Showing papers on "Animal mortality published in 2001"

I am not an animal: mortality salience, disgust, and the denial of human creatureliness.

Abstract: The present research investigated the need to distinguish humans from animals and tested the hypothesis derived from terror management theory that this need stems in part from existential mortality concerns. Specifically, the authors suggest that being an animal is threatening because it reminds people of their vulnerability to death; therefore, reminding people of their mortality was hypothesized to increase the need to distance from animals. In support, Study 1 revealed that reminders of death led to an increased emotional reaction of disgust to body products and animals. Study 2 showed that compared to a control condition, mortality salience led to greater preference for an essay describing people as distinct from animals; and within the mortality salient condition but not the control condition, the essay emphasizing differences from other animals was preferred to the essay emphasizing similarities. The implications of these results for understanding why humans are so invested in beautifying their bodies and denying creaturely aspects of themselves are discussed.

Interleukin-12 promotes pathologic liver changes and death in mice coinfected with Schistosoma mansoni and Toxoplasma gondii.

Abstract: We previously demonstrated that mice concurrently infected with Schistosoma mansoni and Toxoplasma gondii undergo accelerated mortality which is preceded by severe liver damage. Abnormally high levels of serum tumor necrosis factor alpha (TNF-alpha) in the dually infected mice suggested a role for this and related proinflammatory mediators in the pathologic alterations. In order to evaluate the factors involved in increased inflammatory-mediator production and mortality, interleukin-12(-/-) (IL-12(-/-)) mice were coinfected with S. mansoni and T. gondii, and survival and immune responses were monitored. These IL-12(-/-) mice displayed decreased liver damage and prolonged time to death relative to wild-type animals also coinfected with these parasites. Relative to the response of cells from the coinfected wild-type animals, levels of TNF-alpha, gamma interferon, and NO produced by splenocytes from coinfected IL-12(-/-) mice were reduced, and levels of IL-5 and IL-10 were increased, with the net result that the immune response of the dually infected IL-12(-/-) mice was similar to that of the wild-type mice infected with S. mansoni alone. While dually infected wild-type animals succumb in the absence of overt parasitemia, the delayed death in the absence of IL-12 is associated with relatively uncontrolled T. gondii replication. These data support the view that S. mansoni-infected mice are acutely sensitive to infection with T. gondii as a result of their increased hepatic sensitivity to high levels of proinflammatory cytokines; IL-12 and TNF-alpha are implicated in this process.

Counter-protective role for interleukin-5 during acute Toxoplasma gondii infection.

Abstract: The role of interleukin-5 (IL-5) during Toxoplasma gondii infection was investigated by comparing disease progression in IL-5 gene deficient (IL-5-/-) mice and their wild-type (WT) counterparts on a C57BL/6 background. IL-5-/- mice infected orally with T. gondii were less susceptible to infection than WT mice as demonstrated by reduced mortality rates. Consistent with this data, orally infected IL-5-/- mice had less severe pathological changes in their small intestines than WT mice at 8 days postinfection. At this time, splenocytes and mesenteric lymph node cells derived from IL-5-/- mice produced levels of IL-12, interferon-gamma (IFN-gamma), IL-4, IL-10, and nitric oxide (measured as nitrite) similar to those derived from WT mice when stimulated with Toxoplasma lysate antigen. However, peak serum IL-12 and IFN-gamma levels (at days 6 and 8, respectively) were significantly higher in IL-5-/- mice than in WT mice. In addition, WT mice but not IL-5-/- mice had raised levels of eosinophils in their peripheral blood between days 5 and 8 following infection. Oral administration of N omega-nitro-L-arginine methyl (from day 4 postinfection) increased mortality rates in both IL-5-/- and WT mice, indicating a protective role for nitric oxide during the early stages of oral T. gondii infection. In comparison with oral infection, no difference in mortality was observed between IL-5-/- and WT mice following intraperitoneal infection with T. gondii, with all mice surviving until 35 days postinfection. Similarly, no significant differences were observed in the severity of the meningitis, perivascular cuffing, or number of microglial nodules or parasites in the brains of intraperitoneally infected mice. Together, these results demonstrate a detrimental role for IL-5 during the early stage of oral infection with T. gondii which is associated with increased small-intestine pathology, eosinophilia, and reduced plasma IL-12 and IFN-gamma levels.

Pathogenicity of different serogroups of avian salmonellae in specific-pathogen-free chickens.

Abstract: The pathogenicity of one isolate of Salmonella typhimurium, four isolates of Salmonella heidelberg, three isolates of Salmonella kentucky, two isolates of Salmonella montevideo, one isolate of Salmonella hadar, and two isolates of Salmonella enteritidis (SE), one belonging to phage type (PT)13a and the other to PT34, was investigated in specific-pathogen-free chicks. Three hundred eighty-four chicks were separated into 16 equal groups of 24 chicks. Thirteen groups were inoculated individually with 0.5 ml of broth culture containing 1 x 10(7) colony-forming units (CFU) of either S. typhimurium (one source), S. heidelberg (four sources), S. montevideo (two sources), S. hadar (one source), S. kentucky (three sources), SE PT 13a (one source) or SE PT 34 (one source) by crop gavage. Two groups of 24 chicks were inoculated in the same way with 1 x 10(7) CFU of SE PT4 (chicken-CA) and Salmonella pullorum. Another group of 24 chicks was kept as an uninoculated control group. The chicks were observed daily for clinical signs and mortality. Isolation of salmonella was done from different organs at 7 and 28 days postinoculation (DPI). All the chicks were weighed individually at 7, 14, 21, and 28 DPI. Two chicks chosen at random from each group were euthanatized and necropsied at 7 and 14 DPI and all the remaining live chickens, at 28 DPI. Selected tissues were taken for histopathology at 7 and 14 DPI. Dead chicks were examined for gross lesions and tissues were collected for histopathology. Chicks inoculated with S. pullorum had the highest mortality (66.66%), followed by S. typhimurium (33.33%). Chicks inoculated with S. heidelberg (00-1105-2) and SE PT4 (chicken-CA) had 12.5% mortality and 8.3% mortality, respectively, with SE PT 13a. Ceca were 100% positive for salmonellae at acute or chronic infection compared with other organs. Mean body weight reduction ranged from 0.67% (inoculated with S. kentucky 00-926-2) to 33.23% (inoculated with S. typhimurium 00-372) in the inoculated groups at different weeks compared with uninoculated controls. Gross and microscopic lesions included peritonitis, perihepatitis, yolk sac infection, typhilitis, pneumonia, and enteritis in some groups, especially those inoculated with S. typhimurium, S. heidelberg (00-1 105-2), SE PT4 (chicken-CA), and S. pullorum.

The role of parasitic diseases as causes of mortality in small ruminants in a high-potential farming area in central Kenya.

Abstract: A 15-year retrospective study was performed to determine the role of parasitic diseases in causing mortalities in small ruminants. In total, 115 (32 %) sheep were diagnosed as having been killed by parasitic diseases out of 366 that died as a result of disease. The major cause of mortality was helminthosis (63 %of all parasitic cases). Most of the helminthosis cases were attributed to haemonchosis (40 % of parasitic cases). Heartwater was the second most important parasitic disease (27 %of all parasitic cases). Ninety-five (26 %) goats were diagnosed to have been killed by parasitic diseases out of 365 cases presented at the post mortem facility. Helminthosis was the most frequent cause of mortality (55 % of the total parasitic diseases). Twenty-six goats were killed by haemonchosis (27 % of all parasitic diseases). Heartwater was the second most important parasitic disease, accounting for about 20 % of all parasitic diseases. These findings indicate that viable helminth and tick control strategies should be devised in order to reduce mortality caused by helminthosis and heartwater and thereby achieve improved productivity.

An Overview of Early Anthrax Outbreaks in Northern Canada: Field Reports of the Health of Animals Branch, Agriculture Canada, 1962-71

Abstract: Between 1962 and 1971, six outbreaks of anthrax occurred in the bison herds of the Northwest Territories and northern Alberta. In response, the federal Health of Animals Branch dispatched staff veterinarians to oversee carcass disposal operations and later to take part in bison depopulation and vaccination programs. Recently, a collection of documents from that agency concerning the outbreaks was discovered in the federal archives. The collection includes field reports from the veterinarians that provide valuable, detailed, first-person accounts of the outbreaks and later programs, information which has generally been lacking in the published literature. The reports identify at least 1102 bison that died of anthrax during the six outbreaks, dozens more than reported previously. They also indicate that the disease spread into Wood Buffalo National Park in 1963, rather than in 1964, as reported previously. A minimum of 598 healthy bison were also killed in depopulation programs aimed at preventing the spread of anthrax into the Park, even though anthrax carcasses had already been discovered within the Park and the targeted regions would be repopulated within weeks. Coverage and revaccination rates were low throughout the vaccination program, and a further 828 bison died during the vaccine roundups.

Contagious bovine pleuropneumonia in Tanzania: current status.

Abstract: CBPP reappeared in Arusha, Northern Tanzania in 1990, having been introduced from Kenya. The disease spread rapidly to Mara region through rustling of sick or infected animals. In November 1992, an unrelated outbreak occurred in Kagera, having spread from Southern Uganda. Up to the end of December 1994, the disease appeared to be confined to Kagera and Arusha. In January 1995, CBPP was observed in Morogoro region, south of the central railway line. Thereafter, the disease spread through western Tanzania. More recently, further disease has occurred in the Southern Highlands and Central regions. The contaminated area now stretches roughly between latitudes 1° and 9°S and longitudes 30° and 37°E, with a cattle population of about 10 million. The direct losses incurred as a result of animal mortality, and vaccination campaign and disease surveillance costs have been assessed at over US$11 million. Indirect losses resulting from chronic disease are much more difficult to assess but are believed to be even higher. Control of the disease has been through restricting animal movements and a mass vaccination campaign. Uncontrolled animal movement during transhumance, trade, cattle thefts and vaccination breakthroughs facilitated the spread of the disease.

Experimental myocardial hypertrophy induced by a minimally invasive ascending aorta coarctation.

Abstract: Ascending aorta coarctation was produced by a minimally invasive technique in rabbits. Animal mortality was 5%. Morphometric and hemodynamic parameters were evaluated. A parabiotically isolated heart model was used to assess the hemodynamic parameters. Left ventricular weight/body weight ratio and muscle area showed clear evidence of hypertrophy when compared to control. The hemodynamic changes in the isolated heart model suggested decreased diastolic and systolic function in the coarcted group. The present model produced hypertrophy with low mortality rates as a result of its less invasive nature.

Factors influencing road-related amphibian mortality in Southern California

Abstract: Roads constitute a direct and often permanent loss of wildlife habitat; they can serve as physical or psychological barriers to animal movements, and are often the source of exceedingly high levels of animal mortality Our goal was to better understand the effects of roads on amphibian populations in a planned landscape corridor in southern California Road cruising was employed to examine the usage of roadways and related mortality levels of amphibians Two hundred and fifty four evening road cruising surveys were conducted between February and April 1999 and 2000 During 93 road nights with “wet roads,” we recorded 465 dead animals and 505 live animals on roadways, yielding an overall mortality rate of 48% In contrast, during 161 road nights that were classified as having “dry roads,” we recorded only 25 dead animals and 105 live animals, yielding an overall mortality rate of 19% In addition to rainfall, the type of road surveyed also influenced road mortality; as expected, the highest mortality rates occurred on highly traveled roads, with small two-lane roads exhibiting the lowest mortality rates Our results suggest that roadways in the region are negatively impacting amphibian populations, particularly when roads are wet in areas of high traffic volume

Factors influencing the movement, spatial patterns, and wildlife underpass use of coyotes and bobcats along State Route 71 in Southern California

Abstract: Funding Source: California Department of Transportation Total Budget: $130,000 Project Period: February 1998-February 2000 Mammalian carnivores may be sensitive to habitat fragmentation due to roadway construction. As a solution, roadway underpasses have received increasing attention; however, relatively little data exist on how carnivores respond to roadways or use the underpasses. We present results from a study of movement patterns and underpass use of coyotes and bobcats along CA 71, a freeway bisecting the eastern end of the Puente-Chino Hills wildlife corridor in urban Los Angeles. Recent reconstruction of a 5-km segment included installation of wildlife fencing, three large wildlife culverts, and 20 smaller water culverts. From February 1998 to February 2000, we captured and radio-tracked 29 coyotes and 4 bobcats and fitted an additional 24 coyotes with dog collars. Telemetry data were augmented by remotely triggered camera surveys at the culverts. Mean home range sizes for 15 coyotes and 3 bobcats were 13.72±3.92 and 8.89±3.45 km2 while core-use area sizes were 1.71±0.48 and 1.31±0.40 km2, respectively; both area sizes differed between age and social classes. Nine individuals maintained core-use areas that overlapped roadways and several had linear home ranges paralleling the roadways. Buffer zones established alongside roadways were not used proportional to their availability by 10 individuals. Telemetry and remotely triggered cameras documented 320 roadway crossings, which included 150 confirmed uses of underpasses by 16 collared individuals. However, hourly traffic volume influenced frequency of culvert use. In addition, surface crossings, particularly in areas where wildlife fencing was absent, accounted for 67 percent of study animal mortality. Mortality patterns for age classes and traffic direction differed. Overall, our study has provided valuable information for the California Department of Transportation on factors influencing underpass use and the effectiveness of roadway design for target species in fragmented landscapes.

New experimental model of multiple myeloma.

Abstract: NSO/1 (P3?63Ay 8Ut) and SP20 myeloma cells were inoculated to BALB/c OlaHsd mice. NSO/1 cells allowed adequate stage-by-stage monitoring of tumor development. The adequacy of this model was confirmed in experiments with conventional cytostatics: prospidium and cytarabine caused necrosis of tumor cells and reduced animal mortality.