show_page.php1 : pb18.jpg
2 : pb18.jpg
3 : pb18.jpg
4 : pb18aa02.jpg
5 : pb18aa10.jpg
6 : pb18aa10.jpg
7 : pb18aa40.jpg
8 : pb18ab02.jpg
9 : pb18ab02.jpg
10 : pb18ab10.jpg
11 : pb18ab10.jpg
12 : pb18ab40.jpg
13 : pb18ac02.jpg
14 : pb18ac10.jpg
15 : pb18ac40.jpg
16 : pb18ad10.jpg
17 : pb18ad40.jpg
18 : pb18ae40.jpg
19 : pb18af40.jpg
Read-Only Case Details Reviewed: Sep 2008

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: 

 

PATHOGENESIS:  

 

TYPICAL CLINICAL FINDINGS:

 

TYPICAL GROSS FINDINGS:  

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

 

ADDITIONAL DIAGNOSTIC TESTS:  

 

DIFFERENTIAL DIAGNOSIS:

 

COMPARATIVE PATHOLOGY:

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

 

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

 

References:

  1. 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.  
  2. 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. 
  3. 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.
  4. 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.
  5. 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. 
  6. Jimenez Martinez MA et al. Suidae and Tayassuidae. Terio KA, McAloose D, G. SLJ., eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018: 219. 
  7. Lopez A, Martinson SA. Respiratory System, Thoracic Cavities, Mediastinum, and Pleurae. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:624,626, 629, 630.
  8. Miller AD, Porter, BF. Nervous System. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:925. 
  9. Olson EJ, Dykstra JA, Armstrong AR, Carlson CS. Bones, Joints, Tendons, and Ligaments. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:1086.
  10. Schlafer DH, Foster RA. Female Genital System. In: Maxie MG, ed. Jubb, Kennedy & Palmer's Pathology of Domestic Animals. Vol 3. 6th ed. St. Louis, MO: Elsevier; 2016:424. 
  11. Salogni C, Capucchio MT, Colombino E, et. al. Bacterial polyarthritis in post-weaning pigs in a high-density swine breeding area in Italy. J Vet Diagn Invest. 2022;34(4):709-711.
  12. 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. 
  13. 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.
  14. Stanton JB, Zachary JF. Mechanisms of Microbial Infections. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:218.
  15. Uzal FA, Plattner BL, Hostetter JM. Alimentary System. In: Maxie MG, ed. Jubb, Kennedy & Palmer's Pathology of Domestic Animals. Vol 2. 6th ed. St. Louis, MO: Elsevier; 2016:252.

 


Click the slide to view.



Back | Home | Contact Us | Links | Help |