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                                                                                 TINEA CAPITIS

T. Capitis is a worldwide problem fungal infection of the scalp. It is primarily a disease in young children where, males are more infected than females. This may be due to shortness of the hair, which facilitates easy reach of the fungal spores to the scalp.

Adults are rarely infected; this is believed to be due to the higher fatty acid of the scalp, which have dermatophytes inhibiting property.

It was established many years ago that some saturated fatty acids, from adult human hair (and derived from sebum) were inhibitory to dermatophytes fungi.

Fungal scalp infection may be endemic, sporadic or epidemic, where involvement of large number of school children or in crowded low hygiene refugee camps is not uncommon.

The tendency of scalp ringworm to clear spontaneously at puberty was believed to be due to the change in sebum composition at this age.

Modes of Infection

T. Capitis infections are common in temperate countries.

            Fig. 60a. Tinea capitis (Black dot)


                       Fig. 60c.Tinea capitis           Fig.60d. After treatment     


                       Fig. 60b.Tinea capitis
                     (Cicatricial alopecia)                                    





  Fig. 61. Kerion                                                          

Contact with infected persons or their fomites such as combs, brushes, or headgears.

Contact with infected pets or animals such as cats, dogs or cattle.

Minor trauma is an important predisposing factor for seeding of the fungi on the scalp to cause infection.

Curiously, human-to-human infection of M. canes infections seems to be low and once treatment is established children can go back to school.

Different Fungal strains causing infection

Microsporon auduini - is the most common strain to cause T. Capitis.

Microsporon canis - is often contracted from animals, can cause highly inflammatory lesions.

Trichophyton mentagrophyte - causes highly inflammatory T. Capitis.

Tricophyton Tonsurans - causes an exceedingly chronic infection. The fungal infections often are familial.

T. Violaceum - causes the clinical lesion called "black dot" ring worm

T. Schoenleini - causes the clinical type of T. Capitis known as favus.

Clinical Features

The clinical picture usually varies according to the causative dermatophyte.

Some strains such as Microsporon Canis and T. Mentagrophtes cause highly inflammatory lesions, while T. Tonsurans lesions have a very chronic course.

The clinical picture may be sometimes confusing and cannot be easily diagnosed except by detection of the dermatophyte by potassium hydroxide smears.

Different clinical types of Tinea Capitis:

  1. Dry Type - lesion may be dry and scaly simulating dandruff of the scalp, psoriasis and lichen planus.

  2. Black Dot Type - usually the lesion is dry where the hair is cut short from the stumps, and the bases of infected hairs are prominent. There is a variable degree of erythema, itching and scaling. The individual lesion may persist for a long time or resolve spontaneously.

  3. Kerion - Other lesions may be highly inflammatory which show swollen, edematous, oozing and crusting lesion in the form of boggy inflammation of the scalp called "kerion". This type may be mis-diagnosed and treated as an abscess of the scalp. Hair loss may be permanent causing cicatricial alopecia.

  4. Favus - the clinical picture of favus is characteristic where solid crust is formed on the infected area, which may spread to cover the whole scalp. The scalp has special mouse smell. The condition is very chronic and may end with cicatricial alopecia. The infection may spread to other areas away from the scalp such as to the abdomen and extremities.


Diagnosis of T. capitis can be settled by different methods:

  1. The clinical picture - fungi causing T. capitis characteristically beginn the pathological manifestations in the center feeding on the keratin and spreading peripherally away from the center. There is central clearing where the periphery of the lesion shows active edges either papular, vesicular or papulovesicular edge with scaling surface.

  2. Wood‘s light - microsporon gives strong green fluorescence.
    Trichophyton groups such as T. Schoenleini give dull green fluorescence under a filtered ultra violet, Wood‘ light in a dark room. This is very helpful in rapid screening of large number of school children.

  3. Smear - this is a simple method and can be done easily in the office. Microscopic examination of the specimen by potassium hydroxide smears can detect the hyphae of the causative dermatophyte.


Collection of scrapings from the infected skin should be taken from the active edge of the lesion using a blunt scalpel blade or by the edge of a slide. Infected hairs should be depilated from their roots especially in favus.

The specimen is placed on a slide and a drop of 30 percent potassium hydroxide is added and covered by a cover slip . This is heated gently in order to soften and clear the material . Care should be taken in order not to heat the specimen too much and not to boil .

The specimen is examined with low power microscope without staining. This may show the branched septate hyphae.

Hair invasion by dermatophyte is ectothrex in Microsporon, T. Mmentagrophyte and T. Verrucosum, while it is endothrix in T. Tonsurans and T. Violaceum.

  1. Culture - Culture is on petri dishes or cotton wool - plugged test tubes with Sabouraud‘s dextrose agar containing antibiotics to inhibit bacterial and saprophyte contamination. Incubation is kept at 26-30 C for one to two weeks. Different colonies can be identified morphologically and microscopically.

Differential Diagnosis

  1. Alopecia areata - the area involved is smooth, free of hair and if there is some hair growing in the patch it is not short cut at the surface and without scaling . The exclamation mark sign of some hairs growing on the periphery of the patches are an aid to diagnose alopecia areata. Detection of the causative fungi is diagnostic for T. Capitis.

  2. Seborrheic dermatitis - the lesion is more diffuse and with greasy scales, diffuse hair loss and negative microscopic examination are important criteria for differential diagnosis .

  3. Impetigo and carbuncles of the scalp may simulate kerion . Bacterial lesions are more inflammatory , has shorter course , the hair is not loose and cut short. Dermatophytes can be detected on microscopic examination .

  4. Discoid lupus erythematosus : The condition has a chronic course ending with cicatricial alopecia. The scales are adherent , shows stibbling and other exposed areas such as the face may be involved. Microscopic examination for any fungal elements is negative .

  5. Lichen planus: Flat topped ,violaceous papules may be seen in the lesion, which ends with cicatricial alopecia . The extremities and the buccal cavity may have the characteristic lesions of lichen planus.


Preventive measures

Topical treatment

Systemic treatment

  1. Griseofulvin

    Griseofulvin was discovered in the late 1940s and it was used after 1958 for treatment of fungal lesions in man. This was the first oral antimycotic drug used in the past till nowadays .

    Despite its long history as a fungastatic preparation, it has the most limited spectrum of activity of all the available antifungal drugs, meanwhile it has no effect on bacteria.

Mode of action:

The mode of action of griseofulvin appears to be in part by inhibition of formation of microtubules and it is most apparent in the active metabolizing cells near the hyphal tip.

In man, griseofulvin is fairly rapidly metabolized and conjugated with glucuronide in the liver, excreted by the kidney and by the liver in bile.


Griseofulvin interacts with certain drugs such as anticoagulants, warfarin, cyclosporin , barbiturates and oral contraceptives.


Griseofulvin is available in the standard microcrystalline form as 125 mg and 500 mg tablets and as a pediatric oral suspension, 125 mg per 5 ml given after meals preferably after a fatty meal , which increase drug absorption.

In Tinea capitis a single dose, 2 g. of griseofulvin especially in young children (in order to be sure that the effective dose was given), is frequently enough to clear most of the lesions .

The recommended daily dose is: A. Infants and children:

  1. Infants and children :

    125mg/)day up to the age of 1 year.(one teaspoonful )

    187mg/day from 1 to 5 years (one and a half teaspoonful), and

    250-375mg/day (2-3 teaspoonful) from 6 to 12 years divided into two doses or as one dose after a fatty meal .

    In children the daily dose is 10mg/kg/day given in two divided doses daily. It should be after meals (after fatty meal as after eating an egg).

    The duration of treatment varies from ten to twenty days according to the type and severity of the fungal infection .

  1. Adult dose :

    0ne to two 500mg tablet daily or at least 10 mg/ kg /day.

    Small adults (55 kg). one tablet 250 mg. twice daily

    Medium-sized adults, one tablet 250 mg. three times daily.

    For large adults (over 100-kg), one tablet 500 mg. twice daily).

  1. Azoles
    The newer oral azoles, particularly itraconazole, are effective substitutes for griseofulvin but more expensive .

Special indications of Azoles

Widespread Tinea corporis due to T. rubrum , azoles are the treatment of choice.

Cases that failed to respond or cannot tolerate griseofulvin

Type of azoles available

Itraconazole - these are effective new anti-fungal preparations.


Adult: 100-200mg. /day for few weeks in skin fungal infection and for several months in onychomycosis..

Side effects of itraconazole:

  • Gastro-intestinal disturbances .

  • Headache

  • Rarely exfoliative dermatitis .

  1. Ketoconazole 

    This orally active imidazole is a broad-spectrum anti-fungal agent.


    Adult: 200-400 mg/day with food and is usually well tolerated.

Side effects:

  • Headache and nausea are relatively common minor side effects.

  • Liver enzymes should be measured at monthly intervals with

    prolonged courses .Treatment should be stopped if ALT or SGPT rise two- to threefold.

  • Ketoconazole may inhibit androgen biosynthesis.


The drug interacts with the following:

  • Antihistamines. Ketoconazole may interact with certain antihistamines such as Astemazole and Terfenadine .

  • Corticosteroids

  • Anticholinergic

  • Antispasmodics

  • Anti-acids

  • Warfarin

  • Phenytoin

  • Isoniazides

  • Alcohol


Severe hepatocellular failure .

Terfenadine or astemazole concurrent use .



Allergy to the drug .

  1. Allylamine

    These are antifungal drugs that act by inhibition of squalene epoxidase formation of the fungal cell membrane.

    The two main compounds are Terbinafine and Naftifine.

    Both are active against dermatophytes.

5- Terbinafine:

Terbinafine such as Lamasil can be given orally.
Children above 20kg can be given 62.5 mg daily.
20- 40-kg-body weight : 125 mg can be given daily .
Above 40 kg - 250 mg daily.

The adult dose is 250 mg daily. Terbinafine is available also as topical preparation (Lamasil cream). It has produced rapid and long-lasting remissions in both nail disease and persistent Tinea pedais.

There is some evidence to suggest that the frequency of relapse is much lower with Terbinafine than that with other antifungal preparations.

6- Voriconazole:

The anti-fungal agent voriconazole is well tolerated, with only mild to moderate adverse effects, report researchers.

The most common of side effects are headache, rash and abnormal vision. Visual function tests detected no further abnormalities during treatment, report Pfizer researchers in Sandwich, Kent, England, and Brussels, Belgium.




Fungal infection of the nails has a chronic course , slow and may take few months to manifest . The severity and effect of infection of the nail is rather much dependent on the type of infecting dermatophyte .

Different Fungi causing onychomycosis:

  1. T. Tubrum : Causes chronic infection with little inflammatory reaction.

    Clinical manifestations:

    The course of the disease is chronic. The lesion manifests with yellowish discoloration of the nail tip which may spread to involve the whole nail. The nail color is changed and shows dirty debris underneath. Later on the nail becomes brittled and breaks off leaving undermined black remnants .

    The adjacent skin may be invaded by the dermatophyte, leading to characteristically branny, scaly and erythematous well-defined areas.

  2. T. Mentagrophtes infection

    Causes superficial and usually localized nail infection .

  3. Candidal nail infection

  4. The disease is usually mild and begins on the nail fold. The adjacent cuticle is pink, swollen, and tender and characteristically, beads like pus can be expressed from the lesion. The affected nail may become dark, ridged and may become separated from its nail bed.

    Fig. 62. Onychomycosis

    The nail plate remains hard and glossy as the normal nail in contrast to infections caused by dermatophyte, which lead to broken and friable, nails.

Fig. 63. Onychomycosis

Fig. 64. Onychomycos

Fig. 65. Onychomycosis



T. Corporis is an inflammatory mycosis of the glabrous skin. Different species as Trichophyton, Microsporon and Epidermophyton floccosum can cause the disease.

Modes of Infection

  • Infected pet animals. The inflammation is transmitted from infected pets such as cat or dogs .

  • Autoinoculation from a primary fungal focuses elsewhere on the skin.

  • From infected fomites of the patients

  • Direct infection from one patient to another

Clinical Picture

The most  common sites involved are the exposed areas such as face, neck and extremities especially in children, but any site of the body may be involved.

Body ringworm lesions present with erythematous papules, which enlarge to the periphery. The fungus consumes the keratin at the center and retreats away from the primary inoculation site, forming an oval or circular plaque with elevated papulo-vesicular active edges more inflamed than the center. The lesions sometimes form inflamed circles alternating with pale scaly areas.

Fig. 66. Tinea Corporis

Fig. 69. Tinea of the face

Fig. 67. Psoriasis (for differential diagnosis)

Fig.70a. Tinea corporis(Scaly lesion)


Fig. 68. Tinea Manum  (Tinea of the hand)                                        

Fig. 70b. Tinea Corporis


Fig.70b. Peri-oral dermatophytosis

     ( Uncommon site may be mis-diagnosed as Peri-oral contact dermatitis)

*The above is a camel-man who used to suck  directly the infected camel breast to get his needs from camel's milk*

Fig.70c. Wide spread fungal infection of the scalp&skin

Course of Tinea Corporis:

T. corporis lesion may heal spontaneously.

May become a highly inflammatory lesion.

May run a chronic course.

Dissemination may spread to other parts of the body.

Secondary bacterial infection may invade the area.

Differential Diagnosis:


Pityriasis rosea



This is a fungal lesion of the skin that appears as a small papule, which enlarges eccentrically, where the dermatophyte consumes the keratin in the center and then moves to the periphery leaving scaly hypopigmented center and raised active edges.


                                                                                                                                  Fig. 71a. Tinea circinata

                                                                      (Vesiculo-bullous and crusted lesions on the active periphery with central clearing)

Clinical Features

Circinate lesions may fuse together forming large plaques or gyrate lesions. The symptoms are minimal apart from mild itching. The condition is mildly contagious.

These lesions form different clinical varieties:

  1. Plaque type

    Mainly T. Rubrum causes this where large scaly plaques appear on the glabrous skin by fusing of different lesions causing gyrate and arciform patches.

  1. Crusted type

  2. Crusted lesions covering wide areas of the skin and scalp with a mousy smell. The characteristics of this type are Scutula and heavily crusted lesions as that occurring in favus.

Fig. 71. Tinea circinata

Fig. 72. Tinea circinata



This is a boggy inflammation of the glabrous skin as that of the kerion, which occurs on the scalp. The condition is caused by dermatophytes transmitted from animals such as T. verrucosum.

Clinical Features

Different clinical types of Tinea profunda:

  1. Eczematous type

    The lesions are intensely inflammatory, sharply circumscribed with follicular pustules that exude serosanguous or blood tinged secretions.

    Secondary bacterial infection may complicate the condition.

    Scarring may be the end result.

  2. Dry type

    The lesions are round, scaly erythematous without central clearing. This type is caused by Trichophyton species.

  3. Herpetiform type

    This is a vesicular form of body ringworm due to dermatophytes transmitted from animals such as cats and dogs. Vesicular lesions appear which rupture leaving eroded surface.


(Majocchi‘s granuloma)

This is a rare form of follicular and perifollicular granulomatous ring worm which has a chronic course.

Clinical Features

The lesion appears on the glabrous skin mainly on the chins as a circular, raised, circumscribed boggy-crusted lesion in which the follicles are distended with a viscid purulent material.



This is a superficial fungal infection of the glabrous skin. The lesions present with extensive patches that appear as concentric rings with polycyclic borders and scaly edges. The course may take a long time where hyperpigmented and residual hypo-pigmentation appear after healing of the lesions.



Favus is a fungal infection of the scalp, caused by Trichophyton Schoenleini. Children are the main age group infected with favus.

The infection rarely involves the glabrous skin as trunk and neck.

The lesions may present with thick and crusted patches.

Differential Diagnosis of T. Corporis

Different skin lesions may simulate T. Corporis:
Pityriasis Rosea - this is the  most common skin disease that has morphologically some of the clinical picture as T. Corporis mainly in shape.

Fig. 73. Favus

Tinea Corporis lesion has an active vesiculo-papular elevated edges while in pityriasis rosea the edges are smooth. Herald patch (which is a large erythematous plaque preceded the appearance of the skin eruption) may be detected.

The distribution of pityriasis rosea lesions is usually along the line of ribs.

When there is a problem in the differential diagnosis, potassium hydroxide smears can detect the causative fungal species in T corporis.

Discoid Eczema - the lesion is more itchy, round erythematous, scaly and there is no elevated active edge such as in T. corporis and no fungal elements detected on microscopical examination.

Discoid lupus erythematosus - The sites involved are mainly sun-exposed areas. No papulo vesicles appear on the edges. The lesion of discoid lupus erythematosus has adherent scales. Heals with scarring.

Psoriasis - silvery scales covering the patches with no central clearing.


  • Typical clinical picture - the fungal lesions have erythematous-raised edges and usually with a clear center.

  • Microscopic examination - examination of a smear of the scrapings from the active lesion immersed in 20 percent potassium hydroxide and 10 percent sodium sulfide solution shows the septate hyphae as round or oval in shape arranged in chains.

  • Culture: on Sabouraud‘s medium - can detect the pathogenic fungal species.

Treatment of T. Corporis

Topical Preparations

Mild solitary lesion: may need only topical antifungal preparation such as Tolnaftate or imidazole derivatives as Miconazole, Ecanozole nitrate, Clotrimazole and Chlormidazole.

Localized tinea corporis, especially of recent origin, commonly responds usually to topical antifungal preparations, applied twice daily for about a month.

Severe inflammatory fungal lesions: are treated by combination of oral and topical antifungal medications.

Care should be taken in using topical steroids in fungal lesions. Topical steroids may suppress the inflammation and irritation, but it masks the clinical picture besides the side effect causing striae and skin atrophy especially the delicate skin of the intertriginous areas when used for a long time.

Systemic Preparations

Systemic treatment by griseofulvin or the other new generation antifungal drugs the Azole groups should be used in wide spread lesions, or cases not responding to topical preparations or in follicular lesions.

In more widespread infections of recent onset, griseofulvin will generally be preferred and may be expected to clear the condition in about 4 weeks.

Where the infection is long-standing, for example, when caused by T. rubrum, much longer-term intermittent courses for 3-4-weeks intervals, over a period of several months may be required.

Ketoconazole appears to be less satisfactory than griseofulvin in Tinea imbricata, although preliminary data suggest that itraconazole may work better.



Tinea Cruris is a superficial fungal inflammation of the intertriginous areas mainly that of the inguinal, gluteal and the axillary areas. The most common dermatophytes that can cause T. cruris are Epidermophyton floccosum and Trichophyton rubrum.

Severe inflammatory lesions are rare and are due to the species T. Mentagrophtes and T. Verrucosum.

Tinea Cruris occurs mainly in adults but infants and young children are rarely infected.

During the last twenty-five years I have seen a very few cases of Tinea cruris due to dermatophytes in infants and young children. Tinea cruris due to Candida are the most common fungal infections in infants and young children.

Predisposing Factors

Occlusion of the crural area such as by diapers or plastic pants.

Excessive sweating and maceration.

Modes of inection

Infection may be contracted from infected domestic animals such as cats or dogs.

Infected materials such as towels or others.

Auto inoculation from fungal focus elsewhere.

Epidemic infection in school children may occur especially when sharing training suits, swimming kits or infected clothes

Clinical Picture

The lesion may begin in the crural area on the side of one thigh and extends to the other side to become bilateral. Spread of the lesion may extend to the adjacent areas to the intergluteal cleft, groin and upper abdomen.

Scrotum is usually not involved; this may be due to the thin musculature of the area and continuous movement of the scrotal muscles that may cause difficulty for the fungus to seed there.

The lesions begin as an erythematous scaly area spreading to the periphery with an active elevated edge, where itching is a predominant feature.

The lesions in the early stages are in the form of erythematous macules or plaques, arciform with sharp margins extending from the groin down to the thighs. Scaling is variable and occasionally may mask the inflammatory changes.

Central clearance is usually incomplete with nodules scattered throughout the affected area.

Satellite lesions if present are few in number and relatively large.

The course of the lesion depends on the causative dermatophyte.

The clinical picture usually varies according to the type of dermatophyte:

Epidermophyton floccosum infections - are typically acute in onset, rather inflammatory and often primary.

Trichophyton rubrum - lesions are usually chronic. Extension from the groins to other sites is common. T. Rubrum lesions extend to the buttocks, the lower back and the abdomen.

T. interdigitale - infections may be vesicular and inflammatory.

Fig. 74. Tinea cruris

Fig. 75. Tinea cruris


Fig. 76. Tinea cruris

Fig. 76c. Tinea cruris(Widespread lesion)



                 Fig.76d. Erythrasma(For differential diagnosis)          Fig. 76d. Tinea versicolor( For D.D.)

Differential Diagnosis

Seborrheic dermatitis - the lesion presents with diffuse erythematous patch free from central clearing and has no active edges such as the lesions of T. Cruris. Greasy scales cover the lesion in seborrheic dermatitis. No fungal elements are detected on microscopic examination.

Pityriasis rosea: the lesions are oval or rounded discreet patches with few scales on the center. The edges are not raised and herald patch may be detected elsewhere.

Erythrasma - the lesions covers the infected area without central clearing. No active edges as in T. Cruris. Erythrasma gives coral red color with Wood‘s light. Microscopic examination of the scraping of the lesion shows the causative bacteria.

Candidiasis - Satellite lesions appear on the sides of the lesion.



T. pedis is a mycotic infection of interdigital spaces, sub-digital folds, the soles and other areas of the skin. Dermatophytes (T. Rubrum, T. Interdigitale and Epidermophyton floccosum), yeast and moulds are the causative fungi. The disease is more common in adult males and mainly in temperate zones.

Modes of Infection

  • Children especially those sharing sport activities in the school or sport clubs may be more exposed to infection.

  • Infected fomites such as stockings, slippers and shoes.

  • Moist sandy beaches, swimming pools, common bathrooms and showers used by infected persons predispose to the spread of T. Pedis.

Fig. 77. Tinea pedis


Fig.77b. T. pedis & Onychomycosis(due to dermatophytes)


                                                                         Fig.77c. T. pedis ( due to Candida )


                                                                    Fig.77c. T. pedis ( due to dermatophytes)

  • Walking barefoot may precipitate infection in areas where there is contamination by fungi disseminated by animals and man.

Epidemic cases of T. Pedis may occur especially in school children and other groups under certain conditions facilitating spread of fungal infection.

Predisposing Factors

  1. Hot humid climate may precipitate sweating and maceration of the feet that may act as an optimum medium for the dermatophytes.

  2. Wearing of nylon socks or wearing the shoes for a long time may lead to occlusion of the foot and predispose to infection.

  3. Strong alkaline soaps will change the pH of the skin and make the skin more susceptible to the infection.

  4. Peripheral circulatory problems or factors causing hyperhidrosis as in certain endocrine disturbance will lead to more maceration of the interdigital areas.

  5. Chronic diseases such as diabetes or chronic debilitating diseases.

  6. Topical antibacterial and steroid preparations used for a long time may predispose to T. Pedis.

Fig. 78. Tinea pedis (Hyperkeratosis)

Clinical picture

Maceration of the interdigital area between the third or fourth toe web space or beneath the interphalangeal crease of the last three toes accompanied by inflammation and vesiculation.

The clinical picture usually depends on the type of the fungus causing the disease.

T. Interdigitale causes the acute vesicular lesions predisposed by excessive maceration of the interdigital area.

Vesicular eruption appears in the interdigital area with vesicles on an erythematous base containing clear yellow liquid.

Secondary infection of the vesicles may cause more inflammation accompanied by itching and pain.

T. Rubrum causes the chronic dry and scaly type of T. Pedis. The infection may spread to the adjacent tissue and nail causing onychomycosis.

Treatment of Tinea Pedis

  1. Correction of the predisposing factors such as excessive sweating, occlusion of the feet, and proper hygiene to the feet.

  2. Topical antifungal powder dusted in the socks or between the interdigital areas in the morning before wearing the socks.

  3. Topical antifungal preparations alone or in combination with antibacterial when secondary infections are suspected.

  • Tolnaftate powder has proven value and the imidazole are equally effective topical antifungal preparations.

  • Potassium permanganate solution 1: 9000 or aluminium chloride solution 20-30% applied twice daily has considerable advantages in drying the wet oozing lesions.

  1. :If there is any evidence of bacterial infection, swabs should be taken for culture and sensitivity.

  2. Griseofulvin
    Using griseofulvin in the treatment of Tinea pedis is sometimes difficult to evaluate. In the chronic type (usually due to T. rubrum) it is of great value but may need to be continued for 2 or 3 months.

  1. Azoles

    Imidazole, Itraconazole and Terbinafine are effective medications. There is some evidence that the speed of recovery is faster and relapsing rates are less with these compounds.

    Other drugs in this group, Miconazole, Isoconazole, Tioconazole and Sulconazole are equally effective.

    Cases complicated with onychomycosis may need longer period of treatment.

    The dose is:

    • Children up to age 1 year: 10 mg /kg/day (5 mg/lb./day) or 125 mg/day

    • From 1 to 5 years: 187 mg/day

    • From 6 to 12 years: 250-375 mg/day.

    Itraconazole is an effective new antifungal preparation and is given for adults in a dose of 200 mg./day. The drug should always be given after meals. Single daily dose can be used however twice daily is preferred.

    The duration of treatment varies considerably with the type of infection and the site involved.

    Imidazole compounds in particular have considerable antibacterial properties.



Tinea versicolor is a superficial fungal infection caused by Malassezia Furfur. The infection is most prevalent in the tropics predisposed by excessive sweating.

T. Versicolor is unusual in children and young age. Infection occurs from using infected clothes, towels and bed sheets.

Autoinfection is also common.

Clinical Picture

T. Versicolor has a chronic course and recurrence is common due to auto- infection or due to re-infection.

Erythematous scaly macules and patches appear on the trunk shoulders, upper neck and upper limbs. Pityriasis versicolor is usually asymptomatic. The condition rarely forms a distinct problem except for cosmetic. Hyperpigmented patches intermingled with hypopigmented areas appear on the affected site.

Pruritus is minimal but may increase with excessive sweating and bathing. The condition may have a chronic course extending months and even years recurring every summer if not properly treated.


  • Typical clinical picture

  • Smear prepared from skin scaling of fresh lesion on a glass slide.
    The organisms can be detected microscopically.

                                                                              Fig. 79. Tinea versicolor

Fig. 80. Tinea versicolor (Fresh lesion)

  • T. Versicolor lesions show yellow dull color with Wood‘s Light.



                                                                            Fig. 80b Tinea versicolor (Uncommon wide spread lesion)



                                                        Fig. 80 Tinea versicolor 


                                                 Fig. 80b. Tinea versicolor

                                               ( chronic lesion misdiagnosed as vitilligo)

Differential Diagnosis

Tinea corporis - the lesion is more inflammatory with raised active edges and the dermatophytes can be detected microscopically.

Vitilligo - the pigmentary loss in vitilligo is complete and the patches are white, smooth and without the branny scales.

Tuberculoid leprosy - the clinical picture may sometimes simulate the hypo-pigmented plaques of tuberculoid leprosy and the diagnosis can be settled by laboratory finding of the causative bacteria. The neurological signs show anesthesia of the hypopigmented patches of tuberculoid leprosy.

Pityriasis rosea - the herald patch, the distinct distribution of the eruption along the line of the ribs and the negative microscopic examination for any fungal element will help in the differential diagnosis.

Erythrasma - the two conditions may co-exit together. Diagnosis can be confirmed by microscopic detection of the causative organism and the pink fluorescence with Wood‘s Light in erythrasma.

Seborrheic dermatitis - the condition is more inflammatory and the sites involved are localized to certain areas as the intertriginous. The greasy scales covers lesions of seborrheic dermatitis.

Secondary stage of syphilis - the history, the clinical features, the color of the lesions and positive serological tests of syphilis confirm the differential diagnosis.


Preventive measures: are very important to prevent re-infection.

  • Boiling and ironing of the clothes in contact with the infected areas.

Certain expensive clothes can be washed the ordinary way by adding Nizoral shampoos to hot water and soak the clothes for one hour, then wash and rinse. Towels and bed sheets should be also boiled and ironed to destroy the fungus.

  • Avoid excessive sweating.

  • Proper body hygiene.

Active treatment

Selenium sulfide 2.5 per cent (Selsun shampoo) applied every other day for two weeks clear most of the lesions. Take care of the genitalia and eyes due to the possibility of local irritations.

Topical azoles such as Ecanozole (Pevaryl spray) and other anti- fungal preparations are also effective, but are more expensive.

Spray or shampoo preparations are easier to use than creams or ointments. Once or twice daily application of the medication is usually required for several weeks.

Topical Corticosteroids, which may improve the condition temporary, are not recommended.

Treatment of Recurrent Cases

Most failures of topical therapy are either due to inaccurate diagnosis, inadequate treatment, missing out some lesions or re-infection either auto-infection or from other sources.

Treatment with one percent Ecanozole citrate spray (Pevaryl) is effective and easy to be used especially on widespread areas.

Oral Itraconazole used in a single dose of 400 mg and ketoconazole total adult dose 800-1000 is very effective. Children are given smaller doses depending on their weight.

The value of oral treatment with 400 mg. of Fluconazole (adult dose) in a single dose proved to be effective in the treatment of pityriasis versicolor. These medications are expensive and some patients can not afford the cost. Oral azoles are better kept as a reserve for reluctant or recurrent cases of T. versicolor.

Oral antifungal medications are not usually recommended as a routine in T. Versicolor where the lesion may clear with topical preparations such as Ecanozole cream, spray and shampoo alone.

In recurrent cases, treatment may take a longer time and it is better to use topical Ecanozole (Pevaryl sachets). One sachet can be used to rub the skin twice weekly for one month and later once weekly for three months or for longer periods

Care and precautions to prevent auto or re-infection from contacts.


(Trichomycosis nodularis)

This is a fungal infection confined to the hair shafts and resulting in the formation of superficial nodules on the infected hair.

Young girls are frequently affected.

Familial outbreaks may occur.

Clinical features

There are two varieties of Piedra, the black and the white (asteroid), which are caused by Piedra hortae and Trichosporon beigelii, respectively.

Black Piedra

Black Piedra is characterized by the presence of firmly adherent black, hard, gritty nodules, which are composed of a mass of fungus cells on the hair shaft, which causes its disintegration , britling and breaking. These nodules vary in size from microscopic to 1 mm or more in diameter. This type occurs in tropical countries and affects monkeys as well as man.

White Piedr

White Piedra lesions are soft, white or light-brown nodules on the hair shaft. The fungus grows both within and outside the hair shaft and like Black Piedra, the hair shaft may be weakened and break off.
The underlying skin is not affected and there is no fluorescence under Wood‘s light.

Fig. 81. White piedra

Systemic infections due to Trichosporon may affect many different sites including the liver, spleen and heart. Occasionally deep dermal nodules may occur.



Microscopically hyphae, arthrospores and budding cells are present.


In culture, the fungus has slow growth, dark and compact, and usually heaped at the center. In cultures of T. beigelii the colonies develop rapidly and are creamy and wrinkled, later becoming deeply furrowed and folded.


The organisms of White Piedra are surprisingly resistant in vitro to the Azole antifungal drugs.

Shaving or cutting the hair is an effective method of treatment.

To prevent recurrence, antifungal preparations such as Benzoic Acid Compound Ointment BPC or a 1:2000 solution of mercury perchloride may be applied to the scalp after shampooing.

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