Small Animal Dermatology, 3rd edition

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chapter 23 Eosinophilic Disease (Granuloma) Complex...................


DEFINITION/OVERVIEW


 Cats: Feline eosinophilic dermatitis or eosinophilic granuloma complex (EGC) is


often a confusing term for four distinct syndromes grouped primarily according to
their clinical similarities as a disease complex, their frequent concurrent (and recur-
rent) development, and their positive response to antiinflammatory therapeutics.
EGC is a description, not a diagnosis:
Eosinophilic plaque
Eosinophilic granuloma
Indolent ulcer
Allergic miliary dermatitis.

 Dogs: canine eosinophilic granuloma (CEG) uncommon; not part of a disease com-


plex; specific differences from cats are listed within the text.


ETIOLOGY/PATHOPHYSIOLOGY


 Eosinophilic plaque: hypersensitivity reaction, most often to insects (fleas,


mosquitoes), food or environmental allergens; exacerbated by mechanical trauma.


 Eosinophilic granuloma: multiple causes; idiopathic, genetic predisposition, and


hypersensitivity.


 Indolent ulcer: may have both hypersensitivity and genetic causes.


 Allergic miliary dermatitis: not always included within the EGC; very common hyper-


sensitivity reaction, most often to fleas.


 Eosinophil: major infiltrative cell for eosinophilic granuloma, eosinophilic plaque,


and allergic miliary dermatitis, but not indolent ulcer; most often associated with
allergic or parasitic conditions, as well as a more general role in the inflammatory
reaction.

 Several reports of related affected individuals and a study of disease development in


a colony of specific pathogen-free cats indicate that genetic predisposition may be a
significant component for development of eosinophilic granuloma and indolent ulcer.

 A heritable dysfunction of eosinophil regulation has been proposed.


 CEG (dogs): may have both a genetic predisposition and a hypersensitivity cause;


insect bite often incriminated.


Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Small Animal Dermatology, Third Edition.
Karen Helton Rhodes and Alexander H. Werner.
©2018 John Wiley & Sons, Inc. Published 2018 by John Wiley & Sons, Inc.


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