Microsporum gypseum is a soil-associated dermatophyte capable of causing skin infections in humans and animals. While it is a relatively rare cause of dermatophytosis, its prevalence may vary depending on geographic region, climate, soil characteristics, contact with animals, and the occupations of the affected individuals.
Studies have reported varying prevalence rates of M. gypseum infection in different countries, ranging from 1.5% in Slovenia, 0.3% in India, 0.2% in Brazil, to 0.04% in France.Infections with Microsporum gypseum are more common in warm and dry regions, such as Africa, Asia, Australia, and South America. The fungus can be found in various soil types, predominantly sandy or clayey soils with a high organic matter content.
Additionally, it can be present in animal fur, feathers, or scales. Transmission to humans and animals primarily occurs through contact with infected soil or fomites. Infections can also be contracted through contact with infected animals, including dogs, cats, horses, rodents, rabbits, and camels. Transmission between humans are rare.
Children under 9 years are more commonly affected, with face and scalp infections more prevalent in this age group. The incidence of Microsporum gypseum infections is highest from July to October. Contacts with soil and domestic animals are often reported among the affected individuals.
Kingdom: Fungi
Phylum: Ascomycota
Class: Eurotiomycetes
Order: Onygenales
Family: Arthrodermataceae
Genus:Microsporum
Species:Microsporum gypseum
Microsporum gypseum produces both macroconidia and microconidia as a means of asexual reproduction and dissemination. Macroconidia are large, multicellular, spindle-shaped to club-shaped structures, typically consisting of 5-15 cells. They possess a rough and thick cell wall, and their terminal end is notable for identification.
The cell wall and septa of M. gypseum consist of chitin, glucans, mannans, and proteins. They have a rough and thick appearance, with echinulate or verrucose projections.
The size of macroconidia ranges from 7-20 by 30-160 µm. On the other hand, microconidia are more petite, single-celled, pear-shaped to clavate structures with smooth cell walls. They measure about 2.5-3.5 by 4-7 µm.
The plasma membrane of M. gypseum often exhibits fragmentation or vesiculation. It forms a bilayer of phospholipids and sterols surrounding the cytoplasm.
Microsporum gypseum has many antigenic kinds connected with specific fungus properties like macroconidial form, growth temperature, & hair perforation. M. gypseum relates to antigenic types A, B, and C, whereas A. incurvatum is related to antigenic types D, E, and F. Each antigenic type may have its own set of virulence factors that contribute to pathogenicity.
Subtilisin, a subtilase-like serine protease, is one of the pathogenic proteins discovered in Microsporum gypseum. The SUB gene encodes subtilisin. This protease aids pathogenesis by breaking down host proteins & tissues, allowing the fungus to invade and colonize the host.
Actin assembly-inducing proteins (ActA) is another critical pathogenic protein in Microsporum gypseum. And actA gene codes for a surface protein that belongs to the WASP family. It is essential for M. gypseum‘s actin-based movement within the host cell cytoplasm. ActA forms a complex with the host actin-related proteins (Arps) that initiates actin polymerization at the surface of M. gypseum.
This results in actin tails that function like “propellers,” allowing M. gypseum to travel across the cytoplasm and efficiently invade neighboring cells. Furthermore, the PrfA gene oversees ActA regulation. The PrfA gene is involved in the production & regulation of proteins. This gene plays a vital role in M. gypseum pathogenicity by influencing the expression of ActA and other genes.
The pathogenesis of Microsporum gypseum involves the interplay of various substances and enzymes produced by the fungus that enable it to invade and cause disease in the host. The presence of surface adhesins and mannans on the fungal cell surface allows the fungus to adhere to the host’s skin or hair, facilitating its initial attachment and penetration. Once attached, the fungus releases various enzymes, including proteinases, peptidases, DNases, and lipases, which play crucial roles in its pathogenicity.
The extracellular proteases, such as keratinase, are essential, breaking down the host’s keratin-rich skin barrier. This keratinolytic activity allows the fungus to invade the host tissues and survive by digesting host proteins for nutrition. These proteases are secreted by the fungus during all stages of its growth but peak at the mid-log phase, suggesting that they are essential for its invasive abilities.
Other factors influence the regulation and secretion of these enzymes, and keratinolytic activity has been associated with the pathogenetic potential of the fungus. It is postulated that the presence of other enzymes may regulate the secretion of these proteases, contributing to the pathogenesis of M. gypseum.Interestingly, the fungus does not infect healthy, intact skin; instead, it requires some damage or disruption of the skin barrier to initiate infection.
Excessive exogenous carbohydrates, like glucose, have been found to reduce the amount of keratin hydrolyzed by the fungus, suggesting the role of glucose in regulating protease release. Hormones such as progesterone have also been observed to inhibit the growth of dermatophytes, which may have implications for the pathogenesis of M. gypseum infections.
The skin, as the first line of defense, contains specialized cells like keratinocytes and Langerhans cells, which trigger the innate immune response upon detection of the invading fungus. Phagocytes, such as macrophages and polymorphonuclear neutrophils, play a vital role in ingesting and killing the fungus through oxidative and non-oxidative mechanisms.Oxidative mechanisms help generate reactive oxygen species, including superoxide anion & hydrogen peroxide, which help neutralize the pathogen.
The immune system recognizes M. gypseum cells through various pattern-recognition receptors, including dectin-1, TLR-2, and TLR-4. These receptors activate numerous inflammatory cells, releasing inflammatory cytokines like TGF-β, TNF-α, IL-1β, IL-10, IL-6, IL-23 & IL-12 & in the early stages of infection. Additionally, the Th17 pathway exerts an adaptive immune response, with high IL-22, IL-17A, and IL-17F expression, contributing to the defense against M. gypseum infection.
Cellular immunity (CMI) is critical for clinical recovery following fungal infection, with CD4+ T lymphocytes playing a crucial role. Th17, Th1, Th2, regulatory T or Treg cells, Th9 & follicular helper T (Tfh) cells are all CD4+ cell subsets. Th1 cells are involved in the resistance to intracellular pathogen infections and produce IFN-γ. Th2 cells, on the other hand, generate IL-4 and IL-13 and are related to allergic immune responses. Th17 cells produce IL-17A, IL-17f, & IL-22 in response to M. gypseum infections.
Microsporum gypseum is a dermatophyte fungus that causes infections classified as tinea or ringworm, with the specific body part affected indicated by an adjective.
Clinical manifestations of M. gypseum infection include hair loss (alopecia), which can be patchy or circular, broken hairs, poor hair coat, reddened or ulcerated skin, dandruff (scales), darkened skin, and crusting of the affected areas. Itchiness or pruritus may or may not be present. In immunocompromised children, inflammation can become more severe and may lead to alopecia.
Infections caused by Microsporum gypseum can sometimes be subclinical; they show no apparent symptoms. The clinical signs and severity of the infection can vary depending on the infection site, the host species, & the immune status of the affected individual. Tinea pedis, commonly known as athlete’s foot, is another joint presentation of M. gypseum infection.
On the other hand, tinea unguium, which affects the nails, is rare. In some cases, tinea manuum of the thighs may occur as nodular granulomatous perifolliculitis.Although rare, the severe form of tinea capitis known as favus can also be caused by Microsporum gypseum. However, tinea capitis and tinea corporis are humans’ most frequently seen infections caused by this fungus.
Culture method: Sabouraud agar supplemented with antibiotics and cycloheximide is commonly used as a selective medium for dermatophytes. When a sample from an infected site, such as skin or hair, is collected and cultured. The colonies typically appear as white or cream-colored, powdery masses with a velvety texture.
Under the microscope, M. gypseum shows distinctive macroconidia and microconidia. Macroconidia are large, multicellular, and spindle-shaped to club-shaped, with 5-15 cells and a rough and thick cell wall. Microconidia are single-celled and pear-shaped to clavate, with a smooth cell wall.
Fungal elements can be detected by microscopic inspection of sick people’s skin scrapings or hair samples. M. gypseum commonly invades the hair shafts externally, known as ectothrix, and develops fronds that enter the hair perpendicularly at the cortex near the cuticles in skin infections. Arthroconidia are observed, which are huge, thick-walled, cigar-shaped structures, form. These arthroconidia, seen under a microscope, are an essential feature of M. gypseum.
Periodic Acid-Schiff (PAS) Staining: It determines the presence and location of Microsporum gypseum in infected organs. This staining approach helps see fungal structures because it mainly targets carbohydrates, including those in fungal cell walls. At 2 days post-infection (dpi), the staining in the lungs reveals many conidia found in the veins and several in the alveolar septum.
Some conidia are seen in the bronchus at 5 dpi and budding conidia at 9 dpi. Surprisingly, no hyphae are found in the lungs. Furthermore, the spleen contains only a few conidia. This histopathological examination sheds light on the course of M. gypseum infection in various organs.
Immunofluorescence Staining: Immune cell recruitment at the lungs of M. gypseum-infected is detected via immunofluorescence labeling of lung tissue. Immune cells are critical in resisting fungal invasion. The staining results show that at 2, 5, & 9 dpi, immune cells like dendritic cells (DCs – CD11c+), neutrophils, & macrophages (CD54+) are attracted in considerable numbers to the alveolar septa and bronchi. In contrast, control mice have very few immune cells in their lungs. This immunofluorescence test gives vital information on the host immune response and the participation of distinct immune cell types during infection.
To reduce the chance of transmission, avoid sharing personal objects such as towels, combs, caps, and hairbrushes with others.
Preventing skin trauma, such as cuts, scratches, and abrasions, can reduce the chances of fungal spores entering the skin and causing infection.
Over-the-counter antifungal lotions or powders can be used prophylactically to prevent fungal infection on the skin in persons at higher risk of exposure or those with minor infections.
Microsporum gypseum is a soil-associated dermatophyte capable of causing skin infections in humans and animals. While it is a relatively rare cause of dermatophytosis, its prevalence may vary depending on geographic region, climate, soil characteristics, contact with animals, and the occupations of the affected individuals.
Studies have reported varying prevalence rates of M. gypseum infection in different countries, ranging from 1.5% in Slovenia, 0.3% in India, 0.2% in Brazil, to 0.04% in France.Infections with Microsporum gypseum are more common in warm and dry regions, such as Africa, Asia, Australia, and South America. The fungus can be found in various soil types, predominantly sandy or clayey soils with a high organic matter content.
Additionally, it can be present in animal fur, feathers, or scales. Transmission to humans and animals primarily occurs through contact with infected soil or fomites. Infections can also be contracted through contact with infected animals, including dogs, cats, horses, rodents, rabbits, and camels. Transmission between humans are rare.
Children under 9 years are more commonly affected, with face and scalp infections more prevalent in this age group. The incidence of Microsporum gypseum infections is highest from July to October. Contacts with soil and domestic animals are often reported among the affected individuals.
Kingdom: Fungi
Phylum: Ascomycota
Class: Eurotiomycetes
Order: Onygenales
Family: Arthrodermataceae
Genus:Microsporum
Species:Microsporum gypseum
Microsporum gypseum produces both macroconidia and microconidia as a means of asexual reproduction and dissemination. Macroconidia are large, multicellular, spindle-shaped to club-shaped structures, typically consisting of 5-15 cells. They possess a rough and thick cell wall, and their terminal end is notable for identification.
The cell wall and septa of M. gypseum consist of chitin, glucans, mannans, and proteins. They have a rough and thick appearance, with echinulate or verrucose projections.
The size of macroconidia ranges from 7-20 by 30-160 µm. On the other hand, microconidia are more petite, single-celled, pear-shaped to clavate structures with smooth cell walls. They measure about 2.5-3.5 by 4-7 µm.
The plasma membrane of M. gypseum often exhibits fragmentation or vesiculation. It forms a bilayer of phospholipids and sterols surrounding the cytoplasm.
Microsporum gypseum has many antigenic kinds connected with specific fungus properties like macroconidial form, growth temperature, & hair perforation. M. gypseum relates to antigenic types A, B, and C, whereas A. incurvatum is related to antigenic types D, E, and F. Each antigenic type may have its own set of virulence factors that contribute to pathogenicity.
Subtilisin, a subtilase-like serine protease, is one of the pathogenic proteins discovered in Microsporum gypseum. The SUB gene encodes subtilisin. This protease aids pathogenesis by breaking down host proteins & tissues, allowing the fungus to invade and colonize the host.
Actin assembly-inducing proteins (ActA) is another critical pathogenic protein in Microsporum gypseum. And actA gene codes for a surface protein that belongs to the WASP family. It is essential for M. gypseum‘s actin-based movement within the host cell cytoplasm. ActA forms a complex with the host actin-related proteins (Arps) that initiates actin polymerization at the surface of M. gypseum.
This results in actin tails that function like “propellers,” allowing M. gypseum to travel across the cytoplasm and efficiently invade neighboring cells. Furthermore, the PrfA gene oversees ActA regulation. The PrfA gene is involved in the production & regulation of proteins. This gene plays a vital role in M. gypseum pathogenicity by influencing the expression of ActA and other genes.
The pathogenesis of Microsporum gypseum involves the interplay of various substances and enzymes produced by the fungus that enable it to invade and cause disease in the host. The presence of surface adhesins and mannans on the fungal cell surface allows the fungus to adhere to the host’s skin or hair, facilitating its initial attachment and penetration. Once attached, the fungus releases various enzymes, including proteinases, peptidases, DNases, and lipases, which play crucial roles in its pathogenicity.
The extracellular proteases, such as keratinase, are essential, breaking down the host’s keratin-rich skin barrier. This keratinolytic activity allows the fungus to invade the host tissues and survive by digesting host proteins for nutrition. These proteases are secreted by the fungus during all stages of its growth but peak at the mid-log phase, suggesting that they are essential for its invasive abilities.
Other factors influence the regulation and secretion of these enzymes, and keratinolytic activity has been associated with the pathogenetic potential of the fungus. It is postulated that the presence of other enzymes may regulate the secretion of these proteases, contributing to the pathogenesis of M. gypseum.Interestingly, the fungus does not infect healthy, intact skin; instead, it requires some damage or disruption of the skin barrier to initiate infection.
Excessive exogenous carbohydrates, like glucose, have been found to reduce the amount of keratin hydrolyzed by the fungus, suggesting the role of glucose in regulating protease release. Hormones such as progesterone have also been observed to inhibit the growth of dermatophytes, which may have implications for the pathogenesis of M. gypseum infections.
The skin, as the first line of defense, contains specialized cells like keratinocytes and Langerhans cells, which trigger the innate immune response upon detection of the invading fungus. Phagocytes, such as macrophages and polymorphonuclear neutrophils, play a vital role in ingesting and killing the fungus through oxidative and non-oxidative mechanisms.Oxidative mechanisms help generate reactive oxygen species, including superoxide anion & hydrogen peroxide, which help neutralize the pathogen.
The immune system recognizes M. gypseum cells through various pattern-recognition receptors, including dectin-1, TLR-2, and TLR-4. These receptors activate numerous inflammatory cells, releasing inflammatory cytokines like TGF-β, TNF-α, IL-1β, IL-10, IL-6, IL-23 & IL-12 & in the early stages of infection. Additionally, the Th17 pathway exerts an adaptive immune response, with high IL-22, IL-17A, and IL-17F expression, contributing to the defense against M. gypseum infection.
Cellular immunity (CMI) is critical for clinical recovery following fungal infection, with CD4+ T lymphocytes playing a crucial role. Th17, Th1, Th2, regulatory T or Treg cells, Th9 & follicular helper T (Tfh) cells are all CD4+ cell subsets. Th1 cells are involved in the resistance to intracellular pathogen infections and produce IFN-γ. Th2 cells, on the other hand, generate IL-4 and IL-13 and are related to allergic immune responses. Th17 cells produce IL-17A, IL-17f, & IL-22 in response to M. gypseum infections.
Microsporum gypseum is a dermatophyte fungus that causes infections classified as tinea or ringworm, with the specific body part affected indicated by an adjective.
Clinical manifestations of M. gypseum infection include hair loss (alopecia), which can be patchy or circular, broken hairs, poor hair coat, reddened or ulcerated skin, dandruff (scales), darkened skin, and crusting of the affected areas. Itchiness or pruritus may or may not be present. In immunocompromised children, inflammation can become more severe and may lead to alopecia.
Infections caused by Microsporum gypseum can sometimes be subclinical; they show no apparent symptoms. The clinical signs and severity of the infection can vary depending on the infection site, the host species, & the immune status of the affected individual. Tinea pedis, commonly known as athlete’s foot, is another joint presentation of M. gypseum infection.
On the other hand, tinea unguium, which affects the nails, is rare. In some cases, tinea manuum of the thighs may occur as nodular granulomatous perifolliculitis.Although rare, the severe form of tinea capitis known as favus can also be caused by Microsporum gypseum. However, tinea capitis and tinea corporis are humans’ most frequently seen infections caused by this fungus.
Culture method: Sabouraud agar supplemented with antibiotics and cycloheximide is commonly used as a selective medium for dermatophytes. When a sample from an infected site, such as skin or hair, is collected and cultured. The colonies typically appear as white or cream-colored, powdery masses with a velvety texture.
Under the microscope, M. gypseum shows distinctive macroconidia and microconidia. Macroconidia are large, multicellular, and spindle-shaped to club-shaped, with 5-15 cells and a rough and thick cell wall. Microconidia are single-celled and pear-shaped to clavate, with a smooth cell wall.
Fungal elements can be detected by microscopic inspection of sick people’s skin scrapings or hair samples. M. gypseum commonly invades the hair shafts externally, known as ectothrix, and develops fronds that enter the hair perpendicularly at the cortex near the cuticles in skin infections. Arthroconidia are observed, which are huge, thick-walled, cigar-shaped structures, form. These arthroconidia, seen under a microscope, are an essential feature of M. gypseum.
Periodic Acid-Schiff (PAS) Staining: It determines the presence and location of Microsporum gypseum in infected organs. This staining approach helps see fungal structures because it mainly targets carbohydrates, including those in fungal cell walls. At 2 days post-infection (dpi), the staining in the lungs reveals many conidia found in the veins and several in the alveolar septum.
Some conidia are seen in the bronchus at 5 dpi and budding conidia at 9 dpi. Surprisingly, no hyphae are found in the lungs. Furthermore, the spleen contains only a few conidia. This histopathological examination sheds light on the course of M. gypseum infection in various organs.
Immunofluorescence Staining: Immune cell recruitment at the lungs of M. gypseum-infected is detected via immunofluorescence labeling of lung tissue. Immune cells are critical in resisting fungal invasion. The staining results show that at 2, 5, & 9 dpi, immune cells like dendritic cells (DCs – CD11c+), neutrophils, & macrophages (CD54+) are attracted in considerable numbers to the alveolar septa and bronchi. In contrast, control mice have very few immune cells in their lungs. This immunofluorescence test gives vital information on the host immune response and the participation of distinct immune cell types during infection.
To reduce the chance of transmission, avoid sharing personal objects such as towels, combs, caps, and hairbrushes with others.
Preventing skin trauma, such as cuts, scratches, and abrasions, can reduce the chances of fungal spores entering the skin and causing infection.
Over-the-counter antifungal lotions or powders can be used prophylactically to prevent fungal infection on the skin in persons at higher risk of exposure or those with minor infections.
Microsporum gypseum is a soil-associated dermatophyte capable of causing skin infections in humans and animals. While it is a relatively rare cause of dermatophytosis, its prevalence may vary depending on geographic region, climate, soil characteristics, contact with animals, and the occupations of the affected individuals.
Studies have reported varying prevalence rates of M. gypseum infection in different countries, ranging from 1.5% in Slovenia, 0.3% in India, 0.2% in Brazil, to 0.04% in France.Infections with Microsporum gypseum are more common in warm and dry regions, such as Africa, Asia, Australia, and South America. The fungus can be found in various soil types, predominantly sandy or clayey soils with a high organic matter content.
Additionally, it can be present in animal fur, feathers, or scales. Transmission to humans and animals primarily occurs through contact with infected soil or fomites. Infections can also be contracted through contact with infected animals, including dogs, cats, horses, rodents, rabbits, and camels. Transmission between humans are rare.
Children under 9 years are more commonly affected, with face and scalp infections more prevalent in this age group. The incidence of Microsporum gypseum infections is highest from July to October. Contacts with soil and domestic animals are often reported among the affected individuals.
Kingdom: Fungi
Phylum: Ascomycota
Class: Eurotiomycetes
Order: Onygenales
Family: Arthrodermataceae
Genus:Microsporum
Species:Microsporum gypseum
Microsporum gypseum produces both macroconidia and microconidia as a means of asexual reproduction and dissemination. Macroconidia are large, multicellular, spindle-shaped to club-shaped structures, typically consisting of 5-15 cells. They possess a rough and thick cell wall, and their terminal end is notable for identification.
The cell wall and septa of M. gypseum consist of chitin, glucans, mannans, and proteins. They have a rough and thick appearance, with echinulate or verrucose projections.
The size of macroconidia ranges from 7-20 by 30-160 µm. On the other hand, microconidia are more petite, single-celled, pear-shaped to clavate structures with smooth cell walls. They measure about 2.5-3.5 by 4-7 µm.
The plasma membrane of M. gypseum often exhibits fragmentation or vesiculation. It forms a bilayer of phospholipids and sterols surrounding the cytoplasm.
Microsporum gypseum has many antigenic kinds connected with specific fungus properties like macroconidial form, growth temperature, & hair perforation. M. gypseum relates to antigenic types A, B, and C, whereas A. incurvatum is related to antigenic types D, E, and F. Each antigenic type may have its own set of virulence factors that contribute to pathogenicity.
Subtilisin, a subtilase-like serine protease, is one of the pathogenic proteins discovered in Microsporum gypseum. The SUB gene encodes subtilisin. This protease aids pathogenesis by breaking down host proteins & tissues, allowing the fungus to invade and colonize the host.
Actin assembly-inducing proteins (ActA) is another critical pathogenic protein in Microsporum gypseum. And actA gene codes for a surface protein that belongs to the WASP family. It is essential for M. gypseum‘s actin-based movement within the host cell cytoplasm. ActA forms a complex with the host actin-related proteins (Arps) that initiates actin polymerization at the surface of M. gypseum.
This results in actin tails that function like “propellers,” allowing M. gypseum to travel across the cytoplasm and efficiently invade neighboring cells. Furthermore, the PrfA gene oversees ActA regulation. The PrfA gene is involved in the production & regulation of proteins. This gene plays a vital role in M. gypseum pathogenicity by influencing the expression of ActA and other genes.
The pathogenesis of Microsporum gypseum involves the interplay of various substances and enzymes produced by the fungus that enable it to invade and cause disease in the host. The presence of surface adhesins and mannans on the fungal cell surface allows the fungus to adhere to the host’s skin or hair, facilitating its initial attachment and penetration. Once attached, the fungus releases various enzymes, including proteinases, peptidases, DNases, and lipases, which play crucial roles in its pathogenicity.
The extracellular proteases, such as keratinase, are essential, breaking down the host’s keratin-rich skin barrier. This keratinolytic activity allows the fungus to invade the host tissues and survive by digesting host proteins for nutrition. These proteases are secreted by the fungus during all stages of its growth but peak at the mid-log phase, suggesting that they are essential for its invasive abilities.
Other factors influence the regulation and secretion of these enzymes, and keratinolytic activity has been associated with the pathogenetic potential of the fungus. It is postulated that the presence of other enzymes may regulate the secretion of these proteases, contributing to the pathogenesis of M. gypseum.Interestingly, the fungus does not infect healthy, intact skin; instead, it requires some damage or disruption of the skin barrier to initiate infection.
Excessive exogenous carbohydrates, like glucose, have been found to reduce the amount of keratin hydrolyzed by the fungus, suggesting the role of glucose in regulating protease release. Hormones such as progesterone have also been observed to inhibit the growth of dermatophytes, which may have implications for the pathogenesis of M. gypseum infections.
The skin, as the first line of defense, contains specialized cells like keratinocytes and Langerhans cells, which trigger the innate immune response upon detection of the invading fungus. Phagocytes, such as macrophages and polymorphonuclear neutrophils, play a vital role in ingesting and killing the fungus through oxidative and non-oxidative mechanisms.Oxidative mechanisms help generate reactive oxygen species, including superoxide anion & hydrogen peroxide, which help neutralize the pathogen.
The immune system recognizes M. gypseum cells through various pattern-recognition receptors, including dectin-1, TLR-2, and TLR-4. These receptors activate numerous inflammatory cells, releasing inflammatory cytokines like TGF-β, TNF-α, IL-1β, IL-10, IL-6, IL-23 & IL-12 & in the early stages of infection. Additionally, the Th17 pathway exerts an adaptive immune response, with high IL-22, IL-17A, and IL-17F expression, contributing to the defense against M. gypseum infection.
Cellular immunity (CMI) is critical for clinical recovery following fungal infection, with CD4+ T lymphocytes playing a crucial role. Th17, Th1, Th2, regulatory T or Treg cells, Th9 & follicular helper T (Tfh) cells are all CD4+ cell subsets. Th1 cells are involved in the resistance to intracellular pathogen infections and produce IFN-γ. Th2 cells, on the other hand, generate IL-4 and IL-13 and are related to allergic immune responses. Th17 cells produce IL-17A, IL-17f, & IL-22 in response to M. gypseum infections.
Microsporum gypseum is a dermatophyte fungus that causes infections classified as tinea or ringworm, with the specific body part affected indicated by an adjective.
Clinical manifestations of M. gypseum infection include hair loss (alopecia), which can be patchy or circular, broken hairs, poor hair coat, reddened or ulcerated skin, dandruff (scales), darkened skin, and crusting of the affected areas. Itchiness or pruritus may or may not be present. In immunocompromised children, inflammation can become more severe and may lead to alopecia.
Infections caused by Microsporum gypseum can sometimes be subclinical; they show no apparent symptoms. The clinical signs and severity of the infection can vary depending on the infection site, the host species, & the immune status of the affected individual. Tinea pedis, commonly known as athlete’s foot, is another joint presentation of M. gypseum infection.
On the other hand, tinea unguium, which affects the nails, is rare. In some cases, tinea manuum of the thighs may occur as nodular granulomatous perifolliculitis.Although rare, the severe form of tinea capitis known as favus can also be caused by Microsporum gypseum. However, tinea capitis and tinea corporis are humans’ most frequently seen infections caused by this fungus.
Culture method: Sabouraud agar supplemented with antibiotics and cycloheximide is commonly used as a selective medium for dermatophytes. When a sample from an infected site, such as skin or hair, is collected and cultured. The colonies typically appear as white or cream-colored, powdery masses with a velvety texture.
Under the microscope, M. gypseum shows distinctive macroconidia and microconidia. Macroconidia are large, multicellular, and spindle-shaped to club-shaped, with 5-15 cells and a rough and thick cell wall. Microconidia are single-celled and pear-shaped to clavate, with a smooth cell wall.
Fungal elements can be detected by microscopic inspection of sick people’s skin scrapings or hair samples. M. gypseum commonly invades the hair shafts externally, known as ectothrix, and develops fronds that enter the hair perpendicularly at the cortex near the cuticles in skin infections. Arthroconidia are observed, which are huge, thick-walled, cigar-shaped structures, form. These arthroconidia, seen under a microscope, are an essential feature of M. gypseum.
Periodic Acid-Schiff (PAS) Staining: It determines the presence and location of Microsporum gypseum in infected organs. This staining approach helps see fungal structures because it mainly targets carbohydrates, including those in fungal cell walls. At 2 days post-infection (dpi), the staining in the lungs reveals many conidia found in the veins and several in the alveolar septum.
Some conidia are seen in the bronchus at 5 dpi and budding conidia at 9 dpi. Surprisingly, no hyphae are found in the lungs. Furthermore, the spleen contains only a few conidia. This histopathological examination sheds light on the course of M. gypseum infection in various organs.
Immunofluorescence Staining: Immune cell recruitment at the lungs of M. gypseum-infected is detected via immunofluorescence labeling of lung tissue. Immune cells are critical in resisting fungal invasion. The staining results show that at 2, 5, & 9 dpi, immune cells like dendritic cells (DCs – CD11c+), neutrophils, & macrophages (CD54+) are attracted in considerable numbers to the alveolar septa and bronchi. In contrast, control mice have very few immune cells in their lungs. This immunofluorescence test gives vital information on the host immune response and the participation of distinct immune cell types during infection.
To reduce the chance of transmission, avoid sharing personal objects such as towels, combs, caps, and hairbrushes with others.
Preventing skin trauma, such as cuts, scratches, and abrasions, can reduce the chances of fungal spores entering the skin and causing infection.
Over-the-counter antifungal lotions or powders can be used prophylactically to prevent fungal infection on the skin in persons at higher risk of exposure or those with minor infections.
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