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The third virus affecting the wide spectrum of endemic disease is swine influenza. This agent primarily has effects on the respiratory system and sometimes produces severe damage to the respiratory tract facilitating secondary infections with a whole range of other respiratory pathogens, opportunist organisms and commensals. It has been regarded as a disease of the winter months associated with colder climatic conditions and poor ventilation.
Pigs appear to be affected as a herd rather than as individuals with a variety of signs including high temperature, prostration, lethargy, inappetance, reluctance to move to even drink, conjunctivitis and with cough or dyspnoea (difficult breathing) or both. Susceptible sows may run very high temperatures leading to abortion and infertility. Quite often, they will, unless affected by secondary infections, spontaneously recover after a period of several days.
Epidemiology and emergence of new viruses
All the influenza viruses are RNA viruses with 8 RNA segments that code for at least 10 viral proteins. Although there are type A, B and C viruses all the pig viruses have been type A viruses. The types are subdivided by their surface glycoproteins haemagglutinin (HA) and neuraminidase (NA). There are 16 haemagglutinins (H1-16) and 9 neuraminidases(N1-9).
Unfortunately, humans have influenza viruses and so do pigs and so do avians. All of these are known as influenza A strains. The most important point is that they can all swap genetic material. This is especially true as pigs, birds and humans live in close relationship. One of the major differences however, is that influenza infection in avians is also an alimentary disease and viruses may be recovered from both cloacal and nasal swabs in affected animals. It is also one of the reasons that pig units should if possible be protected from the roosting of large numbers of birds..
The first swine influenza viruses were classified on the basis of the above glycoproteins and were all H1N1 and were for about 60 years in North America.
In the middle 1980’s, there appeared in European pigs H3N2 viruses that were derived originally from humans and had adapted to pigs and were therefore known as human-like H3N2 viruses. These viruses have since appeared in other parts of the world most notably as H3N2 in the USA in 1998. These viruses however contained bits of human, avian and swine viruses and were therefore called triple re-assortants.
New viruses emerge or strains occur by one of three mechanisms. The first is by interspecies transmission, ie a bird virus moving to the other species which is what happened in the 1990’s when an avian strain 195852 became wholly adapted to the pig and became widespread in the pig population in the UK.
The second is by one of the viruses mutating and causing changes in its major proteins and this is what is known as ‘antigenic drift’ a change which can lead to small or large changes in the virus.
The third and last type of change is where the virus shares its genetic material with another different virus by re-assortment and this process is known as ‘antigenic shift’. All of these three types of change have occurred in Europe.
Thus, in pigs in Europe we have had classical H1N1 like the original Wisconsin strains for long periods of time, we had the emergence of human-like H3N2 viruses, then we had the avian viruses that wholly adapted to pigs and finally the H1N2 viruses which are a re-assortant of H1 and N2 from old human viruses and middle segments from avian viruses. If you look you will find!. You will also find that the viruses disappear as it seems that the H3N2 has not been found in the UK since 1997. For example, in the USA in recent times since 2005 an H1N1 of human origin has been found in pigs but the rest of the genes are similar to the usual triple assortant genes. Also in 2006 an H2N3 virus was found in Missouri with the H2 and N3 being avian in origin and again the rest of the genes being from the customary swine triple re-assortant found at the time.
There have been suggestions that the incorporation of the internal avian genes into the viruses circulating in the pig has facilitated the spread of the external H1 and N1 segments of avian origin. In any event it is the worldwide expansion of all three populations (avian, porcine and human) that is enabling the appearance of these new strains to appear. Most of the viruses circulating at the moment carry H and N segments of porcine origin with a variety of avian, human, and porcine internal genes.
As far as the pig and swine influenza is concerned the most common threat to the pig is considered to be the avian virus. In the last decade there have been significant changes to the avian viruses, subtypes H5, H7 and H9 have been widely reported in poultry to have shown increased virulence. For example the H9 strains have spread widely worldwide and the first H9N2 viruses were found in pigs in Hong Kong in 1998. These viruses often appear in pigs but it is difficult to establish whether they are being passed from pig to pig. However in the case of the H9N2 virus Chinese and Korean studies have suggested that the virus may be able to transmit from pig to pig.
Similarly, the incursion of highly pathogenic H5N1 avian influenza into the Netherlands was extremely worrying in that pigs on 5 farms that kept both poultry and pigs showed evidence of infection probably as a result of being exposed to large concentrations of the virus. From the point of view of the swine population we are therefore extremely vigilant about the occurrence of virulent avian influenza viruses.
