Tetanus is considered an uncommon disease in dogs.4 Following localization of Clostridium tetani in an anaerobic environment, the spores vegetate and produce a toxin (tetanospasmin) that is released into tissues and absorbed at the peripheral neuromuscular junction.1 Tetanospasmin inhibits neurotransmitter release centrally from CNS inhibitory interneurons, and release of extensor muscles from inhibition results in increased involuntary activity ranging from tremors to opisthotonos. In domestic dogs, tetanus can occur following surgery, deep or neglected wounds, replacement of deciduous teeth in puppies, dental disease, and complications from parturition.4 Diagnosis is based on the patient’s history and clinical signs. Clinical features of disease include increased muscle tone, cranial nerve signs, tonic spasms, and autonomic signs. Classic presentation is that of gait stiffness, a “sawhorse stance,” an elevated tail and excessive contraction of facial muscles. Facial changes include the characteristic sneering appearance (“risus sardonicus”), erect ears, wrinkled forehead, protrusion of the membrana nictitans, and contraction of masticatory muscles (trismus).1 Treatment of tetanus is via a combination of immunotherapy, antimicrobial therapy, sedatives, muscle relaxants, and nursing care.1,4
Hiatal hernia has been reported as a complication of tetanus in domestic dogs.2,5 Sliding hiatal hernia is the most commonly reported type of hiatal hernia reported in domestic pets, and is characterized by cranial displacement of the abdominal esophagus, esophagogastric junction and, often, a portion of the stomach through the esophageal hiatus.3 In domestic dogs, sliding hiatal hernia may be asymptomatic, or may result in signs of gastro-esophageal reflux and esophagitis. Reflux esophagitis is a disorder in which esophageal inflammation occurs as a result of mucosal contact with gastric or duodenal fluid or ingesta. Most hiatal hernia patients have some degree of reflux esophagitis, resulting from decreased lower esophageal sphincter pressure;3 however, clinical signs may be subtle or inapparent. Clinical signs of esophagitis may include hypersalivation, frequent attempts to swallow, regurgitation, and behaviors that suggest esophageal pain. Medical management is directed towards increasing the tone of the lower esophageal sphincter, decreasing gastric secretions, and increasing the rate of gastric emptying.6 Complications of severe or persistent esophagitis include esophageal stricture and aspiration pneumonia.
An 18-wk-old, 11.3-kg, male maned wolf (Chrysocyon brachyurus) presented with mild coughing and hypersalivation. Signs of facial muscle contracture became evident 24 h later. No wounds were detected during examination under anesthesia; however, there were several sites where deciduous teeth had been recently shed. Treatment for suspected tetanus was initiated at this time, including administration of 16,000 IU IV of equine-derived tetanus antitoxin (Equivac TAT CSL Limited, Parkville, VIC, Australia), 40,000 U/kg penicillin G IV, and 15 mg/kg IM amoxicillin-clavulanate (Clavulox injection, Pfizer Animal Health, West Ryde, NSW, Australia). Forty-eight hours after initial presentation, the patient developed gait stiffness, and auditory and tactile stimulation resulted in periods of extensor muscle spasm in hindlimbs, progressing to opisthotonos. Severe muscle spasms were controlled using IV diazepam 0.25–0.5 mg/kg IV (Pamlin injection, Parnell Laboratories Pty Ltd., Alexandria, NSW, Australia) and 0.1–0.2 mg/kg IM acepromazine (A.C.P. 10, Delvet Pty Ltd., Seven Hills, NSW, Australia). The animal was housed in a dark, quiet cage and maintained on intravenous fluids. Metronidazole (10–15 mg/kg slow IV BID) (Metrin solution, Parnell Laboratories) was used as the primary antimicrobial therapy thereafter.
The maned wolf had improved after 4 days of therapy, and was resting quietly without the need for administration of tranquilizers or sedatives. Marked hypersalivation remained a prominent clinical sign. At that time, pharyngeal dysphagia was the presumed cause of hypersalivation; however, the animal began to regurgitate, and endoscopic examination of the esophagus confirmed the presence of esophageal mucosal inflammation and ulceration. Thoracic radiographs revealed a hiatal hernia. Because the animal was unable to prehend solid foods (the result of trismus) and was losing body condition, a gastrostomy tube was placed to allow feeding. Medical therapies for esophagitis were initiated at this time, including the promotility agent, cisapride (0.5 mg/kg via gastrostomy tube TID; Prepulsid, Janssen-Cilag Pty Ltd., North Ryde, NSW, Australia), to increase lower esophageal sphincter pressure and stimulate more rapid gastric emptying, and the H2-receptor antagonist, ranitidine (0.5 mg/kg slow IV BID; Zantac injection, GlaxoSmithKline Australia Pty Ltd, Boronia, VIC, Australia), to decrease gastric acid production. During the course of treatment, a decision was made to use omeprazole (1 mg/kg via gastrostomy tube SID; Losec tablets, Astra Pharmaceuticals Pty Ltd., North Ryde, NSW, Australia), in place of ranitidine, because omeprazole is considered a more potent and long-lasting gastric acid suppressor than the H2-receptor antagonists. A second promotility agent, metoclopramide (0.5 mg/kg SC PRN; Maxolon injection, ICN Pharmaceuticals Pty Ltd., Auburn, NSW, Australia), was used as adjunctive therapy during episodes of apparently severe esophageal discomfort following tube feeding. There was acute onset of a right hindlimb proprioceptive deficit 7 days after commencement of intravenous metronidazole. Metronidazole therapy was ceased and within 72 h the proprioceptive deficit had significantly improved. After 18 days of antimicrobial and supportive therapy, all clinical signs of tetanus had resolved; however, clinical signs of reflux esophagitis persisted despite aggressive medical therapy. Movement of the sliding hiatal hernia resulted in persistent tension on the gastrostomy tube. This resulted in breakdown of the surgical wound in the abdominal wall, necessitating removal of the tube after it had been in place for 15 days.
After 24 days of intensive medical therapy, the maned wolf presented acutely with clinical signs of systemic inflammatory response syndrome, including tachypnea, hypoglycemia, hypothermia, and collapse, resulting in death. Necropsy examination findings were consistent with acute aspiration pneumonia with severe pulmonary edema. Sliding hiatal hernia (with displacement of approximately 60% of the stomach, the spleen and a liver lobe through the esophageal hiatus) and megaesophagus were grossly evident.
1. Coleman, E.S. 1998. Clostridial neurotoxins: tetanus and botulism. Compend. Contin. Educ. 20:1089–1093.
2. Dierenger, T.M., and A.M. Wolf. 1991. Esophageal hiatal hernia and megaesophagus complicating tetanus in two dogs. J. Am. Vet. Med. Assoc. 199:87–89.
3. Sivacolundhu, R.K., R.A. Read, and A.M. Marchevsky. 2002. Hiatal hernia controversies—a review of pathophysiology and treatment options. Aust. Vet. J. 80:48–53.
4. Soubasis, N., A.F. Koutinas, M.N. Saridomichelakis, and Z.S. Polizopolou. 2002. Tetanus in the dog: a study of six cases. Eur. J. Comp. Anim. Pract. 12:19–23.
5. Van Ham, L., and H. van Bree. 1992. Conservative treatment of tetanus associated with hiatus hernia and gastro-oesophageal reflux. J. Small Anim. Pract. 33:289–294.
6. Willard, M.D., and E.A. Weyrauch. 2000. Esophagitis. In: Bonagura, J.D. (ed.). Kirk’s Current Veterinary Therapy XIII, Small Animal Practice. W.B. Saunders Co., Philadelphia, PA. Pp. 607–614.