Caudal Occipital Malformation Syndrome in a 6‐Year‐Old Female Huacaya Alpaca

A 58-kg, 6-year-old, female Huacaya alpaca presented to the Washington State University Veterinary Teaching Hospital with a history of gradual developing lethargy, reluctance to rise, anorexia, blindness, and respiratory distress. A presumptive diagnosis of dorsal displacement of the soft palate was made and a tracheostomy tube was surgically placed by the referring veterinarian. Supportive treatment included crystalloid fluids (lactated Ringer’s solution) administered IV and antimicrobial (certiofur sodium, unknown dose) therapy. The tracheotomy tube was removed and the respiratory distress appeared to have resolved. For the 2 months prior, the alpaca had been housed at an out-of-state breeding facility. Marginal feed quality during this period was believed to be related to the alpaca’s poor body condition score (1/5). The alpaca’s vaccination (Clostridium perfringens C/D, Cl. tetani toxoids) and deworming (Ivermectin) history were deemed appropriate and current. The owner thought that the alpaca might be pregnant. Upon examination, the alpaca was dull, lethargic (reluctant to rise when stimulated), and had not eaten for at least 1 day. The alpaca was thin (body condition score 1/5) and adequately hydrated. Vital signs (heart rate, respiratory rate, and temperature), capillary refill time, and mucus membrane color were normal. The alpaca urinated and defecated normally and had normal compartment 1 (C1) contractions upon auscultation. The tracheostomy site was patent, healing, and no abnormal respiratory sounds were asculted. Neurologic examination revealed an absent menace response in the left eye, with normal palpebral reflexes and pupilary light reflexes (direct and consensual). No other abnormal cranial nerve signs were detected. The alpaca held her head in an abnormally low position and moved her head slowly in response to stimuli. There were no signs of pain upon neck manipulation. Although it was difficult to maintain the alpaca in a standing position, conscious proprioceptive (CP) deficits were observed in all 4 legs. Flexor reflexes (thoracic and pelvic) and patellar reflexes were normal. Abnormalities identified on clinical pathology included decreased serum activity of SDH and AST and serum concentration of cholesterol, BUN, and albumin, most likely a result of decreased feed intake. No fecal parasite ova were observed and serum bile acids were within the normal limits. Virus neutralization testing for EHV-1, West Nile virus, and cELISA for Bluetongue virus from blood were all negative. CSF protein concentration, cell count, and cell morphology were within normal limits. Because of the continued anorexia, the alpaca was transfaunated with 2 L of rumen fluid and administered IV lactated Ringer’s solution supplemented with KCl (20 mEqs/L) and Vitamin B complex (2 mls/L) at 1.39 maintenance (4 L/d). Ceftiofur sodium (1.1 mg/kg IV q12h) and flunixin meglumine (1.1 mg/kg IV q12h) were administered. Because of the dam’s lack of milk production and substantial time spent in recumbency, the cria was weaned. Magnetic resonance imaging (MRI) examination revealed malformation of the caudal occipital bone with herniation/caudal displacement of the caudal cerebellum through the foramen magnum. There was also a T2-weighted hyperintensity within the cervical spinal cord (from C1-C3) that became hypointense on the T1-weighted images consistent with syringohydromyelia (Fig 1). Follow-up neurologic examination findings were consistent with the changes found on MRI examination. CP deficits were most likely caused by the extensive syringohydromyelia in the cervical spinal From the Department of Veterinary Clinical Sciences, Washington State University, Pullman, WA (Allen, Chen, Barrington); and is presently affiliated with Department of Veterinary Clinical Sciences, Iowa State University (Bagley). Corresponding author: Andrew J. Allen, Department of Veterinary Clinical Sciences Veterinary Teaching Hospital, P.O. Box 647060, Pullman, WA 99164-7060; e-mail: [email protected]. Submitted August 15, 2013; Revised November 26, 2013; Accepted December 31, 2013. Copyright © 2014 by the American College of Veterinary Internal Medicine 10.1111/jvim.12316 Abbreviations: