Carotid Taenia solium Oncosphere Infection: A Novel Porcine Neurocysticercosis Model.

Neurocysticercosis (NCC), the infection of the human central nervous system (CNS) with larval cysts of Taenia solium causes widespread neurological morbidity. Animal models are crucial for studying the pathophysiology and treatment of NCC. Some drawbacks of current NCC models include differences in the pathogenesis of the model and wild-type parasite, low rates of infection efficiency and lack of reproducibility. We describe a novel porcine model that recreates infection in the CNS with high efficiency. Activated oncospheres, either in a high (45,000-50,000) or low (10,000) dose were inoculated in the common carotid artery of 12 pigs by ultrasound-guided catheterization. Following oncosphere injection, either a high (30 mL) or low (1-3 mL) volume of saline flush was also administered. Cyst burden in the CNS was evaluated independently according to oncosphere dose and flush volume. Neurocysticercosis was achieved in 8/12 (66.7%) pigs. Cyst burden in the CNS of pigs was higher in the high versus the low oncosphere dose category (median: 4.5; interquartile ranges [IQR]: 1-8 and median: 1; IQR: 0-4, respectively) and in the high versus the low flush volume category (median 5.5; IQR: 1-8 and median: 1; IQR: 0-2, respectively), although not statistically different. All cysts in the CNS were viable, whereas both viable and degenerated cysts were found in the musculature. Carotid injection of activated oncospheres in pigs is effective in reproducing NCC. Oncosphere entry into the CNS by way of vasculature mimics wild-type infection, and provides a useful alternative for future investigations on the pathogenesis and antiparasitic treatment of NCC.

Elaeophora schneideri in moose (Alces alces) from Colorado.

Two adult moose (Alces alces) from Colorado (USA) were naturally infected with Elaeophora schneideri. Both animals had patent infections indicating that moose may serve as definitive hosts. Gross and histological lesions were characterized by fibromuscular intimal proliferation within the carotid arteries and rete mirabile cerebri. This is the first report of Elaeophora schneideri in moose from Colorado.

Elaeophorosis in Barbary sheep and mule deer from the Texas Panhandle.

Adult Elaeophora schneideri were recovered from the common carotid artery and its branches in 14 of 14 mule deer, Odocoileus hemionus, and 3 of 9 Barbary sheep or aoudads, Ammotragus lervia, from Palo Duro Canyon in the Texas Panhandle. Gross cutaneous lesions attributable to elaeophorosis in the Barbary sheep varied from small circumscribed scars up to 10 cm in diameter usually on the poll or orbital region to extensive proliferative irregular encrustations on the frontal, temporal and orbital regions, sometimes extending to the ears and muzzle. Individual lesions varied from slate-gray scarred areas to brown proliferative edematous and hyperemic encrustations, sometimes with depigmented pustules a few millimeters in diameter. Microscopic lesions ranged from granulation tissue to severe pyogranulomatous reactions with neutrophils, eosinophils, lymphocytes and plasma cells as the primary infiltration. Foreign body giant cells and/or microfilariae were not observed. Microscopic changes in the carotid arteries and their branches were limited to small villous projections on the intimal surface apparently resulting from medial hyperplasia. Cutaneous lesions attributable to elaeophorosis were not observed in mule deer. Histopathologic lesions in the carotid arteries of mule deer were similar to those observed in Barbary sheep. The comparative pathology of elaeophorosis in various hosts is reviewed and discussed in terms of its pathology in Barbary sheep. The potential ramifications of this infection on the expanding aoudad population in the southwestern United States require that elaeophorosis be considered in the management of this species, particularly in areas with sympatric mule deer populations.