The population of ring-necked pheasants (Phasianus colchicus) is decreasing all over Germany since the years 2008/2009. Besides impacts of habitat changes caused by current rates of land conversion, climatic influences or predators, a contribution of infectious pathogens needs also to be considered. Infectious and non-infectious diseases in free-living populations of ringnecked pheasants have been scarcely investigated so far. In the present study, carcasses of 258 deceased free-ranging pheasants of different age groups, predominantly adult pheasants, collected over a period of 4 years in the states of Lower Saxony, North Rhine-Westphalia and Schleswig-Holstein, were examined pathomorphologically, parasitologically, virologically and bacteriologically, with a focus set on infectious pathogens. A periocular and perinasal dermatitis of unknown origin was present in 62.3% of the pheasants. Additional alterations included protozoal cysts in the skeletal musculature (19.0%), hepatitis (21.7%), enteritis (18.7%), gastritis (12.6%), and pneumonia (11.7%). In single cases, neoplasms (2.6%) and mycobacteriosis (1.7%) occurred. Further findings included identification of coronaviral DNA from trachea or caecal tonsils (16.8%), siadenoviral DNA (7.6%), avian metapneumoviral RNA (6.6%), and infectious bursal disease viral RNA (3.7%). Polymerase chain reaction (PCR) on herpesvirus, avian influenza virus (AIV), paramyxovirus type 1 (PMV-1), avian encephalomyelitis virus (AEV), and chlamydia were negative. Based on the present results, there is no indication of a specific pathogen as a sole cause for population decline in adult pheasants. However, an infectious disease can still not be completely excluded as it may only affect reproduction effectivity or a certain age group of pheasants (e.g., chicks) which were not presented in the study.

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.

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.