Mycology Lec2superficial

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MICROBIOLOGY LECTURE M2 – Superficial Mycoses Lecture and Notes by Dr. Ng USTMED ’07 Sec C – AsM SUPERFICIAL MYCOSES INFECTIONS DUE TO Malassezia Species 3 Species of Medical Importance Malassezia furfur Malassezia pachydermatis Malassezia sympodialis MALASSEZIA FURFUR - causes Pityriasis versicolor – a chronic, usually asymptomatic fungal infection of the stratum corneum - synonyms for Pityriasis versicolor - tinea versicolor, tinea flava, dermatomycosis furfuracea, “liver spots” - member of the normal skin flora HISTORY 1846 - detected by Eichstedt & named the disease pityriasis versicolor 1853 - Robin named the fungus Microsporon furfur 1874 - Malassez described the yeast-like cells from lesions of the scalp 1889 - Baillon created genus Malassezia 1939 - Benham described the lipophilic nature of the fungus EPIDEMIOLOGY worldwide distribution but more prevalent in the tropics & subtropics some countries - 50% of people are infected occurs in both sexes, all ages, all races major factor - excessive sweating other factors - poor hygiene, malnutrition, poor health, pregnancy, systemic steroids, Cushing’s syndrome CLINICAL MANIFESTATIONS Pityriasis versicolor Folliculitis Sepsis other conditions o Peritonitis o Nipple discharge o Dacryoliths o Sinusitis Pityriasis versicolor - usually: asymtomatic, hyperpigmented macules or patches - common sites - chest, upper back, shoulder, upper arms, abdomen - may extend to - thighs, neck, forearms - rare in - scalp, palms, feet - hair shafts & nails - not infected - color varies according to : (1) pigmentation (2) exposure to sunlight (3) severity CLINICAL PRESENTATION OF PITYRIASIS VERSICOLOR Hyperpigmented Tinea Versicolor Round, hyperpigmented, barely palpable plaques and some perifollicular patches are evident on the upper abdomen. (A) Hyperpigmented Tinea Versicolor Perifollicular round patches of hyperpigmented lesions are tightly grouped on the upper back. (B) Hyperpigmented Tinea Versicolor The fine, branny scaling is not readily evident until lesions are gently scraped with the end of a glass microscope slide. (C) Inflammatory Tinea Versicolor Folliculitis - uncommon variant - lesions resemble acne - papules & pustules - history of antibiotic or steroid intake - may resolve spontaneously or evolve into abscesses Sepsis - catheter-acquired - neonates & adults on prolonged IV lipid hyperalimentation - peripheral blood is usually negative - usual source - patient’s skin or medical personnel other conditions Other Conditions - peritonitis - nipple discharge - dacryoliths - sinusitis

Transcript of Mycology Lec2superficial

Page 1: Mycology Lec2superficial

MICROBIOLOGY LECTURE M2 – Superficial MycosesLecture and Notes by Dr. NgUSTMED ’07 Sec C – AsM

SUPERFICIAL MYCOSES

INFECTIONS DUE TO Malassezia Species

3 Species of Medical Importance Malassezia furfur Malassezia pachydermatis Malassezia sympodialis

MALASSEZIA FURFUR- causes Pityriasis versicolor – a chronic, usually

asymptomatic fungal infection of the stratum corneum

- synonyms for Pityriasis versicolor - tinea versicolor, tinea flava, dermatomycosis furfuracea, “liver spots”

- member of the normal skin flora

HISTORY

1846 - detected by Eichstedt & named the disease pityriasis versicolor

1853 - Robin named the fungus Microsporon furfur

1874 - Malassez described the yeast-like cells from lesions of the scalp

1889 - Baillon created genus Malassezia 1939 - Benham described the lipophilic nature of

the fungus

EPIDEMIOLOGY

worldwide distribution but more prevalent in the tropics & subtropics

some countries - 50% of people are infected occurs in both sexes, all ages, all races major factor - excessive sweating other factors - poor hygiene, malnutrition, poor

health, pregnancy, systemic steroids, Cushing’s syndrome

CLINICAL MANIFESTATIONS

Pityriasis versicolor Folliculitis Sepsis other conditions

o Peritonitiso Nipple dischargeo Dacryolithso Sinusitis

Pityriasis versicolor- usually: asymtomatic, hyperpigmented macules or

patches- common sites - chest, upper back, shoulder, upper

arms, abdomen- may extend to - thighs, neck, forearms- rare in - scalp, palms, feet- hair shafts & nails - not infected- color varies according to :

(1) pigmentation(2) exposure to sunlight (3) severity

CLINICAL PRESENTATION OF PITYRIASIS VERSICOLOR

Hyperpigmented Tinea VersicolorRound, hyperpigmented, barely palpable plaques and some perifollicular patches are evident on

the upper abdomen. (A)

Hyperpigmented Tinea VersicolorPerifollicular round patches of hyperpigmented lesions are tightly grouped on the upper back. (B)

Hyperpigmented Tinea VersicolorThe fine, branny scaling is not readily evident until lesions are gently scraped with the

end of a glass microscope slide. (C)

Inflammatory Tinea Versicolor

Folliculitis- uncommon variant- lesions resemble acne - papules & pustules- history of antibiotic or steroid intake- may resolve spontaneously or evolve into

abscesses

Sepsis- catheter-acquired- neonates & adults on prolonged IV lipid

hyperalimentation- peripheral blood is usually negative- usual source - patient’s skin or medical

personnel other conditions

Other Conditions

- peritonitis- nipple discharge- dacryoliths- sinusitis

DIAGNOSIS

Direct Examinationo KOH mount - short, angular, occasionally

branching, septate hyphae & clusters of budding yeast

o Wood’s light - most lesions fluoresce yellow

Skin scrapings stained with periodic-acid schiff’s stain showing typical yeast-like and hyphal fragments of Malassezia furfur, the etiology agent of Pityriasis Versicolor

KOH wet mount of Tinea VersicolorAbundant short hyphae and round spores, so-called Spaghetti and meatballs are apparent. (A)

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Adding a small amount of Parker’s blue-black ink to the KOH stains Pityrosporon organisms blue and facilitates their identification from the skin scrapings.

Culture o often

not necessary, tedious & meticulouso Sabouraud’s agar with antibiotics at 37Co overlay with olive oil or whole-fat milko colonies appear dry, smooth or lightly

wrinkled, glistening or dull, white to creamy

Gram stain and calcofluor white preparation of Malassezia furfur

DIFFERENTIAL DIAGNOSIS

steroid-induced acne acne vulgaris vitiligo pigmentary disorders eg. Chloasma inflammatory conditions eg. tinea circinata,

seborrheic dermatitis, pityriasis rosea, erythrasma, syphilis, pinta

IMMUNOLOGY

rare in children under 10 years, associated with increase sebaceous gland activity

sweating - predisposing factor genetics - may play a role antibodies - detectable in chronic cases indirect IF - organism in skin scales & culture

PATHOLOGY

limited to the stratum corneum moderate hyperkeratosis may be seen increase in melanosome size but not in number other changes - mild acanthosis & perivascular

lymphocytic infiltrate

TREATMENT

selenium sulfide Na thiosulfate salicylic acid benzoyl peroxide the azole family eg. Ketoconazole NB. recurrence rate - very high despite treatment

MALASSEZIA PACHYDERMATIS- first isolated in 1925 from Indian rhinoceros- often associated with otitis externa of dogs- in man - associated with psoriasis or mycosis

fungoides, febrile systemic syndrome (neonates)...- isolated from urine, CSF, blood, vaginal, eye & ear

discharge, tracheal aspirate - also reported in patients receiving IV lipid

hyperalimentation (esp. neonates)- grows on agar at 37C without the addition of oil

MALASSEZIA SYMPODIALIS- isolated from the scalp of an AIDS patient with

tinea capitis (1990)

PIEDRA ( Black & White)

DEFINITIONS

a chronic, fungal infection of the hair shaft, forming firm, irregular nodules or encrustations composed of fungal elements

2 varieties - black & white, produced by 2 different species

synonyms - tinea nodosa, trichomycosis nodularis, trichomycosis nodosa, Beigel’s disease, Chignon disease

ETIOLOGY

Black Piedra - Piedraia hortai White Piedra - Trichosporon beigelii

Hair infected wth Piedraia hortae. The hard black nodule contains asci and ascospores, the sexualphase of the fungus.

Clinical presentation of white piedra

BLACK PIEDRAPiedraia hortai on hair

HISTORY

1865 - Beigel first observed white piedra 1901 - Malgoi-Hoes described black piedra 1911 - Horta differentiated black from white

piedra 1928 - Fonseca & Leao named the etiology of

black piedra, Piedraia hortai 1936 - Langeron summarized findings on both

varieties

EPIDEMIOLOGY – BLACK PIEDRA

tropics & subtropics males = females common among regular swimmers

EPIDEMIOLOGY – WHITE PIEDRA

more common in the temperate zone affects both sexes of all age group lower incidence than black variety

CLINICAL MANIFESTATION – BLACK PIEDRA

usually on scalp hair only infected hair - rough, sandy or granular

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nodules - hard, fusiform, firmly attached to hair shaft

thick part - layers of fungal cells cemented thin part - single layer of cells & hyphae does not penetrate cortex of hair hair follicles not involved

CLINICAL MANIFESTATION – WHITE PIEDRA

usually on facial & genital hair nodules are softer, mucilaginous, white to light

brown in color nodules are not as adherent hair follicles not affected

DIFFERENTIAL DIAGNOSIS

pediculosis (pubic hair) trichomycosis axillaries

o Gram stain - cocci & short bacillio UV light - (+) fluorescence o due to Corynebacterium tenuis

nits & lice tinea capitis

LABORATORY DIAGNOSIS

Direct Examination]o KOH mount – Black Piedra

nodules are composed of tightly packed, regularly arranged, thick-walled cells

dichotomously branching, dematiaceous hyphae

central part - fungal cells cemented

periphery - aligned hyphal strands

asci are found within the locules containing up to 8 ascospores

o KOH mount – White Piedra nodules are softer, less

adherent, not as discrete often - transparent, greenish,

rregular sheath cells are not as organized one sees only blastospores &

arthrospores Culture

o Culture - Piedraia hortai compact, dark-brown to black,

conical colonies with short aerial hyphae

grows slowly on Sabouraud’s agar (2-4wk) at 25-30C

some colonies : reddish-brown, diffusable pigment on agar

examination - dematiaceous, septate, branching hyphae with asci & ascospores

o Culture - Trichosporon beigelii grows moderately on

Sabouraud’s agar (1-2 weeks) at 25-30C

colonies appear smooth, highly-wrinkled or radially folded, yeastlike, cream-colored

examination - hyaline, septate hyphae with many arthrospores

TREATMENT – BLACK & WHITE

shaving affected area or cutting infected hair topical medication in lotion

TINEA NIGRA

DEFINITION

a chronic, superficial, usually asymtomatic, fungal Infection usually of the palms

synonyms - keratomycosis nigricans palmaris, cladosporiosis epidermica, pityriasis nigra, microsporis nigra

primary medical importance - often misdiagnosed as melanoma

ETIOLOGY

Cladosporium werneckii or Exophiala werneckii

HISTORY

1891 - first observed in Brazil by Cerqueira 1916 - Cerqueira-Pinto reported his own

observation & his father’s 1921 - Ramos e Silva reported first case in Rio de

Janeiro; Horta isolated a fungus from the same patient: Cladosporium werneckii

1970 - von Arx transferred the genus to Exophiala

EPIDEMIOLOGY

considered a tropical disease but extends to the temperate zone (esp. WH)

occurs in any age group but more common under 20

male:female (1:3) no known predisposing factor although many

patients are hyperhydrotic transmission not known to occur

CLINICAL MANIFESTATION

usually asymptomatic lesion - usually, a dark patch on the palm

of one hand with well-defined, irregular margin about 1-5 cm in diameter

other locations - sole of foot, interdigits, wrists, forearm, trunk, neck

no induration, no erythema, and has the characteristic “stained appearance”

ocassionally - pruritus & scaling

TINEA NIGRA: Dark pigmentation in the center of palm

TINEA NIGRA: Dark pigmentation in the center of palm

TINEA NIGRA: Dark pigmentation in the center of palm

DIFFERENTIAL DIAGNOSIS

melanoma junctional nevus contact dermatitis

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pigmentation of Addison’s disease post-inflammatory melanosis syphilis pinta staining from chemicals

PATHOLOGY

confined to the upper layers of the stratum corneum

mild hyperkeratosis may be seen

pigmentation is due to the fungus

TINEA NIGRA: Hematoxylin-eosin-stained section of palmar skinShow abundant dark-colored fungal elements.

LABORATORY DIAGNOSIS

Direct Examinationo KOH mount - long, sinuous, strongly

dematiaceous branching, septate hyphae & elongated budding cells

Yeastlike cells of Exophiala werneckii, the causative agent of tinia nigra

Cultureo Sabouraud’s agar with antibiotics at 25-

30Co colonies appear shiny, moist,

yeastlike, dirty white to brown, covered with masses of conidia & budding cells

o will turn black in 2-3 weeks

TREATMENT

sulfur salicylic acid Na thiosulfate the azoles eg. Ketoconazole NB. recurrence rate – low

MYCOTIC KERATITIS (KERATOMYCOSIS)

- FUNGAL INFECTIONS OF THE CORNEAo cause: History of trauma leading to the

inoculum of eyes with a fungus

ETIOLOGIC AGENTS

Histoplasma capsulatum Fusarium solani

EPIDEMIOLOGY

More often in males and individual below the age of 50 years.

CLINICAL MANIFESTATIONS

Raised cornea ulcers with occassional satellite lesions, plaques or hypopyon

DIAGNOSIS

Direct examination (demonstration of hyphae)o corneal scrapings

o Surgical

specimens Culture

o Fusarium species grow rapidly in: Sabourauds medium Enriched medium

Fusarium spp. Colony on potato dextrose agar. The colonies appear to be cottonlike, usually white, turning pink-violet or brown at the center with age

Fusarium spp. Stained with lactophenol cotton blue. Typical Fusarium spp: Microconidia with a fusiform or oval shape extending from delicate lateral phialides. Macroconidia are fusiform, usually curved, giving the appearance of a sickle and have three to five septae.

-fin-

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