Symptoms of elaeophorosis include necrosis of the muzzle, ears, and optic nerves; lack of coordination (ataxia); facial or lower limb dermatitis; horn deformities; blindness; and death.

Symptoms of elaeophorosis were first observed in 1933, in sheep (New Mexico) and mule deer (Utah) infested by an unknown nematode worm.

Within a few weeks, the microfilariae develop into infective third-stage larvae (called L3) in the fly's fat body tissue and haemocoel.

In these smaller arteries, they obstruct blood flow to various parts of the head, face, and brain; which leads to the clinical symptoms of elaeophorosis [citation needed] In the United States, E. schneideri has been reported from various wild hosts in 19 states: Arizona, Arkansas, California, Colorado, Florida, Georgia, Louisiana, Missouri, Montana, Nebraska, New Mexico, North Dakota (in imported animals), Oklahoma, South Carolina, South Dakota, Texas, Utah, Washington and Wyoming.

[12] Field surveys of wild mammal populations have shown wide variation in the percentage of animals infested with E. schneideri.

However, blockage and thickening of coronary, cephalic, brachial and femoral arteries and sublingual food impaction have been reported in this host.

Blockage of the carotid and other arteries of the head and face region by E. schneideri adults restricts local bloodflow, leading to ischemic damage to the brain, optic nerve, ears, muzzle and other facial areas.

The results are often blindness; walking in circles or poor coordination (ataxia); dermatitis or gangrene of the ears, muzzle or nostrils; abnormal antler growth; or death.

[6] Diagnosis involves recovering either adult worms from the arteries after the death of the infested host, or microcercariae from the skin of the face or head.

A combination of tartar emetic (antimony potassium tartrate) and emetine hydrochloride healed the skin lesions.

[24] However, repeated administration of diethylcarbamazine runs the risk of fatality due to accumulation of dead worms in the arteries.