Spirocercosis has resurfaced in various parts of the world as an important disease of dogs. Although it has a worldwide distribution, spirocercosis is most prevalent in warm climates. It appears however, that in some countries this is an urban disease while in others it is a rural disease. Dogs become infected with Spirocerca lupi by ingesting the intermediate host, coprophagous beetles in which Spirocerca larvae have developed, or by ingesting the paratenic host (transport host); birds, hedgehogs, lizards, mice and rabbits which have swallowed the beetles and in which larvae from beetles have reencysted. The dog is the definitive host and after ingesting larval cysts becomes infected when the larvae is freed and invades the gastric mucosa. The larvae then migrate within the walls of the gastric arteries to the thoracic aorta. About 3 months post-infection, the larvae leave the aorta and migrate to the esophagus where they provoke the development of granulomas. As the larva mature to adults over the next 3 months the adult female lays eggs in the wall of the esophagus. These eggs enter the esophageal lumen and pass through the alimentary tract to exit the body in the feces. The larvae containing eggs do not hatch unless ingested by a coprophagous beetle in which they encyst.
Aberrant migration of S. lupi larvae is not uncommon and Spirocerca larvae have been found in many different organs primarily in the thoracic cavity but also in the skin, kidney, heart and the eye to name a few.
The lesions caused by S. lupi are mainly due to the migration and persistent presence of larvae and adults in the tissues. Esophageal granulomas, aortic scars and aneurysms are the lesions most frequently seen. Spondylitis and spondylosis of the caudal thoracic vertebrae are additional typical lesions, however they occur in fewer cases. When large enough, the esophageal granuloma appears as a caudal thoracic mass on radiography. Neoplastic transformation of the granulomas to fibrosarcoma or osteosarcoma may occur in dogs with spirocercosis. In rare cases these neoplasms have been associated with the development of hypertrophic osteopathy
The clinical manifestations of canine spirocercosis depend on the location and severity of the lesions. Esophageal lesions are associated with regurgitation and/or persistent vomiting, ptyalism, difficult swallowing, followed by weakness and emaciation. Sudden death may be caused by rupture of an aortic aneurysm induced by migration of worms in the aortic wall.
A definitive diagnosis of spirocercosis is made by detection of characteristic eggs by fecal flotation, demonstration of typical esophageal granulomas as areas of increased density in the caudodorsal mediastinum and occasionally spondylitis of the caudal thoracic vertebrae. The radiological findings may be seen in survey thoracic radiographs and contrast esophagrams which appear as filling defects. Recently, esophagoscopy has proven to be a most useful diagnostic modality allowing direct visualization of the typical broad-based protuberances with a distinct nipple-like orifice. This procedure has proven to be the most sensitive diagnostic aid in our practice.
Several anti-helminthics have been used with limited efficacy for the treatment of canine spirocercosis. These include: diethylcarbamazine, disophenol, levamisole, albendazole and fenbendazole. In the past few years the avermectins; ivermectin and doramectin have been tested. The latter has been shown to be highly efficacious at the dose of 400µg/kg subcutaneously at bi-weekly intervals for 12 weeks, followed by monthly injections until the disappearance of the esophageal granulomas as judged by endoscopy. In the event of very large esophageal masses or neoplasia that results in severe esophageal obstruction, surgical excision of esophageal granulomas and sarcomas has been attempted with guarded prognosis. Prophylactic therapy for spirocercosis may be appropriate in endemic areas and recent work to be reported here using doramectin and selamectin have shown promising results.