Pediatric Annals

Fungal Infections of the Skin in Children

William Watson, MD

Abstract

Fungal organisms cause a great variety of diseases in human beings, sometimes systemic and fatal and sometimes only annoying. This discussion will be limited to entities that are manifest solely on the skin and mucous membranes and will not include cutaneous manifestations of the systemic mycoses. In children, superficial fungal infections of the skin are caused by two groups of organisms - the dermatophyte fungi, which cause disease only in the skin and its appendages, the hair and nails, and Candida albicans, a yeast, which can produce severe systemic disease but most often limits itself to the skin and mucous membranes.

Fungal infections of the skin are usually manifested by erythema and scaling, but they may also be vesicular and pustular. It is important to note that many other inflammatory diseases of the skin may present identical findings - for example, contact dermatitis and psoriasis. Because of this, there is a great tendency for misdiagnosis. The tendency is to overdiagnose fungal infections. Many nonfungal dermatoses are diagnosed as fungal infections, and treated as such, because very simple diagnostic techniques available to all physicians are not utilized.

DIAGNOSIS OF FUNGAL INFECTIONS OF THE SKIN

The materials required for accurate diagnosis are inexpensive; the techniques are simple and not time consuming. They are as follows:

A 15 to 20 per cent potassium hydroxide solution (KOH).

A scalpel blade.

A microscope.

Sabouraud or Mycosel® agar for culture.

A Wood's lamp.

Potassium hydroxide wet-mount preparation. The affected skin is swabbed gently with alcohol. Scrapings from skin lesions are taken, preferably from the active border. If the lesion is scaly, a small quantity of scale is placed on a glass slide, a drop of 15 to 20 per cent KOH added, and a cover slip applied. If the lesion is vesicular, the roof of the vesicle should be shaved and placed on the slide with the KOH. The slide is then heated very gently and briefly with a Bunsen burner or a match. The underside of the slide should be warm, not hot. If too much heat is applied, the KOH will crystallize and completely distort the mount. The slide should then be set aside for a few minutes so that the KOH can dissolve the horny layer cells, allowing the fungal elements to be easily identified. If the KOH preparation is examined before the skin cells dissolve, the cell walls may be mistaken for fungal elements.

1. Blank. H., and Roth, F. J. The treatment of dermatomycoses with orally administered griseofulvin. Arch. Dermatol. 79 (1959), 259.

2. Keddie. F., and Shadomy, S. Etiological significance of Pityrosporum orbiculare m tinea versicolor. Sabouraudia 3 (1963). 21.

3. Burke. RC. Tinea versicolor: Susceptibility factors and experimental infection in human beings. J. Invest. Dermatol. 36 (1961 ). 389.

4. Demis, D. J., Dobson. R. L. and McGu ire, J. Clinical Dermatology, Volume 3. Hagerstown, Md,: Harper & Row, 1976.

5. Canales, L.. et al. Immunological observations in chronic mucocutaneous candidiasis. Lancet 2 (1969), 567.

6. Chilgren, R. A., et al. The cellular immune defect in chronic mucocutaneous candidiasis. Lancet 1 (1969). 1286.…

Fungal organisms cause a great variety of diseases in human beings, sometimes systemic and fatal and sometimes only annoying. This discussion will be limited to entities that are manifest solely on the skin and mucous membranes and will not include cutaneous manifestations of the systemic mycoses. In children, superficial fungal infections of the skin are caused by two groups of organisms - the dermatophyte fungi, which cause disease only in the skin and its appendages, the hair and nails, and Candida albicans, a yeast, which can produce severe systemic disease but most often limits itself to the skin and mucous membranes.

Fungal infections of the skin are usually manifested by erythema and scaling, but they may also be vesicular and pustular. It is important to note that many other inflammatory diseases of the skin may present identical findings - for example, contact dermatitis and psoriasis. Because of this, there is a great tendency for misdiagnosis. The tendency is to overdiagnose fungal infections. Many nonfungal dermatoses are diagnosed as fungal infections, and treated as such, because very simple diagnostic techniques available to all physicians are not utilized.

DIAGNOSIS OF FUNGAL INFECTIONS OF THE SKIN

The materials required for accurate diagnosis are inexpensive; the techniques are simple and not time consuming. They are as follows:

A 15 to 20 per cent potassium hydroxide solution (KOH).

A scalpel blade.

A microscope.

Sabouraud or Mycosel® agar for culture.

A Wood's lamp.

Potassium hydroxide wet-mount preparation. The affected skin is swabbed gently with alcohol. Scrapings from skin lesions are taken, preferably from the active border. If the lesion is scaly, a small quantity of scale is placed on a glass slide, a drop of 15 to 20 per cent KOH added, and a cover slip applied. If the lesion is vesicular, the roof of the vesicle should be shaved and placed on the slide with the KOH. The slide is then heated very gently and briefly with a Bunsen burner or a match. The underside of the slide should be warm, not hot. If too much heat is applied, the KOH will crystallize and completely distort the mount. The slide should then be set aside for a few minutes so that the KOH can dissolve the horny layer cells, allowing the fungal elements to be easily identified. If the KOH preparation is examined before the skin cells dissolve, the cell walls may be mistaken for fungal elements.

Figure 1. KOH preparation demonstrating branching hyphae of a dermatophyte.

Figure 1. KOH preparation demonstrating branching hyphae of a dermatophyte.

In dermatophyte infections, the branching fungal hyphae are easily discernible (Figure 1). In C. albicans infections, round spores and short "pseudohyphae" are seen (Figure 2).

If a KOH preparation is positive, it can be assumed that one is dealing with a fungal infection. Contaminant or saprophytic fungi rarely give a positive KOH. Therapy can be begun immediately. Ideally, the species should be identified by culture confirmation, but this is not absolutely necessary. Occasionally, KOH preparations will be negative despite the presence of pathogenic fungi. In most of these instances, the culture will be positive.

Fungal culture. All pathogenic fungi have growth characteristics in culture that permit precise species identification (Figure 3). This can be important, since different species connote different prognoses and, possibly, different therapy.

Scrapings from lesions are placed on agar. Mycosel® agar is preferable because it contains antibacterials that prevent contamination of the culture. Interpreting fungal cultures requires some experience, since contaminant fungi must be differentiated from pathogens. Recently a new medium called DTM has been developed. The agar will turn red if a dermatophyte sensitive to griseofulvin is present. Most dermatophytes require two or three weeks to grow. C. albicans can be identified in two or three days.

Wood's light examination. Wood's lamp emits ultraviolet light with wavelengths in the range of 365 nm. Certain fungi that commonly cause scalp ringworm (Microsporum species) will fluoresce a brilliant blue-green under Wood's lamp. Aside from cases of tinea capitis, most fungal infections of the skin do not fluoresce upon Wood's light examination. Erythrasma, a bacterial infection of the skin of intertriginous areas - such as the axilla, groin, and interdigital spaces - will fluoresce a coral red. Since erythrasma is often clinically mistaken for fungal infection. Wood's light is a valuable screening device. It is also very useful in screening school-age children for epidemic tinea capitis caused by Microsporum species.

Figure 2. KOH preparation demonstrating spores and pseudohyphae of C. albicans.

Figure 2. KOH preparation demonstrating spores and pseudohyphae of C. albicans.

I must emphasize that examination by Wood's light should always be complemented by a KOH examination and usually by a fungus culture.

DERMATOPHYTE INFECTIONS

Dermatophytes belong to three species. Figure 4 demonstrates the tissues affected by each species. Dermatophytes reside only in keratin, the horny protein outer covering of the skin. Hair and nails are also composed of keratin. They produce inflammation of the skin by elaboration of toxins. The term used to designate this group is tinea. Tinea is usually modified by a word that describes either the location of the infection (tinea capitis, tinea corporis, tinea cruris, tinea pedis) or the morphology of the lesions (tinea versicolor, tinea circinata). This terminology is more specific than, and preferable to, such terms as "athlete's foot," "crotch itch," or "jock itch," since these may be caused by dermatophyte fungi, yeast, bacteria, or contactants.

Tinea capitis (scalp "ringworm"). Tinea capitis is caused by infection of the hair and epidermis of the scalp by the Microsporum and Trichophyton species. It is almost exclusively a disease of prepubertal children and will usually not persist past puberty, even if untreated. The clinical presentation varies depending on the causative fungus. The most common etiologic fungi in the United States are M. audouini, M. cants, and T. tonsurans.

Tinea capitis caused by M. audouini is the least inflammatory type and usually presents as oval or circular patches of hair loss with scaling of the scalp. There may be slight redness and broken hair shafts (Figure 5). This type of tinea capitis seldom resolves spontaneously and may progress to involve the entire scalp. Yellow-green fluorescence is seen on Wood's light examination, and fungal elements are seen on KOH examination of fluorescent hairs. Differential diagnoses of this nonscarring type of hair loss must be differentiated clinically from alopecia areata and trichotillomania (hair pulling), neither of which exhibits scaling of the scalp. Seborrheic dermatitis and psoriasis are scaly but usually do not cause hair loss.

Tinea capitis caused by M. canis (a misnomer, since the main reservoir is the cat) tends to be much more inflammatory and, in addition to patches of hair loss, may have pustules that resemble a bacterial folliculitis.

Kerion is a highly inflammatory tinea capitis most commonly caused by M. canis but occasionally by other organisms. This usually presents as a red boggy circumscribed area of inflammation and hair loss. There is often a purulent or serous drainage (Figure 6). Because of the highly inflammatory and pustular nature of the kerion, it must be differentiated from pyoderma caused by staphylococci. Kerions may also become secondarily infected by bacteria. The intense inflammatory response often destroys fungal elements, making Wood's light examination, KOH examination, and culture occasionally negative despite the presence of fungi.

Figure 3. Dermatophyte fungal culture.

Figure 3. Dermatophyte fungal culture.

Figure 4. Tissues invaded by dermatophyte fungi.

Figure 4. Tissues invaded by dermatophyte fungi.

Figure 5. Tinea capitis caused by M. audouini. Note circular patches of hair loss with scaling.

Figure 5. Tinea capitis caused by M. audouini. Note circular patches of hair loss with scaling.

Figure 6. Kerion. Inflammatory, boggy purulent lesion.

Figure 6. Kerion. Inflammatory, boggy purulent lesion.

"Black-dot ringworm" caused by T. tonsurans is also seen in the United States. Its appearance is characteristic and is caused by breakage of hairs at the skin surface. This type of tinea capitis does not fluoresce on Wood's light examination.

Treatment of tinea capitis. Before the discovery of griseofulvin in 1959, * treatment of tinea capitis was difficult and not very successful. Drastic measures, such as x-ray epilation and systemic administration of thallium, were often used.

Tinea capitis cannot be successfully treated with topical medication because the fungi are embedded in and around the hair shaft, where the agents will not penetrate. Orally administered griseofulvin is the treatment of choice. This antibiotic has the property of combining with healthy keratin in the hair, protecting the hair from further invasion by fungi. As the healthy hair grows outward, the affected portion of the hair shaft is shed. Adequate treatment requires two or three months' administration of griseofulvin, usually in a dose of 250-500 mg. of microparticulate drug daily. This should be given with meals, because dietary fats facilitate absorption from the gastrointestinal tract. Griseofulvin has proved to be a safe drug with few severe side reactions. Nausea, diarrhea, headache, and photosensitivity are the most frequently encountered.

In the presence of a highly inflammatory kerion, one should consider a short course of systemic corticosteroids to reduce the inflammation and thereby reduce the possibility of permanent hair loss due to scarring. If secondary bacterial infection is present, it should be treated with a 10-day course of systemic antibiotic, usually penicillin or erythromycin.

Figure 7. Annular tinea corporis.

Figure 7. Annular tinea corporis.

Figure 8. Tinea corporis caused by M. gypseum lacking annular configuration.

Figure 8. Tinea corporis caused by M. gypseum lacking annular configuration.

Figure 9. Kerion of the face.

Figure 9. Kerion of the face.

Tinea corporis. The clinical appearance of dermatophyte infections of the glabrous (nonhairy) skin is variable. They are common in young children. The most common causative organism is M. canis, usually transmitted by cats. The classic tinea corporis has an annular, or ring, shape. The borders are usually erythematous and scaly, and there is central clearing (Figure 7). In some cases, small vesicles border the lesion. AU lesions of tinea corporis, however, do not have the ring configuration. Some present as nonspecific redness with papules and scaling (Figure 8) and others as highly inflammatory kerion, as seen on the scalp (Figure 9).

Differential diagnosis includes eczematous conditions, such as contact dermatitis and nummular eczema; pityriasis rosea (the herald patch); and, if lesions are on the face, lupus erythematosus.

Figure 10. Tinea cruris. Note active border and central clearing.

Figure 10. Tinea cruris. Note active border and central clearing.

Figure 11. Tinea pedis. Interdigital maceration.

Figure 11. Tinea pedis. Interdigital maceration.

Figure 12. Low-grade tinea pedis with mild erythema and scaling.

Figure 12. Low-grade tinea pedis with mild erythema and scaling.

Figure 13. Vesiculopustular tinea pedis.

Figure 13. Vesiculopustular tinea pedis.

Tinea cruris. This disorder appears in the groin and is not usually seen in préadolescent children. It is not uncommon, however, in teenage boys. There is usually a peripheral zone of papules or vesicles with scaling and central clearing (Figure 10). Pruritus is common. This type of intertrigo must be differentiated from candidiasis and erythrasma. Candidiasis usually has satellite vesicles and pustules and has yeast forms on KOH preparation. Erythrasma, caused by Corynebacterium, fluoresces a coral red on Wood's light examination. Psoriasis and seborrheic dermatitis also occur in the groin, but there is usually involvement elsewhere, such as in the scalp or nails.

Tinea pedis. "Athlete's foot" is uncommon in younger children but becomes more common in adolescents. The simplest form consists of maceration and fissuring between the toes (Figure 11). C. albicans, erythrasma, and Pseudomonas infections can have an identical clinical pattern.

Tinea pedis may involve one or both feet and may extend to the entire plantar and part of the dorsal surface. There may be mild erythema and scaling (Figure 12) or a marked vesicuiopustular inflammatory response (Figure 13). The degree of inflammation is usually dependent on the causative fungus.

Differential diagnosis includes contact dermatitis (usually seen on the dorsal rather than the plantar surface), psoriasis (which may be scaly or vesicuiopustular), and localized atopic dermatitis. Again, the diagnosis must be confirmed by KOH examination and culture.

Tinea manus. Dermatophyte infections of the palm are unusual. When they are present, there is usually concomitant tinea pedis. The "twofoot, one-hand syndrome" is a common pattern. Tinea manus must be differentiated from psoriasis, contact dermatitis, and dyshidrosis (Figure 14). Tinea nigra palmaris is an unusual dermatophyte infection of the palm that presents as a brown to black discoloration.

Onychomycosis. Two of the dermatophyte species, Trichophyton and Epidermophyton, can invade nails. This is referred to as tinea unguium or onychomycosis. Fingernails and toenails may be affected. There is usually a loss of luster, white or yellow discoloration, onycholysis (separation of the distal nail from the nail bed), crumbling, and subungual hyperkeratosis (Figure 15).

Definite laboratory confirmation is necessary to make this diagnosis. Psoriasis, eczema of the fingertips, congenital ectodermal syndromes, and mechanical trauma can cause identical changes. C. albicans can also cause similar nail dystrophy.

Figure 14. "Eczematous" tinea manus.

Figure 14. "Eczematous" tinea manus.

Figure 15. Early onychomycosis with loss of luster, yellowish discoloration, and thickening.

Figure 15. Early onychomycosis with loss of luster, yellowish discoloration, and thickening.

KOH preparations from nails are difficult to interpret. The entire thickness of the nail must be examined. The nail is poorly dissolved by the KOH. A fungal culture is the most reliable way to confirm the diagnosis of onychomycosis.

As with tinea capitis, topical therapy of onychomycosis is ineffective. Griseofulvin, 250-500 mg. daily, can clear this infection, but it must be given for six to nine months for fingernails and 12-18 months for toenails. Unfortunately, onychomycosis tends to recur after clearing with griseofulvin.

Treatment of tinea of the glabrous skin. Tinea corporis, tinea cruris, tinea pedis, and tinea manus can usually be successfully treated with topical medication.

If the reaction is highly inflammatory or vesiculopustular, compresses with Burow's solution 1:20 or potassium permanganate 1:16,000 should be applied for 20 minutes three times daily. Secondary bacterial infection should be treated with systemic antibiotic.

If there is marked scaling and hyperkeratosis, often seen in tinea pedis, keratolytic preparations are very effective. Whitfield's ointment (6 per cent salicylic acid, 6 per cent benzoic acid), applied twice daily, works well.

Preparations containing undecylenic acid (Desenex,® Verdefam®) are also effective; however, they may be irritating on intertriginous skin, especially in the groin. They have the advantage of being inexpensive, over-the-counter preparations.

Castellani's paint (carbol-fuchsin) works well for interdigital, macerated tinea pedis.

Recently, extremely effective topical antifungal preparations have been developed. They all have the advantage of being effective against C. albicans as well as the dermatophytes. They are applied sparingly to the affected areas twice daily. The agents are clortrimazole solution or cream (Lotrimin®), haloprogin solution or cream (Halotex®), and miconazole nitrate cream (MicaTin®).

Tolnaftate (Tinactin®), for many years the most prescribed topical antifungal agent, does not seem to be quite as effective as these newer products and is not active against C. albicans.

In addition to specific antifungal therapy, care should be taken to keep the affected areas dry. This is particularly true in tinea pedis and tinea cruris. Antifungal powders can be used in socks and in the groin area to absorb moisture.

If dermatophyte infections involve large areas of skin, griseofulvin, 250 mg. twice a day for two or three weeks, may be given.

Tinea versicolor. Tinea versicolor is very common, especially in warm, humid climates. The most superficial of the cutaneous fungal infections, it is caused by a yeastlike organism, Malassezia furfur. Many believe that this organism is identical with Pityrosporon orbiculare, a normal inhabitant of human skin.2 Patients with exogenous or endogenous Cushing's disease are particularly prone to extensive tinea versicolor.3

Tinea versicolor characteristically affects the upper trunk and arms, neck, and face. It consists of macular (nonpalpable) lesions with a branny scale (Figure 16). The lesions have minimal inflammation and are a fawn color on white skin and often hyperpigmented on darker skin. After sun exposure and tanning, the lesions become hypopigmented (Figure 17); hence the name versicolor. Many of the lesions have a perifollicular distribution. They are usually asymptomatic.

Diagnosis is made by KOH preparations, where there are usually abundant hyphae with clusters of round yeast cells, the so-called spaghetti-and-meatballs pattern (Figure 18).

Differential diagnosis includes pityriasis rosea, secondary syphilis, and seborrheic dermatitis. The hypopigmented lesions must be differentiated from vitiligo.

The simplest therapy for tinea versicolor is 2.5 per cent selenium sulfide shampoo (Selsun,® Exsel®) as a cleaner in the bathtub or shower. The affected areas are lathered with the shampoo and then rinsed off after about five minutes. This is done daily for one or two weeks and then weekly for maintenance. The weekly maintenance treatment should be continued indefinitely, particularly during warm weather, since tinea versicolor usually returns on discontinuance of therapy. Selenium should not be left in contact with young children's skin, since absorption with toxicity has been reported. Alternative treatments include daily application of 20 per cent aqueous solution of sodium thiosulfate or one of the more expensive topical antifungals mentioned in treatment of tinea of the glabrous skin. Tinea versicolor tends to recur when treatment is discontinued, particularly in hot climates.

CANDIDIASIS

Candidiasis is an infection of skin and mucous membranes caused by the yeastlike fungus C. albicans. This organism occasionally involves internal organs, usually in immunosuppressed hosts. Diabetics are more susceptible to C. albicans infections. C. albicans is isolated from the gastrointestinal tract of up to 59 per cent of healthy persons.4

Candidiasis of the skin and mucous membranes is more common in infancy than in later childhood. The manifestations of candidiasis are varied. The most common will be discussed here.

Oral candidiasis (thrush). Thrush is seen most commonly in the newborn, usually at about one week of age. It affects approximately 5 per cent of infants.4 Trie infection is acquired by passage through a vaginal canal inhabited with C. albicans. The lesions are white and raised with a cheesy appearance and are usually located on the buccal mucosa, tongue, and palate. When they are scraped lightly, there is an eroded, bleeding site (Figure 19).

Figure 16. Tinea versicolor with fine, branny scaling.

Figure 16. Tinea versicolor with fine, branny scaling.

Figure 17. Tinea versicolor after suntan. The lesions are hypopigmented.

Figure 17. Tinea versicolor after suntan. The lesions are hypopigmented.

Figure 18. KOH preparation demonstrating "spaghetti and meatballs" pattern of tinea versicolor.

Figure 18. KOH preparation demonstrating "spaghetti and meatballs" pattern of tinea versicolor.

Figure 19. Cheesy-appearing lesions of oral candidiasis on buccal mucosa.

Figure 19. Cheesy-appearing lesions of oral candidiasis on buccal mucosa.

Figure 20. Diaper candidiasis complicating ammoniacal diaper dermatitis.

Figure 20. Diaper candidiasis complicating ammoniacal diaper dermatitis.

Thrush may also be seen in debilitated patients or those on antibiotic, corticosteroid, or cytotoxic drug therapy.

Occasionally there will be extension to the perioral skin, particularly the angles of the mouth, causing angular cheilitis (perleche).

Thrush is treated with nystatin oral suspension (Mycostatin®), 100,000 units/ml. Two to 4 ml. is given with a medicine dropper and allowed to remain in the mouth as long as possible. This is done three times daily for at least 10 days. If this treatment fails, the mouth can be painted with 1 per cent gentian violet aqueous solution daily.

"Diaper candidiasis." C. albicans is a frequent primary and secondary invader of the diaper area of infants, owing to its presence in the lower gastrointestinal tract. Usually candidiasis complicates pre-existing ammoniacal dermatitis, seborrheic dermatitis, or atopic dermatitis. All persistent diaper eruptions should be examined for the presence of C. albicans with a KOH wet mount. If C. albicans is a factor in the eruption, there are often satellite vesicopustules near the border of the lesion (Figure 20). Occasionally, candidiasis may spread from the diaper area to involve large areas of the skin surface.

Candidiasis of the diaper area may be treated with creams, lotions, and powders containing nystatin or amphotericin B (Fungizone®). If topical treatment fails, an attempt should be made to eliminate C. albicans from the intestinal tract with oral nystatin, which is not absorbed.

Candidal paronychia. A painful, red, and swollen nailbed and periungual area may be caused by C. albicans, although not commonly in healthy children. It usually occurs in "wet workers" or diabetics. If candidal paronychia becomes chronic, permanent nail dystrophy may result (Figure 21).

This condition is difficult to treat. A solution of 4 per cent thymol in chloroform, dropped into the space between the nail and the posterior and lateral nail folds, helps to dry the space, making a poor environment for moisture-loving C. albicans. Nystatin cream or amphotericin B lotion should be massaged into the area. Hands should be protected from water.

Figure 21. Candidal paronychia.

Figure 21. Candidal paronychia.

Figure 22. Nail dystrophy in chronic mucocutaneous candidiasis.

Figure 22. Nail dystrophy in chronic mucocutaneous candidiasis.

Acute candidal paronychia must be differentiated from staphylococcal paronychia with a KOH examination, Gram's stain, and bacterial culture.

Miscellaneous Candida albicans infections. Candidiasis should be considered in the differential diagnosis of tinea cruris, erythrasma, intertriginous psoriasis, seborrheic dermatitis, and interdigital tinea pedis.

The diagnosis is made by finding pseudohyphae and budding yeasts on KOH examination. Cultures from the oral cavity and the anogenital area have little value because C. albicans is frequently part of the normal flora of these areas.

Chronic mucocutaneous candidiasis (candidal granuloma). There is a group of chronic and progressive candidal infections of skin and mucous membranes, characterized by a variety of immunologic defects.5,6 Many of these children seem to have a specific defect with regard to C. albicans, since they do not have problems with other microorganisms. They have been successfully treated with transfer factor. Some children with hypoparathyroidism develop this syndrome.

The candidiasis usually begins in the oral cavity in infancy but then proceeds to involve the skin of the face, scalp, trunk, and distal fingers. There is plaquelike erythema with crusting and scaling and granulomatous-appearing lesions, often with bizarre patterns. Chronic paronychia on all fingers usually results in severe nail dystrophy (Figure 22). Fortunately, the invasion seems to limit itself to the skin and oral mucosa.

SUMMARY

Fungal infections of the skin in children are common and may mimic many other dermatoses. Diagnostic techniques are simple and inexpensive; Wood's light examination, KOH wet mounts, and preferably fungal culture should be performed on all suspected lesions.

BIBLIOGRAPHY

1. Blank. H., and Roth, F. J. The treatment of dermatomycoses with orally administered griseofulvin. Arch. Dermatol. 79 (1959), 259.

2. Keddie. F., and Shadomy, S. Etiological significance of Pityrosporum orbiculare m tinea versicolor. Sabouraudia 3 (1963). 21.

3. Burke. RC. Tinea versicolor: Susceptibility factors and experimental infection in human beings. J. Invest. Dermatol. 36 (1961 ). 389.

4. Demis, D. J., Dobson. R. L. and McGu ire, J. Clinical Dermatology, Volume 3. Hagerstown, Md,: Harper & Row, 1976.

5. Canales, L.. et al. Immunological observations in chronic mucocutaneous candidiasis. Lancet 2 (1969), 567.

6. Chilgren, R. A., et al. The cellular immune defect in chronic mucocutaneous candidiasis. Lancet 1 (1969). 1286.

10.3928/0090-4481-19761201-10

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