Tinea Capitis

How Does One Define Tinea Capitis?

Tinea capitis is the medical term pertaining to scalp ringworm. It is an infection with a ring like lesion brought about by fungi known as dermatophytes, particularly those originating from the genera Trichophyton and Microsporum. This fungi usually affects not only the scalp, but the hair follicles and the surrounding skin as well. [1, 2]

tinea capitis, more commonly known as scalp ringworm image

Picture 1 : An image of tinea capitis, more commonly known as scalp ringworm.
Image Source: www.scripps.org

Tinea capitis: Its History

During the Roman era, the term tinea is used to indicate the insects nibbling on books and clothes, and infesting the skin. Later on, the word was then utilized to describe the illnesses of the hair and scalp in the 12th century. It was in Europe that a man named Turner first described tinea capitis as the disease affecting scalp hairs.

Since then, it was alternately used with ringworm for diseases of the scalp with which lesions are arranged in rings. To date, it is considered as one of the most common causes of hair loss among children. [3, 4]

Causes of Tinea capitis and Risk Factors

  • Usually affecting children in their toddler and school age years, Tinea capitis is said to be highly contagious. It was found to be an endemic disease in Madras (now Chennai) in Southern India during the 1970s, but is still a significant health problem among children in Africa. [5, 6, 7, 8]
  • As previously stated, the etiologic agents spreading the disease are dermatophytes from the Trichophyton and Microsporum genera. The Trichophyton species involved in scalp ringworm diseases include T. verucusom, T. mentagrophytes, T. violaceum, T. rubrum, T. schoenleinii, T. megninii, T.tonsurans, T. soudanense, and T. yaoundei.
  • On the other hand, those belonging in the genus Microsporum include: M. nanum, M. distortum, M. canis, M. audouinii, M. ferrugineum, M. gypseum, and M. fulvum. Infections caused by the Trichophytons usually prevail in Central America, Western Europe, and the United States, while those infested by the Microspora are found in the Southern parts of America, Africa, Middle East, and the Central and Southern Europe. [9, 10]
  • Tinea capitis accounts for 92.5% of dermatophyte infections in children below ten years of age. It predominates among children 3 to 7 years of age. This can be acquired from other humans through skin to skin contact, by using the clothings, towels, and combs of infected persons, and thru contact with carrier animals such as cats, dogs, horses and even pigs. [ 11, 12]
  • These fungi adapt and reproduce well in moist and warm areas. Hence, the risk of tinea increases in the presence of excessive sweating, skin and scalp injuries, poor hygienic practices, overcrowding, and low socioeconomic status. [13, 14, 15]

Pathophysiology of the Scalp Ringworm

Both dermatophytes causing tinea capitis produce spores. These can usually be discarded into one’s clothing, combs, and even into the surroundings through the air. The spores can survive for months, thus they can easily be transmitted through contact. [15]Once infected, the ringworm initially manifests as a sore, or pimple, in the scalp. It then forms into a ring-like shape, with hairs becoming brittle and having a propensity to break and fall out. Hence, these may often present with alopecia or hair loss. [16, 17]

Signs and Symptoms of Tinea capitis

Common clinical manifestations of scalp ringworm include the following:

  • These may begin as erythematous papules progressing into grayish ring-shaped patches with perifollicular papules. See : Folliculitis
  • Also noted are pus-filled skin lesions called kerions, usually evolving to a patchy or diffuse loss of hair with concomitant scarring alopecia. These are due to an exaggerated immune response of the body from the fungi.
  • Small erythematous papules around hair shaft are usually present. These later on become scaly, causing hair breakage. They are usually caused by Microsporum species, hence are often coined as microsporosis.
  • There are also dry, angular patches, without any inflammation.This is associated with hair breakages, leaving a black dot in tow. This is a commonly a manifestation of trichophytosis.
  • Favus are caused by T. scheonleinii. They are commonly present as yellowish, round, crusted, cup shaped lesions clustered and formed like a honeycomb. Each of these lesions are sized like a pea, with a hair protruding at the middle of it.
  • Skin lesions on the scalp may extend to the eyebrows and eyelashes.
  • Lymphadenopathies of the cervical region may occur at episodes of severe infection with complicated kerions. [9, 10, 11, 13, 15]

kerion, pus filled skin lesion with an surrounding area of alopecia seen in a patient with tinea capitis picture

Picture 2 : A picture of a kerion, pus filled skin lesion with an surrounding area of alopecia seen in a patient with tinea capitis.
Pic Source: www.edoctoronline.com

A child infected with tinea capitis, having patches of baldness or air loss, leaving a black dot as remnant image

Picture 3 : A child infected with tinea capitis, having patches of baldness or air loss, leaving a black dot as remnant.
Source: www.avantderm.com

An illustration of a patient with tinea capitis shown to have favus, the yellowish, crusted lesions with a honeycomb appearance image

Picture 4 : An illustration of a patient with tinea capitis shown to have favus, the yellowish, crusted lesions with a honeycomb appearance.
Source: www.dermaamin.com

Diagnostic Tests In Evaluating Tinea capitis

Tinea capitis infection may be diagnosed clinically. It should be considered in children older than 3 months presented with a scaly scalp, until a negative test for mycology ruled out the disease. [2] Once scalp ringworm is considered, specimen for further workup should be gotten. In doing so, a blunt scalpel may be used to obtain affected hair strands, broken off hair and scales from the scalp. Alternatives to which are the use of a toothbrush or a moistened swab to sweep and rub the area gently for specimen extraction. These then are sent to the laboratory for mycology tests. [2, 18, 19]

Hair samples can also be utilized for potassium hydroxide (KOH) examinations. In such tests, hair samples are cultured in 10-20% KOH prior to microscopic examination. This test is usually done to screen for the presence of tinea infections. [11]

In a Wood Lamp examination, the black light (Wood Lamp) is filtered, allowing only the passage of long ultraviolet rays. Hairs infected with M. canis, M. audouinii, M. rivalieri, and M. ferrugineum have a resulting bright green to yellow green fluorescence. Those with T. Schoenleinii fluoresce with a dull green or bluish white hue. However, infections due to T. tonsurans have negative fluorescence on Wood Lamp, hence the availability of other options for diagnosis. [20]

tinea capitis picture

Picture 5 : As a diagnostic test for tinea capitis, this wood lamp result showed positive fluorescence of the hairs examined, hence, a scalp ringworm is confirmed.
Image Source: www.usmlepathslides.tumbler.com

Kerion skin lesions may also be utilized as samples for diagnostics. A bacteriologic swab can be derived from the pustules and inoculated as culture. This, however, may carry false negative results from its difficult sampling derivation. [21]

Precise identification of the species involved may be done thru culture. This is usually done with the use of Saboraud agar with antibacterial and the antifungal cycloheximide to suppress the growth of contaminant organisms. Identification of dermatophytes usually takes 2 weeks. [22]

Treatment for Tinea capitis Infection

The main goal in treating scalp ringworm is to eradicate and eliminate the fungi in the shortest possible time. This may only be done with the use of the following oral antifungal medications: [2]


This drug is a fungistatic agent capable of stopping the synthesis of nucleic acid, arresting cell division and impairing the synthesis of fungal walls. This is available in tablet and suspension forms and is administered for 8 to 10 weeks.


Terbinafine focuses on destroying fungal cell membranes. It is fungicidal and is effective versus all dermatophytes.


This has both fungistatic and fungicidal activities. It interferes with permeabililty of the fungal cell membranes and at the same time, depletes the substance ergosterol found within these membranes.


It is usually used for tinea capitis among children. With a dose of 3 to 5 mg/kg per day, this is usually administered for 4 weeks.

Treatment for Tinea capitis Carriers

Tinea capitis is a very contagious disease. If a member of the family is diagnosed of such infection, all members of the family should be screened for the said condition. Once carriers of the disease are discovered, they should be treated to prevent further spread of the fungal infection.

Use of antifungal shampoos can be advised. This should be applied to hair two times a week for a month. The preferred shampoos include those with 2.5% selenium sulfide, with povidone –iodine, with 1 to 2% zinc pyrithione, and with 2% ketoconazole. If cultures remain positive despite the 4 weeks use of the shampoo, oral treatment is then recommended. [2]

Preventing Tinea capitis

To diminish the risk of this highly contagious fungal infection, one should be reminded of the following:

  • Wash and shampoo the hair regularly. Make sure the scalp is completely washed and rinsed out.
  • Regular haircuts are recommended.
  • Good hygienic practice is a must.
  • Thorough washing of the hands must be done to avoid the spread of this fungal infection.
  • Avoid infected animals
  • Avoid sharing personal items like towels, combs and clothes.
  • Health education is necessary. [12, 16]


  1. Rapini, R, et al. Dermatology: 2 –Volume Set. St. Louis: Mosby. 2007.
  2. Higgins, EM, et al. Guidelines for the Management of Tinea Capitis. British Journal of Dermatology. 2000; 143: 53-58.
  3. Donald, GF. The History, Clinical Features, and Treatment of Tinea capitis due to Trichophyton tonsurans and Trichophyton violaceum. Eleventh Annual Meeting of the Dermatological Association of Australia. Melbourne. October 1959.
  4. http://www.thebaldtruth.com
  5. http://www.mayoclinic.com
  6. Kamalam, A. Tinea capitis an Endemic Disease in Madras. Mycopathologia. 1980 May; 71 (1): 45-51.
  7. Morar, M, et al. Tinea capitis in Kwa-Zulu Natal, South Africa. Pediatric Dermatology. 2004; 21: 444-7.
  8. Ngwogu, A, et al. Epidemiology of Dermatophytoses in a Rural Community in Eastern Nigeria and Review of Related Literature from Africa. Mycopathologia. 2007; 164:149-58.
  9. http://www.dermnetnz.org
  10. http://www.en.wikipedia.org
  11. http://www.emedicine.medscape.com
  12. http://www.mayoclinic.com
  13. http://www.nlm.nih.gov
  14. http://www.patient.co.uk
  15. http://www.about.com
  16. http://www.who.int
  17. http://www.africandiseases.org
  18. Head, E, at al. The Cotton Swab Technique for the Culture of Dermatophyte Infections—Its Efficacy and Merit. Journal of American Academy of Dermatology. 1984; 11:797-801.
  19. Akbaba, M, et al. Comparison of Hairbrush, Toothbrush and Cotton Swab Methods for Diagnosing Asymptomatic Dermatophyte Scalp Carriage. Journal of European Academy of Dermatology and Venereology. 2008 March. ; 33(3): 165-8.
  20. Torvato, M, et al. Tinea capitis: Current Concepts in Clinical Practice. Cutis. 2006 February; 77(2): 93-99.
  21. Friedlander, S, at al. Use of the Cotton Swab Method in Diagnosing Tines Capitis. Pediatrics. 1999 August; 104 (2): 276-9.
  22. Bonifaz, A, et al. Cytobrush-Culture Method to Diagnose Tinea Capitis. Mycopathologia. 2007 June; 163(6): 309-13.
Tinea Capitis
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Published on by under Skin and Hair.
Article was last reviewed on September 26th, 2017.

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