Athletes' Foot?

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My eleven year old grandson has been complaining of severe itching and cracks between his toes, his mother took him to the GP who gave him Daktarin, but his foot became swollen and there are blisters not only underneath on the soles but even on top of his foot. Only one foot is affected. The GP took swabs and a week later gave him penicillin. He has been using the Daktarin for over a week now and still new blisters break out.

Any ideas?

 

Hi zsuzsanna,

I think maybe the second pic could be your answer. The vesicles look like the second phase of an irritant contact dermatitis, that is; allergic contact dermatitis with the usual suspects of localised erythema, inflammation and pruritic papules associated with prolonged exposure to a sensitizing agent. In this case, probably the rubber in the flip-flops. My son manifested similar unilateral symptoms a couple of summers ago. He ditched the itch by ditching the rubber footwear.
If you`re interested, during the primary irritant phase (first exposure, leading to recognition of an antigen) the skin responds with localised erythema, often on the toes and dorsum of the foot, yet rarely interdigitally (unlike tinea). If the pt is exposed to the sensitizing agent for a sufficient time, an allergic phase occurs as the T cell-mediated immune response is triggered in response to the antigen.

Interesting that the GP prescribed ABs. Did you ask which bacterium was isolated from the swab?

Hope this helps your grandson.

Cheers,
Bel

 

Just a thought Bel,

Why if it is contact dermatitis are the blisters not at the points of contact, ie between 1 and 2 and across the dorsum?

Also why only one foot?

 

Good question, Bob.:drinks

That is why I made a point of saying `Allergic Contact Dermatitis*` (ACD), which is the next phase after Irritant Contact Dermatitis (ICD). It can be difficult to differentiate between ICD and ACD; however acute ACD generally presents with intense erythema, oedema and pruritic vesicles may spread beyond and around the site of contact, due to allergens spreading with increased vascularity and perspiration. ICD is more localised and looks rather like a burn with blistering. Ivan put it well in his Text Atlas of Podiatric Dermatology(2001); “Allergens which are absorbed into the circulation on the sensitized lymphocytes travel to other parts of the body where it may appear without direct contact”. So, although the dermatitis is often confined to the site of contact, at least on initial/first exposure, Gary Dockery (another of my favourite Dermy Pods) explained that "prolonged exposure to a sensitizer can cause the dermatitis to extend to adjacent areas or in more severe cases, may even become widespread". He also said; “In many instances the proper diagnosis is delayed due to extended treatment of the condition with topical antifungal creams, which exacerbate symptoms". The pics didn`t look particularly fungal to me and rubber components, or rubber accelerators used in footwear manufacture, are listed amongst the top ten deejay stylie sensitizers associated with ICD and ACD of the foot.

You`re right, bilateral symmetrical presentation is usually the norm in footwear related Contact Dermatitis, although Johansen et al state that it `may be patchy and even unilateral`, so did these guys, as did Nardelli et al - The relation between the localization of foot dermatitis and the causative allergens in shoes: a 13-year retrospective study (nudge me if you want a copy of the full text). Interestingly, the aforementioned also said;” ...in chronic cases, the specific pattern of the disease may no longer be present. For example, allergens can leach out of the shoe to affect parts of the foot that are not normally in contact with it".

Cheers,
Bel

*Dermatitis is interchangable with eczema, in this instance.

 

Bel,

Thanks for the comprehensive reply.

I think I would want a bit more information about the onset and duration of the lads problem before reaching any conclusion.

You describe acute ACD as 'puritic vesicles may spread beyond and around the site of contact', but I conclude from that that they would also appear at the point of contact? Also mainly the interdigital spaces are spared.

All very interesting.

Of course there is no problem in stopping wearing the flip flops or doing some patch testing.

As yet we do not know the results of the penicillin treatment and I'm not convinced that Daktarin is a very good antifungal.

Once got caught out by the initial stages of a psoriasis flare up, looked very fungal.

Bob

 

Indeed. That is why I said "could be" , "probably" and "may". Without medical and social history, detailed description of onset and duration we can only make wild stabs in the dark

With regard to the initial contact phase with any sensitizer (probably rubber), this may have been confined to the footbed of the flip flop as the 'thong' bit, which is in contact with the dorsum and between the 1st and 2nd, is often made from plastic rather than rubber components. Only an idea, of course. And by no means a diagnosis.

I'm also keen to hear the results of the swab and the clinical reasoning for prescribing ABs. If pathological tinea was not isolated then I don't understand why the continuation of an anti-fungal was recommended. And I agree with you, Bob. Daktarin is only fungistatic so pretty useless anyway.

 

Bel, Bob

Saw the pictures and immediately thought pompholyx...then read your debate.

Agree that the debate needs more input from Zsuszanna and if her location is correct (SE England) I doubt that her grandson's choice of footwear has been flipflops...more likely flippers which I know, still rubber.

Given Bel's input I do see a dermatitis/eczema reaction but not convinced of a "simple" contact allergy. The cause of pompholyx is not a definite, it is thought to be triggered by contact with certain allergens so perhaps could account for the random areas affected?

A swab has obviously revealed infection, probably secondary. Trust the Path Lab guys. Knowing what I got up to as an 11 year old, a good old itch and scratch with grubby fingernails on damaged skin, I can see how easily a secondary bacterial infection can take a hold.

GB

 

Hi George,

Yep, pompholyx certainly falls within the dermatitis/eczema umberella, which is what I was alluding to. However, having briefly stepped into the world of immunology for literature reviews, I would not really describe any hypersensitivity, or contact allergy, as "simple".

I would agree that secondary bacterial infection was probably identified by the swab, hence the AB prescription, but would be interested to hear why anti-fungal treatment was continued.

Your mentioning flippers reminded me of a pic that my hairdresser sent me. Apparently this is what they`re all wearing in Bridport these days;



Guess we`re all waiting for zsuszanna`s input now, before we can go any further with this. Good discussion guys :drinks

 

Bel

Guess why I put simple in inverted commas? Agree totally that no contact allergy is simple...it can be a precursor to the positively drastic. But how many times does it get dismissed as such? Not in my clinic for all the reasons you state.

I do believe that this young man's (OP grandson) GP is absolutely on the ball. Isn't there evidence to support the need to treat fungal infections as a potential trigger for eczema/Pompholyx? Agree Daktarin is not the best choice. Is Terbinafine Cream licensed for use on the under 16's yet? Maybe GP is organising allergy testing as we all debate....come on Zsuszanna help us out.

Always appreciate the references you give, Bel, especially as I tend towards the practical side of treatment and pick the brains of others for the evidence base...we can't all be "good" scholars!

GB

 

Sorry, George. Not good at guessing games. I don’t know why you put simple in inverted commas. Perhaps you could explain?

I don’t think we are in a position to say whether the GP is on the ball, or not, without further input from zsuszanna. I`d still like to know the results of the swab.

Not where there is no evidence of tinea infection, so far as I am aware. Do you know of any? In fact, as I posted earlier, Gary Dockery stated in his book Cutaneous Disorders of the Lower Extremity (p137); “Appropriate treatment of contact dermatitis is frequently delayed because of misdiagnosis and long-term treatment of this condition with topical antifungal agents.” Which is supported by these guys who discuss sensitization to topicals containing miconazole, which is, coincidentally, the active ingredient in Daktarin.

I do believe it is. Dermatologists are now prescribing oral terbinafine for under 16`s.

Maybe igs:

Thank you for the compliment, I think. I would hope that I am also practical in a clinical setting. I certainly don`t consider myself an above average scholar. I may have said this before; I simply have an unhealthy interest in skin.

Cheers,
Bel

 

Bel

Please do take my appreciation as a compliment. It was intended as such. The rest of the statement I made refers to my choice to turn up to lectures/CPD events, be spoonfed the evidence rather than creating it then turning it into practical applications within the clinic setting.

As for the use of inverted commas or quotation marks...no hidden agenda here either. They were used as a touch of irony... lifted from Wiki:

Hope this better explains my last posting to you.

GB

 

DERMATOLOGICAL COMORBIDITIES AND ASSOCIATED DISORDERS

Atopic eczema may predispose to and coexist with other dermatological disorders that may complicate diagnosis, such as hyper-IgE syndrome, scabies, herpes simplex infection,staphylococcal and streptococcal infection, superficial fungal infection and contact dermatitis(irritant and allergic). Widespread herpes simplex (eczema herpeticum) should be considered in any patient with rapidly deteriorating atopic eczema. Some rare genetic disorders are associated with a pattern of cutaneous inflammation that resembles atopic eczema. These include Wiskott-Aldrich syndrome, anhidrotic ectodermal dysplasia, phenylketonuria, Netherton’s syndrome, ataxia-telangiectasia and agammaglobulinaemia.

http://www.sign.ac.uk/pdf/sign125.pdf

Not very good at this hyperlink thing but hopefully it will show in my post. The paragraph above is what I was remembering from when looking up current NICE and SIGN guidelines on the treatment of eczema. This is taken from point 3.3 of the SIGN Guideline 125.

I seem to get an inordinate amount of dermatitis/eczema/psoriasis patients passing through my clinic and as part of my self directed learning a wee while ago, the guidelines made for interesting reading. I don't have access to any papers that support the statement in the SIGN 125.

Does coexist indicate a happily ever after or fungus irritants can cause eczema or vice versa, eczema breaks down skin integrity allowing secondary infection? Unsure.

My other half just happens to be a Biomed Scientist, is involved in the identification of fungal infection and was happy to answer my questions: The biggest single problem for obtaining an appropriate result within the path lab is having a large enough sample to work with. In this case, I doubt I would have been able to obtain a suitable sized sample for microscopy and culture. If hyphae are present (microscopy) the GP will be advised immediately and he/she can expect results within 2 to 3 days of sending to lab. The choice of treatment is then based on the presence of hypae not the actual infecting dermatophyte. For culture, the result can take 2 to 3 weeks to obtain then the GP can be directed to the appropriate treatment plan.

Given the highlighted concerns about the use of Miconazole should the GP not treat for fungal infection until the culture results are obtained or should he/she risk treatment based on the ability for eczema and superficial fungal infections to co-exist?

I certainly do work on a process of elimination with patients who present with undiagnosed skin conditions ie lets try antifungals 1st, corticosteroids, emollients etc. Should they be referred straight to dermatology in the future?

Good debate and thank you for making me think.

GB