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.

Winter mortality of common loons in Florida coastal waters.

Diagnostic findings are presented for 434 common loons (Gavia immer) found sick or dead on Florida beaches from 1970 through 1994, primarily during the months of December to April. The most commonly recognized problem was an emaciation syndrome (66%), followed by oiling (18%), aspergillosis (7%), trauma (5%) and miscellaneous disease entities (1%). The cause-of-death for 3% of the birds was not determined. Many of the carcasses examined (n = 173) were obtained during an epizootic which occurred from January to March of 1983 in which more than 13,000 loons were estimated to have died. An emaciation syndrome, characterized by severe atrophy of pectoral muscles, loss of body fat and hemorrhagic enteritis, was the primary finding in this epizootic. It was postulated to have a complex etiologic basis involving synergistic effects and energy costs of migration, molting and replacement of flight feathers, food resource changes, salt-loading, intestinal parasitism, environmental contaminants, and inclement weather.

Winter poisoning of coyotes and raptors with Furadan-laced carcass baits.

Three bald eagles (Haliaeetus leucocephalus), a red-tailed hawk (Buteo jamaicensis), 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.

Suspected fusariomycotoxicosis in sandhill cranes (Grus canadensis): clinical and pathological findings.

In 1985 and 1986, large-scale natural die-offs of sandhill cranes in Texas were attributed to fusariomycotoxicosis. These birds demonstrated a progressive loss of motor control to the neck, wings, and legs. Based on necropsy and/or histopathology of 31 cranes, the most common lesions involved skeletal muscle and included hemorrhages, granulomatous myositis, thrombosis, and vascular degeneration. Serum chemistry results revealed that levels of creatinine kinase, aspartate aminotransferase, and alanine aminotransferase were above published normals. However, only alanine aminotransferase was higher in clinically affected cranes than in normal cranes collected from the same area.

Presumed drowning of Aleutian Canada geese on the Pacific coast of California and Oregon.

Carcasses of 42 and 17 Aleutian Canada geese (Branta canadensis leucopareia), a federally listed endangered species, were found on ocean beaches near Crescent City, California, and near Pacific City, Oregon, respectively, following severe storms. Necropsies and other information suggest that the birds were flushed during the storms and somehow entered the water where they were washed into the surf and drowned.

Selenium toxicosis in wild aquatic birds.

Severe gross and microscopic lesions and other changes were found in adult aquatic birds and in embryos from Kesterson Reservoir (a portion of Kesterson National Wildlife Refuge), Merced County, Calif., during 1984. Adult birds from that area were emaciated, had subacute to extensive chronic hepatic lesions, and had excess fluid and fibrin in the peritoneal cavity. Biochemical changes in their livers included elevated glycogen and non-protein-bound sulfhydryl concentrations and glutathione peroxidase activity but lowered protein, total sulfhydryl, and protein-bound sulfhydryl concentrations. Congenital malformations observed grossly in embryos were often multiple and included anophthalmia, microphthalmia, abnormal beaks, amelia, micromelia, ectrodactyly, and hydrocephaly. Mean concentrations of selenium in livers (94.4 ppm, dry weight) and kidneys (96.6 ppm) of birds collected at the Kesterson ponds were about 10 times those found at a nearby control area (8.3 and 12.2 ppm). We conclude that selenium present in the agricultural drainage water supplied to the Kesterson ponds accumulated in the food chain of aquatic birds to toxic concentrations and caused the lesion and other changes observed.

Salt toxicosis in waterfowl in North Dakota.

About 150 waterfowl died and another 250 became weak and lethargic from suspected salt poisoning after using White Lake, a highly saline lake in Mountrail County, North Dakota. Frigid temperatures made fresh water unavailable, forcing the birds to ingest the saline waters with resultant toxic effects. Sick birds recovered when removed from the salt water and released into fresh water marshes. Brain sodium levels were higher in dead geese submitted for necropsy than in controls.

Blastomycosis in an African lion.

Using fluorescent antibody techniques, Blastomyces dermatitidis was identified in pyogranulomatous lesions in the lungs, mediastinum, trachea, and cerebrum of an African lion (Panthera leo). Clinical signs included anorexia and dry inspiratory rales. Signs of nervous system dysfunction were not reported prior to death even though a large lesion was found in the cerebrum at necropsy. The lion was shipped from a geographic area where B dermatitidis infection is endemic. It was evident from histologic studies that organisms were being shed from lesions in the trachea into the environment. We were unable to culture the organism because freezing apparently destroyed its viability.

Lymphosarcoma in a harbor seal (Phoca vitulina richardii).

Lymphosarcoma is described in a wild juvenile harbor seal (Phoca vitulina richardii). Gross lesions included hepatomegaly, splenomegaly and lymphadenopathy. Neoplastic lymphoid cells were observed histologically in lung, kidney, liver, spleen, adrenals, bone marrow and visceral and peripheral lymph nodes.

Salmonella meningoencephalomyelitis in a northern fur seal (Callorhinus ursinus).

Salmonella enteritidis was isolated from the brain of a neonatal northern fur seal (Callorhinus ursinus) with gross and microscopic lesions of meningoencephalomyelitis. Microscopic lesions in the liver and lung suggested septicemia.

Causes of death in marine mammals stranded along the Oregon coast.

Sixty-eight marine mammals stranded on the Oregon beaches were examined at necropsy. Gunshot was the primary cause of death in 30% of the pinnipeds examined. Bacterial infections (27%) and parasitism (27%) were also of major importance in the death and debilitation of Oregon marine mammals. Traumatic death or debilitation other than gunshot was observed in 11 animals (16%). Predation, starvation due to neonatal abandonment, viral encephalitis (presumptive diagnosis), dystocia and neoplasia were diagnosed as primary or contributory causes of stranding.

Isolation of Edwardsiella tarda from three Oregon sea mammals.

Edwardsiella tarda was isolated from the peritoneal exudate of a Steller's sea lion (Eumetopias jubata) with peritonitis resulting from a perforating colonic ulcer; from the liver of a harbor porpoise (Phocena phocena) with metritis and peritonitis sequela to dystocia; and from the liver of a California sea lion (Zalophus californianus) with peritonitis following fracture and necrosis of a lumbar vertebrae. These findings indicate E. tarda is a common opportunistic invader in sick or injured marine mammals.

Parasites and associated pathology observed in pinnipeds stranded along the Oregon coast.

Forty-two seals and sea lions found dead along the Oregon Coast were examined for parasites and associated pathology. Nematode infections of the lung and/or gastrointestinal tract were the primary cause of death in 5 of 42 animals examined. New distribution records were established for Pricetrema zalophi and Zalophotrema hepaticum. New host records include Z. hepaticum and Diphyllobothrium cordatum in the Steller's sea lion (Eumetopias jubatus); Nanophyetus salmincola in the California sea lion (Zalophus californianus); P. zalophi in the harbor seal (Phoca vitulina); and P. zalophi, Trigonocotyle sp. and Otostrongylus circumlitus in the northern elephant seal (Mirounga angustirostris).