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.

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 three 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 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 fifth 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.

Isolation of poxvirus from debilitating cutaneous lesions on four immature grackles (Quiscalus sp.).

Poxvirus was isolated from nodules on four immature grackles (Quiscalus sp.) collected in two residential areas of Victoria, Texas. All of the birds were emaciated and had nodules on the eyelids, bill, legs, toes, and areas of the skin on the wings, neck, and ventral abdomen. These pox nodules were extensive and probably interfered with both sight and flight. The preliminary diagnosis was confirmed by virus isolation, histopathology, and electron microscopy. Poxvirus was isolated on the chorioallantoic membrane of embryonated hen's eggs and in Muscovy duck embryo fibroblast cell culture. Phaenicia calliphoridae (blowfly) larvae were found in one of the pox nodules, raising the possibility of mechanical transmission of the virus by contaminated adult blowflies.

Kidney lesions associated with mortality in chickens inoculated with waterfowl influenza viruses.

Seventy-six type A influenza viruses recovered from waterfowl in Wisconsin, California, South Dakota, Florida, Texas, Alabama, and Nebraska were tested for virulence in chickens. The challenge to chickens was intravenous inoculation of first-, second-, or third-egg-passage virus. Each of the virus strains was tested separately in three or four chickens. Eighteen of the 76 viruses caused the death of one or more chickens following inoculation. Postmortem lesions were similar in all dead birds. In decreasing order of frequency, gross lesions included: swollen kidneys evident as accentuated lobular patterns, urates in the pericardial sac, and urates on the surface of the liver. Microscopic lesions present in kidneys were consistent with visceral gout. Mortality was associated with inoculations having higher concentrations of infectious virus. These results indicate that the influenza A viruses circulating in duck populations may include strains potentially pathogenic for chickens.

Lead poisoning in common loons (Gavia immer).

Two emaciated common loons (Gavia immer) were believed to have died of lead poisoning when fragments of fishing lines and lead sinkers were discovered in their stomachs. Later a third emaciated loon, which had only the remnants of fishing line in its stomach, was suspected of being a possible lead-poisoning victim when all other test results were negative. The liver lead levels in the first two loons were 20.6 ppm and 46.1 ppm (wet weight), and the level in the third was 38.52 ppm (wet weight). Thirteen common loons dying of other causes had liver lead levels of less than 1 ppm (wet weight).

Organochlorine residues and mortality of herons.

Since 1966, 72 herons found dead or moribund in the field have been analyzed for organochlorine chemicals. In addition, 36 herons were obtained through systematic collections, and carcasses were analyzed to determine sublethal exposure to organochlorines. Brains of birds found dead or moribund were analyzed to determine whether the birds had died of organochlorine poisoning. Residues of DDE were found most frequently (96 of 105 carcasses analyzed), PCBs were second (detected in 90 carcasses), and dieldrin and TDE (detected in 37 and 35 carcasses, respectively) were about equal as third and fourth most frequent. Endrin, mirex, toxaphene, and HCB were found least often (8, 9, 9, and 9 carcasses, respectively). At least one organochlorine was found in each carcass, except for six heron chicks found dead in a Maryland heronry. DDE and PCBs were present in highest concentrations; they exceeded 100 ppm in two birds each. Organochlorine concentrations were almost always higher in adult herons than in immature birds. All birds that had hazardous or lethal concentrations in the brain were adults, and most were great blue herons (Ardea herodias). Dieldrin was the chemical most often considered responsible for death. Herons died of suspected DDT and dieldrin poisoning years after the chemicals were banned in the United States. More than 20 percent of the herons found dead or moribund had lethal or hazardous concentrations of organochlorines in the brain.

Epizootic of coccidiosis in free-flying lesser scaup.

A coccidiosis epizootic has occurred in lesser scaup (Aythya affinis) at Bluestem Reservoir in eastern Nebraska during the spring in each of three recent years: 1976-1978. Losses peaked during the period from mid-March through April. As much as 29% of the peak population of scaup using the reservoir died. Necropsies of 72 of the nearly 1390 scaup that died revealed destruction and sloughing of the intestinal mucosa and associated hemorrhaging. Fibrinonecrotic cores were frequently found in the intestinal lumens. Scrapings from the intestinal mucosal contained massive numbers of oocysts of the coccidian Eimeria aythyae. This is the first report of recurrent epizootics of coccidiosis in freeflying waterfowl.

Organochlorine pesticide, PCB, and PBB residues and necropsy data for bald eagles from 29 states--1975-77.

During 1975-77, 168 bald eagles (Haliaeetus leucocephalus) found moribund or dead in 29 states were analyzed for organochlorine pesticides and polychlorinated biphenyls (PCBs); 32 specimens from 13 states were analyzed for polybrominated biphenyls (PBBs). PCBs were present in 166 bald eagle carcasses and DDE was found in 165. TDE and dieldrin were identified in 137 samples, trans-nonachlor in 118, and oxychlordane in 90. Brains of five eagles contained possible lethal levels of dieldrin, and two eagles possibly died of endrin poisoning. Nine eagle livers, analyzed because of suspected lead poisoning, contained high levels of lead. Twenty percent of the eagles died from shooting, the most common cause of death; this cause of death, however, has declined.

Residues of organochlorine pesticides and polychlorinated biphenyls and autopsy data for bald eagles, 1973-74.

Eighty-six bald eagles found sick or dead during 1973-74 in 24 States were analyzed for organochlorine compounds. DDE was detected in all caracasses; polychlorinated biphenyls (PCB's) were found in all but two. Seventy-five carcasses contained TDE and/or dieldrin. Four eagles had possibly lethal levels of dieldrin in the brain. Bald eagles continue to retain high residue levels of organochlorine pollutants. Illegal shooting remained the most common cause of death but accounted for a smaller percentage of the mortalities than in the two previous biennial collections.

Ruptured-yolk peritonitis and organochlorine residues in a royal tern.

Ruptured-yolk peritonitis was responsible for the death of a royal tern. Lodgment of eggs in the oviduct was probably due to reverse peristalsis brought about by breakage of the thin-shelled eggs and secondary bacterial infection. The thin shells were apparently not related to the low levels of DDE and other organochlorine pollutants found in tissues and egg contents.

Lead in tissues of mallard ducks dosed with two types of lead shot.

Mallard ducks (Anas platyrhynchos) were sacrificed one month after ingesting one number 4 all-lead shot or one number 4 lead-iron shot. Livers, kidneys, blood, wingbones, and eggs were analyzed for lead by atomic absorption. Necropsy of sacrificed ducks failed to reveal any of the tissue lesions usually associated with lead poisoning in waterfowl. Lead levels in ducks given all-lead shot averaged about twice those in ducks given lead-iron shot, reflecting the amount of lead in the two types of shot. Lead in the blood of ducks dosed with all-lead shot averaged 0.64 ppm, and 0.28 ppm in ducks given lead-iron shot. Lead residues in livers and kidneys of females given all-lead shot were significantly higher than in males. In both dosed groups, lead levels in wingbones of females were about 10 times those in males, and were significantly correlated with the number of eggs laid after dosage. Lead levels in contents and shells of eggs laid by hens dosed with all-lead shot were about twice those in eggs laid by hens dosed with lead-iron shot. Eggshells were found to best reflect levels of lead in the blood. Our results indicate that mallards maintained on a balanced diet and dosed with one lead shot may not accumulate extremely high lead levels in the liver and kidney. However, extremely high lead deposition may result in the bone of laying hens after ingesting sublethal amounts of lead shot as a result of mobilization of calcium from the bone during eggshell formation.

Sublethal effects of chronic lead ingestion in mallard ducks.

Mallard drakes (Anas platyrhynchos) fed 1, 5, or 25 ppm lead nitrate were bled and sacrificed at 3-wk intervals. No mortality occurred, and the pathologic lesions usually associated with lead poisoning were not found. Changes in hematocrit and hemoglobin concentration did not occur. After 3-wk ducks fed 25 ppm lead exhibited a 40% inhibition of blood delta-aminolevulinic acid dehydratase activity that persisted through 12 wk exposure. After 12 wk treatment similar enzyme inhibition was present in the ducks fed 5 ppm lead. At 3 wk there was a small accumulation of lead (less than 1 ppm) in the liver and kidneys of ducks fed 25ppm lead; no further increases occurred throughout the exposure. No significant accumulation of lead occurred the the tibiae or wing bones. Groups of ducks fed 5 and 25 ppm diets for 12 wk were placed on clean feed and examined through a 12 wk posttreatment period. After 3 wk on clean diet delta-aminolevulinic acid dehydratase activity and lead concentrations in the blood had returned to pretreatment levels. Even though lead concentrations in the blood, soft organs and bone were low, a highly significant negative correlation between blood lead and blood enzyme activity was obtained. This enzyme bioassay should provide a sensitive and precise estimate for monitoring lead in the blood for waterflow.

Brain lesions in mallard ducklings from parents fed methylmercury.

Methylmercury dicyandiamide was fed to mallard ducks at 3 ppm mercury. Mercury accumulated in the eggs to an average of 7.18 and 5.46 ppm on a wet-weight basis in 2 successive years. Mercury in the eggs is believed to have caused brain lesions in the hatched ducklings. Lesions included demyelination, neuron shrink-age, necrosis, and hemorrhage in the meninges overlying the cerebellum. Brains of dead ducklings contained an average of 6.17 and 5.19 ppm mercury on a wet-weight basis in 2 successive years.

Residues of organochlorine pesticides and polychlorinated biphenyls and autopsy data for bald eagles, 1971-72.

Thirty-seven bald eagles found sick or dead in 18 States during 1971-72 were analyzed for organochlorine pesticides and polychlorinated biphenyls (PCB's). DDE and PCB's were detected in all bald eagle carcasses; 30 carcasses contained DDD and 28 contained dieldrin. Four eagles contained possibly lethal levels of dieldrin and nine eagles had been poisoned by thallium. Autopsies revealed that illegal shooting was the most common cause of mortality. Since 1964 when data were first collected, 8 of the 17 eagles obtained from Maryland, Virginia, South Carolina, and Florida possibly died from dieldrin poisoning; all four specimens from Maryland and Virginia were from the Chesapeake Bay Tidewater area.