ABSTRACT
Previous reports on skeletal pathology in captive snakes did not clarify the relationship of lesions to captive or free-ranging status. In this study, post-cranial skeletons from 7,950 captive and free-ranging snakes in nine of the major North American collections were examined macroscopically, microscopically and radiologically for the presence of pathology. Micro-computerized tomography was performed on two skeletons on which surface microscopy failed to provide a definitive diagnosis. Osteomyelitis was identified in the vertebrae of 24 snakes and spondyloarthropathy in one snake. Neoplasia or congenital anomalies were not found. Osteomyelitis was four times as common in Viperidae than in Colubridae and twice as common as in Boidae, independent of captive or free-ranging status. A lytic lesion in the vertebrae of one snake was suggestive of fungal disease. The progression of bone lesions was greater in captive snakes, but the prevalence was independent of captive or free-ranging status. The results of this study indicate that bone alterations, previously proposed as neoplastic disease, in archival snake skeletons were most likely of infectious aetiology, and establish macroscopic examination as a useful technique for characterizing skeletal pathology in snakes.
Subject(s)
Boidae , Colubridae , Skeleton/pathology , Viperidae , Animals , Mycoses/veterinary , Osteomyelitis/veterinary , Prevalence , Spine , Spondylarthropathies/veterinaryABSTRACT
Spondyloarthropathies, the second most frequently occurring form of chronic inflammatory arthritis, affects young adults in particular. However, a proper model with which to study the biology of this disease and to develop therapeutics is lacking. One of the most accepted animal models for this disease uses HLA-B27/Hu-ß2m transgenic rats; however, only 30%-50% of male HLA-B27/Hu-ß2m rats develop spontaneous, clinically apparent spondylitis and have a variable time until disease onset. Here, we report a high-incidence, low-variation spontaneous mouse model that delineates how the combination of inflammatory cytokine interleukin-27 (IL-27) signaling deficiency and mitogenic signaling (mutant p53R172H) in vivo, leads to bone loss in the vertebral bodies and ossification of the cartilage in the intervertebral discs. In this human disease-like mouse model, bone loss and pathogenic bone development are seen as early as 4 months of age in the absence of inflammatory aggregates in the enthesis or intervertebral disc.
Subject(s)
Disease Models, Animal , Receptors, Cytokine/genetics , Spondylarthropathies/pathology , Tumor Suppressor Protein p53/genetics , Animals , Humans , Male , Mice , Mutation , Rats , Receptors, Interleukin , Signal Transduction , Spondylarthropathies/diagnostic imaging , Spondylarthropathies/genetics , Spondylarthropathies/veterinary , X-Ray Microtomography/veterinarySubject(s)
Spondylarthropathies/veterinary , Whales , Animals , Paleontology , Species Specificity , Thoracic Vertebrae/pathologyABSTRACT
Spondyloarthropathy is a common occurrence in Old World primates, with only limited presence in New World monkeys. Clearly distinguished from rheumatoid arthritis, this erosive arthritis afflicts 20% of great apes, baboons, and rhesus macaques and had been increasing in frequency. Habitat-dependent infectious agent diarrhea-induced reactive arthritis is implicated on a background of genetic predisposition. A gorilla-derived therapeutic preventative approach has possible application in human clinical medicine.
