Canine spirocercosis: clinical, diagnostic, pathologic, and epidemiologic characteristics
Introduction
The nematode Spirocerca lupi is primarily a parasite of dogs, although other animals, particularly carnivores may be affected. It has a worldwide distribution, but is most prevalent in warm climate (Bailey, 1972). The adult S. lupi is found in a nodular mass in the wall of the host’s thoracic esophagus. The female lays embryonated eggs that are transferred through a tract in the nodule and excreted in the host’s feces. Eggs are ingested by the intermediate host, corprophagus beetles, and develop to infective (L3) stage within 2 months. Carnivores are infected by ingestion of a beetle or a variety of parathenic hosts including: birds, hedgehogs, lizards, mice, and rabbits. In the carnivore host, the infective larvae penetrate the gastric mucosa, and 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 they mature to adults over the next 3 months (Bailey, 1972, Soulsby, 1986, Fox et al., 1988, Urquhart et al., 1996).
The lesions caused by S. lupi are mainly due to the migration and persistent presence of larvae and adults in the tissues. Esophageal nodular masses and granulomas, and aortic scars and aneurysms are the most frequent lesions. Spondylitis and spondylosis of the caudal thoracic vertebrae are additional typical lesions (Soulsby, 1986, Fox et al., 1988, Urquhart et al., 1996). Neoplastic transformation of the granulomas to fibrosarcoma or osteosarcoma has been reported in dogs with spirocercosis sometimes with the development of hypertrophic osteopathy (Bailey, 1972, Grant et al., 1979, Johnson, 1992). Less frequently, lesions may occur due to the aberrant migration of the worms. S. lupi worms and nodules have been reported in almost every thoracic organ (Fischer and Carneiro, 1974, Garg et al., 1989, Harrus et al., 1996), the gastrointestinal tract (Babero et al., 1965; Georgi et al., 1990; Brodey et al., 1977), the urinary system (Turk, 1960, Thanikachalam et al., 1984), and the subcutaneuos tissues (Chandrasekharon et al., 1958, Turk, 1960, Harrus et al., 1996).
The clinical signs reported in canine spirocercosis depend on the location and severity of the lesions. Esophageal lesions are associated with persistent vomiting and/or regurgitation followed by weakness and emaciation (Bailey, 1972, Chhabra, 1973, Fox et al., 1988). Sudden death may be caused by rupture of an aortic aneurysm induced by migration of worms in the aortic wall (Ndiritu, 1976, Ivoghli, 1977).
A definite diagnosis of spirocercosis is made by detection of characteristic eggs by fecal flotation (Soulsby, 1986, Markovics and Medinski, 1996). Survey thoracic radiographs of affected dogs show esophageal granulomas as areas of increased density in the caudodorsal mediastinum and contrast esophograms may outline granulomas. Spondylitis of the caudal thoracic vertebrae occasionally may be seen on radiorgraphs (Fox et al., 1988). Esophagoscopy and gastroscopy allow direct visualization of the nodules, which appear as broad-based protuberances with a distinctly nipple-like orifice.
Several anti-helminthics have been suggested for the treatment of canine spirocercosis. These include: diethylcarbamazine, disophenol, levamizole, albedazole, ivermectin and doramectin (Seneviranta et al., 1966, Fox et al., 1988, Berry, 2000). Surgical excision of esophageal granulomas and sarcomas is often not possible due to extensive or multiple lesions (Fox et al., 1988).
Canine spirocercosis had been a rare diagnosis in Israel until 1988. In the period of 1980–1988 only two cases of spirocercosis, a fox from the Jerusalem area and a dog from Tel Aviv, were diagnosed. However during 1989, four dogs were diagnosed with spirocercosis on necropsy (Harmelin et al., 1991), and since then, the frequency of diagnosis of this infection has increased remarkably.
A limited number of case studies on spirocercosis have been published describing the clinical presentation, diagnosis and management of S. lupi infection in the dog (Berry, 2000, Lobetti, 2000, Dvir et al., 2001). The emergence of an outbreak of spirocercosis and the lack of detailed large studies on this disease warranted an in-depth clinical and epidemiological investigation on this infection in Israel.
The goals of this retrospective study were to describe the clinical, hematological, and biochemical findings in 50 dogs diagnosed with spirocercosis at the Hebrew University Veterinary Teaching Hospital (HUVTH) in Israel during 1991–1999, and to document the emergence and spread of this disease in Israel, as expressed by the hospital medical records.
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Materials and methods
The medical records of all dogs diagnosed with spirocercosis at the HUVTH in Israel during 1991–1999 were retrospectively reviewed. The HUVTH is the only veterinary teaching hospital in Israel and it accepts referrals and emergency cases from the whole state. Criteria for inclusion in the study were the detection of S. lupi eggs by fecal examination, visualization of a typical granuloma by esophagoscopy, or findings of typical lesions of spirocercosis at necropsy. Age, sex, breed, geographic
Diagnosis
Fifty dogs met the criteria of diagnosis with spirocercosis. The initial diagnosis was made by fecal flotation in 32 dogs, at necropsy in 9, by endoscopy in 8 and by identification of an adult S. lupi worm in the vomitus in 1 dog. Five dogs had the following concurrent diseases: ehrlichiosis in two dogs, lymphosarcoma, lymphocytic thyroiditis, and intervertebral disc disease each in one dog.
Annual diagnosis of new cases
The number of dogs diagnosed with spirocercosis at the HUVTH increased significantly (P=0.00093) from 2
Discussion
The increase in the number of dogs diagnosed with spirocercosis at the HUVTH during the course of this study suggests that an outbreak of this disease has occurred in Israel. Spirocercosis was first reported in Israel in 1934 (Witenberg, 1934), but it had been a rare clinical and pathologic diagnosis until 1988. The esophageal lesions caused by adult S. lupi are prominent and it is unlikely that a large number of infected dogs would have been overlooked at necropsies performed prior to 1988. In
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