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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.

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.

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. /// Se evaluó en pollos la virulencia de 76 cepas de virus de influenza tipo A aisladas de aves acuáticas en los estados de Wisconsin, California, Dakota del Sur, Florida, Texas, Alabama y Nebraska. El desafío de los pollos se hizo por inoculación intravenosa de virus de primero, segundo o tercer pasaje en embrión. Cada una de las cepas fue evaluada separadamente en tres o cuatro pollos. Después de la inoculación, 18 de los 76 virus causaron la muerte de uno o más pollos. Las lesiones encontradas a la necropsia fueron similares en todos los pollos. En orden decreciente de presentación, las lesiones macroscópicas incluyeron: inflamación del riñón con acentuación de la configuración lobular, uratos en el saco pericárdico y uratos en la superficie del hígado. Las lesiones microscópicas presentes en los riñones fueron compatibles con gota visceral. La mortalidad se asoció con la inoculación de altas concentraciones de virus infeccioso. Estos resultados indican que dentro de los virus de influenza tipo A circulantes en las poblaciones de patos, se pueden encontrar cepas potencialmente patógenas para los pollos.

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).

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 shrinkage, 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.

Streptococcus zooepidemicus was isolated from the intestinal tract of an adult male bald eagle (Haliaeetus leucocephalus) found dead in Minnesota in 1974. /// Se aisló Streptococcus zooepidemicus del tracto intestinal de un águila adulta (Haliaeetus leucocephalus) que se encontró muerta en Minnesota en 1974.

Ethyl mercury p-toluene sulfonanilide (active ingredient of Ceresan M) at a dietary concentration of 30 parts per million (12.5 parts of mercury per million) was lethal to adult ring-necked pheasants. Egg production and survival of third-week embryos were sharply reduced when breeders were maintained on feed containing 10 parts of this compound per million (4.2 parts of mercury per million).

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 blow-files

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.