Survival of a Foal with Type A Botulism

A 10-day-old female, 42 kg pony/Paint horse cross filly was presented to the University of California Davis, William R. Pritchard Veterinary Medical Teaching Hospital (VMTH) for low head and neck carriage, suspected to be caused by a fractured cervical vertebrae. For 3 days after parturition, no abnormalities were noted. At 4 days of age, the foal began to exhibit progressive weakness, an inability to rise unassisted, low head carriage, and an inability to nurse without manual support of the head. Radiographs of the cervical vertebrae, complete blood count (CBC), and serum biochemistry profile obtained 4 days before admission did not reveal abnormalities. The foal had received no medications nor had serum IgG concentrations been measured. The dam had one previous foal with no complications and had not been vaccinated in 2 years. On presentation, the foal was in lateral recumbency and unable to rise unassisted. The owners had assisted her to rise, and supported her head in order to nurse every 2 hours while en route to the hospital. No abnormalities were noted on physical examination other than weakness and an inability to maintain the head and neck in a normal position and posture. Cranial nerve examination was within normal limits. With assistance to stand, the foal was able to ambulate but the gait was short and stiff, and the foal tired quickly. The neck was extended with the head held in a neutral position. No evidence of pain could be elicited on flexion of the neck in either a vertical or horizontal plane. There was a decrease in tone through the dorsal cervical musculature that allowed abnormal hyperextension of the nuchal ligament and neck. The foal was able to suckle well with the head supported, with normal tongue tone and no signs of aspiration. Repeat radiographs of the cervical vertebrae, CBC, and arterial blood gas analysis did not reveal abnormalities. Because of an inability to nurse unassisted and concerns over the potential for aspiration, an intravenous catheter was placed in the jugular vein and a nasogastric feeding tube was placed. Serum and whole blood submitted for vitamin E and selenium testing, respectively, showed a low whole blood selenium concentration (0.051 ppm; ref: 0.08–0.5 ppm) and a normal vitamin E concentration (3.7 ppm; ref >2 ppm adequate). Ultrasonography of the umbilical structures showed asymmetric umbilical arteries and a mildly hyperechoic left umbilical artery, although both measured within normal limits (<9 mm). Because of the progressive weakness, without other clinical or hematologic abnormalities, toxicoinfectious botulism was suspected. Botulism types A and C were considered the most likely serotypes in this foal, having been born on the West coast of the United States. Initial therapy included administration of divalent plasma (18 mL/kg, IV), containing antibodies to C. botulinum Type B and C toxins. When it became available 24 hours later, trivalent plasma, with antibodies to Types A, B, and C (12 mL/kg), was administered. The foal was administered polyionic fluids at 4 mL/kg/h for 48 hours and the rate was adjusted to maintain 6 mL/kg/h total rate in combination with the plasma. Additional therapeutics included: potassium penicillin (22,000 mg/kg, IV, q6h), selenium (2.5 mg or 1 mL/50 kg, IM, once), omeprazole (4 mg/kg, PO, q24h), and vitamin E (10 IU/kg, PO, q24h). The foal was assisted to stand, or the recumbent side was alternated, every 2 hours. She was fed 12% of body weight daily as a mixture of mare milk and a commercial milk replacer. The foal was weaned onto the commercial milk replacer, and the amount fed was increased to 25% of body weight as she became more active. The transition to milk replacer was initiated because of the unavailability of mare’s milk. To treat constipation, a frequent complication of botulism, the foal was administered enemas as well as mineral oil (1 mL/kg, through NG administration) once. A fecal sample collected at the time of admission was submitted for PCR detection From the William R. Pritchard Veterinary Medical Teaching Hospital, School of Veterinary Medicine, Davis, CA (Prutton, Plummer, Williams); and the Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA (Magdesian, Aleman). Work performed at: The William R. Pritchard, Veterinary Medical Teaching Hospital, University of California, Davis, CA 95616. Corresponding author: Dr K.G. Magdesian, Department of Medicine and Epidemiology, School of Veterinary Medicine, One Shields Avenue, University of California, Davis, CA 95616; e-mail: [email protected] Submitted November 6, 2015; Revised December 9, 2015; Accepted January 18, 2016. Copyright © 2016 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. DOI: 10.1111/jvim.13840 Abbreviations: