Abstract
A 13-year-old female red kangaroo (Macropus rufus) was presented with a history of chronic, intermittent vomiting. The kangaroo was immobilized for diagnostic examination. Complete blood count, serum chemistry, and fibrinogen were within normal limits. Radiographs revealed two mixed-density radiopaque masses in the right cranioventral abdomen. The masses were of granular, mineral opacity and were ovoid in shape, with long axes of 10 cm and 5 cm. Exploratory laparotomy performed several days after diagnosis of suspected gastrolithiasis revealed no foreign objects, and intraoperative radiographs confirmed this finding. After surgery, the kangaroo continued to expel ingesta passively, characterizing the clinical sign as regurgitation rather than vomiting. Bloodwork parameters remained unremarkable. Symptomatic treatment with a variety of antiemetics, including parenteral metoclopramide (dosage: 0.2–0.4 mg/kg BID) and maropitant citrate (dosage: 1 mg/kg SID) did not decrease frequency of regurgitation. Treatment for gastritis was initiated with parenteral famotidine (dosage: 0.5 mg/kg BID) and oral omeprazole (dosage: 3.5 mg/kg SID). Intermittent episodes of presumed gastric tympany with audible borborygmus were treated with chewable simethicone tablets (dosage: 9 mg/kg BID), which the kangaroo consumed readily. Pain related to these episodes was managed with flunixin meglumine (1 mg/kg SID) and butorphanol (0.3 mg/kg PRN). A barium study revealed esophageal dilation with suspected decreased esophageal motility. Diagnostic tests for hypothyroidism and myasthenia gravis were negative. Symptomatic treatment for megaesophagus was initiated by feeding gruel from an elevated platform and frequent hand feeding, which required the kangaroo to extend vertically. The kangaroo continued to lose weight despite showing a good appetite, and endoscopy performed under anesthesia confirmed a severely dilated esophagus that contained a moderate amount of ingesta and fluid despite a 12-h fast. On necropsy, the proximal 30 cm (about 50%) of the esophagus was severely dilated and had thin, flaccid walls. The esophagus became more normal in appearance at the diaphragmatic hiatus, although no stricture was evident. Esophageal histopathology revealed chronic, multifocal myofiber degeneration with fibrosis. Aspiration pneumonia, a common sequela to megaesophagus, was also diagnosed on histopathology.
Vomiting occurs occasionally in macropods through a process termed merycism. In this process, ingesta moves up the esophagus and into the oral cavity through obvious abdominal contractions that appear as heaving. Typically, the ingesta is swallowed immediately rather than chewed, and some material may fall from the oral cavity.7 Although a few episodes of heaving were described in this kangaroo, the predominant clinical sign was simple regurgitation with no perceptible abdominal contracture, pointing to the esophageal etiology. To the author’s knowledge, megaesophagus has never been diagnosed in a macropod. Megaesophagus has been described in several large animal and exotic species, including a Bengal tiger, a wood bison, and a llama, but in all of these cases, megaesophagus was diagnosed as a consequence of persistent right aortic arch.1,4,5 No such vascular anomalies were apparent in this kangaroo. Myasthenia gravis has been previously diagnosed as a cause of megaesophagus in a ferret, polar bear, and Siberian tiger.2,3,6 In all of these cases, serum acetylcholine receptor (AChR) antibody levels were assessed at the Comparative Neuromuscular Laboratory of the University of California San Diego and were well above canine and feline reference ranges. In the polar bear and tiger cases, serum AChR antibody titers were also several times higher than those of healthy conspecifics.3,6 Although normal ranges for AChR antibody titers have not been established in macropods, antibody levels for this kangaroo were far lower than canine and feline reference intervals for myasthenia gravis-positive animals. The titer was also comparable with levels from a juvenile, healthy female red kangaroo, making myasthenia gravis highly unlikely as the cause of megaesophagus in this case.
Literature Cited
1. Butt, T.D., D.G. MacDonald, and W.H. Crawford. Persistent right aortic arch in a mature llama. Vet Rec. 2001;148(4):118–119.
2. Couturier, J., M. Huynh, D. Boussarie, L. Cauzinille, and G.D. Shelton. Autoimmune myasthenia gravis in a ferret. J Am Vet Med Assoc. 2009;235(12):1462–1466.
3. Kenny, D.E., J. Baier, F. Knightly, D. Steinheimer, D.M. Getzy, and G.D. Shelton. Myasthenia gravis in a polar bear (Ursus maritimus). J Zoo Wildl Med. 2004;35(3):409–411.
4. Ketz, C.J., M. Radlinsky, L. Armbrust, J.W. Carpenter, and R. Isaza. Persistent right aortic arch and aberrant left subclavian artery in a white Bengal tiger (Panthera tigris). J Zoo Wildl Med. 2001;32(2):268–272.
5. Peters, M., R. Koch, J. Kammerling, and P. Wohlsein. Persistent right aortic arch in a yearling captive wood bison (Bison bison athabascae). J Zoo Wildl Med. 2002;33(4):386–388.
6. Wallace, R.S., and J.A. Teare. Myasthenia gravis in a Siberian tiger. Proc. Assoc. Rept. and Amph. Vet. and Am. Assoc. Zoo Vet. 1994:154–155.
7. Vogelnest, L., and T. Portas. Macropods. In: Vogelnest L., and R. Woods (eds.). Medicine of Australian Mammals. CSIRO Publishing, Collingwood, Victoria, Australia; 2008:138.