Fungal Infection of the Hair

Overview

Tinea capitis represents one of the most prevalent fungal infections worldwide, particularly in developing countries and urban areas with overcrowded living conditions. The infection affects millions of children globally, with prevalence rates varying from 1-20% depending on geographic location, socioeconomic factors, and local hygiene practices. In some African countries, prevalence can reach up to 40% among school-aged children.

The causative organisms are dermatophyte fungi that have a unique ability to invade and digest keratin, the protein that makes up hair, nails, and the outer layer of skin. These fungi can be classified as anthropophilic (human-loving), zoophilic (animal-loving), or geophilic (soil-loving), with anthropophilic species causing the majority of scalp infections. The specific fungal species causing infection varies by geographic region, with Trichophyton tonsurans being most common in North America and Microsporum canis prevalent in Europe and other regions.

The clinical presentation of tinea capitis can vary significantly, ranging from mild scaling similar to dandruff to severe inflammation with painful, boggy masses called kerion. Without proper treatment, the infection can lead to permanent hair loss and scarring. The condition's contagious nature means it can spread rapidly through families, schools, and communities, making early diagnosis and treatment essential for both individual health and public health control.

Symptoms

The symptoms of fungal hair infection can vary depending on the type of fungus involved, the host's immune response, and the severity of infection. Presentation ranges from subtle scaling to severe inflammatory reactions.

Scalp and Hair Symptoms

• Itchy scalp - Often the first symptom, ranging from mild to severe
• Irregular appearing scalp - Patchy areas with different textures or appearances
• Hair loss (alopecia) - In circular patches or diffuse patterns
• Broken hair shafts - "Black dot" appearance where hair breaks at scalp level
• Gray or white scales - Similar to severe dandruff
• Pustules or papules - Small bumps that may contain pus

Skin Manifestations

• Skin lesion - Circular or irregular patches on the scalp
• Skin irritation - Redness, tenderness, and inflammation
• Skin dryness, peeling, scaliness, or roughness - Flaking and scaling of affected areas
• Skin rash - May extend beyond the scalp to face and neck
• Abnormal appearing skin - Changed texture or color
• Skin swelling - Particularly with inflammatory types

Types of Presentation

• Gray patch type: Round patches of alopecia with gray scales
• Black dot type: Multiple areas where hair breaks at scalp surface
• Kerion: Severe inflammatory type with boggy, tender masses
• Favus: Rare chronic type with yellow crusts and musty odor
• Diffuse scale type: Generalized scaling resembling seborrheic dermatitis

Associated Symptoms

• Lymph node enlargement - Especially occipital and cervical nodes
• Secondary bacterial infection - With increased pain and discharge
• Id reaction - Allergic rash on body in response to fungal antigens
• Skin growth - Nodular lesions in severe cases
• Itching of skin - May extend beyond scalp
• Fever - In severe inflammatory cases

Some patients may also experience acne or pimples around affected areas due to follicular involvement, and rarely, pelvic pain from systemic inflammatory response in severe cases.

Causes

Fungal infections of the hair are caused by dermatophyte fungi that have evolved to digest keratin. Understanding the various causative organisms and transmission methods is crucial for prevention and treatment.

Common Causative Fungi

• Trichophyton tonsurans: Most common in North America, causes black dot tinea capitis
• Microsporum canis: Common worldwide, transmitted from cats and dogs
• Trichophyton violaceum: Endemic in Africa and Middle East
• Microsporum audouinii: Once common, now rare due to improved hygiene
• Trichophyton schoenleinii: Causes favus, rare in developed countries
• Trichophyton verrucosum: From cattle, causes severe inflammatory response

Transmission Methods

• Direct contact: Person-to-person transmission most common
• Fomites: Contaminated combs, brushes, hats, pillows, towels
• Animals: Pets (especially cats and dogs) and farm animals
• Environment: Fungal spores can survive on surfaces for months
• Asymptomatic carriers: Adults may carry fungi without symptoms

Predisposing Factors

• Age: Children 3-14 years most susceptible
• Immunosuppression: HIV/AIDS, chemotherapy, immunosuppressive drugs
• Overcrowding: Schools, daycare centers, orphanages
• Poor hygiene: Infrequent hair washing, sharing personal items
• Warm, humid climate: Promotes fungal growth
• Malnutrition: Weakens immune defenses
• Trauma to scalp: Creates entry points for infection

Pathophysiology

• Spore attachment: Fungal spores adhere to hair shaft or scalp
• Germination: Spores germinate and produce hyphae
• Invasion: Hyphae penetrate hair shaft and follicle
• Endothrix vs. Ectothrix: Fungi grow inside or outside hair shaft
• Immune response: Determines clinical presentation severity
• Hair destruction: Fungal enzymes digest keratin, weakening hair

Risk Factors

Multiple factors increase the risk of developing fungal hair infections:

• Age: Highest risk in children aged 3-14 years
• Gender: Boys affected more often than girls before puberty
• Race: African American children at higher risk in the US
• Socioeconomic status: Poverty and overcrowding increase risk
• Geographic location: Urban areas with high population density
• Climate: Hot, humid environments favor fungal growth
• Pet ownership: Especially cats and dogs with ringworm
• Personal hygiene: Sharing combs, brushes, hats, or pillows
• Hair care practices: Tight braiding, use of hair oils
• Immunocompromised state: Increased susceptibility and severity
• Diabetes mellitus: Higher risk of fungal infections
• Contact sports: Wrestling, martial arts with skin contact
• Family history: Genetic susceptibility factors
• Previous infection: Risk of reinfection if not properly treated

Diagnosis

Accurate diagnosis of fungal hair infection requires clinical examination combined with laboratory confirmation, as many scalp conditions can mimic tinea capitis.

Clinical Examination

• Visual inspection: Pattern of hair loss, scaling, inflammation
• Wood's lamp examination: Some fungi fluoresce blue-green (limited utility)
• Dermoscopy: Magnified view of hair shafts and scale
• Lymph node palpation: Check for regional lymphadenopathy
• Assessment of contacts: Family members, classmates, pets

Laboratory Tests

• KOH preparation: Direct microscopy of hair and scale
  • Endothrix: Spores inside hair shaft
  • Ectothrix: Spores outside hair shaft
  • Favus: Hyphae and air spaces in hair
• Fungal culture: Gold standard for diagnosis
  • Sabouraud dextrose agar
  • Dermatophyte test medium (DTM)
  • Takes 2-4 weeks for results
  • Identifies specific species for treatment
• PCR testing: Rapid molecular diagnosis (where available)
• Histopathology: Rarely needed, shows fungal elements in hair

Sampling Techniques

• Hair plucking: Remove affected hairs with forceps
• Scalp brushing: Sterile toothbrush or brush technique
• Adhesive tape: For collecting scale samples
• Scalp swab: Moistened swab for culture

Differential Diagnosis

• Alopecia areata
• Seborrheic dermatitis
• Psoriasis
• Trichotillomania
• Bacterial infections (impetigo)
• Lupus erythematosus
• Secondary syphilis
• Nutritional deficiencies

Treatment Options

Treatment of fungal hair infections requires systemic antifungal therapy, as topical treatments alone cannot penetrate the hair shaft adequately. The choice of treatment depends on the causative organism, patient age, and severity of infection.

Systemic Antifungal Medications

• Griseofulvin:
  • Traditional first-line treatment
  • Microsize: 20-25 mg/kg/day for 6-12 weeks
  • Ultramicrosize: 10-15 mg/kg/day
  • Take with fatty meal for better absorption
  • Less effective against T. tonsurans
• Terbinafine:
  • Often more effective than griseofulvin
  • Weight-based dosing for 4-8 weeks
  • Particularly effective for T. tonsurans
  • Granules available for children
• Itraconazole:
  • Pulse therapy or continuous dosing
  • 5 mg/kg/day for 4-6 weeks
  • Effective for most dermatophytes
  • Liquid formulation for children
• Fluconazole:
  • 6 mg/kg/day for 3-6 weeks
  • Once-weekly dosing option
  • Good safety profile

Adjuvant Topical Therapy

• Antifungal shampoos:
  • Ketoconazole 2% shampoo twice weekly
  • Selenium sulfide 1-2.5% shampoo
  • Ciclopirox 1% shampoo
  • Reduces spore shedding and transmission
• Topical antifungals: Limited efficacy alone, used as adjuvant
• Corticosteroids: For severe inflammation (kerion)

Management of Kerion

• Systemic antifungals (may need higher doses)
• Oral corticosteroids for severe inflammation
• Antibiotics if secondary bacterial infection
• Gentle debridement of crusts
• Avoid surgical drainage

Treatment of Contacts

• Screen all household members
• Treat asymptomatic carriers with antifungal shampoo
• Examine and treat infected pets
• Simultaneous treatment of infected family members

Monitoring and Follow-up

• Clinical improvement usually seen within 4-6 weeks
• Continue treatment for 2 weeks after clinical cure
• Repeat culture if no improvement after 4 weeks
• Monitor for side effects of systemic antifungals
• Hair regrowth may take several months

Treatment Failure Considerations

• Incorrect diagnosis
• Inadequate dose or duration
• Poor compliance
• Reinfection from untreated contacts
• Antifungal resistance (rare)
• Immunocompromised state

Prevention

Preventing fungal hair infections requires a combination of personal hygiene measures, environmental controls, and community education:

• Personal hygiene:
  • Regular hair washing with shampoo
  • Avoid sharing combs, brushes, hats, pillows
  • Use personal towels and hair accessories
  • Keep scalp clean and dry
• Environmental measures:
  • Disinfect combs and brushes regularly
  • Wash bedding and towels in hot water
  • Vacuum carpets and furniture regularly
  • Improve ventilation in living spaces
• School and daycare:
  • Screen for infected children
  • Educate about not sharing personal items
  • Notify parents of outbreaks
  • Maintain clean facilities
• Pet care:
  • Regular veterinary check-ups
  • Treat infected animals promptly
  • Limit contact during treatment
  • Wash hands after handling pets
• Community education:
  • Awareness programs in schools
  • Early recognition of symptoms
  • Importance of completing treatment
  • Reducing stigma
• High-risk situations:
  • Extra precautions in contact sports
  • Screening in residential facilities
  • Prophylactic shampoo in outbreaks

When to See a Doctor

Seek medical attention if you or your child experience:

• Persistent itchy scalp that doesn't improve with regular shampoo
• Patches of hair loss or broken hairs
• Scaling, crusting, or skin lesions on the scalp
• Red, swollen, or tender areas on the scalp
• Pus-filled bumps or drainage from the scalp
• Enlarged lymph nodes in the neck
• Fever accompanying scalp symptoms
• Spreading of symptoms to other body parts
• No improvement after 2 weeks of over-the-counter treatment
• Multiple family members with similar symptoms
• Contact with someone diagnosed with scalp ringworm

Urgent care is needed for:

• Large, painful, swollen areas on scalp (kerion)
• Signs of spreading bacterial infection
• High fever with scalp infection
• Rapid spread despite treatment

Related Conditions

Frequently Asked Questions

References

1. Elewski BE. Tinea capitis: a current perspective. J Am Acad Dermatol. 2000;42(1):1-20.
2. Gupta AK, et al. Systematic review of systemic treatments for tinea capitis. Pediatr Dermatol. 2018;35(5):615-621.
3. Fuller LC, et al. British Association of Dermatologists' guidelines for the management of tinea capitis 2014. Br J Dermatol. 2014;171(3):454-463.
4. Hay RJ. Tinea Capitis: Current Status. Mycopathologia. 2017;182(1-2):87-93.
5. Chen X, et al. Systematic review of the treatment of tinea capitis with griseofulvin versus terbinafine. J Dermatolog Treat. 2020;31(6):628-634.