Jump to content

User:Nairndan/sandbox

From Wikipedia, the free encyclopedia

Microsporum audouinii is an anthropophilic fungus in the genus Microsporum.[1] It is a type of dermatophyte that colonizes keratinized tissues (primarily hair) causing infection. [2] The fungus is characterized by its spindle shaped macroconidia (7-30 X 35-160µm), clavate microconidia (2.5-3.5 X 4-7µm) as well as its pitted or spiny external walls. [3]

Microsporum audouinii
Scientific classification
Kingdom:
Fungi
Division:
Ascomycota
Class:
Eurotiomycetes
Order:
Onygenales
Family:
Arthrodermataceae
Genus:
Microsporum
Species:
Microsporum audouinii

Gruby (1843)

Factors required for growth

[edit]

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, humidity, organic carbon, nitrogen and temperature.[4] M.audouinii appears to prefer a neutral pH in the range of 6.8 - 7 and room temperature.[4] Drastic increases or decreases in temperature can inhibit its growth.[5] M.audouinii is effective in utilizing its carbon sources, but growth is strongest in the hexoses (glucose, mannose and fructose) and weakest in maltose,sucrose, lactose and galactose.[5] It is unable to synthesize the vitamins thiamine, niacin and riboflavin, however they are essential for its growth.[5] M. audouinii is only able to utilize organic nitrogen sources, particularly nitrogen from arginine and urea.[5]

Epidemiology

[edit]

Microsporum audouinii causes the infections Tinea capitis (scalp ringworm) and Tinea 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 to to M. audouinii. Differences in the chemical composition and quantity of the triglycerides in hair sebum 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 of Pityrosporum ovale decreases the ability for M. audouinii to thrive.[8][9] Pityrosporum ovale is an opportunistic lipophilic yeast that is a part of the human cutaneous flora in adults[9]. In most cases of adult onset Tinea capitis due to M. audouinii, there is at least one predisposing factors. Examples include, an immunocompromised system (diabetes mellitus, systemic lupus, organ transplant and HIV), zoophilic sources and hormonal changes in postmenopausal women.[8][7]

Generally, Tinea capitis is primarily seen in areas where there is high immigration. Especially 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.[11][10] With the advent of antimycotic 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] A recent increase in the M. audouinii-related Tinea capitis in Europe is thought to be related to migration of infected individuals from Africa.[4]

Pathology

[edit]

Tinea capitis develops when an inoculum from another individual or animal comes into a 'compromised scalp.' A compromised scalp can occurs when the stratum 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 the stratum corneum is continues to invade the epidermis, it then enters a hair follicle, penetrates the hair shaft and grows down the length of the hair.[3] The hyphae grow distally until they reach the upper limits of the zone of keratinization where the nucleated hair shaft cornifies completely and is convertedinto hard anucleated keratin. [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) and arthroconidia are produced.[7] Eventually due to mechanical forces (the movement of the fungi) and keratinase (a chymotrypsin-like enzyme with optimal activity at an acidic pH), all but 1 to 2 mm of the diseased hair follicle weakens and falls off.[3][2] The remaining hair has a characteristic dark grey appearance due to the Adamson's Fringe.[3]

Diagnostic tests

[edit]

There is an array of different tests to differentiate between fungi. Direct microscopy with 10% KOH would show small to medium conidia 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 would show artifactual clefts that form between the inner root sheath and hair.[14]

Microsporum audouinii fluoresces when examined in ultraviolet light (Wood's lamp).[15] The two main growth media employed to test for M. audouinii are Sabouraud's Dextrose agar and potato 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 similar M. canis by culture on autoclaved rice. Under these conditions, M. canis typically yields abundant growth and little to know pigmentation whereas M. 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]

Treatment

[edit]

A symptomatic patient will present an unusual amount of itching and alopecia.[11] Primary treatment involves griseofulvin, an antimycotic agent. For patients who don't respond to Griseofulvin, other drugs, Itraconazole, fluconazole, and terbinafine 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 have drug-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 its mechanism 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 or selenium 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.[18][4] 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 inhibits nucleic acid synthesis. Both Itraconazole and Fluconazole inhibits the synthesis of ergosterol which is an important component of fungal cell membranes. Consequently, Fluconzole 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]

References

[edit]
  1. ^ a b Roque HD, Vieira R, Rato S, Luz-Martins M (December 2006). "Specific primers for rapid detection of Microsporum audouinii by PCR in clinical samples". J. Clin. Microbiol. 44 (12): 4336–41. doi:10.1128/JCM.00759-06. PMC 1698423. PMID 17005755. Retrieved 2008-12-16.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link)
  2. ^ a b c Kibbler, edited by C.C. (1996). Principles and practice of clinical mycology (Repr ed.). Chichester: Wiley. p. 13,105. ISBN 0471961043. {{cite book}}: |first= has generic name (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  3. ^ a b c d e f g Schwartz, W. (24 January 2007). "Emmons, Chester W., Chapman H. Binford und John P. Utz, Medical Mycology 380 S., 388 Abb., darunter 2 Farbtafeln, Philadelphia 1963: Lea & Febiger. $ 14.-". Zeitschrift für allgemeine Mikrobiologie. 5 (3): 256. doi:10.1002/jobm.19650050318.
  4. ^ a b c d e f Jain, N.; Sharma, M. (2011). "Distribution of dermatophytes and other related fungi in Jaipur city, with particular reference to soil pH". Mycoses. 54 (1): 52–58. doi:10.1111/j.1439-0507.2009.01751.x. PMID 19638000. S2CID 38921416. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: date and year (link)
  5. ^ a b c d Rippon, J. W.; Lebeau, L. J. (1965 Aug 10). "Germination and initial growth of Microsporon audouinii from infected hairs". Mycopathologia et Mycologia Applicata. 26 (2): 273–88. doi:10.1007/BF02049781. PMID 5876965. S2CID 5746363. {{cite journal}}: Check date values in: |date= (help)
  6. ^ KLIGMAN AM; GINSBERG D (1950 May). "Immunity of the adult scalp to infection with Microsporum audouinii". The Journal of Investigative Dermatology. 14 (5): 345–58. doi:10.1038/jid.1950.43. PMID 15422183. {{cite journal}}: Check date values in: |date= (help)
  7. ^ a b c d e f g h i j Gupta, A. K.; Summerbell, R. C. (2000 Aug). "Tinea capitis". Medical Mycology : Official Publication of the International Society for Human and Animal Mycology. 38 (4): 255–87. doi:10.1080/mmy.38.4.255.287. PMID 10975696. {{cite journal}}: Check date values in: |date= (help)
  8. ^ a b Narang, Kirti; Pahwa, Manish; Ramesh, V. (2012). "Tinea capitis in the form of concentric rings in an HIV positive adult on antiretroviral treatment". Indian Journal of Dermatology. 57 (4): 288–290. doi:10.4103/0019-5154.97672. PMC 3401845. PMID 22837564.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: unflagged free DOI (link)
  9. ^ a b Faergemann, J (1993 Sep). "Pityrosporum ovale and skin diseases". The Keio Journal of Medicine. 42 (3): 91–4. PMID 8255067. {{cite journal}}: Check date values in: |date= (help)
  10. ^ a b c d e Arenas, R.; Torres, E.; Amaya, M.; Rivera, E. R.; Espinal, A.; Polanco, M.; Fernández, R.; Isa-Isa, R. (2010 May). "[Emergence of Microsporum audouinii and Trichophyton tonsurans as causative organisms of tinea capitis in the Dominican Republic]". Actas Dermo-sifiliograficas. 101 (4): 330–5. doi:10.1016/j.ad.2009.12.004. PMID 20487688. {{cite journal}}: Check date values in: |date= (help)
  11. ^ a b c d Vella Zahra, L.; Vella Briffa, D. (2003). "Tinea capitis due to Microsporum audouinii in Malta". Mycoses. 46 (9–10): 433–5. doi:10.1046/j.0933-7407.2003.00913.x. PMID 14622396.
  12. ^ Rezusta, A.; Betrán, A.; Querol, I.; Palacián, M. P.; Revillo, M. J. (2011). "Tinea capitis caused by Trichophyton soudanense and Microsporum audouinii in an adult: a case report". Mycoses. 54 (1): 89–90. doi:10.1111/j.1439-0507.2009.01749.x. PMID 19712077. S2CID 205448257. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: date and year (link)
  13. ^ Joshi, Rajiv (2011). "Adamson′s Fringe, Horatio George Adamson, and Kligman′s experiments and observations on Tinea capitis". International Journal of Trichology. 3 (1): 14–19. doi:10.4103/0974-7753.82120. PMC 3129117. PMID 21769230.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  14. ^ Joshi, Rajiv (1 January 2011). "Adamson′s Fringe, Horatio George Adamson, and Kligman′s experiments and observations on Tinea capitis". International Journal of Trichology. 3 (1): 14–19. doi:10.4103/0974-7753.82120. PMC 3129117. PMID 21769230.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  15. ^ a b Griffin, Craig E.; Muller, George H.; Kirk, Robert Warren; Scott, Danny W.; Miller, William L. (2001). Muller and Kirk's Small Animal Dermatology. Philadelphia: Saunders. p. 347. ISBN 0-7216-7618-9.{{cite book}}: CS1 maint: multiple names: authors list (link)
  16. ^ a b c Ellis, Dr.David. "Microsporum audouinii". The University of Adelaide. Retrieved 18 October 2013.
  17. ^ a b Coulibaly, Oumar (April 2013). "activity of aminosterols against dermatophytes". Medical Mycology. 51 (3): 309–312. doi:10.3109/13693786.2012.724773. PMID 22998181. S2CID 12440878. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: date and year (link)
  18. ^ a b c d E. Elewski, Boni (June 1999). "Treatment of tinea capitis: beyond griseofulvin". J Am Acad Dermatol. 40 (6 Pt 2): S27-30. doi:10.1016/S0190-9622(99)70394-4. PMID 10367913.{{cite journal}}: CS1 maint: date and year (link)
[edit]

Category:Parasitic fungi Category:Eurotiomycetes

Stub icon

This Eurotiomycetes-related article is a stub. You can help Wikipedia by expanding it.

Stub icon

This article related to parasites is a stub. You can help Wikipedia by expanding it.

Retrieved from "https://en.wikipedia.org/w/index.php?title=User:Nairndan/sandbox&oldid=1168295774"