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Title: DEVELOPMENT AND PATHOGENESIS OF PARELAPHOSTRONGYLUS ODOCOILEI (NEMATODA: PROTOSTRONGYLIDAE)IN EXPERIMENTALLY INFETED THINHORN SHEEP (OVIS DALLI)

Author
item JENKINS, E - SASKATCHEWAN, CANADA
item Hoberg, Eric
item POLLEY, L - SASKATCHEWAN, CANADA

Submitted to: Journal of Wildlife Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/10/2005
Publication Date: 8/8/2005
Citation: Jenkins, E.J., Hoberg, E.P., Polley, L. 2005. Development and pathogenesis of parelaphostrongylus odocoilei (nematoda: protostrongylidae)in experimentally infeted thinhorn sheep (ovis dalli). Journal of Wildlife Diseases. 41:669-682.

Interpretive Summary: Parasitic nematodes continue to be recognized as significant pathogens among ungulates in both managed and natural ecosystems. A definition of life history, the interface between a host and parasite, and behavior of parasites within ungulate hosts are necessary to understand substantial issues about host association, and diseases attributable to nematodes and other pathogens. Recently, the muscle-dwelling nematode Parelaphostrongylus odocoilei has been reported in wild ungulates at many locations in north-western North America, including in a new genus of host, thinhorn sheep (Ovis d. dalli and O. d. stonei).For the first time, we completed the life cycle of P. odocoilei in Stone's sheep (O. d. stonei) thinhorn sheep hybrids (O. d. stonei x O. d. dalli), each experimentally infected with 200 third-stage larvae. The pre-patent period (time of development prior to release of first larvae) ranged from 68-74 days, and shedding of first-stage larvae (L1) peaked at >10,000 L1 per gram of feces between 90 and 110 days post infection. Starting in the pre-patent period, all infected sheep lost weight and developed peripheral eosinophilia. At two weeks prior to patency, two thinhorn sheep hybrids developed neurological signs (hind end ataxia, loss of conscious proprioception, and hyperesthesia) that resolved at patency The migration route of the 'muscleworm' P. odocoilei may involve the central nervous system, altering our current understanding of the life history and phylogenetic relationships of the elaphostrongylines. Neurological signs associated with infections of Parelaphostrongylus had not been observed previously and suggest that occurrence of such disease in domestic hosts that may become infected in zones of geographic contact with naturally infected wild ungulates. Multiple parenteral treatments with ivermectin neither immediately nor completely eliminated larval shedding in one experimentally infected thinhorn sheep hybrid. P. odocoilei and related species of elaphostrongyline nematodes remain important pathogens in ungulates in both North America and across Europe and parts of Asia. Our studies provide important new insights into migratory behavior of nematodes in the ungulate definitive host, and suggest that regimes for effective treatment require further evaluation.

Technical Abstract: Recently, the muscle-dwelling nematode Parelaphostrongylus odocoilei has been reported in wild ungulates at many locations in north-western North America, including in a new genus of host, thinhorn sheep (Ovis d. dalli and O. d. stonei). Between August 2000 and December 2004, for the first time, we completed the life cycle of P. odocoilei in three Stone's sheep (O. d. stonei) and two thinhorn sheep hybrids (O. d. stonei x O. d. dalli), each experimentally infected with 200 third-stage larvae. The pre-patent period ranged from 68-74 days, and shedding of first-stage larvae (L1) peaked at >10,000 L1 per gram of feces between 90 and 110 days post infection. Sequence of the ITS-2 region of nuclear DNA of L1 shed in feces, and morphology of adult male nematodes from the muscles of three Stone's sheep, from which we recovered a total of 14, 17, and 75 adult nematodes, were consistent with P. odocoilei. Starting in the pre-patent period, all infected sheep lost weight and developed peripheral eosinophilia. At two weeks prior to patency, two thinhorn sheep hybrids developed neurological signs (hind end ataxia, loss of conscious proprioception, and hyperesthesia) that resolved at patency. Eosinophilic pleocytosis and antibody to Parelaphostrongylus spp. were detected in the cerebrospinal fluid of infected, but not control, thinhorn sheep hybrids, which showed no clinical abnormalities at any time. During patency, two Stone's sheep with heavy burdens of eggs and larvae of P. odocoilei in the lungs died of respiratory failure following anesthesia or exertion. Multiple parenteral treatments with ivermectin neither immediately nor completely eliminated larval shedding in one experimentally infected thinhorn sheep hybrid. The migration route of the 'muscleworm' P. odocoilei may involve the central nervous system, altering our current understanding of the life history and phylogenetic relationships of the elaphostrongylines.