PRACTICAL THE RA P E U TICS
Drugs 43 (5): 674-682, 1992 00 12-6667/92/0005-0674/$04.50/0 © Adis International Limited, All rights reserved. DRUl150
Superficial Fungal Infections of the Skin Diagnosis and Current Treatment Recommendations George H. Rezabek and Allan D. Friedman Department of Pediatrics, St Louis University School of Medicine, Cardinal Glennon Children's Hospital, St Louis, Missouri, USA
Contents 674 675 675 677 677 678 678 678 678 679 679 679 680 680 680 681 681 681 681 681 681 682 682
Summary
Summary I. Dermatophyte Infections I.l Tinea Capitis 1.2 Tinea Pedis 1.3 Tinea Corporis 1.4 Tinea Cruris 1.5 Tinea Unguium 2. Tinea Versicolor Infection 2.1 Presentation and Diagnosis 2.2 Treatment 3. Candida Skin Infections 3.1 Presentation and Diagnosis 3.2 Treatment 4. Drugs Used to Treat Superficial Fungal Infections 4.1 Griseofulvin 4.2 Ketoconazole 4.3 Itraconazole 4.4 Miconazole 4.5 Econazole 4.6 Nystatin 4.7 Selenium Sulfide 4.8 Haloprogin 5. Conclusion
Superficial fungal infections are common. Most diagnoses of fungal infections of the skin can be made by physical examination, assisted by the use of a Wood's lamp, skin scrapings for microscopic examination, and fungal cultures. Dermatophyte infections are common at all ages, in both sexes, and they have a worldwide distribution, These infections include tinea capitis, tinea cruris, tinea pedis, tinea corporis, tinea manuum and tinea barbae. Tinea versicolor, caused by Malasseziafurfur, and candidal infections are also common. Treatment modalities include oral and topical agents. Good personal hygiene is an important adjunct to antifungal therapy. Decisions regarding the appropriateness of therapy in a given patient
Superficial Fungal Infections
675
must take into account the extent and location of the infection, the benefits and risks of each of the treatments, and cost. Oral therapies include griseofulvin, ketoconazole, and itraconazole. There are a large variety of topical treatments, including nystatin, selenium sulfide, tolnaftate, haloprogin, miconazole, clotrimazole, and sodium thiosulfate. Important to successful treatment is compliance with what is sometimes a long course of treatment, and good personal hygiene.
1. Dermatophyte Infections Dermatophytes are fungi that cause superficial infections of the skin, commonly referred to as tinea infections. Transmission of these infections can be via person to person spread, by soil contact or from animal contact. Fungal infections of the scalp are referred to as tinea capitis; tinea pedis is a superficial fungal infection of the foot; groin infections are referred to as tinea cruris; and most other superficial skin infections due to tinea are categorised as tinea corporis. Superficial fungal infections are seen worldwide. The distribution of the different species of dermatophytes, however, varies widely by geographical area. Since dermatophyte infections are not generally reportable diseases, few statistics are available regarding incidence. Chronic superficial fungal infections probably occur in about 20% of the population and over 90% of adult males probably have had one or more superficial fungal infection sometime during their lives. Infection rates appear to be highest in tropical, humid climates. These infections occur more commonly in males
Fig. 1. Tinea capitis caused by Microsporum audouinii.
Fig. 2. Branching hyphae inside hair shaft (endothrix) that when degenerated appear as empty spaces (X492).
than females. Age incidence varies with anatomical site of infection. 1.1 Tinea Capitis 1.1.1 Presentation and Diagnosis Tinea capitis is primarily a disease of childhood. The peak incidence is between 3 and 9 years of age (Frieden 1987), and is more common in nonWhites (Prevost 1983). Most tinea capitis infections are due to either Microsporum or Trichophyton spp. (fig. I). Trichophyton tonsurans is the most common aetiological agent in the United States, whereas M. canis is more common in the South Pacific and Europe (Fitzpatrick & Newcomer 1987). Other common agents responsible for tinea capitis include M. audouinii and T. mentagrophytes. Tinea capitis results from invasion of the hair shaft. If the spores stay within the shaft it is referred to as an endothrix infection (fig. 2), usually resulting in a noninflammatory tinea capitis. These
676
Fig. 3. Fungal spores (5 to IOl'm) in sheath or in isolated chains on hair (ectothrix) [X400j.
patients have hair loss without erythema, scales, or pustules. This form of tinea capitis is usually a result of a Trichophyton infection. If the spores spread beyond the hair shaft it is referred to as an ectothrix infection (fig. 3). In this infection a sheath of arthrospores forms on the outside of the hair, often leading to an inflammatory tinea capitis. Both Microsporum and Trichophyton infections can be responsible for ectothrix tinea disease. These infections may result in the formation of an inflammatory lesion called a kerion (fig. 4). A kerion is a swollen, purulent, crusty lesion which is hairless, and may be associated with suppurative folliculitis. It is not clear why some patients develop kerions and others do not. The pus that can be expressed is due to the fungus and not a secondary bacterial infection. Although kerions may be caused by any of the dermatophytes that cause tinea capitis, it is most commonly associated with T. verrucosum. Occasionally the presence of a kerion may lead to a hypersensitivity reaction (an 'id reaction') which presents as a rash on the face and trunk (Stein 1983). Not a great deal is known about precipitating factors for kerion formation except that it appears that a tinea capitis infection is almost always present prior to development of the kerion. In the past a kerion was thought to be a secondary infection but it now appears to clearly be an inflammatory
Drugs 43 (5) 1992
response. The first step in the diagnosis of tinea capitis is the physical examaination. Areas of alopecia often associated with a characteristic 'black· dot' appearance will suggest the diagnosis. In certain fungal scalp infections the use of a Wood's lamp which emits filtered ultraviolet light can be helpful. Typically M. audouinii, M. canis and other small spore-forming fungi which cause ectothrix will fluoresce (fig. 5), while T. tonsurans and other producers of large spores that cause ectothrix or endothrix infections will not fluoresce. Diagnosis can also be made from scrapings of the lesion. Under the microscope, a potassium hydroxide preparation will show the presence of arthroconidia filling the hair shaft in T. tonsurans and other endothrix infections (fig. 2), and spores surrounding the hair shaft can be seen in ectothrix infections such as M. canis (fig. 3). Definitive diagnosis can be made by culturing the scraping for fungus. Also available is a simple diagnostic aid called the dermatophyte test medium. This has a colour indicator that turns red in the presence of a fungal infection (Frieden 1987). Tinea barbae is a fungal infection of the hair of the beard, and is a variant of tinea capitis. It is predomina~tly seen in rural men infected from animals. The clinical manifestations and treatment are similar to tinea capitis. 1.1.2 Treatment Tinea capitis can be challenging to treat. The infection may be self-limiting in some patients but can be present for months to years before resolving. In order for therapy to be effective it must
Fig. 4. Kerion caused by T. mentagrophytes.
Superficial Fungal Infections
Fig. 5. M. audouinii under Wood's lamp examination.
penetrate into the hair follicles (Lucky 1985). Topical agents penetrate poorly, thus the treatment of tinea capitis is best accomplished with the use of oral antifungal agents such as microcrystalline griseofulvin 10 to 15 mg/kg once daily for I to 2 months (Nelson 1991), ketoconazole, or itraconazole. For over 30 years griseofulvin has been the standard of care. Adverse reactions to griseofulvin include hypersensitivity reactions (rashes, urticaria, angioneurotic oedema), paraesthesias, nausea, vomiting, epigastric distress and mental confusion. Less commonly granulocytopenia, proteinuria, nephrosis and hepatic toxicity may occur. Oral ketoconazole 6 mg/kg/day given in divided doses every 12 to 24 hours (Nelson 1991) has been shown to be a safe alternative (Gan et al. 1987; Martin-Roig et al. 1988; Tanz 1985). All oral therapy often does require at least 6 weeks. Patients should be reevaluated after 3 or 4 weeks of therapy to ensure compliance and safety. In addition, application of a 2.5% selenium sulfide shampoo may decrease spore shedding and therefore help curb the spread (Allen et al. 1982). Furthermore, tinea capitis that is complicated by kerion formation may heal more rapidly if oral prednisone is given in a dose of I to 2 mg/kg/day for 2 weeks (Frieden 1987). 1.2 Tinea Pedis 1.2.1 Presentation and Diagnosis Tinea pedis is infrequently seen in preadolescents. It increases in frequency with age and is more frequently seen in men than women. Its distribu-
677
tion is worldwide and is primarily seen in people who wear shoes. Tinea manuum, a fungal infection of the palmar surface of the hands, is frequently seen in conjunction with tinea pedis. Tinea pedis is most frequently caused by T. rubrum and T. mentagrophytes. both of which are spread human to human. In addition, T. mentagrophytes can also be spread through rodent to human contact. These organisms proliferate in the stratum corneum by utilising the lipid present there. Characteristically, tinea pedis can present in a moccasin-like distribution in which there is dry scaling plantar skin extending up the sides of the feet. In addition, there may be involvement of the intertriginous areas of the feet which occasionally may lead to secondary bacterial infection 1.2.2 Treatment Topical agents in the form of cream or lotions are usually most appropriate for the treatment of tinea pedis. These agents include c1otrimazole, miconazole, haloprogin, and econazole. Application of these antifungal agents is usually twice a day until clear (Peter et al. 1991). If there is a large amount of oozing from the lesions, topical astringents such as aluminium acetate solution (Burow's solution) will be helpful. Wearing heavy cotton socks with frequent changes may aid fungal eradication. Resistant cases may respond to oral griseofulvin, and if there is an id reaction to the infection, oral prednisone I mg/kg/day may prove beneficial (Caravati et al. 1976). 1.3 Tinea Corporis 1.3.1 Presentation and Diagnosis Tinea corporis, also referred to as ringworm, has a worldwide distribution but is more commonly found in hot, humid climates. It occurs in both males and females of all ages. Transmission has been reported from human to human, animal to human and from inanimate objects. The fungi responsible for this form of tinea include Microsporum. Trichophyton. and Epidermophyton spp. This infection may be asymptomatic. When symptomatic it typically presents as a character-
678
Drugs 43 (5) 1992
may be helpful, but false-negative microscopic examinations can occur.
Fig. 6. Tinea corporis caused by M. audouinii.
istic pruritic annular plaque (fig. 6). Scaling, crusting, vesicule formation and papules on non-hairy skin may be present (Caputo 1986). 1.3.2 Treatment Tinea corporis usually responds to topical treatment with agents such as haloprogin, clotrimazole, miconazole or econazole, applied twice daily for 2 to 4 weeks (Peter et al. 1991). The application of topical steroids to the lesions should be avoided, since this may result in the formation of multicentric, large ringed lesions that have advancing borders (Caputo 1986). 1.4 Tinea Cruris 1.4.1 Presentation and Diagnosis Tinea cruris is a dermatophyte infection of the groin and thighs, more common in males than in females. The disease is more likely to recur if moisture, trauma or occlusion are present. Predisposing factors include obesity, and tight-fitting pants, pantyhose, athletic supports, and wet swimsuits. Organisms frequently causing tinea cruris include E. floccasum, T. mentagrophytes and T. rubrum. Erythrasma, which is colonisation of the affected area with Corynebacterium minutissimum, may mimic tinea cruris. However, under Wood's light erythrasma will fluoresce a bright red (Tunnessen 1985). Laboratory confirmation of the clinical diagnosis is best made by fungal culture. Potassium hydroxide preparation and microscopic examination
1.4.2 Treatment Treatment of tinea cruris generally consists of topical agents such as miconazole or clotrimazole as a lotion gently rubbed into the affected areas twice daily for 3 to,4 weeks, or topical ketoconazole once daily. Loose-fitting cotton undergarments and good hygiene are important in successfully treating this infection. Oral griseofulvin may be needed in unresponsive cases (Peter et al. 1991). 1.5 Tinea Unguium 1.5.1 Presentation and Diagnosis Tinea unguium is a dermatophyte infection of the nail. If the nail plate is directly invaded the term used to describe the infection is leuconychia mycotia. Conversely, if the nail bed is invaded first with secondary spread to the plate, it is called subungual dermatophytosis. Most cases of tinea unguium are associated with tinea pedis or tinea manuum and are usually found in adults. Clinical findings include nail discolouration, subungual hyperkeratosis, and separation of the nail from the be'd. As the infection progresses the plate may become brittle and friable. 1.5.2 Treatment Systemic therapy with either ketoconazole or griseofulvin is acceptable for 3 to 4 weeks. Griseofulvin is still accepted as the drug of choice, with ketoconazole usually reserved for those cases not responsive to griseofulvin. Topical agents do not appear to be effective (Fitzpatrick et al. 1987).
2. Tinea Versicolor Infection 2.1 Presentation and Diagnosis Tinea versicolor is a superficial fungal infection which is sometimes confused with other dermatological disorders such as pityriasis alba, secondary syphilis, and vitiligo. Predisposing factors include excessive sweating, malnutrition, chronic illnesses, immunosuppression, and a warm en-
Superficial Fungal Infections
Fig. 7. Tinea versicolor caused by Malassezia /wfur.
vironment. This infection is a mycotic invasion of the stratum corneum by the lipophylic, dimorphic yeast Malassezia furfur. This yeast, also known as Pityrosporum orbiculare, is believed to be a skin saprophyte that normally colonises the hair follicle. After converting to its mycelial form it spreads into the superficial dermal layers, resulting in the appearance of a rash. As with many other superficial skin infections the organisms, be they bacteria or fungi, may reside on the skin on some patients without causing disease. Why some otherwise healthy patients develop symptomatic infection and others do not, may relate to the integrity of the skin, i.e. small breaks in the skin may allow for invasion and disease. It is not clear what other factors are involved. Tinea versicolor is commonly seen on the head and neck as small oval or round hyper- or hypopigmented patches (fig. 7). In children the rash may be seen on the face as well. The patches may be covered with a fine scale. Diagnosis is aided by Wood's light examination which will demonstrate the typical yellow-orange fluorescence. Potassium hydroxide preparation for microscopic examination is also useful; culture is rarely necessary for diagnosis. 2.2 Treatment Treatment options include shampoos and topical antifungal agents; systemic therapy is rarely required. Selenium sulfide shampoo is usually applied to the affected area daily for 10 to 15 minutes for 7 to 14 days. In warmer, humid weather the
679
application may need to be repeated biweekly to prevent recurrences. It should be remembered that abnormalities in pigmentation will resolve slowly over several weeks even after fungal colonisationhas been eradicated. More frequent or prolonged application of treatment will not hasten the resolution of the pigmentation abnormality (Friedman 1990). Topical sodium thiosulfate 25% solution, to 1naftate, halprogin, miconazole and clotrimazole can also be used, although the latter agents may be expensive. In more difficult cases, oral agents may be necessary. Ketoconazole once a day for 2 to 4 weeks is effective, but the potential hepatotoxicity must be considered. Griseofulvin does not appear to be effective for tinea versicolor (Stein 1983).
3. Candida Skin Infections 3.1 Presentation and Diagnosis Candida skin rashes occur at all ages, but they are most commonly manifested as diaper dermatitis in infants. Although there are at least 80 species of Candida. the vast majority of human disease is due to Candida albicans. C. albicans colonises the gastrointestinal tract, the vagina and the skin, and it is at these sites that most infection occurs. Oral infections with C. albicans are common in infants. Passage of the yeast through the intestine can result in seeding to the perineum, which can give rise to diaper dermatitis. If the perineum is moist and somewhat macerated, this creates an environment conducive to the development of Candida dermatitis. Candidal diaper dermatitis usually appears as bright red confluent patches with well demarcated serpiginous borders. Satellite lesions are frequently present. The inguinal folds are often involved. Perleche, also known as candidal angular cheilitis, results from Candida infection and presents as erythematous, macerated corners of the mouth. Indeed there is usually some degree of maceration of the angle of the mouth as a predisposing factor. Children and adults who wear braces on their teeth are predisposed to this as the braces distort the an-
Drugs 43 (5) 1992
680
Table I. Treatment of superficial fungal infections Disease
Organism
Treatment
Tinea capitis or barbae
M. canis, T. tonsurani, others
Griseofulvin 10-20 mg/kg/d PO (max 1 g/day) or Ketoconazole 3-4 mg/kg/d PO (max 1.6 g/day) plus selenium sulfide 2.5% for 10 min twice weekly plus Prednisone 1 mg/kg/day PO
Tinea corporis
T. rubrum, Microspora, Epidermophyton spp.
Topical miconazole, haloprogin, clotrimazole or tolnaftate bid or Topical ketoconazole qd or Griseofulvin 10-20 mg/kg/day PO (max 1 g/day) for 4w in unresponsive cases
Tinea pedis, manuum or cruris
Microspora, Epidermophyton, Trichophyton spp. Trichophyton, Epidermophyton spp.
Topical clotrimazole, haloprogin, miconazole or econazole bid or Topical ketoconazole or sulconazole qd or Aluminium acetate solution or Griseofulvin 10-20 mg/kg/day PO (max 1 g/day)
Tinea versicolor
Malassezia furfur
Topical selenium sulfide 2.5% for 1-2w or Topical sodium thiosulfate 25% bid for 2-4w or Topical ketoconazole or sulconazole
with kerions
Abbreviations: d
= day; w = wee\
Drugs 43 (5): 674-682, 1992 00 12-6667/92/0005-0674/$04.50/0 © Adis International Limited, All rights reserved. DRUl150
Superficial Fungal Infections of the Skin Diagnosis and Current Treatment Recommendations George H. Rezabek and Allan D. Friedman Department of Pediatrics, St Louis University School of Medicine, Cardinal Glennon Children's Hospital, St Louis, Missouri, USA
Contents 674 675 675 677 677 678 678 678 678 679 679 679 680 680 680 681 681 681 681 681 681 682 682
Summary
Summary I. Dermatophyte Infections I.l Tinea Capitis 1.2 Tinea Pedis 1.3 Tinea Corporis 1.4 Tinea Cruris 1.5 Tinea Unguium 2. Tinea Versicolor Infection 2.1 Presentation and Diagnosis 2.2 Treatment 3. Candida Skin Infections 3.1 Presentation and Diagnosis 3.2 Treatment 4. Drugs Used to Treat Superficial Fungal Infections 4.1 Griseofulvin 4.2 Ketoconazole 4.3 Itraconazole 4.4 Miconazole 4.5 Econazole 4.6 Nystatin 4.7 Selenium Sulfide 4.8 Haloprogin 5. Conclusion
Superficial fungal infections are common. Most diagnoses of fungal infections of the skin can be made by physical examination, assisted by the use of a Wood's lamp, skin scrapings for microscopic examination, and fungal cultures. Dermatophyte infections are common at all ages, in both sexes, and they have a worldwide distribution, These infections include tinea capitis, tinea cruris, tinea pedis, tinea corporis, tinea manuum and tinea barbae. Tinea versicolor, caused by Malasseziafurfur, and candidal infections are also common. Treatment modalities include oral and topical agents. Good personal hygiene is an important adjunct to antifungal therapy. Decisions regarding the appropriateness of therapy in a given patient
Superficial Fungal Infections
675
must take into account the extent and location of the infection, the benefits and risks of each of the treatments, and cost. Oral therapies include griseofulvin, ketoconazole, and itraconazole. There are a large variety of topical treatments, including nystatin, selenium sulfide, tolnaftate, haloprogin, miconazole, clotrimazole, and sodium thiosulfate. Important to successful treatment is compliance with what is sometimes a long course of treatment, and good personal hygiene.
1. Dermatophyte Infections Dermatophytes are fungi that cause superficial infections of the skin, commonly referred to as tinea infections. Transmission of these infections can be via person to person spread, by soil contact or from animal contact. Fungal infections of the scalp are referred to as tinea capitis; tinea pedis is a superficial fungal infection of the foot; groin infections are referred to as tinea cruris; and most other superficial skin infections due to tinea are categorised as tinea corporis. Superficial fungal infections are seen worldwide. The distribution of the different species of dermatophytes, however, varies widely by geographical area. Since dermatophyte infections are not generally reportable diseases, few statistics are available regarding incidence. Chronic superficial fungal infections probably occur in about 20% of the population and over 90% of adult males probably have had one or more superficial fungal infection sometime during their lives. Infection rates appear to be highest in tropical, humid climates. These infections occur more commonly in males
Fig. 1. Tinea capitis caused by Microsporum audouinii.
Fig. 2. Branching hyphae inside hair shaft (endothrix) that when degenerated appear as empty spaces (X492).
than females. Age incidence varies with anatomical site of infection. 1.1 Tinea Capitis 1.1.1 Presentation and Diagnosis Tinea capitis is primarily a disease of childhood. The peak incidence is between 3 and 9 years of age (Frieden 1987), and is more common in nonWhites (Prevost 1983). Most tinea capitis infections are due to either Microsporum or Trichophyton spp. (fig. I). Trichophyton tonsurans is the most common aetiological agent in the United States, whereas M. canis is more common in the South Pacific and Europe (Fitzpatrick & Newcomer 1987). Other common agents responsible for tinea capitis include M. audouinii and T. mentagrophytes. Tinea capitis results from invasion of the hair shaft. If the spores stay within the shaft it is referred to as an endothrix infection (fig. 2), usually resulting in a noninflammatory tinea capitis. These
676
Fig. 3. Fungal spores (5 to IOl'm) in sheath or in isolated chains on hair (ectothrix) [X400j.
patients have hair loss without erythema, scales, or pustules. This form of tinea capitis is usually a result of a Trichophyton infection. If the spores spread beyond the hair shaft it is referred to as an ectothrix infection (fig. 3). In this infection a sheath of arthrospores forms on the outside of the hair, often leading to an inflammatory tinea capitis. Both Microsporum and Trichophyton infections can be responsible for ectothrix tinea disease. These infections may result in the formation of an inflammatory lesion called a kerion (fig. 4). A kerion is a swollen, purulent, crusty lesion which is hairless, and may be associated with suppurative folliculitis. It is not clear why some patients develop kerions and others do not. The pus that can be expressed is due to the fungus and not a secondary bacterial infection. Although kerions may be caused by any of the dermatophytes that cause tinea capitis, it is most commonly associated with T. verrucosum. Occasionally the presence of a kerion may lead to a hypersensitivity reaction (an 'id reaction') which presents as a rash on the face and trunk (Stein 1983). Not a great deal is known about precipitating factors for kerion formation except that it appears that a tinea capitis infection is almost always present prior to development of the kerion. In the past a kerion was thought to be a secondary infection but it now appears to clearly be an inflammatory
Drugs 43 (5) 1992
response. The first step in the diagnosis of tinea capitis is the physical examaination. Areas of alopecia often associated with a characteristic 'black· dot' appearance will suggest the diagnosis. In certain fungal scalp infections the use of a Wood's lamp which emits filtered ultraviolet light can be helpful. Typically M. audouinii, M. canis and other small spore-forming fungi which cause ectothrix will fluoresce (fig. 5), while T. tonsurans and other producers of large spores that cause ectothrix or endothrix infections will not fluoresce. Diagnosis can also be made from scrapings of the lesion. Under the microscope, a potassium hydroxide preparation will show the presence of arthroconidia filling the hair shaft in T. tonsurans and other endothrix infections (fig. 2), and spores surrounding the hair shaft can be seen in ectothrix infections such as M. canis (fig. 3). Definitive diagnosis can be made by culturing the scraping for fungus. Also available is a simple diagnostic aid called the dermatophyte test medium. This has a colour indicator that turns red in the presence of a fungal infection (Frieden 1987). Tinea barbae is a fungal infection of the hair of the beard, and is a variant of tinea capitis. It is predomina~tly seen in rural men infected from animals. The clinical manifestations and treatment are similar to tinea capitis. 1.1.2 Treatment Tinea capitis can be challenging to treat. The infection may be self-limiting in some patients but can be present for months to years before resolving. In order for therapy to be effective it must
Fig. 4. Kerion caused by T. mentagrophytes.
Superficial Fungal Infections
Fig. 5. M. audouinii under Wood's lamp examination.
penetrate into the hair follicles (Lucky 1985). Topical agents penetrate poorly, thus the treatment of tinea capitis is best accomplished with the use of oral antifungal agents such as microcrystalline griseofulvin 10 to 15 mg/kg once daily for I to 2 months (Nelson 1991), ketoconazole, or itraconazole. For over 30 years griseofulvin has been the standard of care. Adverse reactions to griseofulvin include hypersensitivity reactions (rashes, urticaria, angioneurotic oedema), paraesthesias, nausea, vomiting, epigastric distress and mental confusion. Less commonly granulocytopenia, proteinuria, nephrosis and hepatic toxicity may occur. Oral ketoconazole 6 mg/kg/day given in divided doses every 12 to 24 hours (Nelson 1991) has been shown to be a safe alternative (Gan et al. 1987; Martin-Roig et al. 1988; Tanz 1985). All oral therapy often does require at least 6 weeks. Patients should be reevaluated after 3 or 4 weeks of therapy to ensure compliance and safety. In addition, application of a 2.5% selenium sulfide shampoo may decrease spore shedding and therefore help curb the spread (Allen et al. 1982). Furthermore, tinea capitis that is complicated by kerion formation may heal more rapidly if oral prednisone is given in a dose of I to 2 mg/kg/day for 2 weeks (Frieden 1987). 1.2 Tinea Pedis 1.2.1 Presentation and Diagnosis Tinea pedis is infrequently seen in preadolescents. It increases in frequency with age and is more frequently seen in men than women. Its distribu-
677
tion is worldwide and is primarily seen in people who wear shoes. Tinea manuum, a fungal infection of the palmar surface of the hands, is frequently seen in conjunction with tinea pedis. Tinea pedis is most frequently caused by T. rubrum and T. mentagrophytes. both of which are spread human to human. In addition, T. mentagrophytes can also be spread through rodent to human contact. These organisms proliferate in the stratum corneum by utilising the lipid present there. Characteristically, tinea pedis can present in a moccasin-like distribution in which there is dry scaling plantar skin extending up the sides of the feet. In addition, there may be involvement of the intertriginous areas of the feet which occasionally may lead to secondary bacterial infection 1.2.2 Treatment Topical agents in the form of cream or lotions are usually most appropriate for the treatment of tinea pedis. These agents include c1otrimazole, miconazole, haloprogin, and econazole. Application of these antifungal agents is usually twice a day until clear (Peter et al. 1991). If there is a large amount of oozing from the lesions, topical astringents such as aluminium acetate solution (Burow's solution) will be helpful. Wearing heavy cotton socks with frequent changes may aid fungal eradication. Resistant cases may respond to oral griseofulvin, and if there is an id reaction to the infection, oral prednisone I mg/kg/day may prove beneficial (Caravati et al. 1976). 1.3 Tinea Corporis 1.3.1 Presentation and Diagnosis Tinea corporis, also referred to as ringworm, has a worldwide distribution but is more commonly found in hot, humid climates. It occurs in both males and females of all ages. Transmission has been reported from human to human, animal to human and from inanimate objects. The fungi responsible for this form of tinea include Microsporum. Trichophyton. and Epidermophyton spp. This infection may be asymptomatic. When symptomatic it typically presents as a character-
678
Drugs 43 (5) 1992
may be helpful, but false-negative microscopic examinations can occur.
Fig. 6. Tinea corporis caused by M. audouinii.
istic pruritic annular plaque (fig. 6). Scaling, crusting, vesicule formation and papules on non-hairy skin may be present (Caputo 1986). 1.3.2 Treatment Tinea corporis usually responds to topical treatment with agents such as haloprogin, clotrimazole, miconazole or econazole, applied twice daily for 2 to 4 weeks (Peter et al. 1991). The application of topical steroids to the lesions should be avoided, since this may result in the formation of multicentric, large ringed lesions that have advancing borders (Caputo 1986). 1.4 Tinea Cruris 1.4.1 Presentation and Diagnosis Tinea cruris is a dermatophyte infection of the groin and thighs, more common in males than in females. The disease is more likely to recur if moisture, trauma or occlusion are present. Predisposing factors include obesity, and tight-fitting pants, pantyhose, athletic supports, and wet swimsuits. Organisms frequently causing tinea cruris include E. floccasum, T. mentagrophytes and T. rubrum. Erythrasma, which is colonisation of the affected area with Corynebacterium minutissimum, may mimic tinea cruris. However, under Wood's light erythrasma will fluoresce a bright red (Tunnessen 1985). Laboratory confirmation of the clinical diagnosis is best made by fungal culture. Potassium hydroxide preparation and microscopic examination
1.4.2 Treatment Treatment of tinea cruris generally consists of topical agents such as miconazole or clotrimazole as a lotion gently rubbed into the affected areas twice daily for 3 to,4 weeks, or topical ketoconazole once daily. Loose-fitting cotton undergarments and good hygiene are important in successfully treating this infection. Oral griseofulvin may be needed in unresponsive cases (Peter et al. 1991). 1.5 Tinea Unguium 1.5.1 Presentation and Diagnosis Tinea unguium is a dermatophyte infection of the nail. If the nail plate is directly invaded the term used to describe the infection is leuconychia mycotia. Conversely, if the nail bed is invaded first with secondary spread to the plate, it is called subungual dermatophytosis. Most cases of tinea unguium are associated with tinea pedis or tinea manuum and are usually found in adults. Clinical findings include nail discolouration, subungual hyperkeratosis, and separation of the nail from the be'd. As the infection progresses the plate may become brittle and friable. 1.5.2 Treatment Systemic therapy with either ketoconazole or griseofulvin is acceptable for 3 to 4 weeks. Griseofulvin is still accepted as the drug of choice, with ketoconazole usually reserved for those cases not responsive to griseofulvin. Topical agents do not appear to be effective (Fitzpatrick et al. 1987).
2. Tinea Versicolor Infection 2.1 Presentation and Diagnosis Tinea versicolor is a superficial fungal infection which is sometimes confused with other dermatological disorders such as pityriasis alba, secondary syphilis, and vitiligo. Predisposing factors include excessive sweating, malnutrition, chronic illnesses, immunosuppression, and a warm en-
Superficial Fungal Infections
Fig. 7. Tinea versicolor caused by Malassezia /wfur.
vironment. This infection is a mycotic invasion of the stratum corneum by the lipophylic, dimorphic yeast Malassezia furfur. This yeast, also known as Pityrosporum orbiculare, is believed to be a skin saprophyte that normally colonises the hair follicle. After converting to its mycelial form it spreads into the superficial dermal layers, resulting in the appearance of a rash. As with many other superficial skin infections the organisms, be they bacteria or fungi, may reside on the skin on some patients without causing disease. Why some otherwise healthy patients develop symptomatic infection and others do not, may relate to the integrity of the skin, i.e. small breaks in the skin may allow for invasion and disease. It is not clear what other factors are involved. Tinea versicolor is commonly seen on the head and neck as small oval or round hyper- or hypopigmented patches (fig. 7). In children the rash may be seen on the face as well. The patches may be covered with a fine scale. Diagnosis is aided by Wood's light examination which will demonstrate the typical yellow-orange fluorescence. Potassium hydroxide preparation for microscopic examination is also useful; culture is rarely necessary for diagnosis. 2.2 Treatment Treatment options include shampoos and topical antifungal agents; systemic therapy is rarely required. Selenium sulfide shampoo is usually applied to the affected area daily for 10 to 15 minutes for 7 to 14 days. In warmer, humid weather the
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application may need to be repeated biweekly to prevent recurrences. It should be remembered that abnormalities in pigmentation will resolve slowly over several weeks even after fungal colonisationhas been eradicated. More frequent or prolonged application of treatment will not hasten the resolution of the pigmentation abnormality (Friedman 1990). Topical sodium thiosulfate 25% solution, to 1naftate, halprogin, miconazole and clotrimazole can also be used, although the latter agents may be expensive. In more difficult cases, oral agents may be necessary. Ketoconazole once a day for 2 to 4 weeks is effective, but the potential hepatotoxicity must be considered. Griseofulvin does not appear to be effective for tinea versicolor (Stein 1983).
3. Candida Skin Infections 3.1 Presentation and Diagnosis Candida skin rashes occur at all ages, but they are most commonly manifested as diaper dermatitis in infants. Although there are at least 80 species of Candida. the vast majority of human disease is due to Candida albicans. C. albicans colonises the gastrointestinal tract, the vagina and the skin, and it is at these sites that most infection occurs. Oral infections with C. albicans are common in infants. Passage of the yeast through the intestine can result in seeding to the perineum, which can give rise to diaper dermatitis. If the perineum is moist and somewhat macerated, this creates an environment conducive to the development of Candida dermatitis. Candidal diaper dermatitis usually appears as bright red confluent patches with well demarcated serpiginous borders. Satellite lesions are frequently present. The inguinal folds are often involved. Perleche, also known as candidal angular cheilitis, results from Candida infection and presents as erythematous, macerated corners of the mouth. Indeed there is usually some degree of maceration of the angle of the mouth as a predisposing factor. Children and adults who wear braces on their teeth are predisposed to this as the braces distort the an-
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Table I. Treatment of superficial fungal infections Disease
Organism
Treatment
Tinea capitis or barbae
M. canis, T. tonsurani, others
Griseofulvin 10-20 mg/kg/d PO (max 1 g/day) or Ketoconazole 3-4 mg/kg/d PO (max 1.6 g/day) plus selenium sulfide 2.5% for 10 min twice weekly plus Prednisone 1 mg/kg/day PO
Tinea corporis
T. rubrum, Microspora, Epidermophyton spp.
Topical miconazole, haloprogin, clotrimazole or tolnaftate bid or Topical ketoconazole qd or Griseofulvin 10-20 mg/kg/day PO (max 1 g/day) for 4w in unresponsive cases
Tinea pedis, manuum or cruris
Microspora, Epidermophyton, Trichophyton spp. Trichophyton, Epidermophyton spp.
Topical clotrimazole, haloprogin, miconazole or econazole bid or Topical ketoconazole or sulconazole qd or Aluminium acetate solution or Griseofulvin 10-20 mg/kg/day PO (max 1 g/day)
Tinea versicolor
Malassezia furfur
Topical selenium sulfide 2.5% for 1-2w or Topical sodium thiosulfate 25% bid for 2-4w or Topical ketoconazole or sulconazole
with kerions
Abbreviations: d
= day; w = wee\
