What You Should Know About Treating Tinea Capitis

Tinea capitis is the most common pediatric dermatophyte infection. Currently, there is a 3 to 8 percent prevalance in the pediatric population. We tend to see it in 3- to 7-year-olds. Adults may also get tinea capitis, but not as frequently. According to the most recent data, there is an equal incidence between boys and girls.
The most common organism we’re seeing today with tinea capitis is Tricophyton tonsurans. A study in Cleveland really sums up the state of tinea capitis today.16 They looked at children in eight elementary schools, did cultures from 937 children and found that 13 percent or 122 children actually had positive cultures. All of them except one were for Trichophyton tonsurans. All of these children were African-American and 60 percent of these patients were asymptomatic with positive cultures and no clinical signs of infection.
What they found is that race, scaling and the use of anti-dandruff shampoo was a factor in terms of determining who was going to have a positive culture.16 This group had its own way of determining susceptibility to the known antifungals today and found that they were all sensitive to these medications. However, currently there really is no established way to determine the susceptibility of these organisms that we culture now.
We know the incidence of tinea capitis is increasing in this country. A study done in California looked at the number of griseofulvin prescriptions written for children from 1984 to 1993.17 For the African-American population, there was over a 200 percent increase in the number of prescriptions for griseofulvin suspension. In Caucasian children, there was an approximately 140 percent increase. In the overall population, there was an increase of 84 percent.

A Few Thoughts On The Etiologic Evolution Of Tinea Capitis
Dr. Shin: The etiologic organism has changed through the years. Prior to the 1900s, it was Microsporum canis. From the 1900s to the 1950s, it was Microsporum audouinii. When griseofulvin was first developed around the 1950s, Microsporum audouinii was the prevalent organism for tinea capitis. The recommended dosing of griseofulvin was based on the treatment of Microsporum audouinii tinea capitis. Today, most cases of tinea capitis in the United States are caused by Trichophyton tonsurans. It is believed that this organism was brought into this country via the large immigrant population from Central and South America.18
Some people feel that because Microsporum audouinii responded well to treatment with griseofulvin, perhaps we were able to eradicate it and treat it more effectively.18 The other thought is that with Microsporum species, you can use a Woods light to identify it and patients tend to have much more of an obvious inflammatory response. They were able to identify the tinea capitis more readily and be on top of the treatment. Trichophyton tonsurans isn’t as obvious a clinical picture. It does not fluoresce with a Woods light. Sometimes all you’ll have is this very subtle, fine scale that looks like dandruff and it’s not picked up. The issue with the carrier state is a problem too because patients are colonized with spores. They may not have active clinical infections, but they are infected.

Understanding The Etiology
Dr. Shin: In tinea capitis, the dermatophyte is usually transmitted from infected person to infected person. Fallen infected hairs can have the dermatophyte. There are select animal vectors in which you tend to see the Microsporum species, more in cats and dogs and children pick it up from those animals. They have also found dermatophytes on fomites like barbershop instruments, hairbrushes and combs.19
The carrier state is somewhat of a controversial issue. We know it exists in the at-risk population, mostly African-American children. In some studies, they’ve shown there is an approximately 15 percent incidence.20-22 Up to 34 percent of household contacts of infected patients have been found to be carriers with positive cultures and no clinical signs and symptoms.
Essentially, people with a carrier state can be divided into three groups. They either remain in the carrier state, go on to develop overt infection or the condition just resolves spontaneously. These people in the population are reservoirs for infection and I think that’s contributing to why we’re seeing so much tinea capitis today.

Reviewing Different Types Of Tinea Capitis
Dr. Shin: There are a number of different clinical types of tinea capitis. There is gray patch scaling. There are very obvious patches of alopecia with a thick scale. We rarely see these patients today. What you will see more often is a little patch of fine scale. This seborrheic dermatitis-like scale type of tinea capitis is very subtle and very easy to miss.
Another type of tinea capitis is the black dot alopecia type. The fungus probably causes fragility within the hair shaft and what you’re getting is breakage of the hair right at the scalp, which leaves these little black dots. Another type of tinea capitis is the localized pustular form in which you see clusters of small follicular pustules. You don’t see this as commonly because with the Trichophyton species, it’s not as inflammatory. In children, pustules in the scalp is tinea capitis until proven otherwise.
One other thing I want to mention is the ID reaction. I don’t know if you see this as much in tinea pedis. Patients can get this ID reaction, whether they are on treatment or not. What they get is this fine, papular eruption. Patients think it’s actually a drug reaction and want to stop the medication, but you can just treat through it. It’s usually an ID reaction to the dying dermatophyte.

What About The Differential Diagnosis?
Dr. Shin: There are a number of different entities to consider in the differential diagnosis for tinea capitis.
A patient with atopic dermatitis may present with diffuse scaling on the scalp. These patients will also have eczematous patches and plaques on other parts of the body characteristic for atopic dermatitis.
Psoriasis can also appear as scaling on the scalp and what you typically see are very discreet erythematous plaques with some thick scale on top. With seborrheic dermatitis, you get this brown, greasy, caked-on scale whereas you may have more diffuse fine scale in the older patients.
Alopecia areata presents as discreet patches of hair loss. Usually, there is minimal inflammation and no scale. There is very little surface change. Unlike the black dot alopecia that you see in tinea capitis, there are exclamation point hairs in alopecia areata. There is an inherent weakness in the hair, causing breakage at the level of the scalp. Sometimes, you will notice a peachy color to the skin with alopecia areata.

Using Griseofulvin To Treat Tinea Capitis
Dr. Shin: We know topical treatment alone is not enough to cure tinea capitis. There may be a rare case in which you can get it to clear. We know the dermatophyte is either within or outside of the hair shaft and goes deep into the hair follicle. That’s why we require a minimum of six to eight weeks of treatment because we know it takes that long for the hair at the base of the hair follicle to grow out to be properly treated.

We talked a lot about the mechanism of action, but I just want to mention that griseofulvin is the only FDA-approved treatment for tinea capitis in children. Unfortunately, the FDA-approved dosage was based on the original studies done in the 1950s for the treatment of Microsporum audouinii tinea capitis and was much lower than what we actually need today to treat Trichophyton tonsurans tinea capitis. We know it comes in a number of different tablet strengths in both microsize and ultramicrosize form. The microsized form comes in a suspension as well.
In treating children, we always mention to the parents that there is an improved absorption with microsized griseofulvin when it is taken with fatty foods. We find patients who don’t respond sometimes are taking it on an empty stomach or with not enough fatty foods, and it definitely affects the efficacy of the medication.
In terms of dosing, back in the 1970s, 10 mg/kg/day of microsize griseofulvin for four weeks was enough to eradicate tinea capitis. The recommended dose was increased in the 1990s to 15 to 20 mg/kg/day for four to six weeks. We know today that you cannot effectively treat Trichophyton tinea capitis unless you have a treatment dose of 20 to 25 mg/kg/day for a minimum of six weeks, and sometimes it requires a longer duration.
If you use the ultramicrosize form of griseofulvin, you can cut back on the dose by about 25 percent. You can probably cut that to about 15 to 20 mg/kg/day for the ultramicrosize form. Since griseofulvin does not remain in the keratinized tissue for extended periods, the treatment of tinea capitis requires longer dosing periods and compliance becomes an issue. We are seeing treatment failures as well and that is why people are looking into alternative treatment options. However, none of these are FDA-approved for tinea capitis at this time.

Exploring The Alternative Agents For Tinea Capitis
Dr. Shin: Dr. Gupta participated in many of the studies that looked at alternate agents — such as fluconazole, itraconazole and terbinafine — for tinea capitis. Back in the late ‘80s, they looked at treating Microsporum tinea capitis with ketoconazole and found that there was really no advantage over griseofulvin.23 Given the risk of hepatic toxicity, it wasn’t really looked into much after that.
A retrospective literature review of the treatment of tinea capitis with these various agents was published in Pediatric Dermatology.24 They found that in order to effectively treat tinea capitis — no matter what the organism — higher doses of griseofulvin were required. They found that it’s not as effective as it was just a few years ago. In regard to these newer agents, there is more experience with them in Europe and in the Middle East. Most of these studies looked at tinea capitis caused by organisms other than Trichophyton tonsurans.
There are a number of drug interactions with the newer agents as we discussed before. Overall the side effect profile for all of these agents is pretty good. The downfall to terbinafine is that it only comes in tablets and children prefer to use syrup. It’s recommended that you don’t crush these tablets. The tablets can be scored. Dosing is based on weight category. In the studies that are out today, this is a wide range—3 to 6 mg/kg/day. Patients with Microsporum tinea capitis who were dosed on the higher end of the spectrum tended to respond better to treatment. We just don’t have enough safety data at these varied doses so you need to monitor at initiation.
In terms of studies done with terbinafine for the treatment of Trichophyton species tinea capitis, there was one in San Francisco that looked at 172 patients in a multi-centered trial with the same dosing regimen based on the weight.25 They dosed them for either one week, two weeks or four weeks. An effective treatment was a negative culture or minimal clinical symptoms. The data was not so impressive with effective treatment in only two-thirds of the patients overall. When you extrapolate the data, patients who are on the higher end of the scale in terms of dosing did better than the ones on the lower end of the scale. This is just one of the few studies that are out there.
Itraconazole comes in a capsule and is best taken with a full meal, particularly with something acidic. There is a suspension available. However, it was developed in a cyclodextran vehicle that has been shown to cause pancreatic cancer in rats.26 The theory is that this phenomenon is species-specific. They haven’t been able to show this in other animals. However, it’s a concern and when parents read that in the package insert, they’re not so happy to be administering this medication to children.
Yet it has been used for other systemic fungal infections and it is absorbed better with an empty stomach. There are anecdotes of patients that have gotten severe diarrhea from this, but Dr. Gupta noted in one of his reviews that it’s more of a loosening of the stool.27 The recommended dosing is 5 mg/kg/day, either in a continuous or pulsed basis. Again, we don’t have enough data to really know how how long to dose this medication so we need to monitor.
In a study, Boni Elewski, MD, looked at 120 patients who either failed griseofulvin treatment or were unable to tolerate it.28 They all had Trichophyton species tinea capitis. They were dosed at 3 to 5 mg/kg/day for one month. The patients were permitted to use adjunctive ketoconazole shampoo two to three times per week. At four weeks, they all had negative cultures and clinical improvement. At eight weeks, they all had clinical cure.
Fluconazole has the same issues in terms of drug interactions. There are a number of different strength tablets as well as a suspension. The suspension happens to have a fruity flavor so it’s well tolerated by pediatric patients. The suspension needs to be reconstituted every two weeks. There is continuous dosing at 6 mg/kg/day versus pulsed dosing of once a week for an extended number of weeks. We monitor these children. Fluconazole is approved by the FDA for treatment of oropharyngeal candidiasis in children, but not for tinea capitis.
In this particular study involving fluconazole, there were 42 patients with Trichophyton tonsurans tinea capitis.29 They were treated with 6 mg/kg/day for two weeks and then they were evaluated at the four-week point. If they still had clinical disease, they were given an additional dose. Half of these patients required an additional dose. At the 12-week point, they found that 88 percent of the treated patients had both mycological and clinical clearing.
We know there are drugs that are absolutely contraindicated for some of these antifungal medications. For children, I’d say we would worry most when they are on anticonvulsants. In this situation, what you choose can be an issue because the anticonvulsant can affect the metabolism of the antifungal and vice versa.

A Few Thoughts About Cost-Effectiveness
Dr. Shin: A six- to eight-week course of griseofulvin tablets is probably going to run you less than $100. For children, the tablets can be crushed and then mixed with pudding or ice cream. It’s actually much more cost-effective than the suspension itself if you’re able to administer it to a patient that way.
Itraconazole and fluconazole run somewhere between $250 or $300 for a four-week course. It’s not really established how many weeks of therapy you need, but the cost is definitely an issue. When you look at the liquid form, griseofulvin suspension is not inexpensive. A six-week course can cost around $200 and this is for a 25 kg child so that’s probably treatment for your average 5-year-old. Itraconazole suspension is also very expensive and can run between $250 and $300 for a four-week course. When you think about cost, the griseofulvin tablets are much more cost-effective than the actual suspension.

Is There A Role For Topical Therapy?
Dr. Shin: There is a role for topical therapy in treating tinea capitis. There were a few studies that looked at shampooing with either selenium sulfide or ketoconazole two or three times per week.30,31 They were able to reduce the frequency of positive cultures as well as the shedding of spores. The hope is that you’ll minimize the spread of infection. It’s very controversial whether patients who are in the carrier state should be treated or not. I think the current recommendation is not to treat them. When you have patients with tinea capitis, close contacts need to be checked carefully. If there is any sign of disease, then you need to treat them as well, but I don’t think there is any current recommendation to prophylactically treat them with either orals or topicals to minimize this spread of spores.

Final Notes
Dr. Shin: In summary, griseofulvin is still the first line of therapy for tinea capitis. It is the only agent that is FDA approved for this condition. There are a number of newer agents that are out there, but we just don’t have enough experience with them in this country to show efficacy and safety for Trichophyton tinea capitis. At this point, you should reserve them for griseofulvin failures because this is off-label use. We know there is a need for future studies to determine proper dosing and the duration of therapy, as well as the safety of these agents in children. It is also important to use adjunctive topical therapies to minimize the spread of infection.

A Closer Look At Anti-Dandruff Shampoos
Dr. Joseph: I was reading the new study about the kids in Cleveland.16 They found that anti-dandruff shampoos are a pre-disposing factor, yet isn’t this selenium sulfide an anti-dandruff shampoo? Why would an anti-dandruff shampoo be a major predisposing factor?
Dr. Shin: I think it’s a predictive factor but not necessarily a predisposing one. What I took from that was that patients who have tinea capitis are more likely to have scaling. They think it’s dandruff and end up using an anti-dandruff shampoo. I don’t think the patients put themselves on it because they think they have tinea capitis. It’s a predictive factor. An anti-dandruff shampoo can have selenium sulfide or zinc pyrithione.
Dr. Gupta: Again, the old studies are not really being done as rigorously as you and I would like in this area. More work needs to be done in this area.

Has There Been A True Increase In Tinea Capitis?
Dr. Blass: When you were talking about the incidence of tinea capitis going up so dramatically, do you feel that is really a true increase? Years ago, nobody really cared about looking at kids’ heads in school. Now because of lice, kids are examined on a regular basis in school. Braiding, although it was around, was not nearly as common and braiding forces you to look at the scalp. Do you think that it’s an actual marked increase or do you think it’s just an increase in noticing what was there before subclinically and now it’s being noticed because people are looking at kids’ heads more?
Dr. Shin: It’s probably both. Years ago, tinea capitis was caused by a different species. There was much more of an inflammatory response when patients had an infection so it was obvious. Now a number of people are just carriers and they have the spores there but not evidence of active infection, and that’s more likely to spread the disease and lead to a higher incidence of tinea capitis.
Dr. Gupta: The other thing to add to that has to deal with the population. In Canada, it’s kind of interesting. One could make a case that in the United States, there’s a difference in access with health care. In Canada, that’s not the case and yet we find that certain segments of the population carry tinea capitis a lot more than others. It may be due to certain populations moving from certain countries to other countries, genetic predisposition, hairstyles, shampooing and the oils and pomades and other things that they use. I think those kind of factor into it quite a bit. This is something to keep in mind.
Dr. Shin: The issue of hair care practice is controversial. Recent studies show that it does not predispose to tinea capitis.32 Furthermore, the Cleveland study also did not find that hair practices like braiding increased the chances of having tinea capitis.16

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