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Biomedical subjects

L Sileo

Publications and source records attributed to L Sileo.

At least 37 records · Page 2Linked to original sources
PubMed1987

Embryotoxicity, teratogenicity, and aryl hydrocarbon hydroxylase activity in Forster's terns on Green Bay, Lake Michigan.

Known reproductive problems, including congenital malformations and poor hatching success, exist for the state endangered Forster's tern (Sterna forsteri) in Green Bay, Wisconsin. Twenty Forster's tern eggs were collected from separate nests at a natural colony with documented reproductive problems, situated at Green Bay, Lake Michigan, and an inland colony at Lake Poygan (control) where reproduction was documented as normal. Eggs from the two locations were placed in the same laboratory incubator and candled throughout incubation. Hatching success of Green Bay eggs was 52% of that for controls. Several early embryonic deaths occurred, but most mortality occurred close to the time of hatching. Liver microsomal aryl hydrocarbon hydroxylase activity was elevated approximately threefold in Green Bay hatchlings compared to controls. Green Bay terns that hatched weighed less than controls, had an increased liver to body weight ratio, and had a shorter femur length. Two Green Bay embryos that failed to hatch had anomalies, one with a crossed beak and one with poor ossification of the foot. One Green Bay hatchling had an abnormally ossified ilium. These effects were observed in eggs where there were measureable levels of aryl hydrocarbon hydroxylase inducers including polychlorinated biphenyls and polychlorinated dibenzo-p-dioxins.

Animals↗
PubMed1987

Paint chip poisoning of Laysan albatross at Midway Atoll.

Epizootic mortality occurred in Laysan albatross (Diomedea immutabilis) fledgings at Midway Atoll in 1983. Heavy metal toxicity from ingestion of weathered paint chips was one of the causes. Sick albatrosses were unable to retract their wings, causing a "droop-wing" appearance. Five normal and 12 droop-winged fledglings were captured, killed, and examined. Paint chips found in the proventriculus of the affected fledglings contained up to 144,000 ppm lead. Blood, liver, and kidney concentrations of lead in affected birds were higher than in normal fledglings, and acid-fast intranuclear inclusion bodies were present in the kidneys. Degenerative lesions were present in the myelin of some brachial nerves. Weathered paint samples collected from 12 buildings contained up to 247,250 ppm lead and 101 ppm mercury. Lead poisoning was diagnosed in 10 of the droop-winged albatrosses and was one of the causes of morbidity. Mercury toxicosis and plastic impaction were other possible causes.

Animals↗
PubMed1986

Inclusion body disease of cranes: comparison of pathologic findings in cranes with acquired versus experimentally induced disease.

Inclusion body disease of cranes was the cause of death in 17 immature and mature cranes of 5 different species in Wisconsin. A herpesvirus of unknown origin was the apparent cause. An isolate of this herpesvirus was used to experimentally infect 3 species of cranes. Macroscopic and microscopic lesions associated with naturally acquired and experimentally induced disease were essentially identical. Multifocal hepatic and splenic necrosis was found in all cranes evaluated. Necrosis of the gastrointestinal tract, thymus, and bursa of Fabricius also was seen in some of the cranes. Eosinophilic intranuclear inclusion bodies often were commonly associated with hepatic lesions, sometimes with the splenic lesions, and rarely with the thymic or gastrointestinal tract lesions. The lesions of this inclusion body disease were similar to those reported for cranes in Austria from which a crane herpesvirus was isolated.

Animals↗
PubMed1985

Heavy metals in white-tailed deer living near a zinc smelter in Pennsylvania.

White-tailed deer (Odocoileus virginianus (Zimmermann) shot within 20 km of the zinc smelters in the Palmerton, Pennsylvania area contained extremely high renal concentrations of cadmium (372 ppm dry weight (dw] and zinc (600 ppm dw). The deer with the highest renal zinc concentration was shot 4 km from the smelters and had joint lesions similar to those seen in zinc-poisoned horses from the same area. The highest concentrations of lead in both hard and soft tissues were relatively low, 10.9 ppm dw in a sample of teeth, 17.4 ppm dw in a metacarpus, and 4.9 ppm dw in a kidney.

Age Factors↗
PubMed1984

Subchronic organophosphorus ester-induced delayed neurotoxicity in mallards.

Eighteen-week-old mallard hens received 0, 10, 30, 90, or 270 ppm technical grade EPN (phenylphosphonothioic acid O-ethyl-O-4-nitrophenyl ester) in the diet for 90 days. Ataxia was first observed in the 270-ppm group after 16 days, in the 90-ppm group after 20 days, in the 30-ppm group after 38 days; 10 ppm failed to produce ataxia. By the end of 90 days all 6 birds in the 270-ppm group exhibited ataxia or paralysis whereas 5 of 6 birds in the 90-ppm group and 2 of 6 birds in the 30-ppm group were visibly affected. Treatment with 30 ppm or more resulted in a significant reduction in body weight. Brain neurotoxic esterase activity was inhibited by averages of 16, 69, 73, and 74% in the 10-, 30-, 90-, and 270-ppm groups, respectively. Brain acetylcholinesterase, plasma cholinesterase, and plasma alkaline phosphatase were significantly inhibited as well. Distinct histopathological effects were seen in the 30-, 90-, and 270-ppm groups which included demyelination and degeneration of axons of the spinal cord. Additional ducks were exposed in a similar manner to 60-, 270-, or 540-ppm leptophos (phosphonothioic acid O-4-bromo-2,5-dichlorophenyl-O-methylphenyl ester) which resulted in similar behavioral, biochemical, and histopathological alterations. These findings indicate that adult mallards are probably somewhat less sensitive than chickens to subchronic dietary exposure to organophosphorus insecticides that induce delayed neurotoxicity.

Acetylcholinesterase↗
PubMed1984

Neurotoxic and teratogenic effects of an organophosphorus insecticide (phenyl phosphonothioic acid-O-ethyl-O-[4-nitrophenyl] ester) on mallard development.

Phenyl phosphonothioic acid-O-ethyl-O-[4-nitrophenyl] ester (EPN) is one of the 10 most frequently used organophosphorus insecticides and causes delayed neurotoxicity in adult chickens and mallards. Small amounts of organophosphorus insecticides placed on birds' eggs are embryotoxic and teratogenic. For this reason, the effects of topical egg application on EPN were examined on mallard (Anas platyrhynchos) embryo development. Mallard eggs were treated topically at 72 hr of incubation with 25 microliter of a nontoxic oil vehicle or with EPN in the vehicle at concentrations of approximately 12, 36, or 108 micrograms/g egg, equivalent to one, three, and nine times the agricultural level of application used to spray crops. Treatment with EPN resulted in 22 to 44% mortality over this dose range by 18 days of development compared with 4 and 5% for untreated and vehicle-treated controls. EPN impaired embryonic growth and was highly teratogenic: 37-42% of the surviving embryos at 18 days were abnormal with cervical and axial scoliosis as well as severe edema. Brain weights were significantly lower in EPN-treated groups at different stages of development including hatchlings. Brain neurotoxic esterase (NTE) activity was inhibited by as much as 91% at 11 days, 81% at 18 days, and 79% in hatchlings. Examination of brain NTE activity during the course of normal development revealed an increase of nearly sixfold from Day 11 through hatching. The most rapid increase occurred between Day 20 and hatching. Brain acetylcholinesterase (AChE) activity was inhibited by as much as 41% at 11 days, 47% at 18 days, and 20% in hatchlings. Plasma cholinesterase and alkaline phosphatase activities were inhibited and plasma aspartate aminotransferase activity was increased at one or more stages of development. Hatchlings from EPN-treated eggs were weaker and slower to right themselves. Histopathological examination did not reveal demyelination and axonopathy of the spinal cord that was characteristic of delayed neurotoxicity in adult birds.

Animals↗
PubMed1983

Effects of dietary cadmium on mallard ducklings.

Mallard (Anas platyrhynchos) ducklings were fed cadmium in the diet at 0, 5, 10, or 20 ppm from 1 day of age until 12 weeks of age. At 4-week intervals six males and six females from each dietary group were randomly selected, bled by jugular venipuncture, and necropsied. Significant decreases in packed cell volume (PCV) and hemoglobin (Hb) concentration and a significant increase in serum glutamic pyruvic transaminase (GPT) were found at 8 weeks of age in ducklings fed 20 ppm cadmium. Mild to severe kidney lesions were evident in ducklings fed 20 ppm cadmium for 12 weeks. No other blood chemistry measurement, hematological parameter, or tissue histopathological measurement indicated a reaction to cadmium ingestion. Body weight, liver weight, and the ratio of the femur weight to length were not affected by dietary cadmium. Femur cadmium concentration in all ducklings 12 weeks of age declined from the values detected at 4 and 8 weeks of age. Liver cadmium concentrations were significantly higher in relation to the increased dietary levels and in relation to the length of time the ducklings were fed the cadmium diets. At 12 weeks of age the cadmium concentration in liver tissue was twice that in the diet.

Age Factors↗
PubMed1983

Residues of petroleum hydrocarbons in tissues of sea turtles exposed to the Ixtoc I oil spill.

Sea turtles found dead when the Ixtoc I oil spill reached Texas waters were necropsied and tissues were analyzed for residues of petroleum hydrocarbons. Two of three turtles were in poor flesh, but had no apparent oil-caused lesions. There was evidence of oil in all tissues examined and indications that the exposure had been chronic. Comparisons with results of studies done on birds indicate consumption of 50,000 ppm or more of oil in the diet. Some possible mechanisms of mortality are suggested.

Animals↗
PubMed1983

Effects of chronic dietary lead in American kestrels (Falco sparverius).

American kestrels were fed a diet containing 0, 10, or 50 ppm lead (Pb) powder for at least 5 mo. Blood delta-aminolevulinic acid dehydratase (ALAD) activity in birds receiving 50 ppm Pb was as low as 20% of controls but no significant effects were noted in packed cell volume (PCV) or hemoglobin concentration (Hb). Mean liver Pb residues in birds fed 50 ppm Pb were 1.3 and 2.4 ppm (dry wt) for males and females, respectively. Liver Pb residues in birds fed 10 ppm Pb were not significantly greater than controls. There was no significant correlation between blood ALAD activity and blood Pb concentration, no consistent histopathological lesions were noted, and body and organ weights were not affected.

Animals↗
PubMed1983

Hemorrhagic enteritis in captive American kestrels (Falco sparverius).

Hemorrhagic enteritis and hepatitis of suspected adenovirus etiology were the apparent cause of death of nine captive American kestrels. Cloacal hemorrhage was the only prominent gross lesion: disseminated hepatocellular necrosis, and intranuclear inclusion bodies were evident microscopically. Electron microscopy revealed numerous adenovirus-like particles associated with the hepatic lesions. Attempts to serologically identify the agent were unsuccessful.

Animals↗
PubMed1982

Oviposition and the plasma concentrations of LH, progesterone and corticosterone in bobwhite quail (Colinus virginianus) fed parathion.

Bobwhite quail were fed concentrations of parathion (0,50, 100, 200 or 400 p.p.m.) for 10 days. Food intake, body weight change, brain acetylcholinesterase activity, egg production, and ovary weight were reduced in a dose-dependent manner. In a second experiment, birds were fed 0, 25 or 100 p.p.m. parathion or pair-fed control food to equate consumption in the 100 p.p.m. group. Egg production was not affected in birds fed 25 p.p.m. or in the pair-fed group, but the daily time of oviposition was more variable than in the control group. Cessation of egg production, inhibition of follicular development, and reduced plasma LH concentration were observed in birds fed 100 p.p.m. parathion. These findings indicate that exposure to parathion can impair reproduction, possibly by altering gonadotrophin secretion.

Acetylcholinesterase↗
PubMed1981

Iatrogenic salt poisoning in captive sandhill cranes.

Salt poisoning developed in captive sandhill cranes (Grus canadensis) when sea salt was added to normal drinking water to produce a sodium chloride concentration of 1%. Two of 18 cranes died and 2 were euthanatized when moribund. Muscle weakness, paresis, dyspnea, and depression were observed. Brain and serum sodium, serum uric acid, and plasma osmolality values were abnormally high. Lesions were those of visceral gout, renal tubular necrosis, nephrosis, and skeletal muscle necrosis.

Animals↗
PubMed1979

Mycobacteriosis in the lesser flamingos of Lake Nakuru, Kenya.

In 1974, 51 debilitated lesser flamingos (Phoeniconaias minor) were easily captured at Lake Nakuru, Kenya. Nineteen (37%) of these had extensive mycobacterial lesions. Two years later it was difficult to locate any debilitated flamingos and no evidence of mycobacterial infection was found. Possible reasons for the high prevalence of mycobacteriosis in the 1974 collection are discussed.

Animals↗
PubMed1977

Isolation of a hemolytic Actinobacillus from waterfowl.

A previously undescribed species of hemolytic Actinobacillus was isolated from six waterfowl, three with periocular serous exudation and two with airsacculitis and bronchopneumonia. Cultural and biochemical characteristics were compared with those of Actinobacillus and Pasteurella spp, using a numerical technique.

Actinobacillus↗
PubMed1977

Organochlorine poisoning of ring-billed gulls in southern Ontario.

Clinical, necropsy, bacteriologic, parasitologic, histopathologic, toxicologic and animal inoculation studies suggest that organochlorine (PBC, dieldrin and DDE) poisoning was an important factor in causing deaths of free-flying ring-billed gulls (Larus delawarensis) in southern Ontario in 1969 and 1973. The brains of gulls dying with clinical signs of neurologic involvement, and dead gulls with no other apparent cause of death, contained organochlorine residues of significantly greater levels than those found in healthy gulls shot for comparison.

Animals↗