Review
Spirocerca lupi infection in the dog: A review

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Abstract

Spirocercosis is a disease occurring predominantly in Canidae, caused by the nematode Spirocerca lupi. Typical clinical signs are regurgitation, vomiting and dyspnoea. The life-cycle involves an intermediate (coprophagous beetle) and a variety of paratenic hosts. Larvae follow a specific migratory route, penetrating the gastric mucosa of the host, migrating along arteries, maturing in the thoracic aorta before eventually moving to the caudal oesophagus. Here the worm lives in nodules and passes larvated eggs which can be detected using zinc sulphate faecal flotation. Histologically, the mature oesophageal nodule is composed mostly of actively dividing fibroblasts.

Spirocerca lupi-associated oesophageal sarcomas may occur and damage to the aorta results in aneurysms. A pathognomonic lesion for spirocercosis is spondylitis of the thoracic vertebrae. Primary radiological lesions include an oesophageal mass, usually in the terminal oesophagus, spondylitis, and undulation of the aortic border. Contrast radiography and computed tomography are helpful additional emerging modalities. Oesophageal endoscopy has a greater diagnostic sensitivity than radiography. Endoscopic biopsies are not sensitive for detecting neoplastic transformation. Doramectin is the current drug of choice, effectively killing adult worms and decreasing egg shedding. Early diagnosis of infection is still a challenge and to date no ideal regimen for prophylaxis has been published.

Introduction

Spirocercosis is a disease caused by the nematode Spirocerca lupi which has a variety of clinical presentations (Dvir et al., 2001, Lobetti, 2000, Mazaki-Tovi et al., 2002). S. lupi is found worldwide especially in tropical and subtropical regions. This nematode has been found in many species, but affects mostly carnivores, especially Canidae (Dvir et al., 2001, Lobetti, 2000, Mazaki-Tovi et al., 2002). Clinical signs are mostly due to the migration and persistence of the larvae or adult worms within the host and secondary bacterial infections. Diagnosis in the early stages can be challenging and, unfortunately, most animals are only diagnosed once advanced disease is present. The most commonly reported clinical signs are regurgitation and vomiting (Mazaki-Tovi et al., 2002, Ranen et al., 2004). The distribution, life-cycle, pathogenesis and pathology, clinical signs, diagnosis, treatment and prevention of S. lupi will be discussed in this review.

Section snippets

Distribution

Spirocerca lupi is a nematode with a worldwide distribution in regions with a warm climate. The majority of reports are from Israel (Mazaki-Tovi et al., 2002), Greece (Mylonakis et al., 2001), Turkey, India (Ramachandran et al., 1984), Pakistan (Anataraman and Krishna, 1966), the southern United States (Dixon and McCue, 1967), Brazil (Oliviera-Sequeira et al., 2002), Kenya (Brodey et al., 1977) and South Africa (Lobetti, 2000).

In Israel, the majority (62%) of infections are diagnosed in winter

Life-cycle

The lifecycle of S. lupi involves intermediate and paratenic hosts. The adult worms are found coiled within nodules in the oesophageal wall. S. lupi eggs containing larvae (L1) are passed from the oesophagus through the gastrointestinal tract and into the faeces or may be shed in the vomitus. A variety of species of coprophagous beetles act as intermediate hosts. Eggs are ingested by the intermediate host and the larvae encyst within the tissues and develop to infectivity (L3) within 2 months.

Pathogenesis and pathology

Larvae cause necrosis, haemorrhage and neutrophil exudation within the vessel walls in which they migrate, but, except for the thoracic aorta, these lesions usually heal completely. In the thoracic aorta, degenerate elastic and muscle tissue becomes fibrotic, and sometimes mineralised to form permanent intimal scars and aneurysms of varying size and number. These result by the sixth month post infection (Fig. 2) (Hu and Hoeppli, 1936, Johnson, 1992). Tissue damage in the aorta can be severe

Clinical signs

The clinical signs of spirocercosis vary greatly, depending on the stage of disease, aberrant migrations and possible complications. Early migration of larvae through the gastric mucosa is associated with acute onset vomition in experimental cases (Bailey, 1972, Hu and Hoeppli, 1936). An uncomplicated infection may be sub-clinical, or show vomiting or regurgitation, weight loss and dysphagia due to the development of a caudal oesophageal mass (Mazaki-Tovi et al., 2002). The dog may also breathe

Faecal flotation

The female worm produces numerous small (35 × 15 μm) thick shelled larvated eggs (Fig. 5). Several factors affect the results of faecal flotation. Passage of eggs occurs for a relatively short period in the lifespan of the worm and is thus unpredictable. Eggs will only be present in the faeces when the female has a patent passage to the oesophageal lumen thus maturation of the nodule is essential. Eggs are difficult to detect in direct faecal preparations and routine flotation techniques using

Medical treatment

Over the years a number of different drugs have been used for treatment and or prophylaxis but to date no one remedy has been effective in killing both adult and larval stages of S. lupi while being devoid of host side-effects. Diethylcarbamazine, a piperazine derivative, was the first anthelmintic used for the treatment of spirocercosis and was shown to be effective in ameliorating the typical clinical signs of vomiting and regurgitation in animals with oesophageal nodules and improving the

Prevention

Disease incidence can be reduced by disposal of faeces, preventing dogs from hunting, scavenging and eating uncooked viscera and decreasing egg shedding by infected animals. Control of coprophagous beetles and transport hosts is not a feasible form of control due to the variety and ubiquity of transport hosts in an endemic area.

A study by Lavy et al. (2003) to evaluate the prophylactic effect of doramectin showed that treatment at 400 μg/kg, 30 days prior to exposure to infective larvae delayed

Conclusions

Spirocercosis is a serious condition in endemic areas. Clinical signs usually develop late in the disease except in those cases presenting with peracute aortic rupture. Clinical signs, which should be regarded as highly suspicious for spirocercosis in endemic areas include vomiting or regurgitation, dyspnoea, persistent coughing and hypertrophic osteopathy. Radiological lesions regarded as diagnostic for spirocercosis in endemic areas are typical oesophageal nodules, aortic aneurysms and

Acknowledgements

We acknowledge all the clinical staff of the Onderstepoort Veterinary Academic Hospital for allowing the use of their case material.

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