Diagnostic imaging of canine spirocercosis: Wide range of pathologic findings



Knowledge Farm Veterinary Specialists Referral Centre, Beit Berl Campus, Kfar Saba, Israel




Spirocerca lupi is a nematode parasite of dogs and other carnivores. It has world wide distribution but is most prevalent in warm climates. Dogs are the definite host and become infected by ingesting the corpophageous beetle intermediate host. After being released in the stomach of the final host (e.g. dog), the larvae penetrate the stomach wall and migrate in the wall of the arteries to the thoracic aorta, where they remain for three months. The worms reach the oesophagus from this site by direct migration through the thoracic cavity. Typically, the worms become encapsulated in nodules (granulomas) within the esophageal wall where they reach their sexual maturity.




Migrating larvae cause hemorrhages, inflammatory reactions, necrosis and abscesses in the tissues in which they migrate. Most of these lesions are not serious and heal rapidly. Larvae migrating in the walls of the thoracic aorta cause purulent panarteritis with thickening of the intima and granuloma of the adventitia. Degeneration of the elastic tissue may lead to thromboembolism, stenosis or formation of aneurysm with possible rupture of the vessel. Calcification and ossification of the aortic wall is often seen (CT imaging).

The adult worms live in nodules in the esophageal and sometime stomach wall. These nodules eventually reach the size of a pigon egg, in which several worms are embedded in a pus-like, crumbly, brownish mass. Large nodules in the oesophageal wall may cause obstruction and thereby interfere with prehension of food. Massive infestation may lead to esophageal rupture with consequent of mediastinitis, pneumothorax and pyothorax.

Spondylitis involving the thoracic vertebrae is often associated with the infection.

S. Lupi appears to be an important factor in malignant tumourigenesis (oesophageal fibrosarcoma and osteosarcoma).

Affected dogs may present with lameness and thickening of the distal limbs due to hypertrophic osteopathy (HO).

Aberrant migration  via arterial or venous walls or possibly via  a haematogeneous rout may lead to the formation of nodules in the pleura, mediastinum, diaphragm, lung, trachea, bronchi, thymus, heart, lymphatics, subcutaneous tissues, Stomach, spinal cord, renal capsule, urinary bladder, small intestine and rectum.


Clinical signs


Clinical signs vary depending on the stage of the disease and possible complications. An uncomplicated infection may either be subclinical, or more commonly, if the oesophageal granuloma is big enough, regurgitation, vomiting, weight loss, and dysphagia will devellope. Additional common clinical signs may be pyrexia, weakness, respiratory abnormalities, anorexia, melena and paraparesis.




Initial diagnosis of a suspected Spirocerca granuloma is most commonly made radiographically. It can then be confirmed by means of fecal examination and endoscopy. Althogh endoscopic biopsy is a useful tool, its sensitivity for detecting neoplastic transformation is limited. In one study (Dvir et al 2001) biopsy diagnosis proved incorrect after necropsy or surgical excision in 38% of dogs.

Computed Tomography (CT) imaging, due to its tomographic nature and superb contrast capability may provide crucial information with respect to early tomourigenesis, pulmonary metastasis, aortic and other related parencymal lesions.


Diagnostic imaging appearance of lesions attributed to Spirocerca Lupi:


Caudal esophageal mass

Thoracic radiographs, preferably right lateral (RLR) and ventrodorsal (VD) views may show soft tissue mass located in the caudal mediastinal region overlaying the caudal thoracic esophagus (Fig. 1).


Fig. 1. Poor quality practice film, yet of diagnostic value; (A) Lateral thoracic radiograph. Note the typical caudal oesophageal mass and the palisading new bone on the ventral aspect of mid vertebral bodies (spondylitis). Additionally, note the thick periosteal reaction on the distal aspect of the humerus (hypertrophic osteopathy).



Fig. 1. (B) VD view with midline oesophageal mass detected in caudal mediastinum.

Moderate amount of esophageal air may be detected aborally to the mass. Atypical cases may have esophageal masses in the cranial thorax leading to saccular-like esophageal dilation (Fig. 2).



Fig. 2. (A) Lateral view of oesophageal contrast study (50ml of Iohexol 300mgI/ml). Note the cranial oesophageal diverticulum with a large oval filling defect due to intraluminal geanuloma. There are additional filling defects in the caudal oesophagus due to numerous nodules protruding into the lumen. Spondylitis is noted on the ventral aspect of the T7 & T8 vertebral bodies. Marked alveolar lung pattern signify severe aspiration pneumonia.




 Fig. 2. (B) VD view better demonstrate the extent of the aspiration pneumonia.



In many cases, especially at an early stage of the disease, the thoracic radiographs appear unremarkable and therefore the diagnosis of oesophageal spirocerca nodules may be achieved by other means (Fig. 3).Esophageal contrast studies can be useful in the absence of endoscopy to detect small masses which are not visible on survey radiographs. 


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Fig. 3. (A) Lateral and (B) VD views of apparently normal thorax.





Fig. 3. (C) Endoscopic picture of the distal oesophagus of the same dog showing a nodule protruding into the oesophageal lumen. The nodule has a crater-like small opening.


Endoscopically there may be one or several nodules protruding into the esophageal lumen (Fig. 3 &4) that may have polyp or nipple like structure or a small opening. Nodules that have gone malignant transformation tend to appeare lobulated, ulcerated, and partially necrotic. These lesions often do not contain worms and lack a visible opening

Esophageal nodules may be seen ultrasonographically (Fig. 4) using transhepatic window. The nodule may appear as an isoechoic caudal mediastinal mass with internal irregular cavity that is filled with hypoechoic fluid and multiple echogenic interfaces (worms).




Fig. 4. (A) Lateral thoracic radiograph showing large caudal oesophageal mass displacing the heart base cranioventrally and the main stem bronchi craniodorsally. Note the spondylitis on T7 & T8.




Fig. 4. (B) Transhepatic ultrasound image showing a large hypoechoic mass with eccentric cavity that is filled with multiple echogenic interfaces (worms). The mass is located just cranially to the gastro-oesophageal sphincter.




Fig. 4. (C) Endoscopic picture of the distal oesophagus of the same dog. Large ventral nodule with evidence of ulceration protrudes into the oesophageal lumen. The oesophagus appears inflame



Mass mineralization (Fig. 5) may be suggestive of neoplastic transformation (osteosarcoma/  fibrosarcoma). Pulmonary metastasis may be noted on the thoracic radiographs as nodular lung pattern whereas consolidation of the dependent lobes may suggest aspiration pneumonia.


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Fig. 5. (A) Lateral and (B) VD thoracic radiographic views showing distinct caudal oesophageal mass. The mass has central patchy amorphous mineralization. Such finding may have high index of suspicion for neoplastic transformation. Not the spondylitis on the ventral aspect of T7 &T8 vertebras.


CT examination should be performed while the dog is in sternal recumbency as it allows more normal positioning of the heart and other mediastinal structures. Slice thickness and intervals of 5mm should be sufficient in large breed dogs. Survey scan should be repeated after intravenous contrast administration. Distending the esophagus with air and administration of small amount of iodinated contrast fluid (e.g. Iohexole 300mg/ml I) may better delineate the nodules.

Esophageal nodule is typically seen as mural cavitary mass with isodense thick irregular wall and eccentric hypodense fluid filled cavity. Post contrast administration, the mass will show moderate contrast uptake at the periphery with the cavity remaining slightly hypodense and unenhanced. If the esophagus is distended with air the nodules may be seen protruding into the lumen. Hypodense tract may be seen connecting the centre of the mass to the esophageal lumen.

CT is extremely sensitive tool for detecting early tumour mineralization and pulmonary matastasis. Masses that are mineralized, have amorphous architecture, lack distinct cavity, and have complex pattern of contrast uptake are more likely to be neoplastic. 



Spondylitis appears on lateral thoracic radiogrphs as an active periosteal/bony proliferation often involving the ventral aspect of the T8-L1 vertebrae. It must be distinguished from spondylosis, a non- inflammatory bridging of the intervertebral disk space. It is postulated that the aberrant parasite migration or the severe periaortic inflammation may be responsible.

CT is superior to radiography for identifying early spondylitis due to its improved contrast resolution and tomographic nature.


Hypertrophic Osteopathy (HO)

Some cases may present soft tissue swelling of the extremities and complaint of shifting lameness. Radiography may show periosteal proliferation along the diaphyses of the affected bones (Fig. 6) with adjacent soft tissue swelling. Periosteal pattern may vary from smooth to palisading. The changes are usually bilaterally symmetrical and the joints are not affected. Occasionally the periosteal changes also involve other bones (i.e., vertebra, pelvis, humerus, femur, and patella).


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Fig. 6. Practice films of a dog with endoscopically confirmed spirocercosis. (A) Lateral radiographic view of the radius/ulna showing soft tissue swelling and palisade (proximally) to thick (distally) periosteal proliferation on the caudal aspect of the ulna

Fig. 6. (B) VD radiographic view of the pelvis and femurs of the same dog showing thick periosteal proliferation along the femoral diaphyses also involving the ischium. These finding are indicative of Hypertrophic Osteopathy.

The pathogenesis of HO is incompletely understood. The most consistent pathologic finding in affected animals is increased blood flow to the extremities leading to overgrowth of the vascular connective tissue and subsequent subperiosteal new bone formation.


Aortic pathology

Parasitic migration in the aorta can cause extensive intimal damage leading to aortic aneurysm, thromboembolysm and dystrophic calcification of the aortic wall.

Aortic aneurysm (Fig. 7) is defined as abnormal irreversible dilation of the aortic lumen. It is weakening and destruction of the elastic fibers that results in aneurysm formation. Fuciform aneurysms involve the entire aortic circumference, thus appearing cylindrical. Saccular aneurysms are sharply delineated and usually involve a localized segment of the aorta. They can be present as eccentric out pouching from one side of the aortic wall.

On lateral thoracic radiographs the border of the aorta may be poorly demarcated due to the inflammation of the aorta and its surrounding tissue. On the DV projection the left border of the aorta may bulge or have a vaguely undulant outline. If there was partial rupture of the aortic wall there may be evidence of mediastinal and pleural effusion and subsequent mediastinal widening and effacement of the aortic outline.


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Fig. 7. (A) Transverse CT-angiogram image of the caudal thorax illustrating marked aortic aneurismal dilation. Note the cavitary ventral oesophageal mass. (B) Transverse image of the thorax a level slightly cranially to the previous image showing hypodense tract connecting the mass with the oesophageal lumen. 




Fig. 7.(C) sagittal and (D) coronal reconstruction images illustrating the extent of the aortic aneurysm also vaguely showing the lobulated oesophageal mass.

Aortic aneurysm in the caudal thorax and cranial abdomen may be seen ultrasonographicaly using intercostals approach as focal increase in the caliber of the vessel. Concentric layers of thrombus may line the interior of the aneurysm, and this thrombus may generate emboli that occlude distal arteries. A large aneurysm is very pulsatile as the change in radius over the change in pressure, from systolic to diastolic, is also large. Flow velocities seen in aneurysms are often very low. This is because the vessel diameter is wide and flow is similar to the sluggish flow seen in a wide river. Distal wave forms often look as pulsatile as normal, and other than the problem of blood stasis the low velocities are not in themselves significant. The colour-flow patterns (Fig. 7) seen in aneurysms are often very complex and the wave forms obtained may have odd peaks and reverse flow component. This varies from point to point within the aneurysm.


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Fig. 7.(E) Ultrasound image of the cranial abdominal aorta and (F) colour-doppler image at the same level illustrating extensive fuciform aneurysm with very complex colour-flow patterns.

The demonstration of mediastinal or retroperitoneal haematoma provides direct evidence of aortic rupture. The haematoma is hypoechoic and usually asymmetric. Free fluid may also be present if the aneurysm has leaked into the adjacent space.

Aortic thrombus may be seen as an intaluminal structure which may be adhered to the aortic wall. The appearance of thrombosis can vary from hypoechoic in the early stage to more heterogenically echogenic structure.  Linear hyperechoic foci with acoustic shadowing along the aortic wall suggest dystrophic mineralization.  

CT angiography (Fig. 8) will demonstrate circumscribed dilatation of the aorta and is extremely helpful in assessing the location and magnitude of the aneurysms.

CT findings indicating aortic rupture include; streaks and puddles of contrast outside of the aorta within the mediastinum. Unenhanced CT scan is extremely sensitive for detection of intimal calcifications. Thrombus within an aneurysm or hematoma adjacent to leaking aneurysm may appear higher in attenuation than aortic blood on unenhanced scans. With contrast infusion, the lumen of the aorta, the aneurysm and a protruding thrombus can be defined clearly.

Fig. 8. (A) Transverse CT-angiogram image of the thorax illustrating aorta filling defect due to mural thrombus formation at 9-12 o'clock. Note the midline oesophageal mass.

Fig. 8. (B)
Sagittal reconstruction. Note the irregular oesophageal mass. There is a plaque-like dorsally located aortic thrombus. There is mild aneurismal dilation cranially to the thrombus.

Fig. 8.  (C) Coronal reconstruction. The plaque-like aortic thrombus is visible. Note the ill demarcated and undulant lateral border of the thoracic aorta.

Pathology related to aberrant migration of the parasites.


Reported areas of larval migration include most of the thoracic structures (lung, trachea, bronchus, aorta, pleura, diaphragm and vertebral bodies), stomach small intestine, rectum, urinary system and sub cutis.

Aberrant migration seems to occur via arterial or venous wall migration or possibly via haematogeneous rout, which may explain distant aberrant sites like the skin. Aberrant migration to the abdominal structures may be seen as hypoechoic cystic nodules or hypoechoic cavitary small mass which may be surrounded by an echogenic zone of reactive tissue (Fig. 9).


Fig. 9. Ultrasound image of the cranial abdominal aorta. Note the ill defined mass adhered to the outer aortic wall, constituted of multiple small cysts. Ultrasound needle aspirate yielded serosnguineous fluid which was filled with Spirocerca larvae.


Migration to the thoracic spinal area (Fig. 10) possibly occurs via intercostals arteries, which originate from the thoracic aorta, through their spinal branches and into the extra dural space or into the spinal cord parenchyma. Here they elicit clinical neurological signs typical of thoracolumbar IVD disease or spinal trauma, either by their physical presence, blood vessel rupture and subsequent haematoma formation, or inflammatory reaction.

The diagnosis of intramedullary spirocercosis may be challenging as in one study (Dvir et al 2007) a myelogram and CT investigation of one case did not demonstrate the intraspinal lesion. In such case MRI investigation is likely to be informative.

Aberrant migration to the thoracic structures is best investigated with CT imaging.

On contrast-enhanced CT the peri nodule may enhance. If infection or haemorrhage occurs, the clear demarcation with adjacent parenchyma is lost and the parasite may stimulate pneumonia. In these cases a dense halo is seen on CT imaging, representing surrounding inflammatory change.


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Fig. 10. (A) Sagittal and (B) coronal reconstruction myeloCT images of the thoracolumbar spin. A uniform widening of the spinal cord on all planes was indicative of intramedullary lesion. CSF findings of inflammatory pleocytosis and the detection of oesophageal spirocerca granuloma were highly suggestive of aberrant parasitic migration to the L1 spinal cord segment.

Further complications may be pleural or mediastinal effusions (inflammatory or haemorragic) and pneumothorax.




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