JPC SYSTEMIC PATHOLOGY
RESPIRATORY SYSTEM
September 2023
P-B18
SIGNALMENT (JPC #2741839): Pig
HISTORY: Unknown
HISTOPATHOLOGIC DESCRIPTION:
Lung: The pleura is diffusely expanded up to 500µm by large aggregates of extracellular eosinophilic finely beaded fibrillar material (fibrin) admixed with degenerate neutrophils, fewer lymphocytes, plasma cells, and macrophages, multifocal aggregates of karyorrhectic and cellular debris (lytic necrosis), and mineral, which extends into the subpleural pulmonary parenchyma. Alveolar and intralobular septa are expanded up to 3 times normal by a similar fibrinocellular infiltrate. Multifocally affecting 40% of the section, alveolar and bronchiolar lumina contain an inflammatory exudate as previously described admixed with fibrin and necrotic debris that occasionally obscures normal architecture. Bronchiolar epithelial cells are multifocally shrunken and hypereosinophilic with pyknotic nuclei (necrotic), occasionally sloughed into the lumen, and discontinuous (ulceration), 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 fibrillar material (fibrin), neutrophils, and fewer lymphocytes, macrophages, and rare eosinophils admixed with scant 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).
MORPHOLOGIC DIAGNOSIS:
1. Lung: Pleuropneumonia, fibrinosuppurative and necrotizing, subacute, multifocal, moderate, breed unspecified, porcine.
2. Heart: Epicarditis and subepicardial myocarditis, fibrinosuppurative, necrotizing, histiocytic, subacute, diffuse, moderate.
ETIOLOGIC DIAGNOSIS: Pleural, epicardial, and myocardial haemophilosis
CAUSE: Glaesserella parasuis (formerly Haemophilus parasuis)
CONDITION: Glasser’s disease (primary causative agent, there are other possible causes of polyserositis in swine)
SYNONYMS: Porcine polyserositis and arthritis
GENERAL DISCUSSION:
- Pleomorphic gram-negative bacteria; ranges from single coccobacilli to long, thin filamentous chains in the family Pasteurellaceae
- Peracute (1-2 day course), septicemic disease of 8-16 week old weaner to grower pigs that causes fibrinous meningitis, polyserositis, and/or polyarthritis
- Predilection sites (in descending order)
- Meninges > joints > peritoneum > pleura > pericardium
- Meningitis occurs in >80% of pigs
- Polyarthritis is most severe in the atlanto-occipital joint and large limb joints
- A strong positive correlation between coinfection by G. parasuis and M. hyorhinis and also by G. parasuis with PRRSV (Salogni, et. al JVDI 2020)
PATHOGENESIS:
- Opportunistic commensal organisms of respiratory tract (nasopharynx and tonsils)
- Environmental stress (weaning, shipping, cold weather) and/or concurrent viral infection (SIV, PCV-2, PRRSV) or mucosal damage predisposes to disease
- Mechanisms of injury:
- Vasculitis affecting microvasculature in serosal membranes
- Inhaled > trapped in conducting airway mucus layer > adhesion to epithelial cells/cilia > colonization > toxin-mediated mucosal epithelial injury & lysis > bacteremia (cell-free or in leukocytes) > bacterial endotoxin > vasculitis of serosal surfaces > fibrinous polyserositis, pleuritis, pericarditis, and peritonitis
- Virulence factors: LPS, neuraminidase-like toxin
TYPICAL CLINICAL FINDINGS:
- Peracute septicemia, high mortality in 1-2 day course
- High fever
- Lameness (septic arthritis)
- Coughing and abdominal breathing
- Neurologic abnormalities: Paresis; stupor; hyperesthesia (fibrinous meningitis)
- Purple skin discoloration
TYPICAL GROSS FINDINGS:
- Serofibrinous meningitis, pericarditis, pleuritis, peritonitis, and synovitis of multiple joints, acute cellulitis and myositis in some cases
- Meningitis- More severe around the brain than the spinal cord
- Synovitis
- Gray/yellow/white friable material (fibrin) within the joint space
- Most severe in the atlanto-occipital joint and large limb joints
- Red gastric fundic mucosa (venous infarcts; multiple septicemic agent differentials in swine)
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Septicemia and fibrinous inflammation
- Fibrinous to fibrinopurulent polyserositis
- Fibrinopurulent meningitis
- Prominent vascular thrombosis in the skin, meninges, and glomeruli
- Suppurative bronchopneumonia (a separate presentation from Glasser’s disease)
ADDITIONAL DIAGNOSTIC TESTS:
- Isolation of the organism is required to differentiate Glaesserella parasuis from other causes of Glasser’s disease; Streptococcus suis, Mycoplasma hyorhinis
- Bacterial culture (visceral pleura only reliable site)
- Polymerase chain reaction (PCR)
DIFFERENTIAL DIAGNOSIS:
- 3 main rule-outs for polyserositis in pigs are:
- Glaesserella parasuis
- Mycoplasma hyorhinis
- Streptococcus suis
- Both M. hyorhinis and S. suis are more chronic and less frequently cause meningitis when compared with G. parasuis
- Causes of pneumonia, polyserositis, and polyarthritis in pigs:
- Mycoplasma hyorhinis – Most frequent isolate in young pigs with arthritis (Salogni et. al, JVDI 2022)
- Streptococcus suis (zoonotic)
- Actinobacillus suis
- Pasteurella multocida
- E. coli (edema disease) and Salmonella choleraesuis septicemia can also cause fibrinous polyserositis
COMPARATIVE PATHOLOGY:
Wild boars: H. parasuis infection has been reported in the wild boar
- Fibrinosuppurative polyserositis/arthritis +/- meningoencephalitis, pneumonia
- No fibrinous exudate as seen in domestic pigs so not called “Glasser’s disease”
Pasteurellaceae: Gram (-) coccobacilli, many are normal upper respiratory tract inhabitant of healthy animals but cause pneumonia and septicemia in animals with impaired pulmonary and systemic defenses respectively
- Pasteurella multocida (swine, ruminants, cats, chickens, turkeys)
- Mannheimia haemolytica and Bibersteinia trehalosi (ruminants)
- Actinobacillus pleuropneumoniae and A. suis (swine)
- A. equuli (horses)
- Histophilus somni (cattle and sheep)
References:
- Caswell JL, Williams KJ. Respiratory System. In: Maxie MG, ed. Jubb, Kennedy & Palmer's Pathology of Domestic Animals. Vol 2. 6th ed. St. Louis, MO: Elsevier; 2016:521-522, 524, 532, 543.
- 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.
- Cooper BJ, Valentine BA. Muscle and Tendon. In: Maxie MG, ed. Jubb, Kennedy & Palmer's Pathology of Domestic Animals. Vol 1. 6th ed. St. Louis, MO: Elsevier; 2016:230.
- Dickerman A, et al. Phylogenic analysis of Haemophilus parasuis and proposed reclassification to Glaesserella parasuis, gen. nov., comb. nov. Int J Syst Evol Microbiol. 2020; 70(1):180-186.
- Gal A, Castillo-Alcala F. Cardiovascular System, Pericardial Cavity, and Lymphatic Vessels. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:689.
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- Salogni C, Lazzaro M, Giovannini S, et. al. Causes of swine polyserositis in a high-density breeding area in Italy. J Vet Diagn Invest. 2020;32(4):594-597.
- Spagnoli ST, Gelberg HB. Alimentary System and the Peritoneum, Omentum, Mesentery, and Peritoneal Cavity. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:409, 480.
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