An assessment of post-plague reintroduced native white-clawed crayfish, a Ustropotamobius pallipes, in the Sherston Avon and Tetbury Avon, Wiltshire

This article reports on the success of reintroducing native crayfish (Austropotamobius pallipes) in the Sherston and Tetbury Avon, following extinction of the population from crayfish plague. The authors describe and review the survey methods that were used and identify a survey technique that was found to be the most rapid and robust for monitoring crayfish populations. Such a survey technique could be adopted as a standard method.

Aphanomycosis of crayfish: crayfish plague

This is the Aphanomycosis of crayfish: crayfish plague report produced by the Environment Agency in 2000. Crayfish plague is an extremely virulent fungal disease of European crayfish species, the white clawed or stone crayfish of Western Europe Austropotamobius pallipes, the Noble crayfish of northern Europe Astacus astacus and the narrow clawed crayfish of Eastern Europe, Astacus leptodactylus. The white claw crayfish A. pallipes is the indigenous native crayfish of the British Isles. Until the early 1980s there were extensive healthy populations of this crayfish in almost all suitable alkaline river and lake environments in England and Wales as far north as Northumberland. The conservation importance of this native crayfish is widely recognised. This report provides a general review of the literature of crayfish plague, including an overview of its spread through the British Isles from CEFAS records. Information on current diagnostic methods from the Office International des Epizooties (OIE) Aquatic Disease Manual is provided. Information on the taxonomy, morphology and physiology of the pathogen is reviewed, together with the pathogenicity and pathology of the disease and current means of prevention and control.

The great plague : an eyewitness account.

A través del escritor Daniel Defoe, que vivió en su niñez la enfermedad de la peste negra, conocemos la historia de esta Gran Plaga. Con textos ilustrados se explica a los alumnos de Primaria el origen de esta enfermedad que asoló Londres en 1665, causó muchos muertos y era transmitida por las ratas a los hombres.

Plague of diagrams

Group exhibition curated by Plastique Fantastique. Organised by David Burrows and Dean Kenning in collaboration with Ami Clarke, Andrew Conio, John Cussans and David Osbaldeston. Contributors: David Burrows, Rachel Cattle & Jenna Collins, Neil Chapman & Gillian Wylde, Ami Clarke, Richard Cochrane, Andrew Conio, John Cussans, David Burrows, Benedict Drew, English Heretic, Nikolaus Gansterer, Joey Holder, Dean Kenning, Christoph Lueder, Stine Llungdalh, Adelheid Mers, Mike Nelson, Paul O'Kane, David Osbaldeston, Plastique Fantastique, Patricia Reed, John Russell, Erica Scourti, Andy Sharp, Kamini Vellodi, Martin Westwood and Carey Young.

Ovarian morphology and oogenesis dynamic of the diplopod Urostreptus atrobrunneus Pierozzi & Fontanetti, 2006 (Spirostreptidae), a potential plague in urban centers

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Ultrastructure of oocytes of the Urostreptus atrobrunneus (Diplopoda, Spirostreptida, Spirostreptidae): A potential urban centers plague

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

THE CURRENT STATUS OF PLAGUE IN CALIFORNIA

At the first Vertebrate Pest Control Conference in 1964, I traced the history of plague control in California and outlined a revised approach, based on newer concepts of plague ecology. In our state of relative ignorance, this required a number of unproved assumptions about plague occurrence in California that verged on crystal ball gazing. These were principally that (1) plague persists in relatively resistant rodent species in certain favorable locations, (2) ground squirrels and chipmunks experience periodic epizootics, but are not permanent reservoirs, (3) plague "foci" of the past were merely sites of conspicuous epizootics, they did not necessarily correspond to permanent foci, and could result from epizootic migrations over considerable distances, and (4) a number of assumptions about areas of greatest epizootic potential can be made by analyzing the pattern of recurrent plague outbreaks in the past. Since then the validity of these assumptions has been tested by the largest outbreak of plague since the early 1940's. We believe that the results have proved the crystal ball largely correct, resulting in much more precise and efficient epizootic surveillance and deployment of control measures than in the past. The outbreak was for us an administrative emergency that exceeded the capacities of the State Health Department. We greatly appreciated the vital help and cooperation of other agencies and individuals. The U.S, Public Health Service accepted a heavy burden of laboratory testing through its San Francisco Field Station, and provided emergency field personnel. The contributions of State Department of Agriculture, Bureau of Weed and Vertebrate Pest Control; U.S. Parks, Forest Service and Bureau of Land Management; local health and agriculture department; and State Division of Parks personnel were essential in accomplishing control work, as well as epizootic surveillance.

Autumn Leaves: Curing the Window Plague in IDEs

Navigating large software systems is difficult as the various artifacts are distributed in a huge space, while the relationships between different artifacts often remain hidden and obscure. As a consequence, developers using a modern interactive development environment (IDE) are forced to open views on numerous source artifacts to reveal these hidden relationships, leading to a crowded workspace with many opened windows or tabs. Developers often lose the overview in such a cluttered workspace as IDEs provide little support to get rid of unused windows. AutumnLeaves automatically selects windows unlikely for future use to be closed or grayed out while important ones are displayed more prominently. This reduces the number of windows opened at a time and adds structure to the developer's workspace. We validate AutumnLeaves with a benchmark evaluation using recorded navigation data of various developers to determine the prediction quality of the employed algorithms.

Yersinia pestis, the cause of plague, is a recently emerged clone of Yersinia pseudotuberculosis

Plague, one of the most devastating diseases of human history, is caused by Yersinia pestis. In this study, we analyzed the population genetic structure of Y. pestis and the two other pathogenic Yersinia species, Y. pseudotuberculosis and Y. enterocolitica. Fragments of five housekeeping genes and a gene involved in the synthesis of lipopolysaccharide were sequenced from 36 strains representing the global diversity of Y. pestis and from 12–13 strains from each of the other species. No sequence diversity was found in any Y. pestis gene, and these alleles were identical or nearly identical to alleles from Y. pseudotuberculosis. Thus, Y. pestis is a clone that evolved from Y. pseudotuberculosis 1,500–20,000 years ago, shortly before the first known pandemics of human plague. Three biovars (Antiqua, Medievalis, and Orientalis) have been distinguished by microbiologists within the Y. pestis clone. These biovars form distinct branches of a phylogenetic tree based on restriction fragment length polymorphisms of the locations of the IS100 insertion element. These data are consistent with previous inferences that Antiqua caused a plague pandemic in the sixth century, Medievalis caused the Black Death and subsequent epidemics during the second pandemic wave, and Orientalis caused the current plague pandemic.

Molecular and cell biology aspects of plague

A 70-kb virulence plasmid (sometimes called pYV) enables Yersinia spp. to survive and multiply in the lymphoid tissues of their host. It encodes the Yop virulon, a system consisting of secreted proteins called Yops and their dedicated type III secretion apparatus called Ysc. The Ysc apparatus forms a channel composed of 29 proteins. Of these, 10 have counterparts in almost every type III system. Secretion of some Yops requires the assistance, in the bacterial cytosol, of small individual chaperones called the Syc proteins. These chaperones act as bodyguards or secretion pilots for their partner Yop. Yop proteins fall into two categories. Some are intracellular effectors, whereas the others are “translocators” needed to deliver the effectors across the eukaryotic plasma membrane, into eukaryotic cells. The translocators (YopB, YopD, LcrV) form a pore of 16–23 Å in the eukaryotic cell plasma membrane. The effector Yops are YopE, YopH, YpkA/YopO, YopP/YopJ, YopM, and YopT. YopH is a powerful phosphotyrosine phosphatase playing an antiphagocytic role by dephosphorylating several focal adhesion proteins. YopE and YopT contribute to antiphagocytic effects by inactivating GTPases controlling cytoskeleton dynamics. YopP/YopJ plays an anti-inflammatory role by preventing the activation of the transcription factor NF-κB. It also induces rapid apoptosis of macrophages. Less is known about the role of the phosphoserine kinase YopO/YpkA and YopM.