Reference: May 2026 | Issue 5 | Vol 12 | Page 30
Skin diseases often present with overlapping clinical signs. This can result in confusion and misdiagnosis, which in turn can lead to choosing the incorrect treatment. When it comes to managing disease, an accurate diagnosis is an essential starting point. Disc-shaped lesions present one such conundrum for the diagnostician.
As a general practitioner, when faced with a disc-shaped lesion, one has to ask: Is it a fungal infection, discoid eczema, psoriasis or perhaps something else? In my experience these three entities are easily confused, and I hope these illustrations will help improve your diagnostic accuracy.
Before reading this article, consider having a look at the clinical cases illustrated and before you read the captions, ask yourself: Is it a fungal infection, discoid eczema, psoriasis, or perhaps something else?
Discoid eczema
Discoid eczema is a common eczematous disorder characterised by scattered, circular or oval, exudative plaques with well-defined borders. With its coin-like shape it is often referred to as nummular eczema (derived from the Latin word for coin).
Similar lesions can occur with atopic eczema (Figure 8), asteatotic eczema, and stasis eczema, leading some to question whether discoid eczema is an independent clinical entity. It may be complicated by secondary bacterial infection, and seems to be particularly susceptible to Staphylococcus aureus colonisation. However, although the exact relation between Staphylococcus aureus colonisation and discoid eczema remains unknown; it does seem to flare the eczema lesions.
Pruritus is usually severe. All age groups can be affected, especially older adults. Eczema lesions usually start as small papules and papulovesicles on a red base. Over time, more and more papules and papulovesicles develop and become confluent to form the characteristic plaques of discoid eczema. Vesicles are thin walled and rupture easily, producing a prominent exudate which dries, leaving a crusted surface over the eczema plaques (exudative acute discoid eczema).
Over time, plaques become less vesicular and are dry with a covering of scale (dry discoid eczema). Some plaques develop central clearing to produce annular lesions that may be confused with tinea infection, especially as distribution of discoid eczema can sometimes mimic the asymmetrical distribution of tinea.
Discoid eczema most commonly affects the extremities, but involvement may be widespread. Distribution is usually bilateral. Most cases follow a relapsing/remitting course over months or years. In darker skin, clearance may leave patches of post-inflammatory hyperpigmentation or hypopigmentation. All phases of eczema may be seen. Lesions may be acute (vesicles and weeping) or chronic (lichenified, scaling, and hyperkeratotic). Subacute lesions (combining oozing and scaling) are common.
Management
Emollients: Patients with discoid eczema tend to have a dry background skin and a defective skin barrier function. Irritants such as soaps, shower gels, shampoos, detergent, washing up liquid, and polish need to be avoided. When washing hair in the shower, suds should be allowed run down the plughole directly, avoiding contact with the body as much as possible. If taking a bath, the hair should be washed separately, not allowing bathing in water mixed with shampoo. Before a bath or a shower, a greasy moisturiser might be applied if the skin is particularly dry. For the body, a liquid moisturiser should be substituted for soap and shower gel. Following a shower or bath, the skin should be moisturised. A regular moisturising regimen, outside bath or shower time, should be started.
Topical corticosteroids: Topical corticosteroids(TCSs) have potent anti-inflammatory effects and constitute the first-line therapy for acute flares of discoid eczema. TCSs are safe when the appropriate potency is employed, depending on the body area being treated (Table 1).
Most discoid eczema occurs in adults and involves the limbs and trunk. Potent or very potent TCSs are needed to get control. Clobetasol propionate ointment (or as a cream if lesions are very wet – creams tend to dry oozing lesions) may be applied daily. After about a week you will hopefully have had a good response and may step down the potency to betamethasone butyrate ointment once daily.
In the event of frequent recurrences, consider suppressive TCS use combining betamethasone butyrate ointment daily for two days each week with ongoing with irritant avoidance and moisturisation.
Tinea corporis
Tinea corporis is a superficial fungal infection of the trunk and limbs. It presents as ring-shaped lesions with an advancing, scaly, and a slightly raised edge. As the advancing edge looks like a worm, it is commonly referred to as ‘ringworm’. The causative dermatophytes constitute a group of fungi that produce keratinases, which break down keratin, allowing the dermatophytes penetrate keratinised human tissue such as hair, nail, and skin.
Tinea corporis starts as a single red patch with a raised scaly leading edge that gradually advances from the centre to give the classic ring-shape rash with central clearing.
The clinical signs of tinea skin infection vary, depending on the degree of inflammatory host response. Trichophyton rubrum (from humans) induces a mild response. Trichophyton verrucosum (from cattle) induces a vigorous inflammatory response, while in Trichophyton tonsurans (from humans), the response may vary from mild to severe.
Microsporum canis (from cats and dogs) does not usually give a brisk inflammatory response, although a high infection load may. The case illustrated in Figure 13 was associated with a prod from a sharp piece of hedging associated with a cat spending a lot of time in the patient’s lap.
Tinea incognito
If tinea skin infection is misdiagnosed (as dermatitis, psoriasis etc) and treated with a topical steroid, the clinical features are markedly modified (Figure 10). As the name suggests, tinea is in disguise, and is sometimes called ‘steroid-modified tinea’. It was first described and named by Dr Adrian Ive and Prof Ronnie Marks. Those of you who participated in the early years of the Diploma in Practical Dermatology in Cardiff will remember Prof Marks, who was quite a character. They later admitted that their classical education had let them down. They should have termed it tinea incognita as tinea is feminine.
When we examine a rash, we rely on the inflammatory reactions provoked in the skin by tinea infection. This inflammatory reaction may be suppressed by corticosteroids. In addition, steroids may have an immunosuppressive effect, leading to spreading of the rash. Suppression of inflammation leads to relief of pruritus, encouraging the patient to continue steroid use. You end up with a rash that feels better, but is spreading, and as it extends it may mimic other skin diseases.
Clinically, the extending rash with a raised, continuous edge is broken up and is less raised. Scaling at the rash margins is lost, nodules and, more rarely, pustules may develop and concentric arcs are common. All potencies of TCSs may induce tinea incognito with potent, and very potent, TCSs carrying a higher risk. The mild potency, hydrocortisone, may lead to tinea incognito, especially on the face (Figure 11).
With loss of scaling, scrapings may be difficult to obtain. Stopping the TCSs for a few days prompts a rapid return of inflammation and scale production. The clinical appearance may again resemble tinea and scrapings are more easily collectable. The diagnosis should always come to mind when faced with a unilateral or asymmetric, scaly or pustular rash with an irregular border that is spreading with the application of a topical steroid.
Management
Tinea incognito is best managed with oral terbinafine or itraconazole. The topical steroid may be continued for the first few days of oral antifungal to reduce the risk of a severe flare.
Kerion
As outlined, the clinical signs of tinea skin infection vary depending on the degree of inflammatory host response. With a milder response, the typical picture of circular lesions with a scaly, advancing edge are seen. If the immune response to the dermatophyte is dramatic, a severe inflammatory reaction called a kerion may result.
Trichophyton verrucosum, the most common culprit, is not unusual in rural Ireland. It presents as an inflammatory mass, sometimes studded with pustules or a boggy abscess discharging puss. With this appearance it is often misdiagnosed as a bacterial infection (Figure 14). It arises most commonly on the scalp, but can occur on the face, upper limbs, and other body sites. This is usually caused by one of the zoophilic species (from animals), typically Trichophyton verrucosum, Microsporum canis, Trichophyton tonsurans, or Trichophyton mentagrophyte.
Management: Six to eight weeks of oral terbinafine or itraconazole.
Palmoplantar pustulosis
Palmoplantar pustulosis is a chronic, and often relapsing, dermatosis affecting typical sites on the palms and soles. (Figures 15 and 16). It is still sometimes referred to as palmoplantar pustular psoriasis, but it is now accepted as representing a distinct clinical entity.
The rash has a sharp, non-raised margin. Sterile pustules resolve to leave distinctive, brown macules, a most useful diagnostic clue. Scaling and peeling may be evident on the background, over the erythematous plaques. Itch is not usually prominent, and many complain of a more stinging discomfort.
It usually presents between the ages of 20 and 60 years, and is more common in females. About 80 per cent of patients are cigarette smokers. Stopping smoking may benefit.
Management: Emollients containing keratolytics (salicylic acid or urea) to moisturise and help break down thickened keratin. Topical potent or very potent steroid ointment formulations are first-line. After application at night, they may be covered with cling film or polyethylene gloves, left on overnight. This increases the potency of the topical steroid by a factor of five, and occlusion should be stopped after one week, while the steroid may be continued. Morning application of tar or calcipotriol added to the topical steroid at night may impact to the therapeutic response. Response to topical treatment is frequently disappointing. Early referral to secondary care is encouraged.
Figure 1: Early discoid eczema with scaling and oozing from ruptured vesicles.
Figure 2: Same patient (Fig 1) with papules and vesicles coalescing to form a patch of subacute eczema with marked redness and oozing.
Figure 3: Discoid eczema mistaken for tinea. One month of oral terbinafine ineffective. The picture is of a more chronic eczema with less redness and no vesicles or oozing.
Figure 4: Lichenification, lack of central clearing, and lack of a raised advancing edge suggest discoid eczema rather than tinea.
Figure 5: Extensive discoid eczema. Staphylococcal infection.
Figure 6: Close up of lesions in the same patient (Fig 5). Note the inflammatory papules of spreading eczema beyond the margins.
Figure 7: Lower limb dscoid eczema with oozing, crusting, and papules coalescing beyond the margins forming new patches.
Figure 8: Two year old with a history of atopic eczema, now presenting with discoid pattern near the shoulders. Honey coloured crusts suggest staphylococcal infection.
Figure 9: Typical early tinea corporis due to Microsporum canis in a young boy. Note the advancing, raised, inflamed edge with central clearing.
Figure 10: Look what happens when a mild potency topical steroid was applied to a similar rash
(Fig 9), but different
patient – tinea incognito.
Figure 11: Tinea incognito on the face may be difficult to appreciate. Think of it if faced with inflamed nodules in a spreading rash while applying a topical steroid.
Figure 12: Tinea incognito. Groin rash misdiagnosed as psoriasis. Betamethasone plus calcipotriol applied and followed by rapid spread over buttock and leg.
Figure 13: A rapidly advancing, vesicular edge.with pustules. Mistaken
for cellulitis. Micrisporum canis was the suprising cause. A puncture wound facilitated fungal entry.
Figure 14: Trichophyton verrucosum causing a kerion on the forearm. Remember if you find pustules or a boggy swelling think kerion.
Figure 15: Early palmoplantar pustulosis on hands. More lesions develop and coalesce to a plaque. There may be only a few pustules and brown macules, so always examine carefully.
Figure 16: Palmoplantar pustulosis. Note pustules fade to brown macules. Margin is discrete and without a raised edge.