Occurrence: Worldwide, some herds free.
Age affected: Piglets pre-weaning, weaners.
Causes: Bacterium - Haemophilus parasuis.
Effects: Fever, inappetence, arthritis, breathing difficulty, cough, nervous signs, death.
Glässer’s disease is caused by the bacterium Haemophilus parasuis. The organisms produce fimbriae and capsules and pathogenic organisms appear to possess a particular outer membrane protein. A cytotoxin has been described but not defined. H. parasuis can be grown easily in the laboratory, but the media used must be supplemented with nicotinamide adenine dinucleotide (NAD). Small translucent 1 mm colonies develop within 48 hours. The species is currently divided into 15 serovars. Serovars 1, 4, 5, 10, 12, 13, 14 cause Glässer’s disease, 15 is less virulent and 3, 6, 7, 8 9, and 11 appear to be avirulent. Infection is by the respiratory route, either by aerosol or by inhalation of infected droplets and the bacteria can soon be found in the blood. The incubation period may be as little as 12 hours and septicaemia results in fibrinous polyserositis, polyarthritis and purulent meningitis within 36 hours of infection. Bronchopneumonia may develop and organisms appear to colonise the tracheal mucus. Patchy ciliary loss is seen and a purulent rhinitis develops. H. parasuis pneumonias often accompany infection with swine influenza and PRRS. Protective immunity develops to the infecting serovar, but this may not protect against other serovars. Passive immunity may protect piglets for up to 4 weeks.
Mode of transmission
H. parasuis infection is transmitted from pig to pig directly by contact or by aerosol and is inhaled. As the organism is delicate and does not survive drying well, indirect contact with clothing and pen furniture is less important. The infection (or a new strain of the organism) is usually introduced into a herd in carrier pigs. Infection may be present in a farm for some time without resulting in clinical disease.
Outbreaks of the disease occur in young pigs 3-6 weeks of age as maternal immunity wanes. The disease begins suddenly with fever (40-41˚C, 104-107˚F), complete loss of appetite, shallow, laboured breathing and extension of the head. There may be a serous (clear) nasal discharge and coughing may occur. Lung sounds and pericardial rubbing can be heard when using a stethoscope Animals become lame and shuffle. All joints are swollen, warm and painful. There may be swelling of the face and one or both ears. Pigs may die within 2-5 days of the onset of the disease and show a red to blue skin discolouration before death or signs of head tilt and other indications that meningitis is present. Survivors may develop chronic arthritis, pericarditis and heart failure, meningitis or intestinal obstruction once the fibrinous exudate become fibrous. Those with inguinal hernias are at particular risk of strangulation of the bowel. Animals of any age may be affected in non-immune herds. Coughing, bronchitis and meningitis may occur in gilts or older finishers and sudden death has been recorded in this age group. Clinical signs may be overlooked until death or signs of chronic disease appear.
The disease is a common cause of fever, purulent (cloudy) nasal discharge, and coughing in pigs 3-6 weeks old. Lameness may lead to suspicion of Glässer’s disease in some cases, the skin may be flushed or there may be sudden deaths. Glässer’s disease should be suspected when sudden death, coughing and fever occur in high health finishers or gilts.
Inside the carcass of a swine affected by fibrinous pleuropneumonia (A.pleuropneumoniae).
Photo credit: Ricardo A. Soncini.
Affected piglets which have died suddenly are often in good condition. At post-mortem examination, yellowish jelly-like fibrin is present on the lungs (pleurisy), heart (pericarditis) and peritoneum and abdominal organs (peritonitis). Bronchopneumonia may also occur. The spleen and liver are enlarged and petechial haemorrhages may be seen on the kidneys. The joint fluid is turbid and yellowish-green fibrin deposits may be present in the joint cavities. A purulent meningitis is often present. Animals which have died from chronic disease have fibrous pericarditis accompanied by signs of chronic heart failure, enlarged heart, oedema of the lungs, enlarged liver and spleen with excess straw-coloured peritoneal fluid. Fibrous pericarditis and pleurisy are frequently recorded at meat inspection.
Pure cultures of H. parasuis may be isolated from the nasal cavity, tracheobronchial tree, joint fluids, heart blood or, if meningitis is present, from the cerebrospinal fluid. The organism may be present in lesions initiated by other agents.
Treatment and prevention
Early cases of Glässers disease may be treated by injection with penicillin, ampicillin, tetracycline, ceftiofur, enrofloxacin and trimethoprim: sulphonamide where allowed. Spread to other animals at risk may be prevented and treatment continued by water medication with one of the above drugs for the appropriate treatment period. Feed medication over the period of risk may prevent infection. The disease may be reduced in its severity by using all-in, all-out husbandry at weaning and may also be controlled by using Isowean management. Treatment of a group of pigs on entry to an airspace will also reduce the likelihood disease. Vaccination is now perhaps the control method of choice. Killed vaccines containing serotypes 4 and 5 are commercially available and may be used to vaccinate sows or piglets. Vaccine failure has occurred when there has been infection with serovars not included in the vaccine and successful protection depends upon inclusion of appropriate serovars. Serotypes 4 and 5 are important in most countries surveyed to date. Vaccines made from the herd’s own organisms are also effective. Eradication has not been reported, although treatment during segregated early weaning may leave animals uninfected.