Pigs can be colonized by different microorganisms before weaning, but some of those early colonizing agents are potentially pathogenic. This is the case with Haemophilus parasuis, a commensal organism of the upper respiratory tract of swine that causes severe systemic disease characterized by fibrinous polyserositis, arthritis, and meningitis. Disease caused by has a sudden onset, short course, and high morbidity and mortality. Young animals (4–8 wk of age) 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 (see Porcine Reproductive and Respiratory Syndrome).
The causal agent, H 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, H parasuis grows on enriched chocolate agar; it can also be cultured in blood agar with a Staphylococcus nurse streak. However, H parasuis is fastidious and its isolation in pure culture from diseased animals is usually difficult and frequently complicated due to 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 serovar 3 and other non-typed isolates are frequently isolated from the upper respiratory tract. The factors involved in systemic invasion by H parasuis are still unknown. Moreover, the correlation between serovar and virulence is not clear, and strains belonging to the same serovar may vary in virulence. Serotyping has been also used as the basis for establishing 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).
Clinical signs are observed mainly in pigs 4–8 wk old, 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's disease 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.
Dyspnea and coughing not usually associated with Glässer's disease have been described, together with H parasuis isolation from the lungs of pigs with catarrhal purulent bronchopneumonia and even fibrinohemorrhagic pneumonia.
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 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 antero-ventral consolidation (catarrhal-purulent bronchopneumonia). 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 be present in the peritoneal cavity.
Diagnosis is based on the observation of characteristic clinical signs and lesions, in association with detection of H parasuis in affected swine by isolation or by molecular methods such as PCR.
Because current diagnostic methods do not differentiate virulent from nonvirulent isolates, it is important to sample only from systemic sites such as pleura, pericardium, peritoneum, joints, and brain. Isolation of H parasuis from the upper respiratory tract has no relevance in the diagnosis of systemic infection. Samples collected from clinically affected animals that were euthanized increase the chances of isolation.
Differential diagnoses of Glässer's disease include infections by Streptococcus suis, septicemic Escherichia coli, Actinobacillus suis, Mycoplasma hyorhinis, Erysipelothrix rhusiopathiae, and Salmonella Choleraesuis.
Treatment and Control
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, ampicillin, enrofloxacin, erythromycin, tiamulin, tilmicosin, florfenicol, and potentiated sulfonamides. Individual treatments must be given parenterally to see a significant effect, and all pigs in the affected group (not just those showing clinical signs) should be treated. Preventive treatments can be given via water or feed medication. Either commercial or autogenous vaccines can be used to control H 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 H parasuis. Homologous protection between isolates from the same serovar group is relatively satisfactory, while heterologous protection is restricted to a few serovars.
In the near future, genotyping and genomic studies should help determine cross immunity between strains, identify virulent clone lines and virulent genes, and assist with development of more reliable disease control methods.
Last full review/revision March 2012 by Joaquim Segalés, DVM, PhD, DECVP, DECPHM