Virulence Factors of Microsporum canis: Enzymes, Genes, and Clinical Implication Original paper
Researched by:
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Karen Pendergrass
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Karen Pendergrass
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
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Microbes
Microbes
Microbes, short for microorganisms, are tiny living organisms that are ubiquitous in the environment, including on and inside the human body. They play a crucial role in human health and disease, functioning within complex ecosystems in various parts of the body, such as the skin, mouth, gut, and respiratory tract. The human microbiome, which is […]
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Microsporum canis (M. canis)
Microsporum canis (M. canis)
OverviewMicrosporum 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 […]
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Karen Pendergrass
Researched by:
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Karen Pendergrass
ID
Karen Pendergrass
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Karen Pendergrass
What was reviewed?
This systematic review examined the phenotypic virulence factors of Microsporum canis, a dermatophyte responsible for superficial fungal infections in humans and animals. The authors compiled and synthesized data from 46 original research articles published between 1988 and 2023, focusing on enzymatic and non-enzymatic factors that contribute to fungal adhesion, invasion, immune evasion, and survival within keratinized tissues. Key attention was given to extracellular and intracellular virulence mechanisms, associated gene expression, and implications for infection control and antifungal resistance.
Who was reviewed?
The review drew upon experimental and clinical studies investigating M. canis strains isolated from both symptomatic and asymptomatic animals (especially cats and dogs) and human hosts, including pediatric and immunocompromised individuals. The reviewed studies encompassed diverse methodological approaches—ranging from enzymatic profiling and gene expression analyses to in vivo and in vitro infection models using tissues from humans, cats, and guinea pigs.
Most important findings
The review identified a broad range of virulence factors grouped into extracellular and intracellular categories. Among the extracellular factors, three key protease classes—keratinases, metalloproteases (fungalisins), and subtilisins—were most frequently characterized. These enzymes enable M. canis to degrade host keratin, collagen, and elastin, facilitating nutrient acquisition and tissue colonization. Subtilisin Sub3 was notably linked to fungal adhesion and chronic infection persistence. Other extracellular factors included dipeptidylpeptidases (DppIV, DppV), aminopeptidases (Lap1, Lap2), aspartyl proteases, catalases, hemolysins, ureases, and serine hydrolases, each contributing variably to tissue invasion, immune modulation, and environmental stress resistance. Biofilm formation and thermotolerance were also identified as phenotypes enhancing antifungal resistance and deeper tissue penetration.
The review also highlighted a set of intracellular virulence genes, including:
| Gene | Protein | Function |
|---|---|---|
| FSH1 | Serine hydrolase | Metabolism regulation and macroconidia production |
| NADH1 | NADH dehydrogenase | Respiratory chain function |
| AreA | GATA transcription factor | Nitrogen metabolism and proteolytic regulation |
| SUB1–SUB3 | Subtilisins | Arthroconidia adhesion and anchorage |
| MEP1–MEP5 | Metalloproteases | Collagen/elastin/keratin degradation |
| DPPIV/V | Dipeptidylpeptidases | Collagen and elastin degradation, nutrient acquisition |
| LAP1/LAP2 | Aminopeptidases | Conversion of long-chain peptides to amino acids |
| SSU1 | Sulfite efflux pump | Detoxification of sulfur metabolites |
| PacC | pH-responsive TF | Regulation of proteolytic gene expression |
Key implications
The review underscores the complexity and adaptability of M. canis as a pathogen, facilitated by its diverse enzymatic arsenal and environmentally responsive gene expression. While keratinases, subtilisins, and metalloproteases are well-characterized, less attention has been given to dipeptidylpeptidases, biofilm formation, thermotolerance, and sulfite detoxification—all of which may be crucial for chronicity, deep invasion, and treatment resistance. The authors emphasize the need to expand research beyond the canonical virulence enzymes to uncover novel targets for antifungal therapy. This has clinical relevance not only for treating dermatophytosis but also for addressing M. canis as an emerging threat in immunocompromised populations.
Urease
Urease is a nickel-dependent microbial enzyme that breaks down urea into ammonia, altering local pH and nitrogen availability. While essential for microbial survival in acidic niches and nutrient-limited environments, urease activity also contributes to conditions like ulcers, urinary stones, colitis, and hepatic encephalopathy.