Microsporum canis (M. canis)

Overview

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 as inflammatory tinea capitis (including Celsus’ Cherion), favus, tinea barbae, and tinea corporis.^[3] It is also reported as the primary agent of dermatophytosis in domestic cats in the US and a common cause of tinea capitis in humans in parts of Europe.^[4]

Antifungal Resistance

The increasing use of antifungal agents has led to rising drug resistance, posing a significant barrier to effective treatment.^[5] Resistance mechanisms include efflux pump overexpression, mutation of drug target enzymes, and biofilm formation. M. canis and generally have lower resistance rates relative to other dermatophytes.^[6] However, recalcitrant infections are well-documented for M. canis. ^[7]

Pathogenicity

Dermatophytes such as Microsporum canis exhibit a unique capacity to invade, colonize, and derive nutrients from keratinized host tissues through the secretion of proteolytic enzymes and other virulence factors.^[8] The infection begins with the adherence of arthroconidia to the host epidermis via specialized fungal surface proteins, a process facilitated by disruptions in the stratum corneum such as maceration or occlusion.^[9] Remarkably, these arthrospores can remain infectious in the environment for up to 18 months, contributing to their high transmissibility.^[10] A central feature of dermatophyte pathogenicity is their ability to degrade keratin, a complex structural protein, using a class of enzymes known as keratinases. These enzymes solubilize keratin and are considered key virulence determinants during tissue invasion. Keratinase production is typically enhanced under alkaline conditions (pH ~7.5) and at temperatures ranging from 35°C to 50°C. M. canis, in particular, synthesizes a keratinase enzyme known as Ecasa, which facilitates its ability to colonize and persist within host tissues.^[11][12]

Morphology

Microsporum canis is a filamentous, anamorphic dermatophyte that primarily reproduces asexually and exhibits distinct morphological and physiological traits optimized for keratin degradation and host adaptation.^[13][14] Macroscopically, colonies grown on Sabouraud Dextrose Agar (SDA), Sabouraud Glucose Agar (SGA), or Potato Dextrose Agar (PDA) appear white with a bright yellow periphery or lemon-yellow base and display a silky center; the reverse side may range from yellow to orange.^[15] These colonies grow rapidly, with increased diameters observed under zinc-sufficient conditions (e.g., 1000 nM Zn), while growth is markedly impaired under zinc deficiency. ^[16][17] Microscopically, M. canis produces thick-walled, spindle-shaped macroconidia with up to 15 septa and smaller microconidia, but conidiation is suppressed in zinc-limiting environments (200–800 nM), where only unstructured “flake fungus blocks” may form.^[18] A ZafA-knockout strain further demonstrates the zinc dependence of conidiogenesis, with severely diminished hyphal and conidial development.^[19] The fungus thrives at 28–30 °C but shows optimal keratinase activity at 35–50 °C and pH ~7.5.^[20]

Virulence Factors

M. canis employs a multifaceted arsenal of virulence factors to colonize keratinized tissues and evade host defenses. These include extracellular enzymes like keratinases, subtilisins, metalloproteases, and aminopeptidases, which degrade host proteins for nutrient acquisition and tissue invasion.^[21] Dipeptidyl peptidases, siderophores, and hemolysins further facilitate colonization by promoting immune evasion and iron acquisition.^[22] Catalases, ureases, and heat shock proteins enhance fungal survival under oxidative and thermal stress, while biofilm formation contributes to chronicity and antifungal resistance.^[23] Intracellularly, virulence is driven by conserved genes like ZafA, SUB3, and SSU1, which regulate metal acquisition and proteolytic activity essential for pathogenicity.^[24][25] Together, these factors enable M. canis to adapt to host environments, resist immune clearance, and maintain infection, particularly under nutrient-limited or stressed conditions. Targeting these virulence mechanisms—especially metal acquisition pathways—may offer novel antifungal strategies.

Virulence Factor	Description and Role

Keratinases (e.g., Ecasa)

Proteases that degrade keratin to enable tissue invasion. Optimal activity at pH ~7.5 and 35–50°C. Higher expression in symptomatic cases.

Metalloproteases (MEP1–3)

Zinc-dependent M36 fungalysins with keratinolytic, elastinolytic, and collagenolytic activity; essential for adhesion and tissue invasion.

Subtilisins (Sub1–3)

Serine proteases contributing to keratin degradation and adhesion. Sub3 is a well-characterized virulence marker.

Aminopeptidases (Lap1–2)

Involved in keratin breakdown and nitrogen assimilation under alkaline conditions.

Dipeptidyl Peptidases (DppIV, DppV)

Facilitate nutrient acquisition and tissue colonization; degrade elastin and collagen.

Aspartyl Proteases

Less characterized in M. canis; suspected to degrade host defense proteins based on in vitro/ex vivo data.

Hemolysins

Contribute to iron acquisition and cytotoxicity. Correlated with azole resistance.

Catalases

Detoxify reactive oxygen species; higher activity in lesion-associated strains and correlated with antifungal susceptibility.

Ureases

Provide nitrogen source; increase pH; used taxonomically. Activity varies by strain.

Serine Hydrolase (FSH1)

Functions as an esterase regulating growth, pigmentation, and conidiation; knockout reduces virulence.

Biofilms/Dermatophytomas

Structured hyphal networks embedded in ECM; increase antifungal resistance and promote chronic infection.

Heat Shock Proteins (HSPs)

Chaperones that support stress tolerance, antifungal resistance, and tissue colonization.

ZafA Gene

Zinc-responsive transcription factor regulating zinc uptake; essential under zinc-restricted conditions.

SSU1 Gene

Encodes sulfite efflux pump; involved in early infection stages. Highly conserved.

SUB3 Gene

Encodes subtilisin 3; crucial for adhesion and keratin degradation. Also highly conserved.

Metallomics

Vulnerabilities

^[26] A potential antifungal bioproduct for Microsporum canis- Bee venom.pdf

^[27] Secreted Metalloprotease Gene Family of Microsporum canis.pdf

^[28] Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review .pdf

^[29] Genetic Characterization of Microsporum canis Clinical Isolates in the United States.pdf

^[30]Synergistic Anti-Dermatophytic Potential of Nanoparticles and Essential Oils Combinations.pdf

^[31] Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review .pdf

^[32] Therapy_and_Antifungal_Susceptibility_Profile_of_M.pdf

^[33] Dermatophyte infection: from fungal pathogenicity to host immune responses.pdf

^[34] Evaluation of the antidermatophytic activity of potassium salts of N-acylhydrazinecarbodithioates and their aminotriazole-thione derivatives.pdf

^[35] Molecular detection and in vitro antifungal study of Microsporum canis isolated from cat- A case report.pdf

^[36] Virulence and Antifungal Susceptibility of Microsporum canis Strains from Animals and Humans.pdf

^[37] RNA-Seq Analysis of the Effect of Zinc Deficiency on Microsporum canis, ZafA Gene Is Important for Growth and Pathogenicity.pdf

^[38] Therapy_and_Antifungal_Susceptibility_Profile_of_M.pdf

Update History

References

1. A potential antifungal bioproduct for Microsporum canis: Bee venom.. Ütük AE, Güven Gökmen T, Yazgan H, Eşki F, Turut N, Karahan Ş, et al.. (Onderstepoort J Vet Res. 2024;91(1):a2191.)
2. Secreted Metalloprotease Gene Family of Microsporum canis.. Brouta F, Descamps F, Monod M, Vermout S, Losson B, Mignon B.. (Infect Immun. 2002 Oct;70(10):5676–5683.)
3. Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review.. Vite-Garín T, Estrada-Cruz NA, Hernández-Castro R, Fuentes-Venado CE, Zarate-Segura PB, Frías-De-León MG, Martínez-Castillo M, Martínez-Herrera E, Pinto-Almazán R.. (Int J Mol Sci. 2024;25(5):2533.)
4. Genetic Characterization of Microsporum canis Clinical Isolates in the United States.. Moskaluk A, Darlington L, Kuhn S, Behzadi E, Gagne RB, Kozakiewicz CP, VandeWoude S.. (J Fungi. 2022;8(7):676.)
5. Synergistic anti-dermatophytic potential of nanoparticles and essential oils combinations.. Sayed MA, Ghazy NM, El-Bassuony AAH.. (J Inorg Organomet Polym Mater. 2025;35:1021–1035.)
6. Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review.. Vite-Garín T, Estrada-Cruz NA, Hernández-Castro R, Fuentes-Venado CE, Zarate-Segura PB, Frías-De-León MG, Martínez-Castillo M, Martínez-Herrera E, Pinto-Almazán R.. (Int J Mol Sci. 2024;25(5):2533.)
7. Therapy and Antifungal Susceptibility Profile of Microsporum canis.. Aneke CI, Otranto D, Cafarchia C.. (J Fungi. 2018;4(3):107.)
8. Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review.. Vite-Garín T, Estrada-Cruz NA, Hernández-Castro R, Fuentes-Venado CE, Zarate-Segura PB, Frías-De-León MG, Martínez-Castillo M, Martínez-Herrera E, Pinto-Almazán R.. (Int J Mol Sci. 2024;25(5):2533.)
9. Dermatophyte infection: from fungal pathogenicity to host immune responses.. Deng R, Wang X, Li R.. (Front Immunol. 2023 Nov 2;14:1285887.)
10. A potential antifungal bioproduct for Microsporum canis: Bee venom.. Ütük AE, Güven Gökmen T, Yazgan H, Eşki F, Turut N, Karahan Ş, et al.. (Onderstepoort J Vet Res. 2024;91(1):a2191.)
11. Evaluation of the antidermatophytic activity of potassium salts of N-acylhydrazinecarbodithioates and their aminotriazole-thione derivatives.. Ciesielska A, Kowalczyk A, Paneth A, Stączek P.. (Sci Rep. 2024;14:3521.)
12. Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review.. Vite-Garín T, Estrada-Cruz NA, Hernández-Castro R, Fuentes-Venado CE, Zarate-Segura PB, Frías-De-León MG, Martínez-Castillo M, Martínez-Herrera E, Pinto-Almazán R.. (Int J Mol Sci. 2024;25(5):2533.)
13. A potential antifungal bioproduct for Microsporum canis: Bee venom.. Ütük AE, Güven Gökmen T, Yazgan H, Eşki F, Turut N, Karahan Ş, et al.. (Onderstepoort J Vet Res. 2024;91(1):a2191.)
14. Molecular detection and in vitro antifungal study of Microsporum canis isolated from cat: A case report.. Prajapati P, Gangil R, Pal S, Chhabra DK, Sharda R, Jogi J, Sikrodia R.. (Int J Vet Sci Anim Husbandry. 2025;10(4):225-231.)
15. Molecular detection and in vitro antifungal study of Microsporum canis isolated from cat: A case report.. Prajapati P, Gangil R, Pal S, Chhabra DK, Sharda R, Jogi J, Sikrodia R.. (Int J Vet Sci Anim Husbandry. 2025;10(4):225-231.)
16. Virulence and Antifungal Susceptibility of Microsporum canis Strains from Animals and Humans.. Aneke CI, Rhimi W, Hubka V, Otranto D, Cafarchia C.. (Antibiotics. 2021;10(3):296.)
17. RNA-Seq analysis of the effect of zinc deficiency on Microsporum canis, ZafA gene is important for growth and pathogenicity.. Dai P, Lv Y, Gong X, Han J, Gao P, Xu H, Zhang Y, Zhang X.. (Front Cell Infect Microbiol. 2021;11:727665.)
18. Molecular detection and in vitro antifungal study of Microsporum canis isolated from cat: A case report.. Prajapati P, Gangil R, Pal S, Chhabra DK, Sharda R, Jogi J, Sikrodia R.. (Int J Vet Sci Anim Husbandry. 2025;10(4):225-231.)
19. RNA-Seq analysis of the effect of zinc deficiency on Microsporum canis, ZafA gene is important for growth and pathogenicity.. Dai P, Lv Y, Gong X, Han J, Gao P, Xu H, Zhang Y, Zhang X.. (Front Cell Infect Microbiol. 2021;11:727665.)
20. Therapy and Antifungal Susceptibility Profile of Microsporum canis.. Aneke CI, Otranto D, Cafarchia C.. (J Fungi. 2018;4(3):107.)
21. https://doi.org/.
22. https://doi.org/.
23. https://doi.org/.
24. https://doi.org/.
25. Genetic Characterization of Microsporum canis Clinical Isolates in the United States.. Moskaluk A, Darlington L, Kuhn S, Behzadi E, Gagne RB, Kozakiewicz CP, VandeWoude S.. (J Fungi. 2022;8(7):676.)
26. A potential antifungal bioproduct for Microsporum canis: Bee venom.. Ütük AE, Güven Gökmen T, Yazgan H, Eşki F, Turut N, Karahan Ş, et al.. (Onderstepoort J Vet Res. 2024;91(1):a2191.)
27. Secreted Metalloprotease Gene Family of Microsporum canis.. Brouta F, Descamps F, Monod M, Vermout S, Losson B, Mignon B.. (Infect Immun. 2002 Oct;70(10):5676–5683.)
28. Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review.. Vite-Garín T, Estrada-Cruz NA, Hernández-Castro R, Fuentes-Venado CE, Zarate-Segura PB, Frías-De-León MG, Martínez-Castillo M, Martínez-Herrera E, Pinto-Almazán R.. (Int J Mol Sci. 2024;25(5):2533.)
29. Genetic Characterization of Microsporum canis Clinical Isolates in the United States.. Moskaluk A, Darlington L, Kuhn S, Behzadi E, Gagne RB, Kozakiewicz CP, VandeWoude S.. (J Fungi. 2022;8(7):676.)
30. Synergistic anti-dermatophytic potential of nanoparticles and essential oils combinations.. Sayed MA, Ghazy NM, El-Bassuony AAH.. (J Inorg Organomet Polym Mater. 2025;35:1021–1035.)
31. https://doi.org/.
32. Therapy and Antifungal Susceptibility Profile of Microsporum canis.. Aneke CI, Otranto D, Cafarchia C.. (J Fungi. 2018;4(3):107.)
33. Dermatophyte infection: from fungal pathogenicity to host immune responses.. Deng R, Wang X, Li R.. (Front Immunol. 2023 Nov 2;14:1285887.)
34. Evaluation of the antidermatophytic activity of potassium salts of N-acylhydrazinecarbodithioates and their aminotriazole-thione derivatives.. Ciesielska A, Kowalczyk A, Paneth A, Stączek P.. (Sci Rep. 2024;14:3521.)
35. Molecular detection and in vitro antifungal study of Microsporum canis isolated from cat: A case report.. Prajapati P, Gangil R, Pal S, Chhabra DK, Sharda R, Jogi J, Sikrodia R.. (Int J Vet Sci Anim Husbandry. 2025;10(4):225-231.)
36. Virulence and Antifungal Susceptibility of Microsporum canis Strains from Animals and Humans.. Aneke CI, Rhimi W, Hubka V, Otranto D, Cafarchia C.. (Antibiotics. 2021;10(3):296.)
37. RNA-Seq analysis of the effect of zinc deficiency on Microsporum canis, ZafA gene is important for growth and pathogenicity.. Dai P, Lv Y, Gong X, Han J, Gao P, Xu H, Zhang Y, Zhang X.. (Front Cell Infect Microbiol. 2021;11:727665.)
38. Therapy and Antifungal Susceptibility Profile of Microsporum canis.. Aneke CI, Otranto D, Cafarchia C.. (J Fungi. 2018;4(3):107.)