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Loh Xin Hui 01/07/09
Ringworm (tinea capitis) is a superficial fungal infection of the scalp, eyebrows, and eyelashes, with a propensity for attacking hair shafts and follicles. Caused by fungi of species of genera Trichophyton and Microsporum that invade the hair shaft. In New Zealand, M. canis is the commonest dermatophyte fungus to cause tinea capitis. This fungus is zoophilic i.e. it grows naturally on an animal rather than a human. M canis tinea capitis is due to contact with a cat or dog. In the United States, T. tonsurans has also become a common cause of tinea capitis; this is passed on from one person to another as it naturally infects humans (i.e. it is anthropophilic) through human-to-human contact with fomites, such as combs, hats, pillows and sofas. It frequently causes no symptoms and is commonly found in adult carriers. Predominantly seen in pre-pubertal children, most commonly in children younger than 10 years. Peak age range is in patients aged 3-7 years, more often in boys than girls. Uncommon in adults.
Infection begins as a small erythematous papule around a hair shaft on the scalp, eyebrows, or eyelashes. Within a few days, the red papule becomes paler and scaly, and the hairs appear discolored, lusterless, and brittle. They break off a few millimeters above the scalp skin surface. The lesion spreads, forming numerous papules in a typical ring form. Ringformed lesions may coalesce with other infected areas. Pruritus usually is minimal but may be intense at times. Alopecia is common in infected areas. Inflammation may be mild or severe. Cats and dogs are natural reservoirs of M. canis fungal infections of the commonly inflammatory type. Infected cats contaminate the environment with microsporum through airborne arthrospores. The organism is transmitted through direct contact of an exposed area, such as the face, scalp, or arms, with an infected animal or its dander.
Tinea capitis may present in several ways. Dry scaling – like dandruff but usually with moth-eaten hair loss Black dots – the hairs are broken off at the scalp surface, and the black tips of the hair follicles remain and looks scaly Smooth areas of hair loss Kerion – very inflamed, thickened, pus-filled area Favus – yellow crusts and matted hair Carrier state no symptoms and only mild scaling (T. tonsurans). The clinical presentation is typically a single or multiple patches of hair loss, sometimes with a 'black dot' pattern (often with broken-off hairs). The infection continues (for 8-10 wk) to spread in the stratum corneum to involve other hairs, at which point, the infected area is approximately 3.5-7.0 cm in diameter. Common symptoms include: - Areas that appear bald, due to hair that has broken off - Itching of the scalp - Pus-filled sores (lesions) on the scalp (kerions) - Round, scaly lesions on the scalp that may be red or swollen (inflamed)
In the scalp, fungal infections often form circular, scaly, inflamed patches. Frequently, there can be temporary hair loss (hair returns when infection clears but if treatment is delayed and scarring results, permanent hair loss can be seen). This is a classical example of ringworm (tinea capitis) in a young child.
These pictures show the characteristic rash of a tinea capitis (scalp ringworm) infection. Note the round, scaly patches with hair loss. Other children may just have a scaly rash on their scalp without hairloss and others may have small black dots on their scalp.
Three types of in vivo hair invasion are recognized.
characterized by the development of spores (arthroconidia) on the exterior of the hair shaft. The cuticle of the hair is destroyed. infected hairs usually fluoresce a bright greenish-yellow color under a Wood lamp ultraviolet light. Common agents include Microsporum canis, Microsporum gypseum, Trichophyton equinum, and Trichophyton verrucosum.
characterized by the development of arthroconidia within the hair shaft only. The cuticle of the hair remains intact. infected hairs do not fluoresce under a Wood lamp ultraviolet light. all endothrix-producing agents are anthropophilic (eg, Trichophyton tonsurans, Trichophyton violaceum).
usually caused by T. schoenleinii, produces favus-like crusts or scutula and corresponding hair loss, which can be seen as dull green or blue-white color of hairs.
Treatment of carriers
If the child has an anthropophilic infection, all family members should be examined for signs of infection. Brushings of scaly areas of the scalp should be taken for mycology. Sometimes it is best for the whole family to be treated whether or not fungal infection is proven. It is advisable for parents of classmates and other playmates to be informed, so their children may be examined and treated if necessary. In some countries, infected children are not allowed to attend school. Elsewhere children with tinea capitis can attend school providing they are receiving treatment. Carriers may have no symptoms. Treatment of carriers is necessary to prevent spread of infection. Antifungal shampoo twice weekly for four weeks may be sufficient but if cultures remain positive, oral treatment is recommended. Suitable shampoos include:
2.5% selenium sulfide 10% povidone-iodine solution 2% ketoconazole
Treatment of tinea capitis
Tinea capitis requires treatment with an oral antifungal agent. Topical treatment alone usually is ineffective and is not recommended for the management of tinea capitis. Some patients may need short oral courses of corticosteroids. Bacterial superinfections are common, and antibiotic treatments may be neccesary. Topical therapy with ketoconazole, selenium sulfide or povidone-iodine shampoo, may reduce infectivity in the course of therapy by reducing the number of viable spores that are shed, but should not be used as the sole therapeutic agents. Keep the area clean. Other family members and pets should be examined and treated, if necessary.
Griseofulvin has been the treatment of choice in all ringworm infections of the scalp. (safe and inexpensive) Griseofulvin must be taken orally to be effective; this allows the drug to penetrate the hair shaft where the fungus lives. The effective therapy rate of this treatment is generally high, in the range of 88–100%. The effective dosage of griseofulvin often prescribed is 10-20 mg/kg/day for 6-8 weeks. Griseofulvin accumulates in keratin of the horny layer, hair, and nails, rendering them resistant to invasion by the fungus. Treatment must continue long enough for infected keratin to be replaced by resistant keratin, usually 4-6 weeks. In inflammatory lesions, compresses often are required to remove pus and infected scale. Therapy progress is monitored by regular clinical examination with the aid of a Wood lamp for fluorescent species such as M audouinii and M canis. Adverse effects include nausea and rashes in 8-15%.
Other oral antifungal treatments for tinea capitis include terbinafine, itraconazole and fluconazole.
These drugs have the advantage of shorter treatment durations than griseofulvin. However, concern has been raised about the possibility of rare side effects like liver toxicity or interactions with other drugs; furthermore, the newer drug treatments tend to be more expensive than griseofulvin.
Oral fluconazole (6mg/kg stat, then 3mg/kg daily) seems to have similar efficacy to griseofulvin. A meta-analysis suggested that terbinafine is at least as effective as griseofulvin for treating tinea capitis due to Trichophyton infections, while griseofulvin appears to be superior to terbinafine for treating tinea capitis due to Microsporum infections. Itraconazole can be used in children as continuous therapy at a dose of 2-4 mg/kg 12-24H orally for four to six weeks.
Good general hygiene is important to prevent and treat tinea infections. Shampoo the scalp regularly, especially after haircuts. A medicated shampoo, such as one containing ketoconazole or selenium sulfide, may reduce the spread of infectionearly in the course of therapy by reducing the number of viable spores that are shed. Other family members and pets should be examined and treated, if necessary. Avoid contact with infected pets or people. Do not exchange headgear, combs, and similar items unless they are first thoroughly cleaned and dried.
Parents play the most critical role. First, they need education to understand why they must insist on preventive measures (i.e., having all family members use antifungal shampoos) or if necessary, insist on getting the entire family tested (and treated with antifungals if cultured positive for tinea capitis). Parents need to understand that sharing brushes, combs, hats, hair ties, headbands, or any other items in contact with the head (i.e., pillows or sheets) is to be strictly policed and avoided. Occasionally, children may develop a fine pink pruritic, papular, or vesicular exanthem on the head, neck, and shoulders once griseofulvin is initiated. Parents need to know this is a hypersensitivity reaction to a fungal agent and not a drug reaction. True allergic urticaria and angioedema are rare.
http://emedicine.medscape.com/article/1091351overview http://dermnetnz.org/fungal/tinea-capitis.html Goldstein AO, Goldstein BG. Dermatophyte (tinea) infections. Available at 2007 UpToDate. http://www.doctorfungus.org/mycoses/human/other/tine a_capitis_favosa.htm
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