Infection by Elaeophora schneideri, the arterial worm, is found in a variety of wild and domestic ruminants. Clinical signs (endothelial damage, thrombosis, and infarction) result from obstructed blood flow in the carotid and cephalic arteries. Diagnosis is based on histological examination of necropsy specimens and PCR assay. There is no effective treatment; however, restricting movement of susceptible wildlife from endemic areas can help limit spread of the disease.
Elaeophorosis is the disease resulting from disruption of the arterial circulation due to infection with the arterial worm Elaeophora schneideri.
Etiology and Pathogenesis of Elaeophorosis in Animals
E schneideri, commonly referred to as the arterial worm, is a filarial nematode that causes elaeophorosis. E schneideri adults are stout, white worms frequently found within the common carotid or maxillary artery of their hosts (see carotid artery image).
Courtesy of Dr. Nick DeCesare.
E schneideri adult females measure 60–120 mm × 0.6–0.9 mm, and males are slightly smaller (55–85 mm × 0.4–0.7 mm). Microfilariae, which reside within the dermal capillary beds of the forehead and poll region, are 239–279 mcm × 11–15 mcm, with a rounded anterior end and a posterior end tapering to a blunt point.
E schneideri is transmitted via the bite of an infected horse fly in the genus Tabanus or Hybomitra. As the fly feeds, infective larvae migrate to the leptomeningeal arteries, where the nematodes develop into immature adults in approximately 3 weeks. Immature adults migrate against blood flow to establish in larger arteries of the head and neck, where approximately 6 months later they reach sexual maturity, mate, and release microfilariae into the bloodstream. E schneideri adults are relatively long-lived, with an estimated lifespan of 3–4 years.
E schneideri infections have been reported in a variety of domestic, wild, and exotic game species. Mule deer and black-tailed deer are considered to be definitive hosts but might have minimal clinical signs. However, atypical hosts, including domestic and wild sheep, moose, elk, sika deer, sambar deer, and white-tailed deer, can develop clinical signs of elaeophorosis when infected.
Clinical Findings of Elaeophorosis in Animals
Elaeophorosis is characterized by obstructed blood flow, endothelial damage, thrombosis, and infarction resulting from the presence of nematodes in the carotid and cephalic arteries. Parasite-mediated disruption of arterial circulation can lead to blindness; to ischemic necrosis of the brain, ears, muzzle, and other cephalic tissues (see ear tip necrosis image); and to poor antler development, oral impactions, and sudden death.
Courtesy of Dr. Nick DeCesare.
Elaeophorosis in sheep commonly manifests as dermatitis of the head ("sorehead") in reaction to microfilariae dwelling in skin.
Diagnosis of Elaeophorosis in Animals
Ear tip necrosis or cheek impaction
Finding the worm in carotid arteries
Histological identification in arterial and CNS tissues
Elaeophorosis is diagnosed during necropsy by identification of parasites in animal tissues. E schneideri adults or larval forms are found within the carotid, internal maxillary, cerebral, and leptomeningeal arteries.
Molecular identification of nematodes in tissues can be done by PCR assay to support the diagnosis of elaeophorosis. In addition, histological examination can be used to observe arterial surface lesions produced by previous parasite infections. Recovery of microfilariae from skin lesion biopsies confirms suspected elaeophorosis in sheep.
Differential diagnoses for elaeophorosis include the following:
For deer with cheek impactions (see cheek impaction image): tooth wear in older deer, or previous trauma to the mandible and associated muscles or the cranial nerves innervating the buccal cavity
For moose and elk: epizootic Hemorrhagic disease infection with bluetongue virus, trauma, or meningeal worm (Parelaphostrongylus tenuis) infection
For sheep: trauma, fly strike, or caustic chemical reactions
Courtesy of Dr. Kevin Keel.
Epidemiology and Control of Elaeophorosis in Animals
The impact of E schneideri on ruminant host populations is not well defined. E schneideri is endemic to much of the western and southwestern US; however, additional population pockets have been identified, including portions of the southeastern US and areas of Minnesota.
E schneideri infection rates in domestic sheep are relatively low, likely because of the use of anthelmintics for routine parasite control. However, wild sheep populations sympatric with mule deer could have a greater risk of infection.
Reports of elaeophorosis in elk suggest that E schneideri infections can lead to calf deaths (1). The effects of E schneideri infections on moose are undetermined. A high prevalence of E schneideri in apparently healthy moose of Wyoming and Colorado suggests that infections can be tolerated; however, several cases of disease and death attributed to E schneideri have been documented (1). According to one source, moose populations in Montana are more likely to have health-related deaths in areas with higher prevalence and intensity of E schneideri (2).
Because of the complexity of the E schneideri life cycle and the potential for multiple ruminants to serve as competent hosts, the possibility that E schneideri will be transmitted to new locations via migration of host animals, especially mule deer and black-tailed deer, must be considered. Movement of atypical hosts such as elk, white-tailed deer, moose, and sheep from enzootic areas to nonendemic locations could introduce elaeophorosis into naive populations, because E schneideri can produce patent infections in these host species.
Key Points
Elaeophora schneideri is transmitted via bites of various tabanid horse flies and can lead to varying levels of disease and, in some cases, death.
Lesions can consist of dermatitis, ear tip necrosis, abnormal mastication, neurological damage, or vision impairment.
More research is needed to understand the geographical distribution and clinical impact of this parasite in domestic and wild animals.
For More Information
Grunenwald CM, Butler E, Wünschmann A, et al. Emergence of the arterial worm Elaeophora schneideri in moose (Alces alces) and tabanid fly vectors in northeastern Minnesota, USA. Parasit Vectors. 2018;11(1):507.
References
Anderson RC. Filarioid nematodes. In: Samuel WM, Pybus MJ, Kocan AA, eds. Parasitic Diseases of Wild Mammals. Iowa State University Press; 2001:342-356. doi:10.1002/9780470377000
DeCesare NJ, Harris RB, Peterson CJ, Ramsey JM. Prevalence and mortality of moose (Alces alces) infected with Elaeophora schneideri in Montana, USA. J Wildl Dis. 2023;59(4):748-752. doi:10.7589/JWD-D-22-00075
