1N1 virus.
The CDC developed a PCR diagnostic test to detect novel H1N1 virus. Photo courtesy of the CDC


What treatment is available for swine flu (H1N1)?

The best treatment for influenza infections in humans is prevention by vaccination. Work by several laboratories has recently produced vaccines. The first vaccine released in early October 2009 was a nasal spray vaccine. It is approved for use in healthy individuals ages 2 through 49. This vaccine consists of a live attenuated H1N1 virus and should not be used in anyone who is pregnant or immunocompromised. The injectable vaccine, made from killed H1N1, became available in the second week of October. This vaccine is approved for use in ages 6 months to the elderly, including pregnant females. Both of these vaccines have been approved by the CDC only after they had conducted clinical trials to prove that the vaccines were safe and effective. However, caregivers should be aware of the vaccine guidelines that come with the vaccines, as occasionally, the guidelines change. Please see the sections below titled "Can novel H1N1 swine flu be prevented with a vaccine?" and the timeline update for the current information on the vaccines.

Two antiviral agents have been reported to help prevent or reduce the effects of swine flu. They are zanamivir (Relenza) and oseltamivir (Tamiflu), both of which are also used to prevent or reduce influenza A and B symptoms. These drugs should not be used indiscriminately, because viral resistance to them can and has occurred. Also, they are not recommended if the flu symptoms already have been present for 48 hours or more, although hospitalized patients may still be treated past the 48-hour guideline. Severe infections in some patients may require additional supportive measures such as ventilation support and treatment of other infections like pneumonia that can occur in patients with a severe flu infection. The CDC has suggested in their interim guidelines that pregnant females can be treated with the two antiviral agents.

Picture of oseltamivir (Tamiflu)
Oseltamivir (Tamiflu) is an antiviral agent that may prevent or reduce influenza A and B symptoms. Photo courtesy of the CDC

Picture of zanamivir (Relenza)
Zanamivir (Relenza) has been reported to help prevent or reduce the effects of swine flu. Photo courtesy of the CDC


What is the history of swine flu (H1N1) in humans?

In 1976, there was an outbreak of swine flu at Fort Dix. This virus is not the same as the 2009 outbreak, but it was similar insofar as it was an influenza A virus that had similarities to the swine flu virus. There was one death at Fort Dix. The government decided to produce a vaccine against this virus, but the vaccine was associated with neurological complications (Guillain-Barré syndrome) and was discontinued. Some individuals speculate that formalin, used to inactivate the virus, may have played a role in the development of this complication in 1976. There is no evidence that anyone who obtained this vaccine would be protected against the 2009 swine flu. One of the reasons it takes a few months to develop a new vaccine is to test the vaccine for safety to avoid the complications seen in the 1976 vaccine. New vaccines against any flu virus type are usually made by growing virus particles in eggs. A serious side effect (allergic reaction such as swelling of the airway) to vaccines can occur in people who are allergic to eggs; these people should not get flu vaccines. Individuals with active infections or diseases of the nervous system are also not recommended to get flu vaccines.

Can novel H1N1 swine flu be prevented with a vaccine?

The best way to prevent novel H1N1 swine flu would be the same best way to prevent other influenza infections, and that is vaccination. The CDC has multiple recommendations for vaccination based on who should obtain the first doses when the vaccine becomes available (to protect the most susceptible populations) and according to age groups. The CDC based the recommendations on data obtained from vaccine trials and infection reports gathered over the last few months. The current (October 2009) vaccine recommendations from the CDC say the following groups should get the vaccine as soon as it is available:

  • pregnant women,


  • people who live with or provide care for children younger than 6 months of age,


  • health-care and emergency medical services personnel,


  • people between 6 months and 24 years of age, and


  • people from the ages of 25 through 64 who are at higher risk because of chronic health disorders such as asthma, diabetes, or a weakened immune system.

Currently, the CDC is stating that people ages 10 and above are likely to need only one vaccine shot to provide protection against novel H1N1 swine flu and further suggest that these shots will be effective in about 76% of people who obtain the vaccine. New vaccine trial data showed that healthy adults produce protective antibodies in about 98% of people in 21 days. Unfortunately, the vaccine shot in children ages 6 months to 9 years of age is not as effective as it is in older children and adults. Consequently, the CDC currently recommends that for ages 6 months up to and including 9 years of age, the children obtain two shots of the novel H1N1 vaccine, the second shot 21 days after the first shot.

Pregnant women are strongly suggested to get vaccinated as stated above. Although some vaccine preparations (multidose vials) contain low levels of thimerosal preservative (a mercury-containing preservative), the CDC still considers the vaccine safe for the fetus and mother. However, some vaccine preparations that are in single-dose vials will not have thimerosal preservative, so those pregnant individuals who are concerned about thimerosal can get this vaccine preparation when it is available.

Another type of vaccine (currently named Influenza A [H1N1] 2009 Monovalent Vaccine Live, Intranasal) has been made available during the first week in October 2009. It is a live attenuated novel H1N1 flu vaccine that contains no thimerosal, is produced by MedImmune, LLC, and is sprayed into the nostrils. This vaccine is only for healthy people 2-49 years of age, and some data suggest that it is less effective in generating an immune response in adults than the vaccine injection. The dosing schedule is as follows:

  • Children 2-9 years of age should receive two doses (0.1 ml in each nostril; total equals 0.2 ml per dose) -- the second dose should be given the same way about one month after the first dose


  • Children, adolescents and adults, 10-49 years of age should receive one dose -- (0.1 ml in each nostril; total equals 0.2 ml per dose)

The CDC occasionally makes changes and updates its information on vaccines and other recommendations about the current flu pandemic. The CDC states, "for the most accurate health information, visit http://www.cdc.gov or call 1-800-CDC-INFO, 24/7." Caregivers should check the vaccine package inserts for more detailed information on the vaccines when they become available. This article has an updated timeline for novel H1N1 swine flu attached (see below) and provides the reader with current details about the pandemic. The following is a list of the CDC-approved H1N1 vaccines and the companies that name and manufacture them as of 10/29/09:

  • Influenza A (H1N1) 2009 Monovalent Vaccine by Sanofi Pasteur


  • Influenza A (H1N1) 2009 Monovalent Vaccine by Novartis


  • Influenza A (H1N1) 2009 Monovalent Vaccine Live, Intranasal by MedImmune, LLC


  • Influenza A (H1N1) 2009 Monovalent Vaccine by CSL Limited

The CDC says that a good way to prevent any flu disease is to avoid exposure to the virus; this is done by frequent hand washing, not touching your hands to your face (especially the nose and mouth), and avoiding any close proximity to or touching any person who may have flu symptoms. Since the virus can remain viable and infectious for about 48 hours on many surfaces, good hygiene and cleaning with soap and water or alcohol-based hand disinfectants are also recommended. Some physicians say face masks may help prevent getting airborne flu viruses (for example, from a cough or sneeze), but others think the better use for masks would be on those people who have symptoms and sneeze or cough. The use of Tamiflu or Relenza may help prevent the flu if taken before symptoms develop or reduce symptoms if taken within about 48 hours after symptoms develop. Some investigators say that administration of these drugs is still useful after 48 hours, especially in high-risk patient populations .However, taking these drugs is not routinely recommended for prevention for the healthy population because investigators suggest that as occurs with most drugs, flu strains will develop resistance to these medications. Recently, the CDC made further suggestions about the use of these antiviral medications. Dr. Schuchat, a CDC official, indicated that three modifications were being suggested (Sept. 8, 2009) to the interim guidelines for use of Tamiflu and Relenza:

    1. Patients with high-risk factors should discuss flu symptoms and when to use antiviral medications; doctors should provide a prescription for the antiviral drug for the patient to use if the patient is exposed to flu or develops flu-like symptoms without having to go in to see the doctor.

    2. "Watchful waiting" was added as a response to taking antiviral medications, with the emphasis on the fact that those people who develop fever and have a preexisting health condition should then begin the antiviral medication.

    3. The antiviral medications are the first-line medicines for treatment of novel H1N1 swine flu, and most current cases of flu are novel H1N1 and are, to date, susceptible to Tamiflu and Relenza.

Your doctor should be consulted before these drugs are prescribed.

In general, preventive measures to prevent the spread of flu are often undertaken by those people who have symptoms. Symptomatic people should stay at home, avoid crowds, and take off from work or school until the disease is no longer transmittable (about two to three weeks) or until medical help and advice is sought. Sneezing, coughing, and nasal secretions need to be kept away from other people; simply using tissues and disposing of them will help others. Quarantining patients is usually not warranted, but such measures depend on the severity of the disease. The CDC recommends that people who appear to have an influenza-like illness upon arrival at work or school or become ill during the day be promptly separated from other people and be advised to go home until at least 24 hours after they are free of fever (100 F [37.8 C] or greater), or signs of a fever, without the use of fever-reducing medications. The novel H1N1 swine flu disease takes about seven to 10 days before fevers stop, but new research data (Sept. 14, 2009) suggests waiting until the cough is gone since many people are still infectious about one week after fever is gone. The CDC has not yet extended their recommendations to stay home for that extra week.


Can H1N1 be prevented if the H1N1 flu vaccine is not readily available?

Although vaccination is the best way to "prevent" H1N1, currently (November 2009), there is not enough available for everyone who wants or needs H1N1 vaccination. Until H1N1 vaccine supplies meet demand, there are some things people can do to try and prevent infection. Without vaccination, the best strategy is to not allow H1N1 virus to contact a person's mucus membranes because if the virus does not reach cells in which it can grow, it cannot cause infection. Quarantining H1N1-infected people is an extreme measure that may work in some instances (for example, China uses this method), but even with quarantining, the virus may still spread by people who have minimal or no symptoms.

The next step that is easier to be implemented by individuals is for people with the disease to self-quarantine until they become noninfectious (about seven to 10 days after flu symptoms abate). Infected people can wear surgical masks to reduce the amount of droplet spray from coughs and sneezes and throw away contaminated tissues. Unfortunately, these approaches depend on the compliance of many other people, and the likelihood that such methods will be highly successful in preventing H1N1 infections, at best, is only fair. Such methods have not stopped the current pandemic. Yet there are still some other methods available to individuals. Perhaps the best way for individuals to try to prevent H1N1 infection is a combination of methods that are aimed at fulfilling the very basic principle that if H1N1 doesn't reach an individual's mucus membrane cells, infection will be prevented. The methods are as follows:

    1. Kill or inactivate the virus before it reaches a human cell by using soap and water to clean your hands; washing clothing and taking a shower will do the same for the rest of your body.

    2. Use an alcohol-based hand sanitizer if soap and water are not readily available.

    3. Use sanitizers on objects that many people may touch (for example, doorknobs, computer keyboards, handrails, phones).

    4. Do not touch your mouth, eyes, nose, unless you first do items 1 or 2 above.

    5. Avoid crowds, parties, and especially people who are coughing and sneezing (most virus-containing droplets do not travel more than 4 feet, so experts suggest 6 feet away is a good distance to stay). If you cannot avoid crowds (or parties), try to remain aware of people around you and use the 6-foot rule with anyone coughing or sneezing. Do not reach for or eat snacks out of canisters or other containers at parties.

    6. Avoid touching anything within about 6 feet of an uncovered cough/sneeze, because the droplets that contain virus fall and land on anything usually within that range.

    7. Studies show that individuals who wear surgical or N95 particle masks may prevent inhalation of some H1N1 virus, but the masks may prevent only about 50% of airborne exposures and offer no protection against surface droplets. However, masks on H1N1 infected people can markedly reduce the spread of infected droplets.

These seven steps can help prevent individuals from getting H1N1 infection, but for many people, adherence to them may be difficult at best. However, there are some additional strategies that may also help prevent H1N1 infections in unvaccinated people according to some investigators. Saline nasal washes and gargling with saline (or a commercial product) as a way to reduce or eliminate H1N1 virus from mucus membranes has been suggested. Proponents of these methods base their rationale on the fact that flu viruses usually take about two to three days to proliferate in nasal/throat cells. While nasal washes and gargling may be soothing to some people, there are no studies that indicate H1N1 is killed, inactivated, or completely removed by these methods; conversely, there are no data suggesting these methods cannot have any effect on H1N1. However, with long-term nasal washes using Neti pots, sinus infection with other pathogens may be encouraged.

Other investigators and physicians have offered additional methods that may help reduce exposure to H1N1 virus. For example, Dr. Gerberding, a former CDC director, had several suggestions about how to avoid H1N1 infection on an airplane. She suggested the following:

    1. If a person is next to you or near (within 6 feet) and is coughing/sneezing, ask the flight attendant to offer the person a mask.

    2. If there are available seats 6 feet or more away from the coughing/sneezing person, ask to change your seat (planes are good means of travel because the air is recirculated through HEPA filters that can capture viruses, but even the filters will not help if people touch areas where droplets have landed; HEPA filters are usually not available in buses, cars, ships, or trains).

    3. Turn away from the coughing/sneezing person and turn the air vent toward the person to blow the droplets away from yourself.

Variations of her suggestions may be applicable in many different social, work, or travel situations, but there are no data to prove these methods are effective. In addition, common-sense precautions such as not drinking or eating things touched by others, avoiding casual physical contacts (for example, handshakes, social hugs or kisses, public water fountains [these are OK if you touch nothing and lips only touch flowing water], banisters on stairways, and restroom door handles) will limit exposure to H1N1. Again, these common sense suggestions lack data substantiation.

Many investigators suggest that people stay well hydrated, take vitamins, and get plenty of rest, but these precautions will not prevent H1N1 infections although they may help reduce the effects of infection by strengthening the person's immune system to fight infection. Similarly, current antiviral medications (described in the preceding section) act on H1N1 viruses that have already infected cells; they work by preventing or reducing viral particles from aggregating and being released from infected cells. Timing is important; if only a few cells are infected and the antiviral medications are administered quickly (usually before flu symptoms develop or within 48 hours), the viruses are reduced in number (they cannot easily bud out from the cell surface), so few, if any, other respiratory or mucus membrane cells become infected. This can result in either no flu symptoms or, if a larger number of cells were initially infected, less severe symptoms. The overall effect for the person is that the H1N1 infection was prevented (it was not; the symptoms were prevented from developing) or that symptoms were reduced.

In the strictest sense of the word prevention, even effective vaccines do not "prevent" infections. What they do accomplish is to alert the immune system to be on guard for certain antigens that are associated with a pathogen (for example, H1N1 virus, pneumococcal bacteria). When the pathogen first infects the host, its antigens are recognized, and these cause a rapid immunoprotective response to occur that prevents the pathogen from proliferating and developing symptoms in the host. People, including physicians and researchers, often term this complex response to vaccination as "prevention of infection" but what actually occurs is the prevention of further infection so well that symptoms do not develop or are minimal in the host.

In summary, if H1N1 viruses fail to contact cells they can infect, the disease will be prevented. As stated above, this is difficult, but not impossible, to do in almost all societies. Prevention of H1N1 symptoms of infection is possible with antiviral medications if these are given very early in the infection. There are many other methods that may reduce the chance of getting the virus on a person's mucosal surface, but most methods have not been backed up with objective data. Most doctors and investigators suggest that items that help boost or allow the immune response to function well will help people resist H1N1 infections and reduce symptoms, but these also do not prevent infections. Consequently, while waiting for H1N1 vaccine, these are some ways individuals can improve their chances of preventing or reducing the symptoms of H1N1 infections.

Is swine flu (H1N1) a cause of an epidemic or pandemic in 2009?

An epidemic is defined as an outbreak of a contagious disease that is rapid and widespread, affecting many individuals at the same time. The swine flu outbreak in Mexico fit this definition. A pandemic is an epidemic that becomes so widespread that it affects a region, continent, or the world. As of April 2009, the H1N1 swine flu outbreak did not meet this definition. However, as of June 11, 2009, WHO officials determined that H1N1 2009 influenza A swine flu reached WHO level 6 criteria (person-to-person transmission in two separate WHO-determined world regions) and declared the first flu pandemic in 41 years. To date, the flu has reached over 74 different countries on every continent except Antarctica in about three month's time; fortunately, the severity of the disease has not increased.

What is the prognosis (outlook) for patients who get swine flu (H1N1)?

The following is speculation on the prognosis for swine flu (H1N1) because this disease has only been recently diagnosed and the data is changing daily. This section is based on currently available information.

In general, the majority (about 90%-95%) of people who get the disease feel terrible (see symptoms) but recover with no problems, as seen in patients in both Mexico and the U.S. Caution must be taken as the swine flu (H1N1) is still spreading and has become a pandemic. So far, young adults have not done well, and in Mexico, this group currently has the highest mortality rate, but this data could quickly change.

People with depressed immune systems historically have worse outcomes than uncompromised individuals; investigators suspect that as swine flu (H1N1) spreads, the mortality rates may rise and be high in this population. Current data suggest that pregnant individuals, children under 2 years of age, young adults, and individuals with any immune compromise or debilitation are likely to have a worse prognosis. Unfortunately, the problem with the prognosis is still unclear. If the mortality is like the conventional flu that causes mortality rates of about 0.1%, the result would be about 36,000 deaths per year because of the huge number of people who get infected. If the Mexico swine flu (H1N1) ends up with a mortality rate of about 6% and infects the same number of millions of people as conventional flu viruses, the projected numbers could be as high as 2 million deaths in the U.S. alone. This is a bad prognosis for about 2 million people and their families; these potential deaths are major reasons that health officials are so concerned about the spread of this new virus. As of September 2009, the current estimates are that about 90,000 deaths will occur in the U.S. from novel H1N1 swine flu (estimated by the president's advisory committee). As of October, these estimates have not been revised by the advisory committee or the CDC.

Another confounding problem with the prognosis of swine flu (H1N1) is that the disease is occurring and spreading in high numbers at the usual end of the flu season. Most flu outbreaks happen between November to the following April, with peak activity between late December to March. This outbreak is not following the usual flu pattern since novel H1N1 began its outbreak in April and had spread throughout the world by September. Some scientists think that swine flu (H1N1) will die down but return with many more cases in the fall, and still others speculate the current pandemic will eventually resemble the outcomes similar to the 1918 influenza pandemic. Some suggest it may resemble the SARS (severe acute respiratory syndrome caused by a coronavirus strain) outbreak in 2002-2003 in which the disease spread to about 10 countries with over 7,000 cases, over 700 deaths, and had a 10% mortality rate. Effective isolation of patients was done in this case, and many investigators think the outbreak was stopped due to this measure. Because swine flu (H1N1) is a new virus and does not seem to be following the usual flu disease pattern, any prognosis is speculative, although as of October 2009, the numbers of people with flu-like illness are higher than usual and the illness is affecting a much younger population than the conventional flu. As the pandemic progresses, this article will be updated. The best news about this novel H1N1 swine flu is that the majority of people, as of October 2009, who have caught the flu recover without medical treatment and have an excellent prognosis.


http://www.medicinenet.com/swine_flu/article.htm

Bird flu

Bird Flu (Avian Influenza, Avian Flu)

Bird Flu Symptoms

Read about the outbreak of bird flu in Hong Kong

Medical Author: Melissa Conrad Stöppler, MD
Medical Editor: Dennis Lee, MD

Bird flu (also referred to as avian flu), as the name implies, is an infection in birds caused by an influenza virus. Influenza viruses that infect birds often do not cause illness in birds. Since the viruses are highly contagious, danger to humans arises when domesticated birds (for example chickens, ducks, and turkeys) become infected. While bird flu usually poses no threat to humans, instances of transmission of bird flu to humans have been reported since 1997, and over 100 people were infected in an outbreak that began in Southeast Asia in mid-2003. In November 2010, officials in Hong Kong announced that a woman had contracted bird flu, the first reported case of the condition in seven years. The 59-year-old woman had recently traveled to mainland China but reported no contact with live poultry or visits to farms.

Learn about avian flu (H5N1) symptoms in humans »

Bird flu facts

  • Bird flu refers to strains of influenza that primarily affect wild and domesticated birds.
  • Bird flu is also known as avian flu or avian influenza.
  • Although bird flu is contagious and spreads easily among birds, it is uncommon for it to be transmitted to humans.
  • In the late 1990s, a new strain of bird flu arose which was unusually severe ("highly pathogenic"), resulting in the deaths of hundreds of millions of birds, including poultry.
  • Control efforts, including culling infected flocks and vaccinating healthy birds, have limited the spread of highly pathogenic bird flu.
  • In 2011, a mutated strain of highly pathogenic bird flu appeared, which is concerning because the existing poultry vaccines are not very effective against the new strain.
  • Human infection with the highly pathogenic strain of bird flu is uncommon, with fewer than 600 cases reported since 1997.
  • Human infection occurs primarily in people who have close contact with sick poultry in countries where the virus is found. There have been isolated cases of human-to-human transmission.
  • Human infection with bird flu is fatal in approximately 60% of cases.
  • Bird flu from the highly pathogenic strain is not found in the United States at this time.

What is bird flu?

Bird flu (avian influenza) is a disease caused by an influenza virus that primarily affects birds. In the late 1990s, a new strain of bird flu arose that was remarkable for its ability to cause severe disease and death, especially in domesticated birds such as ducks, chickens, or turkeys. As a result, this strain was called highly pathogenic (meaning very severe) avian influenza.

Since the identification of highly pathogenic influenza, infected birds have been found in Asia, Europe, the Middle East, and Africa. Careful control measures, including destroying infected flocks and vaccinating healthy birds, have reduced the number of cases, but the virus continues to exist in poultry flocks in areas of Asia and Africa. Bird flu from the highly pathogenic strain is not found in the United States at this time.

The virus spreads from bird to bird through infected birds shedding the virus in their saliva, nasal secretions, and droppings. Healthy birds get infected when they come into contact with contaminated secretions or feces from infected birds. Contact with contaminated surfaces such as cages might also allow the virus to transfer from bird to bird. Symptoms in birds range from mild drops in egg production to failure of multiple major organs and death.

The first human case of illness from highly pathogenic avian influenza was identified in 1997, and more than 560 cases have been identified since then, with deaths worldwide exceeding 300. Human cases of highly pathogenic bird flu have been largely confined to Southeast Asia and Africa. However, mutations often occur in the virus, and it is possible that some mutations could create a more contagious virus that could cause a regional epidemic or a worldwide pandemic of bird flu among humans. Fortunately, the mutations that have occurred to date have not made the virus more contagious, although the concern remains.

What causes bird flu?

Bird flu is caused by strains of the influenza virus that have evolved to be specially adapted to enter avian cells. There are three main types of influenza: A, B, and C. The virus that causes bird flu is an influenza A type with eight RNA strands that make up its genome. Influenza viruses are further classified by analyzing two proteins on the surface of the virus. The proteins are called hemagglutinin (H) and neuraminidase (N). There are many different types of hemagglutinin and neuraminidase proteins. The current highly pathogenic bird flu virus has type 5 hemagglutinin and type 1 neuraminidase. Thus, it is a "H5N1" influenza A virus.

There are many types of influenza viruses, and most prefer to live in a limited number of animals. Thus, swine flu primarily infects swine and bird flu primarily infects birds. Human influenza is best adapted to humans. A few cases may occur in an accidental host, such as when people who have extensive contact with sick birds get the bird flu. In addition to humans and birds, we know that pigs, tigers, leopards, ferrets, and domestic cats can sometimes be infected with avian influenza viruses.

Influenza viruses mutate easily and often. These mutations can arise spontaneously in a single virus or can occur when two different influenza strains get close enough together to exchange genetic material. There are two major types of mutations in influenza viruses: antigenic shifts, where large RNA segments are interchanged between different influenza virus type, and antigenic shifts, where small RNA sequences are changed. The antigenic shifts are usually responsible for developing new strains. For example, the 2009 swine flu pandemic was caused by a virus that included genetic material from pig influenza, avian influenza, and human influenza strains. New mutations can allow the virus to evade the body's immune system and makes older vaccines ineffective. In 2011, one strain of the highly pathogenic avian influenza virus mutated in this way, making the existing vaccine used against avian flu ineffective against the new strain. Sometimes a flu virus will mutate in a way that makes it able to infect a new species.

Serious pandemic influenza occurs when a relatively new strain of the influenza virus arises that is highly contagious to humans. The most deadly pandemic in modern history was the 1918 influenza, also known as the Spanish flu (although it did not originate in Spain). The 1918 virus spread rapidly and killed tens of millions of people worldwide. Mortality was especially high in healthy young adults. Although the 1918 virus was a human influenza virus it, had many genes that likely came from a strain of bird flu. One reason that health officials carefully watch for and try to limit human contact with birds that develop avian flu is to avoid chances for a new strain to arise that may prefer to develop in human tissue.

What are risk factors for bird flu?

Humans may get bird flu from contact with infected birds (chickens, for example) or their droppings or surfaces with infected droppings. Risk factors include caring for sick birds, killing sick birds, and preparing sick birds for consumption. Despite the large number of people who have contact with poultry every day in the world, human cases of bird flu remain rare. This highlights how difficult it is for the bird flu virus to infect human cells, but mutations like antigenic shifts may reduce such difficulties.

Although direct contact with sick poultry poses the highest risk, indirect exposure to bird feces is also a risk. Thus, contact with unwashed eggs from sick birds or water contaminated by poultry feces poses a potential risk of disease.

Human to human spread has occurred in isolated cases. Thus, caring for a person infected with bird flu is also a risk factor for the disease. There is a theoretical risk in laboratory workers who handle the avian flu virus. One alleged incident in 2009 occurred when a company inadvertently sent live avian flu virus samples to research laboratories, which subsequently were used to vaccinate ferrets. The contaminated vaccine did not result in any human cases of infection.

What are bird flu symptoms and signs?

Symptoms occur approximately two to eight days after exposure, on average. Infected people experience typical flu-like symptoms, including fever, cough, sore throat, and muscle aches. Some people also have nausea, vomiting, diarrhea, or eye infections. This can progress to pneumonia and even respiratory failure. Bird flu causes a very aggressive form of pneumonia (acute respiratory distress syndrome or ARDS) that is often fatal.

How is bird flu diagnosed?

Routine tests for human influenza A will be positive in patients with bird flu but are not specific for the avian virus. To make a specific diagnosis of bird flu, specialized tests are needed. In the United States, local health departments and the Centers for Disease Control and Prevention can provide access to the specialized testing. The virus can be detected in sputum by several methods, including culture or polymerase chain reaction (PCR). Culture should be done in laboratories that have an appropriate biosafety certification. PCR detects nucleic acid from the influenza A virus. Specialized PCR testing is available in reference laboratories to identify avian strains.

During and after infection with bird flu, the body makes antibodies against the virus. Blood tests can detect these antibodies, but this requires one sample at the onset of disease and another sample several weeks later. Thus, results are not available until the patient has recovered or died.

What is the treatment for bird flu?

Because of the small number of human cases, it has not been possible to conduct rigorous treatment trials for bird flu. The current recommendation from the World Health Organization is to use an antiviral medication called oseltamivir (Tamiflu). In Sept. 2011, the CDC stated the following: "Two other antiviral medications, oseltamivir and zanamivir, would probably work to treat influenza caused by H5N1 virus, but additional studies still need to be done to demonstrate their effectiveness."


What is the prognosis of bird flu?

The prognosis in human cases of bird flu remains poor. Many cases occur in people who are poor, live in rural areas in underdeveloped countries, and do not have access to modern intensive care units or antiviral therapy. Approximately 60% of people diagnosed with bird flu eventually die from the disease.

Can bird flu be prevented?

Bird flu can be prevented by avoiding contact with sick poultry originating in countries known to be affected by the virus. In 2011, Egypt has the most reported cases to date. Prevention also includes poultry safety measures such as destroying flocks when sick birds are identified and vaccinating healthy flocks. Combined with import bans, this culling has effectively limited the spread of bird flu in outbreak situations but naturally has negative effects on the poultry and egg industry. Unlike SARS which some investigators suggest has been eliminated from the world or Ebola which has a narrow geographic range, the bird flu continues to exist in significant areas of the world and can be spread widely by migrating birds.

Properly handling and cooking of poultry and eggs can kill viruses like the bird flu virus. Hands should be washed before and after handling poultry and eggs, and surfaces that have come in contact with the food should be cleaned thoroughly with hot soapy water. Cooked poultry should have an internal temperature of at least 165 F.

Masks and other respiratory protection should be used when caring for patients with bird flu. If a person has close contact with an infected patient, the exposed person may be offered oseltamivir in an attempt to prevent infection.

In 2007, the FDA licensed the first vaccine in the United States for humans against the highly pathogenic bird flu virus. The vaccine is made from inactivated viruses and does not contain any live viruses. It has been shown to stimulate the immune system to make antibodies against the bird flu virus that could presumably protect a person from the bird flu. The vaccine has been purchased by the federal government for inclusion within the CDC's Strategic National Stockpile. It is not available to the general public in part because the United States does not currently have a problem with the highly pathogenic strain of bird flu. Vaccine side effects include a sore arm, fatigue, or temporary muscle aches. The vaccine has not been tested in large numbers of patients, however, and there may be other side effects that have not yet been detected. The current vaccine is effective against the strain that has caused the large outbreaks of bird flu, but it may not be as effective against a newly mutated strain found in 2011.

Research on vaccines against influenza viruses is ongoing, and new developments such as a vaccine that is directed against the common and relatively unchanging antigens on the influenza viruses may lead to a vaccine that is protective against most if not all influenza viruses. If such research is successful, potential influenza outbreaks, including avian flu, may be reduced or prevented in the future.

Where can people find more information about bird flu?

The World Health Organization (http://www.who.int/csr/disease/avian_influenza/en/) provides current information about outbreaks and management of bird flu.

http://www.medicinenet.com/bird_flu/article.htm

Foot and mouth disease

Foot-and-mouth disease

Foot-and-mouth disease
Classification and external resources

Ruptured nasal blister in diseased cow.
ICD-10 B08.8 (ILDS B08.820)
ICD-9 078.4
DiseasesDB 31707
MeSH D005536

Foot-and-mouth disease or hoof-and-mouth disease (Aphtae epizooticae) is an infectious and sometimes fatal viral disease that affects cloven-hoofed animals, including domestic and wild bovids. The virus causes a high fever for two or three days, followed by blisters inside the mouth and on the feet that may rupture and cause lameness.

Foot-and-mouth disease is a severe plague for animal farming, since it is highly infectious and can be spread by infected animals through aerosols, through contact with contaminated farming equipment, vehicles, clothing or feed, and by domestic and wild predators.[1] Its containment demands considerable efforts in vaccination, strict monitoring, trade restrictions and quarantines, and occasionally the elimination of millions of animals.

Susceptible animals include cattle, water buffalo, sheep, goats, pigs, antelope, deer, and bison. It has also been known to infect hedgehogs, elephants,[1][2] llama, and alpaca may develop mild symptoms, but are resistant to the disease and do not pass it on to others of the same species.[1] In laboratory experiments, mice and rats and chickens have been successfully infected by artificial means, but it is not believed that they would contract the disease under natural conditions.[1] Humans are very rarely affected.

The virus responsible for the disease is a picornavirus, the prototypic member of the genus Aphthovirus. Infection occurs when the virus particle is taken into a cell of the host. The cell is then forced to manufacture thousands of copies of the virus, and eventually bursts, releasing the new particles in the blood. The virus is highly variable,[3] which limits the effectiveness of vaccination.

Contents

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History

The cause of FMD was first shown to be viral in 1897 by Friedrich Loeffler. He passed the blood of an infected animal through a Chamberland filter and found that the fluid that was collected could still cause the disease in healthy animals.

FMD occurs throughout much of the world, and whilst some countries have been free of FMD for some time, its wide host range and rapid spread represent cause for international concern. After World War II, the disease was widely distributed throughout the world. In 1996, endemic areas included Asia, Africa, and parts of South America; as of August 2007, Chile is disease free,[4] and Uruguay and Argentina have not had an outbreak since 2001. North America and Australia have been free of FMD for many years. New Zealand has never had a case of foot-and-mouth disease.[5] Most European countries have been recognized as disease free, and countries belonging to the European Union have stopped FMD vaccination.

However, in 2001, a serious outbreak of FMD in Britain resulted in the slaughter of many animals, the postponing of the general election for a month, and the cancellation of many sporting events and leisure activities such as the Isle of Man TT. Due to strict government policies on sale of livestock, disinfection of all persons leaving and entering farms and the cancellation of large events likely to be attended by farmers, a potentially economically disastrous epizootic was avoided in the Republic of Ireland[citation needed], with just one case recorded in Proleek, Co. Louth. In August 2007, FMD was found at two farms in Surrey, England. All livestock were culled and a quarantine erected over the area. There have since been two other suspected outbreaks, although these seem now not to be related to FMD. The only reported cases in 2010 were a false alarm from GIS Alex Baker, as proven false by the Florida Farm and Agricultural Department, and confirmed quarantine/slaughter of cows and pigs has been reported from Miyazaki prefecture in Japan in the month of June after three cows tested positive. A total of some 270,000 cattle have been ordered slaughtered following the disease's outbreak.

[edit] Clinical signs

Ruptured blisters on the feet of a pig

The incubation period for foot-and-mouth disease virus has a range between 2 and 12 days.[6] The disease is characterized by high fever that declines rapidly after two or three days; blisters inside the mouth that lead to excessive secretion of stringy or foamy saliva and to drooling; and blisters on the feet that may rupture and cause lameness. Adult animals may suffer weight loss from which they do not recover for several months as well as swelling in the testicles of mature males, and in cows, milk production can decline significantly. Though most animals eventually recover from FMD, the disease can lead to myocarditis (inflammation of the heart muscle) and death, especially in newborn animals. Some infected animals remain asymptomatic, but they nonetheless carry FMD and can transmit it to others.

Evolution

Of the seven serotypes[7] of this virus, A, C, O, Asia 1 and SAT3 appear to be distinct lineages; SAT 1 and SAT 2 are unresolved clades.[8] The mutation rate of the protein-encoding sequences of strains isolated between 1932 and 2007 has been estimated to be 1.46 × 10(-3) substitutions/site/year, a rate similar to that of other RNA viruses. The most recent common ancestor appears to have evolved ~481 years ago (early 16th century). anestor then diverged into two clades which have given rise to the extant circulating Euro-Asiatic and South African. This event occurred ~1800.[9] Skyline plot analysis shows a population expansion in the early 20th century, which was then followed by a rapid decline in population size in the late 20th century.

There are at least 7 genotypes of serotype Asia 1.[10]

Transmission

The foot-and-mouth disease virus can be transmitted in a number of ways, including close contact animal-to-animal spread, long-distance aerosol spread and fomites or inanimate objects, typically fodder and motor vehicles. The clothes and skin of animal handlers, such as farmers, standing water, and uncooked food scraps and feed supplements containing infected animal products can harbor the virus as well. Cows can also catch FMD from the semen of infected bulls. Control measures include quarantine and destruction of infected livestock, and export bans for meat and other animal products to countries not infected with the disease.

Just as humans may spread the disease by carrying the virus on their clothes and bodies, animals that are not susceptible to the disease may still aid in spreading it. This was the case in Canada in 1952, when an outbreak flared up again after dogs had carried off bones from dead animals.[1] Wolves are thought to play a similar role in the former Soviet Union.[11]

Foot-and-mouth disease infecting humans

Humans can be infected with foot-and-mouth disease through contact with infected animals, but this is extremely rare. Some cases were caused by laboratory accidents. Because the virus that causes FMD is sensitive to stomach acid, it cannot spread to humans via consumption of infected meat, except in the mouth before the meat is swallowed. In the UK, the last confirmed human case occurred in 1966,[12][13] and only a few other cases have been recorded in countries of continental Europe, Africa, and South America. Symptoms of FMD in humans include malaise, fever, vomiting, red ulcerative lesions (surface-eroding damaged spots) of the oral tissues, and sometimes vesicular lesions (small blisters) of the skin. According to a newspaper report, FMD killed two children in England in 1884, supposedly due to infected milk.[14]

Another viral disease with similar symptoms, hand, foot and mouth disease, occurs more frequently in humans, especially in young children; the cause, Coxsackie A virus, is different from FMDV. Coxsackie viruses belong to the Enteroviruses within the Picornaviridae.

Because FMD rarely infects humans, but spreads rapidly among animals, it is a much greater threat to the agriculture industry than to human health. Farmers around the world can lose huge amounts of money during a foot-and-mouth epizootic, when large amounts of animal capital is destroyed, and revenues from milk and meat production go down.

Vaccination

Like other viruses, the FMD virus continually evolves and mutates, thus one of the difficulties in vaccinating against it is the huge variation between, and even within, serotypes. There is no cross-protection between serotypes (meaning that a vaccine for one serotype will not protect against any others) and in addition, two strains within a given serotype may have nucleotide sequences that differ by as much as 30% for a given gene. This means FMD vaccines must be highly specific to the strain involved. Vaccination only provides temporary immunity that lasts from months to years.

Currently, the World Organisation for Animal Health recognizes countries to be in one of three disease states with regards to FMD: FMD present with or without vaccination, FMD-free with vaccination, and FMD-free without vaccination. Countries designated FMD-free without vaccination have the greatest access to export markets, and therefore many developed nations, including Canada, the United States, and the UK, work hard to maintain their current status.

Reasons cited for restricting export from countries using FMD vaccines include, probably most importantly, routine blood tests relying on antibodies cannot distinguish between an infected and a vaccinated animal,[15] which severely hampers screening of animals used in export products, risking a spread of FMD to importing countries. A widespread preventive vaccination would also conceal the existence of the virus in a country. From there, it could potentially spread to countries without vaccine programs. Lastly, an animal infected shortly after being vaccinated can harbor and spread FMD without showing symptoms itself, hindering containment and culling of sick animals as a remedy.

Many early vaccines used dead samples of FMDV to inoculate animals, but those early vaccines sometimes caused real outbreaks. In the 1970s, scientists discovered that a vaccine could be made using only a single key protein from the virus. The task was to produce enough quantities of the protein to be used in the vaccination. On June 18, 1981, the U.S. government announced the creation of a vaccine targeted against FMD, the world's first genetically engineered vaccine.

The North American FMD Vaccine Bank is housed at the United States Department of Agriculture's (USDA) Foreign Animal Disease Diagnostic Laboratory (FADDL) at Plum Island Animal Disease Center. The Center, located 1.5 miles (2.4 km) off the coast of Long Island, NY, is the only place in the United States where scientists can conduct research and diagnostic work on highly contagious animal diseases such as FMD. Because of this limitation, US companies working on FMD usually use facilities in other countries where such disases are endemic.

Epizootics

United States 1914-1929

The US has had nine FMD outbreaks since 1870; the most devastating one happened in 1914. It originated from Michigan, but its entry into the stockyards in Chicago turned it into an epizootic. About 3,500 livestock herds were infected across the US, totaling over 170,000 cattle, sheep and swine. The eradication came at a cost of US$4.5 million. A 1924 outbreak in California resulted not only in the slaughter of 109,000 farm animals, but also 22,000 deer. The US saw its latest FMD outbreak in Montebello, California in 1929. This outbreak originated in hogs that had eaten infected meat scraps from a tourist steamship that had stocked meat in Argentina. Over 3,600 animals were slaughtered and the disease was contained in less than a month.[16][17]

United Kingdom 1967

In October 1967, a farmer in Shropshire reported a lame sow, which was later diagnosed with FMD. The source was believed to be remains of legally-imported infected lamb from Argentina and Chile. The virus spread and, in total, 442,000 animals were slaughtered and the outbreak had an estimated cost of £370 million.

Taiwan 1997

Taiwan had previous epidemics of FMD in 1913-14 and 1924–29, but had since been spared epidemics,[18] and considered itself free of FMD as late as in the 1990s. On the 19th of March 1997, a sow at a farm in Hsinchu prefecture, Taiwan was diagnosed with a strain of FMD which only infects swine. Mortality was high, nearing 100% in the infected herd. The cause of the epidemic was not determined, but the farm was near a port city known for its pig-smuggling industry and illegal slaughterhouses. Smuggled swine or contaminated meat are thus likely sources of the disease.

The disease spread fast among swine herds in Taiwan, with 200-300 new farms being infected daily. Causes for this include the high swine density in the area, with up to 6,500 hogs per square mile, feeding of pigs with untreated garbage, and the farm's proximity to slaughterhouses. Other systemic issues, such as lack of laboratory facilities, slow response and initial lack of a vaccination program, contributed. The farmers allegedly intentionally introduced FMD to their flocks, because the payment offered to farmers for culled swine was at the time higher than the market value of the swine.

A complicating factor is the endemic spread of swine vesicular disease (SVD) in Taiwan. The symptoms are indistinguishable from FMD, which may have led to previous misdiagnosing of FMD as SVD. Laboratory analysis was seldom used for diagnosis, and FMD may thus have gone unnoticed for some time.

The swine depopulation was a massive undertaking, with the military contributing substantial manpower. At peak capacity, 200,000 hogs per day were disposed of, mainly by electrocution. Carcasses were disposed of by burning and burial, but burning was avoided in water resource protection areas. In April, industrial incinerators were running around the clock to dispose of the carcasses.

Initially, 40,000 combined vaccines for the strains O-1, A-24 and Asia-1 were available and administered to zoo animals and valuable breeding hogs. At the end of March, half a million new doses of vaccines for O-1 and Asia-1 were made available. On the May 3rd, 13 million doses of O-1 vaccine arrived, and both the March and May shipments were distributed free of charge. There was a danger of vaccination crews spreading the disease; therefore, trained farmers were allowed to administer the vaccine under veterinary supervision.

Taiwan had previously been the major exporter of pork to Japan, and among the top 15 pork producers in the world in 1996. During the outbreak, over 3.8 million swine were destroyed at a cost of US$6.9 billion. The Taiwanese pig industry was devastated as a result, and the export market was in ruins.[16][19] In 2007, Taiwan was considered free of FMD, but was still conducting a vaccination program, which restricts the export of meat from Taiwan.

United Kingdom 2001

The epidemic of foot-and-mouth disease in the United Kingdom in the spring and summer of 2001 was caused by the "Type O pan Asia" strain of the disease.[20] This episode resulted in more than 2,000 cases of the disease in farms throughout the British countryside. Around seven million sheep and cattle were killed in an eventually successful attempt to halt the disease. The county of Cumbria was the worst affected area of the country, with 843 cases. By the time the disease was halted in October 2001, the crisis was estimated to have cost Britain £8 billion ($16 billion) in costs to the agricultural and support industries, and to the outdoor industry. What made this outbreak so serious was the amount of time between infection being present at the first outbreak loci, and the time when countermeasures were put into operation against the disease, such as transport bans and detergent washing of both vehicles and personnel entering livestock areas. However, the extreme overkill of many disease-free animals (80% of culled livestock were clean) was a result of inappropriate poor mathematical modelling that did not reflect the epidemiology of the epidemic.[21] The epidemic was probably caused by pigs which had been fed infected garbage that had not been properly heat-sterilized. It is further believed that the garbage contained remains of infected meat which had been illegally imported to Britain.[22]

China 2005

In April 2005, an Asia-1 strain of FMD appeared in the eastern provinces of Shandong and Jiangsu. During April and May, it spread to suburban Beijing, the northern province of Hebei, and the Xinjiang autonomous region in northwest China. On 13 May, China reported the FMD outbreak to the World Health Organization and the OIE. This was the first time China has publicly admitted to having FMD.[23][24] China is still reporting FMD outbreaks. In 2007, reports filed with the OIE documented new or ongoing outbreaks in the provinces of Gansu, Qinghai and Xinjiang. This included reports of domestic yak showing signs of infection.[25] FMD is endemic in pastoral regions of China from Heilongjiang Province in the northeast to Sichuan Province and the Tibetan Autonomous region in the southwest. Chinese domestic media reports often use a euphemism "Disease Number Five" (五号病) rather than FMD in reports because of the sensitivity of the FMD issue. In March 2010, Southern Rural News (Nanfang Nongcunbao), in an article "Breaking the Hoof and Mouth Disease Taboo", noted that FMD has long been covered up in China by referring to it that way.[26] FMD is also called canker (口疮) or hoof jaundice (蹄癀) in China, so information on FMD in China can be found online using those words as search terms.[27][28] One can find online many provincial orders and regulations on FMD control predating China's acknowledgment that the disease existed in China, for example Guangxi Zhuang Autonomous Region 1991 regulation on preventing the spread of Disease No.5.[29]

United Kingdom 2007

An infection of foot-and-mouth disease in the United Kingdom was confirmed by the Department for Environment, Food and Rural Affairs, on 3 August 2007, on farmland located in Normandy, Surrey.[30][31] All livestock in the vicinity were culled on 4 August. A nationwide ban on the movement of cattle and pigs was imposed, with a 3 km (1.9 mi) protection zone placed around the outbreak sites and the nearby virus research and vaccine production establishments, together with a 10 km (6.2 mi) increased surveillance zone.[32]

On 4 August, the strain of the virus was identified as an "01 BFS67-like" virus, one linked to vaccines and not normally found in animals, and isolated in the 1967 outbreak.[33] The same strain was used at the nearby Institute for Animal Health and Merial Animal Health Ltd at Pirbright, 2.5 miles (4.0 km) away which is an American/French owned research facility, and was identified as a possible source of infection.[34]

On 12 September, a new outbreak of the disease was confirmed in Egham, Surrey, 19 km (12 mi) from the original outbreak,[35] with a second case being confirmed on a nearby farm on 14 September.[36]

These outbreaks caused a cull of all at-risk animals in the area surrounding Egham, including two farms near to the famous four-star Hotel Great Fosters. These outbreaks also caused the closure of Windsor Great Park due to the park containing deer; the park remained closed for three months. On 19 September 2007, there was a suspected case of FMD in Solihull, where a temporary control zone was set up by Defra.

Japan and Korea 2010–2011

In April 2010, a report of three incursions of FMD in Japan and South Korea led the United Nations Food and Agriculture Organization (FAO) to issue a call for increased global surveillance. Japan veterinary authorities confirmed an outbreak of type O FMD virus, currently more common in Asian countries where FMD is endemic.

South Korea was hit by the rarer type A FMD in January, and then suffered type O infection in April.[37] The most serious case of foot-and-mouth outbreak in South Korea's history started in November 2010 in pig farms in Andong city of Gyeongsangbuk-do, and has since spread in the country rapidly.[38][39] More than 100 cases of the disease have been confirmed in the country so far,[38] and in January 2011, South Korean officials started a mass cull of approximately 12 percent, or around 3 million in total, of the entire domestic pig population and 107,000 of three million cattle of the country to halt the outbreak.[38]

On 10 Feb 2011, North Korea reported an outbreak affecting pigs in the region around Pyongyang, by then ongoing since at least December 2010. Efforts to control the outbreak have been hampered by illicit sales of infected meat.[40]

Bulgaria 2011

The outbreak was recognised when a wild boar was shot, which had crossed the Bulgarian-Turkish border near the village of Kosti, Burgas Province in the Strandzha Mountains.[41] The autopsy discovered foot-and mouth disease.[41] After this, 37 infected animals were discovered in the village of Kosti, and all susceptible animals there were culled. Burgas Province and seven other neighboring provinces declared a quarantine.[42]

On 14 January, a further outbreak was discovered in the neighboring village of Rezovo.[41] It is thought to have been carried by a Turkish cattle herd. On 17 January, the presence of the disease was confirmed.[41] The Bulgarian authorities ordered culling of all susceptible livestock in Rezovo.[43] Compensation for the losses in the two villages has been promised.[41]

On 31 January, a third focus of infection was discovered in the southeastern Bulgarian village of Gramatikovo.[44] On 25 March, two new outbreaks were discovered in the villages of Granichar and Kirovo.[45]

Economic and ethical issues

Epidemics of FMD have resulted in the slaughter of millions of animals, despite this being a frequently nonfatal disease for adult animals (2-5% mortality), though young animals can have a high mortality. The Taiwan outbreak that only affected pigs also showed a high mortality for adults. The destruction of animals is primarily to halt further spread, as growth and milk production may be permanently affected, even in animals that have recovered. Due to international efforts to eradicate the disease, infection would also lead to trade bans being imposed on affected countries. Critics of current policies to cull infected herds argue that the financial imperative needs to be balanced against the killing of many animals,[46] especially when a significant proportion of infected animals, most notably those producing milk, would recover from infection and live normal lives, albeit with reduced milk production. On the ethical side, one must also consider that FMD is a painful disease for the affected animals.[47] The vesicles/blisters are painful in themselves, and restrict both eating and movement. Through ruptured blisters, the animal is at risk from secondary bacterial infections [47] and, in some cases, permanent disability.

https://en.wikipedia.org/wiki/Foot-and-mouth_disease