Epidermis as a Platform for Bacterial Transmission

The epidermis constitutes a continuous external layer covering the body, offering protection against bacteria, the most abundant living organisms that come into contact with this barrier. The epidermis is heavily colonized by commensal bacterial organisms that help protect against pathogenic bacteria. The highly regulated and dynamic interaction between the epidermis and commensals involves the host’s production of nutritional factors promoting bacterial growth together to chemical and immunological bacterial inhibitors. Signal trafficking ensures the system’s homeostasis; conditions that favor colonization by pathogens frequently foster commensal growth, thereby increasing the bacterial population size and inducing the skin’s antibacterial response, eliminating the pathogens and re-establishing the normal density of commensals. The microecological conditions of the epidermis favors Gram-positive organisms and are unsuitable for long-term Gram-negative colonization. However, the epidermis acts as the most important host-to-host transmission platform for bacteria, including those that colonize human mucous membranes. Bacteria are frequently shared by relatives, partners, and coworkers. The epidermal bacterial transmission platform of healthcare workers and visitors can contaminate hospitalized patients, eventually contributing to cross-infections. Epidermal transmission occurs mostly via the hands and particularly through fingers. The three-dimensional physical structure of the epidermis, particularly the fingertips, which have frictional ridges, multiplies the possibilities for bacterial adhesion and release. Research into the biology of bacterial transmission via the hands is still in its infancy; however, tribology, the science of interacting surfaces in relative motion, including friction, wear and lubrication, will certainly be an important part of it. Experiments on finger-to-finger transmission of microorganisms have shown significant interindividual differences in the ability to transmit microorganisms, presumably due to genetics, age, sex, and the gland density, which determines the physical, chemical, adhesive, nutritional, and immunological status of the epidermal surface. These studies are needed to optimize interventions and strategies for preventing the hand transmission of microorganisms.

The Host-Guest Complexes of Various Carbon Nanotubes (CNTs) and Boron Nitride Nanotubes (BNNTs) with Water at DFT Levels

We have investigated the various nanotube (NT)-water complexes as important host-guest complexes via the DFT method using B3LYP/6-31G* and M06/6-31G* levels of theory. These NTs include single-walled and double-walled carbon nanotubes (SWCNT and DWCNT, respectively). In addition, the boron nitride nanotube (BNNT) and tip-functionalized CNTs are also designed. All geometries turn out as minima on their energy surfaces. Calculated structural and thermodynamic parameters, along with atoms in molecules (AIM) and natural bond orbital (NBO) analyses, indicate that water inside the SWCNTs shows a higher interaction with NT where the nature of interactions is partially electrostatic-partially covalent. Therefore, the SWCNTs turn out as the best candidates for carrying and storage the water molecules.

Disruption of vacuolin microdomains in the host Dictyostelium discoideum increases resistance to Mycobacterium marinum-induced membrane damage and infection

Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, manipulates the host phagosome maturation pathway to replicate intracellularly. Mycobacterium marinum, a closely-related species, and Dictyostelium discoideum, a social amoeba and alternative phagocytic host, have been used as models to study host-pathogen interactions occurring during mycobacterial infections. Vacuolins, functional homologues of the mammalian flotillins, organize membrane microdomains and play a role in vesicular trafficking. Various pathogens have been reported to manipulate their membrane association and function. During infection of D. discoideum with M. marinum, Vacuolin C was specifically and highly induced and all three vacuolin isoforms were enriched at the mycobacteria-containing-vacuole (MCV). In addition, absence of vacuolins reduced escape from the MCV and conferred resistance to M. marinum infection. Moreover, ESAT-6, the membrane-disrupting virulence factor of M. marinum, was less associated with membranes when vacuolins were absent. Together, these results suggest that vacuolins are important host factors that are manipulated by mycobacteria to inflict membrane damage and escape from their compartment.

Selective Host Attachment by Ixodes scapularis (Acari: Ixodidae): Tick–Lizard Associations in the Southeastern United States

Questing behavior and host associations of immature blacklegged ticks, Ixodes scapularis Say, from the southeastern United States are known to differ from those in the north. To elucidate these relationships we describe host associations of larval and nymphal I. scapularis from 8 lizard species sampled from 5 sites in the southeastern U.S. Larvae and nymphs attached in greater numbers to larger lizards than to smaller lizards, with differential levels of attachment to different lizard species. Blacklegged ticks are generally attached to skinks of the genus Plestiodon in greater numbers per unit lizard weight than to anoles (Anolis) or fence lizards (Sceloporus). The broad-headed skink, Plestiodon laticeps (Schneider), was a particularly important host for immature I. scapularis in our study and in several previous studies of tick–host associations in the southeast. Blacklegged ticks show selective attachment to Plestiodon lizard hosts in the southeast, but whether this results from behavioral host preferences or from ecological factors such as timing or microhabitat distributions of tick questing and host activity remains to be determined.

A SYSTEMATIC REVIEW AND META-ANALYSIS TO ASSESS THE SIGNIFICANCE OF MICROBIAL INFECTIONS IN ZEBRA

Wild equids can harvest multiple-host infectious agents that are able to affect other wildlife species, but also domestic animals and humans. The contact between wild and domestic equids is constantly increasing due to the depletion of natural areas, climate and land-usage changes, which could result in burdensome epidemics. Nevertheless, currently there is a lack of adequate epidemiological data from zebra. Three electronic databases were searched from 10 to 20 March 2021 for publications reporting bacterial, viral and protozoan infections in zebra. Data for a total of 12 nominal variables were extracted from reviewed papers to undergo a qualitative analysis on microbial infections in zebra. Prevalence-reporting studies were subjected to meta-analysis for estimating the pooled prevalence and seroprevalence of infectious agents in wild zebra populations. We identified 29 pathogen species and the most represented were Equine Herpesvirus 1 and 9, Bacillus anthracis, African Horse Sickness virus and Theileria equi. They were reported from all the three zebra species, both in captivity and wilderness. Pooled seroprevalences were estimated for the equine Orbiviruses AHSV (70%; 95%CI: 35-96%) and EEV (21%; 95%CI: 8-38%) and for the equine α -Herpesviruses EHV-1 (72%; 95%CI: 43-93%), EHV-4 (40%; 95%CI: 0-100%) and EHV-9 (58%; 95%CI: 9-98%), and pooled prevalences for the equine piroplasms T. equi (100%; 95%CI: 94-100%) and B. caballi (8%; 95%CI: 0-28%). Zebra is most probably a reservoir from which AHSV, EHV-1 and T. equi can be transmitted to horse populations, potentially causing disastrous epidemics. Zebra can also harvest zoonotic pathogens like B. anthracis, A. phagocytophylum, CCHFV and T. brucei. Other agents like EHV-9, BPV-1 and BPV-2 have the potential to spread from zebra to other wild endangered animal species. We conclude that zebra is an important host for multiple and dangerous pathogens. Alert and epidemiological research should be increased on infectious agents of zebra.

The IL-33-ILC2 pathway protects from amebic colitis

Entamoeba histolytica is a pathogenic protozoan parasite that causes intestinal colitis, diarrhea, and in some cases, liver abscess. Through transcriptomics analysis, we observed that E. histolytica infection was associated with increased expression of IL-33 mRNA in both the human and murine colon. IL-33, the IL-1 family cytokine, is released after cell injury to alert the immune system of tissue damage. Treatment with recombinant IL-33 protected mice from amebic infection and intestinal tissue damage; moreover, blocking IL-33 signaling made mice more susceptible to amebiasis. IL-33 limited the recruitment of inflammatory immune cells and decreased the pro-inflammatory cytokine IL-6 in the cecum. Type 2 immune responses were upregulated by IL-33 treatment during amebic infection. Interestingly, administration of IL-33 protected RAG2–/– mice but not RAG2−/−γc−/− mice, demonstrating that IL-33-mediated protection required the presence of innate lymphoid cells (ILCs). IL-33 induced recruitment of ILC2 but not ILC1 and ILC3 in RAG2−/− mice. At baseline and after amebic infection, there was a significantly higher IL13+ILC2s in C57BL/J mice, which are naturally resistant to amebiasis, than CBA/J mice. Adoptive transfer of ILC2s to RAG2−/−γc−/− mice restored IL-33-mediated protection. These data reveal that the IL-33-ILC2 pathway is an important host defense mechanism against amebic colitis.

SigV mediates lysozyme resistance in Enterococcus faecalis via RsiV and PgdA

Enterococcus faecalis is a gut commensal but transitions to a pathogenic state as a consequence of intestinal dysbiosis and/or the presence of indwelling medical devices causing a wide range of infections. One of the unique features of E. faecalis is its ability to display high level resistance to lysozyme, an important host defense of the innate immune response. Lysozyme resistance in E. faecalis is known to be mediated by the e xtra c ytoplasmic f unction (ECF) sigma factor, SigV. PgdA and RsiV expression is directly regulated by SigV, but pgdA and rsiV mutants display nominal changes in lysozyme resistance, suggesting that additional gene products in the SigV regulon contribute to lysozyme resistance. Using RNA-seq analysis, we compared the transcriptional profile of the parental strain to an isogenic sigV mutant and show that apart from sigV , only rsiV and pgdA expression was induced upon lysozyme exposure. The combined deletion mutant of both rsiV and pgdA rendered E. faecalis sensitive to lysozyme at a level comparable to the sigV mutant, highlighting the limited SigV regulon. Several additional genes were also induced upon lysozyme exposure, but in a SigV-independent fashion. Overexpression of pgdA from a SigV-independent promoter restored lysozyme resistance in a sigV deletion mutant and also induced cell chaining. Overexpression of rsiV from a SigV-independent promoter only partially restored lysozyme resistance in a sigV mutant. Overall, we provide evidence for a simple adaptation to lysozyme stress, in which SigV controls the expression of rsiV and pgdA , and that both gene products contribute to lysozyme resistance. Importance Enterococcus faecalis causes healthcare-associated infections and displays resistance to a variety of antibiotics and molecules of the innate immune system. SigV has been shown to play an important role in enterococcal lysozyme resistance. Even though several proteins have been implicated in enterococcal lysozyme resistance, a complete SigV-dependent regulon has not been functionally characterized as being responsible for the dramatic increase in lysozyme susceptibility displayed by a sig V mutant. Using RNA-seq, we have identified the SigV regulon to be comprised of two gene loci, sigV - rsiV and pgdA . Deletion of both rsiV and pgdA renders E. faecalis susceptible to lysozyme on par with a sigV mutant. We also demonstrate that overproduction of rsiV and pgdA contribute to lysozyme resistance in susceptible strains.

Differentiated Archean Dolerites: Igneous and Emplacement Processes that Enhance Prospectivity for Orogenic Gold

Magnetite-bearing granophyre and quartz dolerite are the evolved fractions of differentiated dolerite (diabase) sills and are an important host to Archean gold deposits because they are chemical traps for orogenic fluids. Despite their economic importance, there is a poor understanding of how melt composition, crystal fractionation, sill geometry, and depth of emplacement increase the volume of host rock that is most favorable for gold precipitation during orogenesis. We use drill core logging, whole-rock geochemistry, magnetic susceptibility, gold assay, and thermodynamic modeling data from 11 mineralized and unmineralized ca. 2.7 Ga differentiated dolerites in the Eastern Goldfields superterrane (Yilgarn craton, Western Australia) to better understand the influence of igneous and emplacement processes on gold prospectivity. Orogenic gold favors differentiated dolerites, derived from iron-rich parental magmas, that crystallize large volumes of magnetite-bearing quartz dolerite (>25% total thickness). Mineralized sills are commonly >150 m thick and hosted by thick and broadly coeval sedimentary sequences. Sill thickness is an important predictor for gold prospectivity, as it largely controls cooling rate and hence fractionation. The parental melts of gold mineralized sills fractionated large amounts of clinopyroxene and plagioclase (possibly up to 50%) at depth before emplacement in the shallow crust. A second fractionation event at shallow levels (<3 km) operated both vertically and laterally, resulting in an antithetic relationship between quartz (magnetite) dolerite and cumulates (pyroxenites and peridotites). By comparison with younger mafic sills emplaced in synsedimentary basins, we argue that the geometry of these high-level sills was more irregular than the often-assumed tabular form. Any irregularities in the lower sill margin act as traps for early formed (dense) ferromagnesian minerals, now represented by pyroxene and peridotite cumulates. In contrast, irregularities in the upper sill margin trap the buoyant fractionated liquids when the sill is more crystalline, through magma flow on the scale of <1 km. Sills derived from iron-poor melts are rarely mineralized and, all else being equal, probably have to be thicker than Fe-rich sills to be similarly prospective for orogenic gold. Finally, we provide a list of quantifiable parameters that can be incorporated into an exploration program targeting differentiated dolerites that host orogenic gold.

Community structure of protozoan parasites in Heteropneustes fossilis (Bloch 1794) in Bangladesh

The study was conducted to prepare a database for the infection status of protozoan parasites on an important host fish species of Bangladesh, Heretropneustes fossilis. Host samples were collected from the freshwater habitats of six different districts of Bangladesh- Manikganj, Faridpur, Mymensingh, Kishoreganj, Bogura, and Jashore. H. fossilis was noted to be infected by 6 parasite species, of which 3 belonged to myxozoa (Henneguya singhi, Henneguya qadrii and Henneguya mystusia); 1 belonged to ciliophora (Trichodina siddiquae) and 2 (Trypanosoma singhii and Piscinoodium pillulare) belonged to mastigophora.The parasites, Trypanosoma singhii and Henneguya singhi were recorded as new locality record in H. fossilis. The three parasites Piscinoodium pillulare, Henneguya qadrii and Henneguya mystusia were the first recorded parasites in this fish and the first locality record in Bangladesh. The parasites were observed to occupy gill, body slime, and blood. Gill parasites were abundantly found compared to body slime and blood parasites. The highest prevalence (67.21%) of infection of H. fossilis was observed in Manikganj and the lowest prevalence (54.67%) of infection was observed in Bogura. Parasites of H. fossilis showed the highest diversity in fishes of Faridpur (2.63). Species richness of parasites was highest in Manikganj (0.38) and species evenness was relatively low (0.13-0.19) in almost all the study sites. Dhaka Univ. J. Biol. Sci. 30(2): 307-316, 2021 (July)

Systems Biology and Bile Acid Signalling in Microbiome-Host Interactions in the Cystic Fibrosis Lung

The study of the respiratory microbiota has revealed that the lungs of healthy and diseased individuals harbour distinct microbial communities. Imbalances in these communities can contribute to the pathogenesis of lung disease. How these imbalances occur and establish is largely unknown. This review is focused on the genetically inherited condition of Cystic Fibrosis (CF). Understanding the microbial and host-related factors that govern the establishment of chronic CF lung inflammation and pathogen colonisation is essential. Specifically, dissecting the interplay in the inflammation–pathogen–host axis. Bile acids are important host derived and microbially modified signal molecules that have been detected in CF lungs. These bile acids are associated with inflammation and restructuring of the lung microbiota linked to chronicity. This community remodelling involves a switch in the lung microbiota from a high biodiversity/low pathogen state to a low biodiversity/pathogen-dominated state. Bile acids are particularly associated with the dominance of Proteobacterial pathogens. The ability of bile acids to impact directly on both the lung microbiota and the host response offers a unifying principle underpinning the pathogenesis of CF. The modulating role of bile acids in lung microbiota dysbiosis and inflammation could offer new potential targets for designing innovative therapeutic approaches for respiratory disease.