Immunization against Receptor Binding Domains of an Intracellular Bacterium’s Adhesins Paves a Path towards Vaccine Development
Adhesin-receptor interactions that facilitate entry into host cells are essential for obligate intracellular pathogens to survive and cause disease, making them attractive targets for protecting against infection. Anaplasma phagocytophilum is the obligate intracellular bacterium that invades neutrophils to cause granulocytic anaplasmosis, a severe disease for which no vaccine exists. Naimi et al. (e00106-20) demonstrate that immunizing mice against peptides corresponding to two adhesins’ receptor binding domains elicits B and T cell responses and pronouncedly reduces bacterial loads following challenge. This study confirms the adhesin domains’ relevance to infection in vivo and establishes them as protective antigens against granulocytic anaplasmosis.
Genetic Determinants of Enterococcal Vaginal Colonization and Persistence
Enterococcus faecalis is a vaginal pathobiont that outgrows following antibiotic perturbation of the microbiota or in patients with aerobic vaginitis. The genes that enable enterococcal colonization within the vaginal tract are undefined. Alhajjar et al. (e00270-20) provide a comprehensive genome-wide analysis of the enterococcal vaginal fitness determinants through the colonization of mice with an E. faecalis transposon mutant library. Specifically, mutants in genes encoding ethanolamine utilization and the type VII secretion system were attenuated in vaginal colonization. This study provides insight into mechanisms of E. faecalis vaginal colonization and provides a platform to explore interactions of enterococci with the vaginal mucosa.
A Microbial Prison Break in the Aerodigestive Tract
ESKAPE (Enterococcus, Staphylococcus, Klebsiella, Acinetobacter, Pseudomonas, Enterobacter) pathogens are a concerning collection of bacterial culprits, having emerged as major global health threats with a proclivity for developing antimicrobial resistance. These pathogens interact with bile, a naturally bactericidal component of digestion produced in the gastrointestinal tract and found in the lungs under certain pathological conditions. Interactions between ESKAPE pathogens and bile encourage antimicrobial tolerance and bile resistance, enabling these troublesome species to break free and cause persistent infections. Gipson et al. (e00865-19) highlight mechanisms by which ESKAPE pathogens resist bile in the aerodigestive tract and discuss important implications for human health.
Intratracheal Infection of the Pregnant Guinea Pig Is an Improved Model for Reproductive Brucellosis and Vaccine Development
Brucella spp. are intracellular bacterial pathogens of significant concern both in animals and in humans. Reproductive failure is the predominant sign of infection in animals, and new evidence indicates that Brucella can contribute to adverse pregnancy events in women. Hensel et al. (e00204-20) demonstrate that the intratracheal inoculation of pregnant guinea pigs can generate clinical disease that more closely resembles natural infection. They also demonstrate its usefulness for evaluating safety and efficacy of improved vaccines. This model offers an exciting potential to serve as an improved tool for understanding how Brucella spp. cause reproductive disease and to evaluate new vaccines for both animal and human disease.
Staphylococcus aureus Induces a Diverse Interferon Response
Staphylococcus aureus is known to activate the type I and III interferon (IFN) pathways, which contribute to its pathogenesis in acute pneumonia. The extent of this activation among different strains is unknown. In this issue, Peignier et al. (e00352-20) examine a broad collection of S. aureus isolates and observe differential interferon induction. They characterize a strain that shows very limited type I IFN induction and identify it as a vancomycin-intermediate S. aureus (VISA) isolate, going on to show that additional VISA strains have reduced capacity to activate the pathway.
Loss of the Phosphotransferase System for the β-Glucoside Salicin Affects Group A Streptococcal Virulence during Invasive Infections
Human pathogens not only have to contend with host immune defenses but must also obtain necessary nutrients found within the host for successful infection. Braza et al. (e00346-20) demonstrate that in Streptococcus pyogenes (group A Streptococcus [GAS]), the phosphotransferase system (PTS) for uptake and metabolism of the β-glucoside sugar salicin is required for GAS growth in human blood. Mutants in this operon also show altered ability to regulate virulence attributes such as biofilm formation, hemolysis, and lesion severity. Thus, GAS appears to rely on β-glucoside carbohydrates in vivo, supporting a link between sugar availability/uptake and growth/damage balance during infection.
Mutagenesis and Infection Assessment in a Physiologically Relevant Canine-Tick Infection Model Identified Genes/Genomic Regions Essential for Persistent Ehrlichia chaffeensis Infection
Understanding tick-borne diseases, including human monocytic ehrlichiosis caused by Ehrlichia chaffeensis, is hampered by inefficient mutagenesis and lack of physiologically relevant infection models. Wang et al. (e00316-20) describe Himar1 mutagenesis in E. chaffeensis coupled with canine-tick infection assessment to identify vital pathogen genes. The authors demonstrate that disruptions in the majority of pathogen genes/genomic regions are detrimental. They identify essential genes encoding outer membrane, protein synthesis, fatty acid and biotin biosynthesis, DNA repair, oxidoreductase, and multidrug resistance efflux pump proteins. This study opens novel research in defining pathogenesis, prevention, and therapeutics in E. chaffeensis and other important Anaplasmataceae pathogens.
Interleukin-1β Fuels Streptococcal Pharyngitis
Group A Streptococcus causes half a billion annual cases of pharyngitis (strep throat). In this issue, LaRock et al. (e00356-20) show that the hallmark inflammation, swelling, pain, and neutrophil influx during infections of the upper respiratory tract depend on the proinflammatory cytokine interleukin-1β (IL-1β). The streptococcal protease SpeB directly matures pro-IL-1β, leading to neutrophilic inflammation that promotes pathogen growth. Immune inhibition blocks streptococcal infection, suggesting that group A Streptococcus uses inflammation to remodel the upper respiratory tract and the symptoms of strep throat are purposeful manipulations by the pathogen to support its growth.
- Copyright © 2020 American Society for Microbiology.
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- Article
- Immunization against Receptor Binding Domains of an Intracellular Bacterium’s Adhesins Paves a Path towards Vaccine Development
- Genetic Determinants of Enterococcal Vaginal Colonization and Persistence
- A Microbial Prison Break in the Aerodigestive Tract
- Intratracheal Infection of the Pregnant Guinea Pig Is an Improved Model for Reproductive Brucellosis and Vaccine Development
- Staphylococcus aureus Induces a Diverse Interferon Response
- Loss of the Phosphotransferase System for the β-Glucoside Salicin Affects Group A Streptococcal Virulence during Invasive Infections
- Mutagenesis and Infection Assessment in a Physiologically Relevant Canine-Tick Infection Model Identified Genes/Genomic Regions Essential for Persistent Ehrlichia chaffeensis Infection
- Interleukin-1β Fuels Streptococcal Pharyngitis
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