ABSTRACT
A retrospective study was carried out to define the spectrum of spontaneous diseases in ostriches and few other captive ratites, order Struthioniformes, in northwestern Germany. The investigation included 71 ratites necropsied between 1968 and 2014. They consisted of 54 ostriches, 5 emus, and 12 rheas with 37 adults, 23 juveniles and 11 neonates and embryonated eggs. Necropsy reports were reviewed, histologic preparations were re-examined and additional histochemical and immunohistochemical stains were carried out in selected cases. In many animals more than one morphologic diagnosis attributable to different disease processes was found. In adult animals (n = 37), the most commonly altered organ systems were the musculoskeletal system (49%), the digestive system (46%), and the cardiovascular system (46%) affected by traumatic lesions, inflammatory and degenerative changes, respectively. A spongy degeneration was found in the brain (35%); however, immunohistochemistry and western blotting failed to detect pathological prion protein. In juvenile animals (n = 23), the musculoskeletal (44%) and the digestive system (43%) were mainly affected by traumatic and inflammatory lesions, respectively. In embryonated eggs and neonates (n = 11) the major cause of death was circulatory failure associated with generalized subcutaneous edema as described for improper incubation conditions (64%). Summarized, most of the findings observed in adult and juvenile ratites in northwestern Germany are related to trauma, inflammatory and degenerative disorders, whereas death in embryonated eggs and neonates was most likely related to breeding conditions. A spongy encephalopathy awaits further studies to elucidate cause and pathogenesis.
Subject(s)
Bird Diseases/pathology , Struthioniformes , Animals , Bird Diseases/epidemiology , Bird Diseases/etiology , Female , Germany , MaleABSTRACT
A female, 5-year-old American Staffordshire Terrier with severe progressive neurological deficits, particularly in terms of ataxia and keeping balance, was examined pathomorphologically and a genetic analysis was performed. In neurons of various localizations of the central nervous system an accumulation of a finely granular pale eosinophilic or light brown material was found. In addition, the cerebellum revealed marked degeneration and loss of Purkinje and inner granule cells. The accumulated PAS-positive, argyrophilic, autofluorescent material showed ultrastructurally a lamellar appearance suggestive of lipofuscin. Genetic analysis revealed the presence of a sequence variant in the ARSG gene encoding the lysosomal enzyme arylsulfatase G. This case report describes an adult-onset of a neuronal ceroid lipofuscinosis that shows similarities with a human disorder termed Kufs disease.
