Parelaphostrongylus tenuis (Nematoda) and Fascioloides magna (Trematoda) in moose of southeastern Manitoba

1974 ◽  
Vol 52 (2) ◽  
pp. 235-239 ◽  
Author(s):  
Murray W. Lankester

Neurologic disease caused by the meningeal worm, Parelaphostrongylus tenuis (Dougherty 1945), is reported in moose of southeastern Manitoba, where the ranges of moose (Alces alces) and white-tailed deer (Odocoileus virginianus) overlap. Moose of this area are also infected commonly with the large American fiver fluke, Fascioloides magna (Bassi 1875). The moose cannot be considered a suitable host of F. magna since extensive liver damage results from infection, thick-walled cysts are formed, and mature flukes with eggs were not found in moose examined. Trematode eggs were found in liver sections of one animal but were not present in the faeces. It is suggested F. magna may be unable to persist in moose populations in the absence of a more suitable cervid host such as white-tailed deer.

2021 ◽  
Vol 57 (3) ◽  
Author(s):  
Amanda M. McGraw ◽  
Ron A. Moen ◽  
Louis Cornicelli ◽  
Michelle Carstensen ◽  
Véronique St-Louis

2005 ◽  
Vol 119 (3) ◽  
pp. 330 ◽  
Author(s):  
Norman W. S. Quinn

The history of White-tailed Deer, Odocoileus virginianus, Moose, Alces alces, and Beaver, Castor canadensis, in Algonquin Park since the 1860s is reviewed and placed in the context of changes to the forest, weather, and parasitic disease. Deer seem to have been abundant in the late 1800s and early 1900s whereas Moose were also common but less so than deer. Deer declined through the 1920s as Moose probably increased. Deer had recovered by the 1940s when Moose seem to have been scarce. The deer population declined again in the 1960s, suffered major mortality in the early 1970s, and has never recovered; deer are essentially absent from the present day Algonquin landscape in winter. Moose increased steadily following the decline of deer and have numbered around 3500 since the mid-1980s. Beaver were scarce in the Park in the late 1800s but recovered by 1910 and appear to have been abundant through the early 1900s and at high numbers through mid-century. The Beaver population has, however, declined sharply since the mid-1970s. These changes can best be explained by the history of change to the structure and composition of the Park's forests. After extensive fire and logging in the late 1800s and early 1900s, the forest is now in an essentially mature state. Weather and parasitic disease, however, have also played a role. These three species form the prey base of Algonquin's Wolves, Canis lycaon, and the net decline of prey, especially deer, has important implications for the future of wolves in the Park.


2002 ◽  
Vol 38 (4) ◽  
pp. 796-803 ◽  
Author(s):  
Oladele A. Ogunremi ◽  
Murray W. Lankester ◽  
Shaun J. Dergousoff ◽  
Alvin A. Gajadhar

1971 ◽  
Vol 49 (2) ◽  
pp. 159-166 ◽  
Author(s):  
Roy C. Anderson

In May, 1969, a small herd of reindeer (Rangifer tarandus tarandus) from Norway was placed in a recently enclosed area formerly inhabited by white-tailed deer (Odocoileus virginianus). The animals subsequently developed signs of neurologic disease. An analysis of clinical and pathologic findings, as well as a consideration of the history of the introduction, indicates the reindeer became infected in June with meningeal worm (Pneumostrongylus tenuis Dougherty, 1945) harbored by molluscs which had survived during the winter in the enclosure.


2012 ◽  
Vol 19 (7) ◽  
pp. 1019-1026 ◽  
Author(s):  
S. R. Purdy ◽  
L. F. Gagliardo ◽  
S. Lefman ◽  
P. J. S. Hamel ◽  
S. Ku ◽  
...  

ABSTRACTThe parasitic nematodeParelaphostrongylus tenuisis an important cause of neurologic disease of camelids in central and eastern North America. The aim of this study was to determine whether alpacas develop resistance to disease caused byP. tenuisin response to a previous infection or a combination of controlled infection and immunization. Alpacas were immunized with a homogenate of third-stage larvae (L3) and simultaneously implanted subcutaneously with diffusion chambers containing 20 live L3. Sham-treated animals received adjuvant alone and empty chambers. The protocol was not effective in inducing resistance to oral challenge with 10 L3, and disease developed between 60 and 71 days following infection. Immediately following the onset of neurologic disease, affected animals were treated with a regimen of anthelmintic and anti-inflammatory drugs, and all recovered. One year later, a subset of alpacas from this experiment was challenged with 20 L3 and the results showed that prior infection induced resistance to disease. Primary and secondary infections induced production of conventional and heavy-chain IgGs that reacted with soluble antigens in L3 homogenates but did not consistently recognize a recombinant form of a parasite-derived aspartyl protease inhibitor. Thus, the latter antigen may not be a good candidate for serology-based diagnostic tests. Antibody responses to parasite antigens occurred in the absence of overt disease, demonstrating thatP. tenuisinfection can be subclinical in a host that has been considered to be highly susceptible to disease. The potential for immunoprophylaxis to be effective in preventing disease caused byP. tenuiswas supported by evidence of resistance to reinfection.


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