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How parasites hamper livestock growth.

Farmers and scientists have long known that livestock animals with parasites grow poorly and never reach their full growth potential. They are called runts or poor doers, and no matter how much they eat they remain undersized.

Although veterinarians and researchers have known for many years that parasites cause these problems, the underlying mechanisms by which infectious agents restrict growth are just beginning to be understood, say ARS scientists Ronald Fayer and Theodore H. Elsasser.

Historically, we have thought that large parasites such as tapeworms in the gut simply robbed the host animal of nutrients needed for normal growth. However, in many cases where animals grow poorly, the parasites or other organisms are too small and too few to directly consume enough food to affect the nutritional status of the host animal. Furthermore, some animals continue to grow poorly long after the parasite is gone.

"For these reasons, we figured parasites and other infectious agents had to be influencing their hosts in ways that we had not detected," says Fayer, a zoologist at the Zoonotic Diseases Laboratory in Beltsville, Maryland.

Recent studies on calves at ARS' Beltsville Agricultural Research Center have provided insight into the complexities of parasite infections as related to poor growth. "We now know that the immune system responds, in part, to invading organisms by producing chemical signals that modify host metabolism," says Elsasser, an endocrinologist with ARS' Ruminant Nutrition Laboratory, Beltsville, Maryland.

These immune response signals--small proteins called cytokines--manipulate the hormones that regulate feed intake, nutrient use, and ultimately, growth of the animals.

"Dairy and beef calves infected with a protozoan parasite called Sarcocystis run a fever, lose their appetite, and become emaciated. But even after they recover from an acute illness, some calves simply fail to grow normally," says Fayer.

Experiments designed to uncover why this is so were set up using three groups of calves.

A control group was made up of uninfected calves that were allowed to eat as much as they desired.

A second group consisted of Sarcocystis-infected calves that were also permitted to eat as much as they desired.

Uninfected calves formed the third group.

These calves were fed exactly the same amount of feed that the infected calves ate. This last group of "pair-fed" control calves was used to determine the effect of nutritional intake on growth, separate from other effects on the parasite.

The studies showed that uninfected calves with no feed restriction grew best and flourished, as expected. But uninfected calves fed just the amount of feed the infected calves received still grew at a near-normal rate, diminishing the possibility that reduction in the quantity of feed eaten by infected calves was the sole cause for poor growth.

In contrast, the infected calves grew to only half the size of the uninfected, unrestricted control animals.

Some Explanations Emerge

Before, during, and after acute infection with the parasite, the concentration of growth-regulating hormones in the blood was measured. "We found that the concentration of a hormone essential for growth--an insulin-like growth factor (IGF-I)--decreased at the same time that another hormone that blocks growth hormone secretion, somatostatin, increased," says Elsasser.

Furthermore, these hormone changes persisted in the infected calves even after the symptoms of infection were gone.

Other researchers have shown that symptoms such as fever, poor appetite, and emaciation in human patients with malaria or cancer are caused by a cytokine released by cells of the immune system.

This cytokine was called both cachectin, because it causes cachexia (emaciation), and tumor necrosis factor (TNF), because it attacks and kills some types of tumors.

Says Fayer, "When we noticed many of the same symptoms--as well as premature growth cessation in cattle infected with Sarcocystis--we decided to see if TNF played a role by affecting those growth-regulating hormones that we had found altered in the parasitized calves."

"Tumor necrosis factor is only one of many cytokines produced by white blood cells in response to infections," says Elsasser. "We found that white blood cells grown in culture tubes could be stimulated to produce and release TNF when Sarcocystis was added to the culture.

"Then we found that calves infected with Sarcocystis had an elevated concentration of TNF in their blood. This finding potentially linked the response of the immune system to an effect on the endocrine system. Soon it was clear to us and others that cells throughout the body had receptors where TNF and other cytokines could attach and influence the activities of those cells," says Fayer.

To clearly establish the link between Sarcocystis, TNF production, and changes in the growth-regulating hormones, the scientists injected healthy, parasite-free calves with bovine TNF, then measured the concentrations of hormones in the blood. They found that TNF could cause changes in growth-regulating hormones parallel to those they observed in parasitized calves.

Overall, it appeared that TNF could depress bone growth, muscle growth, feed intake, and pituitary hormone secretion.

The calves' immune and hormonal responses to parasitic infection may ultimately be a mechanism for self-preservation," says Fayer. In theory, the following sequence of events takes place: The body's immune system recognizes the parasite proteins as foreign, or not belonging in the body, and the white blood cells, the first line of the body's defense, responds by secreting TNF.

TNF attaches to cells throughout the body, stimulating some and depressing the activity of others, so that nutrients and energy can be used to fight infection while maintaining just the basic life support systems.

Since energy is derived by using stored fat, carbohydrate, and proteins in muscle, growth is suppressed to conserve both energy and nutrients.

Based on this theory and the newfound understanding--at least in part--of one of the underlying molecular mechanisms of communication between the immune and endocrine systems, Elsasser and Fayer think it may be possible to come up with ways to prevent permanent damage or to restore normal function and growth to those animals that have been infected by parasites.
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Author:Mazzola, Vince
Publication:Agricultural Research
Date:Apr 1, 1993
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