Swine influenza is caused by a number of closely related influenza A viruses that are noted for their ability to change their antigenic structure and create new strains.
Each serotype is identified by surface proteins referred to as “H” and “N”. The three common strains that affect the pig are described as H1 N1, H1 N2 and H3 N2. There are also different strains within these serotypes with differing pathogenicity (capacity to produce disease).
The incubation period of the disease is very short, as little as 12-48 hours and the onset is usually rapid and dramatic.
It is virtually impossible to maintain a population of pigs that is influenza virus free.
SI in large herds may become endemic with intermittent bouts of disease and infertility and different strains may also sequentially infect the herd. Immunity to influenza viruses is often short lived (6 months) and the immunity profile in the breeding herd varies considerably with time.
Symptoms
Piglets
- It would be unusual to see any signs of swine flu in the sucking pig unless disease entered the herd for the first time.
- Colostrum may prevent infection during the sucking period.
- Coughing.
- Pneumonia.
- Fever.
Sows
- High temperatures which cause abortions.
- Widespread coughing.
- Pneumonia
When the virus first enters the herd two or three animals may be observed sick for the first two days, followed by:
- A rapid explosive outbreak of inappetence and clinically very ill pigs.
- The effects on the reproductive system follow the sudden onset of a rapid spreading respiratory disease with coughing, pneumonia, fevers and inappetence.
- Acute respiratory distress persists over a period of 7-10 days (depending on the amount of contact between groups of sows).
At a herd level the following may also be seen:
- A sudden and rapid onset of acute illness in sows.
- Coughing and pneumonia spreading rapidly.
- A return to clinical normality over 7-10 days.
- Delayed returns to heat after weaning.
- Increased repeats at 21 days.
- Increased repeats outside the normal cycle.
- Increased numbers of sows coming through not in-pig.
- Increased numbers of abortions, particularly late term.
- Increased numbers of stillbirth rates and slow farrowings.
- Premature farrowings.
- Occasionally an increase in mummified pigs.
- During the phases of high temperatures other diseases present in the herd may be triggered off. A typical example would be an increase in abortions associated with leptospira infection.
Weaners & Growers
Acute disease:
- Classically the pigs suddenly become prostrate.
- Breathing heavily.
- Severe coughing.
- Most of them look as if they are going to die but most of them survive without treatment unless the herd already has a respiratory disease problem.
- SI causes severe pneumonia on its own but when it is combined with other infections such as App, EP and PRRS an intractable chronic respiratory disease syndrome can develop. Severely affected individuals or groups of pigs are therefore best given antibiotic cover to prevent secondary pneumonias developing.
Endemic disease:
- Here the virus remains in the herd, affecting small groups of pigs often weaners. It may be responsible for continuing respiratory diseases with symptoms as in acute disease but less dramatic.
Causes / Contributing factors
SI can be introduced by:
- Infected animals including people, pigs and birds.
- Carrier pigs.
- Probably on the wind although this has not been proved.
- Birds particularly water fowl, are reservoirs of infection.
- Secondary bacterial infections.
- Fluctuating temperatures.
- Stress.
- Wet bedding and floor surfaces.
- Poor nutrition.
Diagnosis
This can often be made reliably on clinical grounds with acute disease because there are no other diseases that are so dramatic in their onset and clinical effects. No other disease affects so many pigs so quickly. Blood samples taken at the time of onset of disease from affected sows and repeated 2-3 weeks later show rising levels of antibody to the specific virus. SIV can be readily grown from nasal and throat swabs and identified in the laboratory. This is often the best approach to confirm the diagnosis.
In acute disease the spread is so dramatic across all ages that little else can be confused with it. In endemic disease however differentiation from other viral infections can be difficult, but PRRS, PRCV, AD and also erysipelas should be considered.