| Microsporum audouinii | |
|---|---|
 | |
Scientific classification | |
| Kingdom: | Fungi |
| Division: | Ascomycota |
| Class: | Eurotiomycetes |
| Order: | Onygenales |
| Family: | Arthrodermataceae |
| Genus: | Microsporum |
| Species: | M. audouinii |
| Binomial name | |
| Microsporum audouinii Gruby (1843) | |
Microsporum audouinii is an anthropophilic fungus in the genusMicrosporum.[1]It is a type ofdermatophyte that colonizeskeratinized tissues (primarily hair) causing infection.[2] The fungus is characterized by its spindle-shapedmacroconidia (7–30 × 35–160 μm), clavatemicroconidia (2.5–3.5 × 4–7 μm) as well as its pitted or spiny external walls.[3]
This fungus is often found in soil that is rich in keratinous material.[4] However, there are other factors that can influence its growth, such as pH, relative humidity, organic carbon, nitrogen and temperature.[4]Microsporum audouinii appears to prefer a neutral pH in the range of 6.8-7.0 and room temperature for growth.[4] Drastic increases or decreases in temperature can inhibit its growth.[5]Microsporum audouinii is effective in utilizing its carbon sources, but growth is strongest in the hexoses (glucose,mannose andfructose) and weakest inmaltose,sucrose,lactose andgalactose.[5] It is unable to synthesize the vitaminsthiamine,niacin andriboflavin and requires an exogenous supply of these materials to support its growth.[5] The fungus is only able to utilize organic nitrogen sources, particularly nitrogen fromarginine andurea.[5]
Microsporum audouinii causes the infectionsTinea capitis (scalp ringworm) andTinea corporis.[2] These superficial dermal diseases are generally found in prepubescent children (starting at 6 months) and rarely affect adults.[3] There are a few reasons why children are more susceptible toM. audouinii. Differences in the chemical composition and quantity of thetriglycerides in hairsebum secreted are the primary reasons.[6] In instances whereby the triglyceride content in the sebum decreases so does the susceptibility of a person to the fungus.[7] Cases like those are seen in postmenopausal women of whom suffer hormonal changes which can contribute to triglyceride reduction.[7] In addition, increased sweat production as well as the presence ofMalassezia furfur decreases the ability forM. audouinii to thrive.[8][9]Malassezia furfur is an opportunistic lipophilic yeast that is a part of the humancutaneous flora in adults.[9] In most cases of adult onset Tinea capitis due toM. audouinii, there is at least one predisposing factor such asimmunocompromise (e.g.,diabetes mellitus, systemiclupus, organ transplant andHIV), a local animal reservoir (e.g., infected pet or farm animal) and hormonal changes in postmenopausal women.[7][8]
Tinea capitis is seen in tropical, rural and suburban regions.[10] In the 19th and early 20th centuries,M. audouinii was the primary fungus responsible for Tinea capitis throughout the US and Western Europe.[10][11] With the advent ofantimycotic agents, its prevalence has decreased.[10] But in the poorer parts of Africa, especially Central and West Africa,M. audouinii remains the primary dermatophyte responsible for this disease.[10][12]
Tinea capitis develops when aninoculum from another individual or animal comes into a 'compromised scalp', which can occur when thestratum corneum of the scalp is exposed.[7] This can be due to trauma of the scalp, tight hair braiding or hair styling with infected tools.[7] In general, fungal spread is facilitated by poverty, poor hygiene and overcrowding.[7]
Once the fungus has entered thestratum corneum it continues to invade the epidermis; it then enters a hairfollicle, penetrates the hair shaft and grows down the length of the hair.[3] Thehyphae grow distally until they reach the upper limits of the zone of keratinization where the nucleated hair shaft cornifies completely and is converted into hard, anucleatedkeratin.[13] The terminal end of the growing hyphae forms a ring (Adamson's Fringe).[3] As the hair continues to grow outwards, hyphae are brought to the surface (scalp) andarthroconidia are produced.[7] Eventually due to mechanical forces (the movement of the fungi) andkeratinase (achymotrypsin-like enzyme with optimal activity at an acidic pH), all but 1–2 mm of the diseased hair follicle weakens and falls off.[2][3] The remaining hair has a characteristic dark grey appearance due to the Adamson's Fringe.[3]
There is an array of different tests to differentiate between fungi. Direct microscopy with 10% KOH would show small to mediumconidia with ectothrix hair invasion.[11] Performing a wet mount would show 'racquet shaped hyphae' with few macro and microconidia.[11] Histological examination of a diseased hair shows clefts that between the innerroot sheath and hair.[14]
Microsporum audouinii fluoresces when examined in ultraviolet light (Wood's lamp).[15] The two main growth media employed to test forM. audouinii areSabouraud's Dextrose agar andpotato dextrose agar. On the former, growth is slow with and poor sporulation with most strains producing a few abortive macroconidia and sparse microconidia.[3] The colonies are flat, dense and cottony in texture with a greyish-white to reddish brown hue.[16] On Potato Dextrose agar, colonies are white with a silky texture and a peach-coloured underside.[10][16]
Microsporum audouinii can be differentiated from non-sporulating strains of the similarM. canis by culture on autoclaved rice. Under these conditions,M. canis typically yields abundant growth and little to no pigmentation whereasM. audouinii produces no visible growth and abundant brown pigment on the rice grains.[16]PCR fingerprinting is a fairly new diagnostic tool for the rapid identification of these fungi.[1][15]
A symptomatic patient will present an unusual amount of itching andalopecia.[11] Primary treatment involvesgriseofulvin, an antimycotic agent. For patients who don't respond to griseofulvin, other drugs,itraconazole,fluconazole, andterbinafine can be used as a replacement to or in conjunction with griseofulvin. These drugs are preferred over griseofulvin as they have a shorter duration for treatment.[4] However, these agents havedrug-drug interactions and over a prolonged period of time can cause liver damage.[17] Currently,squalamine, an aminosterol with fungicidal properties is being researched as itsmechanism of action is different from that of the aforementioned medicines, making it a good drug for those who don't respond well to itraconazole, fluconazole, or terbinafine.[17] Systemic treatment with oral medication and anti-fungal shampoos has also been effective.[18] Antifungal shampoos (ketoconazole 2% shampoo orselenium sulfide 2.5% ) are effective as they reduce the transmission of the diseased hair by preventing its shedding.[18] Other treatments include, epilation of the infected follicles, topical ointments and steroidal treatments. Topical ointments immobilize the fungus and reduce shedding but they do not penetrate the hair follicle and hence must be used in conjunction with other treatment methods.[4][18] Steroidal treatments aid in inflammation and pain reduction.[18]
Griseofulvin inhibits fungal cell mitosis via disruption of the mitotic spindle structure and preventing cell division at the metaphase stage.[7] In addition, it inhibitsnucleic acid synthesis. Both itraconazole and fluconazole inhibits the synthesis of ergosterol which is an important component of fungal cell membranes. Consequently, fluconazole use leads to changes in the permeability and function of the cell membrane.[7] Squalene epoxidase contributes to the formation of ergosterol. Terbinafine inhibits squalene epoxidase thereby preventing cell membrane formation.[7]
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