Glässer’s Disease


Causal agent

Haemophilus parasuis alone or a combination with various streptococci spp and Mycoplasma hyorhinis.  A bacteria.  There are at least 15 types of H. parasuis, many are none virulent and the types have little immunological similarities.  One virulence factor may be recognised – VtaA – Virulence associated trimeric autotransporter.

Age group

All ages are susceptible, however generally causes disease in weaned pigs.  Classic clinical signs in 10-25 kg pigs.

Clinical signs

Naive herds

Very rare

The disease creates a devastating acute meningitis

This is normally seen when a naive adult is introduced to a normal herd.

Within 48 hours the adult demonstrate severe pneumonia, depression, anorexia, high rectal temperature 42°C. 

Terminally the animal demonstrates incoordination, prostration, meningitis and dies.  Death can occur very quickly after arrival

Normal Herds

Usually sudden and often affects the better pig.  The animal presents with depression, anorexia, the rectal temperature rises to 40.5ºC. Cyanosis may appear on the extremities.  The animal may appear as if walking is painful.  Terminally meningitis may be seen.  Quite often the animal presents only as a sudden death



Loss of part of the ear associated with failure of the circulation supply to the ears

Wasting piglets who fade and die or grow very poorly

Can be found as a diagnosis in late growers who die

 Glassers weaner problem run off kr

Glassers weaner ears

Hairy pig1

Weaners running off with Glässer's disease

Cardiac insufficiency

Hairy pig post-weaning



The organism lives in the nasal cavities of most normal piglets/weaners

Stress factors


Since PRRSv introduction, Glässer's disease has become more common/severe

Vit E deficiency is often associated with the disease, particularly in otherwise healthy herds.

Environmental stress can play a role, characterised by draughts, chilling and a damp environment. Particularly if the nursery is poorly set up.  The poor environment places a great stress on the newly weaned piglet

Variation in diurnal temperatures or poor adherence to cooling curves

Incubation period


Can be within 24 hours


Post-mortem lesions


The organism infects all the serosal membranes and produces a polyserositis. The clinical signs are dependent on which serosal membrane is affected

The following organs are covered in a serosal membrane:


The disease causes pericarditis seen as tags and fluid around the heart


The disease creates extensive pleurisy


The disease infects the abdominal cavity resulting in peritonitis


When the joints become infected synovitis and arthritis with swollen joints are seen


The meninges of the brain become infected resulting in a meningitis

The pleurisy may be very extensive.  Note that pleurisy takes over 6 months to resolve – so may be present at slaughter

Glassers pleura B

Glassers pericarditis severe

Chronic pericarditis

Acute peritonitis can appear as increased volume of peritoneal fluid

Glassers acute peritonitis detail

Glassers B3

Chronic peritonitis with adhesions between intestinal loops and peritoneum.  The degree of fibrous peritonitis may be seen in 60-70 kg pigs which die for other issues – an influenza outbreak for example



Clinical and postmortem signs

Culture of the organism is difficult and requires special media.  The presence of antibiotics in the pig makes isolation additionally difficult

PRC is available, but does not differentiate pathogenic and none pathogenic strains

Treatment and control


Antimicrobial agents, in particularly penicillin or amoxycillin based, initially via the water supply.  However death can be very rapid before treatment can be initiated

Removal of as many stress factors as possible

Good gilt introduction routines to reduce PRRSv and Swine Influenza flair ups

Vaccination is possible.  Autogenous vaccines are often more effective owing to the large number of serotypes and little protection between the different types.  Note a farm can be infected with multiple serotypes

Common differentials


Actinobacillus pleuropneumonia, Vit E deficiency



There are no zoonotic implications