Case 3 - 170623

Domestic pig of unknown age or sex.

This slide has one section of spleen in which a regionally necrotic foci extends from the serosal surface, affecting approximately 20% of the parenchyma. The area of necrosis is characterized by extensive hemorrhage intermixed with coalescing nodules of remnant fragmented cellular debris and fibrillar eosinophilic strands and mats (fibrin). Remnant vessels within the affected region and at the margin of necrotic and normal parenchyma, are expanded by eosinophilic smudgy to fibrillar material, and infiltrated by lymphocytes and neutrophils (fibrinoid necrosis). There are decreased numbers of lymphoid follicles and those present are variably depleted.

Gross lesions were not reported by the submitter.

This slide has two similarly affected sections of ileum. Peyer’s patches are severely depleted with central hyalinosis, abundant macrophages with loss of central lymphocytes and occasional lymphocytolysis. Crypts are frequently dilated and contain variable amounts of necrotic cellular debris. They are lined by cuboidal to flattened (attenuated) enterocytes with an increased number of mitotic figures and single cell to segmental necrosis. Cuboidal, basophilic (regenerative) crypt enterocytes have moderate anisokaryosis, frequently large nuclea and prominent, central nucleoli. Rare crypt epithelial cells have amphophilic intranuclear inclusions that fill the nucleus and marginalize the chromatin. The lamina propria is infiltrated by a moderate number of lymphocytes, plasma cells and macrophages, which also form a thin band that mildly elevate the crypts from the submucosa. There is marked goblet cell hyperplasia, particularly affecting the villi. The villous goblet cells are intermixed with hypereosinophilic, poorly preserved enterocytes. The intestinal lumen is filled by mucous which separates villi and often fills ectatic crypts.

No special stains.

Spleen: Acute, regionally extensive and marginal, hemorrhagic infarction with associated multifocal vascular fibrinoid necrosis

This changes in this section of spleen are not necessarily definitive for a single disease, however, the importance is recognizing classical swine fever (CSF) as a differential given its importance in veterinary medicine and lack of existence currently in certain regions of the world, including the United States. Classical swine fever is an acute hemorrhagic disease characterized by disseminated intravascular coagulation, thrombocytopenia and immunosuppression. This virus is maintained in wild boar populations in endemic regions, such as Asia. Classical swine fever is currently eradicated in the United States and Canada. Classical swine fever is secreted and transmitted through bodily fluids and mucous membranes.

There are a number of described clinical presentations including acute, subacute, chronic and persistently infected. Clinical signs vary depending on these listed presentations. The discussion revolved around the possible differentials including African swine fever, septicemia and other coagulation dysfunction or systemic inflammation. Some features discussed that may differ between classical and African swine fever include the presence of marginal splenic infarcts in CSF with more generalized splenomegaly and lack of infarcts in ASF. ASF is associated with pulmonary edema while CSF is not typically. Another importance pathogenesis distinction is that CSF infects epithelium, while ASF does not. Both cause endothelial damage with fibrinoid necrosis. Another key point discussed is the importance of evaluating lymphoid tissues, particularly the tonsils in pigs presenting for necropsy, as this is a key route and site of infection for a number of these listed reportable diseases and should be examined and collected in all pig cases. It is also a good site for identifying lesions consistent with other viral etiologies, including porcine circovirus 2, a commonly identified agent.

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