Tinea capitis
Tinea capitis is a superficial dermatophyte infection of the scalp and hair shafts, primarily affecting prepubertal children and caused by keratinophilic fungi such as species of Trichophyton and Microsporum.[1] It typically presents with pruritic, scaly patches of alopecia, and may evolve into inflammatory variants featuring pustules, nodules, or kerion formation with secondary bacterial infection.[2] Transmission occurs via direct person-to-person contact or fomites like combs, hats, and bedding, with higher incidence in crowded urban environments and among certain ethnic groups due to hair characteristics facilitating fungal invasion.[3] In North America, Trichophyton tonsurans accounts for the majority of cases, reflecting an endothrix pattern of hair infection, whereas ectothrix infections from Microsporum canis or Microsporum audouinii predominate in Europe and other regions.[4] Recent epidemiological shifts, including increased adult cases and variations linked to migration, underscore the need for ongoing surveillance.[5] Diagnosis relies on clinical examination, supplemented by microscopy, culture, or Wood's lamp for confirmation, as misdiagnosis can delay treatment and promote spread.[1] Management necessitates oral antifungal therapy, with griseofulvin or terbinafine as first-line agents for 6-8 weeks, since topical treatments fail to penetrate hair follicles adequately.[6] Adjunctive selenium sulfide shampoo reduces infectivity, and public health measures emphasize hygiene and screening in outbreaks, particularly in schools.[7]Etiology and Pathogenesis
Causative Fungi
Tinea capitis is caused by keratinophilic dermatophyte fungi, predominantly species within the genera Trichophyton and Microsporum, which invade the hair shaft and follicle.[1] These anthropophilic (human-adapted) or zoophilic (animal-adapted) pathogens produce arthroconidia—infectious spores formed by hyphal fragmentation—that facilitate hair invasion.[8] In endothrix infections, arthroconidia form inside the hair shaft without destroying the cuticle, as seen with Trichophyton species; ectothrix infections feature a sheath of spores around the exterior, typically from Microsporum species.[8] [9] Trichophyton tonsurans, an anthropophilic endothrix dermatophyte, predominates in urban North American and UK settings, accounting for 88-96% of cultured isolates in recent US surveillance data.[10] [11] This species rose to dominance in the United States during the 1970s, supplanting prior ectothrix agents like Microsporum audouinii through increased person-to-person spread in densely populated areas.[12] [8] Anthropophilic fungi such as T. tonsurans exhibit host adaptation, resulting in chronic, less inflammatory infections compared to zoophilic counterparts.[8] Microsporum canis, a zoophilic ectothrix species primarily hosted by cats and dogs, remains a key pathogen where animal contact is common, comprising the majority of European cases per multicenter reports.[13] [14] It produces abundant ectothrix spores on the hair surface, often eliciting pronounced inflammatory responses due to zoonotic mismatch.[8] Regional variants include Trichophyton violaceum, another anthropophilic endothrix agent prevalent in immigrant communities from Africa or the Middle East, identified in up to 20-30% of cases in affected European cohorts.[15] Culture-based identification confirms these distributions, with T. tonsurans exceeding 90% in US pediatric isolates from 2010-2020 studies.[9] [16]Transmission Mechanisms
Tinea capitis spreads primarily through direct contact with infected individuals or animals, facilitating person-to-person or zoonotic transmission. Close physical contact, such as in households or play settings, allows dermatophytes to transfer from scalp to scalp, while sharing personal items like combs, hairbrushes, hats, or towels provides a common vector for anthropophilic species such as Trichophyton tonsurans. Zoonotic cases often involve direct handling of infected pets, particularly cats and dogs carrying Microsporum canis, which accounts for a significant portion of animal-derived infections in regions where such strains predominate.[1][17][18] Indirect transmission occurs via fomites, including contaminated barber tools, clothing, bedding, or environmental surfaces like gym mats, where arthroconidia shed from infected hairs remain infectious. These spores demonstrate environmental persistence, remaining viable for months on inanimate objects under favorable conditions such as warmth and humidity, thereby sustaining outbreaks even without ongoing direct exposure.[1][19][18] Following exposure, the incubation period for tinea capitis typically spans 1 to 3 weeks, during which fungal elements invade hair follicles without immediate clinical signs, allowing silent dissemination in high-contact settings like schools or communal living arrangements. Crowding exacerbates risk by increasing opportunities for both direct interpersonal transfer and fomite contamination among susceptible children.[20][21]Pathophysiological Processes
Dermatophyte fungi causing tinea capitis invade the stratum corneum and hair follicles by secreting proteolytic enzymes, including keratinases, which hydrolyze keratin into peptides and amino acids for fungal nutrition.[1] This enzymatic degradation enables hyphal penetration of the non-viable keratinized layers, with the fungus colonizing the hair shaft and follicle interior while evading deeper viable tissue invasion due to host temperature barriers and immune factors.[8] The process begins at arthroconidia or hyphal fragments adhering to the scalp, followed by radial growth along the follicle, where the fungus exploits the nutrient-rich environment of newly forming keratin in the hair bulb.[22] Invasion patterns differ by fungal species: ectothrix involves hyphae forming arthrospores that sheath the exterior of the hair shaft beneath the cuticle, often preserving the shaft integrity initially but leading to surface destruction; endothrix features hyphal fragmentation into spores entirely within the hair shaft, compromising internal structure and causing brittleness.[1] These distinctions arise from species-specific adaptations, such as Microsporum spp. favoring ectothrix via external spore production, while Trichophyton tonsurans predominantly causes endothrix by internal proliferation, resulting in hair fragility, breakage at the follicular orifice, or complete shaft dissolution.[8] Follicular colonization disrupts the hair growth cycle, inducing dystrophic changes and mechanical hair loss through enzymatic weakening rather than direct host cell necrosis.[23] Host response is predominantly cell-mediated, involving T-lymphocyte activation and cytokine release (e.g., IL-2, IFN-γ) that recruit neutrophils and macrophages to form granulomatous inflammation.[24] In children, immune immaturity—characterized by underdeveloped Th1 responses and delayed antigen recognition—permits initial fungal proliferation with minimal early inflammation, followed by a hypersensitive reaction in severe cases manifesting as kerion, a boggy abscess from exaggerated delayed-type hypersensitivity.[25] This T-cell-driven response, while aimed at fungal clearance, contributes to tissue damage via inflammatory mediators, potentially leading to follicular scarring if unresolved.[23] Endemic exposure may modulate responses, with repeated low-level contact fostering partial immunity that limits severity in adults compared to children's naive systems.[26]Clinical Features
Primary Symptoms
Tinea capitis primarily manifests as pruritus, scaling, and alopecia in circumscribed scalp patches.[1] Patients commonly report itching and observe dry, flaky skin with hair breakage or loss, often revealing broken hair stubs resembling black dots within the affected areas.[1] [27] Inflammatory variants may feature tender, pustular eruptions or a boggy, suppurative mass accompanied by regional lymphadenopathy.[1] Asymptomatic scalp colonization occurs in some individuals, particularly in high-prevalence settings, without evident hair loss or discomfort.[5] Lesions typically originate as small erythematous papules around hair follicles and expand centrifugally if untreated, potentially enlarging affected zones over weeks to months.[28] Systemic signs such as low-grade fever arise rarely, usually in association with pronounced inflammatory responses.[1]Disease Patterns
Tinea capitis manifests in distinct clinical patterns influenced by the mode of fungal invasion—ectothrix or endothrix—and host immune response, resulting in non-inflammatory or inflammatory presentations.[1] Ectothrix patterns, where arthroconidia sheath the exterior of the hair shaft, typically produce the gray patch variant, featuring circumscribed areas of alopecia with fine scaling and short, broken hairs that appear grayish due to surface spores; these hairs fluoresce bright green under Wood's lamp examination, most commonly from Microsporum species infections.[29] [1] In contrast, endothrix invasion, with hyphae and arthroconidia confined within the hair shaft, yields the black dot pattern, characterized by hairs fracturing at or near the scalp surface, leaving pinpoint black dots amid mild scaling and patchy alopecia; this does not fluoresce under Wood's lamp and predominates in Trichophyton tonsurans cases.[29] [1] Favus represents a specialized non-inflammatory variant linked to Trichophyton schoenleinii, forming yellow, cup-shaped crusts (scutula) around hair follicles amid scarring alopecia, though it remains rare in Western populations due to shifts in dermatophyte ecology.[29] Inflammatory patterns arise from exaggerated hypersensitivity to fungal antigens, culminating in kerion formation—a boggy, tender tumefaction with overlying pustules, crusting, and purulent discharge that can simulate pyogenic bacterial abscesses or cellulitis, often resolving with scarring if untreated.[1] [28] These inflammatory responses occur across invasion types but correlate more with zoophilic fungi or overwhelming anthropophilic loads.[1] While pediatric cases predominate with balanced non-inflammatory and inflammatory forms, adult tinea capitis proves rarer—comprising under 2% of instances—and skews toward severe inflammatory phenotypes like kerion, potentially due to altered sebum production and immune dynamics in post-pubertal scalps.[5] [5] Such patterns underscore the need for pattern-specific evaluation to guide management, as ectothrix forms may respond partially to adjunctive topicals while endothrix variants necessitate systemic therapy.[1]Differential Considerations
Alopecia areata presents with well-demarcated patches of non-inflammatory alopecia, often featuring exclamation-point hairs, without scaling or broken hair shafts characteristic of tinea capitis; it is typically reversible and lacks infectious etiology.[30][23][29]Seborrheic dermatitis manifests as diffuse, greasy yellow scales across the scalp with minimal to no alopecia, differing from the patchy, drier scaling and hair breakage in tinea capitis.[23][31]
Psoriasis of the scalp involves thicker, silvery plaques that often extend beyond the hairline to the forehead or ears, with nail involvement in up to 50% of cases, contrasting the more localized alopecia and potential inflammatory response in tinea capitis.[32]
Bacterial folliculitis or impetigo exhibits pustular or crusted lesions with purulent discharge and rapid progression, unlike the slower-evolving, less exudative patches of tinea capitis; secondary bacterial superinfection can complicate fungal cases but is distinguished by culture.[1][23]
Pediculosis capitis features visible nits or lice along hair shafts with pruritus from infestation, absent in tinea capitis where ectothrix or endothrix hair invasion leads to breakage without macroscopic parasites.[23][18]
Trichotillomania causes irregular, traction-like alopecia from habitual pulling, lacking the scaling, inflammation, or infectious signs of tinea capitis.[23]
Less common mimics include dissecting folliculitis (scarring alopecia with tufted hairs) and secondary syphilis (moth-eaten alopecia with systemic symptoms), which require exclusion via history and serology due to overlapping patchy hair loss.[1][30]
Empirical discriminators for tinea capitis include associated pruritus, posterior cervical lymphadenopathy, and black-dot or stubbed hairs, with confirmation via microscopy revealing hyphae or fluorescence under Wood's lamp for Microsporum species.[18][4]