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CUTANEOUS MYCOSES
(DERMATOMYCOSES)
• Dermatomycoses: Infections affecting keratinized tissues like skin, hair, nails etc.
• Dermatophytes: Fungi infecting epidermis, hair, nails (keratin containing tissues)
• In ancient times, it was thought to be due to worms/lice, therefore called as Ringworm or Tinea ( Latin: worm/ insect larvae)
• Skin lesions: roughly circular with equal expansion in all directions with serpiginous borders.
Nomenclature
Assigned by the area of the skin affected.• Ringworm of scalp: Tinea capitis• Ringworm of body: Tinea corporis• Ringworm of groin: Tinea cruris• Ringworm of feet: Tinea pedis (athlete’s foot)• Ringworm of face: Tinea facei• Nail mycoses: Onchomycosis
Dermatophytes • Dimorphism absent• Infected skin lesions have septate hyphae &
arthrospores (thick walled, asexual spores formed by hyphal septation)
• Keratinases used in industries for hair removal from hides ( leather industries)
• world wide distribution, few spp have local area ditribution
• Increased travel: dispersal of organisms to new regions
Keratinolytic Activity
• Spores/ mycelia injected intravenously into experimental animals (guinea pigs) no lesions developed
• Skin abrasions at time of injection, dermatophytic infection appears in the scarified tissues a few weeks later
• Keratinolysis at low rate under in vitro conditions.
Growth• Simple media: ammonium salts and glucose as
source of N, C and energy• Enriched media: amino acids and proteins. This
shows increased fungal growth• Growth on sterile hair: hyphae from epidermis
grow into hair follicle and then into hair shaft. 2 mechanisms: A) Endothrix: hyphae grow within hair shaft forming long parallel arthrospores’ rows
• B) Ectothrix: growth within & on external surface of hair shaft.
Epidemiology
• Anthropophilic spp: found in human skin. These are about 15 spp.
• Zoophilic spp: indigenous to domesticated and wild animals.
• Geophilic spp: free living saprobes in soil • Egs: Microsporum gypseum, Trichophyton
mentagrophytes, T. ajelloi
Transmission
• Man to man • Man to animal• Direct contact, eg: gardeners affected• Contact with infected tissues like hair, epidermal
scales, eg: barber shops clippers, shower room floors etc.
• Animals: as reservoirs or vectors. These are responsible for infection in children in more than 30% of cases.
Factors involved in infection
• Age: children susceptible to ringworm of scalp, whereas, adults infected with athletes foot
• Resistance to scalp infection: 1) secretory activity of sebaceous gland in adults. 2) antifungal action of C7-C11 unsaturated fatty acids in sebum.eg: undecylenic acid
• Immunity: fungistatic factor ( not an Ig) present in normal serum which prevents penetration of dermatophytes in host tissue.
Hypersensitivity
• Allergic reactions due to fungal antigens• Ags spread from site of infection• Skin lesions caused, these called as
Dermatophytids, which are sterile and appear as vesicles on hands.
Diagnosis
• Microscopic examination of skin scrapings or fungal cultures in KOH preparation (15%-20%)
• Differentiation is based on hyphal morphology, microconidia and macroconidia.
• Molecular biology techniques: PCR
a Microsporum canis. Lactophenol blue preparation: large, fusiform macroconidia. b Trichophyton mentagrophytes. Lactophenol blue preparation: thin-walled, cylindrical macroconidia; numerous microconidia, often in clumps; spiral hyphae.
Macroconidia from the Epidermophyton floccosum
KOH mount of infected skin scales (left) and nail material (right) showing typical dermatophyte hyphae breaking up into arthroconidia
KOH mount of infected hairs showing "small spored" ectothrix invasion by M. canis and "large spored" ectothrix invasion by M. gypseum.
Treatment• Griseofulvin: orally administered. Binding to microtubules prevents
mitosis of the fungal cell• Oral allylamine terbinafine and azoles block ergosterol production,
which is a necessary component of fungal cell membrane. egs. Tolnaftate, itracomzole, fluconazole etc.
• Topical agents: scalp and smooth skin cured within few weeks, but feet (toenails) take months of continuous treatment since action is dependent on keratin layer thickness and rate of replacement. Egs: miconazole, clotrimazole, ketoconazole etc.
• Other important antifungal compound is tinactin, which inhibits squalene epoxidase (necessary for ergosterol synthesis)
• Amphotericin B• Undecylenic acid interfere with hyphae formation, therefore used
as topical treatment
Prophylaxis
• Avoid direct contact with the pathogen• Regular disinfection of shower rooms and
wardrobes• Keeping the infecting area dry• Avoid sharing of clothes, towels and other items
of personal use• Use of cotton clothes • Promote and practise personal hygiene• Use of fungicidal soaps and powders.
References• http://www.lexic.us/definition-of/dermatomycosis• http://en.wikipedia.org/wiki/Dermatomycosis• http://medical-dictionary.thefreedictionary.com/dermatomycosis• http://www.as.ysu.edu/~crcooper/Dermatomycosis-2010.pdf• http://answers.yahoo.com/question/index?qid=20080128094815AA1VW
G4• http://fampra.oxfordjournals.org/content/16/6/611.full• http://www.ncbi.nlm.nih.gov/pubmed/15305713• http://www.merriam-webster.com/medical/dermatomycosis• http://www.vita.bg/zab_en.php?zab=101&d=31• http://www.vetmed.wisc.edu/pbs/courses/PBS517/facdocuments/
pic_glossary.pdf• http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/
71300.htm• Mycology by Davis
