Cutaneous Mycoses of skin Flashcards
Otomycoses caused by
aspergillus
penicillium
mucor
rhizopus
(opportunistic molds that cause outer ear infections
epi otomycoses
world wide
soil
humans and animals are NOT reservoirs
transmission otomycoses
coming in contact with contaminated fomites
path otomycoses
accumulation of large masses of fungi or bacteria in external ear canal
s/s otomycoses
chronic ear infection itching pain inflammation and loss of hearing
dx otomycoses
fragments of mycelium with or without septa
conidiophores and sporangiospores may be seen
tx otomycoses
ketoconazole
wax hook
tinea faciei caused by
trycophyton mentagrophytes
trycophyton rubrum
infection on glabrous skin of face (hair less)
epi of tinea facial
worldwide
p2p p2m fomite and aerial
pathogenesis of tinea facei
by trycophyton
hypae growing release enzymes producing edema and leukocytic infiltrations
mold allergins cause granuloma formations
tinea facei immunity
PARTIAL protective immunity
s/s of tinea facei
calin annular or circular lesions with raised margins and papule
pruritus burning and erythema are present
dx tinea facei
hyphae with microconida
tx tinea facie
myconazole
tinea barbae
aka
trycophyton interdigitale
trycophyton violaceum
aka barbers itch
epi of tinea barbae
transmission
worldwide
commonly in rural areas (farmers) with high temp and humidity
p2p m2p fomite and aerial
pathogenesis of tinea barbae
trycophyton
mycelia grow into pores of hair shafts causing edema and leukocyte infiltrations
immunity tinea barbae
partial
s.s tinea barbae
trycophyton
mild superficial- scaly lesions with vesiculopusturlar borders bearded areas
- deep pustular- follicular pustules on bearded areas of skin
dx tinea barbae
trycophyton
microconida on hyphae
tx tinea barbae
trycophyton
terbinafide
tinea capitis ectothrix caused by
AKA
microsporum
(audouini and canis) `
aka grey patch ring worm
tinea capitis ecto epi
by microsporum
ecothrix world wide
tina favosa- africa and europe
tinea Capitis ecto transmisison
p2p m2p fomite airborne
tinea capitis ecto immunity
partial
tinea capitis ecto s/s
microsporum
begin as coalesced papule and develop into legions (weeping) and keloids (scars)
allergic reaction – causing severe itching and alopecia
tinea favosa
type of tinea capitis caused by tricophyton schoenleini - mycelia interact with s camp proteins producing dead cell masses in mats of hair– yellowing brown cup shaped skin crusts
tx tinea capitis exto
microsporum
tx- griseofulvin
dx tinea capitis exto
hyphae with macroconida
difference between tinea capitis endo and exo
exo- microsporum
endo- trichophyton (harder to get rid of)
tinea capitis endo caused by
AKA?
trichophyton
(tonsurans and violaceum)
aka black dot ring worm*
path tinea capitis endo
trichophyton
conidia found inside hair shaft
if cuticle involved- initial lesions that develop into erythematous circular lesions
immunity tinea capitis endo
by trichophyton
partial
s/s tinea capitis endo
erythematous scaling circular lesions w black dots (broken off hairs)— infection can result in hair loss
dx tinea capitis endo
conydia and hyphae inside hair shafts
tx tinea capitis endo
terbinafine
tinea corporis caused by
trichophyton (interdigital and rubrum )
epidermophyton floccosum
microsporum canis
epi tinea corporis
world wide
transmission (4)
path tinea corporis
hyphae or conydia infect horny layer of skin – spread out in glabrous skin
s.s tinea corporis
- annular
- small spreading circular areas of erythema that become scaly in center with red margins
BECOME CHRONIC - vesicular
- Vesicles and pustules behind erythematous border
dx tinea corporis
mycelia and conidiospores
microsporum canis cas club shaped macroconidia with rough walls
tx tinea corporis
terbinafine
tinea unguium caused by
epidermophyton flocosum
trichophyton interdigitale
tinea unguium associated with
tinea pedis and magnum infections in males after puberty
tinea unguium pathogenesis
unknown incubation period, nail injury predisposes infection
infection starts under nail plate of fingers or toes , grow out of nail plate into stratum corneum
s/s tinea unguiumm
soft friable keratin, THICKENED NAIL
causes white patches/pits
dx tinea unguium
hyphae or macroconida presen t
tx tinea unguium
terbinafide
most infections become resistant and are chronic
sub ungual dermatophytosis
lateral or distal edges of nail are first involved, then develop into nail plate– brittle friable and thickened
tinea manuum caused by
tricophyton interdigitale
epidermophyton flocossum
microsporum gypseum
on palms and fingers
epi tinea manum
world wide
associated with males
pathogenesis tinea manum
infection begins due to maceration ( moisture due to extended wear like gloves) due to occupational activities
infection result in lesions that are exfoliative, erythematous and scaly sheets if stub
s.s. tinea manum
diffuse hyperkeratosis of palms and fencers with concentric exfoliation of skin
scaly sheets develop on dorsal of hand
dx tinea magnum
hyphae macroconida
tx tinea magnum
miconazole
tinea cruris caused by
AKA
trycophyton rubrum
epidermophyton floccosum
jock itch
epidemiology tinea cruris
worldwide p2p areal and fomites
20-30 males commonly infected
pathogenesis tinea cruris
hyphae invade groin and perianal areas causing edematous lesions
s/s tinea cruris
circular lesions in groin and scrotum areas
develops into serpiginous* erythematous lesions
erythema and intense itching occur
dx tinea cruris
epidermophyton- club shaped macroconidia
tricophyton- microconidia
tx tinea cruris
terbinafine
loose clothes and lsoss of weight lessen chance of infection
tinea pedis caused by
aka
tricophytoon interdigitale and rubrum
epidermophyton floccosum
aka athletes foot
epi of tinea pedis
most common fungal infection of humans
p2p aerial and fomites
pathogenesis of tinea pedis
breakdown in host skin promotes invasion of epidermis, localized to keratinized skin ( between toes)
- papulosquamous hyperkeratotic skin is seen
immunity tinea pedis*
poor cel mediated- no partial or protective immunity
s.s tinea pedis
itching
intertriginou dermatitis with peeling maceration and fissuring of skin intertriginous (between 3 4 5 toes)
also vesicular form that ulcerates– cause secondary bacterial infections to develop
dx tinea pedis
stained prep of hyphae with micro or macroconida
tx tinea pedis
terbinafide
onychomycosis caused by
arthroderma aspergillus candidda geotrichum scopulariopsis
epidemiology onychomycosis
transmission
who gets it?
worldwide in soil
transmitted via implantation with spore contaminated fomites
nail infection accompanies disease that causes patient to be immunosuppressed*
pathogenesis of onychomycoses
damage to nail architecture THAT DOES NOT THICKEN
painful with brittleness of nails
dx of onychomycoses
various forms of hyper elements- branching non branchin
tx of onychomycoses
ittraconazole
description of candidiasis
monomorphic opportunistic yeast
epi of candidiasis
normal floral human
p2p nosocomial and fomites
path of candidiasis
farnesol?
gelatinous types of lesions develop – due to mucoid degeneration of tissue — causing formation of large emboli
farnesol helps turn from invasive to non invasive
s/s candidiasis
thrush, etc
paronychia- swelling of paronychial folds
systenic- fever headache anorexia myalgia hepatosplenomegaly heart problems
can be induced due to prolongues antibiotic tx
dx candidiasis
chains of oval budding yeast cells with pseudophyphae and blastospores
in serum* in cheek its part of normal flora
tx candidiasis
fluconazole or amphotericin B
immunity of candidiasis
NONE
allergic rxns can develop