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

Microsporum canis exhibits 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, 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] 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 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.[25]

Metalloproteases (MEP1–3)

Zinc-dependent metalloprotease M36 fungalysins with keratinolytic, elastinolytic, and collagenolytic activity; essential for adhesion and tissue invasion.[26]

Subtilisins (Sub1–3)

Serine proteases contributing to keratin degradation, arthroconidia adhesion, and anchorage to the host surface and tissue invasion. Sub3 is a well-characterized virulence marker.[27]

Aminopeptidases (Lap1–2)

Involved in keratin breakdown and nitrogen assimilation under alkaline conditions.[28]

Dipeptidyl Peptidases (DppIV, DppV)

Facilitate nutrient acquisition and tissue colonization; degrade elastin and collagen.[29]

Aspartyl Proteases

Less characterized in M. canis; suspected to degrade host defense proteins based on in vitro/ex vivo data.[30]

Hemolysins

Contribute to iron acquisition and cytotoxicity. Correlated with azole resistance.[31][32]

Catalases

Detoxify reactive oxygen species; higher activity in lesion-associated strains and correlated with antifungal susceptibility.[33][34]

Ureases

Provide nitrogen source; increase pH; used taxonomically. Urease activity varies by strain.[35]

Serine Hydrolase (FSH1)

Functions as an esterase regulating growth, pigmentation, and conidiation; knockout reduces virulence.[36][37]

Biofilms/Dermatophytomas

Structured hyphal networks embedded in ECM; increase antifungal resistance and promote chronic infection.[38]

Heat Shock Proteins (HSPs)	Chaperones that support stress tolerance, antifungal resistance, and tissue colonization.[39]
Thermotolerance	Thermotolerance allows strains to infect deeper tissue layers by adapting to higher host body temperatures (e.g., 37°C), despite their optimal growth temperature being around 25°C. Strains exhibiting low thermotolerance are frequently observed in animals with lesions and humans with tinea corporis, suggesting a link to the clinical manifestation of the disease.[40]

SSU1 (Sulfite Efflux Pump)

Crucial for the elimination of cytotoxic sulfur compounds that are produced during the degradation of epidermal and dermal components. It is considered an important virulence factor.[41]

ZafA Gene

This gene is significantly upregulated under zinc-deficient conditions and is homologous to Zap1, indicating its role as a main transcription factor regulating M. canis zinc homeostasis. The ZafA gene plays a vital role in zinc absorption, the expression of zinc transporter genes, and the overall growth and pathogenicity of M. canis. Its knockout has been shown to significantly reduce hair biodegradation and skin damage in experimental models.[42]

SUB3 Gene

Encodes subtilisin 3; crucial for adhesion and keratin degradation. Also highly conserved.[43]

Metallomics

M. canis requires multiple metal ions for its growth and virulence, and it has evolved specific mechanisms to acquire, utilize, and regulate these metals. A ferrichrome siderophore circuit (SidA/SidC → MirB) secures iron when the host tries to hide it, while the zinc-starvation regulator ZafA ramps up ZIP importers and keratin-cleaving Zn-metalloproteases.^[44] Copper fuels laccase and Cu/Zn-SOD but turns lethal whenever metallothionein buffering is overwhelmed, a vulnerability that drugs or host immunity can exploit.^[45] Manganese provides a back-up antioxidant route via Mn-SOD, and nickel powers urease-driven pH shifts in urease-positive strains. Together these metal-scavenging, detoxifying, and enzyme-activating systems give the fungus the biochemical leverage it needs to persist on hair and skin, while also offering multiple metabolic choke-points for therapeutic attack.

Metal / Ion	Key Features in M. canis

Iron (Fe)

Secretes hydroxamate siderophores ferrichrome C and ferricrocin for high-affinity Fe³⁺ scavenging.[46] Biosynthetic cluster with sidA (ornithine mono-oxygenase) + sidC (NRPS) confirmed; uptake via MirB-family siderophore transporter.[47] Regulatory circuit presumed HapX (starvation activator) ↔ SreA (surplus repressor). [48] Minor/conditional pathways: reductive Fe assimilation; low, strain-specific hemolysin activity.[49]

Zinc (Zn)

Virulence-linked M36 metalloproteases (MEP1–3) require Zn²⁺ to digest keratin.[50] Master regulator ZafA/ZAF1 induces high-affinity ZIP-family importers under zinc limitation; ΔZafA strains show poor growth, weak keratinolysis, avirulence.[51] Balances excess via a putative ZupT exporter / vacuolar sequestration.[52] Calprotectin-mediated Zn withholding in host skin drives strong ZafA response.[53]

Copper (Cu)

Multi-copper laccase (melanin synthesis, ROS protection) and probable Cu/Zn-SOD need Cu cofactors.[54] Detoxification through a cysteine-rich metallothionein (MT/Cup1); MT transcription surges when Cu rises but is suppressed by fluconazole, which makes Cu synergistically fungicidal.[55]

Manganese (Mn)

M. canis likely possesses manganese-containing superoxide dismutase (Mn-SOD) in mitochondria, as is common in fungi. Mn is also required for enzymes in central metabolism (e.g. some decarboxylases and kinases) and for the function of glycosyltransferases involved in cell wall synthesis.

Nickel (Ni)

Most M. canis strains express nickel-dependent urease (Ni-metalloenzyme) to hydrolyze urea → ammonia (pH increase, N source).[56]

Vulnerabilities

Microsporum canis, though resilient in some environmental conditions, exhibits a broad array of biological and physiological weaknesses that can be therapeutically exploited. From temperature sensitivity and nutrient dependence to pH preference and immune clearance, these vulnerabilities provide clinicians and researchers with a diverse arsenal of intervention points. The following table summarizes key weaknesses of M. canis, paired with potential or existing therapeutic strategies designed to target each one.

Vulnerability	Therapeutic Opportunity

Temperature Sensitivity (Optimal ~25–28 °C; growth inhibited at 37 °C)

Heat-based therapy (laser, localized warming); target heat-shock protein pathways (e.g., Hsp90 inhibitors);

pH Dependence (Optimal pH ~7.5)

Acidifying topical agents (e.g., vinegar rinses, acidic cleansers); maintain skin pH ~5.0–5.5

Humidity Requirement

Environmental dehumidification; drying of infected areas and fomites; sunlight exposure

UV Sensitivity (especially UV-C)

Surface disinfection with UV-C devices; environmental decontamination via sunlight; potential photodynamic therapy

Keratin Dependence

Shaving/debridement to remove keratin substrate; inhibition of keratinases (e.g., Sub3 enzyme blockers)

Iron and Zinc Dependence

Use of metal chelators (e.g., ciclopirox olamine); enhancement of host calprotectin response; iron/zinc deprivation strategies

Biofilm Formation

Anti-biofilm agents (e.g., DNase, glucanase, keratolytics); biosurfactants (e.g., from Beauveria bassiana, Bacillus subtilis)

Superficial Growth Limitation

Boost host immunity (e.g., vaccines, IFN-γ, imiquimod); promote inflammatory response; avoid systemic immunosuppression

Cell Membrane Weakness (ergosterol pathway)

Allylamines (terbinafine), azoles (itraconazole); statins and tamoxifen (repurposed agents) targeting ergosterol biosynthesis

Cell Wall Composition (β-glucans, etc.)

Potential use of echinocandins (e.g., caspofungin) in refractory cases

Metabolic Pathway Targets

Novel agents like olorofim (pyrimidine synthesis inhibitor), oteseconazole (next-gen azole)

Susceptibility to Topical Agents

Broad use of topical antifungals (clotrimazole, terbinafine, ciclopirox); antiseptics (chlorhexidine, povidone-iodine)

Environmental Fragility

Disinfection with bleach (1% NaOCl), phenolics, iodophors; UV-C sterilization; microwave treatment

Limited Defense Against Immune Response

Immunotherapy, monoclonal antibodies, immunomodulators; development of human vaccines

Natural Product Sensitivity

Essential oils (thymol, eugenol, tea tree oil), bee venom, manuka honey, herbal extracts (Mentha piperita)

Microbial Competition

Use of probiotics or microbial antagonists (e.g., Bacillus subtilis, Trichoderma spp.); biocontrol in environments

Interventions

^[57] Contact-free inactivation of Trichophyton rubrum and Microsporum canis by Cold atmospheric plasma (CAP) treatment

^[58] Ciclopirox and Ciclopirox Olamine: Antifungal Agents in Dermatology with Expanding Therapeutic Potential

In vitro Study of Antidermatophytic Activity of Mint (Mentha Piperita) Against Trichophyton rubrum and Microsporum canis

^[59] Hypochlorous acid

Deferoxamine

Clioquinol
TPEN 

^[60] Antifungal activity of berberine hydrochloride and palmatine hydrochloride against Microsporum canis-induced dermatitis in rabbits and underlying mechanism.
^[61] Methylene blue-mediated antimicrobial photodynamic therapy for canine dermatophytosis caused by Microsporum canis: A successful case report with 6 months follow-up

caprylic acid 

^[62] A potential antifungal bioproduct for Microsporum canis- Bee venom.pdf

^[63] Secreted Metalloprotease Gene Family of Microsporum canis.pdf

^[64] Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review .pdf

^[65] Genetic Characterization of Microsporum canis Clinical Isolates in the United States.pdf

^[66]Synergistic Anti-Dermatophytic Potential of Nanoparticles and Essential Oils Combinations.pdf

^[67] Remarkable Phenotypic Virulence Factors of Microsporum canis and Their Associated Genes: A Systematic Review .pdf

^[68] Therapy_and_Antifungal_Susceptibility_Profile_of_M.pdf

^[69] Dermatophyte infection: from fungal pathogenicity to host immune responses.pdf

^[70] Evaluation of the antidermatophytic activity of potassium salts of N-acylhydrazinecarbodithioates and their aminotriazole-thione derivatives.pdf

^[71] Molecular detection and in vitro antifungal study of Microsporum canis isolated from cat- A case report.pdf

^[72] Virulence and Antifungal Susceptibility of Microsporum canis Strains from Animals and Humans.pdf

^[73] RNA-Seq Analysis of the Effect of Zinc Deficiency on Microsporum canis, ZafA Gene Is Important for Growth and Pathogenicity.pdf

^[74] Therapy_and_Antifungal_Susceptibility_Profile_of_M.pdf

^[75] Whole genome sequence analysis of Microsporum canis: A study based on animal strains isolated from India.

^[76] Characterization of siderophores produced by different species of the dermatophytic fungi Microsporum and Trichophyton.

^[77] HapX Mediates Iron Homeostasis in the Pathogenic Dermatophyte Arthroderma benhamiae but Is Dispensable for Virulence.

^[78] Fluconazole downregulates metallothionein expression and increases copper cytotoxicity in Microsporum canis.

^[79] Antifungal activity of berberine hydrochloride and palmatine hydrochloride against Microsporum canis-induced dermatitis in rabbits and underlying mechanism.

^[80] Zinc-Induced Siderophore Production in Penicillium and Rhizosphere Fungi

^[81] Methylene blue-mediated antimicrobial photodynamic therapy for canine dermatophytosis caused by Microsporum canis: A successful case report with 6 months follow-up

Update History

References

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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.)
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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. 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.)
22. 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.)
23. 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.)
24. 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.)
25. 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.)
26. 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.)
27. 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.)
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. 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.)
30. 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.)
31. 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.)
32. 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.)
33. 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.)
34. 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.)
35. 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.)
36. Dermatophyte infection: from fungal pathogenicity to host immune responses.. Deng R, Wang X, Li R.. (Front Immunol. 2023 Nov 2;14:1285887.)
37. 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.)
38. 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.)
39. 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.)
40. 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.)
41. Dermatophyte infection: from fungal pathogenicity to host immune responses.. Deng R, Wang X, Li R.. (Front Immunol. 2023 Nov 2;14:1285887.)
42. 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.)
43. 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.)
44. 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.)
45. Whole genome sequence analysis of Microsporum canis: A study based on animal strains isolated from India.. Nair SS, Thomas P, Abdel-Glil MY, Prajapati SK, Va A, Reddi L, Kumar B, Saikumar G, Dandapat P, Rudramurthy SM, & Abhishek.. (The Microbe, 7, 100329. (2025).)
46. Characterization of siderophores produced by different species of the dermatophytic fungi Microsporum and Trichophyton.. Mor H, Kashman Y, Winkelmann G, Barash I.. (BioMetals. 1992;5(3):213–216.)
47. HapX Mediates Iron Homeostasis in the Pathogenic Dermatophyte Arthroderma benhamiae but Is Dispensable for Virulence.. Kröber A, Scherlach K, Hortschansky P, Shelest E, Staib P, Kniemeyer O, Brakhage AA.. (PLoS ONE. 2016;11(3):e0150701.)
48. HapX Mediates Iron Homeostasis in the Pathogenic Dermatophyte Arthroderma benhamiae but Is Dispensable for Virulence.. Kröber A, Scherlach K, Hortschansky P, Shelest E, Staib P, Kniemeyer O, Brakhage AA.. (PLoS ONE. 2016;11(3):e0150701.)
49. 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.)
50. 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.)
51. 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.)
52. Antifungal activity of berberine hydrochloride and palmatine hydrochloride against Microsporum canis-induced dermatitis in rabbits and underlying mechanism.. Xiao CW, Ji QA, Wei Q, Liu Y, Bao GL.. (BMC Complement Altern Med. 2015;15:177.)
53. Zinc Ions Affect Siderophore Production by Fungi Isolated from the Panax ginseng Rhizosphere.. Hussein KA, Joo JH.. (J Microbiol Biotechnol. 2019;29(1):105-113.)
54. Whole genome sequence analysis of Microsporum canis: A study based on animal strains isolated from India.. Nair SS, Thomas P, Abdel-Glil MY, Prajapati SK, Va A, Reddi L, Kumar B, Saikumar G, Dandapat P, Rudramurthy SM, & Abhishek.. (The Microbe, 7, 100329. (2025).)
55. Fluconazole downregulates metallothionein expression and increases copper cytotoxicity in Microsporum canis.. Uthman A, Rezaie S, Dockal M, Ban J, Soltz-Szots J, Tschachler E.. (Biochem Biophys Res Commun. 2002;299(5):688–692.)
56. 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.)
57. Contact-free inactivation of Trichophyton rubrum and Microsporum canis by cold atmospheric plasma treatment.. Heinlin J, Maisch T, Zimmermann JL, Shimizu T, Holzmann T, Simon M, Heider J, Landthaler M, Morfill G, Karrer S.. (Future Microbiol. 2013;8(9):1097-1106.)
58. Ciclopirox and Ciclopirox Olamine: Antifungal Agents in Dermatology with Expanding Therapeutic Potential.. Mucha P, Borkowski B, Erkiert-Polguj A, Budzisz E.. (Appl Sci. 2024;14(24):11859.)
59. The comparison of ketoconazole and hypochlorous acid (HOCl) applications for the treatment of the fungal infections (dermatophytosis).. Babur M, Karademir B.. (Turk J Agric Food Sci Technol. 2023;11(4):791-798.)
60. Antifungal activity of berberine hydrochloride and palmatine hydrochloride against Microsporum canis-induced dermatitis in rabbits and underlying mechanism.. Xiao CW, Ji QA, Wei Q, Liu Y, Bao GL.. (BMC Complement Altern Med. 2015;15:177.)
61. Methylene blue-mediated antimicrobial photodynamic therapy for canine dermatophytosis caused by Microsporum canis: A successful case report with 6 months follow-up. Fernanda V. Cabral, Fábio P. Sellera, Martha S. Ribeiro.. (Photodiagnosis and Photodynamic Therapy, Volume 36, 2021, 102602, ISSN 1572-1000.)
62. 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.)
63. 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.)
64. 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.)
65. 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.)
66. 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.)
67. 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.)
68. Therapy and Antifungal Susceptibility Profile of Microsporum canis.. Aneke CI, Otranto D, Cafarchia C.. (J Fungi. 2018;4(3):107.)
69. Dermatophyte infection: from fungal pathogenicity to host immune responses.. Deng R, Wang X, Li R.. (Front Immunol. 2023 Nov 2;14:1285887.)
70. 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.)
71. 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.)
72. 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.)
73. 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.)
74. Therapy and Antifungal Susceptibility Profile of Microsporum canis.. Aneke CI, Otranto D, Cafarchia C.. (J Fungi. 2018;4(3):107.)
75. Whole genome sequence analysis of Microsporum canis: A study based on animal strains isolated from India.. Nair SS, Thomas P, Abdel-Glil MY, Prajapati SK, Va A, Reddi L, Kumar B, Saikumar G, Dandapat P, Rudramurthy SM, & Abhishek.. (The Microbe, 7, 100329. (2025).)
76. Characterization of siderophores produced by different species of the dermatophytic fungi Microsporum and Trichophyton.. Mor H, Kashman Y, Winkelmann G, Barash I.. (BioMetals. 1992;5(3):213–216.)
77. HapX Mediates Iron Homeostasis in the Pathogenic Dermatophyte Arthroderma benhamiae but Is Dispensable for Virulence.. Kröber A, Scherlach K, Hortschansky P, Shelest E, Staib P, Kniemeyer O, Brakhage AA.. (PLoS ONE. 2016;11(3):e0150701.)
78. Fluconazole downregulates metallothionein expression and increases copper cytotoxicity in Microsporum canis.. Uthman A, Rezaie S, Dockal M, Ban J, Soltz-Szots J, Tschachler E.. (Biochem Biophys Res Commun. 2002;299(5):688–692.)
79. Antifungal activity of berberine hydrochloride and palmatine hydrochloride against Microsporum canis-induced dermatitis in rabbits and underlying mechanism.. Xiao CW, Ji QA, Wei Q, Liu Y, Bao GL.. (BMC Complement Altern Med. 2015;15:177.)
80. Zinc Ions Affect Siderophore Production by Fungi Isolated from the Panax ginseng Rhizosphere.. Hussein KA, Joo JH.. (J Microbiol Biotechnol. 2019;29(1):105-113.)
81. Methylene blue-mediated antimicrobial photodynamic therapy for canine dermatophytosis caused by Microsporum canis: A successful case report with 6 months follow-up. Fernanda V. Cabral, Fábio P. Sellera, Martha S. Ribeiro.. (Photodiagnosis and Photodynamic Therapy, Volume 36, 2021, 102602, ISSN 1572-1000.)