Superficial Fungal Infections

Abstract

Superficial fungal infections are often mistaken for other common diseases, and the epidemiology of tinea capitis has changed, requiring adaptation in diagnostic techniques.After completing this article, readers should be able to:Infections caused by pathogenic fungi and limited to the human hair, nails, epidermis, and mucosa are referred to as superficial fungal infections. Despite the fact that these infections rarely are dangerous or life threatening, they are important because of their worldwide distribution, frequency, person-to-person transmission, and morbidity. Furthermore, particularly severe infections or those refractory to treatment may be the first indication of an underlying immunodeficiency.Dermatophytosis (tinea or ringworm), pityriasis versicolor (formerly tinea versicolor), and candidiasis (moniliasis) are the three most common types of superficial fungal infections. The dermatophytes are a large group of related fungi that can infect human skin, hair, and nails; they are found in soil (geophilic organisms), on animals (zoophilic), and on humans (anthropophilic). These fungi require keratin for growth and, therefore, they are unable to infect mucosal surfaces. These fungi are found all over the world, although the specific species, and subsequent clinical presentation, vary from region to region.Dermatophytosis is labeled by the involved area of the body (eg, tinea corporis, tinea capitis¸ tinea pedis, tinea unguium). Pityriasis versicolor is caused by the yeast form of a dimorphic fungus that is considered part of the normal human skin flora. Candidiasis is caused by a yeast-like fungus of the genus Candida (most commonly C albicans) that is part of the microflora in the human gastrointestinal tract (including the mouth) and the vagina. Symptoms and signs of candidiasis manifest with a change in the normal host immune system.This article will review a practical approach to the diagnosis and treatment of dermatophytosis, pityriasis versicolor, and other common diseases that often are mistaken for a superficial fungal infection. Candidiasis will not be discussed further in this review. Tinea capitis will be reviewed in detail because of its high incidence in children, need for systemic therapy, and potential for significant morbidity (particularly scarring alopecia).Many clinicians diagnose and treat superficial fungal infections based on clinical presentation alone. However, there are many infectious and noninfectious disorders that can mimic fungal infections. Microscopic confirmation of a dermatophyte or yeast infection is quick and painless and can be reassuring to the patient and parent. Proof of infection by fungal culture is recommended when prolonged systemic antifungal therapy is considered, especially with cases of tinea capitis and onychomycosis.The Wood lamp has been used in dermatology since 1925. It emits long wavelength ultraviolet radiation and can be helpful to the pediatrician for diagnosing a wide variety of dermatologic conditions (Table 1), including tinea capitis and pityriasis versicolor. However, in the United States, a change in the epidemiology of tinea capitis has rendered this technique nearly obsolete for diagnosing this disorder. Tinea capitis in North America is caused predominately by Trichophyton sp and is an endothrix infection. The spores (arthroconidia) exist within the hair shaft in an endothrix infection and, therefore, do not fluoresce under ultraviolet light.Ectothrix infection (usually caused by Microsporum sp), by contrast, has arthroconidia on the outer surface of the hairs and fluoresces a brilliant green with a Wood lamp examination. Microsporum is the most common cause of tinea capitis in many parts of the world (Fig 1). Thus, a hand-held Wood lamp will be useful to the pediatrician practicing in Brazil, central and eastern Europe, Asia, Africa, and Australia.Favus, a rare chronic form of tinea capitis caused by T schoenleinii, will fluoresce a pale green with examination under a Wood lamp. Dermatophyte and Candida infections limited to the skin do not display fluorescence with ultraviolet light. However, tinea cruris and Candida intertrigo can be confused easily with erythrasma. Erythrasma is a bacterial infection caused by Corynebacterium minutissimum, which fluoresces a brilliant coral red when examined with a Wood lamp. This examination also can be helpful in diagnosing pityriasis versicolor. The organism, Malassezia furfur, produces a pale yellow to white fluorescence with a Wood lamp.Microscopic confirmation of a fungal infection is extremely helpful in diagnosing suspected dermatophytosis, pityriasis versicolor, and Candida infection. Superficial scraping or clippings from skin, nails, subungual debris, or hair can be prepared on a slide with potassium hydroxide (KOH) for microscopic review. The KOH destroys the squamous cells without affecting the fungal elements. Skin scraping often is performed with a No. 15 scalpel blade in adults; I prefer to use the edge of a glass slide in children. A thin layer of material is placed on a glass slide and a coverslip is applied. A few drops of 10% to 20% KOH are applied until the area under the coverslip is filled. Gentle heating of the slide will accelerate the destruction of the squamous cells.Gentle pressure applied to the coverslip prior to visualization will help with layering of the fungal elements and remove trapped air. Low-power visualization with a dimmed condenser will reveal branching hyphae with septations when there is a dermatophyte infection. The KOH preparation in a patient with pityriasis versicolor will reveal short hyphae and clusters of spores, often described as a “spaghetti and meatballs” pattern.Fungal culture is the gold standard technique for diagnosing dermatophytosis. Culture usually is unnecessary except in cases of tinea capitis and onychomycosis. Positive results often take 7 to 14 days to develop, and the test is expensive. The sample is placed in a fungal culture media (eg, Sabouraud dextrose agar or Dermatophyte Test Medium) that contain antimicrobials to prevent the growth of saprophytic fungi and bacteria. Samples in suspected tinea capitis are obtained most easily with a tap water–moistened cotton swab rubbed vigorously over the scalp. This technique has proved to be reliable and is much more tolerable for a young child than the traditional hair plucking technique. (1) In suspected onychomycosis, material should be obtained from nail clippings and scraping under the nail.Tinea capitis is the most common superficial fungal infection in North America. In the United States, disease prevalence among inner-city school-age children is 3% to 8%. (2) This infection mainly affects young children (ages 3 to 9 years), although adults are known to be frequent asymptomatic carriers of the dermatophyte. Tinea capitis is more common with crowded living conditions and low socioeconomic and urban settings and in African American children. The prevalence of this disease varies considerably around the world (eg, <1% in Madrid and Palestine to greater than 50% in Ethiopia, where Trichophyton violaceum is endemic). (3)In North America, the epidemiology of this disease has changed dramatically in the past 50 years. Ectothrix infections in the United States with M canis (zoophilic) and M audouinii (anthropophilic) have essentially been eradicated and replaced with the endothrix, anthropophilic dermatophyte T tonsurans. Recent studies in the United States and Canada show that tinea capitis is caused by Trichophyton sp in more than 95% of cases, with T tonsurans the most common species by far. A similar pattern has been noted in Ireland and the United Kingdom.The worldwide incidence of this disease has increased in the past 30 years. Zoophilic organisms, particularly M canis, continue to be a common cause of tinea capitis in South America, central and eastern Europe, the Middle East, Russia, China, and Australia. Only nine of the more than 40 known dermatophyte species are responsible for tinea capitis infections. Within a particular country or region, this disease is caused by only one, two, or three dermatophyte species. Furthermore, species of Epidermophyton (a common cause of tinea corporis) do not appear to infect the hair shaft.Local knowledge of the epidemiology of tinea capitis will help pediatricians who are practicing in international health locales (Fig 1). This knowledge is helpful because the choice of systemic antifungal therapy may be different between Trichophyton-predominant and Microsporum-predominant regions.Tinea capitis is transmitted commonly by indirect contact with fallen hair and epithelial cells. Direct head-to-head transmission among children is thought to be considerably less common. Transmission of dermatophytes from hair brushes, combs, and shared hats also is common. Trichophyton and Microsporum have been isolated from barbershop instruments, combs, hair brushes, bedding, clothing, furniture, theater seats, and towels. Co-sleeping has been associated with the spread of tinea capitis. M canis has been found to be transmitted to humans by both dogs and cats. Rodent pets, especially guinea pigs, may occasionally transmit M canis to humans.Stray cats are thought to be the most important reservoir for M canis infection in urban environments outside of North America. For example, a 2004 Italian study found that 10% of dogs and 28% of cats with a skin condition were infected with a dermatophyte (M canis was the most common isolate in both animal groups). (4) Farmers have a unique exposure to T verrucosum (zoophilic, from cattle) and M gypseum (geophilic), both of which can cause tinea capitis.The presence of asymptomatic carriage among family members is common and of unclear significance. A study done in South London that screened household contacts of patients with tinea capitis caused by T tonsurans found that 44% had asymptomatic carriage of the dermatophyte. (5) Current guidelines do not recommend the routine screening of family members for the presence of dermatophyte carriage.Tinea capitis can present with a wide variety of clinical patterns (Table 2; Figs 2–6). An individual may have one, a few, or many of the following features: alopecia, scale, erythema, pustules, “black dots,” tenderness, pruritus, and lymphadenopathy (suboccipital or cervical). Because of the variability of these features, the differential diagnosis of tinea capitis is broad and case specific.Two US studies have examined the frequency of clinical symptoms and signs in symptomatic children with culture-proved tinea capitis (Table 3). The table shows the prevalence of symptoms or signs in culture-positive groups. Both studies were convenience samples of outpatient children with suspected tinea capitis.Hubbard (6) found that the presence of occipital or posterior auricular lymphadenopathy was predictive of culture-proved T tonsurans infection (positive likelihood ratio = 7.5). In this study, all children with adenopathy and alopecia (100%) and nearly all children with adenopathy and scaling (97%) had cultures confirming T tonsurans infection. Conversely, no child without adenopathy and scaling (0%) and only one child without adenopathy and alopecia (6%) had cultures positive for dermatophytosis. Hubbard concluded that posterior auricular adenopathy in combination with pruritus, scaling, or alopecia was highly predictive of culture-proved tinea capitis.Lorch Dauk et al (2) also found that of the symptoms and signs they studied, occipital adenopathy was the most predictive of culture-proved tinea capitis (positive predictive value = 84%). This study included children with kerion, who are known to have a high false-negative rate for culture-proved disease. Both Hubbard (6) and Lorch Dauk et al (2) concluded that prescribing empiric therapy for tinea capitis was a reasonable approach in an urban setting when presented with a child demonstrating scaling, alopecia, or pruritus associated with adenopathy (occipital or posterior auricular).In a 2005 study of 300 nonselected and largely asymptomatic children, Williams et al (7) found that both lymphadenopathy and scalp scaling are common (53% and 22%, respectively) in the pediatric population. Of the 38 children with both scalp scaling and head or neck lymphadenopathy, only four (11%) had culture-proved dermatophyte infection. Seborrheic dermatitis and atopic dermatitis were the most frequent diagnoses associated with scalp scaling and head/neck lymphadenopathy in this study. The authors conclude that scaling of the scalp and head/neck lymphadenopathy are not specific for tinea capitis in the general (and mostly asymptomatic) pediatric population. However, how this information should be applied to the child who presents to the physician with scalp complaints associated with scaling and significant posterior lymphadenopathy is unclear.Many authors argue that in all cases of suspected tinea capitis, the presence of a dermatophyte should be confirmed by microscopy or culture before starting a prolonged course of systemic therapy. (8)(9)(10) A sample for a KOH preparation can be obtained from a cooperative child using a blunt scalpel or edge of a glass slide. Wiping the area with an alcohol swab may help the material adhere to the scalpel or slide. Alternatively, a toothbrush can be used to collect scale and involved hair.In the United States, one would expect to find spores (arthroconidia) within the hair shaft typical of T tonsurans infection. Microscopy is the quickest and most inexpensive way to confirm the presence of a dermatophyte. However, KOH preps have a high false-negative rate when performed by inexperienced examiners. As mentioned, culturing the scalp can be done with a moist cotton swab. Culture is more sensitive than a KOH prep and less time intensive for the pediatrician, and it does not require the use of an office microscope. However, false-negative cultures do occur, particularly in the setting of a kerion. The culture may take several weeks to become positive and can be costly ($60–$100). (2)There appears to be no clear standard of care in the United States regarding the diagnosis of tinea capitis. A young child presenting with pruritus, scale, or alopecia of the scalp associated with occipital or posterior auricular adenopathy can be treated reasonably with empiric therapy for tinea capitis. With no adenopathy, a dermatophyte infection is less likely and a confirmatory test is prudent before starting therapy. Similarly, when faced with an empiric treatment failure, a fungal culture should be obtained to identify the presence of a dermatophyte and the specific species.Tinea capitis requires systemic antifungal therapy for effective treatment because the dermatophyte is found at the hair follicle root and is not accessible by topical treatments. However, adjunctive topical therapy can decrease transmissibility and improve the mycologic cure rate; see table 4 for dosing of systemic and adjunctive topical therapies. For more than 50 years, griseofulvin has been the treatment of choice for tinea capitis worldwide. This drug has proved to be safe, effective, and relatively well tolerated by children. The availability of griseofulvin has been a major factor in the dramatic reduction of zoophilic dermatophytosis (Microsporum sp) found in North America. However, its effectiveness against anthropophilic organisms, in particular T tonsurans, has waned in recent years.This resistance and the need for a prolonged course of therapy have prompted significant interest in alternative, shorter-course treatment options for tinea capitis. Currently, two systemic antifungal agents have been approved by the Food and Drug Administration (FDA) for the treatment of tinea capitis in children: griseofulvin and terbinafine. In addition, there is considerable evidence that itraconazole and fluconazole are effective and safe therapeutic options for children with tinea capitis.Griseofulvin was first isolated from the mold Penicillium griseofulvin in 1939. The first successful treatment of a superficial fungal infection by griseofulvin in humans was reported in 1958. The drug is active against all common dermatophytes, including Trichophyton, Microsporum, and Epidermophyton spp. Griseofulvin has no effect on bacteria, Candida, M furfur, Aspergillus, and other fungi.Griseofulvin is fungicidal in vitro, but its clinical effect in children and adults with dermatophytosis is fungistatic. This finding is explained by the fact that griseofulvin cannot diffuse into the stratum corneum or hair follicle. Rather, it is absorbed into the keratin precursor cells and prevents the growth of dermatophytes as these cells migrate toward the surface of the skin. Thus, the infection cannot be eradicated until the dermatophyte-infected keratin layers have grown out.Griseofulvin is a mitotic inhibitor and interferes with nucleic acid, protein, and cell well synthesis of replicating dermatophyte cells. There is evidence also that griseofulvin has an anti-inflammatory effect, (11) which is unique among the systemic antifungal agents. Dermatophyte resistance to griseofulvin has been demonstrated, but its frequency and clinical significance are unclear.Recent treatment failures and concerns about increasing resistance (especially in T tonsurans infection) have lead most experts to recommend higher doses of griseofulvin (20 to 25 mg/kg/d vs 11 mg/kg/d) and longer treatment courses (6 to 12 weeks vs 4 to 6 weeks) than in the past. In general, Microsporum infections require a longer treatment course for clinical and mycologic cure than do Trichophyton infections. This difference in course applies to the use of all systemic antifungal agents. Many authors recommend that treatment be continued until mycologic cure is proved. This approach is an expensive and inefficient approach. A more practical approach is to continue griseofulvin therapy for 2 weeks after the symptoms and signs of tinea capitis have resolved. (12) This strategy is endorsed by the American Academy of Pediatrics (AAP).Griseofulvin is not soluble in water and is poorly and variably absorbed from the gastrointestinal tract. Taking the medication with a high-fat meal (eg, whole milk, peanut butter) can significantly improve absorption and double peak serum levels. (11) Absorption is also enhanced by microsizing the formulation, creating microcrystalline griseofulvin, which is available in a suspension for accurate dosing in children. An ultracrystalline formulation increases absorption further and therefore requires a smaller total dose (10 to 15 mg/kg/d). However, this formulation is not available as a suspension, limiting its use in children. All formulations of griseofulvin are given as a once-daily dose. When prescribed at the recommended higher doses and longer courses, griseofulvin continues to be effective for tinea capitis. A recent extensive review quoted mycologic cure rates of 80% to 95% and effective therapy rates of 88% to 100% for griseofulvin. (12) The effective cure rate for griseofulvin, defined as a “negative culture ± negative KOH preparation and few remaining visual signs of infection,” was found to be 73.4% in a recent meta-analysis of seven studies. (12) Importantly, in this study, griseofulvin had a higher effective cure rate when used to treat Microsporum (88.1%) versus Trichophyton (67.9%) infections.Griseofulvin is a safe medication even when prescribed for extended periods of time. Adverse effects generally are mild but not uncommon and include nausea, headache (up to 15%), urticaria, and other rashes. Typically, adverse effects are not severe enough to require discontinuation of the therapy. Life-threatening effects are extremely rare but include Stevens-Johnson syndrome, toxic epidermal necrolysis, and fatal hepatotoxicity. Griseofulvin can induce photosensitivity and photodermatitis.Griseofulvin is contraindicated in pregnancy and in patients who have hepatocellular failure or porphyria. Potential for cross-sensitivity exists in patients who have demonstrated hypersensitivity to penicillin. Griseofulvin may decrease the effectiveness of oral contraceptives. In addition, the manufacturer recommends that women wait at least 1month after griseofulvin therapy before becoming pregnant. Men should wait 6 months after completing therapy before fathering a child.Baseline laboratory tests are unnecessary in children or adults who do not have a history of or evidence of liver disease. The manufacturer recommends “periodic hematologic, hepatic, and renal function tests … in patients on long-term therapy.” If griseofulvin treatment is required for longer than 8 weeks, laboratory testing with a complete blood count and levels of liver transaminases, bilirubin, blood urea nitrogen, and creatinine is recommended. Therapy should be discontinued if evidence of drug toxicity is found. Griseofulvin is FDA-approved for the treatment of dermatophytoses in children (2 years and older) and adults.In 2007, terbinafine became the second FDA-approved drug to treat tinea capitis in children. The drug is an allylamine whose antifungal effect is due to inhibition of squalene epoxidase. This effect leads to decreased synthesis of ergosterol in fungal cell membranes (fungistatic effect) and accumulation of squalene (fungicidal effect). Terbinafine is fungicidal against both Trichophyton and Microsporum spp in vitro. It is highly lipophilic and accumulates in both fat and skin. Terbinafine remains in the stratum corneum above inhibitory levels for 2 months after discontinuation of the drug. The drug is metabolized in the liver and excreted largely in the urine. It can be given once daily.There is good evidence that terbinafine is at least as effective as griseofulvin for tinea capitis caused by T tonsurans. A recent large multicenter international trial showed better clinical (63% vs 55%) and mycologic (62% vs 47%) cure rates with terbinafine vs griseofulvin in children in the United States. (13) However, the dose of griseofulvin used in these studies was less than standard dose used today in the United States. By contrast, effective cure rates are higher for griseofulvin vs terbinafine in children with tinea capitis caused by Microsporum spp. Thus, griseofulvin is considered the first-line systemic therapy for tinea capitis caused by Microsporum spp.Terbinafine, overall, appears to be a very safe drug. A history of allergic reaction to terbinafine is the only contraindication. It is not recommended in patients with chronic or active liver disease. Pretreatment testing of liver transaminases is recommended for all patients. Common adverse effects are nasopharyngitis (10%), headache (7% to 12%), vomiting (5%), and rash (6%). Rare but serious effects include liver failure (1 in 120,000), severe and prolonged disturbance of taste or smell, depression, Stevens-Johnson syndrome, exacerbation of systemic lupus erythematosus, and deceased absolute lymphocyte count. Terbinafine can increase the serum levels of tricyclic antidepressants, selective serotonin reuptake inhibitors, and β-blockers.Terbinafine is approved for the treatment of tinea capitis in children 4 years and older. It is dispensed in individual packets containing 125 mg or 187.5 mg oral granules. The parent should sprinkle the entire content of the packet on a spoonful of nonacidic soft food such as pudding, mashed potatoes, or ice cream. Applesauce or fruit-based foods should not be used. The child should swallow the spoonful without chewing. Recommended length of treatment is 6 weeks. Longer courses may be required with Microsporum infections. A complete blood count with differential should be checked during treatment courses longer than 6 weeks.Fluconazole is a broad-spectrum triazole fungistatic agent that inhibits the production of ergosterol in fungi. The drug is not approved by the FDA for use in patients with dermatophytosis. It is, however, approved for use in children with systemic fungal infection (eg, Candida sp and Cryptococcus).A number of small studies have demonstrated that fluconazole is effective in the treatment of tinea capitis. Gupta et al found that 2 to 3 weeks of daily fluconazole (6 mg/kg) in children resulted in high clinical and mycologic cure rates at a 12 week follow-up visit (90% and 86% respectively). (8) Similarly, Gupta and his colleagues found that once weekly fluconazole (8mg/kg) administered for 8 to 16 weeks produced complete cure (mycologic and clinical) in 98% of children with tinea capitis. In the subgroup with T tonsurans infection, all were cured at 8 weeks. (14)A study conducted in Iran found that children with tinea capitis caused by Trichophyton or Microsporum infection had identical cure rates when treated with daily fluconazole (5 mg/kg) for 4 weeks versus griseofulvin (15 mg/kg/d) for 6 weeks. At 8 weeks, cure rates were 76% and 78%, respectively. (15) A large multicenter randomized controlled trial found that treatment of tinea capitis with 6 weeks of fluconazole 6 mg/kg/d or low-dose griseofulvin (11 mg/kg/d) produced comparable, but low, clinical and mycologic cure rates (successful treatment 54% vs 57% at week 10). (16)Fluconazole, in contrast to other azole antifungals, is very water soluble and, therefore, has excellent bioavailability when taken orally. Fluconazole use is contraindicated in combination with astemizole and terfenadine, both of which have been removed from the US market due to severe adverse effects. The drug is not recommended in patients with liver disease or renal dysfunction or in combination with erythromycin. The FDA considers fluconazole a pregnancy category D medication except for single low-dose therapy for vaginal candidiasis (category C). Adverse effects are less common with fluconazole than with the other systemic antifungals: nausea (4%), vomiting (2%), abdominal pain (2%), diarrhea (2%), headache (2%), and rash (2%). Rare but serious reactions include hepatic failure, anaphylaxis, torsade de pointes, QT prolongation, seizures, exfoliative dermatitis, and agranulocytosis.The major drawback of fluconazole is its potential for drug interactions with many different medications. Commonly used pediatric medications that may interact with fluconazole are alprazolam, amitriptyline, chloral hydrate, cimetidine, citalopram, clarithromycin, and ergotamine. Fluconazole is available in both tablets and oral solution. Pretreatment testing of complete blood count, renal function, and liver function is suggested by some authors.Itraconazole, like fluconazole, is a triazole and exerts its fungistatic effect by inducing ergosterol deficiency. The drug has an extremely broad spectrum of activity against fungi, including Aspergillus and dermatophytes. It is not FDA approved for any indication in children. However, a few studies have shown that itraconazole is as efficacious as terbinafine and griseofulvin in children with tinea capitis. It is contraindicated in patients with congestive heart failure. As with fluconazole, there are many drug-drug interactions with itraconazole. Pretreatment liver function tests should be ordered for all patients. Mild adverse effects are similar to, but more frequent than, adverse effects reported with fluconazole. Rare but serious and life-threatening reactions can occur. Itraconazole is available as capsules or oral solution.Ketoconazole is an imidazole having mainly fungistatic activity against Trichophyton sp. The drug is ineffective against Microsporum. It has been studied in children with tinea capitis and its effectiveness is comparable to griseofulvin in children with infections caused by T tonsurans. However, the risk of hepatotoxicity is unacceptably high with long-term use in children for this indication, given the availability of less toxic and more efficacious alternative medications. Systemic ketoconazole should not be used to treat children with tinea capitis. However, ketoconazole shampoo is a useful and safe adjunct treatment for children with tinea capitis.Topical agents alone are not adequate for the treatment of tinea capitis. However, sporicidal shampoos have been found to reduce the carriage of viable spores and may reduce the risk of transmission in the early stages of systemic therapy. (9) Topical therapy also may shorten and improve the mycologic cure rate in conjunction with oral agents. Selenium sulfide (1% and 2.5%) and ketoconazole (2%) are the best studied shampoos for this indication. There is no proven advantage of the prescription strength (2.5%) selenium sulfide over the 1% formulation, which is available over-the-counter.A recent study of children in the United States found ciclopirox shampoo 1% to be as effective as selenium sulfide when used to treat tinea capitis along with oral griseofulvin. Other experts have recommended zinc pyrithione (1% and 2%) and povidone-iodine (2.5%) shampoo. Sporicidal shampoos may aid also in the physical removal of adherent infected scales from the scalp. All shampoos should be applied for 5 minutes 2 or 3 times weekly for 2 to 4 weeks.Virtually all experts and practice guidelines recommend allowing children with tinea capitis to return to school once they have started appropriate systemic and topical treatment. However, children should not be allowed to share headgear (eg, baseball helmets) or participate in sports with scalp-to-scalp contact (eg, wrestling) until they are cured. Personal items (eg, combs, brushes, scissors, hats) should be disinfected with bleach. Bedding (pillow cases, sheets) should be washed in hot water with or without bleach. In the rare child in the United States who had M canis infection, the family pet (cat, dog, guinea pig) is the likely source of the infection and should be evaluated by a veterinarian. Anthropophilic species such as T tonsurans are more contagious than zoophilic species. A US