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J. Larry Ludke

Publications and source records attributed to J. Larry Ludke.

14 recordsLinked to original sources
USGS2002

Invasive plant species: Inventory, mapping, and monitoring - A national strategy

America is under siege by invasive species of plants and animals, and by diseases. The current environmental, economic, and health-related costs of invasive species could exceed $138 billion per year-more than all other natural disasters combined. Notorious examples include West Nile virus, Dutch elm disease, chestnut blight, and purple loose- strife in the Northeast; kudzu, Brazilian peppertree, water hyacinth, nutria, and fire ants in the Southeast; zebra mussels, leafy spurge, and Asian long-horn beetles in the Midwest; salt cedar, Russian olive, and Africanized bees in the Southwest; yellow star thistle, European wild oats, oak wilt disease, Asian clams, and white pine blister rust in California; cheatgrass, various knapweeds, and thistles in the Great Basin; whirling disease of salmonids in the Northwest; hundreds of invasive species from microbes to mammals in Hawaii; and the brown tree snake in Guam. Thousands of species from other countries are introduced intentionally or accidentally into the United States each year. Based on past experience, 10-15 percent can be expected to establish free-living populations and about 1 percent can be expected to cause significant impacts to ecosystems, native species, economic productivity, and (or) human health.

Information and Technology Report↗
USGS1979

Bone development in black ducks as affected by dietary toxaphene

Black ducks, Anas rubripes, were exposed to dietary toxaphene concentrations of 0, 10, or 50 μg/g of food for 90 days prior to laying and through the reproductive season. Toxaphene did not affect reproduction or survival, but reduced growth and impaired backbone development in ducklings. Collagen, the organic matrix of bone, was decreased significantly in cervical vertebrae of ducklings fed 50 μg/g, and calcium conentrations increased in vertebrae of ducklings fed 10 or 50 μg/g. The effects of toxaphene were observed only in female ducklings. In contrast to effects on vertebrae, toxaphene exposure did not alter tibia development. Toxaphene residues in carcasses of these ducklings averaged slightly less than the dietary levels.

Pesticide Biochemistry and Physiology↗
USGS1978

Studies on combined effects of organophosphates or carbamates and morsodren in birds. II. Plasma and cholinesterase in quail fed morsodren and orally dosed with parathion or carbofuran

The degree of interaction between mercury and cholinesterase inhibiting pesticides was determined by comparing enzyme responses to sublethal dosages of parathion or carbofuran in quail fed 0.05, 0.5, or 5.0 ppm morsodren for 18 weeks. A statistically significant interaction was defined as greater brain cholinesterase inhibition in morsodren-fed than in clean-fed birds following pesticide dosage. The tissue residues of mercury that accumulated before significant mercury-parathion interactions occurred were higher than levels that might be expected in natural populations, but significant mercury-carbofuran interactions occurred in birds that had only accumulated 1.0 ppm liver mercury. The results indicate that indiscriminate usage of cholinesterase inhibiting pesticides are dangerous, since natural populations of fish-eating birds oftentimes contain this magnitude of mercury.

Bulletin of Environmental Contamination and Toxico↗
USGS1977

DDE increased the toxicity of parathion to coturnix quail

Adult male Japanese quail (Coturnix coturnix) were exposed to DDE or chlordane in the diet and subsequently dosed with parathion or paraoxon. Pretreatment with 5 or 50 ppm DDE in the diet for 12 weeks resulted in increased cholinesterase (ChE) activity in plasma, but not in the brain. Dietary concentrations of 5 and 50 ppm DDE caused increased susceptibility of quail that were challenged with parathion or paraoxon. The increased mortality resulting from DDE pretreatment was reflected in brain ChE inhibition. The synergistic action of DDE was apparent after 3 days of exposure to 50 ppm DDE and 1 week of exposure to 5 ppm DDE. Birds exposed for 3 weeks to 5 or 50 ppm DDE retained their DDE-potentiated sensitivity to parathion after 2 weeks on clean diet. Chlordane pretreatment resulted in decreased susceptibility (antagonism) to parathion, but not to paraoxon dosage. Implications of differing responses in ChE and mortality among controls, DDE-, and chlordane-pretreated birds after parathion or paraoxon dosage are discussed.

Pesticide Biochemistry and Physiology↗
USGS1975

Studies on combined effects of organophosphates and heavy metals in birds. I. Plasma and brain cholinesterase in Coturnix quail fed methyl mercury and orally dosed with parathion

We found that mercury potentiated the toxicity and biochemical effects of parathion. Male Coturnix quail (Coturnix coturnix japonica) were fed a sublethal concentration of morsodren (4 ppm as methyl mercury) for 18 weeks. This resulted in an accumulation of 21.0 ppm of mercury in the liver and 8.4 ppm in the carcass. Birds fed clean feed and those fed morsodren-treated feed were orally dosed with 2, 4, 6, 8,and 10 mg/kg parathion, and their 48-h survival times compared. The computed LD50 was 5.86mg/kg in birds not fed morsodren and 4.24 in those fed the heavy metal. When challenged with a sublethal, oral dose of parathion (1.0 mg/kg), morsodren-fed birds exhibited significantly greater inhibition of plasma and brain cholinesterase activity than controls dosed with parathion. Brain cholinesterase activity was inhibited 41% in morsodren-fed birds and 26in clean-fed birds dosed with parathion, which suggested that the increase in parathion toxicity in the presence of morsodren was directly related to the inhibitation of brain cholinesterase.

Bulletin of Environmental Contamination and Toxico↗
USGS1975

Cholinesterase (ChE) response and related mortality among birds fed ChE inhibitors

Patterns of mortality and inhibition of brain and plasma ChE in birds treated with ChE inhibitors were studied in an attempt to determine the validity of using ChE activity as a monitoring and diagnostic technique. Analysis of brain ChE activity proved to be reliable for diagnosing and monitoring effects of selected ChE inhibitors in birds. Brain ChE inhibition exceeding 20% indicated exposure, and inhibition greater than 50% was sufficient for diagnosing cause of death. Individuals that died from dietary exposure to parathion or carbofuran had brain ChE activities below 55% of normal; although individuals could survive with brain ChE activity lower than 50%. Problems associated with collection, storage, and analysis of tissues for ChE activity are discussed.

Archives of Environmental Contamination and Toxico↗