Glässer’s disease

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Acute septicaemia - note discolouration of extremities
Glassers Disease at post mortem examination
Severe pleurisy and pericarditis at slaughter, typical of chronic Haemophilus parasuis

Glässer’s disease is a bacterial disease of pigs, caused by Haemophilus parasuis.

Haemophilus parasuis is a commensal organism of the upper respiratory tract of swine that cause severe systemic disease characterized by fibrinous polyserositis, arthritis, and meningitis. Disease caused by H parasuis has a sudden onset, short course, and high morbidity and mortality. Young animals (6-8 wk) are primarily affected, although sporadic disease can be observed in adults (eg, introduction of a naive adult to a normal herd). Survivors can develop severe fibrosis in the abdominal and thoracic cavities, which can result in reduced growth rate and carcass condemnation at slaughter. Glässer’s disease is seen worldwide, and its incidence appears to have increased since the introduction of porcine reproductive and respiratory syndrome[1].

Cause

The causal agent, H parasuis, is a gram-negative coccobacillus that requires V factor (NAD) supplementation for growth. Fifteen serovars of H parasuis have been reported, but a high percentage of the evaluated isolates are nontypable. The factors involved in systemic invasion by H parasuis are still unknown.

Clinical signs

Clinical signs are observed mainly in pigs 6-8 wk old, although the age of affected animals may vary, depending on the level of acquired maternal immunity. Acute disease has a short course and may result in sudden death without the presence of characteristic gross lesions. Clinical signs include high fever (41.5°C), severe coughing, abdominal breathing, swollen joints, and CNS signs such as lateral decubitus, paddling, and trembling. These signs may be seen jointly or independently. Chronically affected animals may have a reduced growth rate as a result of severe fibrosis in the thoracic and peritoneal cavities.

Systemic infection is characterized by the development of fibrinous polyserositis, arthritis, and meningitis. The fibrinous exudate can be observed on the pleura, pericardium, peritoneum, synovia, and meninges and is usually accompanied by an increased amount of fluid. Fibrinous pleuritis may be accompanied by anteroventral pneumonia, which is characterized by consolidation of the lung as a result of infiltration of inflammatory cells and severe congestion. Hyperacute cases have increased fluid in the thoracic and abdominal cavities, without the presence of fibrin. Lack of characteristic gross lesions is also common in swine showing CNS signs. Chronically affected animals usually have severe fibrosis of the pericardium and pleura, which may or may not extend to the peritoneal cavity.

Diagnosis

Diagnosis is based on the observation of characteristic clinical signs and lesions, in association with isolation of H parasuis from affected swine. Only samples from systemic sites such as pleura, pericardium, peritoneum, joints, and brain should be submitted for bacterial isolation. Isolation of H parasuis from the upper respiratory tract has no relevance in the diagnosis of systemic infection. H parasuis is a fastidious organism that can disappear quickly following death of affected animals. Samples collected from clinically affected animals that were euthanized increase the chances of isolation. H parasuis is initially isolated using sheep blood agar with V factor supplementation, which can be provided by a nurse streak of Staphylococcus aureus. Growth is characterized by the presence of translucent small colonies near the Staphylococcus streak (satellitism). Differential diagnoses include Actinobacillus pleuropneumonia and Vitamin E deficiency.

Treatment

H parasuis is one of the few gram-negative organisms that can be successfully treated with synthetic penicillin. Other antimicrobials that have been used include ceftiofur and sulfonamides. Individual treatments are given parenterally. Preventive treatments can be given via water or feed medication. Either commercial or autogenous vaccines can be used to control H parasuis infection. The broad range of potentially pathogenic serovars has impaired the development of a universal vaccine for H parasuis. Homologous protection between isolates from the same serovar group is satisfactory, while heterologous protection is restricted to a few serovars.

References

  1. Merck Veterinary Manual
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