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American Journal of Pathology, Vol 92, 23-34, Copyright © 1978 by American Society for Investigative Pathology

REGULAR ARTICLES

The cyclic hematopoietic dog: a model for spontaneous secondary amyloidosis. A morphologic study

EA Machado, RS Gregory, JB Jones and RD Lange

Spontaneous amyloidosis was found in dogs affected with hereditary cyclic hematopoiesis (CH dogs). Early perifollicular deposits of amyloid were observed in the spleens of 15-week-old CH dogs. By the 24th week, amyloid deposits were also found in the liver, kidneys, pancreas, adrenals, and small intestine; the incidence of the condition rose to more than 90%. The visceral involvement and the histologic characteristics of amyloid deposition closely resemble those of the secondary form in humans. A transient lymphoid hypoplasia was noted in the spleens of neonates and pups. This abnormality did not appear to be related to exogenous conditions. In young adult dogs, the initial hypoplastic characteristics were replaced by enlarged marginal zones in the follicles of the spleen, composed of pyroninophilic cells and, in a later stage, of PAS-positive cells. These cellular changes preceded the amyloid deposition. Due to the characteristic cyclic neutropenia of the hereditarily transmitted hematologic syndrome, most CH dogs experience episodes of infectious diseases, although the episodes of infection may be separated by long periods of relatively good health. This may provide the underlying antigenic stimulation which triggers the process of amyloid deposition. However, the lag period for the onset of amyloidosis is extremely short and the type of infections is not considered a predisposing factor for amyloid deposition. It is possible that a peculiar sensitivity of the lymphoid system in the CH dog would facilitate the development of widespread amyloidosis. Since the sequence of splenic lymphoid hypoplasia, follicular activation, and amyloid deposition associated with age are consistently repeated, the CH dog may be a suitable animal model for the study of the pathogenesis of secondary form of amyloidosis in humans.

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