Elaeophora schneideri is a parasite of mule deer and black-tailed deer found in the mountains of western and southwestern USA and in Nebraska; it also has been found in white-tailed deer in southern and southeastern regions. Adult parasites are 60–120 mm long and usually are found in the common carotid or internal maxillary arteries. The microfilariae, ∼275 μm long and 15–17 μm thick, normally are found in skin capillaries on the forehead and face. Development in the intermediate hosts, horse flies of the genera Tabanus and Hybomitra, requires ∼2 wk. Infective larvae invade the host as the horse fly feeds, migrate to the leptomeningeal arteries, and develop to immature adults in ∼3 wk. These young adults migrate against the blood flow and establish in the common carotid arteries, where they continue to grow. The parasites reach sexual maturity ∼6 mo later and begin producing microfilariae. The life span of adults is 3–4 yr.
Clinical disease has not been reported in mule deer and black-tailed deer; therefore, they are considered to be the normal definitive hosts. When horse flies transmit the infective larvae to elk, moose, domestic sheep and goats, sika deer, and possibly white-tailed deer, the larvae develop in the leptomeningeal arteries and cause ischemic necrosis of brain tissue, resulting in blindness, brain damage, and sudden death. Blindness in these animals is characterized by absence of opacities in the refractive media of the eye (“clear-eyed” blindness).
Domestic sheep and goats, especially lambs, kids, and yearlings, may die suddenly 3–5 wk after infection. Death is usually preceded by incoordination and circling and often by convulsions and opisthotonos. Numerous thrombi occur in the cerebral and leptomeningeal arteries. One or more young adult E schneideri accompany each thrombus. If sheep or goats survive the early infection, a raw bloody dermatitis on the poll, forehead, or face (“sorehead”) develops 6–10 mo later. Lesions occasionally develop on the legs, abdomen, and feet. These lesions are an allergic dermatitis in response to the microfilariae lodged in capillaries. Lesions persist, with periods of intermittent and incomplete healing for ∼3 yr, followed by spontaneous recovery. Hyperplasia and hyperkeratosis develop in the epidermis of the parasitized area.
Differential diagnoses include coenurosis (Taenia, see Cestodes Causing CNS Disease), cerebrocortical necrosis (see Polioencephalomalacia), and enterotoxemia (see Enterotoxemias). Elaeophorosis should not be considered unless sheep have been in endemic areas during the summer. Diagnosis in lambs, kids, or elk yearlings or calves usually is made at necropsy; numerous thrombi and parasites are found in the common carotid, internal maxillary, cerebral, and leptome-ningeal arteries. Presumptive diagnosis in mature sheep is based on history and location and type of lesion. The skin lesion must be differentiated from that of ulcerative dermatosis (see Ulcerative Dermatosis of Sheep). Confirmation is by recovery of microfilariae from the lesion or by postmortem recovery of the adult parasites. A skin biopsy of the lesion is macerated in isotonic saline solution and allowed to stand ≥6 hr at room temperature. The skin is strained off and the fluid examined for the typical microfilariae.
Piperazine salts (220 mg/kg, PO) are effective. Complete recovery occurs in 18–20 days. No treatment is available for the cerebral form of the disease.
Last full review/revision July 2011 by Thomas R. Klei, PhD