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pestis fulminans [keywords]
- Embryonic diapause in the australian plague locust relative to parental experience of cumulative photophase decline. [JOURNAL ARTICLE]
- J Insect Physiol 2014 Aug 22.
The Australian plague locust Chortoicetes terminifera (Walker) exhibits facultative embryonic diapause during autumn. To approximate natural photoperiod changes during late summer and autumn, locust nymphs were reared under different total declines in laboratory photophase (-0.5, -0.75, -1.0, -1.25, -1.5, -1.75, -2 h each lowered in 15 min steps) in a 24 h photoperiod to quantify any effect on the subsequent production of diapause eggs. Induction of diapause eggs was significantly affected by accumulated photoperiod decline experienced by the parental generation throughout all development stages from mid-instar nymph to fledgling adult. The incidence of embryonic diapause ranged from nil at -0.5 h to 86.6% diapause at -2 h. Continued declines in photoperiod for post-teneral locusts (transitioned from -1 h until fledging to -1.75 h) produced a further increase in the proportion of diapause eggs. The results were unaffected by time spent at any given photoperiod, despite a previously indicated maximal inductive photoperiod of 13.5 h being used as the mid-point of all treatments. Implications for the seasonal timing processes of photoperiodism in C. terminifera, which has a high migratory capacity and a latitudinal cline in the timing of diapause egg production across a broad geographic range, are discussed.
- Reply: methodologic concerns in reliability of noncalcified coronary artery plague burden quantification. [Journal Article]
- AJR Am J Roentgenol 2014 Sep; 203(3):W344.
- Genome-Wide Mutant Fitness Profiling Identifies Nutritional Requirements for Optimal Growth of Yersinia pestis in Deep Tissue. [Journal Article]
- MBio 2014; 5(4)
Rapid growth in deep tissue is essential to the high virulence of Yersinia pestis, causative agent of plague. To better understand the mechanisms underlying this unusual ability, we used transposon mutagenesis and high-throughput sequencing (Tn-seq) to systematically probe the Y. pestis genome for elements contributing to fitness during infection. More than a million independent insertion mutants representing nearly 200,000 unique genotypes were generated in fully virulent Y. pestis. Each mutant in the library was assayed for its ability to proliferate in vitro on rich medium and in mice following intravenous injection. Virtually all genes previously established to contribute to virulence following intravenous infection showed significant fitness defects, with the exception of genes for yersiniabactin biosynthesis, which were masked by strong intercellular complementation effects. We also identified more than 30 genes with roles in nutrient acquisition and metabolism as experiencing strong selection during infection. Many of these genes had not previously been implicated in Y. pestis virulence. We further examined the fitness defects of strains carrying mutations in two such genes-encoding a branched-chain amino acid importer (brnQ) and a glucose importer (ptsG)-both in vivo and in a novel defined synthetic growth medium with nutrient concentrations matching those in serum. Our findings suggest that diverse nutrient limitations in deep tissue play a more important role in controlling bacterial infection than has heretofore been appreciated. Because much is known about Y. pestis pathogenesis, this study also serves as a test case that assesses the ability of Tn-seq to detect virulence genes.Our understanding of the functions required by bacteria to grow in deep tissues is limited, in part because most growth studies of pathogenic bacteria are conducted on laboratory media that do not reflect conditions prevailing in infected animal tissues. Improving our knowledge of this aspect of bacterial biology is important as a potential pathway to the development of novel therapeutics. Yersinia pestis, the plague bacterium, is highly virulent due to its rapid dissemination and growth in deep tissues, making it a good model for discovering bacterial adaptations that promote rapid growth during infection. Using Tn-seq, a genome-wide fitness profiling technique, we identified several functions required for fitness of Y. pestis in vivo that were not previously known to be important. Most of these functions are needed to acquire or synthesize nutrients. Interference with these critical nutrient acquisition pathways may be an effective strategy for designing novel antibiotics and vaccines.
- Molecular detection and genotyping of Aphanomyces astaci directly from preserved crayfish samples uncovers the Norwegian crayfish plague disease history. [JOURNAL ARTICLE]
- Vet Microbiol 2014 Jul 18.
Aphanomyces astaci causes crayfish plague in European freshwater crayfish, but most historical epizootics lack agent isolation and identification. Although declared as crayfish plague outbreaks by the Norwegian Competent Authorities, only presumptive diagnoses without agent isolation exist from Norwegian epizootics until 2005. Molecular methods now allow both A. astaci detection and genotype determination from preserved samples. We therefore aimed to (1) investigate molecularly if A. astaci was involved in a selection of mass-mortality events in Norwegian noble crayfish populations from 1971 to 2004, and (2) determine the eventually involved A. astaci genotype groups both from these historical and also more recent mass-mortality events. DNA was extracted directly from presumptively infected crayfish tissues, and screened by A. astaci specific qPCR. A representative selection of positive samples was confirmed by ITS-sequencing. Finally, genotype determination was performed with microsatellite markers that distinguish all known A. astaci genotype groups. The molecular examination detected A. astaci in crayfish materials from all examined mass-mortality events. The first event in 1971-1974 was caused by the A. astaci genotype group A, presumably the first genotype group that entered Europe more than 150 years ago. All later outbreaks were caused by the A. astaci genotype group B which was introduced to Europe by importation of signal crayfish in the 1960s. The results suggest that molecular methods can verify the involvement of A. astaci in the vast majority of observed crayfish mass mortalities in Europe whenever preserved materials exist. Moreover, microsatellite genotyping can reveal at least parts of the underlying epidemiology.
- LcrV delivered via Type III secretion system of live attenuated Yersinia pseudotuberculosis enhances immunogenicity against pneumonic plague. [JOURNAL ARTICLE]
- Infect Immun 2014 Aug 11.
Here, we constructed a Y. pseudotuberculosis mutant strain with arabinose-dependent regulated delayed-shutoff of crp expression (araC PBAD crp) and replacement of the msbB gene with the E. coli msbB gene to attenuate it. Then, we inserted the asd mutation into this construction to form χ10057 (Δasd-206 ΔmsbB868::PmsbB msbB (EC) ΔPcrp21::TT araC PBAD crp) for use with a balanced-lethal Asd(+) plasmid to facilitate antigen synthesis. A hybrid protein composed of YopE (1-138aa) fused with full-length LcrV (YopENt138-LcrV) was synthesized in χ10057 harboring an Asd(+) plasmid (pYA5199, yopENt138-lcrV) and could be secreted through a type III secretion system (T3SS) in vitro and vivo. Animal studies indicated that mice orally immunized with χ10057(pYA5199) developed similar titers of IgG response to whole cell lysates of Y. pestis (YpL) and subunit LcrV as χ10057(pYA3332, empty plasmid). However, only immunization of mice with χ10057(pYA5199) developed a significant secretory IgA response to LcrV. The χ10057(pYA5199) induced a higher level of protection (80% survival) against intranasal (i.n.) challenge with ∼240 LD50 (2.4 x 10(4) CFU) of Y. pestis KIM6+ (pCD1Ap) than induced by χ10057(pYA3332) (40% survival). Splenocytes from mice vaccinated with χ10057(pYA5199) produced significant levels of IFN-γ, TNF-α, and IL-17 after restimulation with LcrV and YpL antigens. Our results suggest it is possible to use an attenuated Y. pseudotuberculosis strain delivering the LcrV antigen via T3SS as a potential vaccine candidate against pneumonic plague.
- Chromosomal Rearrangement Features of Yersinia pestis Strains from Natural Plague Foci in China. [JOURNAL ARTICLE]
- Am J Trop Med Hyg 2014 Aug 11.
The Yersinia pestis chromosome contains a large variety and number of insert sequences that have resulted in frequent chromosome rearrangement events. To identify the chromosomal rearrangement features of Y. pestis strains from five typical plague foci in China and study spontaneous DNA rearrangements potentially stabilized in certain lineages of Y. pestis genomes, we examined the linking mode of locally collinear blocks (LCBs) in 30 Y. pestis strains by a polymerase chain reaction-based method. Our results suggest most strains have relatively stable chromosomal arrangement patterns, and these rearrangement characteristics also have a very close relationship with the geographical origin. In addition, some LCB linking modes are only present in specific strains. We conclude Y. pestis chromosome rearrangement patterns may reflect the genetic features of specific geographical areas and can be applied to distinguish Y. pestis isolates; furthermore, most of the rearrangement events are stable in certain lineages of Y. pestis genomes.
- Functional and structural analysis of HicA3-HicB3, a novel toxin-antitoxin system of Yersinia pestis. [JOURNAL ARTICLE]
- J Bacteriol 2014 Aug 11.
The mechanisms involved in the virulence of Y. pestis, the plague pathogen, are not fully understood. In previous research, we found that a Yersinia pestis mutant lacking the HicB3 (YPO3369) putative orphan antitoxin was attenuated for virulence in a murine model of bubonic plague. Toxin-antitoxin systems (TASs) are widespread in prokaryotes. Most bacterial species possess many TASs of several types. In type II TASs, the toxin protein is bound and neutralized by its cognate antitoxin protein in the cytoplasm. Here, we identify the hicA3 gene encoding the toxin neutralized by HicB3, and show that HicA3-HicB3 constitutes a new functional type II TAS in Y. pestis. Using biochemical and mutagenesis-based approaches, we demonstrate that the HicA3 toxin is an RNase with a catalytic histidine residue. HicB3 has two functions: it sequesters and neutralizes HicA3 by blocking its active site and it represses transcription of the hicA3B3 operon. Gel-shift assays and reporter fusion experiments indicate that the HicB3 antitoxin binds to two operators in the hicA3B3 promoter region. We solved the X-ray structures of HicB3 and the HicA3HicB3 complex, thus we present the first crystal structure of a TA complex from the HicAB-family. HicB3 forms a tetramer that can bind two HicA3 toxin molecules. HicA3 is monomeric and folds as a double-stranded-RNA-binding domain. HicB3 N-terminal domain occludes the HicA3 active site, whereas its C-terminal domain folds as a ribbon-helix-helix DNA binding motif.
- Herbicides as weed control agents - state of the art. I. Weed control research and safener technology: the path to modern agriculture. [JOURNAL ARTICLE]
- Plant Physiol 2014 Aug 7.
The purpose of modern industrial herbicides is to control weeds. The species of weeds that plague crops today are a consequence of the historical past and are related to the history of crops and the evolution of farming practices. Chemical weed control began over a century ago with inorganic compounds and transitioned to the age of organic herbicides. Targeted herbicide research has created a steady stream of successful products. However, safeners have proven to be more difficult to find. Once discovered, it became important to determine the mode of action, partly to help the discovery of further compounds within the same class. However, mounting regulatory and economic pressure has changed the industry completely, making it harder to find a successful herbicide. Herbicide resistance has also become an increasing problem and increased the difficulty of controlling weeds. As a result, the development of new molecules has become a rare event today.
- Arthropod-Borne Bacterial Diseases in Pregnancy. [JOURNAL ARTICLE]
- Obstet Gynecol Surv 2013 Sep; 68(9):635-649.
Arthropod-borne bacterial diseases affect more than 25,000 Americans every year and thousands more around the world. These infections present a diagnostic dilemma for clinicians because they mimic many other pathologic conditions and are often low on or absent from the differential diagnosis list. Diagnosis is particularly challenging during pregnancy, as these infections may mimic common pregnancy-specific conditions, such as typical and atypical preeclampsia, or symptoms of pregnancy itself. Concerns regarding the safety in pregnancy of some indicated antibiotics add a therapeutic challenge for the prescriber, requiring knowledge of alternative therapeutic options for many arthropod-borne bacterial diseases. Physicians, especially those in endemic areas, must keep this class of infections in mind, particularly when the presentation does not appear classic for more commonly seen conditions. This article discusses presentation, diagnosis, and treatment of the most common of these arthropod-borne bacterial diseases, including Lyme disease, Rocky Mountain spotted fever, tick-borne relapsing fever, typhus, plague, cat-scratch disease, and Carrión disease.
- A Yersinia pestis tat Mutant Is Attenuated in Bubonic and Small-Aerosol Pneumonic Challenge Models of Infection but Not As Attenuated by Intranasal Challenge. [JOURNAL ARTICLE]
- PLoS One 2014; 9(8):e104524.
Bacterial proteins destined for the Tat pathway are folded before crossing the inner membrane and are typically identified by an N-terminal signal peptide containing a twin arginine motif. Translocation by the Tat pathway is dependent on the products of genes which encode proteins possessing the binding site of the signal peptide and mediating the actual translocation event. In the fully virulent CO92 strain of Yersinia pestis, the tatA gene was deleted. The mutant was assayed for loss of virulence through various in vitro and in vivo assays. Deletion of the tatA gene resulted in several consequences for the mutant as compared to wild-type. Cell morphology of the mutant bacteria was altered and demonstrated a more elongated form. In addition, while cultures of the mutant strain were able to produce a biofilm, we observed a loss of adhesion of the mutant biofilm structure compared to the biofilm produced by the wild-type strain. Immuno-electron microscopy revealed a partial disruption of the F1 antigen on the surface of the mutant. The virulence of the ΔtatA mutant was assessed in various murine models of plague. The mutant was severely attenuated in the bubonic model with full virulence restored by complementation with the native gene. After small-particle aerosol challenge in a pneumonic model of infection, the mutant was also shown to be attenuated. In contrast, when mice were challenged intranasally with the mutant, very little difference in the LD50 was observed between wild-type and mutant strains. However, an increased time-to-death and delay in bacterial dissemination was observed in mice infected with the ΔtatA mutant as compared to the parent strain. Collectively, these findings demonstrate an essential role for the Tat pathway in the virulence of Y. pestis in bubonic and small-aerosol pneumonic infection but less important role for intranasal challenge.