ELAEOPHORA SCHNEIDERI (ARTERIAL WORM)

CAUSATIVE AGENT (CLASSIFICATION, morphology) Elaeophora schneideri is a medium-sized (6 to 9 cm) filarial nematode found in the carotid and other arteries of suscep­tible ungulate hosts (Hibler and Adcock 1971).

HOST RANGE AND DISTRIBUTION Elaeophora schneideri occurs primarily in the Odocoileus hemionus complex, comprising mule deer and black-tailed deer, and is distributed in the west­ern United States as far east as Nebraska, and north to British Columbia, Canada (Anderson 2001, McKown et al. 2007). Less commonly, it occurs among white-tailed deer of the southeast­ern and southwestern United States (Prestwood and Ridgeway 1972, Forrester 1992). Infections among white-tailed deer of the southeastern U.S. are thought to have resulted from interstate movement of animals (Prestwood and Ridgeway 1972). The parasite also has been reported from less well-adapted hosts such as elk (Hibler and Adcock 1971), moose (Worley et al. 1972), bighorn sheep (Ovis canadensis) (Boyce et al. 1999), and domestic sheep and goats (Hibler and Adcock 1971) in the western and southwestern United States, as well as Barbary sheep (Ammotragus lervia) (Pence and Gray 1981) and Sika deer (Cer- vus nippon) (Robinson et al.

life cycles and variations In the normal definitive hosts, E. schneideri typically is found in the common carotid and internal maxillary arteries, but can occur in almost any artery large enough to hold it (Hibler and Adcock 1971). Microfilariae generally are found in cap­illaries of the skin on the forehead and face of infected deer (Anderson 2001). The parasite is transmitted by horseflies (Family Tabanidae) of the genera Hybomitra and Tabanus. Microfi­lariae invade the fat body lining the abdomen of horseflies and develop into L₁ larvae; these, in turn, move to the hemocoel and develop to L₃ larvae before moving to the fly mouthparts for transmission to the next definitive host (Hibler et al. 1971, Hibler and Metzger 1974).

After transmission to mule deer from infected horseflies, the L₃ larvae may enter the venous system from the subcutaneous site of entry to be carried to the heart and lungs before moving to the arterial system. They invade the leptomeningeal arteries of the head, develop into immature adults (“L5” larvae), and move to the carotids, where they mature. The prepatent period is about 5.5 months (Hibler and Adcock 1971, Anderson 2001).

reservoirs and transmission In the western and southwestern United States and in southern British Columbia, Canada, members of the Odocoileus hemionus complex are the res­ervoir (Anderson 2000) of E. schneideri. In the southeastern United States, white-tailed deer appear able to sustain the parasite population, although the host-parasite relationship appears to be tenuous (Hibler and Prestwood 1981).

Transmission occurs by horseflies of the genera Tabanus and Hybomitra (Hibler and Adcock 1971). At least 16 horsefly species have been identified as intermediate hosts, includ­ing seven species of Hybomitra and nine spe­cies of Tabanus; occasionally other flies have been infected, but appear to be insignificant contributors to this life cycle (Longfellow 1984, Pence 1991).

There is some variation in the reported elevations inhabited by horseflies. In the Gila Forest, New Mexico, horseflies occurred almost completely above 2,000 meters and were most abundant at about 2,300 meters (Hibler et al. 1971). In contrast, horseflies were collected in coastal California at elevations ranging from 610 to 760 meters (Longfellow 1984). The horseflies on South Island, South Carolina (Couvillion et al. 1984), likely also were at low coastal elevations.

Depending on the site, reported prevalences in horseflies can range from 0.3% (Couvillion et al. 1984) to over 20% (Hibler et al. 1971, Clark and Hibler 1973). The variation in horse­fly prevalences may reflect parasite prevalences in the reservoir hosts (Pence 1991).

Horseflies in the Gila Forest, New Mexico, first emerged in early June, peaked by the second week of June, and remained stable until early July, when summer rains began (Hibler et al. 1971). Similarly, in southeastern New Mexico, horsefly numbers reached a peak about the third week in June and persisted for 2 to ç weeks after that (Pence 1991). In coastal Humboldt County, California, capture dates for members of the genera Tabanus and Hybomitra ranged from 2 May to 30 September; some spe­cies peaked in June while others reached their peak in July (Longfellow 1984).

Most adult tabanid flies are active during the warmer parts of the year, and activity gener­ally occurs during the warmer hours of the day (Hibler et al. 1971, Allan 2001). There are some sites where the greatest activity has been late in the day (Longfellow 1984); also, some tabanid flies are crepuscular (Allan 2001).

CLINICAL EFFECTS AND IDENTIFICATION Mule deer and black-tailed deer in western North America are well-adapted hosts for E.

While very well adapted in its normal definitive hosts, E. schneideri can cause consid­erable pathology and even mortality in abnor­mal ungulate hosts (Anderson 2001). Most pathology in abnormal hosts is linked to physi­cal blockage of arteries by the nematodes. In elk, blockage of the arterial system of the head can lead to ischemic damage in the brain, optic nerves and eyes, ears, muzzle, and develop­ing antlers (Hibler and Adcock 1971). Bilateral clear-eyed blindness, circling, nystagmus, necrosis of the muzzle and nostrils, dry gan­grene of the ear tips, abnormal antler growth, and emaciation are some of the characteristic clinical effects of elaeophorosis in elk (Hibler and Adcock 1971).

Clinical signs in moose included blind­ness, circling, staggering, and ataxia (Worley et al. 1972, Madden et al. 1991). Moose also had fibromuscular intimal proliferation within the carotid and other arteries (Madden et al. 1991).

Sheep, goats, and Sika deer often are hyper­sensitive to the microfilariae and develop skin lesions of a raw, bloody dermatitis on the forehead or face, called “sorehead” (Robinson et al. 1978, Fraser and Mays 1986). Some thrombi may occur in cerebral and leptomen­ingeal arteries (Fraser and Mays 1986). Domes­tic sheep and goats, especially young animals, may die 3 to 5 weeks after infection following a period of incoordination, circling, and convul­sions (Fraser and Mays 1986).

population effects Between 1960 and 1975, there was an abundance of mule deer in the national forests of the southwestern United States. On the Gila National Forest, New Mexico, elk calf survival was reported to range from 7 to 20% during times of severe tabanid fly and E. schneideri infestation, an inadequate survival for success of the popula­tion (Hibler et al. 1969). In 1975, the mule deer population decreased markedly, and the horsefly population also decreased to goats, but not for the cerebral form of the disease (Fraser and Mays 1986). There are no control procedures currently proposed for this parasite in wild populations. However, finding means to reduce tabanid fly populations could be con­sidered in limited areas if some definitive hosts (e.g., elk, moose) were severely affected.