SCF ENCYCLOPEDIA ENTRY

TINEA CAPITIS (SCALP RINGWORM)

I. SCOPE & POSITIONING

Pathogen / Etiology:

• Trichophyton tonsurans
• Microsporum canis

Classification: Fungal (Dermatophyte infection; keratinophilic fungi)

Transmission:

• Direct person-to-person contact
• Shared objects (combs, hats, bedding)
• Animal contact (zoophilic species)

Primary Tropism:

Scalp hair follicles and keratinized tissue

SCF Classification:

Keratin-Invasive Follicular Dermatophytic Colonization with Inflammatory Alopecic Disruption Disorder (KIFDC-IADD Class)

II. GLOBAL & CLINICAL SIGNIFICANCE

• Most common in children
• Highly contagious in:
• Schools
• Households

Clinical Hallmarks:

• Scalp scaling
• Patchy hair loss (alopecia)
• Broken hairs (“black dots”)

Severe Forms:

• Kerion (inflammatory mass)
• Permanent scarring alopecia (rare)

Aligned SCF Clinical Domains:

• C7: Dermatological Systems
• C2: Infectious & Inflammatory Medicine
• C11: Pediatric Infections

III. ETIOPATHOGENIC CORE

Primary Mechanisms:

• Fungal spores infect hair shaft and follicle
• Keratin digestion via fungal enzymes
• Hair shaft weakening and breakage

Key Drivers:

• Keratinase enzyme activity
• Follicular invasion
• Host inflammatory response (in some cases)

IV. SCF FAULT ARCHITECTURE

Key Insight:

Tinea capitis is a localized structural degradation disorder, where fungi consume keratin and destabilize hair architecture.

V. MULTI-OMICS PATHOGENESIS MAP (Keratin Invasion Model)

A. Genomics

• Dermatophyte genomes encode keratin-degrading enzymes

B. Transcriptomics

• Upregulation of:
• Keratinases
• Proteases

C. Proteomics

• Enzymes:
• Keratinases → digest hair proteins
• Lipases → degrade scalp lipids

D. Epigenomics

• Host inflammatory signaling varies by strain
• Zoophilic strains → stronger immune response

E. Metabolomics

• Breakdown of keratin → nutrient source for fungi
• Minimal systemic metabolic impact

F. Interactomics

• Fungus–hair shaft interaction
• Fungus–immune system interaction (inflammatory vs non-inflammatory types)

G. Follicular Interface

• Endothrix invasion (inside hair shaft)
• Ectothrix invasion (outside hair shaft)

VI. PATHOGENESIS FLOW (SCF LOGIC)

Exposure → Spore adherence → Follicular invasion → Keratin degradation → Hair breakage → Inflammation (optional)

VII. CLINICAL SPECTRUM

VIII. SCF DISEASE-ORIGIN MODEL

A. Core Mechanisms:

• Keratin digestion
• Follicular invasion
• Variable immune response

B. SCF Classification:

• Primary: Dermatophytic Infection
• Secondary: Structural Hair Loss Disorder

IX. SCF TRINITY FRAMEWORK MAPPING

Interpretation:

Tinea capitis represents a structural degradation model, where fungal metabolism breaks down keratin-based tissues.

X. SCF PCR THERAPEUTIC STRATEGY

1. PREVENTATIVE (P)

• Avoid sharing personal items
• Hygiene in schools and households
• Animal screening (zoophilic cases)

2. CURATIVE (C)

First-Line Treatment:

• Oral antifungals:
• Griseofulvin
• Terbinafine

Adjunct:

• Antifungal shampoos (ketoconazole, selenium sulfide)
• Reduce transmission

Key SCF Insight:

Topical therapy alone is insufficient due to follicular penetration requirement

3. RESTORATIVE (R)

• Hair regrowth monitoring
• Anti-inflammatory management (kerion cases)
• Microbiome normalization of scalp

XI. CURRENT STANDARD OF CARE

• Systemic antifungal therapy
• Adjunct topical treatment
• Household contact management

XII. SCF THERAPEUTIC ENGINEERING OPPORTUNITIES

High-Value Targets:

• Keratinase enzymes
• Fungal adhesion mechanisms
• Follicular penetration pathways

SCF Design Strategy:

• Keratinase inhibitors
• Follicle-penetrating antifungal systems
• Biofilm disruption agents

XIII. RHENOVA INTEGRATION (REDOX–HYPOXIA LOGIC)

Core Disruption:

• Local inflammation (kerion cases)
• Minimal systemic stress

SCF–RHENOVA Role:

• Monitor inflammatory severity
• Optimize healing environment

XIV. TRANSLATIONAL BLUEPRINT (FDA-ALIGNED)

Preclinical:

• Dermatophyte growth models
• Antifungal efficacy testing

Clinical:

• Resolution of infection
• Prevention of spread
• Hair regrowth outcomes

Biomarkers:

• Fungal culture
• KOH microscopy
• Dermoscopy

XV. SCF DBI INTERPRETATION

Insight:

Tinea capitis represents a DBI localized structural disruption model, where damage is confined but functionally significant.

XVI. SCF LAYMAN’S TRANSLATION SUMMARY

Tinea capitis is a fungal infection of the scalp, commonly seen in children.

It:

• Spreads through contact or shared items
• Causes hair loss and scalp scaling
• Can become inflamed in severe cases

SCF treatment focuses on:

• Oral antifungal medication
• Preventing spread
• Supporting hair regrowth

XVII. MASTER REGISTRY INDEX

• SCF-FUNG-TINEA-0001 — Tinea Capitis Entry
• SCF-DERMATOPHYTE-0002 — Fungal Module
• SCF-FOLLICULAR-0003 — Hair Registry
• SCF-RHENOVA-LOCAL-0004 — Inflammation Mapping
• SCF-DBI-STRUCTURAL-0005 — Keratin Model

NEXT STEP OPTIONS

If you want to go deeper, I can generate:

• SCF comparison: Tinea capitis vs Tinea corporis vs Tinea pedis
• API discovery targeting keratinase inhibition
• Scalp microbiome restoration protocol (post-antifungal)
• Pediatric dermatophyte infection management system (SCF)