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Glässer Disease in Pigs

(Porcine Polyserositis, Infectious Polyarthritis)

By

Joaquim Segalés

, DVM, PhD, Departament de Sanitat i d’ Anatomia Animals and Centre de Recerca en Sanitat Animals (CReSA), Universitat Autònoma de Barcelona

Last full review/revision Dec 2020 | Content last modified Dec 2020

Glässer disease is caused by infection with Glaesserella (Haemophilus) parasuis. The most common form is characterized by fibrinous polyserositis and polyarthritis, but septicemia with sudden death and bronchopneumonia also can occur. Diagnosis is based on clinical signs and bacterial isolation or PCR. Antibiotic treatment remains the first option to control a disease outbreak, but several vaccines are available for prevention.

Pigs can be colonized by different microorganisms before weaning, but some of those early colonizing agents are potentially pathogenic. This is the case with Glaesserella parasuis, a commensal organism of the upper respiratory tract of swine that causes severe systemic disease characterized by fibrinous polyserositis, arthritis, and meningitis. Disease has a sudden onset, short course, and high morbidity and mortality. Young animals (4–8 weeks old) are primarily affected, although sporadic disease can be seen in adults (eg, introduction of a naive adult to a healthy 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 disease is seen worldwide, and its incidence appears to have increased since the emergence of porcine reproductive and respiratory syndrome.

Etiology

The causal agent of Glässer disease, G parasuis, is a small, gram-negative pleomorphic bacterium of the family Pasteurellaceae that requires V factor (NAD) supplementation but not X factor (hemin) for growth. In the laboratory, G parasuis grows on enriched chocolate agar; it can also be cultured in blood agar with a staphylococcal nurse streak. However, G parasuis is fastidious, and its isolation in pure culture from diseased animals is usually difficult and frequently complicated because of antibiotic treatments.

Fifteen serovars of H parasuis have been reported, but a high percentage of the evaluated isolates cannot be typed. Wide differences in serovar virulence have been described. Serovars 1, 2, 4, 5, 12, 13, 14, and some isolates that cannot be typed are usually isolated from systemic disease cases, while serovars 3, 6, 7, 9, and other nontyped isolates are frequently isolated from the upper respiratory tract. Moreover, the correlation between serovar and virulence is not clear, and strains belonging to the same serovar may vary in virulence.

Serotyping also has been used as the basis to establish vaccination criteria, but the cross-protection between different serovars is variable and difficult to predict. Therefore, current methods of H parasuis identification and characterization are primarily genotyping (fingerprinting or sequencing methods). The identification of virulence genes has received increased attention because of the possibility of differentiating strains with pathogenic potential by means of PCR as well as of developing vaccines.

The factors involved in systemic invasion by G parasuis are not well known, but virulent strains are able to avoid phagocytosis, reduce antigen presentation to pulmonary alveolar macrophages, and delay antibody production.

Clinical Findings

Clinical signs of Glässer disease are seen mainly in 4- to 8-week-old pigs, although the age of affected animals may vary, depending on the level of acquired maternal immunity. Peracute disease has a short course and may result in sudden death without the presence of characteristic gross lesions; petechiae may be seen in some organs in these cases, indicating septicemia.

The typical clinical signs of acute Glässer disease may include:

  • high fever (41.5°C [106.7°F])

  • severe coughing

  • abdominal breathing

  • swollen joints

  • CNS signs (eg, lateral decubitus, paddling, and trembling)

Chronically affected animals may have a reduced growth rate as a result of severe fibrosis in the thoracic and peritoneal cavities. G parasuis can be isolated from the lungs of pigs with suppurative bronchopneumonia, with dyspnea and coughing the most common clinical signs. However, G parasuis is not considered a significant cause of coughing. Disease prevalence is modulated by concomitant environmental stressors as well as by viral infections affecting the immune system, mainly porcine reproductive and respiratory syndrome and porcine circovirus 2 systemic disease.

Lesions

Peracute disease may cause petechiae in some tissues, with no gross lesions observed. Histologically, these pigs show septicemia-like microscopic lesions such as DIC and microhemorrhages. Increased fluid in the thoracic and abdominal cavities, without the presence of fibrin, can also be seen in peracute cases.

Acute systemic infection is characterized by development of fibrinous polyserositis, polyarthritis, and meningitis. The fibrinous exudate can be seen on the pleura, pericardium, peritoneum, synovia, and meninges and is usually accompanied by an increased amount of fluid. Fibrinous pleuritis may be accompanied by cranioventral consolidation (suppurative bronchopneumonia). Lack of characteristic gross lesions is also common in swine showing CNS signs.

Chronically affected pigs usually have severe fibrosis of the pericardium and pleura, which may or may not be present in the peritoneal cavity.

Diagnosis

  • Clinical signs and lesions together with detection of the bacterium

Diagnosis is based on observation of compatible clinical signs and lesions, in association with detection of G parasuis in affected swine by isolation or by molecular methods such as PCR.

Most current diagnostic methods do not differentiate virulent from nonvirulent isolates, so it is important to sample only from systemic sites such as pleura, pericardium, peritoneum, joints, and brain. Samples collected from clinically affected animals that were euthanized increase the chances of isolation. Recently, a multiplex PCR technique able to differentiate between virulent and nonvirulent isolates has been developed. This technique might be used to prevent introduction of pigs carrying potentially virulent strains onto farms that are free of clinical Glässer disease.

Because G parasuis is a common commensal organism, isolation from the upper respiratory tract has no relevance in the diagnosis of systemic infection.

Differential diagnoses of Glässer disease include infections by:

Treatment and Control

  • Antibiotics and vaccination

G parasuis is one of the few gram-negative organisms that can be successfully treated with synthetic penicillin. Other antimicrobials used include ceftiofur, ampicillin, enrofloxacin, erythromycin, tiamulin, tilmicosin, florfenicol, and potentiated sulfonamides. Individual treatments must be given parenterally to see a significant effect, and all pigs in affected groups (not just those showing clinical signs) will eventually require treatment. Preventive treatments should be discouraged to avoid development of resistance to antimicrobials.

Either commercial or autogenous vaccines can be used to control G parasuis infection, although their efficacy has been variable. The broad range of potentially pathogenic serovars and genotypes has impaired the development of a universal vaccine for G parasuis. Homologous protection between isolates from the same serovar group is relatively satisfactory, whereas heterologous protection is restricted to a few serovars. Several “universal” (independent of serovar) vaccine prototypes have been experimentally developed but are not commercially available.

Key Points

  • G parasuis is a commensal bacterium of the upper respiratory tract of pigs but able to cause systemic disease under appropriate circumstances.

  • Glässer disease is characterized by sudden death in its peracute form, but the most usual one is an acute presentation, characterized by wasting and dyspnea as well as fibrinous polyserositis, polyarthritis, and meningitis.

  • Diagnosis is based on clinical signs and detection of the bacterium from systemic sites.

  • Control is based on antibiotic treatment of affected pigs; commercial and autogenous vaccines can be used to prevent the disease.

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