PEERing forward in parasitology.

PEERs in Parasitology (PiP) is a global scientific grassroots organization founded in 2021 to promote equity and inclusion for persons (currently and) historically excluded from science because of ethnicity and/or race. The article details systemic obstacles PEER parasitologists face and current and future strategies of PiP to overcome them.

Phosphoglucomutase 1 contributes to optimal cyst development in Toxoplasma gondii.

Objective: Toxoplasma gondii is a ubiquitous parasite of medical and veterinary importance; however, there exists no cure for chronic toxoplasmosis. Metabolic enzymes required for the production and maintenance of tissue cysts represent promising targets for novel therapies. Here, we use reverse genetics to investigate the role of Toxoplasma phosphoglucomutase 1, PGM1, in Toxoplasma growth and cystogenesis.

mSphere of Influence: No More Excuses-Addressing Race, Racism, and Socioeconomic Issues in the Science Classroom and Laboratory.

Pascale Guiton works in the field of parasitology at a primarily undergraduate institution. In this mSphere of Influence article, she reflects on her difficulties as a faculty of color to discuss socioscientific issues in her classrooms. T.

Transcriptional ups and downs: patterns of gene expression in the life cycle of Toxoplasma gondii.

Toxoplasma gondii reproduces sexually in felines and asexually in virtually all warm-blooded animals, including humans. This obligate intracellular parasite alternates between biologically distinct developmental stages throughout its complex life cycle. Stage conversion is crucial for T.

An in vitro model of intestinal infection reveals a developmentally regulated transcriptome of Toxoplasma sporozoites and a NF-κB-like signature in infected host cells.

Toxoplasmosis is a zoonotic infection affecting approximately 30% of the world's human population. After sexual reproduction in the definitive feline host, Toxoplasma oocysts, each containing 8 sporozoites, are shed into the environment where they can go on to infect humans and other warm-blooded intermediate hosts. Here, we use an in vitro model to assess host transcriptomic changes that occur in the earliest stages of such infections.

AhrC and Eep are biofilm infection-associated virulence factors in Enterococcus faecalis.

Enterococcus faecalis is part of the human intestinal microbiome and is a prominent cause of health care-associated infections. The pathogenesis of many E. faecalis infections, including endocarditis and catheter-associated urinary tract infection (CAUTI), is related to the ability of clinical isolates to form biofilms.

Enterococcus faecalis overcomes foreign body-mediated inflammation to establish urinary tract infections.

Urinary catheterization elicits major histological and immunological changes that render the bladder susceptible to microbial invasion, colonization, and dissemination. However, it is not understood how catheters induce these changes, how these changes act to promote infection, or whether they may have any protective benefit. In the present study, we examined how catheter-associated inflammation impacts infection by Enterococcus faecalis, a leading cause of catheter-associated urinary tract infection (CAUTI), a source of significant societal and clinical challenges.

The metal ion-dependent adhesion site motif of the Enterococcus faecalis EbpA pilin mediates pilus function in catheter-associated urinary tract infection.

Unlabelled: Though the bacterial opportunist Enterococcus faecalis causes a myriad of hospital-acquired infections (HAIs), including catheter-associated urinary tract infections (CAUTIs), little is known about the virulence mechanisms that it employs. However, the endocarditis- and biofilm-associated pilus (Ebp), a member of the sortase-assembled pilus family, was shown to play a role in a mouse model of E. faecalis ascending UTI.

Combinatorial small-molecule therapy prevents uropathogenic Escherichia coli catheter-associated urinary tract infections in mice.

Catheter-associated urinary tract infections (CAUTIs) constitute the majority of nosocomial urinary tract infections (UTIs) and pose significant clinical challenges. These infections are polymicrobial in nature and are often associated with multidrug-resistant pathogens, including uropathogenic Escherichia coli (UPEC). Urinary catheterization elicits major histological and immunological alterations in the bladder that can favor microbial colonization and dissemination in the urinary tract.

Enterococcal biofilm formation and virulence in an optimized murine model of foreign body-associated urinary tract infections.

Catheter-associated urinary tract infections (CAUTIs) constitute the majority of nosocomial UTIs and pose significant clinical challenges. Enterococcal species are among the predominant causative agents of CAUTIs. However, very little is known about the pathophysiology of Enterococcus-mediated UTIs.

Contribution of autolysin and Sortase a during Enterococcus faecalis DNA-dependent biofilm development.

Biofilm production is a major attribute of Enterococcus faecalis clinical isolates. Although some factors, such as sortases, autolysin, and extracellular DNA (eDNA), have been associated with E. faecalis biofilm production, the mechanisms underlying the contributions of these factors to this process have not been completely elucidated yet.