Researchers went into eight Cleveland elementary schools and took scalp cultures from 937 children.
A hundred and twenty-two came back positive for a dermatophyte. Thirteen percent of the school population, and every single one of the positive children was African American.
Sixty percent of them had no symptoms at all.
And among the factors associated with a higher likelihood of infection, alongside scaling, was the use of anti-dandruff shampoo.
Read that last one carefully
That is a cross-sectional survey, so the arrow almost certainly runs backwards. Nobody caught ringworm from a bottle of shampoo. Children whose scalps were flaking got bought anti-dandruff shampoo, and some of those flaking scalps were fungal.
Which makes it the most useful finding in the paper, because it is a photograph of the mistake. The scale was noticed. It was treated. It was treated with the wrong thing, and the treatment continued while the infection did not resolve, because a shampoo cannot cure this.
Tinea capitis lives inside the hair shaft. Topical antifungals do not reach it. Curing it requires a systemic antifungal taken by mouth for weeks, and until somebody prescribes one, the scalp keeps flaking and the household keeps being exposed.
Left long enough, some of these infections become a kerion — a boggy, inflamed, pus-filled mass — and a kerion can scar. Scarred follicles do not grow hair back, which puts an untreated childhood scalp infection in the same permanent category as the tension damage that accumulates over school years.
Scalp flaking in a child is dandruff.
- Source
- Ghannoum M, Isham N, Hajjeh R, et al., J Am Acad Dermatol 2003;48(2):189-93; Williams JV, Honig PJ, McGinley KJ, Leyden JJ, Pediatrics 1995;96(2 Pt 1):265-7; Williams JV, Eichenfield LF, Burke BL, Barnes-Eley M, Friedlander SF, Pediatrics 2005;115(1):e1-6; Pomeranz AJ, Sabnis SS, McGrath GJ, Esterly NB, Arch Pediatr Adolesc Med 1999;153(5):483-6
- Participants
- 937 children cultured in Cleveland; 1,404 hemi-scalp cultures from 224 Philadelphia children over 16 months; 300 children in a San Diego prevalence study; 114 household contacts of 56 index cases
- Measured
- In Cleveland all 122 positive cultures were from African American children. In the San Diego study all nine culture-positive children were Black. The Philadelphia school population was entirely Black.
- Not measured
- Any national incidence estimate. Any trial of screening strategies. The commonest study design here is a single school or clinic, and the newest of these four is from 2005.
Sixty percent of the Cleveland positives were asymptomatic carriers, and 14 percent of the Philadelphia children were carrying spores without any visible sign.
The other half of the picture, which cuts the other way
It would be easy to leave you thinking every flaking scalp is fungal. It is not, and the correction comes from another culture survey.
A cross-sectional study of 300 children in San Diego found scalp scaling in 66 of them — 22 percent. Common. In the under-twos it was mostly seborrheic dermatitis and eczema. In the two to ten year olds, the commonest finding was non-specific fine white scaling, then seborrheic dermatitis, then eczema.
Nine children, three percent, grew a dermatophyte. All nine were Black. All nine grew Trichophyton tonsurans.
So most scaling is not ringworm, and the small proportion that is falls very unevenly. Both of those facts have to be held at once, and the practical consequence of holding them is not more anxiety. It is a culture.
The reservoir nobody sees
The carrier state is what makes this infection behave the way it does.
A Philadelphia school was cultured repeatedly over sixteen months — 1,404 hemi-scalp cultures from 224 children. Three percent were symptomatic index cases. Fourteen percent were asymptomatic carriers, with no black-dot lesions, no hair loss, no scaling, no crusts, no pustules, no redness.
Half of all the positive cultures came from kindergarten and first grade.
The carriers had much lower spore loads than the index cases — 59 percent of carriers were at the lowest grade of one to ten colonies, while 74 percent of index cases were at the highest, over 150 colonies. And of 45 untreated carriers followed for two to five months, 19 became culture-negative on their own, almost all of them from the lightest spore loads.
The household picture matches. Of 114 contacts of 56 index cases, 16 percent were carrying the organism, and a third of families had at least one carrier. But only one of fifteen carriers followed up went on to develop actual disease, and the analysis found no association of carrier state with age, sex or comb sharing.
That last detail is worth pausing on, because sharing combs is the advice everybody gives. In the one study that looked, it was not the variable that separated carriers from non-carriers.
Adults have it too, and almost nobody cultures them
This is the finding I most want in front of anybody reading a beauty site.
A clinic reviewed every positive scalp fungal culture over nearly three years. Seventy-nine cases of tinea capitis. Nine of them were adults — and seven of those nine were African American women, average age 46.
Three had a known exposure to a child with the infection.
The authors’ recommendation is unambiguous: widespread scalp culture is indicated for papulosquamous disease and alopecia in this population.
Sit with what that means in practice. A woman in her forties with a flaking, itchy scalp and hair coming out has a differential that includes seborrheic dermatitis, central centrifugal cicatricial alopecia, discoid lupus, psoriasis, and a curable fungal infection. One of those is diagnosed with a swab that costs almost nothing, and it is routinely the one nobody does.
The organism is changing, and the change follows migration
In North America the dominant species has been T. tonsurans for decades — over 95 percent of infections. Two others, T. violaceum and T. soudanense, are common across Africa and were rare in the United States.
A Mayo Clinic review found 81 children in Rochester, Minnesota, positive for those two species between 1997 and 2014. Sixty-seven of them, 82.7 percent, were of African background. Median time to clinical cure, among those not lost to follow-up, was 2.3 months.
This matters for a mundane reason. Different species behave differently under a Wood’s lamp and in the laboratory, and a clinical service whose mental model was built around one organism can miss another. Migration changes the local mycology faster than the local habits change.
The one randomized trial, and who was in it
There is a randomized controlled trial in this field. It is from 1987, it enrolled 30 children with kerion, and it asked whether injecting a steroid into the inflamed mass alongside oral griseofulvin beat griseofulvin alone.
It did not. No difference in time to negative culture, time to new hair growth, complete regrowth, or scalp clearing. The authors concluded the injection was an unnecessary adjunct.
Now the cohort. All 30 children were Black. Twenty-three of the 30 were girls. The authors note their clinic population was 45 percent Black.
A useful, negative, practice-changing trial — and a sample that tells you exactly whose scalps this disease was landing on, in one American clinic, thirty-nine years ago.
A coda about a harm that did not transfer
Before oral antifungals existed, tinea capitis was treated by irradiating children’s scalps to make the hair fall out.
A cohort of 2,224 such children was followed for up to fifty years, against 1,380 who had only topical treatment. Among irradiated white patients the relative risk of basal cell carcinoma of the head and neck was 3.6, from a scalp dose of around 4.8 gray. Forty percent of the affected cases had multiple tumors.
Twenty-five percent of both the irradiated and the control groups were African American. Among all of them, across fifty years, three skin cancers occurred.
The authors read this as evidence of how much ultraviolet susceptibility matters as a cofactor, and light complexion, severe sunburning and North European ancestry predicted risk within the irradiated group.
It is the only place in this entire section where a medical harm arrived overwhelmingly in white patients and largely spared everyone else. It is worth naming for the same reason all the other asymmetries are worth naming: skin genuinely differs, in specific measured ways, and the honest position is to report the difference in whichever direction it runs.
Before the next bottle of shampoo
If a child’s scalp has been flaking for more than a few weeks, or there is a patch of broken-off hairs, or a bald patch with any scale, ask for a fungal culture before another shampoo. If there is a swollen boggy lump, ask today, because that is the version that scars.
If it comes back positive, the treatment is oral, it takes weeks, and stopping early is how it comes back. Ask whether the household should be checked — a third of families in the contact study had a carrier — and remember that a carrier with no symptoms is the person who reinfects the treated child.
And if you are an adult with a scaly scalp and thinning hair and you have been managing it with medicated shampoo for years, the seven women in that clinic review are the reason to ask, once, whether anybody has actually cultured it.
Evidence check: Moderate
Evidence level: consistent culture surveys across three American cities finding the same concentration and the same carrier fraction. The newest primary prevalence study in this set is from 2005.
Sources reviewed September 14, 2026: Ghannoum M, Isham N, Hajjeh R, Cano M, Al-Hasawi F, Yearick D, “Tinea capitis in Cleveland: survey of elementary school students,” J Am Acad Dermatol 2003;48(2):189-93, PMID 12582387. Williams JV, Honig PJ, McGinley KJ, Leyden JJ, “Semiquantitative study of tinea capitis and the asymptomatic carrier state in inner-city school children,” Pediatrics 1995;96(2 Pt 1):265-7, PMID 7630681. Williams JV, Eichenfield LF, Burke BL, Barnes-Eley M, Friedlander SF, “Prevalence of scalp scaling in prepubertal children,” Pediatrics 2005;115(1):e1-6, PMID 15629960. Pomeranz AJ, Sabnis SS, McGrath GJ, Esterly NB, “Asymptomatic dermatophyte carriers in the households of children with tinea capitis,” Arch Pediatr Adolesc Med 1999;153(5):483-6, PMID 10323628. Silverberg NB, Weinberg JM, DeLeo VA, “Tinea capitis: focus on African American women,” J Am Acad Dermatol 2002;46(2 Suppl Understanding):S120-4, PMID 11807474. Grigoryan KV, Tollefson MM, Olson MA, Newman CC, “Pediatric tinea capitis caused by Trichophyton violaceum and Trichophyton soudanense in Rochester, Minnesota, United States,” Int J Dermatol 2019;58(8):912-15, PMID 30548845. Ginsburg CM, Gan VN, Petruska M, “Randomized controlled trial of intralesional corticosteroid and griseofulvin vs. griseofulvin alone for treatment of kerion,” Pediatr Infect Dis J 1987;6(12):1084-7, PMID 3324039. Shore RE, Moseson M, Xue X, Tse Y, Harley N, Pasternack BS, “Skin cancer after X-ray treatment for scalp ringworm,” Radiat Res 2002;157(4):410-18, PMID 11893243. Tack DA, Fleischer A, McMichael A, Feldman S, “The epidemic of tinea capitis disproportionately affects school-aged African Americans,” Pediatr Dermatol 1999;16(1):75, PMID 10028011. Rucker Wright D, Gathers R, Kapke A, Johnson D, Joseph CL, “Hair care practices and their association with scalp and hair disorders in African American girls,” J Am Acad Dermatol 2011;64(2):253-62, PMID 20728245.
This article is educational and is not a substitute for care from someone who can look at your skin. Anything new, changing, painful or spreading should be assessed rather than researched.
