The unprecedented epidemic-like scenario of dermatophytosis in India: I. Epidemiology, risk factors and clinical features

Incidence and prevalence

Though there have been many studies on superficial dermatophytosis, it is difficult to calculate the exact incidence and prevalence owing to a paucity of community-based surveys. The current reported prevalence in India falls in a very wide range (6.09%⁶– 61.5%⁷). A prevalence of 6.09% to 27.6% has been reported in studies from south India,^6,8 while a high prevalence of 61.5% has been recorded in north India.⁷ Most of this data comes from hospital-based studies over periods ranging from 1- 2 years^6-8 Interestingly, though dermatophytosis is expected to be more prevalent in the hot and humid climates of south India and less so in north India, no such association is apparent. We feel that there has been a rising trend of dermatophytosis all over the country in the last 5–7 years.

Further, there appears to be a steady increase in the incidence of chronic, relapsing and recurrent dermatophytosis; it is not uncommon to encounter disease durations running into months or years. Agarwal et al. in 2014 reported disease of >3 months in 163/300 patients (62.5%).⁹ Of the 300 patients, 28 (9.3%) had had similar episodes in the past and 87 (27.7%) patients had been treated previously with medications other than antifungal drugs. Since then, there has been a rising trend of recurrent and relapsing dermatophytosis [Table 1].^9-16

These trends are unique to the present epidemic-like situation of dermatophytosis in India and are not described in the standard dermatology textbooks from the Western world.

Age and sex

In general, dermatophytosis occurs most frequently in postpubertal hosts, with the exception of tinea capitis. Conventionally, men are more frequently affected than women because of the significantly high incidence of tinea cruris, tinea pedis and tinea unguium in men,¹⁷ and outdoor work predisposes men to hot, humid and sweaty conditions conducive to the growth of dermatophytes. However, in the present epidemic, these boundaries are getting blurred with the rising incidence of dermatophytosis in women and children [Table 2].^{7,12-15,18-25} It is clear that the male:female ratio is < 2 in all the studies published in the last 3–4 years^12-14,18-20 in contrast to earlier studies where the ratio was 3–5, indicating a rising prevalence in women.^24,25 Recent studies have even shown the reversal of the men:women ratio.^13,19 As most Indian studies on superficial dermatophytosis have included only adult patients, the exact incidence of cases among children cannot be ascertained. Only a single study by Noronha et al. from south India has included patients of all age groups.²⁶ This study reported that 21.3% of patients were in the age range of 0–10 years, similar to the proportions of adolescents and adults (21.3% and 22.7% in the age range of 11–20 years and 21–30 years, respectively).²⁶ In our experience, it is not uncommon to see infants, toddlers and children of all age groups presenting with all morphological types of dermatophytosis, viz., extensive tinea cruris, tinea corporis and tinea faciei.

Chronic dermatophytosis (disease for more than 6 months with or without recurrence despite being treated) is more common in the late middle age group, around fifth decade, which is attributed to waning immunity, comorbidities like diabetes and other risk factors such as positive family history, use of topical steroid-antifungal creams, immunosuppressants intake etc.¹⁴ However, in a recent study on 150 patients of recurrent dermatophytosis, the mean age of patients withchronic dermatophytosis was lower (32.5 years).¹²

Familial cases

Recent studies have reported a very high frequency of history of dermatophytosis in close contacts (72-82%)^11,12,19 Chronicity and recurrent infection have probably contributed to the rise in the incidence of familial infection. Connubial dermatophytosis is common.⁵ The spouse and children, often the whole family, have concomitant dermatophytosis. A high prevalence occurs in people living in overcrowded homes, slums, hostel rooms and dormitories. A careful inquiry into family history has become the norm; all affected family members must be treated simultaneously to prevent recurrences.

Urban versus rural areas and literacy

People from both urban and rural areas are at increased risk of dermatophytic infections.Studies from the first half of the past decade reported a rural predominance, possibly due to the high frequency of outdoor work including agriculture predisposing to increased perspiration.^6,27 However, studies in the last 5 years have shown greater proportions of patients from urban areas (around 80% of patients).^7,22 This change was initially attributed to increased awareness, literacy and cosmetic concerns in the urban population leading them to seek medical attention. However, the predominance seems to be dependent on the place and nature of the study. The relatively easy availability of creams containing irrational combinations of potent topical steroids along with antifungal and antibacterial agents in urban areas as compared to rural might be a contributing factor.

Education and literacy have not been commented upon much in reports concerning the increased incidence of dermatophytosis. Kaur et al.⁷ reported the frequency of literate patients (64.6%) to be more than the illiterates (35.3%). Similarly, a recent study showed that the majority of their patients had medium educational qualifications (60.20%).¹⁹ These findings can also perhaps be interpreted as above.

Socioeconomic status

A higher proportion of patients with dermatophyte infections are still from lower socioeconomic groups, with studies reporting an incidence of 61–67%.^6,22,26 This is followed by lower-middle and medium socioeconomic strata.^9.19,26 Poor standards of living, lack of hygiene, overcrowding and poor nutrition in the lower socioeconomic groups promote the growth of dermatophytes, increasing the risks of infection, chronicity and recurrence.

Occupation

People engaged in outdoor activities in hot and humid environments are at a greater risk of infection since this provides a favorable environment for dermatophytes. Recent studies too have reported that manual laborers are most commonly affected.^13,18.22 Farmers are at an additional risk due to increased exposure to fungal pathogens from the environment and frequent contact with soil and animals.⁹

More homemakers with active infection are seen now.¹³ The hot environment of the kitchen with increased sweating favors the growth of dermatophytes, making homemakers susceptible. Rudramurthy et al. found homemakers as the most common affected group (25.1%) in their study.¹⁵

An increased frequency of dermatophytosis has also been reported in students recently.^9,10,22 Increased sweating during school and sport activities along with wearing of school uniform and footwear for prolonged hours might be contributory factors. Moreover, wearing tight-fitting synthetic clothing, common amongst younger individuals, provides damp and warm skin conditions^5,13 possibly contributing to the increased prevalence, recurrence and chronicity of these infections in them.

Topical steroid abuse

Topical steroid misuse may be the most important cause of the current outbreak of chronic and recalcitrant dermatophytosis. A strong temporal association has been observed between the increasing availability and irrational use of the combination creams (antifungal-steroid or antifungal-antibiotic) with the sudden increase in chronic, recurrent and refractory cases in the past 4–5 years.⁵ Potent steroid-containing creams are easily available over the counter without prescription. They are often suggested by pharmacists or friends, or are prescribed by general practitioners, and patients keep using them erratically for months to years. At the time of presentation to the dermatologist, most patients are found to have taken some form of treatment [Table 3]. Oral/topical azoles and topical steroids alone or in combinations are commonly self-administered by patients with dermatophytosis.¹¹ Studies in the last 1-2 years reveal that the frequency of prior application of topical steroid-containing combination creams is very high (42%¹⁶–81%⁴) among patients. Ironically, the use of topical antifungals was lower, seen in 5.7%⁹–47%¹³ of patients [Table 3].

Causative organism

Trichophyton mentagrophytes (mostly Trichophyton interdigitale) used to be the predominant organism responsible for superficial dermatophytosisbefore 1935 worldwide.^28,29 Thereafter, an epidemiological shift began with Trichophyton rubrum replacing Trichophyton. mentagrophytes and emerging as the predominant organism by 1954 in many countries and continents (United States, Australia, Germany, Switzerland and Netherlands) including India with a reported incidence of up to 80%.²⁹ The environmental factors (humidity, temperature, trauma), internal factors (host-parasite relationship, host susceptibility) and immunological factors have been speculated for this shift along with the changing virulence of the organism.^4,29 It remained the most prevalent causative agent till the recent upsurge of dermatophytosis, when Trichophyton mentagrophytes has again emerged as the predominant organism. The same factors have been thought to be responsible as during the previous epidemiological shift.⁴ Moreover, a probability that the zoophilic Trichophyton mentagrophytes has acclimatised itself and has undergone anthropization leading to easy transmission among humans has been suggested.⁴ In the past decade, and especially from the beginning of 2012, the reported prevalence of Trichophyton mentagrophytes has not only increased,6,7,10,12,18,22,26,30 but it has even replaced Trichophyton rubrum in a few studies[Table 4].^9-11,24,26 The most recent studies have found Trichophyton mentagrophytes in more than 90% of their dermatophyte isolates. In a recent large multicentric study, Trichophyton mentagrophytes/ Trichophyton interdigitale complex was identified in 93.2 % and Trichophyton rubrum in only 6.8%.⁴ Yet another study recently demonstrated 97.2% of isolated dermatophytes to be Trichophyton mentagrophytes complex with the most significant species being Trichophyton interdigitale.¹⁴ Singh et al. too identified Trichophyton interdigitale in 94% of cases.¹⁶

Trichophyton mentagrophytes exhibits a rapid growth in primary culture within 5–7 days; this might explain the extensive involvement, inflammatory lesions and fomite transmission frequently seen now.⁵

Changes in clinical behavior

Induction of varying degrees of inflammation

It is common now to find moderate or severely itchy, peripherally spreading, flat, whitish or brownish lesions without erythema which yield profuse powdery scales when scraped [Figure 1a]. Such lesions have been called‘non-inflammatory’ superficial dermatophytosis³⁵, but the term may be inaccurate as the absence of erythema does not necessarily mean the absence of inflammation.

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Figure 1a:

Annular plaques of tinea corporis with minimal inflammation

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Multiple lesions in different anatomical locations exhibiting varying degrees of inflammation are also seen [Figure 1b]. Many patients report noticing diurnal changes, with lesions tending to get more erythematous and raised and the edges becoming more defined at times [Figure 1c]. Heat, humidity, sweating, tight clothing, friction, exercise and topical corticosteroid-containing fixed-dose combinations, are known to modify the appearance of lesions. These observations necessitate further research on host immunity, the virulence of the organism and the nuances of topical steroid use.

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Figure 1b:

Multiple annular erythematous plaques of tinea with peripheral pustular borders suggestive of severe inflammation

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Figure 1c:

Tinea corporis et cruris showing varying degrees of inflammation in the same patient

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Exacerbation of inflammation after starting treatment

An abrupt increase in the number of lesions with increased erythema, edema and occasionally pustulation, is seen on starting oral antifungal drugs like itraconazole in some cases [Figure 2a and b]; many of them have been abusing topical steroid-containing fixed-dose combinations. This phenomenon could be on account of withdrawal of corticosteroid with the administration of oral antifungal agents causing a recovery of the local cell-mediated immunity. Another phenomenon is the abrupt onset of multiple papules, plaques and at times, disseminated eczematous lesions with itching and burning in areas other than those with pre-existing tinea. These lesions appear soon after starting oral antifungal therapy and can cause diagnostic confusion between a dermatophytid and an adverse reaction to the antifungal agent, usually itraconazole.

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Figure 2a:

Sudden exacerbation of tinea with the appearance of multiple eczematous scaly lesions after starting antifungal therapy

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Figure 2b:

Sudden appearance of erythema and edema overlying a plaque of tinea faciei after starting antifungal therapy

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Changes in the morphology of lesions

Well-defined, centrifugally spreading lesions with central clearing and an advancing border, as described in textbooks, are not the rule now. A plausible explanation for this is that treatment-naïve cases are now uncommon.

The following are the morphological forms encountered in the current scenario:

Varying morphology

Unusually large lesions are seen, either due to centrifugal spread or by coalescence of multiple lesions. Circular or annular lesions, [Figure 3], arcuate and dumbbell-shaped lesions where two annular or circular lesions coalesce, annular lesions with pustular borders [Figure 4], and bizarre geographic lesions are common. Erythrodermic presentations of dermatophytosis are seen in immunosuppressed as well as immunocompetent individuals [Figure 5a and b].⁴⁰

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Figure 3a:

Multiple annular lesions coalescing to form a plaque

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Figure 3b:

Multiple annular lesions coalescing to form a plaque

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Figure 4:

Multiple coalescing lesions with pustules

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Figure 5a:

Erythrodermic variant of superficial dermatophytosis

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Figure 5b:

Erythrodermic variant of superficial dermatophytosis

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Incomplete central clearance and eczematous appearance

It is common to see incomplete clearing in the centre of lesions leading to variably defined areas of erythema with or without scaling i.e.,“eczematous tinea” [Figure 6a and b]. The natural course of the disease is for cell-mediated immunity to mount an inflammatory response and increase the epidermal cell turnover to eliminate the fungus by shedding the stratum corneum⁴¹. Lesions treated with steroids show activity in the centre as well as in the peripherally spreading margins.⁵ Topical steroid abuse slows down cell turnover and downregulates beneficial proinflammatory mediators, aiding survival of the fungus.

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Figure 6a:

Eczematous variant of tinea facei

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Figure 6b:

Eczematous variant of tinea corporis

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“Double-edged tinea” and tinea pseudoimbricata

Erratic application of fixed-dose combinations and steroid creams in tinea switches inflammation on and off, leading to “double-edged” tinea [Figure 7 ].⁴² The degree of inflammation in such cases often is high, and residual post-inflammatory hyperpigmented “double edges” persist for a long time after successful treatment too [Figure 7]. At times, the double edges are well-defined, running parallel to each other and with central crusting and erosions, resulting in a pseudoporokeratotic appearance [Figure 8a and b]. Repeated on-and-off cycles of inflammation for long periods can lead to concentric rings of tinea described as “tinea pseudoimbricata”[Figure 9a and b]. A “rings within a ring” appearance is also not uncommon and is characterized by smaller scaly lesions of tinea within a centrifugally spreading larger annular lesion, often with more than one border.⁴³ Double-edged tinea, tinea pseudoimbricata and tinea “rings within rings” lesions are all highly suggestive of steroid abuse, especially erratic use of steroid-containing fixed-dose combinations.⁴⁴

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Figure 7:

Double-edged tinea cruris

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Figure 8a:

Steroid modified tinea corporis with pseudoporokeratotic edges

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Figure 8b:

Steroid modified tinea with pseudoporokeratotic edges

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Figure 9a:

Tinea pesudoimbricata

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Figure 9b:

Tinea pseudoimbricata

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Another uncommon entity is tinea recidivans that describes the appearance of lesions at the periphery of a healed lesion [Figure 10a and b].

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Figure 10a:

Tinea recidivans

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Figure 10b:

Tinea recidivans on upper torso

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Pustular lesions in tinea

Pustular lesions are often seen at the periphery of inflammatory erythematous lesions of tinea being treated with potent topical steroids. In some cases, each ring of a tinea pseudoimbricata lesion can be studded with pustules, giving rise to a cockade pattern [Figure 11].

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Figure 11:

Cockade pattern of pustular lesions in steroid-modified tinea

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Majocchi’s granuloma

Rarely, dermatophytes may invade the dermis owing to the reduced local immunity induced by abuse of topical steroids. Such cases show pruritic papules, pustules and nodules in the areas of preexisting dermatophytic infection [Figure 12], and granulomatous perifollicular inflammation on histology.

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Figure 12:

Majocchi’s granuloma (Picture Courtesy – Dr. Chetan Rajput)

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Change in sites of skin involvement

The involvement of multiple body sites is common. Tinea corporis et cruris is the most common presentation;³ individual tinea corporis and tinea cruris are the next two commonest. Lesions at sites of occlusion like the waist and inframammary areas are frequent in female patients [Figure 13a,b].

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Figure 13a:

Tinea corporis limited to the area of occlusion by wrist band

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Figure 13b:

Tinea corporis presenting as a large annular plaque limited to the area of waistline along the line of occlusion by drawstring

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An interesting observation is the absence of a proportionate increase in tinea unguium, tinea pedis and tinea capitis.⁵

Involvement of unusual locations

Genital dermatophytosis

Genital dermatophytosis is not usually mentioned separately in standard textbooks, probably because of its rarity. Together with tinea cruris, it is referred to as tinea pubogenitalis. There is a male predominance with concomitant tinea cruris or tinea cruris et corporis, and the vast majority of these patients have a history of applying fixed-dose combinations containing topical steroids.⁵⁵ The base of the penis is most often affected, followed by the shaft and rarely, the outer prepuce. The scrotum is affected less commonly. Lesions on the penile shaft vary from well- to ill-defined areas of scaling [Figure 14] to annular lesions with or without pustules, on the dorsal [Figure 15], lateral or ventral aspects. Many cases are detected during the examination because they are asymptomatic and patients have sometimes not even noticed them. These lesions usually resolve within days of application of topical antifungal agents. We would like to stress the importance of identifying and treating them because otherwise they may easily become afocus for recurrence.

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Figure 14:

Tinea cruris with male genital dermatophytosis manifesting as ill-defined scaly plaques

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Figure 15:

Tinea cruris with male genital dermatophytosis manifesting as well-defined annular plaques

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A similar entity has been noticed in women with involvement of only the pubic region, or as a part of a larger plaque of tinea cruris [Figure 16].⁵⁶ Waxing or shaving the area may allow the dermatophyte deeper and cause extension of the infection. Patients must therefore be instructed that trimming the hair with scissors is preferable instead.

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Figure 16:

Tinea cruris with female genital dermatophytosis presenting as a double-edged annular plaque involving the pubic area

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Superficial dermatophytosis of the scalp skin

Tinea of the glabrous scalp is a distinct entity in the current scenario in adults as well as children, where lesions involve the skin of the scalp, most often due to secondary spread, without apparent clinical, dermatoscopic or mycological involvement of the hair [Figure 17a], this last feature differentiating it from tinea capitis. Tinea corporis may extend from the nape of the neck to the lower occipital scalp, and tinea faciei to the lateral and anterior aspects of the scalp. The involvement usually does not extend beyond a centimeter or so into the scalp though occasionally, potassium hydroxide-positive, scaly, well-circumscribed areas may be seen more centrally.⁵⁶ This picture defies the earlier notion that sebum is fungistatic and prevents the proliferation of fungus; the higher virulence of Trichophyton mentagrophytes may be one explanation.

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Figure 17a:

Dermatophytosis of the scalp skin manifesting as an erythematous scaly, ill-defined plaque on the occipital area

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Lesions are better delineated with the hairs on the area trimmed. Dermoscopy [Figure 17b] and potassium hydroxide examination of the scalp skin scrapings help to differentiate this presentation from psoriasis and seborrheic dermatitis of the scalp. More studies are needed to explore whether there is subclinical involvement of hair in this condition.

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Figure 17b:

Dermatoscopy of scalp skin dermatophytosis– manifesting as fine scaling. Dermlite DL4N, polarized mode x10

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Tinea faciei

An increasing frequency of tinea faciei has been noted in adults as well as children.³ While it is often secondary to tinea elsewhere on the body, it can also be the first to occur, followed by disease elsewhere. The face may be the only site involved and remain so in some patients.

Lesions vary from a well-defined, annular, scaly plaque or multiple scaly plaques studding parts of the face to at times, diffuse erythema and scaling with barely discernible edges. The latter are examples of true ‘tinea incognita’ as they are difficult to diagnose and a potassium hydroxide examination is necessary. Tinea faciei often shows photoexacerbation with patients complaining of increased erythema, itching and transient edema of the affected areas when exposed to sunlight.

The following entities need special mention here:

1. Tinea facei involving the external ear and “tinea auricularis”: Tinea faciei often shows extension to the skin of the ear. Lesions often extend to the lateral scalp and beyond when the ear is involved [Figure 18]. Involvement of one ear with a scaly, erythematous, papulosquamous eruption on the same side of the face points strongly towards the diagnosis of tinea faciei. External ear involvement in children with tinea capitis has been referred to in the past as the “ear sign”.⁵⁷ We propose that this “ear sign” be extended to the context of tinea faciei as well, especially in the current scenario where tinea faciei has become so common.

2. Very rarely, involvement of only the ear may occur, which can be difficult to recognise with no clinical clue of dermatophytosis elsewhere on the face or the body. We propose the name “tinea auricularis” for this presentation [Figure 19a and b].⁵⁶

3. Tinea facei extending onto the lips and tinea labialis: Lip involvement can occur due to contiguous spread from tinea faciei [Figure 20 a-c] or as an isolated phenomenon, tinea labialis. It is rare and presents as a well-circumscribed scaly lesion or as diffuse scaling over the entire lip.⁵⁶

4. Tinea blepharitis with tinea ciliaris: The term tinea capitis by definition, includes dermatophyte infections of the scalp, eyebrows and eyelids.⁵⁸ Rarely, dermatophytosis can localize itself to the eyelids⁵⁹ [Figure 21a and b], eyelashes or periocular area [Figure 22] without any involvement of the scalp.⁵⁶ With signs of rubbing and scratching, it can then easily be misdiagnosed as atopic blepharitis/ allergic contact dermatitis or atopic involvement of the periocular area, and treated with topical steroids. The topical steroid perpetuates the infection which can later involve the skin of the face.

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Figure 18:

Tinea faciei with extension to the ear

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Figure 19a:

Tinea auricularis

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Figure 19b:

Tinea auricularis

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Figure 20a:

Tinea faciei presenting as an annular plaque with extension to the upper lip

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Figure 20b:

A close-up view of tinea faciei presenting as an annular plaque with extension to the upper lip

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Figure 20c:

Dermatoscopy of involvement of lip by superficial dermatophytosis showing scaling at the active border with crusting. DermLite DL4N, polarised mode, ×10

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Figure 21a:

Superficial dermatophytosis of the upper eyelid with involvement of the eyelid margin

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Figure 21b:

Dermoscopy of superficial dermatophytosis involving the eyelid margin presenting with fine scaling along the eyelid margin sparing the hair shafts

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Figure 22:

Tinea faciei involving the upper and the lower eyelids as well as the periocular area by extension

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Tinea and immunocompromised districts

Animmunocompromised district is alocalised aberration in the immune control of the skin that has been damaged due to various causes⁶³. Many of us are observing superficial dermatophytosis secondarily appearing over amputation sites, surgical incisions and tattoo sites, which are described as immunocompromised districts.⁶⁴

Some dermatologists have also started documenting sites of healed tinea being immunocompromised districts. This could be explained by regional immune dysregulation at sites of tinea, and also related to topical steroid applications. One of us has documented varicella and herpes zoster appearing over partially as well as completely healed sites of dermatophytosis⁶⁵ [Figure 23a]. Vitiligo has been known to develop at the sites of tinea corporis [Figure 23b] and so has lichen planus.⁶⁶.

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Figure 23a:

Vesicles in a case of varicella predominantly localized to the site of tinea corporis that serves as an immunocompromised district (Photo courtesy - Dr. Sanjeev Gupta)

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Figure 23b:

Vitiligo presenting primarily at the site of active tinea corporis

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Signs of topical/injectable corticosteroid use and irritant applications

Patients show much individual variation in the time taken to develop cutaneous adverse reactions, irrespective of the potency of the steroid molecule. It is also common to see patients seeking treatment of multiple stigmata of potent topical steroid abuse, like striae and hypopigmentation.

One of the commonest side effects of topical steroids is striae. They mostly occur early following the application of fixed-dose combinations containing clobetasol propionate and are most pronounced in the flexures and where the skin is thin, like the inner thighs. They are often initially erythematous (striae rubra) and eventually turn whitish (striae alba). Some striae may ulcerate making them prone to secondary bacterial infection [Figure 24].⁶⁷ Some gradually worsen and ulcerate because patients continue to apply the same creams that caused them. Some striae assume a pseudoedematous appearance [Figure 25].⁶⁸ Others may continue to grow despite the patient having stopped applying fixed-dose combinations. This is indicative of high potency topical steroids having adepot effect.⁶⁹

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Figure 24:

Steroid abuse in dermatophytosis leading to hypopigmentation, striae, atrophy, telangiectasia and ulceration

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Figure 25:

Pseudoedematous appearance of striae

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Striae may even occur in distal areas, where the fixed-dose combinations have not been applied. A clinical picture akin to red scrotum syndrome is also seen in some patients applying fixed-dose combinations containing topical steroids for tinea cruris, due to passive transfer of the creams.

Another common side effect of fixed-dose combinations with topical steroids is lesional and perilesional hypopigmentation; this can be seen within 3–4 weeks and is likely to be accompanied by atrophy and telangiectasia later on. Hypopigmentation and depigmentation can also be seen in patients treated with intralesional injections of triamcinolone acetonide [Figure 26a and b] by unqualified practitioners. These lesions are often linear or follow the course of lymphatics.

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Figure 26a:

Depigmentation at the site of intralesional steroid injection

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Figure 26b:

Close-up of depigmentation at the site of intralesional injection

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Concomitant bacterial infections such as recurrent furunculosis and abscesses can complicate thedermatophyte-infected sites, due to local immunosuppression induced by topical steroids [Figure 27].

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Figure 27:

Superficial dermatophytosis with superadded bacterial infection

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Many patients present with signs of irritant dermatitis over and around the infected sites induced by home remedies made of crushed plants, flowers, balm, battery fluid, or over-the-counter preparations containing salicylic acid, sulfur, or anthralin with salicylic acid. The last combination is particularly irritant, especially in the flexures, leading to erythema, brownish discoloration, scaling and exfoliation, along with burning, pain and tenderness [Figure 28a and b].

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Figure 28a:

Irritant contact dermatitis presenting as erythema, edema and brownish pigmentation over the areas of superficial dermatophytosis due to the application of a dithranol-containing cream

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Figure 28b:

Irritant dermatitis presenting as erythema, edema, erosions and brownish pigmentation over the areas of superficial dermatophytosis due to application of dithranol-containing cream

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Iatrogenic cushingoid syndrome in patients of tinea

Dermatologists are seeing an increasing number of patients, including children, presenting with longstanding lesions of tinea in multiple locations that usually wax and wane. These patients give a prolonged history of applying fixed-dose combination creams containing clobetasol propionate or beclomethasone propionate, sometimes running into hundreds of units. Many also give a history of taking weekly intramuscular injections of triamcinolone for several weeks or small doses of oral prednisolone, methylprednisolone or betamethasone for weeks to months. Many are overweight with truncal obesity and have striking striae (often in areas away from the sites of application of creams), hypopigmentation, telangiectasias, acneiform eruptions, local hypertrichosis and sometimes hirsutism [Figure 29]. Their 8 am and 4 pm serum cortisol levels are often very low, even less than 1 microliter per decaliter.⁷⁰ Further studies are needed to quantify the proportion of patients so affected and the amount/duration of application of topical steroids to induce this phenomenon.

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Figure 29:

Exogenous Cushing’s syndrome presenting with central obesity and broad striae, due to the application of topical steroids in a patient with tinea corporis

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Stopping steroid creams and instituting appropriate antifungal therapy is recommended in these patients. In our observation of a limited number of cases, the serum cortisol levels then return to normal within 3 to 5 months. The infection in such cases may take a much longer time to fully clear despite appropriate treatment.⁷¹ We have had some patients needing treatment for 6–9 months before the infection finally resolved.

Characteristics of itch

Itching is one of the cardinal features of superficial dermatophytosis. It is graded severe in studies and can be very bothersome for adults and children alike. Patients complain of paroxysms of pruritus lasting for a few minutes a few times a day; some have it for longer periods. Another common symptom is ‘burning and itching.” In many cases, it gets aggravated by sweating, heat, hot water and after disrobing (atmokinesis), and can disturb sleep.⁷² A significant number of patients complain of nocturnal exacerbation of pruritus.⁷³ Some fully treated patients complain of persistent itching which is often due to xerosis or impaired barrier function due to scratching and topical corticosteroid abuse. Topical antifungal agents like luliconazole have been anecdotally observed by many dermatologists to cause xerosis which can contribute to itching.

Change in the quality of life of patients

Superficial dermatophytosis is now to be viewed like other chronic and recurrent disorders because of its altered nature. The disease is now seen to have a significant bearing on the quality of life, emotions and personal relationships of affected individuals. It is the experience of dermatologists that many patients with chronic recalcitrant dermatophytosis develop feelings of hopelessness, shame and anger; a minority even express suicidal ideation. It is important to give adequate time to each patient, understand disease impact, and educate the patient about the disease, its management and prognosis in order to improve adherence to treatment and hence their quality of life.¹⁹

Financial impact

Though dermatophytosis in the current context does not spare any socioeconomic group, it is a common observation that chronic widespread dermatophytosis often affects those from the lower socioeconomic strata of society. A majority of these patients have multiple, similarly afflicted household contacts, resulting in a magnification of the financial burden of treatment. Such patients usually start with self-treatment and are later advised inappropriate medication (including steroid-containing creams) by non-dermatologists or unqualified individuals. The treatment continues with little or no benefit, compelling the patient to finally visit a dermatologist. Oral antifungals like itraconazole and topical molecules like luliconazole, sertaconazole, oxiconazole, amorolfine and ciclopirox olamine are currently preferred by dermatologists. They are perceived as more efficacious but are also much more expensive than the older antifungal drugs and are a significant financial burden to the patient, especially when multiple family members are affected. Cheaper brands manufactured by companies with uncertain credentials may lack efficacy, necessitating multiple visits to dermatologists and adding to the financial burden. In widespread disease, extensive application of the newer topical antifungals listed above is inconvenient and expensive. Patients often buy less than the required quantity to cut costs and discontinue treatment upon getting symptomatic relief. Other affected members of the household also may use these medications erratically. Such erratic treatment ironically results in their spending larger amounts of money over long periods. This particular patient population harbors smoldering, inadequately treated tinea that becomes an important pool of infection in the community.⁷⁴