Superficial mycoses mbbs v

1
SUPERFICIAL & CUTANEOUS
MYCOSES
DR A.S. BABA
Dept of Medical Microbiology
UCH Ibadan
DR A.S. BABA

OUTLINE
 Introduction
 Recap anatomy & histology of the skin
 Superficial versus cutaneous mycoses
 Disease
 Epidemiology
 Pathogenesis
 Immunity
 Clinical features/manifestations
 Diagnosis
 Treatment
 Prevention /control
2DR A.S. BABA

INTRODUCTION
 These are very mild but chronic superficial
infections affecting the stratum corneum of
the skin;
 Most superficial, outermost layer.*
 Typically cause chronic infections with very
little or no inflammatory reaction.
 May become extensive in the severely
debilitated causing widespread cutaneous
lesions.
3DR A.S. BABA

THE SKIN;RECAP
 The skin; largest organ in the body
 Covers the subcutaneous tissues.
 Involved in temp control, sensation.
 Excretes waste products of metabolism via sweat.
 2 layers:epidermis & dermis madeup of 5 & 2 sub
layers respectively
• Epidermis:
 Stratum corneum
 Stratum lucidum
 Stratum granulosum
 Stratum spinosum
 Stratum basale
4DR A.S. BABA

THE SUPERFICIAL MYCOSES
 Pityriasis (tinea) versicolor
 occurs in tropical and temperate climates; it is
characterized by discrete areas of hypopigmentation or
hyperpigmentation associated with induration & scaling.
 Lesions are found on the trunk and arms; some assume
pigments ranging from pink to yellow-brown, hence the
term versicolor.
 Members of the genus Malassezia,of which M. furfur is
the most common, are the cause; these organisms can be
seen in skin scrapings as clusters of budding yeast cells
mixed with hyphae.
 They grow in the yeast form in culture media enriched
with lipids.
6DR A.S. BABA

7
Tinea
versicolor
DR A.S. BABA

Pityrisis versicolor
8DR A.S. BABA

Pityriasis
9
 Clinical Diagnosis:KOH- Spaghetti and
meatballs
 Treatment:Azoles
DR A.S. BABA

Tinea versicolor (Spaghetti and meatballs) 10DR A.S. BABA

SUPERFICIAL MYCOSES CONT’D
 Tinea nigra
 (Tinea nigra palmaris) is another tropical infection,
is characterized by brown to black macular lesions,
usually on the palms or soles.There is little
inflammation or scaling, and the infection is confined
to the stratum corneum.
 The cause, Hortaea werneckii, is a black-pigmented
fungus found in soil and other environmental sites.
Scrapings of the lesion show brown–black-pigmented
septate hyphae.
 Microscopic examination of skin scrapings will show
branched septate hyphae & budding yeast cells with
melaninized cell walls.
11DR A.S. BABA

Tinea nigraMicrocsopic
Macroscopic
DR A.S. BABA 13

Piedra
 is a nodular infection of the hair shaft
characterized by black or white nodules
attached to the hair shaft.
 White piedra (caused by Trichosporon spp)
infects the shaft in hyphal forms, which
fragment with occasional buds.
 Black piedra (caused by Piedraia hortae)
shows branched hyphae and ascospores in
sections of the hair.
14DR A.S. BABA

White Piedra
Micriscopic appearance of
infected hair shaft
Macroscopic
DR A.S. BABA 16

MYCOLOGY OF DERMATOPHYTES
 Dermatophytes have been classified as Deuteromycetes
(fungi imperfecti).
 The three genera of medical importance are
Epidermophyton, Microsporum, andTrichophyton, which are
separated primarily by the morphology of their macroconidia
and presence of microconidia.
 The sexual forms have been discovered for many of the
Microsporum andTrichophyton species and assigned to
ascomycete genera.
 Most grow best at 25°C on Sabouraud’s agar,which is
usually used for culture.The hyphae are septate, and their
conidia may be borne directly on the hyphae or on
conidiophores. Small microconidia may or may not be
formed; however, the larger and more distinctive
macroconidia are usually the basis for identification.
21DR A.S. BABA

General characteristics of Macroconidia and
Microconidia of Dermatophytes
Genus Macroconidia Microconidia
Microsporum Numerous, thick
walled,rough
Rare
Epidermophyton Numerous,
smooth walled
Absent
Trichophyton Rare,thin walled,
smooth
Abundant
22DR A.S. BABA

TINEA
Ringworm (moth)
23DR A.S. BABA

TINEA CORPORIS
 TINEA CORPORIS
 Skin lesions begin in a similar pattern and enlarge to
form sharply delineated erythematous borders with
skin of nearly normal appearance in the center.
 Multiple lesions can fuse to form unusual geometric
patterns on the skin.
 Lesions may appear in any location, but are
particularly common in moist, sweaty skin folds.
 Obesity and the wearing of tight apparel increase
susceptibility to infection in the groin and beneath the
breasts.
24DR A.S. BABA

Tinea corporis
(the body)
27DR A.S. BABA

 TINEA PEDIS
 Another form of infection, which involves scaling
and splitting of the skin between the toes, is
commonly known as athlete’s foot. Moisture and
maceration of the skin provide the mode of entry.
 Common amongst individuals whom sweat a lot on
the palms & soles of feet.
 Continuous wearing of covered shoes is a
predisposing factor.
 Cracking & macceration of the inter digital web
maybe followed by bacterial superinfection.
28DR A.S. BABA

Tinea pedis
(feet)
29DR A.S. BABA

Tinea unguium
(nails)
30DR A.S. BABA

TINEA UNGUIUM
 Nail bed infections first cause discoloration of
the sub ungual tissue, then hyperkeratosis and
apparent discoloration of the nail plate by the
underlying infection follow.
 Direct infection of the nail plate is uncommon.
Progression of hyperkeratosis and associated
inflammation cause disfigurement of the nail but
few symptoms until the nail plate is so dislodged
or distorted that it exposes or compresses
adjacent soft tissue.
31DR A.S. BABA

Severe nail infection with Trichophyton rubrum in
a 37-year-old male AIDS patient.
Source: Intern. J. Dermatol. 31(1992): 453.
32DR A.S. BABA

Tinea capitis
(scalp)
34DR A.S. BABA

Tinea cruris
(jock itch)
35DR A.S. BABA

Tinea barbae
(bearded area)
36DR A.S. BABA

CLINICAL FEATURES
 TINEA CAPITIS
 Infection of the hair begins with an erythematous papule
around the shaft which progresses to scaling of the scalp,
discolouration and eventually fracture of the shaft.
 Spread of adjacent hair follicles progresses in a ring like
fashion leaving behind broken discoloured hairs and
sometimes black dots filled with fungal elements.
 In most cases, symptoms beyond itching are minimal.
 Scaling of the scalp with hyper or hypopigmented areas
maybe seen.
37DR A.S. BABA

Ecology of Dermatophytes
To determine the source of infection
 Anthropophilic
 Zoophilic
 Geophilic
40DR A.S. BABA

ANTHROPOPHILIC
Associated with humans only. Person -to-person transmission through
contaminated objects (comb, hat, etc.)
41DR A.S. BABA

ZOOPHILIC
Associated with animals.Transmission to humans by close contact with
animals.
42DR A.S. BABA

GEOPHILIC
Usually found in soil.Transmitted to humans by direct exposure.
43DR A.S. BABA

GEOGRAPHIC
DISTRIBUTION
Worldwide
44DR A.S. BABA

Dermatophytes
3 Genera
 Trichophyton
 Microsporum
 Epidermophyton
45DR A.S. BABA

Trichophyton
(19 species)
 Hair
 Skin
 Nails
46DR A.S. BABA

Trichophyton species
Large, smooth, thin wall, septate,
pencil-shaped
47DR A.S. BABA

TRICHOPHYTON RUBRUM
Causes a chronic infection in patients a cell-mediated immune defect.
(most common in SC blacks)
49DR A.S. BABA

DERMATOPHYTES
 Trichophyton rubrum
 Infects nails and smooth skin (rarely found on hair).
 Most common and widely distributed dermatophyte on man and rarely
isolated from animals, never from soils.
 No teleomorph (possibly lost in transition from saprophytic lifestyle to man).
 Resistant and persistent (some people become carriers for life).
 Slow-growing in culture.
 When intensely pigmented in culture the color is reminiscent of port
burgundy wine or venous blood.
 Production of pigment increased, if fungus grown on corn meal agar.
 Microconidium are clavate or "teardrop" shape with a broad attachment
point of the hyphae.
 Microconidia may develop on sides of macroconidium.
 In vitro - lack of hair penetrating organs, unlike T. mentagrophytes.
 T. violaceum grows poorly without thiamine. T. megninii grows poorly
without L-histidine. T. rubrum requires neither thiamine or L- histidine.
50DR A.S. BABA

Trichophyton rubrum
http://www.mycology.adelaide.edu.au/Fungal_Descriptions/Dermatophytes/Trichophyton/rubrum.htm
51DR A.S. BABA

Microsporum
(13 species)
 Skin
 Hair
52DR A.S. BABA

Microsporum species
Thick wall, spindle shape,
multicellular
53DR A.S. BABA

MICROSPORUM CANIS
.
most common etiology of tinea in SC whites
54DR A.S. BABA

DERMATOPHYTES
 Microsporum canis complex?
 Teleomorph is an ascomycete called
Arthroderma otae. Almost all clinical isolates
are minus mating type.
 Macroconidia are abundant, thick-walled
with many septa, up to 15. Macroconidia are
often hooked or curved at ends.
 Microconidia are small and clavate (club-
shaped).
55DR A.S. BABA

Microsporum canis
Teleomorph: Arthroderma otae
http://www.doctorfungus.org/thefungi/microsporum_canis.htm
http://www.mycology.adelaide.edu.au/Fungal_Descriptions/Dermatophytes/Microsporum/Microsporum_canis.html56DR A.S. BABA

DERMATOPHYTES
 Microsporum gypseum complex
 Teleomorphs are Arthroderma gypseum and A. incurvatum.
 Produces abundant macroconidia brownish-yellow due to large
numbers macroconidia. Surface of culture colony often is
powdery in appearance.
 Reverse of colony often appears ragged around edges.
 Macroconidia usually have 4-6 septa or crosswalls.
 Microconidia are smaller than in M. canis.
 Macroconidia up to 40 µm long
 In lactophenol, water is extracted and can cause the
macroconidia walls to collapse. This is an artifact due to
mounting media. Macroconidia do not form on infected hair!
57DR A.S. BABA

Microsporum gypseum
http://www.mycology.adelaide.edu.au/Fungal_Descriptions/Dermatophytes/Microsporum/Microsporum_gypseum.htm
http://www.doctorfungus.org/thefungi/microsporum_gypseum.htm
58DR A.S. BABA

Epidermophyton floccosum
 Skin
 Nails
61DR A.S. BABA

DERMATOPHYTES
 Epidermophyton floccosum
 Only one pathogenic species in this genus.
 Tinea unguium and tinea cruris are often caused
by this fungus.
 Culture starts out white/turns sulfur color.
 Cultures may be wrinkled to cottony in
appearance.
 No microconidia.
 Shape of macroconidia is a distinguishing
characteristic - clavate macroconidia.
62DR A.S. BABA

http://www.mycology.adelaide.edu.au/Fungal_Descriptions/Dermatophytes/Epidermophyton/
http://www.doctorfungus.org/thefungi/epidermophyton.htm
63DR A.S. BABA

Bifurcated hyphae with multiple,
smooth, club shaped macroconidia
(2-4 cells)
64DR A.S. BABA

Therapy
 Griseofulvin
 Tinactin
 Clotrimazole
 Miconazole
 Ketoconazole
 Itraconazole
 Terbinafine
65DR A.S. BABA

TREATMENT
 Treatment involves thorough removal of infected & dead
epithelial tissues & application of a topical antifungal agent.
 To prevent re-infection, the area should be kept dry &
sources of infection such as infected pet or shared bathing
facilities should be avoided.
 Tinea capitis: griseofulvin or terbinafine given orally over several
weeks. frequent shampooing & topical antifungals maybe of
benefit.
 Tinea corporis/pedis: itraconazole & terbinafine are the drugs of
choice,given over a minimum period of 2-4wks.Topical
preparations are also useful.Treatment should be continued for 1-
2weeks after lesions have cleared.
 Tinea unguium:nail infections are most difficult to treat often
requiring months of oral itraconazole or terbinafine as well as
surgical removal of the nail. Relapses are common.
66DR A.S. BABA

Dermatophytid Reaction
(ID)
 Dermatophyte infection on feet
(not clinically evident)
 Ringworm Lesion on hand
(usually the dominant side)
68DR A.S. BABA

Dermatophytid Reaction
(ID)
 Culture skin scrapings from feet
 Treat the tinea pedis
 The hand lesion (ID phenomenon) will
respond to therapy of the foot.
69DR A.S. BABA

Dermatophyte infection
 Epidemiology
 There are both ecologic and geographic differences in the
occurrence of the various dermatophyte species.
 Some are primarily adapted to the skin of humans, others to
animals, and others to the environment. All may serve as the source for
human infection.
 Many wild & domestic animals are infected with Dermatophytes & serve
as a reservior for infection of humans.
 Due to the fact that dermatophytes are of low virulence & infectivity,human to human
transmission requires very close contact with an individual or infected material esp foamites.
 Transmission usually takes place within families or in situations
involving contact with detached skin or hair, such as barber shops
and locker rooms.
 No special precautions beyond handwashing need be taken by
the medical attendant after contact with an infected patient.
72DR A.S. BABA

PATHOGENESIS
 Dermatophytoses begin when minor traumatic skin lesions
come in contact with dermatophyte hyphae shed from
another infection.
 Once the stratum corneum is penetrated, the organism
proliferates in the keratinized layers of skin without invading
the deeper structures.
 The course of the infection is dependent on the anatomic
location, moisture,the dynamics of skin growth and
desquamation, the speed and extent of the inflammatory
response & the infecting species.
 Inflammation speeds up skin growth & desquamation
thereby limiting infection whereas immunosuppresants like
corticosteroids depress shedding of the keratinized layer &
thus favour ing chronicity of the infection.
73DR A.S. BABA

PATHOGENESIS CONT’D
 Most infections are self limiting but those in which the rate
of fungal growth equals desquamation, the inflammatory
response is poor & such infections tend to be chronic.
 Infection may spread from the skin to other keratinized
tissue mainly the hair or nails or may invade them primarily.
 The hair shaft may be penetrated by hyphae which extend
as arthroconidia exclusively within the hair shaft
(endothrix) or both within & outside (ectothrix).
 The end result is damage to the hair shaft structure, which often
breaks off.
 Loss of hair at the root and plugging of the hair follicle with fungal
elements may result.
 Invasion of the nail bed causes a hyperkeratotic reaction, which
dislodges or distorts the nail.
74DR A.S. BABA

IMMUNITY
 The great majority of dermatophyte infections pass through
an inflammatory stage to spontaneous healing.
 Phagocytes are able to use oxidative pathways to kill the
fungi both intracellularly and extracellularly.
 Little is known about the factors that mediate the host
response in these self-limiting infections or whether they
confer immunity to subsequent exposures.
 Antibodies may be formed during infection but play no
known role in immunity.
 Most clinical and experimental evidence points to the
importance of cell-mediated immunity (CMI).
 Occasionally dermatophyte infections may become
widespread esp in the immunocompromised.
75DR A.S. BABA

DIAGNOSIS
 The goal of diagnostic procedures is to distinguish
dermatophytoses from other causes of skin inflammation.
 Infections caused by bacteria, other fungi, and noninfectious
disorders (psoriasis, contact dermatitis) may have similar
features.
 The most important step is microscopic examination of material
taken from lesions to detect the fungus.
 Skin scrappings are collected from the edge of the lesion &
examined microscopically ff KOH preparation or after being
stained with calcoflour white.
 Examination of infected hairs reveals hyphae and arthroconidia
penetrating the hair shaft. Broken hairs give the best yield.
 Some species of dermatophyte fluoresce, and selection of hairs for
examination can be aided by the use of an ultraviolet lamp (Wood’s
lamp).
 The same material used for direct examination can be cultured for
isolation of the organism using Sabouraud’s dextrose agar.
76DR A.S. BABA

Dermatophyte Culture
77DR A.S. BABA

78DR A.S. BABA

79DR A.S. BABA

Dermatophytes
 It is not necessary to be an athlete to get
athlete’s foot.
 A tinea (moth) does not cause skin lesions
 There are no worms in ringworm
80DR A.S. BABA

Ringworm culture
83DR A.S. BABA

Superficial mycoses mbbs v

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Superficial mycoses mbbs v

Similar to Superficial mycoses mbbs v (20)

Recently uploaded

Recently uploaded (20)

Superficial mycoses mbbs v