UK DIAGNOSTIC LAB NEWS (CONT.)


(Top) Figure 2. Liver. Foci of necrosis within the liver are characterized by infiltration of macrophages, neutrophils, lymphocytes, and plasma cells (center of image) with exudation of abundant fibrin (arrow). Surrounding viable hepatocytes exhibit mild signs of degeneration in this section (asterisk). Hematoxylin and eosin. Original magnification 400x.


(Middle) Figure 3. Lung. Multifocally, edema, fibrin, and macrophages fill alveolar spaces (arrows). The alveolar septa are expanded by fibrin, necrotic cellular debris, and inflammatory cells (arrowheads). There is a focal area of fibrinous necrosis of the pulmonary parenchyma (asterisks). Hematoxylin and eosin. Original magnification 200x.


(Bottom) Figure 4: Spleen. The periarteriolar lymphoid sheet is depleted (arrow). Macrophages are admixed with fibrin and necrotic cellular debris within the lymphoid follicle (arrowhead). Hematoxylin and eosin. Original magnification 400x.


Two biotypes of the virus are recognized and dif- fer based on pathogenicity.3


Te enteric biotype


of FCoV is of low pathogenicity and results in transient enteritis, while the highly virulent bio- type is highly pathogenic and causes FIP.3


Re-


cent work has suggested a mutation in two genes (S and 3c genes) determines the biotype and thus, the expected pathogenicity of the virus.3 Infection with highly pathogenic FCoV results in a sporadic, fatal, and systemic immune-medi- ated inflammatory response.1,2


Te progression


from infection to clinical signs of systemic dis- ease can span from weeks to months.1,2


Cats acquire the enteric form of FCoV from sub- clinical carriers and contaminated litter boxes.4 After ingestion, the virus replicates in intestinal epithelial cells. Mutation of enteric FCoV to the highly virulent biotype responsible for FIP, is thought to occur within macrophages in Pey- er’s patches.4,5


Tese infected macrophages then


spread the mutated FCoV from Peyer’s patches, to lymph nodes, and eventually into circulation via the lymphatic ducts.4


Te resulting clinical


signs are based on the individual’s cell-mediat- ed response.4


virus (FCoV).2,6 between 3-18 months of age.1,2,6


Tis disease is common in young cats Immunocompromised


cats and young cats housed in multicat situations, (cat- teries and shelters), are also at increased risk.1


Affected


breeds vary; however, a higher disease prevalence has been reported in Rexes, Himalayans, Ragdolls, Abyssinians, Bengals, and Birmans.1,7


Non-domestic cats are also sus-


ceptible to this disease, particularly captive cheetahs. 1,6,9 Continued on pg. 16


Tose with a weak cell-mediated


response will develop the “dry” or non-effusive form, resulting in predominantly histiocytic inflammation of various organs.3,4


Te “wet”


or effusive form, is seen in individuals with no cell-mediated response and a more pronounced humoral or antibody response.4


Te effusive


form is characterized by peritoneal and thoracic fluid accumulation. Macrophages infected with viral antigens promote effusion formation. Te infected macrophages drive the formation of immune complexes, activation of complement, Diagnostic Rounds - Fall 2020


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