Controlling Bovine Tuberculosis and Other Infectious Diseases in Cattle With Total Health Management.

8 p

Controlling Bovine Tuberculosis and Other Infectious Diseases in Cattle With Total Health Management.

8 p

Brucella melitensis VjbR and C12-HSL regulons: contributions of the N-dodecanoyl homoserine lactone signaling molecule and LuxR homologue VjbR to gene expression

<p>Abstract</p> <p>Background</p> <p>Quorum sensing is a communication system that regulates gene expression in response to population density and often regulates virulence determinants. Deletion of the <it>luxR </it>homologue <it>vjbR </it>highly attenuates intracellular survival of <it>Brucella melitensis </it>and has been interpreted to be an indication of a role for QS in <it>Brucella </it>infection. Confirmation for such a role was suggested, but not confirmed, by the demonstrated <it>in vitro </it>synthesis of an auto-inducer (AI) by <it>Brucella </it>cultures. In an effort to further delineate the role of VjbR to virulence and survival, gene expression under the control of VjbR and AI was characterized using microarray analysis.</p> <p>Results</p> <p>Analyses of wildtype <it>B. melitensis </it>and isogenic Δ<it>vjbR </it>transciptomes, grown in the presence and absence of exogenous <it>N</it>-dodecanoyl homoserine lactone (C₁₂-HSL), revealed a temporal pattern of gene regulation with variances detected at exponential and stationary growth phases. Comparison of VjbR and C₁₂-HSL transcriptomes indicated the shared regulation of 127 genes with all but 3 genes inversely regulated, suggesting that C₁₂-HSL functions via VjbR in this case to reverse gene expression at these loci. Additional analysis using a Δ<it>vjbR </it>mutant revealed that AHL also altered gene expression in the absence of VjbR, up-regulating expression of 48 genes and a <it>luxR </it>homologue <it>blxR </it>93-fold at stationary growth phase. Gene expression alterations include previously un-described adhesins, proteases, antibiotic and toxin resistance genes, stress survival aids, transporters, membrane biogenesis genes, amino acid metabolism and transport, transcriptional regulators, energy production genes, and the previously reported <it>fliF </it>and <it>virB </it>operons.</p> <p>Conclusions</p> <p>VjbR and C₁₂-HSL regulate expression of a large and diverse number of genes. Many genes identified as virulence factors in other bacterial pathogens were found to be differently expressed, suggesting an important contribution to intracellular survival of <it>Brucella</it>. From these data, we conclude that VjbR and C₁₂-HSL contribute to virulence and survival by regulating expression of virulence mechanisms and thus controlling the ability of the bacteria to survive within the host cell. A likely scenario occurs via QS, however, operation of such a mechanism remains to be demonstrated.</p

Estudios histopatológicos de la encefalomielitis equina venezolana en asnos.

Basado en la tesis con igual título de J. Payán Moreno (Doc 867

Gut inflammation provides a respiratory electron acceptor for Salmonella.

Salmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence factors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response enhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through unknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate. The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S. Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium virulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for the biology of this diarrhoeal pathogen

Phage mediated horizontal transfer of the sopE1 gene increases enteropathogenicity of Salmonella enterica serotype Typhimurium for calves

Epidemiological evidence shows that the sopE1 gene is associated with Salmonella Typhimurium phage types causing epidemics in cattle. In this study we demonstrate that horizontal transfer of the sopE1 gene by lysogenic conversion with the SopEΦ increased enteropathogenicity of S. Typhimurium in the bovine ligated ileal loop model. These data support the hypothesis that phage mediated horizontal transfer of the sopE1 gene contributes to the emergence of epidemic cattle-associated S. Typhimurium clone

Correlative Gene Expression to Protective Seroconversion in Rift Valley Fever Vaccinates

Rift Valley fever Virus (RVFV), a negative-stranded RNA virus, is the etiological agent of the vector-borne zoonotic disease, Rift Valley fever (RVF). In both humans and livestock, protective immunity can be achieved through vaccination. Earlier and more recent vaccine trials in cattle and sheep demonstrated a strong neutralizing antibody and total IgG response induced by the RVF vaccine, authentic recombinant MP-12 (arMP-12). From previous work, protective immunity in sheep and cattle vaccinates normally occurs from 7 to 21 days after inoculation with arMP-12. While the serology and protective response induced by arMP-12 has been studied, little attention has been paid to the underlying molecular and genetic events occurring prior to the serologic immune response. To address this, we isolated RNA from whole blood of vaccinated calves over a time course of 21 days before and after vaccination with arMP-12. The time course RNAs were sequenced by RNASeq and bioinformatically analyzed. Our results revealed time-dependent activation or repression of numerous gene ontologies and pathways related to the vaccine induced immune response and its regulation. Additional bioinformatic analyses identified a correlative relationship between specific host immune response genes and protective immunity prior to the detection of protective serum neutralizing antibody responses. These results contribute an important proof of concept for identifying molecular and genetic components underlying the immune response to RVF vaccination and protection prior to serologic detection.The open access fee for this work was funded through the Texas A&M University Open Access to Knowledge (OAK) Fund

A species independent universal bio-detection microarray for pathogen forensics and phylogenetic classification of unknown microorganisms

<p>Abstract</p> <p>Background</p> <p>The ability to differentiate a bioterrorist attack or an accidental release of a research pathogen from a naturally occurring pandemic or disease event is crucial to the safety and security of this nation by enabling an appropriate and rapid response. It is critical in samples from an infected patient, the environment, or a laboratory to quickly and accurately identify the precise pathogen including natural or engineered variants and to classify new pathogens in relation to those that are known. Current approaches for pathogen detection rely on prior genomic sequence information. Given the enormous spectrum of genetic possibilities, a field deployable, robust technology, such as a universal (any species) microarray has near-term potential to address these needs.</p> <p>Results</p> <p>A new and comprehensive sequence-independent array (Universal Bio-Signature Detection Array) was designed with approximately 373,000 probes. The main feature of this array is that the probes are computationally derived and sequence independent. There is one probe for each possible 9-mer sequence, thus 4⁹(262,144) probes. Each genome hybridized on this array has a unique pattern of signal intensities corresponding to each of these probes. These signal intensities were used to generate an un-biased cluster analysis of signal intensity hybridization patterns that can easily distinguish species into accepted and known phylogenomic relationships. Within limits, the array is highly sensitive and is able to detect synthetically mixed pathogens. Examples of unique hybridization signal intensity patterns are presented for different <it>Brucella </it>species as well as relevant host species and other pathogens. These results demonstrate the utility of the UBDA array as a diagnostic tool in pathogen forensics.</p> <p>Conclusions</p> <p>This pathogen detection system is fast, accurate and can be applied to any species. Hybridization patterns are unique to a specific genome and these can be used to decipher the identity of a mixed pathogen sample and can separate hosts and pathogens into their respective phylogenomic relationships. This technology can also differentiate between different species and classify genomes into their known clades. The development of this technology will result in the creation of an integrated biomarker-specific bio-signature, multiple select agent specific detection system.</p