Karen Pendergrass, Standards Team

O₃ nanoparticles, especially when combined with cinnamon, clove, or lemongrass essential oils, exhibited strong synergistic antifungal effects against multiple dermatophytes, offering a promising strategy against antifungal resistance.

This S-based study reveals that M. canis genotype correlates with disease severity in cats, identifies three genetic clusters, and confirms the dominance of the AT1-1 mating type. Conserved virulence genes (SU1, UB3) offer potential diagnostic utility.

This review details the enzymatic and genetic virulence arsenal of Microsporum canis, highlighting understudied factors like biofilms and dipeptidylpeptidases. Greater insight into these mechanisms could improve treatment and prevention strategies.

This study identified a metalloprotease gene family in Microsporum canis and confirmed in vivo expression of EP2 and EP3 during infection. EP3, a keratinolytic enzyme, was expressed recombinantly and may contribute to fungal virulence, supporting its use in vaccine development.

Bee venom showed partial antifungal activity against resistant M. canis isolates, supporting its evaluation as a potential topical therapeutic. While not as potent as terbinafine, V outperformed fluconazole and amphotericin B in susceptible isolates, highlighting its promise amid rising antifungal resistance.

Microsporum canis (M. canis) is a zoophilic dermatophyte common in cats and dogs, responsible for 90% of feline dermatophytoses worldwide.[1][2] It has significant zoonotic potential, transmitting to humans through fomites or direct animal contact, causing severe superficial mycosis. M. canis is considered anthropo-zoophilic and can infect pediatric or immunocompromised patients, causing severe inflammatory responses such […]

A multi‑ethnic review summarising >80 genetic loci underlying Graves’ disease, their clinical correlates and emerging precision‑medicine applications.

This review maps the immune‑microbial mechanisms driving Graves’ disease and evaluates next‑generation biologics, small molecules and tolerance‑inducing peptides that may replace conventional ablation therapies.

This review links genetics, hormones, environment and especially viral exposures—BV and CV—to the Th1‑centric immunopathology of Graves’ disease, highlighting chemokine signatures relevant to microbiome‑based risk models.

Mendelian‑randomization of 18,340 BioGen participants and > 349k Gen controls identifies 32 gut genera with causal roles—some protective, others harmful—across six thyroid diseases, highlighting therapeutic microbiome targets.