Geology topics

L. A. Baeten

Publications and source records attributed to L. A. Baeten.

3 recordsLinked to original sources

USGS2004

Recombinant F1-V fusion protein protects black-footed ferrets (Mustela nigripes) against virulent Yersinia pestis infection

Black-footed ferrets (Mustela nigripes) are highly susceptible to sylvatic plague, caused by the bacterium Yersinia pestis, and this disease has severely hampered efforts to restore ferrets to their historic range. A study was conducted to assess the efficacy of vaccination of black-footed ferrets against plague using a recombinant protein vaccine, designated F1-V, developed by personnel at the U.S. Army Medical Research Institute of Infectious Diseases. Seven postreproductive black-footed ferrets were immunized with the vaccine, followed by two booster immunizations on days 23 and 154; three control black-footed ferrets received a placebo. After the second immunization, antibody titers to both F1 and V antigen were found to be significantly higher in vaccinates than controls. On challenge with 7,800 colony-forming units of virulent plague by s.c. injection, the three control animals died within 3 days, but six of seven vaccinates survived with no ill effects. The seventh vaccinate died on day 8. These results indicate that black-footed ferrets can be immunized against plague induced by the s.c. route, similar to fleabite injection.

Journal of Zoo and Wildlife Medicine↗

USGS2000

Biological and molecular characterizations of Toxoplasma gondii strains obtained from Southern sea otters (Enhydra lutris nereis)

Toxoplasma gondii was isolated from brain or heart tissue from 15 southern sea otters ( Enhydra lutris nereis ) in cell cultures. These strains were used to infect mice that developed antibodies to T. gondii as detected in the modified direct agglutination test and had T. gondii tissue cysts in their brains at necropsy. Mouse brains containing tissue cysts from 4 of the strains were fed to 4 cats. Two of the cats excreted T. gondii oocysts in their feces that were infectious for mice. Molecular analyses of 13 strains indicated that they were all type II strains, but that they were genetically distinct from one another.

California↗

USGS1997

Sodium toxicity and pathology associated with exposure of waterfowl to hypersaline playa lakes of southeast New Mexico

Cause of mortality was studied in waterfowl in hypersaline playa lakes of southeast New Mexico during spring and fall migration. Mortality was not common in wild ducks resting on the playas during good weather. However, when birds remained on the lakes for prolonged periods of time, such as during experimental trials and stormy weather, a heavy layer of salt precipitated on their feathers. Sodium toxicity was the cause of death for all experimental mallards housed on playa water and for 50% of the wild waterfowl found moribund or dead during the spring of 1995. Gross lesions included heavy salt precipitation on the feathers, ocular lens opacities, deeply congested brains, and dilated, thin-walled, fluid-filled cloacae. Microscopic lesions in the more severely affected birds included liquefaction of ocular lens cortex with lens fiber swelling and multifocal to diffuse ulcerative conjunctivitis with severe granulocytic inflammation, edema, and granulocytic vasculitis resulting in thrombosis. Inflammation similar to that seen in the conjunctiva occasionally involved the mucosa of the mouth, pharynx, nasal turbinates, cloaca, and bursa. Transcorneal movement of water in response to the hypersaline conditions on the playa lakes or direct contact with salt crystals could induce anterior segment dehydration of the aqueous humor and increased osmotic pressure on the lens, leading to cataract formation.

New Mexico↗