Tinea corporis, also known as ringworm of the body, is a common superficial fungal infection that affects the skin. It is caused by dermatophytes, which are fungi that feed on keratin found in the outer layer of the skin, hair, and nails. These fungi thrive in warm, moist environments and can infect humans and animals alike. Tinea corporis presents as circular or oval-shaped lesions on various parts of the body, including the trunk, arms, legs, and face, though it spares the palms, soles, and mucous membranes. This infection is highly contagious and can spread through direct contact with infected individuals, animals, or contaminated objects. Tinea corporis typically presents as a well-defined, circular or oval-shaped, mildly erythematous patch or plaque with a raised, advancing edge.
Initially, it appears as a flat, scaly lesion that spreads outward in a centrifugal pattern, creating an annular appearance commonly referred to as “ringworm.” As the infection progresses, the central area may clear and become hypopigmented or brown, with reduced scaliness compared to the advancing border, which often exhibits an irregular or annular shape. Occasionally, the border may present with papules, vesicles, or pustules. Lesions can vary in shape, such as circinate or arcuate, and tend to be asymmetrically distributed, often coalescing into polycyclic patterns when multiple lesions are present. In adults, tinea corporis frequently affects exposed skin areas, while in children and adolescents, the trunk is commonly involved. Bullous tinea corporis, a rare variant, manifests with vesicles or bullae primarily at the periphery of an erythematous, scaly plaque. Rupture of these vesicles or bullae can lead to erosions and crust formation over the erythematous background. In immunocompromised individuals, tinea corporis may present as a disseminated skin infection or even involve deeper layers, forming subcutaneous or deep abscesses. Rarely, it may present with purpuric macules, known as tinea corporis purpurica, indicating a more severe and potentially systemic fungal involvement. Recognition of these clinical presentations is crucial for accurate diagnosis and appropriate management of tineacorporis, ensuring effective treatment and prevention of complications in affected individuals.
The pathophysiology of tinea corporis involves several mechanisms driven by dermatophytes, such as T. rubrum, that enable the fungus to establish and propagate within the skin. Mannans present in the cell walls of these dermatophytes possess immune-suppressive properties, aiding in adherence to the skin and preventing premature shedding before initiating invasion.
The fungi secrete enzymes including proteases, serine-subtilisins, and keratinases. Proteases facilitate the breakdown of keratin, serine-subtilisins initiate protein degradation through nucleophilic attacks on serine residues, and keratinases enable penetration of keratinised tissues, facilitating the spread of the fungus within the outer, non-living, cornified layers of the skin.
Infections are predominantly cutaneous, remaining confined to the superficial layers due to robust immune defenses in immunocompetent individuals. These defenses include the activation of serum inhibitory factors, polymorphonuclear leukocytes, and complement proteins, which collectively inhibit deeper tissue penetration by the fungus.
The characteristic scaling observed at the active borders of lesions is attributed to heightened proliferation of epidermal cells in response to the fungal presence, contributing to the clinical manifestations of tinea corporis.
Early recognition and prompt treatment of tinea corporis are crucial for optimal outcomes, reducing discomfort, preventing complications, and minimising transmission. Adhering to treatment protocols and practicing good personal hygiene are key to effectively managing and resolving the infection, promoting skin health and well-being.
Case report
A 45-year-old female patient presented to the clinic with a suspected case of tinea corporis, a common dermatophyte infection of the skin. Upon examination, the patient exhibited raised, ring-shaped scaly patches distributed across her back, arms, and the dorsal aspects of her hands. These characteristic lesions strongly indicated tinea corporis. To confirm the diagnosis, a clinical examination was conducted, which corroborated the initial suspicion. Given the confirmed diagnosis of tinea corporis, a decision was made to initiate treatment with itraconazole.
Itraconazole was selected due to its potent systemic antifungal properties, which are particularly effective against dermatophytes—the fungi responsible for tinea corporis.
The patient was prescribed a three-week course of itraconazole, and she adhered to this treatment regimen as directed. Following the initiation of itraconazole therapy, the patient showed significant clinical improvement. The lesions that were initially observed demonstrated a notable reduction in both size and scaling.
This positive response to itraconazole was evident as the treatment progressed, indicating the medication’s efficacy in treating the infection. By the end of the three-week course, the patient experienced a substantial resolution of symptoms, with a marked improvement in the appearance of the affected skin areas.
The successful treatment of tinea corporis in this patient highlights the effectiveness of systemic antifungal therapy with itraconazole. The resolution of the lesions and restoration of skin integrity underscore the importance of appropriate antifungal treatment in managing dermatophyte infections. This case reinforces the clinical utility of itraconazole in achieving favourable outcomes for patients with tinea corporis.
Diagnosis
Laboratory investigations are crucial for diagnosing dermatophytosis, particularly in tinea corporis cases. Collecting skin scrapings from the lesion’s active margin and examining them with 10–20 per cent potassium hydroxide under direct microscopy allows rapid visualisation of dermatophytic elements.
Fluorescent staining enhances sensitivity by binding to fungal cell wall chitin. Culture on Sabouraud dextrose agar (SDA) or modified SDA with antibiotics incubates for 7–14 days, with dermatophyte test medium (DTM) indicating fungal growth through phenol red color change.
Antifungal susceptibility testing (AST) is crucial in diagnosing and managing tinea corporis, especially in recurrent or treatment-resistant cases. Two main methods for AST are the microdilution method and Minimum Fungicidal Concentration (MFC) determination. The microdilution method assesses minimum inhibitory concentrations (MICs) of antifungal agents by diluting them in a microplate with culture medium inoculated with fungal isolates. MIC values indicate the lowest drug concentration inhibiting visible fungal growth after incubation, providing quantitative susceptibility data. MFC determination complements MIC testing by determining the lowest concentration needed to kill rather than inhibit fungi. After MIC determination, subculturing on drug-free media checks for fungal growth inhibition. MFC is the minimum concentration preventing visible growth upon subculture, indicating fungicidal activity crucial for effective tinea corporis management.
Histopathology is essential in diagnosing tinea corporis, revealing characteristic changes like epidermal hyperkeratosis, parakeratosis, and septate hyphae within the stratum corneum and hair follicles. Inflammatory cells such as neutrophils and lymphocytes indicate the immune response against the fungus, with additional features like spongiosis, vesiculation, or dermal inflammation helping to assess infection severity. Dermoscopy aids in distinguishing tinea corporis by noting structureless yellowish scales, an erythematous halo, central clearing, peripheral scaling, and marginal hyperpigmentation, guiding effective treatment strategies for fungal skin infections.
Diagnosis of tinea corporis using Polymerase Chain Reaction (PCR) and nucleic acid sequence-based amplification (NASBA) involves molecular techniques that detect fungal DNA or RNA directly from skin samples. PCR targets specific genetic sequences of dermatophytes, amplifying them to detectable levels for identification. NASBA, on the other hand, amplifies RNA molecules, offering a complementary method to PCR for detecting fungal RNA. These molecular methods provide rapid and sensitive detection of dermatophytes, especially in cases where conventional diagnostic methods like microscopy or culture may be inconclusive or challenging.
Matrix-assisted laser desorption ionisation-time of flight mass spectrometry (MALDI-TOF MS) is a novel molecular method revolutionising the evaluation of tinea corporis. This technique allows rapid identification of fungal species by analysing their protein profiles. By comparing the mass spectra of unknown fungal isolates to a reference database, MALDI-TOF MS accurately identifies dermatophytes causing tinea corporis with high specificity and sensitivity. Reflectance confocal microscopy (RCM) is revolutionising the evaluation of tinea corporis by offering non-invasive, real-time imaging of skin lesions at a cellular level. Dermatologists can visualise fungal structures like hyphae and spores directly on the skin surface, leveraging RCM’s ability to detect epidermal changes such as hyperkeratosis and parakeratosis.
This method also reveals the inflammatory response around fungal elements, aiding in diagnosis by providing detailed assessments of lesion morphology, including scales, erythema, and the characteristic annular pattern of tinea corporis.
The effective diagnosis of tinea corporis relies on a thorough clinical assessment supplemented by appropriate diagnostic tests when needed. Early and accurate identification of this superficial fungal infection allows for prompt initiation of targeted antifungal therapy, thereby facilitating rapid resolution of symptoms and reducing the risk of complications.
Treatment
Treatment of dermatophyte infections, particularly localised tinea corporis, relies on the strategic application of topical or oral antifungal treatments. The primary goal of initial management is to provide a focused approach that directly targets the superficial fungal infection, aiming to eradicate the causative dermatophytes and alleviate accompanying symptoms.
Topical antifungal therapy
Azoles, such as econazole, ketoconazole, miconazole, clotrimazole, oxiconazole, sulconazole, sertaconazole, eberconazole, and luliconazole, exert their antifungal effects by inhibiting lanosterol 14α-demethylase, a key enzyme involved in ergosterol biosynthesis. Ergosterol plays a crucial role in preserving the structural integrity of fungal cell membranes. By blocking this enzyme, azoles disrupt ergosterol synthesis, leading to the accumulation of toxic methylated sterols and causing structural and functional damage to the fungal cell membrane. This disruption ultimately results in impaired fungal growth and survival. Allylamines, including naftifine and terbinafine, exert their antifungal effects by inhibiting squalene epoxidase, a crucial enzyme in the ergosterol biosynthesis pathway of fungi. By blocking this enzyme, allylamines disrupt the formation of fungal cell membranes, leading to the accumulation of squalene and depletion of ergosterol. This disruption compromises the structural integrity and function of the fungal cell membrane, ultimately resulting in fungal cell death.
Terbinafine, in particular, is widely used topically and is well-tolerated, making it a preferred treatment option for localised dermatophyte infections. Butenafine, a benzylamine derivative, exerts its antifungal action by inhibiting squalene epoxidase, an enzyme crucial for ergosterol biosynthesis in fungi.
This ultimately leads to fungal cell death. Ciclopirox, chelates with polyvalent cations, particularly iron (Fe^3+), which are essential for various fungal cellular processes.
By depriving fungi of these essential ions, ciclopirox disrupts the integrity and function of their cell membranes. Tolnaftate acts primarily by inhibiting squalene monooxygenase, an enzyme crucial in the biosynthesis of ergosterol, an essential component of fungal cell membranes. By blocking this enzyme, tolnaftate disrupts the synthesis of ergosterol, leading to structural and functional abnormalities in the fungal cell membrane.Amphotericin B functions by binding to ergosterol, an essential component of fungal cell membranes. This binding disrupts membrane integrity, leading to leakage of cellular contents and ultimately fungal cell death. This mechanism of action is broad-spectrum, effective against a wide range of fungal pathogens, including those resistant to other antifungal agents.
Amorolfine alters the membrane structure, increasing permeability and ultimately leading to fungal cell death. It exhibits broad-spectrum antifungal activity and is well-tolerated, characterised by minimal systemic absorption and fewer side effects compared to systemic antifungal therapies.
Oral antifungal therapy
Oral itraconazole is utilised in the treatment of tinea corporis, a superficial dermatophyte infection. As an azole antifungal, it inhibits ergosterol synthesis in fungal cell membranes, disrupting membrane integrity and causing fungal cell death.
It is administered once daily in capsule or tablet form for a specified treatment duration. Itraconazole demonstrates efficacy against a range of dermatophytes, including resistant strains not responsive to topical therapies.
This systemic approach is particularly beneficial for managing extensive or persistent infections inadequately controlled by topical treatments.
Oral terbinafine is prescribed for severe or resistant cases due to its rapid onset of action and favourable safety profile when used correctly. Fluconazole, a triazole antifungal agent, disrupts fungal membrane integrity, leading to cell death and resolving tinea corporis. Administered orally once daily, it effectively treats a range of dermatophytes causing the infection, particularly suitable for widespread or recurrent cases.
Griseofulvin disrupts fungal cell division and mitosis in the keratinised epidermal layers, targeting dermatophytes responsible for tinea corporis.
Administered orally over several weeks, it clears infections, including those resistant to topical treatments, by preventing fungal growth and spread.
Adjunctive therapies
Adjunctive therapies play a crucial role in the comprehensive management of tinea corporis, a superficial fungal infection of the skin caused by dermatophytes. Topical steroids are often used to alleviate inflammation and itching, which are common symptoms accompanying the infection. They help reduce discomfort and promote patient comfort during treatment. In cases where there is a secondary bacterial infection complicating tinea corporis, antibiotics may be prescribed to address bacterial overgrowth and prevent further complications. Emollients and moisturisers are beneficial adjuncts that soothe and hydrate the skin, promoting healing and restoring skin barrier function compromised by fungal infection and inflammation.
These adjunctive therapies complement antifungal treatments by managing symptoms and supporting skin recovery, contributing to comprehensive care and enhancing patient outcomes in the management of tinea corporis.
Effective treatment of tinea corporis involves a comprehensive approach, combining topical and systemic antifungal therapies as necessary, along with adjunctive measures to alleviate symptoms and aid skin recovery.
Customised treatment plans and patient education on preventive measures are crucial for successful outcomes and minimising recurrence in this prevalent skin condition.
Discussion
Tinea corporis, the most common dermatophytosis globally, exhibits a higher prevalence in tropical regions. The lifetime risk of acquiring tinea corporis ranges from 10 per cent to 20 per cent. It primarily affects post-pubertal children and young adults, although rare cases have been reported in newborns. There is no predilection based on gender. Humans contract the infection through close contact with infected individuals, animals (especially domestic dogs or cats), contaminated objects, or soil. Spread can also occur from other sites of dermatophyte infection (e.g., tinea capitis, tinea pedis, onychomycosis). Household transmission among family members, particularly children from infected household members, is the most common route. Autoinfection from dermatophytes elsewhere on the body is possible. Factors that predispose individuals to tinea corporis include personal history of dermatophytosis (e.g., tinea capitis, tinea pedis, tinea cruris, tinea unguium), presence of affected family members, pets in the home, crowded living conditions, participation in sports involving skin-to-skin contact (e.g., wrestling, martial arts), hyperhidrosis, low β-defensin 4 levels, immunodeficiency, diabetes mellitus, genetic predisposition (particularly tinea imbricata), xerosis, and ichthyosis. Transmission is facilitated by moist, warm environments, sharing of towels and clothing, and wearing occlusive clothing. Tinea corporis, predominantly caused by dermatophytes, is commonly attributed to Trichophyton rubrum, T. tonsurans, and Microsporum canis. T. rubrum is the most prevalent worldwide and the leading cause of tinea corporis in North America. Secondary infections from tinea capitis are typically due to T. tonsurans, whereas contact with dogs or cats often leads to infections caused by M. canis. Other notable pathogens include T. interdigitale (formerly T. mentagrophytes), T. verrucosum, T. violaceum, T. concentricum, Epidermophyton floccosum, M. audouinii, and M. gypseum.5
The differential diagnosis of tinea corporis includes pityriasis rosea, presenting with a non-itchy herald patch followed by a ‘Christmas tree’ pattern rash. Tinea versicolor manifests as scaly macules in fair-skinned individuals and hypopigmented patches in dark-skinned individuals. Nummular eczema shows coin-shaped, pruritic lesions, while plaque psoriasis features erythematous plaques with silvery scales. Atopic dermatitis presents with flexural involvement and intense itching. Contact dermatitis is localised due to irritants or allergens, and seborrheic dermatitis shows greasy scales. Other conditions include granuloma annulare, fixed drug eruptions, lupus erythematosus types, urticaria, pityriasis lichenoides chronica, lichen planus, erythema migrans, erythema multiforme, erythema dyschromicum perstans, erythema marginatum, erythema annulare centrifugum, impetigo contagiosa, erythema gyratum repens, and secondary syphilis with macules or patches on the trunk and limbs. Tinea corporis is highly contagious, leading to significant psychological, social, andoccupational impacts. Scratching and skin abrasions can predispose to secondary bacterial infections. Post-inflammatory changes such as hypopigmentation and hyperpigmentation are common sequelae. Dermatophytid reaction, also known as auto-eczematisation, may occur in response to a fungal infection or antifungal treatment, presenting as widespread, intensely itchy, erythematous papules, vesicles, or pustules. This reaction is thought to involve a delayed-type hypersensitivity response to fungal antigens. Additionally, rare instances of psoriatic flares triggered by tinea corporis have been reported.
Preventing tinea corporis hinges on minimising conditions favourable to fungal growth. Patients should be counselled to wear breathable, loose-fitting clothing to reduce moisture and warmth, which promote fungal proliferation. It’s essential to maintain meticulous personal hygiene practices, including frequent handwashing and ensuring skin remains clean and dry. Avoiding direct contact with items or clothing used by individuals with tinea corporis is crucial to prevent transmission of dermatophytes. These measures are fundamental in controlling the spread of this fungal infection within community and household environments. The prognosis for tinea corporis is generally favourable with adherence to proper treatment and patient compliance. Education plays a crucial role in prevention, emphasising measures such as wearing light and loose-fitting clothing and maintaining clean, dry skin to minimise recurrence. When initiating topical antifungal therapy, patient compliance is essential, although symptomatic relief may not be immediate. Patients should be informed that resolution of symptoms may take several weeks with consistent treatment. Encouraging patient understanding and compliance can lead to successful management of tinea corporis and improve overall outcomes.
Conclusion
Managing tinea corporis effectively demands a holistic approach that addresses its chronic nature and potential for resistance. Utilising advanced therapies such as oral antifungals, combination treatments, and adjunctive medications like corticosteroids and immunomodulators is pivotal in achieving successful outcomes. The availability of newer antifungal agents further broadens treatment options, especially for cases resistant to conventional therapies. Vigilant monitoring of treatment response and resistance is critical to adapting therapies as needed. Patient education on hygiene practices is equally indispensable to prevent recurrence and transmission. By integrating these advanced treatments with thorough patient care and education, healthcare providers can significantly enhance treatment effectiveness, minimise relapse rates, and elevate the overall management of tinea corporis, ultimately improving patient outcomes and quality of life.
• DR HARISH GOTTEMUKKALA is a dermatologist at Oceania Hospital. The views expressed in this article are his and not of this newspaper.
