ISSN 2398-2969      




  • Cause:spirurid nematode,Spirocerca lupi(Rudolphi, 1809).
  • Signs:frequently subclinical; regurgitation, odynophagia, vomiting and melena are prominent clinical manifestations.
  • Diagnosis:fecal examination, thoracic radiography, esophagoscopy-gastroscopy.
  • Treatment:macrocyclic lactones (doramectin, ivermectin) constitute the mainstay of treatment.
  • Prognosis:good to guarded in subclinical or uncomplicated clinical cases; poor if complications (ie esophageal sarcomas) have been developed.



  • Nematode,Spirocerca lupi(S sanguinolenta).

Predisposing factors

  • Higher prevalence in warm climates.
  • Seasonality of spirocercosis (higher prevalence of clinical cases during colder months of the year) implies that most infections acquired during warmer months when intermediate hosts abound in dogs' habitat.


  • Life and hunting styles significantly influenceS lupiprevalence; stray and tracer hunting dogs are overrepresented compared to household pets or scent hunting dogs.
  • Higher incidence of disease in large breed dogs compared to smaller breeds.


  • Spirocerca lupieggs shed in feces of infected dogs.
  • Dung beetles feeding on canine feces take up eggs and developS lupilarvae.
  • Dogs are infected directly by ingesting dung beetles of various spp containingS lupi.larvae or by feeding on paratenic hosts ie birds, small mammals and reptiles that have preyed on beetles and acquired larvae that remain encysted in their tissues. Immature stages can survive in these hosts for an indefinite period of time without further ontogenic development of parasite.
  • S lupilarvae released from vectors in dog's stomach and penetrate gut wall.
  • Larvae migrate along blood vessel walls to aorta.
  • Upon reaching aorta, larvae migrate along aortic wall cranially and eventually may create a granuloma between aorta and esophagus in caudal mediastinum.
  • Adult worms develop in esophageal or extraesophageal granulomas.
  • Adult worms create an orifice in esophageal wall and shed eggs that are excreted in dog's feces.

Clinical manifestations

  • Mainly related to migration pattern of infective larvae, as well as granulomatous nodules induced by adult worms Canine spirocercosis: adult worms in esophagus.
  • Esophageal granulomas or, less frequently,S lupi-associated sarcomas (fibrosarcomas Fibrosarcoma , osteosarcomas Osteosarcoma ) account for esophageal dysphagia manifested by regurgitation and/or vomiting, odynophagia and hypersalivation.
  • Dysphagia may be exacerbated by salivary gland necrosis Salivary gland: necrotizing sialometaplasia , occasionally associated withS lupiinfection.
  • Respiratory distress and/or coughing may be induced by the space-occupying nature of esophageal neoplasms Alimentary tract: neoplasia or their pulmonary metastases Lung: pulmonary neoplasia ; aspiration pneumonia Lung: aspiration pneumonia as well as esophageal wall perforation Esophagus: perforation with resultant mediastinitis Mediastinal disease or pyothorax Pyothorax.
  • Hypertrophic osteopathy Hypertrophic osteopathy may be a sequel of esophageal sarcomas.
  • Melena and chronic hemorrhagic anemia may occur due to ulceration Gastric ulceration of esophageal granulomas.
  • Sudden death may occur due to rupture of a migrating larvae-induced aortic aneurysm.
  • Spondylitis or spondylosis of caudal thoracic vertebrae (T6 to T12) may occasionally account for lameness and/or paraplegia.
  • Wide spectrum of clinical manifestations may occur due to aberrant migrations of worms.Spirocerca lupinodules reported in almost every thoracic and abdominal organ and sc tissues.


  • Prepatent period (time interval between ingestion of infective larvae and development of maturity in definitive host) ranges from 4 - 6 m.
  • Most cases of spirocercosis are considered to be subclinical.
  • Course of clinical illness variable.
  • Self-cure rarely witnessed following death of worms (viable adult worms have been retrieved as long as 738 days after inoculation).


  • Prevalence rates depend mainly on density of canine population and degree of contact between definitive, intermediate and transport hosts.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Mylonakis M E, Rallis T S, Koutinas A F, Leontides L S, Patsikas M, Florou M, Papadopoulos E & Fytianou A (2006) Clinical signs and clinicopathologic abnormalities in dogs with clinical spirocercosis: 39 cases (1996-2004). JAVMA 228 (7), 1063-1067 PubMed.
  • Mylonakis M E, Rallis T S, Koutinas A F, Ververidis H N & Fytianou A (2004) A comparison between ethanol-induced chemical ablation and ivermectin plus prednizolone in the treatment of symptomatic esophageal spirocercosis in the dog: a prospective study on 14 natural cases. Vet Parasitol 120, 131-138 PubMed.
  • Lavy E, Aroch I, Bark H, Markovics A, Aizenberg I, Mazaki-Tovi M, Hagag A & Harrus S (2002) Evaluation of doramectin in the treatment of experimental canine spirocercosis. Vet Parasitol 109, 65-73 PubMed.
  • Mazaki-Tovi M, Baneth G, Aroch I, Harrus S, Kass P H, Ben-Ari T, Zur G, Aizenberg I, Bark H & Lavy E (2002) Canine spirocercosis: clinical, diagnostic, pathologic and epidemiologic characteristics. Vet Parasitol 107, 235-250 PubMed.
  • Mylonakis M E, Koutinas A P, Liapi M V, Saridomichelakis M N & Rallis T S (2001) A comparison of the prevalence of Spirocerca lupi in three groups of dogs with different life and hunting styles. J Helminthol 75, 359-361 PubMed.
  • Berry W L (2000) Spirocerca lupi esophageal granulomas in 7 dogs: resolution after treatment with doramectin. J Vet Intern Med 147, 609-612 PubMed.
  • Bailey W S (1972) Spirocerca lupi: a continuing inquiry. J Parasitol 58, 3-22 PubMed.

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