Robert H. Poppenga

Common loon eggs as indicators of methylmercury availability in North America.

Increased anthropogenic mercury (Hg) deposition since pre-industrial times, and subsequent transformation of inorganic Hg to methylmercury (MeHg) in aquatic environments, has created areas in North America where Hg poses a relatively high risk to wildlife, especially long-lived, piscivorous species. From 1995 to 2001, we opportunistically collected 577 eggs abandoned by Common Loons from eight states. Egg-Hg concentrations ranged from 0.07 to 4.42 µg/g (ww) or 0.10 to 19.40 µg/g (dw). Mercury was higher in eastern than in western North America. Female blood-Hg concentrations strongly correlated with those of eggs from the same territory even though the mean intraclutch Hg difference was 25%. In New England, egg volume declined significantly as egg-Hg concentrations increased. Fertility was not related to egg-Hg concentrations. Based on existing literature and this studys findings, egg-Hg risk levels were established and applied to our US data set and an existing Canadian data set. Regionally, we found the greatest risk levels in northeastern North America. With few exceptions, loon eggs are suitable indicators of methylmercury availability on lakes with territorial pairs.

Comparison of Blood Values in Foraging, Nesting, and Stranded Loggerhead Turtles (Caretta Caretta) Along the Coast of Georgia, Usa

The health status of 83 loggerhead sea turtles (Caretta caretta; 39 foraging, 31 nesting, and 13 stranded turtles) was analyzed using physical examinations, hematology, plasma biochemistry, plasma protein electrophoresis, and toxicologic parameters. Significant differences were noted in a number of health parameters between turtles exhibiting each of these behaviors. On physical examinations, stranded turtles had the highest prevalence of heavy carapace epibiont loads, miscellaneous abnormalities, emaciation, and weakness. Differences in hematologic values included a lower packed cell volume, higher number of lymphocytes, and lower number of monocytes in stranded turtles; lower white blood cell counts in foraging turtles; and significant differences in total solid values among turtles exhibiting all behaviors with the lowest values in stranded turtles and the highest values in nesting turtles. Differences in plasma biochemistry values included the highest uric acid, creatine kinase, and CO2 values in stranded turtles; the highest glucose and potassium values in foraging turtles; and the highest cholesterol and triglyceride values, and lowest alanine aminotransferase, in nesting turtles. Differences in total protein, albumin, and globulin were found using plasma biochemistry values, with lowest values in stranded turtles and highest values in nesting females, whereas differences in blood urea nitrogen between turtles included the lowest values in nesting turtles and the highest in foraging turtles. Plasma organochlorine and polychlorinated biphenyl levels were below their limits of quantification in the 39 foraging, 11 nesting, and three stranded turtles tested. A statistically significant difference was noted in the level of whole blood mercury between the 23 foraging and 12 nesting turtles tested. There was no difference in arsenic or lead levels between turtles exhibiting any of the three behaviors. Although a few limitations exist with the present study and include unknown ambient temperatures, turtle handling times that varied from 15 min to 53 min per turtle, and the use of a different laboratory for processing complete blood counts and plasma biochemistries in stranded versus foraging and nesting turtles, we provide baseline blood values for two cohorts (foraging and nesting) of loggerhead sea turtles on the coast of Georgia. Additionally, we demonstrate significant differences in clinical findings and blood parameters between foraging, nesting, and stranded loggerhead turtles in the region.

Clenbuterol Ingestion Causing Prolonged Tachycardia, Hypokalemia, and Hypophosphatemia with Confirmation by Quantitative Levels

Background: Clenbuterol is a long acting beta2-adrenergic agonist used in the treatment of pulmonary disorders. Acute clenbuterol toxicity resembles that of other beta2-adrenergic agonists. Most previously reported cases of clenbuterol toxicity describe patients who ate livestock illicitly treated with clenbuterol. Case Report: We report a case of human clenbuterol toxicity confirmed and correlated with qualitative and quanitative serum clenbuterol assays. This poisoned patient, a 28-year-old woman, developed sustained sinus tachycardia at 140/min, hypokalemia (2.4 mEq/L, 2.4 mmol/L), hypophosphatemia (0.9 mg/dL, 0.29 mmol/L), and hypomagnesemia (1.52 mg/dL, 0.76 mmol/L) after ingesting a reportedly small quantity of clenbuterol. The patient received repeated doses of metoprolol to treat her cardiovascular stimulation and potassium chloride to treat her hypokalemia. She remained symptomatic for more than 20 hours after the ingestion. Analysis by enzyme-linked immunosorbent assay and liquid chromatography/mass spectrometry revealed a serum clenbuterol concentration of 2.93 mcg/L 3 hours after the ingestion and an undetectable serum concentration 20 hours after ingestion. It is noteworthy that at a serum concentration below the limit of detection by liquid chromatography/mass spectrometry, the patient remained symptomatic. Acute clenbuterol toxicity is rarely reported following illicit use in humans, and this is the first such case to provide confirmatory toxicological analysis.

Mortality of common loons in New England, 1987 to 2000.

Diagnostic findings are presented on 522 common loons (Gavia immer) found dead or moribund in New England (Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island, and Vermont, USA) between 1987 and 2000. Common loon numbers and range in New England have decreased from historic levels over the last century due to a number of proposed factors. Goals of this study were to identify and categorize causes of mortality and quantify natural versus anthropogenic causes. The majority of identifiable mortality in chicks was from intraspecific aggression (25%) and other causes of trauma (32%). Death in immature loons was primarily from fungal respiratory disease (20%) and trauma (18%). Causes of adult loon mortality differed significantly in breeding and wintering habitats. Wintering adults primarily died of trauma (17%) and infection (11%) and had significantly poorer body condition than breeding loons. In breeding adults, confirmed and suspected lead toxicosis from ingested fishing weights accounted for almost half of all mortality. Direct anthropogenic factors accounted for 52% of loon mortality in this study. Because of high carcass recovery rates, we believe these data are a good representation of loon mortality in New England. Results highlight the importance of human influences on conservation and management of the common loon in New England.

Lead poisoning and trace elements in common eiders Somateria mollissima from Finland

We collected carcasses of 52 common eider Somateria mollissima adults and ducklings and blood samples from 11 nesting eider hens in the Gulf of Finland near Helsinki in 1994, 1995 and 1996. Samples of liver tissue were analysed for arsenic, cadmium, chromium, copper, iron, lead, magnesium, manganese, mercury, molybdenum, selenium and zinc. Blood was analysed for lead, mercury and selenium. Most of the 21 adults examined at necropsy were emaciated with empty gizzards, and no ingested shotgun pellets or other metal were found in any of the birds. Three adult females had a combination of lesions and tissue lead residues characteristic of lead poisoning. Two of these birds had acid-fast intranuclear inclusion bodies in renal epithelial cells and high concentrations of lead (73.4 and 73.3 ppm; all liver residues reported on dry weight basis) in their livers. The third was emaciated with a liver lead concentration of 47.9 ppm. An adult male had a liver lead concentration of 81.7 ppm, which is consistent with severe clinical poisoning. Two other adults, one male and one female, had liver lead concentrations of 14.2 and 8.03 ppm, respectively. Lead concentrations in the blood of hens ranged from 0.11 to 0.63 ppm wet weight. Selenium residues of ≥60 ppm were found in the livers of five adult males. Selenium concentrations in the blood of hens ranged from 1.18 to 3.39 ppm wet weight. Arsenic concentrations of 27.5–38.5 ppm were detected in the livers of four adult females. Detectable concentrations of selenium, mercury and molybdenum were found more frequently in the livers of adult males arriving on the breeding grounds than in incubating females, while the reverse was true for arsenic, lead and chromium. Mean concentrations of selenium, copper and molybdenum were higher in the livers of arriving males than in the livers of incubating hens, but hens had greater concentrations of iron and magnesium. Concentrations of trace elements were lower in the livers of ducklings than in the livers of adults.

CLINICAL AND NECROPSY FINDINGS ASSOCIATED WITH INCREASED MORTALITY AMONG AMERICAN ALLIGATORS OF LAKE GRIFFIN, FLORIDA

From December, 1997, through November, 2000, 306 deaths were documented among adult and subadult American alligators (Alligator mississippiensis) of Lake Griffin, Florida (USA). Some live alligators were lethargic and unresponsive to approach. To determine the cause, we examined ten alligators captured from Lake Griffin between December 1997 and June 1999. Initially, four alligators, three of which were clinically unresponsive, were sacrificed for routine diagnostic necropsy. The other six Lake Griffin alligators, and five control alligators captured from Lake Woodruff National Wildlife Refuge, Florida, where mortality was negligible, were studied extensively by clinical neurologic examination, electromyography, hematology, serum chemical analyses, and blood culture, then sacrificed and necropsied. Samples of brain, spinal cord, peripheral nerves, skeletal muscle, and major internal organs were examined by light microscopy for abnormalities. Samples of nervous tissue also were examined by electron microscopy, and samples of various tissues were collected for toxicologic analyses. Clinical signs included swimming in circles, inability to submerge, lethargy, weakness, unresponsiveness, slow reflexes, dragging the dorsal surfaces of the hind feet, head tilt, and anisocoria. Lake Griffin alligators had significantly lower distal sciatic nerve conduction velocities than Lake Woodruff alligators, and the most severely affected alligators had the lowest velocities; but morphologic abnormalities in peripheral nerves were not evident in most cases. Three severely affected alligators had acute focal necrosis of the torus semicircularis in the midbrain, two had skeletal myofiber atrophy, another had diffuse nonsuppurative encephalomyelitis, and one mildly affected alligator had skeletal myodegeneration. The cause or causes have not yet been identified.

Winter Poisoning of Coyotes and Raptors with Furadan-Laced Carcass Baits

Three bald eagles (Haliaeetus leucocephalus), a red-tailed hawk (Buteo jatnaicensis), and two coyotes (Canis latrans) found in a field in north-central Kansas (USA) in December 1992 were poisoned by flowable carbofuran (Furadan® 4F) placed on sheep (Ovis aries) carcasses to kill coyotes. The carbofuran was placed on the carcasses in October 1992, but the coyotes and raptors apparently were killed in late December. Thus, flowable Furadan® can cause direct and secondary deaths of wildlife under some circumstances for at least 60 days following placement.

AVIAN VACUOLAR MYELINOPATHY OUTBREAKS AT A SOUTHEASTERN RESERVOIR

Avian vacuolar myelinopathy (AVM) is a neurologic disease of unknown etiology that affects bald eagles (Haliaeetus leucocephalus), American coots (Fulica americana), and several species of waterfowl. An unidentified neurotoxin is suspected as the cause of AVM, which has been documented at several reservoirs in the southeastern United States. We conducted diagnostic and epidemiologic studies annually during October–March from 1998–2004 at Clarks Hill/Strom Thurmond Lake on the Georgia/South Carolina border to better understand the disease. Avian vacuolar myelinopathy was confirmed or suspected as the cause of morbidity and mortality of 28 bald eagles, 16 Canada geese (Branta canadensis), six American coots, two great-horned owls (Bubo virginianus), and one killdeer (Charadrius vociferus). Active surveillance during the outbreaks yielded annual average prevalence of vacuolar lesions in 17–94% of coots, but not in 10 beavers (Castor canadensis), four raccoons (Procyon lotor), and one gray fox (Urocyon cinereoargenteus) collected for the study. Brain lesions were not apparent in 30 Canada geese collected and examined in June 2002. The outbreaks at this location from 1998–2004 represent the most significant AVM-related bald eagle mortality since the Arkansas epornitics of 1994–95 and 1996–97, as well as the first confirmation of the disease in members of Strigiformes and Charadriiformes.

Zinc Phosphide Intoxication of Wild Turkeys (Meleagris gallopavo)

Zinc phosphide (Zn3P2) is a rodenticide used to control a variety of small mammal species. It is available over-the-counter or as a restricted-use pesticide depending on how it is to be applied. The toxicity of Zn3P2 is dependent on the species exposed, whether the animal is able to vomit or not, and whether it is ingested on a full or empty stomach. Nontarget species can be exposed through inadvertent or intentional product misapplication. In this article we describe four mortality events in which wild turkeys (Meleagris gallopavo) were believed to have been intoxicated following the ingestion of baits containing Zn3P2.

PHARMACOKINETICS OF ORALLY ADMINISTERED TERBINAFINE IN AFRICAN PENGUINS (SPHENISCUS DEMERSUS) FOR POTENTIAL TREATMENT OF ASPERGILLOSIS

Abstract The objective of this study was to determine the pharmacokinetic parameters of orally administered terbinafine hydrochloride based on 3, 7, and 15 mg/kg single- as well as multiple-dosage trials in order to calculate dosing requirements for potential treatment of aspergillosis in African penguins (Spheniscus demersus). Ten adult African penguins were used in each of these trials, with a 2-wk washout period between trials. Mean plasma concentrations of terbinafine peaked in approximately 4 hrs at 0.11 ± 0.017 µg/ml (mean ± SD) following administration of 3 mg/kg terbinafine, while 7 mg/kg and 15 mg/kg dosages resulted in peak plasma concentrations of 0.37 ± 0.105 and 0.33 ± 0.054 µg/ml, respectively. The volume of distribution increased with increasing dosages, being 37 ± 28.5, 40 ± 28.1, and 52 ± 18.6 mg/L for 3, 7, and 15 mg/kg doses, respectively. The mean half-life was biphasic with initial terminal half-life (t½) values of 9.9 ± 4.5, 17.2 ± 4.9 and 16.9 ± 5.4 hrs, for 3, 7, and 15 mg/kg doses, respectively. A rapid first elimination phase was followed by a slower second phase, and final elimination was estimated to be 136 ± 9.7 and 131 ± 9.9 hrs, for 7 and 15 mg/kg doses, respectively. Linearity was demonstrated for area under the curve but not for peak plasma concentrations for the three dosages used. Calculations based on pharmacokinetic parameter values indicate that a 15 mg/kg terbinafine q24h dosage regimen would result in steady-state trough plasma concentrations above the minimum inhibitory concentration (0.8–1.6 µg/ml), and this dosage is recommended as a potential treatment option for aspergillosis in penguins. However, additional research is required to determine both treatment efficacy and safety.