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How do I treat ringworm?

BY: Arku Jasmine

Dear Mirror Doctor, I would appreciate it if you can talk about ringworm and how it can be treated. My son has it; can it affect me? I don’t want to lose my hair so what can I do?

Amina, Kokrobite.


Dear Amina, Tinea capitis is a disease caused by superficial fungal infection of the skin of the scalp, eyebrows, and eyelashes, with a tendency for attacking hair shafts and follicles.
Several synonyms are used, but commonly, ringworm is the term known worldwide. Locally it is often called kaka were were or eyam.

Hairs in the affected areas assume a characteristic dull, grayish, discoloured appearance. Infected hairs are broken and shorter with a rash that starts from the hair shafts and spread to form typical patches of ring forms.

Clinical presentation of tinea capitis varies from a scaly non-inflamed scalp lesion to an inflammatory disease with scaly reddish lesions and hair loss (alopecia) that may progress to severely inflamed deep abscesses called kerion, with the potential for scarring and permanent hair loss.

The type of disease elicited depends on interaction between the host and the causative organism.

Ringworm is caused by fungi. It is the most common fungal skin infection in children worldwide. The preferred age of affliction, childhood, is believed to result from the presence of a particular type of fungus called Pityrosporum orbiculare which is part of normal flora on our skin.

It is hardly seen in pubertal children because there is a particular type of fatty acids produced in the pubertal sweat glands which keeps the proliferation of the fungus in check.

This fatty acid is not produced in the sweat glands of the pre-pubertal children hence the frequency of ringworms in these children.

Other causative agents of tinea capitis include a group of fungi termed dermatophytes. These molds are usually present in nonliving layers of skin and its appendages and are sometimes capable of invading the outermost layer of skin or other skin appendages derived from outer layer of the skin, such as hair and nails.

From the site of inoculation, the fungal roots ( hyphae) penetrate into the deeper layers of skin and other appendages. The fungus continues its downward growth into the hair, invading keratin-a special protein in the skin- as it is formed.

The zone of involvement extends upwards at the rate at which hair grows, and is visible above the skin surface by days 12-14. Infected hairs are brittle, and by the third week, broken hairs are evident.

Ringworm is widespread in some urban areas such as overcrowded areas of Accra and other urban centres with children contracting it from peers in school.

The rate of infection has been reported to have decreased because of improved general sanitary conditions and personal hygiene.

The incidence of tinea capitis may vary by sex, depending on the causative fungal organism. Certain organisms causing tinea capitis have been reported to be up to five times more common in boys than in girls.

Diagnosis is made mainly by observing the lesions clinically. However, for avoidance of doubt, skin rubbing, scrapings and hair plucked from the affected area may be examined under the microscope after treating the specimen with alcohol or potassium hydroxide to identify the fungal roots (hyphae). Culture and sensitivity can be done.

Choice of treatment for tinea capitis is determined by the species of fungus concerned, the degree of inflammation, and in some cases, by the immunologic and nutritional status of the patient.

The most common and effective drug used is Griseofulvin (Fucin). Other medication are certain creams such as ketoconazole (Nizoral) cream or shampoo and miconazole (daktarin) cream.

The shampoo reduces the risk of spreading to other uninfected areas by keeping the number of viable spores that are shed in check.

Griseofulvin accumulates in dead layer of the skin, particularly the keratinised layers of the skin, hair, and nails, rendering them resistant to invasion by the fungus.

Treatment must continue long enough for infected layer to be replaced by resistant one, and this usually takes six to eight weeks.

Household contacts of tinea capitis patients should be screened for clinically silent fungal carriage on the scalp.

Asymptomatic carriers, including adults and siblings in the family of patients with tinea capitis and patient caretakers and playmates, require active treatment, since they may act as a continuing source of infection.

Shampoo and oral antifungal therapy have been advocated for eradication of the carrier state.

Classrooms with young children (ie, kindergarten and nurseries) must be evaluated for tinea capitis infection, since these children are most susceptible and have a greater risk of disease transmission.

Playmates in close physical contact with patients can spread tinea capitis organisms by sharing toys or personal objects including combs and hairbrushes. These individuals need to be evaluated for the presence of infection.

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A member of Paediatric Society of Ghana