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Influenza H1N1 2009
• Several novel features of the new infection have shown in man; (All sorts of issues ie who to treat, who to vaccinate, do we push virus etc? Beyond the scope of this short paper). This virus has HA and internal genes from similar to those found in circulating re-assortant viruses found in man but the M and NA genes were more closely related to the Eurasian avian like influenza A lineage. The questions are a) will it establish itself in pigs world wide-probably, b) acquire oseltamivir resistance –probably, c) re-assort with the highly pathogenic H5N1-hopefully not, d) will it show rapid evolution- hopefully not, and e) will the vaccines be effective in the long term- no reason not to think so.
• The new virus has an interesting gene composition. The PB1, PB2, PA, NP and NS genes come from the triple swine re-assortant, the NA and M come from the Eurasian swine virus (H1N1/H3N2) and the HA comes from the swine H1N2. The virus may have been hiding in birds? , but who knows as yet. The group in Athens Georgia has tested the virus in birds, turkeys, chickens, ducks and Quail) and found that the birds became infected but did not transmit the virus. It may be that the virus has occurred in Central America because there is no surveillance there as there is in the USA or Europe.
We do not know if previous immunity to H1N1 will provide immunity to the new virus or not.
The big question is where did it come from as other pandemics probably originated in birds or pigs and in this case there is as yet no direct evidence as to the origin.
Most of the outbreaks detected in pigs have resulted from infections transmitted to the pigs by humans or have no known cause.
It may be residing in an unidentified pig or poultry reservoir and this may eventually be detected by all the surveillance programmes put into operation since the pandemic started (7 of the 8 genes are porcine and 1 is avian).
In ferrets, the new virus is more pathogenic than the normal seasonal virus with more extensive virus replication occurring in the respiratory tract. Usually, the seasonal ones replicate in the nasal cavity but this one also in the trachea, bronchi and bronchioles. Viral shedding was also more significant from the upper respiratory tract. In the ferret experiments the IHC has been positive in the turbinates, trachea and bronchioles with the new virus whereas with the usual seasonal viruses it is only the turbinates that are IHC positive. The ferret is usually killed by H5, H7 and the 1918 H1N1 but this new virus does not seem to cause anything other than a mild disease, although it is probably more severe than the usual seasonal flu. It is highly likely that it can re-assort as it shares the same receptors.
As a result of this analysis it is suspected that the pig is a more likely suspect than an avian. The other possibility, since the discovery of both avian and mammalian receptors in the respiratory tract of humans, is that the virus has recombined in humans from exposure to both avian and porcine strains of influenza virus.
At the moment the virus has not been found retrospectively in pigs.
Experimental infections in the USA have shown that only the respiratory tract produced infectious virus. Virus does not appear to spread and replicate in other tissues.
The recorded instances in pigs in Canada (several cases), Argentina (two cases), Australia (three cases) and Northern Ireland (3 cases) have all suggested, that the pigs have been infected from infected humans but in most cases this evidence is circumstantial. Recently, the virus has been isolated from pigs in quarantine in Singapore from pigs imported from Indonesia.
There has been no pig to pig natural transmission demonstrated until very recently in the Norwegian outbreak in pigs where upwards of 20 odd herds are believed to have been infected by pig to pig transmission. On this basis we can therefore expect the pig to pig transmission to become more common. It is also possible that two human cases have resulted from these new pig to pig transmissions.
It has been demonstrated in experimental infections. The experimental infections produce quite severe reactions in the pig respiratory tract.
The experimental infections in pigs using the Californian virus have shown that there are similar results. The human virus has not yet had time to change significantly.
The other significant change has been the isolation of the virus from 3 herds in Northern Ireland.
The first unit was a weaner to bacon unit (5000 pigs with 600 sows) and samples were not collected until 3 weeks into the course of the disease by which time there was a moderate respiratory disease in the weaners. There was only a 0.1% mortality but with a 90% morbidity. It rapidly spread to the whole herd within 3-4 days and each batch recovered within 4-5 days.
Farrowing sows had a reduced appetite for a few days. No human infection has been detected in the 5 workers on this farm. One of the workers reported respiratory signs to his GP. The virus isolated was exactly the same as the one circulating in humans, ie it has not yet re-assorted.
The second unit (3000 pigs including 340 sows) was 10km from the first. The first clinical sign was coughing 10-15 week old pigs. Then spread to finishers and weaners with sows still unaffected. Mortality slightly increased to 2-3%. Owner was reported to have had a cold. Both units may have received pigs from the Irish Republic.
Both of these first two herds are said to have a high health status and good biosecurity.
The third herd was detected on serology of 5mth old pigs on testing prior to export.
Since then there has been the report of the virus from Eire. The outbreak in the south is almost as far away as is possible from the outbreaks in the north. This outbreak occurred on the 25th September. The unit had 3050 pigs with 40 pigs affected and no deaths. The breeding unit had 650 sows and 2400 piglets and weaners. Two of the three sow houses had 40 dry sows affected. The sows were off their feed and showed laboured breathing. The results were confirmed by RT-PCR. The morbidity rate was 1.31%. The source of the outbreak is apparently an infected farm worker who attended the pigs whilst sick. This exposure suggests that the incubation period in pigs is 7-10 days.
