Swine influenza

This article covers influenza virus disease found in pigs. For the influenza pandemic known as “swine flu” in humans, see Pandemic H1N1 2009/10 .

Domestic pigs

The swine influenza (also known as Porcine influenza or swine flu hereinafter) is an acutely extending infectious disease of the respiratory tract in domestic swine . This is caused by porcine influenza viruses (belonging to the pig) belonging to the virus genus influenza virus A , species influenza A virus . Due to reassortment of segments of the RNA genome of the porcine and human influenza viruses can in outbreaks of swine influenza rise to new anti genetic variants occur ( antigenic shift) which have new pathogenic properties for animals or humans . However, these newly emerging subtypes (reassortants) are not classic pathogens of swine influenza.

Pathogen

Influenza A viruses in the TEM image

The most common pathogens of swine influenza are influenza A viruses of the subtypes H1N1 , rarely H1N2 and H3N2 . (Human) influenza C viruses are very rarely isolated from pigs. The influenza viruses in pigs were formerly known as SIV ( swine influenza virus ). In 2006 an A / H3N1 subtype was also isolated in pigs in Italy . In an epidemiological investigation in central China from 2004 to 2006, a subtype ( H3N8 ) that otherwise only occurs in horses could be detected in pig herds. In addition to influenza viruses, which also cause disease in pigs, a large number of human, avian and porcine virus subtypes have been isolated from pigs, which can be spread by them without any signs of influenza virus infection.

The first porcine influenza virus (A / swine / Iowa / 15/30 [H1N1]) was isolated in 1930. In Europe, this pathogen disappeared completely at the end of the 1950s, until it was re-introduced into European pig populations in 1976, probably by imported pigs from the USA, where it has been endemic ever since . The porcine H1N1 subtypes have shown high genetic and antigenic stability over the past 60 years. It was not until 1979 that an avian H1N1 subtype appeared for the first time in pigs in Europe, which was very similar to the subtypes in ducks. Since then, a co-circulation of porcine and avian strains has been proven to take place.

At the end of the 1990s, H1N2 reassortants were also isolated in pigs in the USA, which were a mixture of porcine H1N1 and human / avian H3N2 reassortants. The susceptibility of pigs to avian and human influenza viruses is supported not only by the experimental and natural infection, but also by the fact that the epithelium of the trachea in pigs has both types of surface receptors, the avian α2,3 and the human α2,6 sialic acid - Receptor. The propagation of avian influenza viruses in pigs therefore also selects variants that also preferentially bind to human receptors.

Pathogenesis and clinical picture

The porcine influenza viruses are transmitted by droplet infection via the mucous membranes of the respiratory tract, where they first multiply in individual cells of the epithelium. Even in this phase, the infected animal can infect other animals in the herd. The incubation period is given as 1 to 4 days. The infection spreads over the entire respiratory system - and with it the lungs - within a few days. The virus does not pass into the blood ( viraemia ). A rapidly rising, high fever (up to 42 ° C), severe airway inflammation, increased mucus secretion in the nose and tears characterize the full clinical picture. An interstitial pneumonia and acute bronchitis are typical.

Swine influenza is highly contagious and spreads rapidly within an animal population. The disease shows a high morbidity , but a low lethality ; after 5 to 7 days the symptoms subside very quickly. Additional secondary infections ( superinfections ) with bacterial pathogens, which can then determine the clinical picture, often occur as complications . The representatives of the bacteria genera Pasteurella , Mycoplasma and Bordetella which are pathogenic to pigs are often involved in the secondary infection. The porcine influenza viruses can be excreted from the animal for up to 5 weeks after the disease has healed.

Swine influenza and human influenza

Antigen shift

The classic porcine virus strains rarely cause diseases in humans, and then only mild ones. The species barrier of human, avian and porcine virus strains can be broken by virus replication in pigs through genetic mixing of the genome segments. The importance of the pig in the creation of new, pathogenic human strains is often characterized as a “mixing vessel” . In this transition between species, porcine reassortants appear in humans and human and avian reassortants in pigs. However, the latter are not causative agents of classic swine influenza.

Porcine reassortants in humans

That H1N1 subtype, which led to a major pandemic under the name of Spanish flu in 1918/19 , is now regarded as an originally porcine subtype or at least assumed to be a common origin.

A crossing to humans was observed in 1976, when a diseased soldiers of Fort Dix in Burlington County ( New Jersey , the other then when five soldiers were found), a porcine H1N1 strain was isolated. Four soldiers fell ill with viral pneumonia and one patient died. The virus strain resembled a subtype isolated from pigs a year earlier. Extensive serological tests showed that at least 500 people had been infected; however, the source of the infection could not be determined. In 1988, a fatal infection occurred in Wisconsin in which a virus was isolated that resembled a virus endemic to pigs in 7 of the 8 RNA segments. However, no special mutations with regard to increased pathogenicity were found. In Europe, the co-circulation of avian and human H3N2 strains in pigs led to the appearance of a new subtype in 1993, with which two children in the Netherlands were infected.

A newly emerged variant of the influenza A virus H1N1 subtype was isolated in April 2009 in Mexico and the United States. This newly emerged reassortant is effectively transmitted from person to person. Disease in pigs was not observed and the source of infection was not determined. The isolated strain is resistant in vitro to the antivirals amantadine and rimantadine , which are effective in influenza , but in vitro, according to initial indications, is sensitive to the neuraminidase inhibitors oseltamivir and zanamivir . The designation of the H1N1 2009/10 pandemic as “swine flu” is misleading insofar as the isolated virus strains do not represent the causative agent of the actual swine influenza. They have only one of eight genome segments that could be of porcine origin and have therefore been classified as human reassortants with avian and porcine components. However, the virus variant from 2009 is said to have developed years before the actual outbreak by combining different viruses or variants in pigs as a mixing vessel .

Human reassortants in pigs

The infection of pigs with human subtypes was first detected serologically in 1938 . At the beginning of the 1990s, a comparison of circulating human and porcine virus strains from Italy and China was able to show the regularly localized transfer of human viruses to pigs.

Natural reservoir

In nature, latently infected pigs, as well as waterfowl and lungworm larvae ( metastrongylus ) in earthworms are considered pathogen reservoirs .

Diagnosis

Due to the rapid course of the disease, a serological test for antibodies during the disease is not useful. For the detection of porcine influenza viruses, the direct detection of the pathogen by virus isolation in embryonated chicken eggs or by polymerase chain reaction from nasal and throat swabs is usually successful. If typical symptoms occur in an animal population, it is usually sufficient to detect the pathogen in individual animals. An outbreak of infection can be determined retrospectively if the antibody titer is determined from a serum sample at the time of the disease and another sample four weeks later . An increase in the titer of the specific antibodies by a factor of 4 is then considered as evidence.

Prophylaxis and control

A combination vaccine for swine is available against the most common pathogens causing swine influenza. It contains several inactivated subtypes of the influenza viruses (H1N1 and H3N2). The vaccination is carried out in piglets around the 10th week of life, a necessary second vaccination follows four weeks after the first vaccination. In order to increase the antibody concentration in the colostrum and thus to protect particularly endangered newborn piglets, mother sows are vaccinated again four weeks before the farrowing date.

Swine influenza is not subject to any statutory reporting requirements in Germany, Austria and Switzerland.

literature

• Bernd Liess, Oskar-Rüger Kaaden (ed.): Virus infections in domestic and farm animals. Domestic mammals, fish. 2nd, updated and expanded edition. Schlueter, Hannover 2003, ISBN 3-87706-745-X , pp. 88-90.
• Brian WJ Mahy, Marc H. van Regenmortel (Eds.): Encyclopedia of Virology. 3rd ed., San Diego 2008, ISBN 978-0-12-373935-3 , Volume 3, p. 101
• David M. Knipe, Peter M. Howley (Eds.): Fields' Virology. 5th ed., Philadelphia 2007, ISBN 0-7817-6060-7 , Volume 2, pp. 1709 f.

Web links

Wiktionary: swine flu  - explanations of meanings, word origins, synonyms, translations

• Swine Influenza - Centers for Disease Control and Prevention
• organic-chemie.ch H1N1: Origins and evolution of the current epidemic (Genetics article on the possible links between diseases in pigs and humans)

Individual evidence

1. ^ A. Moreno, I. Barbieri et al .: Novel swine influenza virus subtype H3N1 in Italy . In: Vet. Microbiol. April 10, 2009, (in print), PMID 19398171 .
2. ↑ J. Tu, H. Zhou et al .: Isolation and molecular characterization of equine H3N8 influenza viruses from pigs in China. In: Archives Virol. Apr. 26, 2009, (in print) PMID 19396578 .
3. ^ RE Shope : The etiology of swine influenza. In: Science . 1931, 73 (1886), pp. 214-215, PMID 17729823 .
4. ↑ M. Pensaert, K. Ottis et al .: Evidence for the natural transmission of influenza A virus from wild ducts to swine and its potential importance for man . In: Bull. World Health Organization. 1981, Vol. 59, Iss. 1, pp. 75-78, PMID 6973418 .
5. ↑ H. Kida, T. Ito et al .: Potential for transmission of avian influenza viruses to pigs . In: Journal of General Virology. 1994, Vol. 75, Iss. 9, pp. 2183-2188, full text (PDF) , PMID 8077918 .
6. ↑ T. Ito, JN Couceiro et al .: Molecular basis for the generation in pigs of influenza A viruses with pandemic potential . In: Journal of Virology. 1998, Vol. 72, Iss. 9, pp. 7367-7373, full text (PDF) PMID 9696833 , PMC 109961 (free full text).
7. ↑ C. Scholtissek, H. Burger et al .: The nucleoprotein as a possible major factor in determining host specificity of influenza H3N2 viruses . Virology (1985) 147 (2): pp. 287-294 PMID 2416114
8. ↑ OT Gorman, WJ Bean et al .: Evolution of influenza A virus nucleoprotein genes: implications for the origins of H1N1 human and classical swine viruses . In: J. Virol. (1991) 65 (7): pp. 3704-3714 PMID 2041090
9. ^ JK Taubenberger: The origin and virulence of the 1918 "Spanish" influenza virus . In: Proc Am Philos Soc. (2006) 150 (1): pp. 86-112 (Review) PMID 17526158
10. ↑ AP Kendal et al .: Identification and preliminary antigenic analysis of swine influenza-like viruses isolated during an influenza outbreak at Fort Dix, New Jersey . In: J. Infectious Dis. (1977) 136 Suppl: S 381-385 PMID 606762
11. ↑ PA Rocha et al .: Laboratory characterization of a swine influenza virus isolated from a fatal case of human influenza . In: J. Clin. Microbiol. (1989) 27 (6): pp. 1413-1416 PMID 2754013
12. ^ EC Claas, Y. Kawaoka et al .: Infection of children with avian-human reassortant influenza virus from pigs in Europe . In: Virology. (1994) 204 (1): pp. 453-457 PMID 8091678
13. ↑ Swine Influenza A (H1N1) infection in two children - Southern California, March-April 2009 . Centers for Disease Control and Prevention (CDC). MMWR Morb Mortal Wkly Rep. (2009) Apr 24; 58 (15): pp. 400-402 PMID 19390508
14. ↑ Assessment of the RKI , as of April 27, 2009
15. ↑ GenBank sequences of the new H1N1 variant
16. ↑ Gavin JD Smith et al .: Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic. In: Nature. Volume 459, 2009, pp. 1122-1125, doi: 10.1038 / nature08182 . Literally it says: “We show that it was derived from several viruses circulating in swine, and that the initial transmission to humans occurred several months before recognition of the outbreak. ”
    Organ-chemie.ch , June 11, 2009: Genom-Analyze swine flu virus suggests disease surveillance in pigs. H1N1: Origins and Evolution of the Current Epidemic. Genome analysis shows current H1N1 virus spread to humans months before the outbreak became known. Accessed on October 7, 2012. In the summary of Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic it says: “Rambaut was able to show that the current virus is the combination of different viruses in pigs as a mixed vessel, therefore a specific one Origin cannot be established and that transmission to humans must have taken place months before the outbreak became known. Years before the actual outbreak of the disease, genes that are now contained in the virus could have been recombined. "
17. ^ RE Shope: An intermediate host for the swine influenza virus. Science (1939) 89 (2315): pp. 441-442 PMID 17816951
18. ↑ MR Castrucci et al .: Antigenic and sequence analysis of H3 influenza virus haemagglutinins from pigs in Italy . J. Gen. Virol. (1994) 75 (2): pp. 371-379 PMID 8113758
19. ^ H. Kammer, RP Hanson: Studies on the transmission of swine influenza virus with Metastrongylus species in specific pathogen-free swine . J. Infect. Dis. (1962) 110: pp. 99-102 PMID 14453488

This article is about a health issue. It is not used for self-diagnosis and does not replace a diagnosis by a doctor. Please note the information on health issues !