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
Acute
Chronic	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
Weaners running off with Glässer's disease		Cardiac insufficiency	Hairy pig post-weaning
Infectivity
	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:
Heart	The disease causes pericarditis seen as tags and fluid around the heart
Lungs	The disease creates extensive pleurisy
Intestines	The disease infects the abdominal cavity resulting in peritonitis
Joints	When the joints become infected synovitis and arthritis with swollen joints are seen
Brain	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			Chronic pericarditis
Acute peritonitis can appear as increased volume of peritoneal fluid			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
Diagnosis
	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
Zoonotic
	There are no zoonotic implications