Superficial mycoses common in medical dermatology

In internal medicine

1. SUPERFICIAL MYCOSESSUPERFICIAL MYCOSES
Col LitetaCol Liteta

2. Superficial mycosesSuperficial mycoses

DermatophytesDermatophytes
–TineaTinea

Malassezia furfurMalassezia furfur
–Pityriasis versicolorPityriasis versicolor
–Pityrosporum Pityrosporum
folliculitisfolliculitis

CandidaCandida
–CandidiasisCandidiasis

3. TINEATINEA

Classification ~ clinical pictureClassification ~ clinical picture
-Tinea capitis (scalp)Tinea capitis (scalp)
-Tinea barbae (beard)Tinea barbae (beard)
-Tinea faciei (face)Tinea faciei (face)
-Tinea corporis (trunk)Tinea corporis (trunk)
-Tinea inguinalis, cruris (groin)Tinea inguinalis, cruris (groin)
-Tinea manuum (hand)Tinea manuum (hand)
-Tinea pedis (feet)Tinea pedis (feet)

4. TINEATINEA
= ringworm= ringworm
DermatophytesDermatophytes
-MicrosporumMicrosporum
-TrichophytonTrichophyton
-EpidermophytonEpidermophyton
Live in stratum Live in stratum
corneum corneum
Feed on keratinFeed on keratin

5. TINEATINEA
Types of dermatophytes based Types of dermatophytes based
on mode of transmissionon mode of transmission
CategoryCategory Mode of transmissionMode of transmission Typical clinical Typical clinical
featuresfeatures
AnthropophilicAnthropophilic Human to humanHuman to human Mild, noninflammatory, Mild, noninflammatory,
chronicchronic
Zoophilic Zoophilic Animal to humanAnimal to human Intense inflammatory Intense inflammatory
(pustules, vesicles (pustules, vesicles
possible), acutepossible), acute
GeophilicGeophilic Soil to humanSoil to human Moderate inflammationModerate inflammation

6. TINEATINEA

PathogenesisPathogenesis
Factors that determine the clinical pictureFactors that determine the clinical picture
1.1.The nature of the fungusThe nature of the fungus
2.2.The human host: age, gender, immune statusThe human host: age, gender, immune status
3.3.External factors: maceration, occlusion, External factors: maceration, occlusion,
minor skin trauma, warm climateminor skin trauma, warm climate

7. TINEATINEA

PathogenesisPathogenesis
Inoculation Inoculation
Interaction between fungus and skin Interaction between fungus and skin
-Fungus Fungus
-must grow more rapidly than the epidermal turnover ratemust grow more rapidly than the epidermal turnover rate
-produces enzymes to attack and digest keratinproduces enzymes to attack and digest keratin
-Host response: peripherical expanding inflammatory bandHost response: peripherical expanding inflammatory band
Exp 1. No inflammation > Tinea incognito Exp 1. No inflammation > Tinea incognito
Exp 2. Prior treatment with corticosteroïds or antifungal drugs Exp 2. Prior treatment with corticosteroïds or antifungal drugs
> mask inflammation > mask inflammation

8. TINEATINEA

DiagnosisDiagnosis

Clinical pictureClinical picture

Wood’s lampWood’s lamp
darken the room and illuminate affected site with wood’s lampdarken the room and illuminate affected site with wood’s lamp
hairs infected by microsporum spp. fluorescence greenishhairs infected by microsporum spp. fluorescence greenish

9. TINEATINEA
DiagnosisDiagnosis

KOH examinationKOH examination
-Collect scale using a number Collect scale using a number
15 blade15 blade
-Place scale on a slidePlace scale on a slide
-Add 5-20% KOH solutionAdd 5-20% KOH solution
-Place coverslip on topPlace coverslip on top
-Wait 15 min. or heat the Wait 15 min. or heat the
preparation with a matchpreparation with a match
-Examination under the Examination under the
microscopemicroscope
-Dermatophytes: septated, Dermatophytes: septated,
tubelike structures (hypae or tubelike structures (hypae or
mycelia)mycelia)

10. TINEATINEA

DiagnosisDiagnosis

CultureCulture
specimens collected from specimens collected from
scaling skin lesions, hair, scaling skin lesions, hair,
nailsnails

11. TINEATINEA

DiagnosisDiagnosis

BiopsyBiopsy
fungi are best demonstrated with PAS (periodic acid-Schiff) stain fungi are best demonstrated with PAS (periodic acid-Schiff) stain
on dermatopathologyon dermatopathology

12. TINEA CAPITISTINEA CAPITIS

DefinitionDefinition
Infection of the scalp by dermatophytesInfection of the scalp by dermatophytes
Micropsorum spp.Micropsorum spp.
Trichophyton spp.Trichophyton spp.
EpidemiologyEpidemiology
children > adultschildren > adults
more common in blacks than in whitesmore common in blacks than in whites

13. TINEA CAPITISTINEA CAPITIS

Inflammatory formInflammatory form
Etiology: Etiology:
zoophilic/geophilic >> anthropophilic zoophilic/geophilic >> anthropophilic
fungifungi
M.canisM.canis

14. Inflammatory Tinea capitisInflammatory Tinea capitis
““Typical lesion” Typical lesion”
Annular areaAnnular area
erythemaerythema
scalesscales
pustules pustules
local hair losslocal hair loss

15. Inflammatory Tinea capitisInflammatory Tinea capitis
““Kerion”Kerion”
Inflammatory nodule with Inflammatory nodule with

pustulespustules

sinus tractssinus tracts

drainage of pusdrainage of pus

destruction of folliclesdestruction of follicles
+ lymphadenopathy+ lymphadenopathy

16. TINEA CAPITISTINEA CAPITIS

Non inflammatory form (epidemic)Non inflammatory form (epidemic)
EtiologyEtiology
Anthropophilic >> Zoophilic/geophilicAnthropophilic >> Zoophilic/geophilic
M.audouiniiM.audouinii M.canisM.canis
T.tonsuransT.tonsurans

17. Noninflammatory Tinea Noninflammatory Tinea
capitiscapitis
Small areas with Small areas with
- - short stubby hairs on a short stubby hairs on a
scaly backgroundscaly background
-no inflammation no inflammation
> slowly expand, coalesce > slowly expand, coalesce
and cause wide areas of and cause wide areas of
alopeciaalopecia

18. TINEA CAPITISTINEA CAPITIS

DiagnosisDiagnosis
–KOH examinationKOH examination
–CultureCulture
–Wood’s lampWood’s lamp: most Microsporum spp. show : most Microsporum spp. show
greenish fluorescence greenish fluorescence

19. TINEA CAPITISTINEA CAPITIS

Differential diagnosisDifferential diagnosis
–Inflammatory tinea capitisInflammatory tinea capitis
CellulitisCellulitis
Furuncle, carbuncleFuruncle, carbuncle
–Noninflammatory tinea capitisNoninflammatory tinea capitis
Seborrhoic dermatitisSeborrhoic dermatitis
PsoriasisPsoriasis
Atopic dermatitisAtopic dermatitis
Lichen simplex chronicusLichen simplex chronicus
Alopecia areataAlopecia areata

20. TINEA CAPITISTINEA CAPITIS

Therapy Therapy
ALWAYS SYSTEMIC!ALWAYS SYSTEMIC!
Griseofulvin orally 8-12 weeksGriseofulvin orally 8-12 weeks
children: 10-15mg/kg O.D. children: 10-15mg/kg O.D.
adults: 500mg O.D. adults: 500mg O.D.
Alt.: itraconazole, ketoconazole, terbinafine p.o. Alt.: itraconazole, ketoconazole, terbinafine p.o.

21. TINEA CAPITISTINEA CAPITIS

Therapy Therapy
–Treat siblings, friends, pets, farm animals Treat siblings, friends, pets, farm animals
as necessary > ask for it!as necessary > ask for it!
–In case of superinfection: associate In case of superinfection: associate
antibiotics/antisepticsantibiotics/antiseptics

22. TINEA CAPITISTINEA CAPITIS

PrognosisPrognosis
–Usually spontaneous resolution after a Usually spontaneous resolution after a
period of timeperiod of time
–Risk of scarring alopecia, especially for the Risk of scarring alopecia, especially for the
inflammatory formsinflammatory forms

23. TINEA BARBAETINEA BARBAE

EtiologyEtiology
Zoophilic fungi Zoophilic fungi >> >> antropophilicantropophilic
T. verrucosumT. verrucosum T. schoenleiniiT. schoenleinii
T. mentagrophytes var. MentagrophytesT. mentagrophytes var. Mentagrophytes T. violaceumT. violaceum
M. canisM. canis

EpidemiologyEpidemiology
-Males with exposure to large animals (farmers, Males with exposure to large animals (farmers,
veterinarians…)veterinarians…)
Occupational dermatitisOccupational dermatitis
-In the past: a common cause was the contaminated In the past: a common cause was the contaminated
razors in barbershopsrazors in barbershops
-Rare: petowner who sleeps with cat, dogRare: petowner who sleeps with cat, dog

24. TINEA BARBAETINEA BARBAE
Clinical findingsClinical findings
Intense inflammationIntense inflammation
–Multiple follicular pustulesMultiple follicular pustules
–Abcesses, sinus tracts, Abcesses, sinus tracts,
bacterial superinfection, bacterial superinfection,
kerion-like lesions may kerion-like lesions may
developdevelop
–Systemic symptoms: malaise Systemic symptoms: malaise
and regional and regional
lymphadenopathy lymphadenopathy

Less inflammation, Less inflammation,
superficial, ~ tinea corporissuperficial, ~ tinea corporis

25. TINEA BARBAETINEA BARBAE

DiagnosisDiagnosis
–Clinical pictureClinical picture
–KOH examinationKOH examination
–CultureCulture
–Wood’s lampWood’s lamp (greenish fluorescence M. (greenish fluorescence M.
canis infection)canis infection)

26. TINEA BARBAETINEA BARBAE

Differential diagnosisDifferential diagnosis
–Bacterial folliculitisBacterial folliculitis
–RosaceaRosacea
–pseudofolliculitispseudofolliculitis
–Viral infections: herpes zoster, herpes Viral infections: herpes zoster, herpes
simplexsimplex
–Acne vulgarisAcne vulgaris
–Cervicofacial actinomycosisCervicofacial actinomycosis
–Dental sinus tractDental sinus tract

27. TINEA BARBAETINEA BARBAE

TherapyTherapy
–Topical agents: ineffective!Topical agents: ineffective!
–Systemic agents ~ tinea capitisSystemic agents ~ tinea capitis

28. TINEA BARBAETINEA BARBAE

PrognosisPrognosis
Spontaneous resolution after 4-6 weeksSpontaneous resolution after 4-6 weeks
Scarring is much less severe than with Scarring is much less severe than with
inflammatory tinea capitisinflammatory tinea capitis

29. TINEA FACIEITINEA FACIEI
Frequently Frequently
misdiagnosed!misdiagnosed!

EtiologyEtiology
Mostly zoophilic fungiMostly zoophilic fungi

EpidemiologyEpidemiology
Usually small children Usually small children
(close contact with pets)(close contact with pets)

30. TINEA FACIEITINEA FACIEI
Clinical findingsClinical findings
-Usually pruriticUsually pruritic
-Typical annular lesionTypical annular lesion
-central clearingcentral clearing
-accentuation of the borderaccentuation of the border
But …But …
Sometimes atypical Sometimes atypical
presentation and difficult presentation and difficult
to diagnose clinically!to diagnose clinically!

31. TINEA FACIEITINEA FACIEI
DiagnosisDiagnosis
–Clinical findingsClinical findings
–KOH examinationKOH examination
–CultureCulture
Differential diagnosisDifferential diagnosis
–Seborrhoic dermatitisSeborrhoic dermatitis
–Atopic dermatitisAtopic dermatitis
–Discoid lupus erythematodesDiscoid lupus erythematodes
–Psoriasis Psoriasis

32. TINEA FACIEITINEA FACIEI

TherapyTherapy
Topical Topical
= tinea corporis treatment= tinea corporis treatment
+ eradicate dermatophyte infection at + eradicate dermatophyte infection at
other sites such as feet and handsother sites such as feet and hands

33. TINEA INCOGNITOTINEA INCOGNITO

DefinitionDefinition
infection with dermatophytes without infection with dermatophytes without
obvious signs of inflammationobvious signs of inflammation
prior treatment with topical antifungals prior treatment with topical antifungals
or corticosteroids may also mask the or corticosteroids may also mask the
inflammation and produce a similar inflammation and produce a similar
picturepicture

34. TINEA CORPORISTINEA CORPORIS

EtiologyEtiology
Zoophilic/geophilic >> anthropophilicZoophilic/geophilic >> anthropophilic
M. canisM. canis T. rubrumT. rubrum
E. floccosumE. floccosum

EpidemiologyEpidemiology
more common in (sub)tropical regionsmore common in (sub)tropical regions

35. TINEA CORPORISTINEA CORPORIS
Clinical findings Clinical findings
Plaque or patchPlaque or patch
-Slightly induratedSlightly indurated
-Sharply borderedSharply bordered
-Peripherically spreadingPeripherically spreading
-Border more red with Border more red with
prominent scales and prominent scales and
pustulespustules
-Central clearingCentral clearing

36. TINEA CORPORISTINEA CORPORIS

Clinical findingsClinical findings
-Usually: one or a few Usually: one or a few
lesionslesions
Malnutrition, Malnutrition,
immunosuppression, immunosuppression,
delay before seeking delay before seeking
treatment: multiple, large treatment: multiple, large
or widespread lesionsor widespread lesions
-Unilateral or asymmetricalUnilateral or asymmetrical

37. TINEA CORPORISTINEA CORPORIS

TreatmentTreatment
One or a few lesions:One or a few lesions:
-Local: Imidazole cream or Whitfield’s ointment B.D. for minimum 4 Local: Imidazole cream or Whitfield’s ointment B.D. for minimum 4
weeksweeks

Continue until one week after symptoms have clearedContinue until one week after symptoms have cleared
Multiple, widespread lesions:Multiple, widespread lesions:
-Systemically: Systemically: Griseofulvin 500mg O.D. 2-6 weeks (adults)Griseofulvin 500mg O.D. 2-6 weeks (adults)
10-15 mg/kg 2-6 weeks (children)10-15 mg/kg 2-6 weeks (children)
Itraconazole 200mg B.D. 7 daysItraconazole 200mg B.D. 7 days
Terbinafine 250mg/d 14 days Terbinafine 250mg/d 14 days

38. TINEA INGUINALISTINEA INGUINALIS

EtiologyEtiology
Epidermophyton floccosumEpidermophyton floccosum
Trichophyton rubrum, mentagrophytes var. Trichophyton rubrum, mentagrophytes var.
Interdigitale (if patient has tinea pedis as well)Interdigitale (if patient has tinea pedis as well)

EpidemiologyEpidemiology
- Men > women- Men > women
- Uncommon in children- Uncommon in children
- Predisposing factors: obesity, inadequate hygiene, - Predisposing factors: obesity, inadequate hygiene,
hyperhidrosis, prolonged sitting on plastic surface, hyperhidrosis, prolonged sitting on plastic surface,
tight synthetic clothes, diabetes mellitustight synthetic clothes, diabetes mellitus

39. TINEA INGUINALISTINEA INGUINALIS

Clinical findingsClinical findings
–Slowly spreading Slowly spreading
erythematous patches erythematous patches
with scaly border on the with scaly border on the
inner aspects of the inner aspects of the
thighs, where scrotum thighs, where scrotum
touches the legtouches the leg
–Occasionally spread to Occasionally spread to
perineum, perianal area perineum, perianal area
and gluteal cleftand gluteal cleft
–Usually asymetrical, but Usually asymetrical, but
can be bilateral when can be bilateral when
there are stimultating there are stimultating
factors or HIV factors or HIV

40. TINEA INGUINALISTINEA INGUINALIS

Clinical findingsClinical findings
-Almost all patients have tinea pedisAlmost all patients have tinea pedis
> > Always check the feet of patients Always check the feet of patients
with with groin rashesgroin rashes

41. TINEA INGUINALISTINEA INGUINALIS
DiagnosisDiagnosis
–Clinical featuresClinical features
–KOH examinationKOH examination
–CultureCulture
Differential diagnosisDifferential diagnosis
–ErythrasmaErythrasma
–IntertrigoIntertrigo
–Candida intertrigoCandida intertrigo
–Psoriasis inversaPsoriasis inversa

42. TINEA INGUINALISTINEA INGUINALIS

TherapyTherapy
treat groin but also the feet if necessary!treat groin but also the feet if necessary!
- local treatment with antifungals B.D. - local treatment with antifungals B.D.
f.e. imidazole creamf.e. imidazole cream
- systemic treatment- systemic treatment
< if recurrent< if recurrent
< failure of adequate topical therapy< failure of adequate topical therapy
options:options:
griseofulvin 500mg/d 14 daysgriseofulvin 500mg/d 14 days
itraconazole 200mg B.D. 7 daysitraconazole 200mg B.D. 7 days
terbinafine 250mg/d 14 daysterbinafine 250mg/d 14 days

43. TINEA PEDISTINEA PEDIS
= Athlete’s foot= Athlete’s foot

EtiologyEtiology
All are anthropophilicAll are anthropophilic
T.rubrum, mentagrophytes var.interdigitale, T.rubrum, mentagrophytes var.interdigitale,
E.floccosumE.floccosum

EpidemiologyEpidemiology
-One of the most common diseasesOne of the most common diseases
-Predisposing factors: hyperhidrosis, reduced Predisposing factors: hyperhidrosis, reduced
hygiene, increasing age, warm, moist climate …hygiene, increasing age, warm, moist climate …

44. TINEA PEDISTINEA PEDIS

Clinical findingsClinical findings
WIDE VARIETY OF CLINICAL MANIFESTATIONS!WIDE VARIETY OF CLINICAL MANIFESTATIONS!
3 types (there are overlaps)3 types (there are overlaps)
1.1.Chronic interdigital scaling typeChronic interdigital scaling type
2.2.Hyperkeratotic typeHyperkeratotic type
3.3.Dyshidrotic typeDyshidrotic type

45. TINEA PEDISTINEA PEDIS
1.1.Chronic interdigital Chronic interdigital
scaling typescaling type
= intertriginous type= intertriginous type
-swollen grayish-white swollen grayish-white
skin, often with fissures skin, often with fissures
between III-IV or IV-V toesbetween III-IV or IV-V toes
-can extend to the can extend to the
underside of the toesunderside of the toes
-pruritus is minimalpruritus is minimal
-Course: persistentCourse: persistent

46. TINEA PEDISTINEA PEDIS
2. Hyperkeratotic type2. Hyperkeratotic type
= Moccasin type= Moccasin type
- Dry, often thick scales, Dry, often thick scales,
covering the heels, tips of covering the heels, tips of
toes, metacarpal padstoes, metacarpal pads
- On the side of the foot: On the side of the foot:
erythema and advancing erythema and advancing
border can be seenborder can be seen
- One feet is more involved as One feet is more involved as
the other onethe other one
- Often unaware of the Often unaware of the
problemproblem
> regard it as “dry feet”> regard it as “dry feet”
- Course: persistentCourse: persistent

47. TINEA PEDISTINEA PEDIS
3. Dyshidrotic, recurrent 3. Dyshidrotic, recurrent
blistering typeblistering type
-Sudden eruptionSudden eruption
-Pruritic grouped vesiclesPruritic grouped vesicles
-Vesicles can coalesce, Vesicles can coalesce,
forming blisters, erosionsforming blisters, erosions
-Usually on the instepUsually on the instep
-Course: recurrentCourse: recurrent

48. TINEA PEDISTINEA PEDIS

TreatmentTreatment
* Local treatment, special considerations by type of infection:* Local treatment, special considerations by type of infection:
1.1.Intertriginous typeIntertriginous type
-Dry interdigital skin with GV paintDry interdigital skin with GV paint
-Imidazole cream or Whitfield’s ointment B.D. until a week after Imidazole cream or Whitfield’s ointment B.D. until a week after
symptoms have cleared (minimum 4 weeks)symptoms have cleared (minimum 4 weeks)
2.2.Mocassin typeMocassin type
-reduce hyperkeratosis with keratolytic agents (salicylic acid, lactic reduce hyperkeratosis with keratolytic agents (salicylic acid, lactic
acid)acid)
-Topical antifungals f.e. imidazole creams B.D.Topical antifungals f.e. imidazole creams B.D.
-Treat associated tinea unguium Treat associated tinea unguium
3.3.Recurrent bullous, dyshidrotic typeRecurrent bullous, dyshidrotic type
-acute: cool compressesacute: cool compresses
-topical antifungals f.e. imidazole cream B.D.topical antifungals f.e. imidazole cream B.D.

49. TINEA PEDISTINEA PEDIS

TherapyTherapy
* Systemic treatment* Systemic treatment
indication: indication:
- extensive infection- extensive infection
- failure of local treatment- failure of local treatment
- tinea unguium and moccasin type tinea pedis- tinea unguium and moccasin type tinea pedis
Options:Options:
- Griseofulvin 500 mg/d 21 days- Griseofulvin 500 mg/d 21 days
- Itraconazole 200mg B.D. 7 days- Itraconazole 200mg B.D. 7 days
- Terbinafine 250mg/d 14 days- Terbinafine 250mg/d 14 days

50. TINEA PEDISTINEA PEDIS

PreventionPrevention
-Use rubber sandals in community Use rubber sandals in community
showersshowers
-Dry the feet carefully Dry the feet carefully
-Wear clean socks and shoes that are not Wear clean socks and shoes that are not
too tight or hottoo tight or hot
-Use antifungal powdersUse antifungal powders

51. TINEA MANUUMTINEA MANUUM
Always secondary to tinea pedisAlways secondary to tinea pedis

EtiologyEtiology
T.rubrum, mentagrophytes T.rubrum, mentagrophytes
var.interdigitale, (E.floccosum)var.interdigitale, (E.floccosum)

52. TINEA MANUUMTINEA MANUUM

Clinical featuresClinical features
A. lesions on the A. lesions on the
dorsal aspects of the dorsal aspects of the
handshands
= tinea corporis= tinea corporis

53. TINEA MANUUMTINEA MANUUM

Clinical findingsClinical findings
B. lesions on the palmsB. lesions on the palms
- diffuse hyperkeratosis, - diffuse hyperkeratosis,
scale with accentuation scale with accentuation
in the foldsin the folds
~ moccasin type of tinea ~ moccasin type of tinea
pedispedis
- dyshidrotic type with - dyshidrotic type with
papules, vesicles, bullaepapules, vesicles, bullae
often unilateraloften unilateral

54. TINEA MANUUMTINEA MANUUM
DiagnosisDiagnosis
–Clinical featuresClinical features
–KOH examinationKOH examination
–CultureCulture
Differential diagnosisDifferential diagnosis
–Atopic dermatitisAtopic dermatitis
–Allergic contact dermatitisAllergic contact dermatitis
–Irritant contact dermatitisIrritant contact dermatitis
–Psoriasis vulgarisPsoriasis vulgaris

55. TINEA MANUUMTINEA MANUUM

TherapyTherapy
Because of the thickness of palmar stratum corneum Because of the thickness of palmar stratum corneum
and especially if associated with tinea unguium of and especially if associated with tinea unguium of
fingernails: impossible to cure with topical agents fingernails: impossible to cure with topical agents
onlyonly
>> systemic treatment>> systemic treatment
Options:Options:
- terbinafine 250mg/d 14 days- terbinafine 250mg/d 14 days
- itraconazole 200mg B.D. 7 days- itraconazole 200mg B.D. 7 days
- Griseofulvin 500mg/d 21 days- Griseofulvin 500mg/d 21 days

56. ““One hand, two feet disease”One hand, two feet disease”

Diffuse tinea pedisDiffuse tinea pedis

Tinea manuum: only Tinea manuum: only
one hand involved!one hand involved!
= the dominant one, = the dominant one,
suggesting a direct suggesting a direct
inoculationinoculation

57. Fungal Id reactionFungal Id reaction

DefinitionDefinition
a distant skin manifestation of a a distant skin manifestation of a
fungal infection in which the fungal infection in which the
lesions are “allergic”, not lesions are “allergic”, not
infectiousinfectious

Most typical setting:Most typical setting:
–Dyshidrotic reaction with Dyshidrotic reaction with
pruritic blisters on both hands pruritic blisters on both hands
and feetand feet
–Tinea pedis flaring upTinea pedis flaring up
–Sometimes: id reaction Sometimes: id reaction
develops when systemic develops when systemic
antifungal treatment is antifungal treatment is
initiatedinitiated

58. CANDIDIASISCANDIDIASIS

DefinitionDefinition
Infection with Candida albicans, usually Infection with Candida albicans, usually
involving moist areas with occlusioninvolving moist areas with occlusion

EpidemiologyEpidemiology
““every individual in the world experiences every individual in the world experiences
at least one episode of clinically apparent at least one episode of clinically apparent
candidal disease in his/her lifetime”candidal disease in his/her lifetime”

59. CANDIDIASISCANDIDIASIS

PathogenesisPathogenesis
Candida albicansCandida albicans
-May be part of the normal flora of the oral May be part of the normal flora of the oral
cavity, gastrointestinal tract, external genitaliacavity, gastrointestinal tract, external genitalia
-When is it a pathogen?When is it a pathogen?
If erythema and other signs of inflammation If erythema and other signs of inflammation
are present it is more likely that candida is are present it is more likely that candida is
playing a pathogenic roleplaying a pathogenic role

60. CANDIDIASISCANDIDIASIS
““illness of the ill people”illness of the ill people”
Predisposing factors:Predisposing factors:
-Immunosuppression (HIV/AIDS, transplant patients)Immunosuppression (HIV/AIDS, transplant patients)
-Diabetes mellitusDiabetes mellitus
-Local factors that create moist warm milieu (obesity, Local factors that create moist warm milieu (obesity,
diapers, incontinence, …)diapers, incontinence, …)
-Intake of oral contraceptives, pregnancyIntake of oral contraceptives, pregnancy
-Intake of systemic antibiotics (change of normal flora)Intake of systemic antibiotics (change of normal flora)
-Intake of oral corticosteroidsIntake of oral corticosteroids

61. CANDIDIASISCANDIDIASIS
SKINSKIN
Red maculesRed macules
Collarette scalesCollarette scales
Often small pustels on Often small pustels on
the peripherythe periphery
MUCOSAMUCOSA
RednessRedness
Superficial erosionsSuperficial erosions
White plaqueWhite plaque

62. CANDIDIASISCANDIDIASIS

ORAL CANDIDIASISORAL CANDIDIASIS

GENITAL CANDIDIASISGENITAL CANDIDIASIS

INTERDIGITAL CANDIDIASISINTERDIGITAL CANDIDIASIS

CANDIDAL INTERTRIGOCANDIDAL INTERTRIGO

DIAPER CANDIDIASISDIAPER CANDIDIASIS

CANDIDAL PARONYCHIACANDIDAL PARONYCHIA

CANDIDAL FOLLICULITISCANDIDAL FOLLICULITIS

CANDIDAL ESOPHAGITISCANDIDAL ESOPHAGITIS

NEONATAL CANDIDIASISNEONATAL CANDIDIASIS

CANDIDEMIACANDIDEMIA

63. ORAL CANDIDIASISORAL CANDIDIASIS
1. Acute pseudomembranous 1. Acute pseudomembranous
candidiasiscandidiasis
= thrush= thrush
- White, cheesy, easily - White, cheesy, easily
removable plaquesremovable plaques
- Scraping > normal or - Scraping > normal or
reddish underlying mucosareddish underlying mucosa
- Symptoms: xerostomia, - Symptoms: xerostomia,
unpleasant taste, mild unpleasant taste, mild
burning sensationburning sensation

64. ORAL CANDIDIASISORAL CANDIDIASIS
2. 2. Angular cheilitisAngular cheilitis
= perlèche= perlèche
-Children (common)Children (common)
-People with poorly People with poorly
fitting denturesfitting dentures
-Erythema with Erythema with
fissures, white coatfissures, white coat

65. ORAL CANDIDIASISORAL CANDIDIASIS
3.3.Chronic hyperplastic Chronic hyperplastic
candidiasis candidiasis
- Single fixed plaque- Single fixed plaque
- Falls into spectrum - Falls into spectrum
of leukoplakiaof leukoplakia

66. ORAL CANDIDIASISORAL CANDIDIASIS
4. Erythematous (atrophic) 4. Erythematous (atrophic)
candidiasiscandidiasis
acuteacute
- erosive candidiasis- erosive candidiasis
- gingivitis- gingivitis
- median rhomboid - median rhomboid
glossitisglossitis
chronicchronic
- often under denture- often under denture

67. GENITAL CANDIDIASISGENITAL CANDIDIASIS
♀♀
““Almost every woman has at Almost every woman has at
least one attack of vaginal least one attack of vaginal
candidiasis in her life-time”candidiasis in her life-time”
symptoms: pruritus, vaginal symptoms: pruritus, vaginal
discharge, creamy white discharge, creamy white
curds on the vaginal wallcurds on the vaginal wall
>>> erythema of the external >>> erythema of the external
genitalia, spreading onto the genitalia, spreading onto the
inner aspects of the thighinner aspects of the thigh

68. GENITAL CANDIDIASISGENITAL CANDIDIASIS
♂♂
men are less often men are less often
affectedaffected
But…But…
candidal balanitis is candidal balanitis is
a frequent in a frequent in
uncircumcised, older uncircumcised, older
menmen

69. INTERDIGITAL CANDIDIASISINTERDIGITAL CANDIDIASIS
-UncommonUncommon
-Painful erosion Painful erosion
surrounded by swollen surrounded by swollen
macerated tissuemacerated tissue
-Almost always between Almost always between
III and IV finger/toeIII and IV finger/toe
-Reason?Reason?
This web space is the This web space is the
least least mobile > retention of mobile > retention of
sweat, sweat, soap and water >soap and water >
irritation irritation and and
secondary infection with secondary infection with
candidacandida

70. CANDIDAL INTERTRIGOCANDIDAL INTERTRIGO
-Typical sites: groins, Typical sites: groins,
axillae, beneath the axillae, beneath the
breastsbreasts
-Clinical clue:Clinical clue:
satellite pustules at satellite pustules at
the periphery of the the periphery of the
lesionlesion

71. CANDIDAL PARONYCHIACANDIDAL PARONYCHIA
-Infection of the nail fold and Infection of the nail fold and
bed by Candidabed by Candida
-SignsSigns
-Red, swollen, painful Red, swollen, painful
periungual tissueperiungual tissue
-Pressure: pus may ooze from Pressure: pus may ooze from
the lateral, proximal nail foldthe lateral, proximal nail fold
-Secondary: transeverse Secondary: transeverse
ridging of the nail or candidal ridging of the nail or candidal
onychomycosisonychomycosis
-Differential diagnosis with Differential diagnosis with
bacterial paronychia is bacterial paronychia is
difficultdifficult
And mixed infections And mixed infections
frequently occur!frequently occur!

72. CANDIDAL FOLLICULITISCANDIDAL FOLLICULITIS
-RareRare
-Usual patient: Usual patient:
-adult man with immunosuppressionadult man with immunosuppression
-Involvement of the beard areaInvolvement of the beard area
-Pustules, crusts or deeper nodules around Pustules, crusts or deeper nodules around
hairshairs

73. CANDIDAL OESOPHAGITISCANDIDAL OESOPHAGITIS
- Almost entirely restricted to HIV/AIDS - Almost entirely restricted to HIV/AIDS
patientspatients

74. NEONATAL CANDIDIASISNEONATAL CANDIDIASIS
-Congenital candidiasisCongenital candidiasis
-Represents intrauterine infectionRepresents intrauterine infection
-Numerous small erythematous papules, pustulesNumerous small erythematous papules, pustules
-Involvement of palms and soles; diaper area usually sparedInvolvement of palms and soles; diaper area usually spared
-Occurs a few hours after birthOccurs a few hours after birth
-Risk of systemic diseaseRisk of systemic disease
-Diffuse neonatal candiasisDiffuse neonatal candiasis
-Superficial infection acquired in the vaginal canalSuperficial infection acquired in the vaginal canal
-Papules, pustules, collarette scale Papules, pustules, collarette scale
-Occurs several days after birthOccurs several days after birth
-Common candidal infections of mouth or diaper areaCommon candidal infections of mouth or diaper area

75. CANDIDEMIACANDIDEMIA
EpidemiologyEpidemiology
-Immunosuppressed patientsImmunosuppressed patients
-Patients with catheter Patients with catheter
““Systemic candidiasis should always be considered in the Systemic candidiasis should always be considered in the
differential diagnosis of catheter associated sepsis”differential diagnosis of catheter associated sepsis”
-Patients with extensive antibiotic treatmentsPatients with extensive antibiotic treatments
Clinical signsClinical signs
-SepsisSepsis
-Tiny pink macules, papules, pustulesTiny pink macules, papules, pustules
>> more dramatic lesions: larger necrotic areas>> more dramatic lesions: larger necrotic areas

76. CANDIDIASISCANDIDIASIS
DiagnosisDiagnosis
-Clinical picture Clinical picture
- - HistopathologyHistopathology
-Seldom doneSeldom done
-Presence of pseudomycelia in tissue suggests Presence of pseudomycelia in tissue suggests
Candida albicans is pathogenicCandida albicans is pathogenic
- - CultureCulture

77. CANDIDIASISCANDIDIASIS

TherapyTherapy
–Very important: identifying and removing Very important: identifying and removing
predisposing factorspredisposing factors
–GRISEOFULVIN IS NOT AN EFFECTIVE GRISEOFULVIN IS NOT AN EFFECTIVE
TREATMENT FOR CANDIDA INFECTIONSTREATMENT FOR CANDIDA INFECTIONS

78. CANDIDIASISCANDIDIASIS

TherapyTherapy
SKINSKIN
- Oozing lesions: potassium permanganate dressings/baths - Oozing lesions: potassium permanganate dressings/baths
for 10 min. B.D.for 10 min. B.D.
- Smaller wet lesions: Gentian Violet solution O.D. - Smaller wet lesions: Gentian Violet solution O.D.
- Nystatin ointment/cream or Imidazole cream B.D. - Nystatin ointment/cream or Imidazole cream B.D.
- Folds and diaper region: antifungal + zinkoxyde Folds and diaper region: antifungal + zinkoxyde
cream/ointmentcream/ointment
ORAL LESIONSORAL LESIONS
- Nystatin oral suspension F.D. Nystatin oral suspension F.D.
- Miconazol oral gel F.D.Miconazol oral gel F.D.

79. CANDIDIASISCANDIDIASIS

TherapyTherapy
VAGINAL LESIONSVAGINAL LESIONS
-Nystatin pessaries nightly for 2 weeksNystatin pessaries nightly for 2 weeks
-Imidazole pessaries 1-3 nightsImidazole pessaries 1-3 nights
-Fluconazole 150mg single doseFluconazole 150mg single dose
SEVERE CASES AND OESOPHAGAL LESIONS: SEVERE CASES AND OESOPHAGAL LESIONS:
-Itraconazole 100mg O.D. 2 weeksItraconazole 100mg O.D. 2 weeks
-Fluconazole 50-200mg O.D. 1-2 weeksFluconazole 50-200mg O.D. 1-2 weeks
-Ketoconazole 200mg B.D. 1-2 weeksKetoconazole 200mg B.D. 1-2 weeks
IMMUNOCOMPROMISED PATIENTS MAY NEED A PROLONGED TREATMENTIMMUNOCOMPROMISED PATIENTS MAY NEED A PROLONGED TREATMENT

80. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR
Definition: superficial scaly infection Definition: superficial scaly infection
producing hypo- and hyperpigmentionproducing hypo- and hyperpigmention
Epidemiology:Epidemiology:
–young people > elderlyyoung people > elderly
–more often in blacksmore often in blacks
–more common in tropical, humid climatesmore common in tropical, humid climates
–summer > wintersummer > winter
–Predisposing factors: obesity, occlusive clothing, Predisposing factors: obesity, occlusive clothing,
inadequate hygiene, impaired immune statusinadequate hygiene, impaired immune status

81. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR

Etiology: Malassezia furfurEtiology: Malassezia furfur
–Absent in newborns, can be cultured from Absent in newborns, can be cultured from
shoulders of a high proportion of asymptomatic shoulders of a high proportion of asymptomatic
individuals > 1 year of ageindividuals > 1 year of age
–Why disease? Why disease? UnclearUnclear
The organism requires lipids > lipid-rich moist skin = one The organism requires lipids > lipid-rich moist skin = one
factorfactor
Patient’s immune status = second factorPatient’s immune status = second factor
–Disease is common in renal transplant and HIV/AIDS patientsDisease is common in renal transplant and HIV/AIDS patients

82. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR

Hypopigmented Hypopigmented
maculae/patchesmaculae/patches
–Sharply borderedSharply bordered
–HypopigmentedHypopigmented
–Fine scale (by scraping Fine scale (by scraping
the skin by a blade)the skin by a blade)
Reason?Reason?
–M. furfur produces azelaic M. furfur produces azelaic
acid which is capable of acid which is capable of
blocking melanin blocking melanin
synthesissynthesis
–Increased thickness of Increased thickness of
the scale > umbrella-like the scale > umbrella-like
effect preventing tanningeffect preventing tanning

83. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR

Clinical findingsClinical findings
–Localisation: seborrhoic areasLocalisation: seborrhoic areas
Favored sites: upper trunk and shouldersFavored sites: upper trunk and shoulders
Occasionally: reaching the umbilicus, thighs, upper inner Occasionally: reaching the umbilicus, thighs, upper inner
aspects of the armsaspects of the arms
–Lesions: hyperpigmented or hypopigmented Lesions: hyperpigmented or hypopigmented
maculae/patches with a fine scalemaculae/patches with a fine scale
> easy to produce the scale by scraping the skin by > easy to produce the scale by scraping the skin by
a bladea blade
–Symptoms: rarely pruritic, mostly cosmetic problemSymptoms: rarely pruritic, mostly cosmetic problem

84. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR

Hyperpigmented Hyperpigmented
maculae/patchesmaculae/patches
–Sharply borderedSharply bordered
–Dirty yellow, red-brown Dirty yellow, red-brown
or café au laitor café au lait
–Fine scale (by scraping Fine scale (by scraping
the skin with a blade)the skin with a blade)
Reason?Reason?
- Increased scale containing - Increased scale containing
multiple organismsmultiple organisms

85. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR

DiagnosisDiagnosis
–Clinical pictureClinical picture
–Wood’s lampWood’s lamp: faint green-: faint green-
yellow fluorescenceyellow fluorescence
–KOH examinationKOH examination
““spaghetti and spaghetti and
meatballs”meatballs”
= Short thick hyphae = Short thick hyphae
with grape-like clusters with grape-like clusters
of sporesof spores
–CultureCulture: difficult: difficult

86. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR
Differential diagnosisDifferential diagnosis
–Hypopigmented lesionsHypopigmented lesions
Postinflammatory hypopigmentation f.e. pityriasis albaPostinflammatory hypopigmentation f.e. pityriasis alba
Vitiligo Vitiligo
> “abscence of scale”> “abscence of scale”
–Hyperpigmented lesionsHyperpigmented lesions
Tinea corporisTinea corporis
Seborrhoic dermatitisSeborrhoic dermatitis
Pityriasis roseaPityriasis rosea

87. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR
Therapy = Therapy = Local treatmentLocal treatment
Reserve oral therapy for cases that have failed Reserve oral therapy for cases that have failed
topical therapy!topical therapy!
In general: In general:
–stop the use of vaseline, olive oil, palm oilstop the use of vaseline, olive oil, palm oil
–Scrub the skin with a brush (it takes away a lot of Scrub the skin with a brush (it takes away a lot of
the infected scales)the infected scales)

88. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR
Local treatmentLocal treatment

Sodiumthiosulphate 20% overnight 2-4 weeksSodiumthiosulphate 20% overnight 2-4 weeks

Selenium sulphide suspension (e.g. Selsun Selenium sulphide suspension (e.g. Selsun
shampoo) overnight or 10 min. daily 2-4 shampoo) overnight or 10 min. daily 2-4
weeksweeks

Topical imidazoles: Topical imidazoles:
- ketoconazole 2% shampoo 10 min. daily 1 - ketoconazole 2% shampoo 10 min. daily 1
week, then weekly for several weeksweek, then weekly for several weeks
- imidazole creams, lotions B.D. 4 weeks- imidazole creams, lotions B.D. 4 weeks

89. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR
Oral treatmentOral treatment

Itraconazole 200mg (2 tablets) O.D. 1 Itraconazole 200mg (2 tablets) O.D. 1
weekweek

Ketoconazole 400mg once or 200mg Ketoconazole 400mg once or 200mg
O.D. 5 daysO.D. 5 days

90. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR
Success of the treatment?Success of the treatment?
Treatment is complete when all scales have Treatment is complete when all scales have
disappeareddisappeared
Test by stretching the affected skin Test by stretching the affected skin
between 2 fingersbetween 2 fingers
> if scales appear infection is still active> if scales appear infection is still active
After treatment hypopigmentation may be After treatment hypopigmentation may be
persist for some time and will re-pigment persist for some time and will re-pigment
when exposed to the sunwhen exposed to the sun

91. PITYRIASIS VERSICOLORPITYRIASIS VERSICOLOR

PrognosisPrognosis
The risk for recurrence is high!The risk for recurrence is high!
> prophylactic treatment > prophylactic treatment
- imidazole or selenium sulphide - imidazole or selenium sulphide
shampoo shampoo once weeklyonce weekly
- itraconazole 2x 200mg day 1 of every - itraconazole 2x 200mg day 1 of every
monthmonth
- (ketoconazole)- (ketoconazole)

92. PITYROSPORUM FOLLICULITISPITYROSPORUM FOLLICULITIS

DefinitionDefinition
Infection of the hair follicles by Infection of the hair follicles by
Malassezia furfurMalassezia furfur

EpidemiologyEpidemiology
especially in HIV/AIDS patients and especially in HIV/AIDS patients and
other immunocompromised individualsother immunocompromised individuals

93. PITYROSPORUM FOLLICULITISPITYROSPORUM FOLLICULITIS

Clinical findingsClinical findings
–‘‘acne-like’ eruptionacne-like’ eruption
Monomorphous lesions: tiny papules Monomorphous lesions: tiny papules
centered around hair follicles, occasionally centered around hair follicles, occasionally
evolving into pustulesevolving into pustules
–Often involving the backOften involving the back
–Usually very pruritic (may be asymptomatic)Usually very pruritic (may be asymptomatic)

94. PITYROSPORUM FOLLICULITISPITYROSPORUM FOLLICULITIS

DiagnosisDiagnosis
–Clinical pictureClinical picture
–KOH examinationKOH examination: only yeast forms, no hyphae: only yeast forms, no hyphae
–Biopsy Biopsy
–CultureCulture: difficult: difficult

Differential diagnosisDifferential diagnosis
–Acne and acneiform lesionsAcne and acneiform lesions
–Different types of folliculitisDifferent types of folliculitis

95. PITYROSPORUM FOLLICULITISPITYROSPORUM FOLLICULITIS

TreatmentTreatment
–Topical:Topical:
Azole shampoo/creamAzole shampoo/cream
Seleniumsulpide shampooSeleniumsulpide shampoo
–Systemic: if pruritus is severeSystemic: if pruritus is severe
Itraconazole 200mg 7 daysItraconazole 200mg 7 days
(ketoconazole)(ketoconazole)