How to rewire the host cell: A home improvement guide for intracellular bacteria.

Intracellular bacterial pathogens have developed versatile strategies to generate niches inside the eukaryotic cells that allow them to survive and proliferate. Making a home inside the host offers many advantages; however, intracellular bacteria must also overcome many challenges, such as disarming innate immune signaling and accessing host nutrient supplies. Gaining entry into the cell and avoiding degradation is only the beginning of a successful intracellular lifestyle. To establish these replicative niches, intracellular pathogens secrete various virulence proteins, called effectors, to manipulate host cell signaling pathways and subvert host defense mechanisms. Many effectors mimic host enzymes, whereas others perform entirely novel enzymatic functions. A large volume of work has been done to understand how intracellular bacteria manipulate membrane trafficking pathways. In this review, we focus on how intracellular bacterial pathogens target innate immune signaling, the unfolded protein response, autophagy, and cellular metabolism and exploit these pathways to their advantage. We also discuss how bacterial pathogens can alter host gene expression by directly modifying histones or hijacking the ubiquitination machinery to take control of several host signaling pathways

The influence of the accessory genome on bacterial pathogen evolution

Bacterial pathogens exhibit significant variation in their genomic content of virulence factors. This reflects the abundance of strategies pathogens evolved to infect host organisms by suppressing host immunity. Molecular arms-races have been a strong driving force for the evolution of pathogenicity, with pathogens often encoding overlapping or redundant functions, such as type III protein secretion effectors and hosts encoding ever more sophisticated immune systems. The pathogens’ frequent exposure to other microbes, either in their host or in the environment, provides opportunities for the acquisition or interchange of mobile genetic elements. These DNA elements accessorise the core genome and can play major roles in shaping genome structure and altering the complement of virulence factors. Here, we review the different mobile genetic elements focusing on the more recent discoveries and highlighting their role in shaping bacterial pathogen evolution

Can the Gram-negative bacterium Escherichia coli colonize the gut of Lone Star Tick (Amblyomma americanum)?

Ticks are obligate blood feeding ectoparasites and vectors of several mammalian pathogens (Williams-Newkirk et al, 2014). In addition to pathogens they also carry a bacterial community with commensal and symbiotic relationships (Bonnet et al, 2017). Using a culture-dependent approach we previously reported a high prevalence of Gram-positive bacteria in the gut of field collected lone star ticks (Amblyomma americanum). These results suggested that epithelial immunity functions to control Gram-negative bacteria in A. americanum. In this study, we used a culturing and non-culturing approach to measure the outcome of E.coli (Gram-negative) when fed to female adult lone star ticks (n=16). Results showed a significant reduction of E.coli at Days 1, 3 and 7 post bacterial feeding. qPCR of 16S rDNA confirmed reduction of bacterial rDNA when compared to water fed ticks (n=16). Our results suggest that there is a midgut epithelial immune response in place, which mainly targets Gram-negative bacteria

Bacterial resistance to antimicrobial agents and its impact on veterinary and human medicine

Background Antimicrobial resistance has become a major challenge in veterinary medicine, particularly in the context of bacterial pathogens that play a role in both humans and animals. Objectives This review serves as an update on acquired resistance mechanisms in bacterial pathogens of human and animal origin, including examples of transfer of resistant pathogens between hosts and of resistance genes between bacteria. Results Acquired resistance is based on resistance-mediating mutations or on mobile resistance genes. Although mutations are transferred vertically, mobile resistance genes are also transferred horizontally (by transformation, transduction or conjugation/mobilization), contributing to the dissemination of resistance. Mobile genes specifying any of the three major resistance mechanisms – enzymatic inactivation, reduced intracellular accumulation or modification of the cellular target sites – have been found in a variety of bacteria that may be isolated from animals. Such resistance genes are associated with plasmids, transposons, gene cassettes, integrative and conjugative elements or other mobile elements. Bacteria, including zoonotic pathogens, can be exchanged between animals and humans mainly via direct contact, but also via dust, aerosols or foods. Proof of the direction of transfer of resistant bacteria can be difficult and depends on the location of resistance genes or mutations in the chromosomal DNA or on a mobile element. Conclusion The wide variety in resistance and resistance transfer mechanisms will continue to ensure the success of bacterial pathogens in the future. Our strategies to counteract resistance and preserve the efficacy of antimicrobial agents need to be equally diverse and resourceful. This article is based on a State of the Art presentation at the 8th World Congress of Veterinary Dermatology held May 2016 in Bordeaux, France

Diagnosis and Treatment of Infectious Enteritis in Adult Ruminants.

Infectious enteritis in adult ruminants is often a result of 1 or more viral, bacterial, or parasitic pathogens. Diagnosis of etiologic agents causing enteritis is important when considering herd implications and zoonotic potential of some etiologies. Differential diagnoses for enteritis in adult ruminants is not simple based on clinical signs alone. Diagnostic samples include feces, blood, and antemortem and postmortem tissues. Treatment of infectious enteritis is aimed at correcting dehydration and electrolyte imbalances secondary to diarrhea. In cases of some bacterial and parasitic pathogens, additional targeted treatment and control are recommended. Management of enteritis may be instituted while awaiting laboratory test results

Differential in vitro and in vivo effect of barley cysteine and serine protease inhibitors on phytopathogenic microorganisms

Protease inhibitors from plants have been involved in defence mechanisms against pests and pathogens. Phytocystatins and trypsin/α-amylase inhibitors are two of the best characterized protease inhibitor families in plants. In barley, thirteen cystatins (HvCPI-1 to 13) and the BTI-CMe trypsin inhibitor have been previously studied. Their capacity to inhibit pest digestive proteases, and the negative in vivo effect caused by plants expressing these inhibitors on pests support the defence function of these proteins. Barley cystatins are also able to inhibit in vitro fungal growth. However, the antifungal effect of these inhibitors in vivo had not been previously tested. Moreover, their in vitro and in vivo effect on plant pathogenous bacteria is still unknown. In order to obtain new insights on this feature, in vitro assays were made against different bacterial and fungal pathogens of plants using the trypsin inhibitor BTI-CMe and the thirteen barley cystatins. Most barley cystatins and the BTI-CMe inhibitor were able to inhibit mycelial growth but no bacterial growth. Transgenic Arabidopsis plants independently expressing the BTI-CMe inhibitor and the cystatin HvCPI-6 were tested against the same bacterial and fungal pathogens. Neither the HvCPI-6 expressing transgenic plants nor the BTI-CMe ones were more resistant to plant pathogen fungi and bacteria than control Arabidopsis plants. The differences observed between the in vitro and in planta assays against phytopathogenic fungi are discusse