Glässers disease (Haemophilus parasuis)

calendar icon 8 November 2018
clock icon 6 minute read

Background and history

Glässers Disease is caused by the bacterium Haemophilus parasuis, a small organism, of which there are at least fifteen different types. It is ubiquitous, found throughout the world and is present even in high health herds. If such herds are set up using SPF or MEW techniques and are free from Hps it can be devastating when they first become contaminated, producing an anthrax-like disease with high mortality in sows.

In the majority of herds in which the bacterium is endemic, sows produce a strong maternal immunity which normally persists in their offspring until 8 to 12 weeks of age and as a result, the effects of the infection in weaners are usually nil or very minimal. The pigs become sub-clinically infected when still protected and then stimulate their own immune response. If however the maternal immunity wears off before they become infected they may develop severe disease. It can however become a secondary organism where there are other major pathogens and in particular enzootic pneumonia. Outbreaks of disease are sometimes experienced in sucking pigs, particularly in gilt herds.

Clinical signs

Acute disease

Pigs with glässers disease become rapidly depressed, with an elevated temperature, stop eating and are reluctant to rise. Hps attacks the smooth surfaces of the joints, coverings of the intestine, lungs, heart and brain. In young growing pigs meningitis or middle ear infections are common together with pneumonia, heart sac infection, peritonitis and pleurisy.

Hps also causes individual cases of arthritis and lameness with acute pain, fever and inappetence. It is respiratory spread and a characteristic feature is a short cough of only 2-3 episodes. Sudden death in good sucking piglets is not uncommon in herds with a problem and in particular when immunity in gilt litters is low.

Chronic disease

Sucking piglets are often pale and poor growing and 10-15% may be affected in a litter. Such pigs then continue into the growing period with poor growth. When long standing pericarditis is a feature sudden deaths occur.


This is confirmed by clinical observations, post-mortem examinations and isolation of the organism in the laboratory but it is not an easy one to grow.

Similar diseases

These would include:

  • Actinobacillus suis.
  • App.
  • Mulberry heart disease.
  • Streptococcal meningitis.
  • Streptococcal septicaemias.

Post-mortem and bacteriological examinations are required to differentiate.


  • Hps has a wide antibiotic sensitivity including amoxycillin, ampicillin, OTC, sulphonamides, penicillin and ceftiofur.
  • Look for the very early signs of huddling and shivering and identify clinical cases.
  • Treatment must be given early, particularly if cases of meningitis are occurring. It is important to differentiate this disease from streptococcal meningitis and this can only be done by isolating the respective organisms from the brain.
  • Identify the onset of disease in sucking pigs and inject 3 to 4 days prior to this to prevent disease, with long-acting penicillin.
  • Treatments are best, using injections of either penicillin/streptomycin, trimethoprim/sulpha, ceftiofur or synthetic penicillins.
  • Treat for 2 to 3 days.
  • Medicate the water with amoxycillin or phenoxymethyl penicillin for 4-5 days over the period of risk.


  • Where the disease is a problem in sucking pigs the sows feed can be top dressed daily 7 days before and 7 days after farrowing with phenoxymethyl penicillin.
  • Alternatively sows can be injected with long-acting penicillin at point of farrowing.
  • Autogenous vaccines can be produced and given to the sow to stimulate an immunity but the response is serotype specific and in any one herd there may be a number of different serotypes. The vaccines need to be multivalent.
  • The lactating and creep rations can be medicated with 200-300g of phenoxymethyl penicillin.
  • Apply the relevant general principles discussed for the control of respiratory disease in chapter 9.

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