Author
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Gasbarre, Louis |
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Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 6/16/1997 Publication Date: N/A Citation: N/A Interpretive Summary: Infections by the medium brown stomach worm cost the American beef and dairy industries in excess of $2 billion per year. A main reason why this worm causes such losses is that cattle take a very long time to become immune to the parasite. A very important question is why do cattle become immune to some worm parasites very easily, but not to the brown stomach worm. Infections of cattle by the brown stomach worm strongly stimulate the bovine immune system, and the type of response resulting from the stimulation is a type that is usually considered to be the type that protects the animal from infection. Strangely, the response does not work efficiently for the stomach worm, indicating that either the stomach is not a good site for this type of response or that the parasite has found a way to evade the immune response. If the parasite evades the immune response by suppressing it, then the parasites may also interfere with immunity against other infectious organisms, or interfere with vaccinations of cattle. At this time there is speculation that this immunosuppression exists but much more work remains to be done. Definition of how the parasites interact with the immune system will be important in controlling worm infections, and may be important in the overall management of other infectious diseases of cattle. Technical Abstract: Protective immunity against Ostertagia ostertagi (OO) is weak and slow to arise. Responses that reduce egg output, or increase larval inhibition, are seen after brief exposure, but protection against reinfection is not evident until the animal's second year. Even older animals that have grazed for several seasons can show low numbers of OO in their abomasa. In spite of this weak immunity, infections with OO induce profound changes in the host immune system. There is an expansion of lymphocytes in both the local lymph nodes and mucosa of the stomach involving a decrease in T cells and an increase in B cells and GD-T cells. At the same time, the expression of mRNA's is increased for IL4 and G-interferon, and decreased for IL2. The weak protective immune responses are not due to a poor exposure to parasite antigens, or to the stomach being an immunoprivileged site. In fact, the responses elicited are thought to be the type necessary for protection. Several factors may account for this apparent contradiction: 1)the responses are suboptimal, 2)the abomasum cannot function efficiently as an effector organ, 3)OO actively evades the immune response, and 4) classic responses are not protective in this parasite system. Researchers have indicated that OO infections diminish the host's ability to respond to immunization. Inhibition of host immunity could significantly impair productivity in times of marginal nutritional status. To date, much of the data attesting to such parasite-mediated effects are anecdotal, or restricted to experimental studies, and much remains to be defined in this area. |
