JPC SYSTEMIC PATHOLOGY

RESPIRATORY SYSTEM

September 2026 P-B18

HISTOPATHOLOGIC DESCRIPTION:

Lung: The pleura is diffusely expanded up to 580 µm by large aggregates of extracellular eosinophilic finely beaded fibrillar material (fibrin) admixed with numerous lysed 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 expanding the epicardium up to 180 µm 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).

GENERAL DISCUSSION:

• Pleomorphic, non-motile, gram-negative bacteria; ranges from single coccobacilli to long, thin filamentous chains in the family Pasteurellaceae
• Opportunistic commensal organisms of respiratory tract (nasopharynx and tonsils)
• Disease depends on combination of innate resistance mechanism and acquired humoral immunity
• Peracute (1-2 day course), septicemic disease of 8-16 week old weaner to grower pigs that causes fibrinous meningitis, polyserositis, and/or polyarthritis known as Glässer disease
• Predilection sites (in descending order)
  • Meninges > joints > peritoneum > pleura > pericardium
• Meningitis occurs in >80% of pigs; more severe in cranial meninges > spinal
• Polyarthritis is most severe in the atlanto-occipital joint and large limb joints

A major cause of bacterial suppurative bronchopneumonia in pigs that can be fatal; separate serotype from Glässer’s disease

PATHOGENESIS:

• Environmental stress (weaning, shipping, cold weather, air quality) and/or concurrent viral infection (SIV, PCV-2, PRRSV), mycoplasmal infection, or mucosal damage predisposes to disease
• Virulence factors: LPS, neuraminidase-like toxin, bacterial toxin
• Mechanisms of injury:
  • Exact mechanisms that cause polyserositis still unknown
  • Vasculitis affecting microvasculature in serosal membranes
  • Fibrinous loose attachments to fibrous adhesions impede respiratory and cardiac contraction and function
  • Inhaled bacteria through contaminated fomites or droplets → stays in conducting airway mucus layer → secondary triggering event changes mucus layer composition → adhesion to epithelial cells/cilia (bronchi and terminal bronchioles)→ 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
• Pleuritis can be secondary to bronchopneumonia or septicemia
• Erythema multiforme has been associated in pigs with respiratory disease
• Historically associated with atrophic rhinitis

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
• Purple skin discoloration

TYPICAL GROSS FINDINGS:

• Classic gross bronchopneumonia appearance: symmetrical consolidation of the cranioventral lung lobes
• 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
  • High volume turbid fluid with 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)
• Body cavities with fibrinous exudate and edema

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Septicemia and fibrinous inflammation
• Fibrinous to fibrinopurulent polyserositis
• Fibrinopurulent meningitis
• Prominent vascular thrombosis in the skin, meninges, and renal 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)
• ELISA or latex agglutination

DIFFERENTIAL DIAGNOSIS:

• 3 main rule-outs for polyserositis in pigs are:
  • Glaesserella parasuis
  • Mesomycoplasma (Mycoplasma) hyorhinis
  • Streptococcus suis
• Both M. hyorhinis and S. suis are more chronic and less frequently cause meningitis when compared with G. parasuis; meningitis in G. parasuis is neutrophilic vs lymphocytic as in the other agents; M. hyorhinis often have free flattened disks of inssipated fibrin within peritoneal cavity
• Other agents include E. coli (edema disease) and Salmonella choleraesuis, Salmonella agona (S. enterica ss enterica sv agona) septicemia (Menegatt, 2025)
• 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
  • Actinobacillus pleuropneumoniae
  • Pasteurella multocida
• Causes of bronchopneumonia in pigs
  • Streptococcus suis (zoonotic)
  • Actinobacillus suis
  • Actinobacillus pleuropneumoniae
  • Pasteurella multocida
  • Bordetella bronchiseptica
• Causes of fibrinous pericarditis
  • Mesomycoplasma (mycoplasma) hyorhinitis

COMPARATIVE PATHOLOGY:

Wild boars: H. parasuis infection has been reported in European wild boar

• No fibrinous exudate as seen in domestic pigs so not called “Glässer’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)

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