HistoryThis section has been translated automatically.
Swine flu was first observed in 1918 (Koen, 1918) and coincided with the 1918-1919 influenza pandemic in humans. Influenza viruses were identified as the cause of febrile respiratory diseases in pigs as early as 1930. Outbreaks of swine flu were also reported in Europe between 1918 and 1959 (Lange et al. 2014). After these episodes, the virus was not detected for almost 20 years. In 1979, a new H1N1 virus emerged in the European pig population. All eight genes were closely related to avian H1N1 viruses, indicating a reassortment and transmission of avian viruses to pigs (Krumbholz et al. 2014). This "avian-like" A(H1N1) virus, referred to as the "Eurasian avian-like 1C lineage", replaced the classical swine influenza virus in Europe and continues to circulate in pigs today.
Since 1984, outbreaks of swine flu in Europe have also been frequently associated with H3N2 viruses antigenically related to human strains from the early to mid-1970s. In 1994, further reassortants between the avian swine influenza H1N1 virus and the human H3N2 influenza virus were discovered, leading to the establishment of human H1N2 viruses in European pigs (Brown et al. 1998). Triple reassortant swine H3N2 viruses that emerged in the USA in 1998 carried genes of seasonal human H3N2 viruses (HA, NA, PB1), classical swine H1N1 viruses (NP, M, NS) and North American avian influenza viruses (PA, PB2) (Karasin et al. 2000). The first isolation of a swine influenza virus from a human was in 1974. Transmission of swine influenza viruses to humans was suspected, but could only be confirmed after an outbreak of swine influenza in 1976 by antigen and gene analysis of H1N1 viruses isolated from pigs and a human contact.
DefinitionThis section has been translated automatically.
Swine influenza, also known as porcine influenza, A(H1N1) or A(H3N2) is a highly contagious disease for pigs. This virus can also infect humans. However, patients without serious pre-existing conditions usually have a mild course, whereas people with pre-existing conditions often have a severe course with complications.
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PathogenThis section has been translated automatically.
The most common subtypes of swine flu viruses currently circulating in pigs are H1N1, H1N2 and H3N2. Swine flu is known to infect people who are in close contact with infected pigs and in some cases leads to death. Retrospective studies showed that farm workers have higher seroconversion rates for IAV than people without daily contact with pigs (Krumbholz et al. 2014). Overall, this information suggests that farm workers may serve as an important conduit for the transmission of IAV from pigs to humans (Lopez-Moreno et al. 2022).
The virus is transmitted by very fine droplets. It nests in the respiratory tract. The highly complex viruses have hemagglutinin (HA) and neuroaminidase (NA) receptors on their surface. They use the HA receptors to dock onto the surface of mucosal cells.
Pigs can become infected with influenza viruses from birds, pigs and humans, as their respiratory tracts contain both avian α-2,3 and mammalian α-2,6 sialic acid receptors. (Balzli et al. 2016). Therefore, pigs are traditionally considered a "mixing vessel" for transmission between different species, creating new viruses with pandemic potential.
Clinical featuresThis section has been translated automatically.
In 2014, the results of 396 confirmed zoonotic infections with swine flu viruses were presented in a literature review (Freidl et al. 2014). More recent studies have also mainly described the antigenic and/or genetic properties of isolated H1N1v viruses (Deng et al. 2020, Dürrwald et al. 2020). Human infections caused by swine influenza viruses have been associated with clinical illness and occasional hospitalizations and deaths. However, only limited human-to-human transmission has been documented to date, with the exception of the pandemic H1N1 swine influenza virus identified in Mexico and the United States in 2009 (Myers et al. 2007). This novel H1N1 virus was characterized by a unique combination of gene segments that had not previously been observed. The A(H1N1)pdm09 virus contains the NA and M genes of the Eurasian avian swine species and all other genes are derived from the American H1N1 triple reassortant that emerged in 1999. This novel swine virus was well adapted to the human host and spread rapidly to other regions of the US, Canada and other continents.
The case of swine-to-human transmission that occurred in Germany in 2010 was characterized by an unusually severe course, whereas the person (m) infected with an H1N1 swine virus in 2007 experienced a more normal flu-like illness. This indicates that more people were probably involved in these transmission events. Osnabrück is located in the region of Germany with the highest density of pig farms. There is therefore a high risk of infection for farmers, who may not show clinical symptoms due to acquired immunity, but can transmit the virus to the population.
DiagnosisThis section has been translated automatically.
In terms of symptoms, an infection with A/H1N1 is difficult to distinguish from a normal flu. The first symptoms appear after one to a maximum of four days: sudden high fever, loss of appetite, runny nose, possibly also a sore throat, cough, muscle and joint pain. Nausea, vomiting or diarrhea may also occur. These latter symptoms do not occur with normal flu. The virus can be detected by PCR.
Internal therapyThis section has been translated automatically.
As with other type A viruses, neuraminidase inhibitors can be used. Amantadine, on the other hand, is ineffective as A/H1N1 is immune to it. However, the neuraminidase inhibitors Tamiflu and Relenza must be taken within 24 to 48 hours of the first symptoms appearing. If there are signs of a bacterial superinfection, an antibiotic is necessary.
Note(s)This section has been translated automatically.
The H1N1 subtype that led to a major pandemic in 1918/19 under the name of Spanish flu is now considered to be the original porcine subtype, or at least a common strain of origin is assumed.
LiteratureThis section has been translated automatically.
- Balzli C et al. (2016) Susceptibility of swine to H5 and H7 low pathogenic avian influenza viruses Influenza Other Respir. Virus 10: 346-352.
- Brown IH et al. (2001) Pattern of mutation in the genome of influenza A virus on adaptation to increased virulence in the mouse lung: identification of functional themes. Proc Natl Acad Sci USA 98: 6883-6888.
- Deng YM et al. (2020) Locally acquired human infection with swine-origin influenza A(H3N2) variant virus, Australia, 2018. Emerg Infect Di 26: 143-147
- Dürrwald R et al. (2020) Zoonotic infection with swine A/H1(av)N1 influenza virus in a child, Germany, June 2020. Eur. Surveill 25 10.2807/1560-7917.
- Freidl GS et al. (2014) Influenza at the animal-human interface: a review of the literature for virological evidence of human infection with swine or avian influenza viruses other than A(H5N1). Eur. Surveill 19: 10.2807/1560-7917
- Heider A et al. (2024) Characteristics of two zoonotic swine influenza A(H1N1) viruses isolated in Germany from diseased patients. Int J Med Microbiol 314:151609.
- Karasin et al.(2000) Genetic characterization of H3N2 influenza viruses isolated from pigs in North America, 1977-1999: evidence for wholly human and reassortant virus genotypes. Virus Res 68: 71-85.
- Koen J (1918) A practical method for field diagnosis of swine disease. Am J Vet Med 14: 468-470
- Krumbholz et al. (2014) Origin of the European avian-like swine influenza viruses. J Gen Virol 95: 2372-2376.
- Lange J et al. (2014) Circulation of classical swine influenza virus in Europe between the wars Arch Virol 159: 1467-1473.
- Lopez-Moreno G et al. (2022) Evidence of influenza A infection and risk of transmission between pigs and farmworkers Zoonoses Public Health 69; 560-571.
- Myers KP et al. (2007) Cases of swine influenza in humans: a review of the literature. Clin Infect Dis 44: 1084-1088.
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