Pediatrics infectious disease update: Tinea capitis

Sheila Fallon Friedlander, MD

Sheila Fallon Friedlander, MD, with Lisette Hilton

What we know about tinea capitis has changed in recent decades

Tinea capitis is not just a disease of preschoolers. When I was in training, I was told to think about tinea capitis when a young child with a scaling head presented. We now know that although that is the most common age to get this fungal infection, it can infect neonates as young as 1, 2, or 3 weeks of age, and it can affect older people, particularly postmenopausal women, who are often caregivers for young children.
We have also learned that one of the things that protects us from fungal infections in our scalp are medium-chain triglycerides, which are present in sebum. It is the oily sebum in our scalp that we all hate in adolescence
that contains these medium-length free fatty acids and glycerol, which are the components of triglyceride and which appear to protect against infection.
We now know more about the genetics of tinea capitis. Susan Abdel-Rahman, PharmD, performed a beautiful study several years ago that evaluated predisposition to tinea capitis infection utilizing whole-genome genotyping
of both susceptible and less susceptible populations. She found that no one specific genetic mutation predisposes to this disease, but likely several genetic subsets make us more susceptible to the infection, including both leukocyte activation and cutaneous permeability.1
It is important to recognize that the nature of the organism changes over time. When I was a little girl, most infections were caused by microsporum audouinii and those infections could be diagnosed with a Wood’s lamp. A
blue-green fluorescence supports the diagnosis of a microsporum infection.

In the past 20 to 30 years, the predominant organism in the US has been trichophyton
tonsurans. It doesn’t fluoresce with a Wood’s lamp. Trichophyton tonsurans is an anthropophilic organism, transmitted from human to human, while microsporum canis is transmitted from animals to humans.
In the last decade, we have seen a lot of what we are referring to as “African species” in
Europe, Canada, and the US. These organisms include trichophyton violaceum and soudanense, as well as some microsporum species. These organisms seem to be a little less sensitive to terbinafine, which is the drug of choice
in the US.

Which treatment to use when?

If you talk to a dozen pediatric dermatologists in the US, at least 11 of the 12 would say, “I use terbinafine as a first line because more than 90% of our cases are trichophyton tonsurans and terbinafine works better.” But there are important cases in which that doesn’t hold. One is if it is clear that the patient was infected by an animal rather than a human. Then you are going to want to use griseofulvin. A significant number of tinea capitis cases have been transmitted by animals. In the US, those animals tend to be cats or dogs, which often transmit microsporum canis. The good news is that microsporum canis often fluoresces with a Wood’s lamp. The bad news is that it doesn’t seem to respond as well to terbinafine.
People at high risk for being infected with the African species include immigrants from Africa, and I have seen a number of cases in Somalian refugees. These people often have trichophyton violaceum or one of the other
African species. They also will do better with griseofulvin.
The standard of care is to examine the child’s skin as well as scalp. Check lymph nodes, because frequently kids who have tinea capitis will have lymphadenopathy in the neck and the posterior occipital area. Check for evidence of psoriasis in the nails and rashes on the body.
If you are worried about psoriasis, alopecia areata, or trichotillomania, the dermatoscope is very helpful to confirm tinea. If you use your dermatoscope on a patient who has tinea, often you will see beautiful little comma-shaped and corkscrew hairs. In contrast, alopecia areata will show exclamation-point hairs, as well as perifollicular golden or brown ovoid spots.
Take a good history. Is there anyone else in the family who is scaling? When did this scaling start? Ask about pets. Are there pets in the house which are scaling? Or does the family live on a farm? Ask about the child’s friends, daycare center, and school. Are there other people scaling in those environments?
We still recommend culturing. Polymerase chain reaction (PCR) tests for tinea are not widely available yet, so I think all of us are still holding on to rubbing a wet Q-tip over the areas that are involved and over the 4 quadrants of the scalp and sending it off in a transport culture, such as we use for obtaining bacterial cultures of the throat or skin. The type of medicine you are going to use in the meantime depends on whether the scalp has fluoresced with a Wood’s lamp or you have a high index of suspicion for infection transmitted from an animal. (Yes, there are cases that have been transmitted from cows as well as cats and dogs!) Then we are probably dealing with a microsporum and will want to treat with griseofulvin in high dose, using 20 to 25 mg/kg to be taken with food. I never use more than a gram a day, no matter how big the child is. I generally give it as a once daily dose because compliance goes up in this case. Warn parents that particularly with the higher doses kids can get headaches, tummy aches, and rashes when they are out in the sun. Fortunately, it is not common to see any of those in young children.
If you learn that the family is from Somalia or they have immigrated recently from anywhere in Africa, then your index of suspicion for African species is higher. I would culture the patient and utilize griseofulvin. I would also
use a topical sporicidal agent, such as topical ketoconazole shampoo, twice a week.
If the child is not from Africa, the scalp is Wood’s lamp negative, no one else in the family is scaling, there are no pets that are a problem, and the child hasn’t traveled recently, the odds are high that you’re dealing with trichophyton tonsurans. This describes almost 90% of my patients, and I would start out with terbinafine.
There is some controversy about what dose of terbinafine to use. If the child weighs greater than 35 kg, I use adult-sized dosing, which is 250 mg daily. If a child is smaller, I use lower dosing. There are dosing tables in the literature
to which you can refer.
Are blood tests necessary? The standard of care for griseofulvin is that if a child is on more than 10 to 12 weeks of therapy, people order blood tests. Unless the child develops symptoms, has other health problems, or is on other drugs, we don’t get labs with griseofulvin. So, the average patient does not require lab monitoring.
Terbinafine is more controversial. Those who follow the standard of care perfectly would have a baseline set of labs, particularly liver function. My standard of care is that I discuss this with the families, going over the risks and
benefits. In most cases, in a healthy child with no risk factors for liver or hematologic disease, families opt not to have blood tests unless symptoms occur. I, along with some of the world’s experts in tinea capitis, plan to publish
something in the next 6 months to document that it is very reasonable not to do lab tests with terbinafine if a child has no underlying problems and if the family agrees.
Length of treatment varies. In my experience with griseofulvin, I treat at least 6 weeks and rarely use it for fewer than 8 weeks. If you are dealing with microsporum canis, often 12 weeks is required.
For a patient who has trichophyton tonsurans, I will try 4 weeks of terbinafine. If you have a child with significant disease, you may want to go for 6 to 8 weeks. Data in the literature support this approach, and many patients will
respond to 4 weeks of treatment.

Prevention takes the form getting a good history and treating anyone who has evidence of disease. We do not have to keep a child with treated tinea out of school unless he or she has an inflammatory lesion that is oozing pus. All
the recommendations say that after 24 hours of therapy a child with classic tinea capitis is free to go back to school.
As for the future, I am excited about a small study that came out recently in Pediatric Dermatology looking at topical encapsulated terbinafine gel for the treatment of tinea capitis. It was a small pilot study of 10 children but 100% of them were mycologically cured after 4 weeks.2 The hope is that we can find a topical agent with high efficacy.

REFERENCES

  1. Abdel-Rahman SM, Preuett BL. Genetic predictors of susceptibility to cutaneous fungal infections: a pilot
    genome wide association study to refine a candidate gene search. J Dermatol Sci. 2012 Aug;67(2):147-52.
    doi: 10.1016/j.jdermsci.2012. 05.003
  2. Jerasutus S, Vejjabhinanta V, Prapapan O. Treatment of tinea capitis with topical
    1% encapsulated terbinafine hydrochloride gel: A pilot study. Pediatr Dermatol. 2020 Nov;37(6):1090-1093.
    doi: 10.1111/pde.14377.

DISCLOSURES
Dr. Friedlander reports no relevant financial interests.