Glässer's disease

  • Close up of pig's head showing cyanosis to ears
    Close up of pig's head showing cyanosis to ears and snout
  • Young pigs showing lateral recumbency and cyanosis.
    Young pigs showing lateral recumbency (lying on their side) and cyanosis (blue-purple tinge to ears and snout)

General information

Glässer's disease is a polyserositis and arthritis of pigs caused by the bacterium Haemophilus parasuis. The disease is an emerging disease in Australia. Diagnostic submissions of Glässer's disease to our microbiology research group rose from 6% of total submissions in the late 1980s to 29% of the total submissions in the late 1990s. H. parasuis exists in a number of different types (serovar 1-15), with serovars 4 and 5 (based on submissions to the microbiology research group serotyping service in years 2002 and 2003) being the most common types in Australian pigs. A significant percentage of H. parasuis (these being types 3, 6, 7, 8, 9 and 11) are less pathogenic than other types (these being 1, 2, 4, 5, 10, 12, 13, 14 and 15).


Haemophilus parasuis

Clinical signs

A wide range of clinical signs are associated with H. parasuis. The disease can be peracute or acute in form. Typical clinical signs include:

  • sudden death
  • neurological signs
  • lateral recumbency
  • prostration
  • reluctance to move
  • cyanosis (bluish or purplish tinge to skin)
  • difficulty breathing (dyspnoea)
  • coughing
  • nasal discharge
  • anorexia
  • lameness
  • swollen joints
  • fever
  • abortion.

In conventional herds, the disease is often sporadic and generally outbreaks are linked with stress factors. In high-health status pigs, outbreaks can be devastating and are often linked with the introduction of pigs with the organism.

Outbreaks and immunity

H. parasuis can be part of the normal flora of the growing pig. The current belief is that, in conventional herds, the very young piglets are exposed to the bacterium as well as the protective antibodies in sows' milk. This graded exposure to both the pathogen and protective antibodies allows the growing piglet to develop its own protective immunity. Hence, conventional pig herds can contain pigs that are healthy carriers of Glässer's disease. If such pigs are then mixed with high-health pigs that have never been exposed to either the bacterium or protective antibodies from their sows, the results can be a devastating, peracute outbreak.

Similarly, peracute outbreaks can occur in herds using segregated early weaning (SEW). In these SEW systems, the early separation of the piglet from the sow can mean that the majority of the piglets have never been in contact with the organism while under the protection of the maternal antibodies and have not developed immunity to H. parasuis. When the small number of piglets that were exposed to the organism start shedding, a peracute outbreak can occur in the unexposed pigs. Outbreak can occur in all ages and is often linked to stress factors, causing shedding.


The condition may be suspected on the basis of history (mixing pigs of different origin), clinical signs and necropsy findings. The isolation of H. parasuis is required to confirm a diagnosis. It should be noted that bacterial isolation is difficult and can often fail. As H. parasuis can exist in the upper respiratory tract of the normal pig, isolates from this region may not be causing the systemic disease. Samples are best obtained from freshly deceased pigs or (ideally) acutely ill pigs that are sacrificed. Samples should be collected from pigs that have not been treated with antibiotics. Animal-challenge trials performed by our microbiology research group have indicated that the best samples for a peracute disease case are lung, joint and brain. For the acute chronic form of the disease, the best samples are peritoneal fluid, fibrin in the peritoneum, lung and pericardial fluid.

Laboratory culture also allows confirmation of the serovar of H. parasuis, which is necessary if inactivated vaccines are to be used as part of a control or prevention program. Several cultures should be serotyped as the existence of several serovars within a herd has been reported. In addition, DNA-fingerprinting tests can help understand the epidemiology of the outbreak. Currently, no blood tests are available in Australia. Identification, serotyping, DNA-typing and serovar profiling are all available from our microbiology research group.


It is important to start treatment as early as possible. Initial treatment must be given by injecting a suitable antibiotic. All pigs in an affected group must be treated, not just those showing clinical signs. Often, high doses are required as the antibiotic has to reach such sites as the cerebrospinal fluid and joints. The most appropriate antibiotic to use and the details of the treatment program will vary from piggery to piggery. Ask your veterinarian.

It is important to review management practices (stocking rate, shed environment, pig movement) to reduce the impact of stress factors.


Using therapeutic levels of antibiotics, either in the water or in the feed (pulse treatment), at times of high risk can be beneficial.

Vaccines are also available and are regarded as being effective. As of 2009, off-the-shelf vaccines provide protection only against certain serovars. Hence, the serovar of the strain present on a farm should be identified by culture to ensure that the appropriate vaccine is being used. Autogenous vaccines (i.e. a vaccine specifically produced from an isolate obtained from the farm) are also possible. Consultation with your veterinarian is a key step in deciding if vaccination (and the type of vaccine) is a suitable option.

A major control mechanism of the disease is management. Predisposing stress factors, such as overcrowding and poor ventilation, should be identified and corrected.

In high-health herds, mixing pigs from different origins should be avoided. In SEW systems suffering Glässer's disease outbreaks, a step-wise increase in the weaning age to allow a greater number of colonised young piglets (and hence, immune piglets) is an option. Such an approach must be balanced against the possibility that increased weaning age may allow outbreaks of other diseases such as pleuropneumonia.

Further information

Last updated 18 June 2010