Plague outbreaks in prairie-dog colonies associated with El Niño climatic events

The SGS-LTER research site was established in 1980 by researchers at Colorado State University as part of a network of long-term research sites within the US LTER Network, supported by the National Science Foundation. Scientists within the Natural Resource Ecology Lab, Department of Forest and Rangeland Stewardship, Department of Soil and Crop Sciences, and Biology Department at CSU, California State Fullerton, USDA Agricultural Research Service, University of Northern Colorado, and the University of Wyoming, among others, have contributed to our understanding of the structure and functions of the shortgrass steppe and other diverse ecosystems across the network while maintaining a common mission and sharing expertise, data and infrastructure.Plague (Yersinia pestis) was introduced to the western U.S. in the mid-20th century and is a significant threat to the persistence of black-tailed prairie dog (Cynomys ludovicianus) populations. The social, colonial habits of prairie dogs make them particularly susceptible to plague, and many flea species, including known carriers of plague, are associated with prairie dogs or their extensive burrow systems. Mortality during plague epizootics, or outbreaks, is nearly 100% (Cully and Williams 2001; J. Mammal. 82:894), resulting in the extinction of entire colonies. In northern Colorado, prairie dogs exist in metapopulations (Roach et al. 2001, J. Mammal. 82:946), in which colonies naturally isolated by topography, soils and vegetation are connected by dispersal. Dispersal of either infected prairie dogs or plague-resistant reservoir species is hypothesized to spread plague among colonies. Plague outbreaks therefore may disrupt the dynamics of prairie-dog metapopulations and affect regional persistence. In the context of a century of past eradication efforts that have drastically reduced prairie-dog numbers, and increasing agricultural and urban development, plague represents a relatively new and unique threat to prairie dogs and the species that are closely associated with them. Poster presented at the 6th SGS Symposium held on 1/10/03

Shortgrass Steppe LTER VI: examining ecosystem persistence and responses to global change, 2010-2014 proposal

Includes bibliographical references.The SGS-LTER research site was established in 1980 by researchers at Colorado State University as part of a network of long-term research sites within the US LTER Network, supported by the National Science Foundation. Scientists within the Natural Resource Ecology Lab, Department of Forest and Rangeland Stewardship, Department of Soil and Crop Sciences, and Biology Department at CSU, California State Fullerton, USDA Agricultural Research Service, University of Northern Colorado, and the University of Wyoming, among others, have contributed to our understanding of the structure and functions of the shortgrass steppe and other diverse ecosystems across the network while maintaining a common mission and sharing expertise, data and infrastructure.The Shortgrass Steppe Long-term Ecological Research (SGS-LTER) program focuses on how grassland ecosystems function and persist or change in the face of global change. Our conceptual framework asserts that climate, physiography, grazing, fire and landuse, operating over different spatial and temporal scales, are the dominant determinants of the structure, function, and persistence of the SGS. Using the shortgrass steppe (SGS) ecosystem of the North American Great Plains as a model, we seek to (1) identify the ecological attributes of grasslands that historically have resulted in their persistence and (2) understand these attributes in ways that will allow us to identify area of vulnerability and better forecast the future of grasslands in the face of global change. Given its geographic extent and history, the SGS encapsulates many of the features of a system driven by social-ecological interactions and the vulnerabilities of semiarid grasslands to global change. Our overarching question is: How will structure and function of the SGS respond to expected changes in climate, management, and land-use, and what will be the consequences

Classic flea-borne transmission does not drive plague epizootics in prairie dogs

We lack a clear understanding of the enzootic maintenance of the bacterium (Yersinia pestis) that causes plague and the sporadic epizootics that occur in its natural rodent hosts. A key to elucidating these epidemiological dynamics is determining the dominant transmission routes of plague. Plague can be acquired from the bites of infectious fleas (which is generally considered to occur via a blocked flea vector), inhalation of infectious respiratory droplets, or contact with a short-term infectious reservoir. We present results from a plague modeling approach that includes transmission from all three sources of infection simultaneously and uses sensitivity analysis to determine their relative importance. Our model is completely parameterized by using data from the literature and our own field studies of plague in the black-tailed prairie dog (Cynomys ludovicianus). Results of the model are qualitatively and quantitatively consistent with independent data from our field sites. Although infectious fleas might be an important source of infection and transmission via blocked fleas is a dominant paradigm in the literature, our model clearly predicts that this form of transmission cannot drive epizootics in prairie dogs. Rather, a short-term reservoir is required for epizootic dynamics. Several short-term reservoirs have the potential to affect the prairie dog system. Our model predictions of the residence time of the shortterm reservoir suggest that other small mammals, infectious prairie dog carcasses, fleas that transmit plague without blockage of the digestive tract, or some combination of these three are the most likely of the candidate infectious reservoirs. disease modeling ͉ disease reservoir ͉ Yersinia pestis ͉ Cynomys ludovicianu

The Influence of Sylvatic Plague on North American Wildlife at the Landscape Level, with Special Emphasis on Black-footed Ferret and Prairie Dog Conservation

Prairie-dogs are distributed over a large part of the Great Plains and Rocky Mountain regions. Their colonies often number thousands of individuals, and their destruction of grasses and other forage plants makes them of considerable economic importance. Drastic measures are frequently necessary to prevent the destruction of crops of grain and hay. The Biological Survey is exterminating these rodents in national forests and in the public domain. The information in this report, in regards to the several species and their distribution, as indicated by maps, will aid materially in efforts, national or state, to control or exterminate them, said Henry W. Henshaw in 1915 (Hollister 1916)

Long-term ecological research on Colorado Shortgrass Steppe

The SGS-LTER research site was established in 1980 by researchers at Colorado State University as part of a network of long-term research sites within the US LTER Network, supported by the National Science Foundation. Scientists within the Natural Resource Ecology Lab, Department of Forest and Rangeland Stewardship, Department of Soil and Crop Sciences, and Biology Department at CSU, California State Fullerton, USDA Agricultural Research Service, University of Northern Colorado, and the University of Wyoming, among others, have contributed to our understanding of the structure and functions of the shortgrass steppe and other diverse ecosystems across the network while maintaining a common mission and sharing expertise, data and infrastructure.Poster presented at the LTER All Scientists Meeting held in Estes Park, CO on September 10-13, 2012

First Reported Prairie Dog–to-Human Tularemia Transmission, Texas, 2002

A tularemia outbreak, caused by Francisella tularensis type B, occurred among wild-caught, commercially traded prairie dogs. F. tularensis microagglutination titers in one exposed person indicated recent infection. These findings represent the first evidence for prairie-dog-to-human tularemia transmission and demonstrate potential human health risks of the exotic pet trade

Varespladib and cardiovascular events in patients with an acute coronary syndrome: the VISTA-16 randomized clinical trial

IMPORTANCE: Secretory phospholipase A2(sPLA2) generates bioactive phospholipid products implicated in atherosclerosis. The sPLA2inhibitor varespladib has favorable effects on lipid and inflammatory markers; however, its effect on cardiovascular outcomes is unknown. OBJECTIVE: To determine the effects of sPLA2inhibition with varespladib on cardiovascular outcomes. DESIGN, SETTING, AND PARTICIPANTS: A double-blind, randomized, multicenter trial at 362 academic and community hospitals in Europe, Australia, New Zealand, India, and North America of 5145 patients randomized within 96 hours of presentation of an acute coronary syndrome (ACS) to either varespladib (n = 2572) or placebo (n = 2573) with enrollment between June 1, 2010, and March 7, 2012 (study termination on March 9, 2012). INTERVENTIONS: Participants were randomized to receive varespladib (500 mg) or placebo daily for 16 weeks, in addition to atorvastatin and other established therapies. MAIN OUTCOMES AND MEASURES: The primary efficacy measurewas a composite of cardiovascular mortality, nonfatal myocardial infarction (MI), nonfatal stroke, or unstable angina with evidence of ischemia requiring hospitalization at 16 weeks. Six-month survival status was also evaluated. RESULTS: At a prespecified interim analysis, including 212 primary end point events, the independent data and safety monitoring board recommended termination of the trial for futility and possible harm. The primary end point occurred in 136 patients (6.1%) treated with varespladib compared with 109 patients (5.1%) treated with placebo (hazard ratio [HR], 1.25; 95%CI, 0.97-1.61; log-rank P = .08). Varespladib was associated with a greater risk of MI (78 [3.4%] vs 47 [2.2%]; HR, 1.66; 95%CI, 1.16-2.39; log-rank P = .005). The composite secondary end point of cardiovascular mortality, MI, and stroke was observed in 107 patients (4.6%) in the varespladib group and 79 patients (3.8%) in the placebo group (HR, 1.36; 95% CI, 1.02-1.82; P = .04). CONCLUSIONS AND RELEVANCE: In patients with recent ACS, varespladib did not reduce the risk of recurrent cardiovascular events and significantly increased the risk of MI. The sPLA2inhibition with varespladib may be harmful and is not a useful strategy to reduce adverse cardiovascular outcomes after ACS. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01130246. Copyright 2014 American Medical Association. All rights reserved

Transmission Shifts Underlie Variability in Population Responses to Yersinia pestis Infection

Host populations for the plague bacterium, Yersinia pestis, are highly variable in their response to plague ranging from near deterministic extinction (i.e., epizootic dynamics) to a low probability of extinction despite persistent infection (i.e., enzootic dynamics). Much of the work to understand this variability has focused on specific host characteristics, such as population size and resistance, and their role in determining plague dynamics. Here, however, we advance the idea that the relative importance of alternative transmission routes may vary causing shifts from epizootic to enzootic dynamics. We present a model that incorporates host and flea ecology with multiple transmission hypotheses to study how transmission shifts determine population responses to plague. Our results suggest enzootic persistence relies on infection of an off-host flea reservoir and epizootics rely on transiently maintained flea infection loads through repeated infectious feeds by fleas. In either case, early-phase transmission by fleas (i.e., transmission immediately following an infected blood meal) has been observed in laboratory studies, and we show that it is capable of driving plague dynamics at the population level. Sensitivity analysis of model parameters revealed that host characteristics (e.g., population size and resistance) vary in importance depending on transmission dynamics, suggesting that host ecology may scale differently through different transmission routes enabling prediction of population responses in a more robust way than using either host characteristics or transmission shifts alone

Antioxidants Protect Keratinocytes against M. ulcerans Mycolactone Cytotoxicity

BACKGROUND: Mycobacterium ulcerans is the causative agent of necrotizing skin ulcerations in distinctive geographical areas. M. ulcerans produces a macrolide toxin, mycolactone, which has been identified as an important virulence factor in ulcer formation. Mycolactone is cytotoxic to fibroblasts and adipocytes in vitro and has modulating activity on immune cell functions. The effect of mycolactone on keratinocytes has not been reported previously and the mechanism of mycolactone toxicity is presently unknown. Many other macrolide substances have cytotoxic and immunosuppressive activities and mediate some of their effects via production of reactive oxygen species (ROS). We have studied the effect of mycolactone in vitro on human keratinocytes--key cells in wound healing--and tested the hypothesis that the cytotoxic effect of mycolactone is mediated by ROS. METHODOLOGY/PRINCIPAL FINDINGS: The effect of mycolactone on primary skin keratinocyte growth and cell numbers was investigated in serum free growth medium in the presence of different antioxidants. A concentration and time dependent reduction in keratinocyte cell numbers was observed after exposure to mycolactone. Several different antioxidants inhibited this effect partly. The ROS inhibiting substance deferoxamine, which acts via chelation of Fe(2+), completely prevented mycolactone mediated cytotoxicity. CONCLUSIONS/SIGNIFICANCE: This study demonstrates that mycolactone mediated cytotoxicity can be inhibited by deferoxamine, suggesting a role of iron and ROS in mycolactone induced cytotoxicity of keratinocytes. The data provide a basis for the understanding of Buruli ulcer pathology and the development of improved therapies for this disease