Read More: Newsletter May 2019
The diverse functional roles of over 6,000 species of extant mammals that range in body size across eight orders
of magnitude, from blue whales (Balaenoptera musculus) to tiny Etruscan shrews (Suncus etruscus), contribute
to shaping Earth’s ecosystems. Large mammalian herbivores (e.g., African elephants [Loxodonta africana],
American bison [Bison bison], hippopotamuses [Hippopotamus amphibius]) and carnivores (e.g., wolves [Canis
lupus], pumas [Puma concolor], sea otters [Enhydra lutris]) often have significant effects on primary producers in
terrestrial, aquatic, and marine systems through nutrient cycling, energy flow, and the exertion of bottom-up and
top-down processes. Small mammals, like bats, are important pollinators, dispersers of fruits, and consumers of
arthropods, and others, especially rodents and primates, are important predators and dispersers of seeds. Many of
these mammal-mediated processes occur simultaneously in the same ecosystem, and have significant effects on
community structure of primary producers that in turn alter communities of other vertebrates and invertebrates.
Many mammals also are ecosystem engineers (e.g., elephants, American beavers [Castor canadensis], porcupines
[Erithezon dorsatum], prairie dogs [Cynomys spp.]) that create, significantly modify, or destroy habitat, and by
doing so, they alter ecosystem structure and function and increase habitat heterogeneity and biodiversity. The
extensive influence mammals have on ecosystems results in important services that contribute to human wellbeing,
such as pollination, insect pest control, and bioturbation of soils. The rapid declines in abundance of many
mammal populations and the associated increase in extinction risk raise conservation concerns for mammals.
To maintain mammalian diversity and the critical ecosystem processes they provide, scientists need to mobilize
concern for their status and strive for more effective and comprehensive conservation action. We provide insights
and synthesis on the ecological role of mammals and highlight key research questions and future directions for
Read more: Mammal
The Prairie Dog Pals Spring garage sale will be held on Friday and Saturday, 17-18 May 2019, at 917 Morris St. NE, between the hours of 800 AM and 400 PM. Donate, shop, volunteer, or just drop by to chat! All are welcome!
If you want to donate you can drop off your treasures at 917 Morris St. NE. Please contact Debbie S at 505 205 7966 so that she can coordinate the drop-off. Please provide an inventory (with values) if you want a tax receipt. Also it would be extremely helpful if you could price your items. I mean only you can assess the true value of your treasures, right?
1. 1 U.S. Geological Survey National Wildlife Health Center, Madison, Wisconsin.
2. 2 Department of Pathobiological Sciences, University of Wisconsin-Madison, School of Veterinary Medicine, Madison, Wisconsin.
3. 3 Wyoming Game and Fish Department, Laramie, Wyoming.
Plague is a lethal zoonotic disease associated with rodents worldwide. In the western United States, plague outbreaks can decimate prairie dog (Cynomys spp.) colonies. However, it is unclear where the causative agent, Yersinia pestis, of this flea-borne disease is maintained between outbreaks, and what triggers plague-induced prairie dog die-offs. Less susceptible rodent hosts, such as mice, could serve to maintain the bacterium, transport infectious fleas across a colony, or introduce the pathogen to other colonies, possibly facilitating an outbreak. Here, we assess the potential role of two short-lived rodent species, North American deer mice (Peromyscus maniculatus) and Northern grasshopper mice (Onychomys leucogaster) in plague dynamics on prairie dog colonies. We live-trapped short-lived rodents and collected their fleas on black-tailed (Cynomys ludovicianus, Montana and South Dakota), white-tailed (Cynomys leucurus, Utah and Wyoming), and Utah prairie dog colonies (Cynomys parvidens, Utah) annually, from 2013 to 2016. Plague outbreaks occurred on colonies of all three species. In all study areas, deer mouse abundance was high the year before plague-induced prairie dog die-offs, but mouse abundance per colony was not predictive of plague die-offs in prairie dogs. We did not detect Y. pestis DNA in mouse fleas during prairie dog die-offs, but in three cases we found it beforehand. On one white-tailed prairie dog colony, we detected Y. pestis positive fleas on one grasshopper mouse and several prairie dogs live-trapped 10 days later, months before visible declines and plague-confirmed mortality of prairie dogs. On one black-tailed prairie dog colony, we detected Y. pestis positive fleas on two deer mice 3 months before evidence of plague was detected in prairie dogs or their fleas and also well before a plague-induced die-off. These observations of plague positive fleas on mice could represent early spillover events of Y. pestis from prairie dogs or an unknown reservoir, or possible movement of infectious fleas by mice.
|1.||Front Vet Sci. 2019 Mar 28;6:75. doi: 10.3389/fvets.2019.00075. eCollection 2019.|
1. United States Geological Survey, Fort Collins Science Center, Fort Collins, CO, United States.
2. Department of Biology, Colorado State University, Fort Collins, CO, United States.
Plague (caused by the bacterium Yersinia pestis) is a deadly flea-borne disease that remains a threat to public health nearly worldwide and is particularly disruptive ecologically where it has been introduced. We review hypotheses regarding maintenance and transmission of Y. pestis, emphasizing recent data from North America supporting maintenance by persistent transmission that results in sustained non-epizootic (but variable) rates of mortality in hosts. This maintenance mechanism may facilitate periodic epizootic eruptions “in place” because the need for repeated reinvasion from disjunct sources is eliminated. Resulting explosive outbreaks that spread rapidly in time and space are likely enhanced by synergistic positive feedback (PFB) cycles involving flea vectors, hosts, and the plague bacterium itself. Although PFB has been implied in plague literature for at least 50 years, we propose this mechanism, particularly with regard to flea responses, as central to epizootic plague rather than a phenomenon worthy of just peripheral mention. We also present new data on increases in flea:host ratios resulting from recreational shooting and poisoning as possible triggers for the transition from enzootic maintenance to PFB cycles and epizootic explosions. Although plague outbreaks have received much historic attention, PFB cycles that result in decimation of host populations lead to speculation that epizootic eruptions might not be part of the adaptive evolutionary strategy of Y. pestis but might instead be a tolerated intermittent cost of its modus operandi. We also speculate that there may be mammal communities where epizootics, as we define them, are rare or absent. Absence of plague epizootics might translate into reduced public health risk but does not necessarily equate to inconsequential ecologic impact.
PMCID: PMC6447679 Free PMC Article