Virginia Tech Magazine

Volume 17, Number 3
Spring 1995


New, safe bait kills cockroaches

A Virginia Tech researcher has developed a compound that not only wipes out cockroach populations and prevents re-infestation, but does it without the use of toxic chemicals. Heather Wren, a research scientist in the university's entomology department, has discovered a combination of environmentally friendly, natural substances that prevent cockroaches from reproducing. The bait mixture contains an inhibitor that interferes with the cockroach's metabolism of certain nutrients. Male cockroaches use up their life force as they breed, and the females' own bodies sabotage themselves as their eggs develop, so that the females die and the eggs are never laid. "In our tests, they prefer this compound over their regular diets," says Wren. The discovery is a breakthrough in "insect growth regulator" technology. Previous growth regulators were based on killing nymph cockroaches at the molt stage. The new approach is based on the insect's nutrition metabolism and is the only compound to kill adults. It also prevents cockroaches from developing resistance. The bait is not toxic. Initial research was sponsored by the Virginia Pesticide Control Board, which encouraged the development of alternatives to toxic pesticides. Additional research to bring a product closer to commercialization was co-funded by Virginia's Center for Innovative Technology (CIT) and Dominion BioSciences Inc. A U.S. patent is pending on the invention. A commercial product is expected by 1997.

Biting down on gum disease bacteria

We all know what causes gum disease--it's plaque, right? In reality, say University Distinguished Professors W.E.C. Moore and Lillian Moore, the answer is more likely bacteria. The husband and wife research team studied the vast array of bacteria found in the human mouth in an attempt to discover which ones are responsible for gingivitis. The Moores isolated 51,000 bacteria from gingival cervices of 300 people. They detected 509 different kinds of bacteria, with 368 appearing more than once. The diversity of bacterial species found in the mouth and the differences in human response to these bacteria are major reasons the specific cause of periodontal disease has been so hard to establish, the Moores say. In contrast to studies that concentrate only on people with advanced periodontal disease, the Moores' study examined healthy as well as diseased gums. They identified several species found in high numbers in diseased gum sites. Evidence points to F. nucleatum, an acid-producing species, as the most likely initial cause of periodontal irritation. This inflammation induces secretion of blood and fluids that stimulates the growth of other species. Learning how to inhibit the growth of this "trigger" bacteria, W.E.C. Moore says, could be a key to preventing periodontal disease.

Targeting Parkinson's disease

Virginia Tech professor Neal Castagnoli predicts that, as the average age of Americans grows older, the number afflicted with Parkinson's disease will grow. The Harvey W. Peters Professor of Chemistry has been working since 1985 to understand and combat the debilitating illness. When the brain develops certain lesions, Parkinson's is the result. The disease, which afflicts more than a million Americans, causes resting tremors and is often associated with dementia similar to that caused by Alzheimer's disease. Castagnoli and his associates at the on-campus Harvey Peters Research Center for the Study of Parkinson's Disease and Disorders of the Central Nervous System are collaborating with researchers around the world investigating the biochemical processes that cause these lesions. In some people, the lesions seem to occurr spontaneously with age; others result when internal chemicals are activated by body enzymes. The researchers have identified these lesion-causing chemicals and are using them to characterize the loss of neurons leading to lesions. The work so far is promising, and Castagnoli hopes it soon will lead to the design of pro-drugs, which would remain latent in the body until activated by the same enzymes that stimulate formation of lesions. These drugs would prevent the lesions from forming in targeted areas.

Virginia Tech Magazine Volume 17, Number 3 Spring 1995