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Influenza (flu)
H1N1 virus
Types
Vaccines
Treatment
Pandemics
Outbreaks
See also
Pigs can harbor influenza viruses adapted to humans and others that are adapted to birds, allowing the viruses to exchange genes and create a pandemic strain.

Swine influenza virus (referred to as SIV) refers to influenza cases that are caused by Orthomyxoviruses that usually occur (are endemic) to pig populations. SIV strains isolated to date have been classified either as Influenzavirus C or one of the various subtypes of the genus Influenzavirus A.

Swine influenza is known to be caused by influenza A subtypes H1N1, H1N2, H3N1, H3N2, and H2N3.

In swine, three influenza A virus subtypes (H1N1, H3N2, and H1N2) are circulating throughout the world. In the United States, the H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs. As of 2004, H3N2 virus isolates in US swine and turkey stocks were triple reassortants, containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages.

Classification

SIV strains isolated to date have been classified either as Influenzavirus C or one of the various subtypes of the genus Influenzavirus A.

Signs and symptoms

Symptoms include fever, disorientation, stiffness of the joints, vomiting, and loss of consciousness ending in death.


Causes

H5N1

Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. Health experts say pigs can carry human influenza viruses, which can combine (i.e. exchange homologous genome sub-units by genetic reassortment) with H5N1, passing genes and mutating into a form which can pass easily among humans. H3N2 evolved from H2N2 by antigenic shift. In August 2004, researchers in China found H5N1 in pigs. Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 in humans has increased to 92% in 2005.

Chairul Nidom, a virologist at Airlangga University's tropical disease center in Surabaya, East Java, conducted an independent research; he tested the blood of 10 apparently healthy pigs housed near poultry farms in West Java where avian flu had broken out, Nature reported. Five of the pig samples contained the H5N1 virus. The Indonesian government has since found similar results in the same region. Additional tests of 150 pigs outside the area were negative.

Pathophysiology

Influenza viruses bind through hemagglutinin onto sialic acid sugars on the surfaces of epithelial cells; typically in the nose, throat and lungs of mammals and intestines of birds (Stage 1 in infection figure).

Swine flu in humans

People who work with poultry and swine, especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur. Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa. This study among others forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance. The 2009 swine flu outbreak appears to be a result of co-occurring zoonosis and reassortment.

The Centers for Disease Control and Prevention (CDC) reports that the symptoms and transmission of the swine flu from human to human is much like seasonal flu, commonly fever, lethargy, lack of appetite and coughing. Some people with swine flu also have reported runny nose, sore throat, nausea, vomiting and diarrhea. It is believed to be spread between humans through coughing or sneezing of infected people and touching something with the virus on it and then touching their own nose or mouth. The swine flu in humans is most contagious during the first five days of the illness although some people, most commonly children, can remain contagious for up to ten days. Diagnosis can be made by sending a specimen, collected during the first five days, to the CDC for analysis.

The swine flu is susceptible to four drugs licensed in the United States, amantadine, rimantadine, oseltamivir and zanamivir, however, for the 2009 outbreak it is recommended it be treated with oseltamivir and zanamivir. The vaccine for the human seasonal H1N1 flu does not protect against the swine H1N1 flu, even if the virus strains are the same specific variety, as they are antigenically very different.

Diagnosis

Prevention

Recommendations to prevent infection by the virus consist of the standard personal precautions against influenza. This includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers, especially after being out in-public. People should avoid touching their mouth, nose or eyes with their hands unless they've washed their hands. If people do cough, they should either cough into a tissue and throw it in the garbage immediately, cough into their elbow, or, if they cough in their hand, they should wash their hands immediately.

Treatment

CDC recommends the use of oseltamivir or zanamivir for the treatment and/or prevention of infection with these swine influenza viruses. Antiviral drugs are prescription medicines (pills, liquid or an inhaler) that fight against the flu by keeping flu viruses from reproducing in your body. If you get sick, antiviral drugs can make your illness milder and make you feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within 2 days of symptoms).

Prognosis

After the fever disorientation, stiffness of the joints, vomiting and loss of consciousness the most common prognosis of swine influenza which has not been treated effectively is death.

Epidemiology

History

1918 Influenza: the Mother of All Pandemics

The "Spanish" influenza pandemic of 1918–1919 infected one third of the world's population (or ≈500 million persons at that time) and caused ≈50 million deaths. The impact of this pandemic was not limited to 1918–1919. All influenza A pandemics since that time, and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics.

Before and after 1918, most influenza pandemics developed in Asia and spread from there to the rest of the world. Confounding definite assignment of a geographic point of origin, the 1918 pandemic spread more or less simultaneously in 3 distinct waves during an ≈12-month period in 1918–1919, in Europe, Asia, and North America (the first wave was best described in the United States in March 1918).

1976 U.S. outbreak

On February 5, 1976, an army recruit at Fort Dix said he felt tired and weak. He died the next day and four of his fellow soldiers were later hospitalized. Two weeks after his death, health officials announced that swine flu was the cause of death and that this strain of flu appeared to be closely related to the strain involved in the 1918 flu pandemic. Alarmed public-health officials decided that action must be taken to head off another major pandemic, and they urged President Gerald Ford that every person in the U.S. be vaccinated for the disease. The vaccination program was plagued by delays and public relations problems, but about 24% of the population had been vaccinated by the time the program was canceled.

About 500 cases of Guillain-Barré syndrome, resulting in death from severe pulmonary complications for 25 people, were probably caused by an immunopathological reaction to the 1976 vaccine. Other influenza vaccines have not been linked to Guillain-Barré syndrome, though caution is advised for certain individuals, particularly those with a history of GBS.

2007 Philippine outbreak

On August 20, 2007 Department of Agriculture officers investigated the outbreak of swine flu in Nueva Ecija and Central Luzon, Philippines. The mortality rate is less than 10% for swine flu, if there are no complications like hog cholera. On July 27, 2007, the Philippine National Meat Inspection Service (NMIS) raised a hog cholera "red alert" warning over Metro Manila and 5 regions of Luzon after the disease spread to backyard pig farms in Bulacan and Pampanga, even if these tested negative for the swine flu virus.

2009 swine flu outbreak

  Confirmed cases followed by death  Confirmed cases  Unconfirmed or suspected cases See also: H1N1 Swine Flu cases tagged on Google Maps
Main article: 2009 swine flu outbreak

The origins of the new swine influenza strain involved in the 2009 swine flu outbreak remain unknown. One theory is that Asian and European strains traveled to Mexico in migratory birds or in people, then combined with North American strains in Mexican pig factory farms before jumping over to farm workers. The Mexican health agency acknowledged that the original disease vector of the virus may have been flies multiplying in manure lagoons of pig farms near Perote, Veracruz, owned by Granjas Carroll, a subsidiary of Smithfield Foods. The strain is a reassortment of several strains of iinfluenza A virus subtype H1N1 that are, separately, endemic in humans and in swine. 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. Viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, but there is no formal national surveillance system to determine what viruses are circulating in pigs in the U.S.

In other animals

Veterinary swine flu vaccine

Swine influenza has become a greater problem in recent decades as the evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the infection when the virus strains match enough to have significant cross-protection, and custom (autogenous) vaccines made from the specific viruses isolated are created and used in the more difficult cases.

Present vaccination strategies for SIV control and prevention in swine farms, typically include the use of one of several bivalent SIV vaccines commercially available in the United States. Of the 97 recent H3N2 isolates examined, only 41 isolates had strong serologic cross-reactions with antiserum to three commercial SIV vaccines. Since the protective ability of influenza vaccines depends primarily on the closeness of the match between the vaccine virus and the epidemic virus, the presence of nonreactive H3N2 SIV variants suggests that current commercial vaccines might not effectively protect pigs from infection with a majority of H3N2 viruses.

The current vaccine against the seasonal influenza strain H1N1 is thought unlikely to provide protection. The director of CDC's National Center for Immunization and Respiratory Diseases said that the United States' cases were found to be made up of genetic elements from four different flu viruses—North American swine influenza, North American avian influenza, human influenza A virus subtype H1N1, and swine influenza virus typically found in Asia and Europe. On two cases, a complete genome sequence had been obtained. She said that the virus is resistant to amantadine and rimantadine, but susceptible to oseltamivir (Tamiflu) and zanamivir (Relenza).

See also

References

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Further reading

External links

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