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Swine influenza virus (referred to as SIV) refers to influenza cases that are caused by Orthomyxoviruses that 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.[1]
Swine flu, unlike bird flu, is able to pass from human to human contact.[2]
Swine influenza is known to be caused by influenza A subtypes H1N1,[3] H1N2,[3] H3N1,[4] H3N2,[3] and H2N3.[5]
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.[6]
Contents [hide]
1 Classification
2 Signs and symptoms
3 Causes
3.1 H5N1
4 Pathophysiology
4.1 Swine flu in humans
5 Prevention
5.1 Veterinary vaccines
6 Treatment
7 Epidemiology
7.1 Outbreaks in swine
7.1.1 2007 Philippine outbreak
7.2 Outbreaks in humans
7.2.1 1918 Influenza
7.2.2 1976 U.S. outbreak
7.2.3 2009 swine flu outbreak
8 See also
9 References
10 Further reading
11 External links
Classification
SIV strains isolated to date have been classified either as Influenzavirus C or one of the various subtypes of the genus Influenzavirus A.[7]
Signs and symptoms
Main symptoms of swine flu in humans.[8]
The Centers for Disease Control and Prevention (CDC) have stated that the symptoms of swine flu are similar to those of other strains of human flu, including fever, cough, sore throat, body aches, headache, chills and fatigue. A few patients have reported that they also suffered from diarrhea and vomiting.[9]
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.[10] Health experts[who?] 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.[11] H3N2 evolved from H2N2 by antigenic shift.[12] In August 2004, researchers in China found H5N1 in pigs.[13] Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 in humans has increased[14] to 92% in 2005.[15]
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.[16][17]
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).[18]
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.[19] 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.[20] 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.[19] The 2009 swine flu outbreak is an apparent reassortment of several strains of influenza A virus subtype H1N1, including a strain endemic in humans and two strains endemic in pigs, as well as an avian influenza.[21]
The 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.[22] 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.[23] Swine flu cannot be spread by pork products, since the virus is not transmitted through food.[23] 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.[24]
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.[25] 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.[26]
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.[27]
Veterinary vaccines
Please help improve this article or section by expanding it. Further information might be found on the talk page. (April 2009)
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.[28][29]
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.[30][31]
Treatment
The CDC recommends the use of Tamiflu (oseltamivir) or Relenza (zanamivir) for the treatment and/or prevention of infection with swine influenza viruses. The virus isolates that have been tested from the US and Mexico are however resistant to amantadine and rimantadine.[32] If a person gets sick, antiviral drugs can make the illness milder and make the patient 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).
Epidemiology
Outbreaks in swine
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, unless there are 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.[33][34]
Outbreaks in humans
1918 Influenza
Main article: 1918 flu pandemic
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.[35] In the U.S., approximately 675,000 people died of the disease.[36] 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.[37]
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).[38]
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.[39][40]
2009 swine flu outbreak
Main article: 2009 swine flu outbreak
Confirmed cases followed by death
Confirmed cases
Unconfirmed or suspected cases
See also: Live map of swineflu, H1N1 live map
The new strain of influenza involved in the 2009 swine flu outbreak strain is a reassortment of several strains of influenza 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.[14]
The origins of this new strain 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.[41] 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,[42] a subsidiary of Smithfield Foods.[43]
Swine flu, unlike bird flu, is able to pass from human to human contact.[2]
Swine influenza is known to be caused by influenza A subtypes H1N1,[3] H1N2,[3] H3N1,[4] H3N2,[3] and H2N3.[5]
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.[6]
Contents [hide]
1 Classification
2 Signs and symptoms
3 Causes
3.1 H5N1
4 Pathophysiology
4.1 Swine flu in humans
5 Prevention
5.1 Veterinary vaccines
6 Treatment
7 Epidemiology
7.1 Outbreaks in swine
7.1.1 2007 Philippine outbreak
7.2 Outbreaks in humans
7.2.1 1918 Influenza
7.2.2 1976 U.S. outbreak
7.2.3 2009 swine flu outbreak
8 See also
9 References
10 Further reading
11 External links
Classification
SIV strains isolated to date have been classified either as Influenzavirus C or one of the various subtypes of the genus Influenzavirus A.[7]
Signs and symptoms
Main symptoms of swine flu in humans.[8]
The Centers for Disease Control and Prevention (CDC) have stated that the symptoms of swine flu are similar to those of other strains of human flu, including fever, cough, sore throat, body aches, headache, chills and fatigue. A few patients have reported that they also suffered from diarrhea and vomiting.[9]
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.[10] Health experts[who?] 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.[11] H3N2 evolved from H2N2 by antigenic shift.[12] In August 2004, researchers in China found H5N1 in pigs.[13] Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 in humans has increased[14] to 92% in 2005.[15]
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.[16][17]
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).[18]
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.[19] 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.[20] 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.[19] The 2009 swine flu outbreak is an apparent reassortment of several strains of influenza A virus subtype H1N1, including a strain endemic in humans and two strains endemic in pigs, as well as an avian influenza.[21]
The 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.[22] 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.[23] Swine flu cannot be spread by pork products, since the virus is not transmitted through food.[23] 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.[24]
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.[25] 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.[26]
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.[27]
Veterinary vaccines
Please help improve this article or section by expanding it. Further information might be found on the talk page. (April 2009)
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.[28][29]
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.[30][31]
Treatment
The CDC recommends the use of Tamiflu (oseltamivir) or Relenza (zanamivir) for the treatment and/or prevention of infection with swine influenza viruses. The virus isolates that have been tested from the US and Mexico are however resistant to amantadine and rimantadine.[32] If a person gets sick, antiviral drugs can make the illness milder and make the patient 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).
Epidemiology
Outbreaks in swine
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, unless there are 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.[33][34]
Outbreaks in humans
1918 Influenza
Main article: 1918 flu pandemic
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.[35] In the U.S., approximately 675,000 people died of the disease.[36] 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.[37]
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).[38]
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.[39][40]
2009 swine flu outbreak
Main article: 2009 swine flu outbreak
Confirmed cases followed by death
Confirmed cases
Unconfirmed or suspected cases
See also: Live map of swineflu, H1N1 live map
The new strain of influenza involved in the 2009 swine flu outbreak strain is a reassortment of several strains of influenza 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.[14]
The origins of this new strain 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.[41] 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,[42] a subsidiary of Smithfield Foods.[43]