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Can a Fungal Infection Cause Body Odor? What Is Published

The antifungal-shampoo theory is spreading fast in body-odour threads, and the logic behind it is reasonable. The evidence underneath it turns out to be almost entirely absent — and two famously smelly conditions with fungal-sounding names are bacterial.

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Somewhere in the last couple of years, body-odour threads acquired a new theory. It goes like this: you have tried every deodorant, you have tried every soap, and then you borrow the anti-dandruff shampoo out of the shower and use it on your armpits — and something finally shifts. The conclusion follows naturally. If an antifungal worked, the problem must have been fungal.

It is a reasonable inference, and it deserves checking before it becomes received wisdom — the treatment involved is a medicine rather than a cosmetic, and the published record behind it is much thinner than the confidence in the threads.

The short answer, and why it is not quite a no

Start with what is true. The most thorough published characterisation of what grows in the armpit describes four principal groups of bacteria — staphylococci, aerobic coryneforms, micrococci and propionibacteria — “and the yeast genus Malassezia” (Taylor et al., 2003). So anyone who says there is yeast in your armpit is right.

The same study is also the problem with the theory. Having counted everything, the authors compared what they found against how much the volunteers’ armpits actually smelled, and the comparison “demonstrated the greatest association between odour levels and the presence of aerobic coryneforms in the under-arm”. The coryneforms are bacteria. The one investigation that weighed the yeast and the bacteria side by side, then measured smell, found the smell tracking the bacteria. The corresponding author worked at Unilever, which sells deodorants; that does not make the measurement wrong, but it is worth knowing.

That eight-word comment is the whole theory, and the thread it appears in argues with itself rather helpfully.

Both are offered a few comments apart with equal confidence. Only one has a literature behind it.

What the yeast actually does, and where

Here the story gets genuinely interesting, because the mechanism is not silly at all.

Malassezia is lipophilic: it lives on sebum-rich skin and works on fats with its own enzymes. Researchers have tried to turn that against it, designing fatty acid esters that the yeast’s own exo-enzymes cleave into antimicrobial fatty acids — a targeted self-kill (Koch et al., 2020; three authors worked at the fragrance company Symrise). A small joke is buried in that paper: those esters cannot be used at useful topical strengths because of, in the authors’ words, “the disadvantage of strong odour”. The anti-Malassezia agent smells.

More to the point, the yeast makes volatiles of its own. In an experiment whose title does the explaining — Yeast Smell Like What They Eat — Malassezia furfur was grown in four liquid media, one with oleic acid, one with palmitic acid, one with both and one standard, and the headspace above each culture was profiled. Sixty-one volatile organic compounds turned up, dominated by alkanes, alcohols, ketones and furanic compounds, and the authors showed that “each tested growth medium stimulates the production of a different volatiles profile” (Gonzalez et al., 2019). Hexan-1-ol, pentyl acetate, dimethyl sulphide and others separated the treatments.

Two things about that. It is a plausible route to a human smell, and nobody should pretend otherwise. It also happened in liquid medium, with no skin and no nose involved — and 2-nonenal, the compound associated with age-related body odour, is not among the volatiles reported.

Where the yeast and the molecule have actually met in print

There is exactly one indexed paper in which 2-nonenal and Malassezia appear together in the title or abstract, and it is about beef. Researchers profiling flavour development in post-mortem aged beef found nine aroma-active compounds, (E)-2-nonenal among them, enriched in beef wet-aged for seven days, and five microbial genera — Trichosporon, Prauserella, Rhodotorula, Malassezia and Corynebacterium — “constituted the functional microbiota responsible for flavor formation” (Wang et al., 2023).

So in the only place the two have been formally connected, both the yeast and the classic odour bacterium are credited — in a cold room, in meat, by food scientists. That is not evidence about armpits. It is a fair illustration of what the research on this molecule mostly is: chemistry done for commercial reasons in other industries.

What a search for fungal body odour returns

The honest centre of this post is a set of empty result pages.

A PubMed title-and-abstract search pairing Malassezia with “body odor” returns nothing. Pairing “antifungal” with “body odor” returns nothing. Pairing any fungus-word with “axillary odor” returns nothing. Pityriasis versicolor — the signature Malassezia skin disease, the one with the visible patches — has never appeared in a title or abstract alongside odour either, and nor has seborrhoeic dermatitis, except in two false friends where the smell under discussion is coal tar. A search pairing Candida with body odour returns a single record, and that record is a monograph entry titled “Garlic”.

These are absences rather than proof, with one qualification that earns them their place: a trial or case series proposing a fungal cause of body odour would be very unlikely to avoid these particular words in its title or abstract. The silence is not a wording artefact.

Ketoconazole specifically — the drug in the shampoo the threads recommend — appears alongside odour in six papers, and we read all six: an experimental study of Christmas decorations with topical preparations, a cyclodextrin inclusion complex, the antifungal activity of a Brazilian fruit essential oil, a vaginitis treatment trial, a scalp white piedra case report, and a stability study of compounded oral liquids. Not one concerns deodorising human skin.

The official health bodies are silent in both directions, which is the cleanest version of the point. The NHS page on antifungal medicines does not mention smell. The NHS page on ringworm does not mention smell. And the NHS page on body odour does not mention fungus or yeast.

Two smelly conditions named after fungi that are not fungal

If the fungal theory has a real origin, this is probably it, and it is a naming accident twice over.

Trichomycosis axillaris sounds definitive: a condition of the underarm hair, a name ending in -mycosis, and malodour among its symptoms. It is bacterial. A 2025 study of 78 patients describes it as “the most common superficial bacterial infection of hair shaft, mainly of axillary hairs and producing pigmented concretions around hair shaft caused by various species of corynebacteria”. Nineteen had no symptoms; the rest reported “malodor, staining of clothes, and itching”. Cultures grew diphtheroids and staphylococci (Kalimuthu et al., 2025). Gritty yellow nodules clinging along underarm hairs plus a stubborn smell is a thing to show a clinician — and not something an antifungal is for.

Gram-negative toe web infection makes the same mistake in the other direction, and the specialists have said so in print: the 2026 German guideline on what is now called infected interdigital intertrigo records that the old term “misleadingly implied a soft-tissue infection of the foot” and was replaced. The condition itself is the one real place fungi belong in a discussion about smell — a “mixed infection of the toe webs in which gram-negative bacteria … seem prevalent, but in which gram-positive pathogens … and fungi (dermatophytes, yeasts) also occur”, diagnosed clinically from “painful macerated erosions or ulcers with yellow-green exudate, putrid odor and edema”, and treated with antiseptic and antifungal agents together (Zeyen et al., 2026).

Note what that is and is not: an open, weeping, visibly damaged skin surface, on feet, where the smell is attributed to the bacterial side. It is not a vague stale smell in a healthy armpit.

Why the shampoo can help anyway

None of the above says the shampoo did nothing. It says the improvement does not identify the cause, and there are at least three ordinary explanations.

The first is the dullest and probably the strongest. An antifungal shampoo used as a body wash is a surfactant left on the skin for a minute or two, which is a more thorough wash than most armpits get. The same thread reports the same result from rubbing alcohol, witch hazel, glycolic acid toner, benzoyl peroxide and chlorhexidine — five mechanisms, one outcome. When five different chemistries all “work”, the common factor is unlikely to be the chemistry.

The second is that the armpit is not a fixed personal trait. In an experiment where product use was manipulated rather than observed, stopping deodorant and antiperspirant raised culturable bacterial density toward non-user levels, applying antiperspirant again made it “decline dramatically”, and two days off shifted the community toward Staphylococcaceae (Urban et al., 2016). Change what you put on your skin and the population changes over days — which is also why a new product often works for a fortnight and then stops, as we have argued about hypochlorous acid sprays.

The third comes from a proper trial. Thirty volunteers wore zinc oxide on one armpit and placebo on the other, double-blind, for 13 days. Odour-producing Corynebacterium and Staphylococcus hominis fell, and self-judged malodour fell with them — while skin-surface pH moved in the opposite direction to what the acidic-deodorant story predicts (Ågren et al., 2020). A product can work while the explanation for why it works is wrong. That applies to antifungal shampoos, to acidic deodorants, and to soap — including the kind we sell.

That trial design is worth a second look, because it treats a person’s two armpits as each other’s control. They are not quite identical: one typing study of 53 people found left-right differences in the bacterial community in roughly half of them, which is the measured part of the common complaint that one armpit smells worse than the other. What has not been shown is that the difference is usually large enough for anyone else to notice.

How to tell which of the three you are dealing with

There are really three processes competing for the blame, and they sort more easily than they sound.

1. Look before you smell. Fungal skin infection shows up as a rash. The NHS describes the main symptom of ringworm as a rash that “may be scaly, dry, swollen or itchy”, and Malassezia folliculitis — the condition popularly called fungal acne — “presents as pruritic, erythematous papules and pustules” and is routinely mistaken for ordinary acne (Draelos et al., 2026). If your skin looks normal, a fungal explanation has nothing to stand on.
2. If there is a rash, get it identified rather than guessing. That same review warns about “patients inappropriately applying antifungals without a confirmed diagnosis”, driven partly by social media trends — which is, precisely, the Reddit thread. A pharmacist is the NHS’s suggested first stop, and if a rash and a smell arrive together, our note on irritation and underarm rashes covers why treating the smell first is the wrong order.
3. With no rash, sort sweat from oil. Sour, oniony, strongest in the armpit, worst after exertion and responsive to deodorant points to the bacterial route — bacteria acting on precursors secreted in apocrine sweat, ending in a thioalcohol (Minhas et al., 2018). Faint, stale and greasy, strongest on collars and pillowcases and barely touched by deodorant points to the oxidation route, which has no microbes in its mechanism at all (Haze et al., 2001; emission measured against skin rises with age, Kimura et al., 2016).
4. Match the product to the process. A leave-on acidic deodorant is aimed at the bacterial route; we set out why that is a different target from a rinse-off bar. A rinse-off tannin soap is aimed at the oily one. Neither treats an infection, and our list of reasons persimmon soap does not work exists largely because people treat one process with a product built for another.

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One caveat from a different angle. The most recent direct look at fungi on the exact sites people are treating — axillary and groin swabs, sequenced rather than cultured — found the mycobiome dominated by Candida at 69.3 per cent, with Malassezia “rare (0.7%)” (Nascimento et al., 2025). Those were intensive-care patients rather than healthy adults and the authors call it a pilot study, so read it loosely — but it does not describe an armpit teeming with the organism ketoconazole targets.

Bottom line

Can a fungal infection cause body odour? Nobody has published anything showing that it does, and the shape of the silence is unusually complete: not one title-or-abstract pairing of the relevant yeast, the relevant drug class or the word “fungus” with body odour or axillary odour, no mention of smell on the NHS fungal pages, and no mention of fungus on the NHS body-odour page. What exists instead is a yeast that genuinely lives there, genuinely makes smells in a flask, and has never been caught doing it on a person — plus two famously malodorous conditions with fungal-sounding names that turn out to be bacterial.

The practical version is short. If you can see a rash, get it looked at. If you cannot, a fungal diagnosis has nothing to rest on, and the question becomes the ordinary one of sweat versus oil — which is where our comparison of the best persimmon soap options can help. And if the shampoo is working for you, keep using it if a pharmacist is content with that. Just hold the explanation more loosely than the result.

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