Current Status of the Identification and Management of Tinea Capitis

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Current

Status

of the Identification

and

Management

of Tinea

Capitis

Daniel

P. Krowchuk,

MD, Anne

W. Lucky,

MD, Susan

I. Primmer,

MD,

and Joseph

McGuire,

MD

From the Departments of Dermatology and Pediatrics, Yale University School of Medicine, New Haven, Connecticut

ABSTRACT. Tinea capitis due to Trichophyton tonsurans

has become a significant health problem affecting

chil-dren and adolescents. This infection has several different

distinctive clinical patterns which, if not recognized, may

result in delayed diagnosis and therapy. This review is

designed to emphasize the differences between tinea

cap-itis caused by T tonsurans and that caused by other organisms. Current diagnostic and therapeutic measures are discussed. Pediatrics 1983;72:625-631; Trichophyton tonsurans, tinea capitis, scalp, Microsporum.

Tinea capitis, a common disorder in the pediatric

age group, may affect up to 10% to 20% of the

population during epidemics.13 The emergence of

Trichophyton tonsurans as the organism predomi-nantly responsible for this infection has resulted in a clinical pattern not previously described with

Microsporum sp infection.4’5 Our experience in the

Pediatric and Dermatology Clinics at the Yale-New

Haven

Medical

Center

seemed

to indicate

an

in-crease

in the

number

of children

affected

by this

disease. If this is true for other areas of the country,

one may expect that those who provide primary

care for children will observe a similar trend. This discussion is limited to tinea capitis caused by T

tonsurans and how the expression of this infection

differs from tinea capitis caused by Microsporum sp.

DEFINITIONS

Tinea is the general term used to describe an

infection by any of the keratinophilic fungi known

Received for publication Oct 14, 1982; accepted Feb 2, 1983. Reprint requests to (A.W.L.) Division of Pediatric Dermatology, The Children’s Hospital Medical Center, Elland and Bethesda Ayes, Cincinnati, OH 45229.

American Academy of Pediatrics.

as dermatophytes and is synonymous with

ring-worm. Dermatophytes exist in two forms: growing,

elongated hyphae and resting, compact spores. Ti-nea capitis refers to infection involving the scalp and hair shafts. Although a number of different

dermatophytes may cause tinea capitis, three

or-ganisms appear to be responsible for the majority

of disease in the United States: T tonsurans, M

audouini, and M canis. Tinea capitis is almost

exclusively a disease of children and adolescents with only 5% of cases occurring in adults. T ton-surans

appears

to be the

most

common

organism

responsible for adult infection.6

EPIDEMIOLOGY

Transmission of dermatophytic infection usually occurs between humans (anthropophilic) during ep-idemics (ie, T tonsurans and M audouini), or trans-mission is from animals to man (zoophilic) and is

sporadic in nature (ie, M canis).7 In the past 30 years, there has been a gradual shift in the role

played by various organisms responsible for

epi-demic tinea capitis in the United States. Studies

performed in South Carolina in the 1950s revealed

that more than 94% of infections were caused by

members of the genus Microsporum (Table 1). In

contrast, by the 1970s only 9.4% of infections were

caused by Microsporum sp while T tonsurans had

become

the

dominant

organism,

causing

90.6% of all cases.8 T tonsurans has been endemic in Puerto Rico and Mexico in the past, and it is postulated that its increasing incidence in the United States reflects population shifts and subsequent

infec-tion.”9 The shift from Microsporum to T tonsurans is more than an epidemiologic curiosity; the char-acteristics of infection by T tonsurans differ

consid-erably from those of disease caused by Microsporum sp (Table 2).

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ton-TABLE 1. Changing Epidemiology of Tinea Capitis In-fection*

1950-1954

Terreni (N = 278)

1954

Adams and

Riley

(N = 100)

1973-1978

Prevost

(N = 265)

Microsporum audouini canis pseum Trichopkvton tonsurans 96.7% 2.9% . .. 0.4% 50% 39% 5% 5% 9.4% ...

...

90.6%

* From Prevost.5

TABLE 2. Differences Between Trichophyton tonsur-ans and Microsporum Species Infection

T tonsurans Microsporum

-.

Sex predisposition M = F M > F

Racial predisposi- B > W B < W

tion

Natural history Chronic

infec-tion

Spontaneous

resolution at puberty

Age Children and

adults

Prepubertal

children

Alopecia Insidious,

dif-fuse

Well-defined

Fluorescence Absent Characteristic

(Wood’s lamp)

surans affects blacks far more commonly than

whites and is equally distributed between males and

females.H Many reports1”#{176}’5 have documented that infection by members of the genus Microsporum

resolve spontaneously and, in the case of M

au-douini, this often occurs at puberty. The natural

history of Trichophyton sp infection has not been as extensively studied. Although spontaneous cures

have been reported, infection may persist for

months, years, or decades in untreated individu-als.t’17

PATHOGENESIS/PATHOPHYSIOLOGY

The exact manner in which dermatophytic infec-tion of the scalp becomes established is not known. Fallen hairs, scale, and shared fomites (combs, brushes, hats) have been implicated in the trans-mission of fungal elements.7 Human inoculation

studies performed in the 1950s using Microsporum

sp have elucidated some features of tinea capitis. From the site of initial infection, hyphae spread in

a radial fashion and penetrate surrounding hair

follicles. The hyphae may then infect the

keratin-ized portions ofthe hair. During this process, spores are formed within the hair shaft (endothrix infec-tion) or on the surface of the hair shaft (ectothrix

infection))#{176}” Spore formation within the hair in

endothrix infection results in significant weakening

of the hair shaft with subsequent fracture of the

hair at the scalp line. The remnant of hair within the follicle is the so-called “black-dot,” the hallmark of infection by T tonsurans. Dermatophytes prefer actively growing (anagen) hairs; hence, resting (tel-ogen) hairs are relatively immune from infection.

The hair bulb is usually spared after eradication of infection, and hair regrowth usually occurs.

CLINICAL PRESENTATIONS

The clinical presentation of tinea capitis caused by T tonsurans varies substantially from that due

to Microsporum infection. Children with

Micros-porum tinea capitis often exhibit well-defined areas

of alopecia and the diagnosis is aided by hair shaft

fluorescence on exposure to ultraviolet light

(Wood’s lamp). T tonsurans tinea capitis does not fluoresce. In addition, T tonsurans tinea capitis is often more subtle in its appearance. Several pat-terns of infection may be observed.

Seborrheic

Patients with T. tonsurans tinea capitis may

complain of dandruff. The diffuse scaling and as-sociated pruritus may mimic atopic or seborrheic dermatitis of the scalp.18 Diffuse and progressive hair loss may occur after long-standing infection.

In Microsporum infections, well-circumscribed

pat-terns of hair loss are more typical. Fine, white scale

throughout the scalp of a 9-year-old girl with T

tonsurans infection is shown in Fig 1. There had

been slow, progressive, generalized hair loss over a

period

of months.

A more

subtle

presentation

with

only limited involvement of the scalp is shown in

Fig 2.

Black Dot

The black dot is the hallmark of infection by T

tonsurans (Fig 3). These hair remnants within the

follicular orifice may be the only manifestation of

fungal disease and may be hidden beneath scale.

The black dots may be few in number and difficult to find, but they are the most reliable source of material for diagnosis.

Kerion

Any patient with tinea capitis may develop a

kerion. Kerions are erythematous, boggy, tender

masses with perifollicular pustules which develop

rapidly on the scalp (Fig 4). They may be

accom-panied

by systemic

manifestations

including

fever,

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neutrophils and that bacterial cultures are sterile.19

Our experience is that secondary infection with

bacteria, especially Staphylococcus aureus is com-mon. Antibiotic treatment alone, however, does not result in resolution of the kerion.

Kerions represent an immune response to the

dermatophyte and often herald the resolution of

the infection. Rasmussen and Ahmed2#{176} found that

36 patients with noninflammatory tinea capitis had intradermal tests negative to trichoptiytin antigen

at 48 hours in contrast to 15/16 patients with

kerions who manifested delayed hypersensitivity reactions. This finding suggests that, in those pa-tients with kerions, cellular immunity was involved in kerion formation.

Patients with any of the forms of T tonsurans tinea capitis may concurrently exhibit tinea cor-poris, lesions of fungal infection elsewhere on the skin. Such lesions are circular or oval scaling

plaques with erythematous papular-pustular

bor-ders (Fig 5).

DIAGNOSIS

The Wood’s lamp (an ultraviolet or “black light” with a spectrum of 320 to 400 nm) has been a useful tool in the diagnosis of tinea capitis because mem-bers of the genus Microsporum produce substances that accumulate in infected hairs and fluoresce when exposed to ultraviolet light. Patients with

tinea capitis caused by Microsporum sp can be

rapidly and accurately examined for the presence of infection using this procedure. Unfortunately fluorescence is not a characteristic of T tonsurans,

and a Wood’s lamp examination is of no value in

the diagnosis of T tonsurans infection.

Specimens obtained from the scalp are useful for the diagnosis of tinea capitis. The black dot offers the highest yield for both potassium hydroxide

(KOH) preparation and fungal culture. Using a

magnifying glass, one may identify black dot hairs and remove them easily and painlessly using forceps or a needle. The small hair fragment is then trans-ferred to a glass slide for a KOH preparation or to appropriate media for fungal culture. Scale from the scalp may also be useful for diagnosis. This may

be obtained by gently scraping the scalp with a

glass slide or scalpel blade or by brushing vigorously with a sterile toothbrush. The material is collected on a glass slide or sterile Petri dish for subsequent

KOH preparation or transfer to culture medium.

Direct inoculation of toothbrush bristles onto agar may be useful.45’15 Although hairs long enough to

be pulled are not infected in T tonsurans tinea

capitis, spores or hyphae may be present at their base. Thus, several hairs pulled from the scalp in an area of scaling (using a small Kelly clamp that has the teeth covered with rubber tubing for greater

traction) may be useful for diagnostic purposes.

The KOH preparation is useful for the rapid

diagnosis of tinea capitis. The specimen is placed on a glass slide, one or two drops of a 10% to 209 solution of KOH is added and a coverslip applied.

The slide may be briefly heated over a flame or

allowed to remain at room temperature for 15 to 20 minutes. Either process allows the KOH to dissolve cellular material, leaving the hyphae and spores

more easily identifiable. Heating too vigorously will

result in crystallization of the KOH, thus making

interpretation more difficult. A black dot hair with intrapiliary hyphae and spores is shown in Fig 6. The endothrix hyphae of T tonsurans characteris-tically line up in parallel arrays within the hair shaft. The transverse septae produce compact, rec-tangular arthrospores. When densely infected, the hair shaft may be replaced by such spores.

Individ-ual spores, often in short chains, can be seen on

keratin debris obtained by scraping the scalp (Fig

7). Altering the focal plane of the microscope will

cause the fungal elements to appear alternately

refractile or blue-green.

Fungal culture provides a definitive diagnosis and

should be performed in all patients suspected of

having tinea capitis. Specimens employed in

cul-tures are identical with those used for the KOH

preparation: black dots, scale, and pulled hairs.

Specimens may be inoculated directly onto the me-dium or may be transported to the laboratory in a sterile Petri dish or between glass slides. Sabour-aud’s agar, containing chloramphenicol and

cyclo-heximide (Mycosel or Mycobiotic agar) which

re-duce the growth of bacteria and saprophytic fungi, is the medium of choice. Specimens are inoculated

onto the surface of the medium and the caps of

slant tubes are left loose to permit air entry. Growth generally occurs within 1 to 2 weeks at room

tern-perature and the fungus may be identified by

mi-croscopic examination of a fungal colony. A typical culture of T tonsurans on Mycobiotic agar is shown

in Fig 8. This demonstrates the buff-tan, folded,

suede surface and the deep brown pigmented

un-derside. Dermatophyte Test Medium (DTM)

con-tains antibiotics (gentamicin sulfate and chlortet-racycline HC1), an agent to control saprophytic fungi (cyclohexamide), and a phenol red indicator.

Growing dermatophytes produce alkaline

byprod-ucts which cause the medium to change from its

original yellow color to red.2’ This facilitates the identification of dermatophytes by nonmycologists but makes species identification more difficult. Be-cause some saprophytic fungi or bacteria may con-taminate the culture and produce a color change, false-positive reactions may occur. Such reactions are seen in approximately 3% ofall cultures.22

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Fig 2.

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Fig 3.

Fig 1. Seborrheic form of T tonsurans tinea capitis in 9-year-old black girl. Widespread areas of fine, white

adherent scale and diffuse hair loss are present.

Fig 2. More limited form of T tonsurans tinea capitis in 6-year-old male sibling of patient in Fig 1.

Fig 3. Characteristic “black dots” (arrows) of T tonsur-ans infection within areas of hair loss in this 3-year-old black girl. Each black dot represents an infected hair

,r

.

., ,..,.

r

. .

.

‘

..

ii F

h

shaft that has broken off at level of scalp surface.

Fig 4. Kerion, acute inflammatory reaction to scalp in-fection with T tonsurans, over occiput of 2-year-old black

boy. Lesion is tender, boggy, erythematous, oozing, and

crusted with numerous pustules. Regional

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Fig5. Fig 6.

1

Fig 7.

4’, - ,.

C- . . ,

Fig 8.

Fig 5. Girl with T tonsurans tinea capitis with irregular annular plaque with papular border and scaly surface characteristic of body ringworm (tinea corporis).

Fig 6. Photomicrograph of KOH preparation of black

dot showing elongated hyphae within shaft of infected hair (endothrix infection). Hair is beginning to dissolve because of 10% KOH. Each hypha is breaking up into characteristic arthrospores (x620).

Fig 7. Photomicrograph of KOH preparation of scalp

rapidly than saprophytic fungi, interpretation of

DTM cultures at 1 or 2 weeks may eliminate some

false-positive results.1#{176}

When the diagnosis of tinea capitis is made,

family members and close contacts should be

ex-amined. These individuals, although asymptomatic, may exhibit signs of early infection such as mild scaling of the scalp. Early recognition and therapy may reduce morbidity and decrease spread of infec-tion.

scale from patient with tinea capitis showing arthrospores of T tonsurans in chains, clumps, and as single elements (x620).

Fig 8. Fungal cultures of T torisurans grown at room temperature showing characteristic morphology. Top of colony (left) is tan to buff-colored with suede, folded surface whereas underside (right) exhibits brown pig-ment. Cultures are on slants of Sabouraud’s agar with cyclohexamide and chioramphenicol (Mycobiotic agar).

DIFFERENTIAL DIAGNOSIS

Scaling and pruritus of the scalp may be seen in disorders such as psoriasis and atopic or seborrheic dermatitis. Bacterial folliculitis with pustules and

inflammation may be confused with a kerion. In

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Morphea may also be seen with an isolated patch of alopecia. Finally, trichotillornania (compulsive hair pulling) also results in areas of alopecia a!-though the scalp itself is not affected.

THERAPY

Systemic griseofulvin is the drug of choice for the treatment of tinea capitis. Topical therapy alone is not curative. Griseofu!vin is active against all

spe-cies of Trichophvton and Microsporum and inhibits

funga! mitosis by disrupting the mitotic spindle. Because it does not affect the resting spores, the

drug is primarily fungistatic, although in actively

metabolizing hyphae it may prove fungicidal.

Gris-eofulvin is also reported to have a direct

anti-inflammatory activity although the mechanism of

this effect is not known.2t

Griseofu!vin is available in microsize and ultra-microsize forms. Use of the ultramicrosize prepa-ration allows the dose to be reduced by 50%, but there is no evidence of increased efficacy or fewer side effects. The dose is determined by the prepa-ration’s particle size and the patient’s body weight

(Table 3). A suspension containing 125 mg of the

microsize particle form in each 5 mL (Grifulvin V, Ortho Pharmaceutical Corp) is available for

pedi-atric use. Absorption of the drug is reported to

increase when the drug is given with a meal, partic-ularly one high in fat content.24’25 Although the optimal dosing schedule has not yet been

deter-mined, most manufacturers recommend daily

ad-ministration in single or divided doses. Some

stud-ies suggest that resolution of infection may be

achieved with less frequent administration.

How-ever, efficacy of a less frequent dose remains to be

confirmed in children with T tonsurans tinea

capi-tis. Most infections can be controlled with a dosage

of 10 mg/kg of body weight per day of the microsize

TABLE 3. Griseofulvin Preparations (1982)

Particle Size and Dose Products Available

Microsize Grifulvin V*_suspension

Child: 10 mg/kg/d 125 mg/5 mL, tablets

Adult: 500- 1,000 mg/d 250, 500 mg

Fulvicin-U/Ft-tablets

250, 500 mg

Grisactin-capsules 125,

250 mg; tablets 500 mg

Ultramicrosize Fulvicin P/Gt-tablets

Child: 5 mg/kg/d 165, 330 mg

Adult: 250-500 mg/d Grisactin Ultra-tablets 125, 250 mg

Gris-PEG-tablets 125,

250 mg

* Ortho Pharmaceutical Corp. 1 Schering Corp.

1:

Ayerst Laboratories.

§

Dorsey Laboratories.

preparation taken for a 6- to 8-week period. In

resistant cases, both the dose and the duration of therapy may be increased. Following initiation of therapy, patients should be seen at 3-week intervals to evaluate clinical progress. At each visit, a repeat fungal culture is performed; treatment is continued until a negative culture is obtained.

There are potential adverse effects associated with griseofulvin therapy. As many as 15% of adult

patients may experience headache, which is often reversible despite continued therapy. Rare hema-tologic alterations such as neutropenia and

leuko-penia have been observed although these have

sometimes resolved during the treatment course.

Hepatotoxic reactions have been recognized and

griseofulvin is contraindicated in patients with

hep-atocellular damage or porphyria. Other reported

adverse reactions include proteinuria,

photosensi-tivity, urticaria, as well as disturbances of the CNS and gastrointestinal tract. Despite these potential adverse effects, the incidence of serious reactions is low.24’25 Manufacturers suggest that hematologic, hepatic, and renal function be monitored periodi-cally during treatment. The standard of practice by many dermatologists suggests that in otherwise

healthy individuals such monitoring may not be

necessary.26 Clinical studies are needed to assess the nature and frequency of adverse effects, if any,

during griseofulvin therapy in children.

Ketocona-zole is a relatively new antifungal agent currently being used for systemic mycoses. It has not yet been

approved for use in dermatophyte infections such as tinea capitis. Recent reports of severe hepato-toxic reactions during therapy may limit its poten-tial use to the rare griseofulvin-resistant cases.27

A variety of adjunctive agents are available for use in tinea capitis and although not curative alone may prove valuable when combined with oral gris-eofulvin. Topical antifungal agents such as clotri-mazole, haloprogin, and miconazole nitrate are of-ten employed in an attempt to control surface fun-gal elements and reduce infectivity. These products are applied twice daily; consequently, their use may

prove expensive during prolonged therapy.

Re-cently, Allen et a!28 compared the efficacy of

ad-junctive agents and found that shampooing twice

weekly with selenium sulfide lotion 2.5% (Selsun Brown, Exsel) was more effective in decreasing the duration of positive fungal cultures in children with

T tonsurans tinea capitis than either clotrimazole or shampooing with a bland preparation.

Although generally not required, oral or

intrale-sional steroid therapy may hasten the resolution of

severe kerions and possibly prevent scarring.19 In patients with persistent alopecia following kerion

resolution, hair transplantation may be considered.

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epilate, thus removing the substrate for infection.

Recent studies have demonstrated that patients

treated with roentgenography have an increased

incidence of benign and malignant tumors of the

head and neck.2Bf This therapeutic measure has

now been abandoned.

SUMMARY

In recent years, T tonsurans has become the

leading cause of tinea capitis in the United States.

Accompanying the increased importance of this

organism have come changes in the clinical pres-entation of the disease. The subtle signs and symp-toms and insidious course of this disease require that clinicians be aware of the multiple clinical presentations if a correct diagnosis is to be made. Early therapy with griseofulvin and topical agents will reduce morbidity and infectivity.

ACKNOWLEDGMENTS

The authors thank Ortho Pharmaceutical Corporation, Raritan, NJ, for supporting the cost of the color repro-ductions.

REFERENCES

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Demis DJ, Dobson RL, McGuire J (eds): Clinical

Dermatol-ogy. Philadelphia, Harper and Row, 1982, Chap 17-6, pp

1-23

2. Terreni AA: Tinea capitis survey in Charleston, SC. Arch Dermatol 1961;83:88-91

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WHO 1962;26:797-821

4. Gaisin A, Holzwanger JM, Leyden JJ: Endothrix tinea cap-itis in Philadelphia.

mt

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Dermatol 1952;66:9-40

7. Rippon JW: Medical Mycology. Philadelphia, WB Saunders and Co, 1974, pp 96-1 16

8. Prevost E: Nonfluorescent tinea capitis in Charleston, SC.

JAMA 1979;242:1765-1767

9. Joseph HL, Halde C: Tinea capitis due to Trichophyton tonsurans. Arch Dermatol 1955;83:371-375

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Microsporum audouini and Microsporum conic: I. Gross observations following the inoculation of humans. J Invest

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1 1. Kligman AM: Tinea capitis due to M audouini and M canis:

II. Dynamics of the host-parasite relationship. Arch I)er-matol 1955;71:313-337

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14. Whittle CH: Is scalp ringworm in children a self-limiting disease? Lancet 1953;2:10-12

15. Friedman L, Derbes VJ, Hodges EP: The course of untreated tinea capitis in negro children. J Invest I)ermatol 1964;

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16. Seale ER, Richardson JB: Trichophvton tonsurans: A follow-up of treated and untreated cases. Arch I)ermatol

1960;81:87-94

17. Warm RP: Persistent Trichophvton tonsurans infection. Br

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18. Honig PJ, Smith LR: Tinea capitis masquerading as atopic or seborrheic dermatitis. J Pediatr 1979;94:604-605

19. Esterly NB: Fungal infections in children. Pediatr Ret’

1981;3:41-49

20. Rasmussen JE, Ahmed AR: Trichophyton reactions in chil-dren with tinea capitis. Arch Dermatol 1978;114:371-372

21. Taplin D, Zaias N, Rebell G, et al: Isolation and recognition ofdermatophytes on a new medium (DTM). Arch I)ermatol

1969;99:203-209

22. RockoffAS: Fungus cultures in a pediatric outpatient clinic.

Pediatrics 1979;63:276-278

23. D’Arcy PF, Howard EM, Muggleton PW, et al: The anti-inflammatory action of griseofulvin in experimental ani-mals. ,J Pharm Pharmacol 1960;12:659-665

24. Sande ME, Mandell GL: Antimicrobial agents, in Gilman AG, Goodman LS, Gilman A (eds): The Pharmacological Basis of Therapeutics. New York, Macmillan, 1980, pp

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Chi-cago, AMA, 1980, pp 1360-1362

26. Friedman L, Derbes VJ, Tromovitch TA: Single dose ther-apy of tinea capitis. Arch Dermatol 1960;82:415-418

27. Jones HE: Ketoconazole, editorial. Arch Dermatol 1982; 118:217-219

28. Allen HB, Honig PJ, Leyden JJ, et a!: Selenium sulfide: Adjunctive therapy for tinea capitis. Pediatrics 1982;69:81-83

29. Shore RE, Albert RE, Pasternack BS: Follow-up study of patients treated by x-ray epilation for tinea capitis. Arch Environ Health 1976;31:21-28

30. Ron E, Modan B: Benign and malignant thyroid neoplasms after childhood irradiation for tinea capitis. JNCI 1980;65:

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1983;72;625

Pediatrics

Daniel P. Krowchuk, Anne W. Lucky, Susan I. Primmer and Joseph McGuire

Current Status of the Identification and Management of Tinea Capitis

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