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L. Sileo

Publications and source records attributed to L. Sileo.

At least 19 recordsLinked to original sources
USGS2016

Zinc and lead poisoning in wild birds in the Tri-State Mining District (Oklahoma, Kansas, Missouri)

contaminated with Pb, Cd, and Zn from mining, milling and smelting. Metals have been dispersed heterogeneously throughout the District in the form of milled mine waste ('chat'), as flotation tailings and from smelters as aerial deposition or slag. This study was conducted to determine if the habitat has been contaminated to the extent that the assessment populations of wild birds are exposed to toxic concentrations of metals. American robins (Turdus migratorius), northern cardinals (Cardinalis cardinalis), and waterfowl had increased Pb tissue concentrations (p < 0.05) compared with Pb tissue concentrations from reference birds, and the exposure of songbirds to Pb was comparable with that of birds observed at other sites severely contaminated with Pb. Mean activities of the Pb-sensitive enzyme delta-aminolevulinic acid dehydratase (ALAD) were decreased by >50% in red blood cells in these birds (p < 0.05). Several birds had tissue concentrations of Pb that have been associated with impaired biological functions and external signs of poisoning. Cadmium was increased in kidneys of songbirds (p < 0.05), but no proximal tubule cell necrosis associated with Cd poisoning was observed. Zinc concentrations in liver and kidney of waterfowl were significantly higher (p < 0.05) than reference values. The increased environmental concentrations of Zn associated with mining in the District accounted for the pancreatitis previously observed in five waterfowl from the District. The District is the first site at which free-flying wild birds have been found to be suffering severe effects of Zn poisoning.

Kansas, Missouri, Oklahoma↗
USGS2007

Raptor mortality due to West Nile virus in the United States, 2002

West Nile virus (WNV) has affected many thousands of birds since it was first detected in North America in 1999, but the overall impact on wild bird populations is unknown. In mid-August 2002, wildlife rehabilitators and local wildlife officials from multiple states began reporting increasing numbers of sick and dying raptors, mostly red-tailed hawks ( Buteo jamaicensis ) and great horned owls ( Bubo virginianus) . Commonly reported clinical signs were nonspecific and included emaciation, lethargy, weakness, inability to perch, fly or stand, and nonresponse to danger. Raptor carcasses from 12 states were received, and diagnostic evaluation of 56 raptors implicated WNV infection in 40 (71%) of these cases. Histologically, nonsuppurative encephalitis and myocarditis were the salient lesions (79% and 61%, respectively). Other causes of death included lead poisoning, trauma, aspergillosis, and Salmonella spp. and Clostridium spp. infections. The reason(s) for the reported increase in raptor mortality due to WNV in 2002 compared with the previous WNV seasons is unclear, and a better understanding of the epizootiology and pathogenesis of the virus in raptor populations is needed.

Journal of Wildlife Diseases↗
USGS2004

Effects of lead-contaminated sediment and nutrition on mallard duckling brain growth and biochemistry

Day-old mallard (Anas platyryhnchos) ducklings received either a clean sediment (24%) supplemented control diet, Coeur d'Alene River Basin, Idaho (CDARB) sediment (3449 ug/g lead) supplemented diets at 12% or 24%, or a positive control diet (24% clean sediment with equivalent lead acetate to the 24% CDARB diet) for 6 weeks. The 12% CDARB diet resulted in a geometric mean concentration of 396 ppb (WW) brain lead with decreased brain protein and ATP concentrations but increased oxidized glutathione (GSSG) relative to the control diet. The 24% CDARB diet resulted in a concentration of 485 ppb brain lead with lower brain weight and ATP concentration than controls but higher concentrations of reduced glutathione (GSH) and calcium. Lead acetate accumulated twice as well as CDARB derived lead and resulted in histopathological lesions of the brain. With a combination of a suboptimal diet and 24% CDARB, brain lead concentration was higher (594 ppb) than with 24% CDARB in the standard diet, histopathological lesions became apparent and GSH was higher than suboptimal diet controls.

Idaho↗
USGS2004

Effects of lead-contaminated sediment and nutrition on mallard duckling brain growth and biochemistry

Day-old mallard ( Anas platyryhnchos ) ducklings received either a clean sediment (24%) supplemented control diet, Coeur d'Alene River Basin, Idaho (CDARB) sediment ( 3449 μg/g lead ) supplemented diets at 12% or 24%, or a positive control diet (24% clean sediment with equivalent lead acetate to the 24% CDARB diet) for 6 weeks. The 12% CDARB diet resulted in a geometric mean concentration of 396 ppb (WW) brain lead with decreased brain protein and ATP concentrations but increased oxidized glutathione (GSSG) relative to the control diet. The 24% CDARB diet resulted in a concentration of 485 ppb brain lead with lower brain weight and ATP concentration than controls but higher concentrations of reduced glutathione (GSH) and calcium. Lead acetate accumulated twice as well as CDARB derived lead and resulted in histopathological lesions of the brain. With a combination of a suboptimal diet and 24% CDARB, brain lead concentration was higher (594 ppb) than with 24% CDARB in the standard diet, histopathological lesions became apparent and GSH was higher than suboptimal diet controls.

Idaho↗
USGS2003

Toxicity of lead-contaminated sediment to mute swans

Most ecotoxicological risk assessments of wildlife emphasize contaminant exposure through ingestion of food and water. However, the role of incidental ingestion of sediment-bound contaminants has not been adequately appreciated in these assessments. This study evaluates the toxicological consequences of contamination of sediments with metals from hard-rock mining and smelting activities. Lead-contaminated sediments collected from the Coeur d'Alene River Basin in Idaho were combined with either a commercial avian maintenance diet or ground rice and fed to captive mute swans ( Cygnus olor ) for 6 weeks. Experimental treatments consisted of maintenance or rice diets containing 0, 12 (no rice group), or 24% highly contaminated (3,950 μg/g lead) sediment or 24% reference (9.7 μg/g lead) sediment. Although none of the swans died, the group fed a rice diet containing 24% lead-contaminated sediment were the most severely affected, experiencing a 24% decrease in mean body weight, including three birds that became emaciated. All birds in this treatment group had nephrosis; abnormally dark, viscous bile; and significant (p ≤ 0.05) reductions in hematocrit and hemoglobin concentrations compared to their pretreatment levels. This group also had the greatest mean concentrations of lead in blood (3.2 μg/g), brain (2.2 μg/g), and liver (8.5 μg/g). These birds had significant (α = 0.05) increases in mean plasma alanine aminotransferase activity, cholesterol, and uric acid concentrations and decreased plasma triglyceride concentrations compared to all other treatment groups. After 14 days of exposure, mean protoporphyrin concentrations increased substantially, and mean δ-aminolevulinic acid dehydratase activity decreased by more than 95% in all groups fed diets containing highly contaminated sediments. All swans fed diets that contained 24% lead-contaminated sediment had renal acid-fast intranuclear inclusion bodies, which are diagnostic of lead poisoning in waterfowl. Body weight and hematocrit and hemoglobin concentrations in swans on control (no sediment) and reference (uncontaminated) sediment diets remained unchanged. These data provide evidence that mute swans consuming environmentally relevant concentrations of Coeur d'Alene River Basin sediment developed severe sublethal lead poisoning. Furthermore, toxic effects were more pronounced when the birds were fed lead-contaminated sediment combined with rice, which closely resembles the diet of swans in the wild.

Archives of Environmental Contamination and Toxico↗
USGS2001

Lead poisoning of waterfowl by contaminated sediment in the Coeur D'Alene River

The Coeur d'Alene River basin in Idaho has been contaminated by mine tailings that have impaired the health of wildlife since the early 1900s. In other parts of the world, virtually all lead poisoning of waterfowl is caused by the ingestion of manmade lead artifacts, primarily spent lead shotshell pellets or, occasionally, fishing sinkers. However, in the Coeur d'Alene River basin in Idaho, nonartifactual lead poisoning was the ultimate cause of death of most of 219 (77%) of 285 waterfowl carcasses that had been found sick or dead from 1992 through 1997. The majority of these 219 waterfowl (172 tundra swans [Cygnus columbianus], 33 Canada geese [Branta canadensis], and 14 other species) were poisoned by ingesting river sediment that was contaminated with lead. The next most common cause of death (20 instances, 7%) was lead poisoning accompanied by ingested shotshell pellets. The remaining 46 waterfowl succumbed to trauma, infectious diseases (aspergillosis, avian cholera, tuberculosis), or miscellaneous problems, or the cause of death was not determined.

Idaho↗
USGS2000

Toxicity of Anacostia River, Washington, D.C., USA, sediment fed to mute swans (Cygnus olor)

Sediment ingestion is sometimes the principal route by which waterfowl are exposed to environmental contaminants, and at severely contaminated sites waterfowl have been killed by ingesting sediment. Mute swans ( Cygnus olor ) were fed a diet for 6 weeks with a high but environmentally realistic concentration (24%) of sediment from the moderately polluted Anacostia River in the District of Columbia, USA, to estimate the sediment's toxicity. Control swans were fed the same diet without the sediment. Five organochlorine compounds were detected in the treated diets, but none of 22 organochlorine compounds included in the analyses was detected in livers of the treated swans. The concentrations of 24 polynuclear aromatic hydrocarbons measured in the treated diet were as high as 0.80 mg/kg, and they were thought to have been responsible for the observed induction of hepatic microsomal monooxygenase activity in livers. A concentration of 85 mg/kg of lead in the diet was enough to decrease red blood cell ALAD activity but was not high enough to cause more serious effects of lead poisoning. The dietary concentrations of Al, Fe, V, and Ba were high compared to the concentrations of these elements known to be toxic in laboratory feeding studies. However, the lack of accumulation in the livers of the treated swans suggested that these elements were not readily available from the ingested sediment. We did not study all potential toxic effects, but, on the basis of those that we did consider, we concluded that the treated swans were basically healthy after a chronic exposure to the sediment.

District of Columbia↗
USGS2000

Field evaluation of lead effects on Canada geese and mallards in the Coeur d'Alene River Basin, Idaho

Hatch year (HY) mallards ( Anas platyrhynchos ) in the Coeur d'Alene (CDA) River Basin had higher concentrations of lead in their blood than HY Western Canada geese ( Branta canadensis moffitti ) (geometric means 0.98 versus 0.28 μg/g, wet weight). The pattern for adults of both species was similar, although geometric means (1.77 versus 0.41 μg/g) were higher than in HY birds. HY mallards captured in the CDA River Basin in 1987 contained significantly lower lead concentrations in their blood than in 1994–95 (0.36 versus 0.98 μg/g); however, some very young mallards were sampled in 1987, and concentrations in adults were not significantly different in 1987, 1994, or 1995 (1.52, 2.07, 1.55 μg/g, respectively). Both species in the CDA River Basin in 1994–95 showed significantly reduced red blood cell delta-aminolevulinic acid dehydratase (ALAD) activity compared to the reference areas: Canada geese (HY −65.4 to −86.0%, adults −82.3%), and mallards (HY −90.7 to −95.5%, adults −94.1%). Canada goose goslings were divided into size classes, and the two smaller classes from the CDA River Basin had significantly elevated free erythrocyte protoporphyrin (protoporphyrin) levels compared to the reference area (15.2× and 6.9×). HY and adult mallards both had significantly elevated protoporphyrin (5.9× and 7.5×). Recognizing that interspecific differences exist in response and sensitivity to lead, it appears (at least for hemoglobin and hematocrit) that Canada geese were more sensitive to lead than mallards, i.e ., adverse hematologic effects occur at lower blood lead concentrations. Only Canada geese from the CDA River Basin, in spite of lower blood lead concentrations, had significantly reduced mean hemoglobin and hematocrit values. No euthanized Canada geese (all HYs) from CDA River Basin were classified as clinically lead poisoned, but 38 Canada geese found dead in the CDA River Basin during a concurrent study succumbed to lead poisoning between 1992 and 1997. Only 6 (15.8%) of these 38 contained ingested lead shot, which contrasts greatly with the 75–94% incidence of ingested lead shot when mortality was due to lead shot ingestion. Lead from other contaminated sources ( i.e ., sediments and vegetation) in the CDA River Basin was strongly implicated in most Canada goose deaths. Based on the 31 live mallards and Canada geese collected in the CDA River Basin, which were representative of the live populations blood sampled only, the prevalence of subclinical and clinical lead poisoning (as determined by liver lead concentrations, excluding birds with ingested lead shot) was higher in mallards: subclinical (4 of 8, 50% HYs and 6 of 11, 55% adults); clinical (0% HYs and 4 of 11, 36% adults), with less data available for Canada geese (only 1 of 9, 11% HYs marginally subclinical). The clinically lead-poisoned mallards had extremely high concentrations of lead in blood (2.69–8.82 μg/g) and liver (6.39–17.89 μg/g). Eight mallards found dead in the CDA River Basin during a concurrent study were diagnosed as lead poisoned, and only one (12.5%) contained ingested lead shot, which again strongly implicates other lead sources. The finding of dead lead poisoned Canada geese together with the high percentage of live mallards classified as subclinically or clinically lead poisoned, in combination with the low incidence of ingested lead shot causes us concern for both of these species, which live in association with lead-contaminated sediment in the CDA River Basin.

Idaho↗
USGS2000

Developmental toxicity of lead-contaminated sediment to mallard ducklings

Sediment ingestion has been identified as an important exposure route for toxicants in waterfowl. The toxicity of lead-contaminated sediment from the Coeur d'Alene River Basin (CDARB) in Idaho was examined on posthatching development of mallard ( Anas platyrhynchos ) ducklings for 6 weeks. Day-old ducklings received either untreated control diet, clean sediment (24%) supplemented control diet, CDARB sediment (3,449 μg/g lead) supplemented diets at 12% or 24%, or a positive control diet containing lead acetate equivalent to that found in 24% CDARB. The 12% CDARB diet resulted in a geometric mean blood lead concentration of 1.41 ppm (WW) with over 90% depression of red blood cell ALAD activity and over threefold elevation of free erythrocyte protoporphyrin concentration. The 24% CDARB diet resulted in blood lead of 2.56 ppm with over sixfold elevation of protoporphyrin and lower brain weight. In this group the liver lead concentration was 7.92 ppm (WW), and there was a 40% increase in hepatic reduced glutathione concentration. The kidney lead concentration in this group was 7.97 ppm, and acid-fast inclusion bodies were present in the kidneys of four of nine ducklings. The lead acetate positive control group was more adversely affected in most respects than the 24% CDARB group. With a less optimal diet (mixture of two thirds corn and one third standard diet), CDARB sediment was more toxic; blood lead levels were higher, body growth and liver biochemistry (TBARS) were more affected, and prevalence of acid-fast inclusion bodies increased. Lead from CDARB sediment accumulated more readily in duckling blood and liver than reported in goslings, but at given concentrations was generally less toxic to ducklings. Many of these effects are similar to ones reported in wild mallards and geese within the CDARB.

Idaho↗
USGS1999

Toxicity of lead-contaminated sediment to mallards

Because consumption of lead-contaminated sediment has been suspected as the cause of waterfowl mortality in the Coeur d?Alene River basin in Idaho, we studied the bioavailability and toxicity of this sediment to mallards (Anas platyrhynchos). In experiment 1, one of 10 adult male mallards died when fed a pelleted commercial duck diet that contained 24% lead-contaminated sediment (with 3,400 &mu;g/g lead in the sediment). Protoporphyrin levels in the blood increased as the percentage of lead-contaminated sediment in the diet increased. Birds fed 24% lead-contaminated sediment exhibited atrophy of the breast muscles, green staining of the feathers around the vent, viscous bile, green staining of the gizzard lining, and renal tubular intranuclear inclusion bodies. Mallards fed 24% lead-contaminated sediment had means of 6.1 &mu;g/g of lead in the blood and 28 &mu;g/g in the liver (wet-weight basis) and 1,660 &mu;g/g in the feces (dry-weight basis). In experiment 2, we raised the dietary concentration of the lead-contaminated sediment to 48%, but only about 20% sediment was actually ingested due to food washing by the birds. Protoporphyrin levels were elevated in the lead-exposed birds, and all of the mallards fed 48% lead-contaminated sediment had renal tubular intranuclear inclusion bodies. The concentrations of lead in the liver were 9.1 &mu;g/g for mallards fed 24% lead-contaminated sediment and 16 &mu;g/g for mallards fed 48% lead-contaminated sediment. In experiment 3, four of five mallards died when fed a ground corn diet containing 24% lead-contaminated sediment (with 4,000 &mu;g/g lead in this sample of sediment), but none died when the 24% lead-contaminated sediment was mixed into a nutritionally balanced commercial duck diet; estimated actual ingestion rates for sediment were 14% and 17% for the corn and commercial diets. Lead exposure caused elevations in protoporphyrin, and four of the five mallards fed 24% lead-contaminated sediment in a commercial diet and all five fed the contaminated sediment in a corn diet had renal intranuclear inclusion bodies. Lead was higher in the livers of mallards fed 24% lead-contaminated sediment in the corn diet (38 &mu;g/g) than in the commercial diet (13 &mu;g/g).

Idaho↗
USGS1999

Persistence of high lead concentrations and associated effects in Tundra Swans captured near a mining and smelting complex in northern Idaho

Lead poisoning of waterfowl, particularly tundra swans ( Cygnus columbianus ), has been documented in the Coeur d'Alene River Basin in northern Idaho for nearly a century. Over 90% of the lead-poisoned tundra swans in this area that were necropsied have no ingested lead shot. Spent lead shot from hunting activities over the years is therefore a minor source of lead in these swans. The migrating swans accumulated lethal burdens of lead from ingestion of sediments and aquatic vegetation during a short stopover in the spring. The lead originated from mining and smelting activities. Lead concentrations and physiological characteristics of blood were compared in swans captured in swim-in traps, with moribund swans caught by hand in the lead-contaminated area in 1987 and 1994–1995 and with birds captured by night-lighting in reference areas in 1994–1995. Blood lead concentrations in swans were highest in moribund birds (3.3 μg g -1 in 1987 and 1995), intermediate in those trapped in the contaminated area (0.82 μg g -1 in 1987 and 1.8 μg g -1 in 1995), and lowest (0.11 μg g -1 ) in those trapped in the reference areas. δ-aminolevulinic acid dehydratase (ALAD) was significantly inhibited in swans from the contaminated area. Hematocrit and hemoglobin were significantly depressed only in moribund swans. Of the 19 swans found moribund and euthanized, 18 were classified as having lead toxicosis on the basis of lead levels in blood (1.3 to 9.6 μg g -1 ) and livers (6 to 40 μg g -1 ) and necropsy findings. The 19th swan had aspergillosis. There was no evidence that effects of lead on tundra swans had diminished from 1987 to 1995.

Idaho↗
USGS1999

Antibodies against Pasteurella multocida in snow geese in the western arctic

To determine if lesser snow geese (Chen caerulescens caerulescens) are a potential reservoir for the Pasteurella multocida bacterium that causes avian cholera, serum samples and/or pharyngeal swabs were collected from > 3,400 adult geese breeding on Wrangel Island (Russia) and Banks Island (Canada) during 1993-1996. Pharyngeal swab sampling rarely (> 0.1%) detected birds that were exposed to P. multocida in these populations. Geese with serum antibody levels indicating recent infection with P. multocida were found at both breeding colonies. Prevalence of seropositive birds was 3.5% at Wrangel Island, an area that has no recorded history of avian cholera epizootics. Prevalence of seropositive birds was 2.8% at Banks Island in 1994, but increased to 8.2% during 1995 and 1996 when an estimated 40,000-60,000 snow geese were infected. Approximately 50% of the infected birds died during the epizootic and a portion of the surviving birds may have become carriers of the disease. This pattern of prevalence indicated that enzootic levels of infection with P. multocida occurred at both breeding colonies. When no avian cholera epizootics occurred (Wrangel Island, Banks Island in 1994), female snow geese (4.7%) had higher antibody prevalence than males (2.0%).

Journal of Wildlife Diseases↗
USGS1998

Epizootic vacuolar myelinopathy of the central nervous system of bald eagles ( Haliaeetus leucocephalus ) and American coots ( Fulica americana )

Unprecedented mortality occurred in bald eagles ( Haliaeetus leucocephalus ) at DeGray Lake, Arkansas, during the winters of 1994-1995 and 1996-1997. The first eagles were found dead during November, soon after arrival from fall migration, and deaths continued into January during both episodes. In total, 29 eagles died at or near DeGray Lake in the winter of 1994-1995 and 26 died in the winter of 1996-1997; no eagle mortality was noted during the same months of the intervening winter or in the earlier history of the lake. During the mortality events, sick eagles were observed overflying perches or colliding with rock walls. Signs of incoordination and limb paresis were also observed in American coots ( Fulica americana ) during the episodes of eagle mortality, but mortality in coots was minimal. No consistent abnormalities were seen on gross necropsy of either species. No microscopic findings in organs other than the central nervous system (CNS) could explain the cause of death. By light microscopy, all 26 eagles examined and 62/77 (81%) coots had striking, diffuse, spongy degeneration of the white matter of the CNS. Vacuolation occurred in all myelinated CNS tissue, including the cerebellar folia and medulla oblongata, but was most prominent in the optic tectum. In the spinal cord, vacuoles were concentrated near the gray matter, and occasional swollen axons were seen. Vacuoles were uniformly present in optic nerves but were not evident in the retina or peripheral or autonomic nerves. Cellular inflammatory response to the lesion was distinctly lacking. Vacuoles were 8-50 microns in diameter and occurred individually, in clusters, or in rows. In sections stained by luxol fast blue/periodic acid-Schiff stain, the vacuoles were delimited and transected by myelin strands. Transmission electron microscopy revealed intramyelinic vacuoles formed in the myelin sheaths by splitting of one or more myelin lamellae at the intraperiodic line. This lesion is characteristic of toxicity from hexachlorophene, triethyltin, bromethalin, isonicotinic acid hydrazide, and certain exotic plant toxins; however, despite exhaustive testing, no etiology was determined for the DeGray Lake mortality events. This is the first report of vacuolar myelinopathy associated with spontaneous mortality in wild birds.

Arkansas↗
USGS1998

Retrospective study of the diagnostic criteria in a lead-poisoning survey of waterfowl

Between 1983 and 1986 the National Wildlife Health Center (NWHC) conducted a nationwide study of lead poisoning of waterfowl from federal and state refuges. This survey was done to assist in identifying zones with lead-poisoning problems. One thousand forty one moribund or dead waterfowl were collected and examined. The presence or absence of 13 gross lesions selected as indicators of lead poisoning and 3 lesions indicating body condition was recorded. Lead-poisoning diagnoses were based on the finding of at least 6 8 ppm (wet weight) lead in the liver and either lead shot in the gizzard content or at least one convincing gross lesion indicative of lead poisoning. Four hundred and twenty-one of these waterfowl were diagnosed as lead-poisoned. The NWHC survey provided a comprehensive basis for estimating the sensitivities, specificities, and likelihood ratios of the gross lesions of lead poisoning and the associated hepatic lead concentrations for several species of waterfowl. Some of the 13 defined gross lesions were more common than others; frequencies ranged from 3% to 80% in the 421 lead-poisoned waterfowl. The most reliable indicators of lead poisoning were impactions of the upper alimentary tract, submandibular edema, myocardial necrosis, and biliary discoloration of the liver. Each of the 13 lesions occurred more frequently in the lead-poisoned birds, but each of the lesions also occurred in waterfowl that died of other causes. The number of lead shot present in a bird?s gizzard was only weakly correlated with its hepatic lead concentration; however, this weak correlation may have been adequate to account for differences in hepatic lead concentrations among species, once the weights of the species were taken into account. Although lead-poisoned ducks tended to have higher hepatic mean lead concentrations than did lead-poisoned geese or swans, the differences were probably a result of a greater dose of shot per body weight than to kinetic differences between species. Hepatic lead concentrations were independent of age and sex. Ninety-five percent of waterfowl diagnosed as lead-poisoned had hepatic lead concentrations of at least 38 ppm, dry weight (10 ppm, wet weight). Fewer than 1% of the waterfowl that died of other causes had a concentration that high. This 5th percentile, of 38 ppm dry weight (10 ppm wet weight), is a defensible criterion for identifying lead-poisoned waterfowl when interpreting hepatic lead concentrations in the absence of pathological observations.

Archives of Environmental Contamination and Toxico↗
USGS1996

Reproductive success, developmental anomalies and environmental contaminants in double-crested cormorants (Phalacrocorax auritus)

To test an association between environmental contaminants and the prevalence of congenital anomalies in colonial waterbirds, we collected representative eggs for chemical analysis from double-crested cormorant nests at colonies in Lake Michigan, Wisconsin, USA, and Lake Winnipegosis, Manitoba, Canada, and periodically revisited the nests to determine the hatching success, survivorship of hatchlings, and number of deformed hatchlings in the remainder of each clutch. Total concentrations of polychlorinated biphenyls (PCBs) in eggs were determined by capillary gas chromatography. The combined activity of planar chlorinated hydrocarbons (PCHs) in the eggs was measured in an in vitro bioassay based on the induction of ethoxyresorufin- O -deethylase (EROD) activity in rat hepatoma cells. The combined EROD induction activity was expressed as 2,3,7,8–tetrachlorodibenzo- p -dioxin equivalents (TCDD-EQ). Total concentrations of PCBs and TCDD-EQ were seven to eight times greater in eggs from Lake Michigan (7.8 μg/g and 138 pg/g, respectively) than in those from Lake Winnipegosis (1.0 μg/g and 19 pg/g, respectively). The proportion of eggs hatching at the Lake Michigan colony (59%) was less ( p < 0.05) than at Lake Winnipegosis (70%), and the prevalence of hatchlings with deformed bills was greater ( p < 0.001) at Lake Michigan (0.79 vs. 0.06%). However, within the Lake Michigan colony, concentrations of PCBs and TCDD-EQ were not correlated with either hatching success or the occurrence of deformities in nestlings.

Manitoba, Wisconsin↗
USGS1996

Technique for implanting radio transmitters subcutaneously in day-old ducklings

We developed and evaluated a surgical procedure for implanting radio transmitters in 1-d-old Canvasback (Aythya valisineria) ducklings. Transmitters (1.5 g) were implanted subcutaneously on the back of ducklings while under a general anesthetic, isoflurane, within a few hours of hatching. Evaluations indicate that the procedure is a reliable method for radio-marking ducklings.

Journal of Field Ornithology↗
USGS1993

Diagnostic riddles

A bridled white-eye ( Zosterops conspicillata ) was captured in a mist net on the island of Saipan and transported to the island of Guam for an experimental study. Beginning on day three, it was immunosuppressed by intramuscular injections of dexamethasone. It was unexpectedly found dead on day 20, at which time it had lost 0.9 g (12.9% of initial body weight). Gross Pathology: Despite the weight loss, the white-eye was in good flesh, with abundant subcutaneous and visceral fat. The spleen was 3 x 11 mm, about 5 times normal size. The striatum of the forebrain was congested. There were no other lesions. Histopathology: There were microscopic abnormalities in skeletal muscle, brain, and gizzard (Figs. 1 and 2; Figure 2 is from a different white-eye which had virtually identical gizzard lesions).

Wildlife Disease Newsletter↗