Abstract:
BACKGROUND : The pathology of spirocercosis, a disease caused by the infestation of carnivores with the nematode
Spirocerca lupi, has been extensively described in domestic dogs and coyotes. However, it has not been described
in wild carnivores in South Africa. The aim of this study was to evaluate whether black-backed jackals are a host for
Spirocerca species and to provide a detailed description of the associated pathology. Jackals were also stratified
according to age and the Spirocerca species recovered were characterized using molecular techniques.
METHODS : Standard necropsies were performed on routinely culled jackals from three of the nine provinces of
South Africa during the period June 2012 to February 2013. Jackals were screened for the presence of
pathognomonic Spirocerca-induced lesions and for evidence of aberrant migration. Relevant samples were
submitted for histopathology and collected larvae were genotyped at nine microsatellite loci.
RESULTS : Spirocerca lupi-associated aortic lesions were found in 16 of 93 (17%) black-backed jackals. Of these, four
(25%) were associated with S. lupi larvae. Genotyping of the larvae revealed amplification of all nine loci that
amplified dog-derived S. lupi, with the same level of polymorphism in the allele size ranges. Only 1 of 93 jackals
had an esophageal nodule with concurrent S. lupi-induced aortic aneurysms. The single esophageal nodule found
did not contain adult nematodes, nor did it communicate with the esophageal lumen. None of the jackals that
were examined had macroscopically evident spondylitis, which is frequently reported in the dog.
Histopathology of the S. lupi-induced aortic lesions in the jackal revealed replacement of elastic and smooth muscle
fibers by fibrous connective tissue. In cases where inflammation was present, the inflammatory infiltrate consisted
predominantly of eosinophils. The single esophageal nodule histologically resembled the early inflammatory nodule
described in dogs and consisted of fibrous connective tissue, multifocal accumulation of lymphocytes, plasma cells
and rare hemosiderin-laden macrophages.
CONCLUSIONS : These lesions suggest that the life cycle of S. lupi may not or only rarely be completed in jackals. A
possible explanation might be that jackals are relatively resistant to developing significant pathology associated
with S. lupi-infection. However, before any conclusions can be drawn, many more jackals, including those that die
naturally will have to be investigated for evidence of S. lupi infection.
