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Wayne I. Jensen

Publications and source records attributed to Wayne I. Jensen.

8 recordsLinked to original sources
USGS1981

Naturally occurring and experimentally induced castor bean (Ricinus communis) poisoning in ducks

Castor bean ( Ricinus communis ) poisoning accounted for the death of several thousand ducks in the Texas panhandle in the fall and winter months of 1969-1971. Signs of intoxication resembled those of botulism, except for mucoid, blood-tinged excreta. The most common lesions were severe fatty change in the liver, widely distributed internal petechial hemorrhages or ecchymoses, and catarrhal enteritis. Nearly intact castor beans were found in the stomach of one duck during field necropsy. Fragments of seed coat resembling castor bean were found in the stomachs of 10 of 14 ducks examined in the laboratory. Clinical signs and postmortem lesions observed in wild ducks were induced experimentally in mallards ( Anas platyrhynchos ) by force-feeding intact castor beans. Toxicity titrations were erratic, but the LD50 appeared to be between three and four seeds. The mouse toxicity test, used to detect Clostridium botulinum toxin in the blood serum of intoxicated ducks, was negative in every case. Hemagglutination and precipitin tests generally failed to detect castor bean in extracts of excreta or intestinal contents of experimentally intoxicated ducks.

Texas↗
USGS1981

Evaluation of coproexamination as a diagnostic test for avian botulism

Fecal extracts and blood sera from 113 ducks showing clinical signs of botulism were examined for Clostridium botulinum type C toxin by means of the mouse toxicity test to evaluate coproexamination as a diagnostic procedure, as compared with demonstration of toxin in serum. When death of test mice unprotected with type specific antitoxin (while protected controls survived) was the criterion, 78.8% of the sera and 5.3% of the fecal extracts were positive. When characteristic signs of intoxication in the unprotected mice was included as evidence of toxin in the specimens, these percentages increased to 86.7 and 6.2, respectively. Fecal specimens were collected hourly for the first 6 h after peroral dosing of eight mallards ( Anas platyrhynchos ) with 1.0 LD 50 , of type C toxin and at 24, 48, and 72 h from birds surviving that long. From 2 to 4 toxin-positive specimens were passed by all eight ducks during the first 6 h, five specimens were positive at 24 h, and three were positive at 48 h. Only three specimens were collected at 72 h, all of which were negative. These findings suggest that attempts to detect toxin in the feces of wild ducks might have been more successful had the birds been captured earlier in the course of the disease.

Utah↗
USGS1980

The susceptibility of the mallard duck (Anas platyrhynchos) to Clostridium botulinum C2 toxin

Most strains of Clostridium botulinum type C, after having lost their capacity to produce their dominant toxin (C 1 ) as a result of being“cured”of their prophages, continue to produce C 2 , a trypsin-activable toxin reported by other investigators. While of relatively low toxicity when administered perorally to the adult mallard duck ( Anas platyrhynchos ), it was highly toxic when given parenterally. By the intravenous route, for example, it was more than 1, 000 times as toxic as C 1 toxin by the same route, when compared on the basis of mouse intraperitoneal toxicity. The cause of death in every instance was massive pulmonary edema and hemorrhage rather than the respiratory paralysis that occurs in C 1 intoxication. 抄録

Japanese Journal of Medical Science and Biology↗
USGS1979

An outbreak of streptococcosis in eared grebes (Podiceps nigricollis)

An outbreak of streptococcosis ( Streptococcus zooepidemicus ), apparently the first recorded in wild birds, killed an estimated 7,500 eared grebes ( Podiceps nigricollis ) on Great Salt Lake (Utah) in November and December, 1977. Ducks and gulls feeding in the same area were unaffected.

Utah↗
USGS1976

Avian botulism epizootiology on sewage oxidation ponds in Utah

In the microenvironment concept of avian botulism epizootiology, it is hypothesized that invertebrate carcasses may serve both as a substrate for toxin production by Clostridium botulinum type C and as a vehicle for toxin transmission to water birds. We field-tested that hypothesis by attempting to induce botulism in wing-clipped mallard ducks ( Anas platyrhynchos ) on sewage oxidation ponds in Utah. The experimental ponds were inoculated with C. botulinum spores in June 1974. Aquatic insect populations were monitored throughout the summer. Rotenone was used in August to kill insects in two ponds (one served as control), thereby providing potential substrate for clostridial growth and toxin production. Botulism was not detected among the birds even though they routinely ingested invertebrate carcasses. Samples of dead invertebrates contained no botulinum toxin. We concluded that the microenvironment concept, as it now stands, cannot always be a sufficient explanation of how type C botulism epizootics are initiated in nature. Other microbes may inhibit the growth of clostridial cells or destroy botulinum toxin.

Utah↗
USGS1976

An outbreak of erysipelas in eared grebes (Podiceps nigricollis)

An outbreak of erysipelas killed an estimated 5,000 aquatic birds on Great Salt Lake (Utah) in late November, 1975. Although several thousand ducks and gulls were using the lake, at least 99 percent of the victims were eared grebes. A hypothetical explanation for the selective mortality is offered.

Utah↗