JPC SYSTEMIC PATHOLOGY
SIGNALMENT (JPC #2741839): Pig
Lung: The pleura is diffusely and moderately expanded (up to 500um) by large aggregates of eosinophilic, beaded, fibrillar material (fibrin) admixed with moderate numbers of degenerate neutrophils, fewer lymphocytes, plasma cells and macrophages, multifocal aggregates of karyorrhectic and cellular debris, and mineral (necrosis), which extends into the subpleural pulmonary parenchyma. Alveolar and intralobular septae are similarly expanded but to a lesser degree (up to 3 times normal). Multifocally (affecting 40% of the section) alveolar and bronchiolar lumina contain an inflammatory exudate admixed with fibrin and necrotic debris (as described above) that occasionally obscures normal architecture. Bronchiolar epithelial cells are multifocally necrotic (sloughed, shrunken) and discontinuous, with infiltration of inflammatory cells through the bronchiolar wall and into the subepithelial connective tissue. Bronchial subepithelial connective tissue is similarly, though less severely, affected.
Heart: Diffusely and moderately expanding the epicardium and extending into the subepicardial myocardium are large aggregates of eosinophilic finely beaded to fibrillar material (fibrin), neutrophils, and fewer lymphocytes, macrophages, and rare eosinophils admixed with small amounts of cellular and karyorrhectic debris (necrosis). Multifocally, subepicardial cardiac myocytes have pale, swollen, and vacuolated cytoplasm (degeneration) or loss of cross striations, pyknotic nuclei and hypereosinophilic cytoplasm (necrosis).
- Lung: Pleuropneumonia, fibrinosuppurative and necrotizing, subacute, multifocal, moderate, breed unspecified, porcine.
- Heart: Epicarditis and subepicardial myocarditis, fibrinosuppurative, necrotizing, and histiocytic, subacute, diffuse, moderate.
ETIOLOGIC DIAGNOSIS: Pleural, epicardial, and myocardial haemophilosis
CAUSE: Haemophilus parasuis
CONDITION: Glasser’s disease
SYNONYMS: Porcine polyserositis and arthritis
- Glasser’s disease is an economically important disease characterized by severe fibrinous meningitis, polyserositis, and/or polyarthritis in pigs 5 to12 weeks old, often following a stressful event (weaning, shipping, cold weather) or viral infection (swine influenza, PCV-2)
- The organism is commonly found in the upper respiratory tract of swine and is considered an opportunistic secondary invader
- Pleomorphic gram-negative bacteria; ranges from single coccobacilli to long, thin filamentous chains
- A serious problem with introduction of new animals or mixing of animals from different herds
- Commensal organisms of respiratory tract isolated from nasopharynx and tonsils of healthy pigs
- Acquired from the dam or by inhalation of contaminated fomites or fluid droplets
- Colostrum deprived piglets often develop the disease; maternal and natural immunity are critical for disease control
- Environmental stress and/or concurrent viral infection likely influences infection
- Inhaled > trapped in mucus layer > adhesion to epithelial cells/cilia > colonization >toxin-mediated cell injury >access to subepithelial tissues/vasculature > bacteremia > vasculitis and inflammation of serosal surfaces > fibrin, fluid and inflammatory cell accumulation
- Induces apoptosis in endothelial cells and produces IL-6 and IL-8
- Although the factors involved in systemic infection are not known, mucosal damage enhances bacterial invasion
- Bacteremia with subsequent replication at serosal surfaces producing polyserositis, polyarthritis, and meningitis, although acute pneumonia without polyserositis has been reported
- Adhesins, fimbriae, LPS, neuraminidase-like toxin
TYPICAL CLINICAL FINDINGS:
- High fever
- Painful and swollen joints
- Coughing and abdominal breathing
- Muscular tremors and incoordination
TYPICAL GROSS FINDINGS:
A vasculitis that leads to gray-white friable material (fibrin) on serosal surfaces and may also contain a fibrinous exudate and edema
- Fibrinous meningitis (>80%)
- Fibrinous polyarthritis (worse in atlanto-occipital and large-limb joints)
- Fibrinous polyserositis
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Fibrinous to fibrinopurulent serositis
- Thrombosis of vessels in the skin, meninges, and glomeruli
- Fasciitis, myositis and purulent rhinitis may occur
ADDITIONAL DIAGNOSTIC TESTS:
- Bacterial isolation, especially from joints or visceral pleura
- Isolation of the organism is required to differentiate Glasser’s disease from other septicemic bacterial infections
- Polymerase chain reaction (PCR)
3 main rule-outs for polyserositis in pigs are: Haemophilus parasuis, Mycoplasma hyorhinis, and Streptococcus suis type II
- Causes of pneumonia, polyserositis and polyarthritis in pigs:
- Mycoplasma hyorhinis: Milder and more chronic infection; rarely accompanied by meningitis; predominantly lymphocytic infiltration in the lung
- Streptococcus suis type II infections (zoonotic)
- Actinobacillus suis
- Septicemic coli & Salmonella spp can also cause fibrinous polyserositis
Haemophilus parasuis, but not Glasser’s disease, has been reported in the wild boar
Causes of polyserositis in other species:
- Horses: Streptococcus equi and Streptococcus zooepidemicus
- Calves: Escherichia coli
- Sheep and goats: Mycoplasma and Haemophilus sp.
- Ducks: Riemerella anatipestifer (New duck disease; duck septicemia)
Causes of polyarthritis
- Cattle: Histophilus somni (formerly Haemophilus somnus), Mycoplasma bovis
- Goats: Caprine arthritis-encephalitis virus (retrovirus)
- Cuesta-Gerveno JM, Perez, DR, Blanco PG, et al. Fatal infection due to Haemophilus parasuis in a young wild boar (Sus scrofa). J Vet Diagn Invest. 2013;25(2):297-300.
- Boulianne M (ed), Avian Disease Manual, 7th 2013: 44.
- Craig LE, Dittmer KE, Thompson K. Bones and joints. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. St Louis, MO: Elsevier; 2016:151-2.
- Zachary JF. Mechanisms of microbial infection. In: Zachary JF. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2017: 174-175.
- Zachary Jf. Respiratory system, mediastinum, and pleurae. In: Zachary JF. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2017: 544