Fungal skin infections

Fungal infections represent the invasion of tissues by one or more species of fungi. There are many fungal infections, ranging from superficial, localised tissue diseases to deeper, serious diseases involving the lungs, the blood (septicaemia) or the whole body (systemic disease). Some fungi are opportunistic, while others are disease-causing (pathogenic) and cause illness whether or not the immune system is healthy.

Fungi are one of the four main groups of microorganisms (bacteria, viruses, parasites and fungi). In nature they are found in one of two forms: single-celled yeasts or branching moulds. Some fungi take on one or the other form depending on their environment. Although yeasts cannot be seen with the naked eye, moulds may be visible as fine fuzzy spots on overripe fruit or stale bread, as mould on a shower, or as fungi growing on a decaying log. Although there are more than 50,000 species of fungi in the environment, fewer than 200 species cause disease in humans. Of these, only about 20–25 species are common causes of infection.

Most fungal infections occur in people exposed to fungal sources such as spores found on the surfaces of objects, in the air, in soil or in bird droppings. Usually there is a disorder or deficiency of the body's immune system and/or the person has created a "favourable environment" for the fungi to multiply. Although anyone can develop a fungal infection, certain groups of people are at increased risk of fungal infection and recurrence. These include organ transplant recipients, people with HIV/AIDS, those receiving chemotherapy or taking immunosuppressive medicines, and those with underlying conditions such as diabetes or lung disease.

Fungal infections can occur on skin surfaces, in skin folds and in other areas that are warm and moist because of clothing and footwear. They can also develop at the site of an injury, on mucous membranes, in the sinuses and within the lungs. Fungal infections trigger the body's immune system, can cause tissue damage and inflammation, and in some people may trigger an allergic reaction.

Although many infections remain confined to a small area, such as between the toes, they can spread across the skin and/or penetrate deeper tissues. Progressive infections and those originating in the lungs can enter the bloodstream and spread through the body. Although some fungal infections clear up on their own, most may require medical care and long periods of treatment. Infections that penetrate the body typically increase in severity and, if left untreated, can cause permanent organ damage. Some cases may ultimately be fatal. A small number of fungal infections pass easily to other people; others typically affect only the infected person.

Fungal infections can be categorised according to the part of the body they affect, how deeply they penetrate the body, the type of fungus causing the infection and the form(s) the fungus takes. Some fungi can cause both superficial and systemic infections.

The Main Fungal Infections of the Skin

  1. Pityriasis (tinea) versicolor: A superficial infection caused by Malassezia yeasts and confined to the outermost layer of the skin. It is common in young people and appears on the chest, back and upper arms as patches that are lighter than the surrounding skin or reddish-brown.
  2. Dermatophyte infections: The most common superficial fungal infections of the skin, hair and nails, caused by Trichophyton, Microsporum and Epidermophyton species. They can affect the scalp (tinea capitis), the body (tinea corporis), the groin (tinea cruris), the feet (tinea pedis) and the nails (onychomycosis).
  3. Candida infections: These mostly settle in moist skin folds, producing dark red, shiny lesions bordered by a thin white film that burn and itch. They can appear in the nappy area in babies, under the breasts in women and in all skin folds in people who are very overweight; in babies they can also appear inside the mouth as oral thrush.

Tinea Capitis

Tinea Capitis Superficialis (Scalp Ringworm):

The causative agents are Trichophyton species (T. violaceum, T. tonsurans, T. mentagrophytes) and Microsporum species (M. audouinii, M. canis, M. gypseum).

It mostly occurs before puberty, although it has rarely been observed after puberty. On the scalp the disease usually forms round, less often oval or irregular, patches. The patches may be single or multiple, and their size can vary from 2–4 mm to 1–3 cm in diameter. The surface of these patches is slightly erythematous and covered with flour- or bran-sized scales. Grey, broken hairs are found beneath or protruding through the scales. This infection heals without leaving a scar.

Tinea Capitis Profunda (Kerion Celsi):

The most common causative agents are Trichophyton species (T. verrucosum, T. mentagrophytes, T. schoenleinii, T. violaceum) and Microsporum species (M. canis, M. gypseum).

It is seen mostly in children before puberty. The disease begins like superficial scalp ringworm. The fungi then cause a suppurative folliculitis that also involves the hair follicle opening. The nodules formed by this folliculitis can reach the size of a hazelnut, walnut or apple on the scalp. When the nodules are squeezed from the side, pus comes out of the follicle openings, and if the hairs on them are pulled with tweezers, they come out easily and painlessly, like hair being pulled from grease.

After puberty, lesions with the same clinical appearance and features develop in the beard area of adults; this is called tinea barbae (sycosis parasitaria). Rarely, an infection with the same appearance and features occurring in the armpits, genital area, eyebrows and vellus hair is called "folliculitis agminata". These are deep-type dermatophytoses and produce immunity to dermatophytes in the body. It should be known that hair loss and scarring may occur with them.

Tinea Corporis (Ringworm of the Body):

The causative agents are Trichophyton and Microsporum species, and less commonly E. floccosum. It can occur at any age and most often affects exposed areas such as the forehead, cheeks, neck, backs of the hands and knees. Less often it may also settle in covered areas. The patches measure from 2–4 mm to 1–3 cm in diameter. They are most often round, less often oval and sometimes irregular. These patches are sharply demarcated; in the first days they are erythematous and scaly throughout, but after a few days their centres almost return to the appearance of normal skin, while an intense erythema and scaling continue around the edge. If the edges are scraped with a scalpel, vesicles can be seen in places as pinpoint weeping spots. Very rarely, Trichophyton schoenleinii has been observed to present on the skin with scutula (godets).

Favus Capitis

The causative agent is Trichophyton schoenleinii. This infection also begins before puberty and, if untreated, continues after puberty. Typical forms account for 95% of cases, while atypical forms account for only 5%.

The cardinal signs of the typical forms are sulphur-yellow scutula (godets), dull hairs emerging through them, atrophic scars and sometimes a characteristic odour. If the scutula are removed, the skin beneath is pink, slightly moist and atrophic in appearance. These cardinal signs usually establish the diagnosis; only in atypical forms does the appearance not establish it. According to their appearance, these are grouped as impetigoid favus, pityroid favus and alopecic favus. Another feature of favus capitis is the presence of a rim of healthy-looking hair around the forehead, ears and nape.

Tinea Corporis with Majocchi Granuloma

Majocchi granuloma is a special form of deep involvement of tinea corporis caused by zoophilic agents. This condition, also called trichophytic granuloma, arises when fungal elements (most often Trichophyton rubrum) settle in the keratin of the lower part of the hair follicle. When the infected hair follicle ruptures, its contents spill into the dermis and subcutis and provoke a granulomatous inflammatory reaction. Trauma and maceration are thought to be predisposing factors. In women, shaving the legs is the most important cause. It is seen most often on the shins and ankles, and is frequently associated with tinea pedis and onychomycosis. Perifollicular pustules may be found on sharply demarcated, raised, erythematous, scaly, alopecic nodules or plaques. In the picture, the pustules and crusting on the raised erythematous plaque are noteworthy. Fluctuation may be felt in some lesions.

In cases where direct microscopy (native preparation) is inconclusive, histopathological examination and special stains to demonstrate fungi (e.g. PAS, Grocott) may be needed for diagnosis. A granulomatous infiltration is seen around the hair follicle, and fungal elements can be detected in this area and in the hair shaft. Systemic antifungal treatment should be given for Majocchi granuloma. As the condition heals it may leave scarring, and hairs that have fallen out may not regrow.

 

Tinea Barbae

This is an inflammatory dermatophyte infection located on the face and neck, especially the beard area and surrounding skin, characterised by invasion of the hair shaft by fungal elements. It most often develops due to zoophilic strains such as Trichophyton mentagrophytes and Trichophyton verrucosum. T. verrucosum can be transmitted from cattle. It is almost always seen in adult men. Although there is also a superficial form, the typical lesion takes the form of deep suppurative nodules or plaques. It may be itchy or painful. Loss of the hairs over the lesion and the presence of pustules are quite typical.

There are 3 different types:

1. Inflammatory type: The lesions resemble those seen in kerion celsi. There is crusting and a foul odour. The hairs are broken or have fallen out. It can be confused with sycosis non-parasitaria, which is caused by staphylococci; however, sycosis non-parasitaria begins at the philtrum below the nose and the hairs cannot be pulled out easily.

2. Superficial type: The lesions resemble those of tinea corporis.

3. Sycosiform type: Clinically it resembles bacterial sycosis and takes the form of folliculitis. The hairs are mostly broken and do not come out easily when pulled. In the differential diagnosis of tinea barbae, bacterial sycosis, furuncles, deep mycoses, syphilis and tuberculosis should be considered. It generally responds well to topical treatment. Warm compresses and epilation can be applied. In resistant cases systemic treatment is required.

Tinea Faciei

This is a dermatophyte infection of the face other than tinea barbae. It usually develops due to Trichophyton species and sometimes Microsporum canis. Transmission from pets is common. It can occur anywhere on the face and is usually not symmetrical. Tinea faciei caused by Trichophyton rubrum can be difficult to recognise. The main clinical features are similar to tinea corporis: the lesion is red and itchy, but its border is not very distinct. In other cases the lesions may be more distinct.

The lesions can sometimes extend to the ear. In some cases, flare-ups of the lesions may occur after sun exposure. Diagnosis is easy for erythematous plaques with central clearing and an active edge. However, it can sometimes present as pink or red scaly plaques with indistinct borders. In these cases it may be confused with dermatoses such as contact dermatitis, atopic dermatitis, seborrhoeic dermatitis, discoid lupus erythematosus, psoriasis vulgaris and polymorphic light eruption, leading to misdiagnosis. Treatment of tinea faciei with topical antifungal medicines is generally sufficient, and it heals without leaving a mark. However, because ointments are difficult to apply to eyelid lesions, systemic treatment is preferred there.

Dermatophytosis of the Eyebrows, Eyelashes and Eyelids

This rare condition, which usually arises secondarily in the presence of dermatophytosis in neighbouring areas, can cause loss of the eyebrows and eyelashes. It may also cause pustules at the follicular openings of the eyelashes and crusting of these. Systemic antifungals are preferred for treatment.

Tinea Inguinalis (Tinea Cruris)

This is a dermatophyte infection located mainly in the groin. Its most important causative agents are the anthropophilic organisms Epidermophyton floccosum, Trichophyton rubrum and Trichophyton mentagrophytes var. interdigitale. Heat, humidity, obesity and excessive sweating are predisposing factors. It can be transmitted easily through shared towels or bathrooms. It can arise through autoinoculation from foci elsewhere on the body. In a significant proportion of cases it occurs together with tinea pedis. Rarely, it can also be transmitted from person to person through direct contact. Most patients are adult men. The upper inner thighs are most commonly affected. Clinically, involvement of the scrotum and penis is rare.

However, fungal elements can also be demonstrated in these areas by direct microscopy. The plaques are often crescent-shaped and show the typical features of tinea corporis, such as a sharp border, erythema, elevation, an irregular edge and central clearing. Although tinea inguinalis settles on both sides of the groin, it is not always symmetrical. The infection is common worldwide. It is an adult disease that appears after puberty. It is seen particularly in young adult men aged 18–25, but can also occur in women. The reason it is common in men is the occlusion created by the scrotum and men's underwear. Tinea inguinalis is very contagious. It often develops through autoinoculation. It can also be transmitted through other people's clothing, shared toilets and sexual contact. Sweat, heat, wet swimwear and obesity predispose to the disease. It is seen more often in men.

The infection, which begins in the groin or perianal area, spreads over time to the thighs and genitals. The condition is very itchy and lasts quite a long time. It appears as crescent-shaped red or brown plaques, with vesicles at the edge of the plaque. In patients with severe maceration, secondary bacterial infections may develop. When diagnosing tinea inguinalis, inverse psoriasis, seborrhoeic dermatitis, intertrigo, erythrasma and candidiasis in particular should be considered. Candidiasis is distinguished clinically from tinea cruris by involvement of the scrotum and the presence of satellite pustules.

Topical antifungal medicines are usually sufficient to treat lesions that are not widespread. Imidazole derivatives (ketoconazole, clotrimazole, oxiconazole, isoconazole, sulconazole, miconazole, tioconazole, sertaconazole, bifonazole), pyridones (ciclopirox olamine), allylamines (terbinafine, naftifine) and morpholines (amorolfine) are important topical medicines used in the treatment of dermatophytoses. These broad-spectrum antifungal creams are also effective against pityriasis versicolor and candida. Creams containing a combination of an antifungal and a corticosteroid should not be preferred for confirmed dermatophytoses.

Tinea Pedis

Tinea pedis is a fungal infection of the feet and toes caused by dermatophytes. It tends to spread to all members of a household and remains contagious for as long as the infection is present. The causative agent is most often Epidermophyton floccosum, T. rubrum or T. mentagrophytes. Tinea pedis is the most common fungal disease in humans. Communal workplaces, shared clogs and slippers, rubber footwear and nylon socks predispose to the disease. In addition, immunosuppressants and corticosteroids can contribute to its spread. The most troublesome symptoms of tinea pedis are foot odour and itching.

The disease is seen after childhood and is generally common in young adults and adolescents. Males are infected more often; this is because they are more often found in communal living places such as boarding schools, barracks and gyms, and wear closed shoes more than women in the summer months. The infection is transmitted by walking barefoot on infected surfaces; transmission occurs by stepping on infected skin flakes on the floors of shared showers, bathrooms, Turkish baths, saunas, swimming pools, hotel rooms and even rooms at home. There is also a risk of infection in pedicure salons.

The fungal nature of this disease was first demonstrated in 1892 by our master Celal Muhtar, which is why it is also called Celal Muhtar's disease. It is usually asymmetrical, with one foot more noticeably affected. This feature is important in distinguishing it from symmetrical diseases such as psoriasis. Maceration developing between the toes in hot and humid climates plays an important role in the development of the disease. Wearing nylon socks and the increasing use of slippers and shoes made of synthetic materials, especially trainers, are factors contributing to its spread. The infection usually starts between the toes and spreads to the sole.

Clinically and pathophysiologically it is divided into 3 types:

1) Interdigital (intertriginous) type: This condition is also called athlete's foot. Most often the space between the

4th and 5th toes is affected. The dermatophyte infection begins with scaling between the toes (simplex type). If a bacterial infection is added to this, severe maceration, fissures and leukokeratotic, symptomatic lesions develop. Pruritus is usually present, and if fissures develop they cause pain. Heat and occlusion are triggering factors.

Gram-negative species, including in particular Staphylococcus aureus, Micrococcus sedentarius, Brevibacterium epidermidis, Corynebacterium minutissimum and many antibiotic-resistant Pseudomonas and Proteus species, take part in this infection (complex type). These bacteria are resistant to the penicillin and streptomycin synthesised by dermatophytes. They can invade the thick stratum corneum between the toes, which they normally cannot, only because the dermatophytes break down the skin barrier there and create an ecological environment with the antibiotics they produce. By synthesising proteolytic enzymes, these bacteria break down the stratum corneum, which in turn allows the dermatophytes to invade more deeply, and maceration and leukokeratosis develop. Bacteria such as Micrococcus sedentarius and Brevibacterium epidermidis also synthesise methanethiol, ethanethiol, dimethyl sulphide and similar sulphur compounds. These compounds have strong antifungal properties. For this reason, dermatophytes can be grown in only one-third of cultures taken from these macerated toe spaces. While T. mentagrophytes var. interdigitale and E. floccosum frequently play a role in this condition, T. rubrum is also a commonly encountered pathogen and tends to invade the sole of the foot as well. Secondary infections may develop, and erysipelas and lymphangitis may occur.

2) Squamous-hyperkeratotic type: This causes diffuse hyperkeratotic desquamation of the soles. The sole is dry, and the skin lines of the sole are covered with adherent, fine (furfuraceous) scales that give the impression of being powdered. Crescent-shaped scales are seen on the soles. The disease has a chronic, silent course. Nail involvement frequently develops as well. Most patients have a history of atopy and a specific impairment of cell-mediated immune sensitisation to dermatophytes. This type of infection is caused largely by T. rubrum.

3) Vesiculobullous type: These are highly inflammatory eruptions that develop acutely. The eruption is usually one-sided, which is its most important difference from dyshidrotic eczema. The vesicles and bullae are usually located in the middle part of the inner edge of the foot. The disease is often caused by T. mentagrophytes var. mentagrophytes. The severe inflammation results from the cellular reaction against this zoophilic dermatophyte, and is the same picture as classic allergic contact dermatitis produced by the same mechanism. The disease follows a course of recurrent attacks, with mild desquamation between attacks. Increased heat and occlusion are factors that trigger attacks. There is severe pruritus and burning. Hyperhidrosis is also present, particularly in the vesiculobullous form, and id reactions are common.

Dermatophyte spores can remain viable in the environment for a long time, and as a result the infection spreads easily. Places such as showers, saunas and swimming pools, as well as shared slippers, are important sources of transmission of tinea pedis. It can be picked up from contaminated floors when walking barefoot. Excessive sweating and tight clothing make it easier to develop. Lesions may worsen in summer. If left untreated, it can last for months or even years. In untreated cases, onychomycosis may also be added to the picture. When diagnosing tinea pedis, contact dermatitis, palmoplantar pustulosis, dyshidrotic eczema, Reiter's syndrome and, when located between the toes, intertrigo and erythrasma should be considered.

The most important complications of tinea pedis are cellulitis, caused by bacteria entering the tissue through macerated areas or fissures, and spread of the fungal infection by contiguity to the toenails (onychomycosis), the top of the foot and the leg. Topical treatment is useful in tinea pedis, but systemic treatment is more effective. For this reason topical and oral treatment should be given together. Griseofulvin is an effective oral antifungal that has long been used to treat tinea pedis and is approved by the FDA. Its use for 6–8 weeks is generally recommended. Itraconazole (200 mg twice a day) and terbinafine (250 mg once a day for 2 weeks) are oral antifungal medicines that are effective in treatment but are not FDA-approved for this use. Together with oral medicines, topical agents such as 2% miconazole nitrate cream, 1% clotrimazole cream, benzylamines, allylamines, terbinafine, naftifine and ciclopirox olamine should also be used. In addition to topical and oral antifungal treatment, it is important to keep the feet dry, to wear partly open shoes that allow the feet to breathe or to alternate with such shoes 2–3 days a week, and to dry the feet thoroughly after bathing, especially between the toes. As secondary bacterial infection is common, particularly in chronic or recurrent cases, the use of antibacterial medicines should be considered.

In inflamed cases, anti-inflammatory medicines should also be used. In acute tinea pedis, potassium permanganate (1/1000) soaks are very beneficial, and topical medicines can be applied after the potassium permanganate soak. Where tinea pedis has spread to the sole and/or top of the foot, or in cases of acute inflammation, systemic antifungals should be used in addition to topical medicines. Drying is an important factor in treatment; drying powders and peeling antifungal ointments can be used.

Tinea Manuum

Tinea manuum is dermatophytosis of the hands; T. rubrum, T. mentagrophytes var. interdigitale and E. floccosum are the most common causative agents. Zoophilic species such as M. canis and T. verrucosum and the geophilic M. gypseum can also cause infection. The most frequently identified agent in Türkiye is T. rubrum.

The causative agents are transmitted directly from infected people and animals or contaminated soil, or indirectly from contaminated objects, towels and garden tools. Transmission can also occur through autoinoculation from dermatophytosis elsewhere on the body. Manual work, heavy sweating of the hands and conditions such as contact eczema are predisposing factors for tinea manuum. Tinea manuum is usually seen on one hand, most often the right. Patients with tinea manuum frequently also have tinea pedis. The infection most often affects the palm, but can also be seen on the back of the hand. Lesions on the back of the hand or between the fingers resemble those of tinea corporis: itchy, erythematous, sharply demarcated, sometimes vesicular lesions that begin to clear in the centre.

Tinea manuum of the palm has two clinical types:

1) Dyshidrotic or eczematoid type: This is an acute condition with vesicles on the edges of the hand, the sides and palmar surfaces of the fingers, or the palm. On the palm there is usually a single large, firm vesicle or bulla filled with a sticky, clear fluid. When the roof of the vesicle or bulla is removed, a moist erythematous base is revealed. Symptoms are itching, burning and tingling.

2) Hyperkeratotic type: This is a subacute or chronic condition. The vesicles on and around the palm peel and turn into round or irregular, hyperaemic, scaly lesions surrounded by a border of thick white scales. The lesions may cover all or a large part of the surface of the palm and fingers. Hyperkeratosis leads to fissures along the palm creases. Because of the fine scaling, the palm looks as if dusted with coarse flour. The scaling is coarser in the palm creases and darkens over time. Onychomycosis of the fingernails is one of the most common complications of tinea manuum. Patients with palmoplantar keratoderma (tylosis) are particularly susceptible to superinfection of the palms and soles with dermatophytes. This complication can be difficult to diagnose, but vesicle formation and itching of the hands help with the diagnosis.

In such cases, fungi other than T. rubrum may also be responsible. Tinea manuum should be distinguished from other forms of dyshidrosis and from psoriasis. Good results are usually obtained with topical medicines within 4 weeks; however, some resistant cases may require systemic treatment.

Tinea Incognito

Dermatophyte infections of the skin take the prefix "tinea", and after this prefix the infection is named after the site where it is located. An exception to this rule is "tinea incognito". Here, "incognito" does not describe a location, but rather a "state of being unrecognisable", derived from the Latin "incognitus". The term tinea incognito was first used by Ive and Marks in 1968. In their original publication they reported that, in patients who actually had dermatophytosis but used topical corticosteroid ointments or creams because of a misdiagnosis, clinical pictures resembling seborrhoeic dermatitis, lichen planus, folliculitis, scleroderma and rosacea developed. However, they also emphasised that the typical clinical features of dermatophytosis were preserved in one-third of cases.

Tinea incognito occurs when patients with a fungal infection use corticosteroid creams or ointments because of a misdiagnosis. In countries outside Türkiye, where patients do not self-medicate, tinea incognito is mostly iatrogenic; the person prescribing the topical corticosteroid is usually a general practitioner or family doctor. In Türkiye, however, because it is common for patients to use, on their own initiative, "the medicine that works so well for that condition (!)" that they have heard about from relatives or neighbours, they create their own tinea incognito. Next in the list of those causing tinea incognito come pharmacists, general practitioners, other specialists and dermatologists.

Corticosteroid preparations suppress cell-mediated immunity when used topically, just as they do when used systemically. With the suppression of cell-mediated immunity, the clinical signs of the patient's dermatophyte infection initially fade, and subjective complaints such as itching and burning disappear. However, the underlying fungal infection gradually spreads, and when the medicine is stopped the subjective complaints flare up again. The patient is therefore forced to use the same medicine again and again. This "vicious circle" will probably end when the patient sees a dermatologist, because the classic clinical picture of "tinea", with centrifugal vesiculopustules, has been transformed under the suppression of the corticosteroid into other clinical pictures such as eczema, impetigo, psoriasis or rosacea. If the clinician is lucky, careful observation may reveal a limited area resembling tinea, and direct microscopy of a sample from this area may show fungal hyphae.

The lesion is usually asymptomatic, although it may sometimes be itchy or painful. It may be dark red or violaceous in colour. Papular and pustular lesions may be seen, and there may be an atrophic appearance resulting from steroid application. Treatment requires the use of a systemic antifungal.

Tinea Unguium

Onychomycosis is the term used for fungal infections involving the nail bed, matrix and plate. Tinea unguium is the name given to onychomycosis caused by dermatophytes. Apart from these, various agents can cause onychomycosis, chiefly non-dermatophyte moulds such as candida, Scopulariopsis brevicaulis and Aspergillus species. It usually occurs together with tinea pedis and tinea manuum, and sometimes on its own. The most common causative agents are Trichophyton rubrum and Trichophyton mentagrophytes. Strains such as Epidermophyton floccosum, T. soudanense, T. violaceum, M. canis, T. tonsurans and T. erinacei can also be responsible. Among dermatophyte infections, tinea unguium has a special place because of its prevalence, chronicity and difficulty of treatment. It accounts for 50% of all nail diseases. The disease is seen consistently all over the world, and its incidence is steadily increasing. About 30% of patients with a cutaneous fungal infection also have onychomycosis, and onychomycosis accompanies the condition in one-third of patients with tinea pedis. Some 15–20% of people aged 40–60 develop this disease. Most patients are adults. It is more common in the toenails. The infection, which often begins at the distal or lateral parts of the nail and sometimes at the proximal part, may progress over time and lead to extensive involvement of the nail plate. There is also a type of tinea unguium that appears as superficial white spots on the nail plate. Different clinical types may coexist. Tinea unguium can act as a source for fungal infections in other areas.

Pityriasis Versicolor

Pityriasis versicolor is a common, benign, recurrent, chronic infection of the skin caused by yeasts of the Malassezia genus. It is seen widely throughout the world and is more common in tropical regions. While its prevalence varies between countries worldwide from 0.8% to 28.5%, studies carried out in our country in small numbers and in small groups have reported widely varying rates of 15–85%.

Causes of Pityriasis Versicolor

Pityriasis versicolor is a chronic superficial infection caused by the Malassezia yeast. There are 13 species of Malassezia yeast that cause pityriasis versicolor. These are: M. furfur, M. sympodialis, M. slooffiae, M. pachydermatis, M. globosa, M. obtusa, M. dermatis, M. japonica, M. nana, M. restricta, M. equina and M. caprae.

General Features of Pityriasis Versicolor Infections

Pityriasis versicolor, a chronic benign cutaneous disease, mostly follows a mild, chronic and asymptomatic course. It is characterised by fine scaling in variable colours (pink, white, brown) on the trunk. The fungus disrupts the melanocytes: either the cells lose their pigment and an achromic picture appears, or pigment increases and dark, milky-coffee-coloured lesions develop. Pityriasis versicolor therefore causes hypo- and hyperpigmentation of the skin. It is seen on oil-rich areas of the body such as the neck, back and chest. Itching may occur in the lesions. Pityriasis versicolor is asymptomatic and causes a cosmetic problem. Its prevalence in tropical regions is 40–60%. Warm, humid weather is an important factor in the development of this disease. Pityriasis versicolor is usually seen in teenagers aged 13–19 and in young adults. Because Malassezia species require lipids, pityriasis versicolor is rarely seen in young children and older people; it begins to appear in the period when the amount of skin oil increases. Its distribution in the normal flora is related to the density of the sebaceous glands, and the fungus is found in high numbers on the face, chest and back. It is not found in the hair, nails or mucous membranes. This yeast is part of the normal flora of human skin. Pityriasis versicolor develops when the fungus changes from its yeast form to its hyphal form. This transformation is related to endogenous and exogenous factors.

Endogenous factors leading to pityriasis versicolor are malnutrition, use of the contraceptive pill, corticosteroid use, immune system disorders and excessive sweating. Pityriasis versicolor is more common in tropical than in temperate climates, and it is also more widespread in the summer months. Increased heat and humidity play a role in its pathogenesis. Athletes in particular are prone to this disease, although it is not clear whether this is due to excessive sweating. Hygiene is not an important factor in the development of this disease. However, applying creams or lotions to the skin is a facilitating factor. There is no relationship between pityriasis versicolor and malnutrition or socio-economic status. However, the development of pityriasis versicolor may also be related to changes in the body's immune response. It is also a common infection in immunosuppressed people, such as those with AIDS or visceral leishmaniasis. Nevertheless, although other fungal diseases are very common in people with AIDS, the incidence of pityriasis versicolor is lower. Pityriasis versicolor is more common in people receiving radiotherapy and lithium treatment.

 

Diagnosis of Pityriasis Versicolor

The cutaneous pathology caused by the Malassezia yeast is characteristic enough to be recognised easily by dermatologists. Because equipment to grow the fungus in culture is generally not needed, dermatologists do not isolate the fungus from the lesions. However, they frequently confirm its presence by direct microscopic examination of material taken from the lesions. In fact, the yeasts appear very small in the tissues, but repeated unipolar budding leaves a very typical permanent mark (scar) on the mother cell.

The most satisfactory method of visualising it is staining with ink (Parker permanent blue and black ink), mixed in equal parts with 20–30% KOH. Malassezia cells (yeasts and hyphae) take up the stain immediately and appear blue on a white background. Calcofluor white is used as a more selective stain; this stain can only be seen with a fluorescence microscope. This technique also provides a good image in seborrhoeic dermatitis. In the tissues the fungus has a yeast appearance. The presence, absence and frequency of hyphae provide information about the disease.

The variation in the appearance of the lesions can be confusing for an inexperienced clinician. Wood's lamp examination can help in the diagnosis of pityriasis versicolor: under Wood's light, pityriasis versicolor lesions fluoresce yellow-green. This fluorescence covers the clinically visible lesions. Wood's light can be useful for differential diagnosis because the colour of the fluorescence is characteristic of Malassezia hyphae. However, Wood's light gives a positive result in only one-third of cases, mostly those due to Malassezia furfur.

The diagnosis of pityriasis versicolor can be confirmed by mycological examination. Clinical material taken from the lesions should be examined under a light microscope. The affected areas contain large numbers of microorganisms. Besides scraping the lesions with a scalpel, the cellophane tape method can also be used. First, the clinical material taken from the lesions is mounted between a slide and coverslip with 10–15% KOH added and examined under a light microscope. KOH dissolves keratin, making the fungal elements easier to see. After treatment with KOH, 15–20 minutes should be allowed. If the slide is warmed gently, the keratin dissolves faster; it is then examined under the light microscope. Hyphae and yeast cells are seen on light microscopy. This appearance is so characteristic that it is called the "spaghetti and meatballs" appearance.

Treatment of Pityriasis Versicolor

Most treatments for pityriasis versicolor do not essentially have direct activity against the fungal agents. In general, they act physically and/or chemically to remove tissue from the stratum corneum. Selenium sulphide comes as a 2.5% lotion, cream or shampoo and is effective in the treatment of pityriasis versicolor, although some patients complain of the unpleasant smell of these products. Propylene glycol, a keratolytic agent, is often used as a base for other topical medications and has been shown to be effective on its own in pityriasis versicolor. Salicylic acid ointments contain benzoic acid and salicylic acid: benzoic acid for its fungicidal activity and salicylic acid as a keratolytic. This treatment has been shown to be effective against pityriasis versicolor.

 

 

Oral Candidiasis

1. Acute pseudomembranous candidiasis: This can occur in 10% of newborns through transmission from the mother's vaginal canal during birth. This condition is also called thrush. In adults it can develop due to causes such as cachexia, immunosuppression and diabetes. It appears as white plaques on the tongue, palate and buccal mucosa. Because the plaque is fragile it may be confused with milk residue left in the mouth, but the diagnosis is made by the erythematous, inflamed base left after it is scraped off and by direct microscopy.

2. Acute atrophic candidiasis: This is seen as an atrophic area on the tongue and mostly develops after antibiotic use.

3. Chronic atrophic candidiasis: This is present in a quarter of the elderly population who wear dentures. There is erythema and an atrophic appearance, especially on the palate beneath the denture. The disease may be accompanied by angular cheilitis. Candida can be isolated from the palatal surface of the denture.

4. Chronic hyperplastic candidiasis: The white plaques on the mucosa are thick and adherent. Unlike in thrush, they cannot be removed.

5. Angular cheilitis (perlèche): This is a candidal infection of the corners of the mouth characterised by maceration, cracks and crusting. It usually develops in older age when saliva seeps from the corners of the mouth as a result of sagging facial skin. It can also occur in people who habitually lick their lips.

After meals and at bedtime, nystatin solution is swished around the mouth for 3–5 minutes and swallowed. To prevent recurrence, people in risk groups are advised to gargle with a 5% bicarbonate solution in water after meals and at bedtime and spit it out. If there is a severe underlying systemic disease, systemic fluconazole or itraconazole is preferred for treatment.

Candidal Intertrigo: This is a candidal infection of intertriginous areas such as the genito-inguinal folds, the spaces between the fingers and toes, beneath the breasts and the armpits, seen especially in women and overweight people. Pinkish, erythematous, macerated lesions are seen in these areas, with satellite pustules close to the lesion. The presence of satellite pustules is important in distinguishing it from simple intertrigo.

If candidal intertrigo develops between the fingers or toes, maceration is prominent. The form seen between the fingers is called "erosio interdigitalis blastomycetica", in whose development Gram-negative bacteria may play a role together with candida. This condition often occurs in women whose hands are constantly in contact with water and soap. When diagnosing the disease, dermatophyte infections, seborrhoeic dermatitis, flexural psoriasis and intertrigo should also be considered.

Candidal Paronychia: Unlike acute paronychia, candida plays a role in the aetiology of chronic paronychia. Chronic candidal paronychia is very common in homemakers whose hands are constantly in contact with water, and in people who wash dishes or laundry. Bacteria may also be involved in addition to candida. In patients the nail folds are erythematous and oedematous, pus may occasionally form, and the nail later becomes involved: deformity and discolouration develop in the affected nail and the disease takes a chronic course. Unlike tinea unguium, nail involvement begins at the lateral part of the nail where the paronychia is located.

Candidal Onychomycosis: This usually develops in the fingernails, with yellow-brown discolouration and subungual hyperkeratosis. This clinical classification of onychomycosis is only possible in the early stages of the infection. In all types, in the advanced stages of the disease the whole nail is involved and takes on a completely dystrophic appearance.

The best-known diagnostic methods are direct microscopic examination using a standard native (KOH) preparation and fungal culture. A definitive diagnosis is made by seeing fungal elements on direct microscopy and identifying the pathogenic organism in culture. In addition, many sources recommend histopathological examination of the nail plate if onychomycosis is clinically suspected but repeated KOH examinations and cultures are negative.

Onychomycosis is seen especially in older age. In children, the rapid growth of the nails may be a factor protecting them from onychomycosis. Although nail infections due to dermatophytes are more common in men, their frequency in women is steadily increasing; the reason may be the wearing of narrow-toed shoes.

The nail unit has many functions, including protecting the distal phalanx, supporting touch, enhancing tactile sensitivity, grasping objects and taking part in activities such as pressing buttons. In addition to all these, nails are also very important cosmetically. Onychomycosis can be severe enough to impair these functions of the nail. Moreover, the appearance of the affected nail and the fear of transmitting the disease to others lead to psychosocial problems for the patient. The fact that nails with onychomycosis act as a reservoir for dermatophytoses is also an important problem.

Treatment is difficult and lengthy. Two methods are used: systemic medication and nail removal. Griseofulvin should not be given at a dose of less than 10 mg/kg/day. Generally at least 6 months of treatment is required for fingernails and 9–12 months for toenails. Terbinafine usually gives results in a shorter time (3 months for fingernails, 6 months for toenails). Itraconazole is used for at least 3 months for fingernails and at least 5 months for toenails. Liver function tests should be carried out before starting the medicines and monitored throughout treatment. In addition to systemic treatment, concentrated topical solutions formulated for nails are also used.

Despite oral antifungals, relapse occurs in 40–70% of toenail infections, and less often in fingernail infections. Favourable results cannot be obtained with systemic oral antifungals in older people or patients with impaired peripheral circulation.

 

Systemic Mycoses (Deep Mycoses)

Systemic or deep mycoses are infections that involve internal organ systems and are not transmitted between people. The typical route of infection is the respiratory tract. Among systemic infections, blastomycosis, histoplasmosis, coccidioidomycosis and paracoccidioidomycosis are the most dangerous to human health. The main reservoirs of these fungi are soil, rotting leaves, wood, manure, animal shelters, bat droppings, food, grain feed and so on.

The primary site of these infections is the lungs. A high degree of specific resistance to reinfection is acquired. In some cases secondary involvement occurs. The course of the resulting infections is determined by the organism and the body's resistance. The rising incidence of systemic fungal infections has increased the use of antifungal medicines and accelerated work on the development of new medicines. In addition to medicines such as fluconazole and conventional and lipid formulations of amphotericin B, various new azoles (voriconazole, posaconazole and ravuconazole) and echinocandins (caspofungin, anidulafungin and micafungin) have come into use. Despite the many new medicines developed, the treatment of some fungal infections, such as mucormycosis, remains a problem.

Cryptococcosis

This is a systemic infection caused by Cryptococcus neoformans. Of all Cryptococcus species, C. neoformans is the most pathogenic. Cryptococcal meningitis is the most severe life-threatening infection in people with HIV infection. C. neoformans is the sole cause of cryptococcosis and is an opportunistic yeast with a mucopolysaccharide capsule. According to its mucopolysaccharide capsular antigen, C. neoformans has two varieties: C. neoformans var. neoformans and C. neoformans var. gattii.

Madura Foot
Madura foot or maduromycosis (mycetoma) is a tropical disease seen most often in India. Various fungi (and actinomycetes such as Actinomyces and Nocardia) can be the cause. It begins as a swelling on the foot that gradually spreads and forms abscesses. Besides the soft tissues, the fungus also destroys the bone, and openings (sinuses) form in the skin. If not treated properly, amputation of the foot may be required. Sulphones (Avlosulfon), antimycotics (griseofulvin) and antibiotics (penicillin, tetracycline) are used in treatment.

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