History

An approximately 7-year-old 5.6-kg sexually intact male carpet python (Morelia spilota) was evaluated for a more than 7-month history of decreased mobility and abnormal behavior, including dull mentation, reduced righting reflex, and anorexia. The snake had not ingested any whole rats or mice for the previous 2 months; therefore, oral tube-feeding with a liquid diet for carnivores had been performed monthly.

Clinical and Gross Findings

On physical examination, the snake was quiet and dull with an altered head carriage, decreased righting reflex, poor body condition (body condition score of 2 on a scale of 1 to 9), decreased muscle mass (score of 1.5 on a scale of 1 to 3), and decreased cervical range of motion with severe crepitus. The ventral musculature had diffuse bunching and contracture, most severely affecting the cervical region.

A CBC and a serum biochemical profile revealed low heterophil count (1.759 × 10³ cells/μL; reference interval, 1.79 × 10³ to 16.8 × 10³ cells/μL), high activities of aspartate aminotransferase (72 U/L; reference interval, 2 to 45 U/L) and creatine kinase (CK; 3,097 U/L; reference interval, 3 to 1,230 U/L), and mild hypernatremia (154 mmol/L; reference interval, 140 to 152 mmol/L).¹ Bacterial culture performed on a blood sample yielded no growth.

Full-body radiography revealed smooth osseous proliferation of multiple vertebral spinous processes and vertebral bodies as well as sclerotic and ill-defined articular facets consistent with severe multifocal spondylosis and spinal osteoarthritis. These lesions were most severe in the cervical and cranial coelomic portions of the vertebral column. No additional abnormalities were identified with MRI. Treatment with ketoprofen (2 mg/kg, IM, q 48 h) and ceftazidime (20 mg/kg, SC, q 72 h) was prescribed. During the first 1.5 months of treatment, the snake began to eat thawed rats and mice; however, around 4 months after beginning the treatment, the snake became anorexic, and euthanasia was elected.

Necropsy revealed multifocal, hard, tan to white, irregular, raised bony nodular proliferation (range, 1 × 0.5 × 0.5 cm to 10 × 2 × 1 cm) along the ventral aspect of the vertebral column, bridging between and fusing vertebral bodies (moderate to severe multifocal vertebral spondylosis and ankylosis; Figure 1), with the cranial two-thirds of the vertebral column more severely affected. Similar nodules (ranging from 0.2 cm to 1.0 cm in diameter) were present along the dorsal spinous processes of the cranial coelomic vertebrae.

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Postmortem photograph of the ventral aspect of the vertebral column of an approximately 7-year-old 5.6-kg sexually intact male carpet python (Morelia spilota) that had decreased mobility and abnormal behavior, including dull mentation, reduced righting reflex, and anorexia. Prominent, multifocal, tan, irregular, raised, hard proliferations (arrows) span multiple vertebral bodies.

Citation: Journal of the American Veterinary Medical Association 260, 3; 10.2460/javma.21.07.0328

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Histopathologic and Clinicopathologic Findings

Vertebrae had dense mature lamellar bone with irregularly distributed, broad, confluent trabeculae with increased, larger, and irregularly arranged osteocytes and fewer, small medullary cavities (Figure 2). The bone trabeculae had prominent irregular and scalloped basophilic reversal lines (bone remodeling). The medullary cavities were filled by numerous heterophils and fewer lymphocytes, plasma cells, and macrophages representing 80% of the nucleated cell population, and the remaining 20% were adipocytes. Along the ventral aspect of a few vertebrae were anastomosing trabeculae of immature woven bone, occasionally bridging between vertebral bodies (spondylosis). The periosteum was expanded with marked proliferation of the fibrous layer. Connective tissue surrounding vertebral bone was rarely infiltrated by moderate numbers of heterophils and fewer lymphocytes with few adjacent atrophied and rare regenerative myofibers. Sections of the spinal cord had patchy rarefaction of the white matter, especially in the ventral aspect, with occasional dilated myelin sheaths containing a swollen hypereosinophilic axon (spheroid) or Gitter cell (digestion chamber). These changes were consistent with multifocal Wallerian-like (axonal) degeneration and corresponded with the snake’s history of neurologic signs.

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Photomicrographs of sections of vertebrae of the snake described in Figure 1. A—Vertebral bone exhibits marked sclerosis characterized by thick confluent trabeculae (black arrowheads) and few small medullary cavities. Marked bone proliferation (spondylosis; asterisk) expands and bridges ventral aspects of the vertebral bodies. H&E stain; bar = 3 mm. B—The vertebral bone consists of thick trabeculae of mature lamellar bone with multiple prominent irregular and scalloped basophilic reversal lines (bone remodeling; black arrows). H&E stain; bar = 60 μm.

Citation: Journal of the American Veterinary Medical Association 260, 3; 10.2460/javma.21.07.0328

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The connective tissue adjacent to the esophagus had a large granuloma and the small intestine submucosa had a focal microgranuloma; tissue sections of each did not have overt acid-fast bacteria on Ziehl-Neelsen stains. Hepatocytes often contained multiple variably sized discrete colorless lipidic vacuoles with eccentric nuclei.

Liver and splenopancreas were submitted for bacterial culture and Salmonella spp PCR assay. The culture yielded 1+ Enterococcus faecalis (presumed contaminant), and no Salmonella spp was detected by PCR assay.

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: multifocal severe vertebral osteosclerosis with bone remodeling, spondylosis, and periosteal reaction with mild to moderate multifocal Wallerian-like axonal degeneration of the spinal cord.

Case summary: chronic vertebral osteopathy in a snake.

Comments

Vertebral (spinal) osteopathy is a common musculoskeletal disorder of reptiles, but the definitive underlying etiology has not been determined.² Possible causes include trauma, infectious agents, neoplasia, nutritional deficiencies, autoimmune conditions, and degenerative or metabolic conditions; however, how these various conditions fit together into 1 disease process has yet to be completely understood.^3,4 Proliferative neoplastic vertebral lesions, such as osteosarcoma³ and chondrosarcoma,⁵ have been reported in snakes. However, infectious and degenerative etiologies are more frequently observed.⁶ In many reptiles, infectious diseases (especially bacterial) are common causes of skeletal disorders.² Hematogenous dissemination and localization of infections to the bone is a frequent sequela. Although various bacterial species including Pseudomonas spp⁷ have been cultured in spinal lesions, spinal osteomyelitis is most often associated with Salmonella spp, particularly Salmonella enterica subsp arizonae. However, tissue samples from the snake of the present report tested negative for Salmonella spp via PCR assay.

Appropriate nutrition and husbandry are often lacking in reptile species, which contributes to many different disease processes, including obesity, metabolic bone disease, and renal secondary hyperparathyroidism.⁸ Hypovitaminosis A and hypervitaminosis D have been associated with skeletal and spinal bone deformities.⁸ Hypovitaminosis A is less commonly seen in reptiles with long-term anorexia.⁸ Hypervitaminosis D, which can be associated with hyperparathyroidism secondary to renal disease, leads to dysregulation of bone deposition.

Typically, snakes with spinal osteopathy have vertebral column stiffness, decreased mobility, kyphosis, pathological fractures, and, in severe cases, palpable firm and irregular subcutaneous nodules.^2,4,9 Neurologic clinical signs, as seen in the snake of the present report, depend on how much the spinal cord is compressed by bony proliferation.⁶

Spinal osteopathy is frequently diagnosed with radiography, which reveals irregular bony proliferation with mixed radiopacity that often involves multiple vertebrae. These lesions may predominate along the articular processes and ventrolateral aspects of the vertebrae.^2,4,7 Additional diagnostic procedures include bone biopsy, bacterial cultures of blood and tissue samples, CBC, and serum biochemical analyses, including vitamin D concentration. Despite similar clinical and gross appearances, spinal osteopathy has multiple different histologic appearances, depending on chronicity and etiology. In this case, there was no overt histologic evidence of bacterial infection or significant inflammation. Positive results for bacterial culture of a patient’s blood may support a diagnosis of bacterial osteomyelitis; however, results should be interpreted with caution as bacteria have been cultured in blood samples from wild, free-ranging western rat snakes (Pantherophis obsoletus) that showed no signs of disease.¹⁰ Bacterial culture performed on blood samples from the snake of the present report yielded no growth; however, this did not necessarily mean that a bacterial infection was not present. If spinal lesions are secondary to an infectious or inflammatory process, then granulocytosis may be noted on CBC.² Bloodwork abnormalities for the snake of the present report included mildly low heterophil count, which was most likely a normal variation; moderately high CK activity, which was most likely due to muscle damage from handling and IM injections; and mildly high aspartate aminotransferase activity, which was more likely secondary to muscle damage as denoted by high CK activity, although hepatocellular lipid accumulation may have also contributed.¹¹

The snake of the present report had 2 granulomas found on necropsy: 1 near the esophagus and 1 in the small intestine. There was no definitive diagnosis for these granulomas; however, differential diagnoses included perforation or ulceration of the esophagus from multiple tube feedings, parasite migration (considered unlikely because there was no evidence of parasites on necropsy nor histology), or chronic bacterial infection. Staining tissue sections with Ziehl-Neelsen stain did not reveal any acid-fast bacilli within the granulomas; therefore, infection with Mycobacterium spp was considered unlikely.

Findings for the snake of the present report demonstrated the importance of including spinal osteopathy and osteomyelitis on the differential diagnosis list for decreased mobility, neurologic signs, or both in snakes. Because snakes are extremely proficient in hiding clinical signs of illness and pain until they are far along in the disease process, full-body radiography and other diagnostic procedures may be warranted for those with changes in behavior, mobility, or appetite. Definitive etiologic diagnosis of an underlying cause can be challenging and is often not found; however, ruling out potential disease processes that may be treated, such as nutritional deficiencies or osteomyelitis, is vital.