SKIN INFECTIONS









Acne

Overview

  • Epidemiology - acne is a common skin condition that affects 85% of people aged 12 to 25 years. It can persist into middle age with 26% of women and 12% of men in their forties being affected.
  • Pathology - acne is caused by a combination of the following: (1) follicular hyperkeratinization, (2) colonization with Propionibacterium acnes, (3) sebum production, (4) complex inflammatory mechanisms
  • Treatment
    • There are few comparative studies in the treatment of acne; therefore, most recommendations are not evidence-based. The treatment algorithm presented here is derived from the AAP 2013 recommendations and the AAD 2016 guidelines.
    • Acne regimens typically require 6 - 12 weeks to achieve their full effect
    • Oral antibiotics should be prescribed with a retinoid +/- benzoyl peroxide; oral antibiotic monotherapy is discouraged. If a beneficial response to oral antibiotics is seen, they should be continued for 3 - 4 months; however, their use should be limited as much as possible to prevent bacterial resistance.
    • Upon stopping oral antibiotics, a 2.5% benzoyl peroxide cream washout for 2 weeks to eradicate resistant Propionibacterium acnes may be beneficial. Topical antibiotics may then be tried. If acne worsens, a repeat course of oral antibiotics may be indicated.
    • Postinflammatory hyperpigmentation from acne lesions typically resolves over a period of months. Sunscreen can help prevent further darkening. [1,2,27,30]

Treatment

Mild acne (mainly small red spots and/or comedones)
Moderate acne (red inflamed lesions, back acne)
Severe acne (nodular, scarring)

Bites (animal and human)

Treatment overview

  • All animal and human bite wounds should receive prompt and vigorous irrigation and cleansing. If cosmetically desirable, wounds may be sutured close; otherwise, healing by secondary intention may help to prevent infection.
  • The risk of infection from animal bites varies widely with rates as high as 45% in some studies and as low as 2% in others. The effectiveness of antibiotic prophylaxis in preventing infections has had mixed results in trials, but it does appear to be beneficial in hand bites and human bites.
  • Rabies prophylaxis should be given to all patients who were potentially bitten by a rabid animal. Rabies immunoglobulin is injected around the wound site, and any remaining volume should be given intramuscularly at an anatomical site distant from vaccine administration. The rabies vaccine (HDCV or PCECV) is given in the deltoid muscle at days 0, 3, 7, and 14.
  • Purulent bite wounds are often polymicrobial (mixed aerobes and anaerobes). Nonpurulent wounds commonly yield staphylococci and streptococci.
  • Tetanus vaccine should be given to patients who have not had one within 10 years [3,33,34]

Treatment regimens

Animal bites (IDSA 2014)
Human bites (IDSA 2014)
Cat and dog bite prophylactic therapy (IDSA 2014)
  • Prophylactic therapy is recommended in the following patients:
    • Immunocompromised
    • Asplenic
    • Advanced liver disease
    • Preexisting or resultant edema of the affected area
    • Moderate to severe injuries, especially to the hand or face
    • Injuries that may have penetrated the periosteum or joint capsule
  • Therapy should be for 3 - 5 days

Boils and abscesses

Treatment

Boils and abscesses (IDSA 2014)
  • Simple (no systemic signs of infection or cellulitis)
    • Incision and drainage only
    • Children with recurrent abscesses should be evaluated for neutrophil disorders [3]
  • Moderate (systemic signs of infection or cellulitis)
    • Incision and drainage
    • Empiric treatment with sulfamethoxazole-trimethoprim, doxycycline, or culture-guided treatment
    • Children with recurrent abscesses should be evaluated for neutrophil disorders
    • Systemic signs of infection include fever, tachycardia, tachypnea, and elevated white count [3]

Recurrent furunculosis / boils

Overview
  • Recurrent furunculosis is defined as ≥ 3 attacks within a 12 month period
  • Risk factors include positive family history (most important), anemia, previous antibiotic therapy, diabetes, previous hospitalization, multiplicity of lesions, poor personal hygiene, obesity, and associated skin diseases (e.g. leg ulcers, atopic dermatitis)
  • Methicillin-susceptible and methicillin-resistant Staph aureus are the most common pathogens. Nasal colonization with Staph aureus is present in up to 89% of patients. Gastrointestinal and urogenital colonization may also occur. [35]

Preventive measures (IDSA 2014)
  • Five day decolonization regimen that includes the following:
    • Intranasal mupirocin two times a day for 5 days each month
    • Daily chlorhexidine or dilute bleach (1/4 - 1/2 cup per full bath) washes
    • Daily washing of towels, sheets, clothes, combs, and razors
  • Other (regimen based on PMID 30763195)
    • Chlorhexidine 4% rinse-off for daily bathing and showering
    • Chlorhexidine 0.12% mouthwash twice daily
    • Intranasal mupirocin twice daily
    • NOTE: Regimen was performed for 5 days twice monthly over a period of 6 months

Studies

Clindamycin vs Sulfa/TMP vs Placebo for 10 days after I&D in patients with small abscesses, NEJM (2017) [PubMed abstract]
  • Design: Randomized, placebo-controlled trial (N=786 | length = 20 days) in patients with small skin abscesses (≤ 5 cm)
  • Treatment: Clindamycin 300 mg 3 times a day vs Sulfa/TMP 800/160 twice daily vs Placebo for 10 days
  • Primary outcome: clinical cure 7 to 10 days after the end of treatment
  • Results:
    • Primary outcome: Clindamycin - 83%, Bactrim - 82%, Placebo - 69% (p<0.001 for both vs placebo)
  • Findings: As compared with incision and drainage alone, clindamycin or TMP-SMX in conjunction with incision and drainage improves short-term outcomes in patients who have a simple abscess. This benefit must be weighed against the known side-effect profile of these antimicrobials.

Sulfa/TMP vs Placebo for 7 days after I&D in patients with abscesses, NEJM (2016) [PubMed abstract]
  • Design: Randomized, placebo-controlled trial (N=630 | length = 21 days) in patients > 12 years old with skin abscesses
  • Treatment: Four tablets of Sulfa/TMP 400/80 twice daily vs Placebo
  • Primary outcome: clinical cure of the abscess, assessed 7 to 14 days after the end of the treatment period
  • Results:
    • Primary outcome: Bactrim - 81%, Placebo - 74% (p=0.005)
  • Findings: In settings in which MRSA was prevalent, trimethoprim–sulfamethoxazole treatment resulted in a higher cure rate among patients with a drained cutaneous abscess than placebo

Cat scratch disease

Overview

  • Epidemiology - cat scratch disease (CSD) is caused by Bartonella henselae, an intracellular gram-negative rod. Bartonella is carried by cats, particularly those less than one year of age, and it is passed to humans through scratch, bite, or infected saliva on broken skin. Over half of CSD cases are seen in children, and the peak incidence of infection occurs between September and January.
  • Symptoms - symptoms of CSD include fever, skin changes at the inoculation site, and regional lymphadenopathy, a hallmark of the disease. The inoculation site may exhibit erythematous papules, vesicles, or nodules that appear 3 - 30 days following exposure and persist for 1 - 3 weeks. Regional lymphadenopathy occurs about 3 weeks after infection and is characterized by tender lymph nodes with overlying erythema; lymphadenopathy may last for 1 - 4 months.
  • Diagnosis - a CSD diagnosis can typically be made when there are characteristic exam findings and a recent history of a cat bite or scratch. Bartonella henselae IgG and IgM antibody tests are available, as is a serum PCR test. [3,4,36]
  • Treatment - in immunocompetent children, up to 95% of cases resolve spontaneously. Immunocompromised patients are at higher risk for disseminated infection that may involve the liver, spleen, and central nervous system. Corneal scratches can lead to a number of ophthalmic complications.

Treatment (IDSA 2014)

Azithromycin
  • Patients < 45 kg: 10 mg/kg on day 1 and 5 mg/kg for 4 more days ($)
  • Patients > 45 kg: 500 mg on day 1 followed by 250 mg for 4 additional days ($)

Cellulitis / erysipelas

Overview

  • Definitions - cellulitis is a common infection of the skin that affects the dermis and subcutaneous tissue. Erysipelas is a subtype of cellulitis that involves the epidermis and superficial dermis. Impetigo is an infection of the superficial layers of the dermis. Necrotizing fasciitis is an infection of the subcutaneous tissue that extends into the fascia, and from there, it spreads quickly in a planar fashion. Treatment recommendations for cellulitis and erysipelas are the same. Necrotizing fasciitis is a medical emergency that requires surgical debridement and intensive antibiotic therapy.
  • Pathology - cellulitis occurs when bacteria gain access to the dermis through breaks in the skin. Common portals of entry are cuts, bites, tinea pedis infections, toe web space infections, and venous stasis ulcers. Systemic risk factors for cellulitis include advanced age, obesity, and edema (especially lymphedema). The most common pathogens in cellulitis are Streptococcus pyogenes and Staphylococcus aureus. Purulent cellulitis (presence of pustules, abscess, or purulent drainage) is more likely to be caused by S aureus.
  • Symptoms - symptoms of cellulitis include pain, heat, swelling, and poorly-demarcated erythema to the affected area. Fever and leukocytosis may or may not be present. Erysipelas differs from cellulitis in that the erythema is more intense and sharply demarcated. Necrotizing fasciitis spreads rapidly, is very painful, and may cause skin necrosis and bullae formation.
  • Differential - other conditions can mimic cellulitis, particularly in the lower extremities; studies have found that up to 33% of cellulitis diagnoses are incorrect. Conditions that have a similar presentation to cellulitis include deep vein thrombosis, hematoma, insect bite reactions, gout, and stasis dermatitis. Stasis dermatitis can be particularly challenging to differentiate; one helpful caveat is that it is usually bilateral, whereas bilateral cellulitis is rare. Hematomas should be considered in areas of trauma and in people who are taking anticoagulants. In gout, the erythema overlies a joint, and joint manipulation is very painful. [37]

Treatment

Non-MRSA (IDSA 2014)
  • Pediatric
    • Cephalexin 25 - 50 mg/kg/day (max 2000 mg/day) given in 4 divided doses for 5 - 10 days ($)
    • Dicloxacillin 25 - 50 mg/kg/day (max 2000 mg/day) given in 4 divided doses for 5 - 10 days ($)
  • Adults
    • Cephalexin 500 mg four times a day for 5 - 10 days ($)
    • Dicloxacillin 500 mg four times a day for 5 - 10 days ($)
    • Penicillin VK 250 - 500 mg four times a day for 5 - 10 days (streptococcal infections only) ($)
MRSA coverage (IDSA 2014)
  • Pediatric
    • Clindamycin 30 - 40 mg/kg/day (max 1800 mg/day) given in 3 divided doses for 5 - 10 days ($$-$$$)
    • Linezolid 10 mg/kg/dose given twice a day for 5 - 10 days ($$)
    • Sulfamethoxazole-trimethoprim 8 – 12 mg/kg/day (based on trimethoprim component) given in 2 divided doses for 5 - 10 days ($)
MRSA coverage (other)
  • Adults
    • Omadacycline 450 mg once daily for 2 days followed by 300 mg once daily for a total of 7 - 14 days ($$$$)

Studies

Compression Stockings vs Education to Prevent Recurrent Cellulitis, NEJM (2020) [PubMed abstract]
  • Design: Randomized controlled trial (N=84 | length = median 186 days) in patients with ≥ 2 episodes of cellulitis in the same leg within the previous 2 years along with ≥ 3 months of leg edema
  • Treatment: Compression stockings + Education vs Education alone
  • Primary outcome: Recurrence of cellulitis
  • Results:
    • Primary outcome: Compression stockings - 15%, Education alone - 40% (p=0.002)
  • Findings: In this small, single-center, nonblinded trial involving patients with chronic edema of the leg and cellulitis, compression therapy resulted in a lower incidence of recurrence of cellulitis than conservative treatment.
Cephalexin + Sulfa/TMP vs Cephalexin alone for Uncomplicated Cellulitis , JAMA (2017) [PubMed abstract]
  • Design: Randomized, placebo-controlled trial (N=500 | length = 21 days) in outpatients older than 12 years with cellulitis and no wound
  • Treatment: Cephalexin 500 mg 4 times a day + Sulfa/TMP 320/1600 twice daily vs Cephalexin only for 7 days
  • Primary outcome: Clinical cure, defined as absence of these clinical failure criteria at follow-up visits: fever; increase in erythema (>25%), swelling, or tenderness (days 3-4); no decrease in erythema, swelling, or tenderness (days 8-10); and more than minimal erythema, swelling, or tenderness (days 14-21)
  • Results:
    • Primary outcome: Ceph + Sulfa/TMP - 83.5%, Ceph only - 85.5% (p=0.50)
  • Findings: Among patients with uncomplicated cellulitis, the use of cephalexin plus trimethoprim-sulfamethoxazole compared to cephalexin alone did not result in higher rates of clinical resolution of cellulitis in the per-protocol analysis. However, because imprecision around the findings in the modified intention-to-treat analysis included a clinically important difference favoring cephalexin plus trimethoprim-sulfamethoxazole, further research may be needed.
Clindamycin vs Sulfa/TMP for Uncomplicated Cellulitis, NEJM (2015) [PubMed abstract]
  • Design: Randomized, controlled trial (N=524 | length = 20 days) in outpatients with uncomplicated skin infections who had cellulitis, abscesses larger than 5 cm in diameter (smaller for younger children), or both
  • Treatment: Clindamycin 300 mg 3 times a day vs Sulfa/TMP 800/160 mg twice daily for 10 days
  • Primary outcome: clinical cure 7 to 10 days after the end of treatment
  • Results:
    • Primary outcome: Clindamycin - 80%, Sulfa/TMP - 78% (p=0.52)
    • MRSA status did not affect cure rates.
  • Findings: We found no significant difference between clindamycin and TMP-SMX, with respect to either efficacy or side-effect profile, for the treatment of uncomplicated skin infections, including both cellulitis and abscesses

Diabetic foot ulcer

Overview

  • Pathology - diabetic foot ulcers are difficult to treat because their origins and response to therapy are multifactorial. Ulcer formation occurs through the following steps: (1) sensory, motor, and autonomic neuropathies reduce sensation, sweating, and biomechanical offloading over an area of skin, (2) a callus forms over the affected area, (3) repetitive shear stress and/or trauma over the callus causes a subcutaneous hemorrhage to form, (4) hemorrhage leads to callus breakdown and ulcer formation, (5) peripheral vascular disease inhibits wound healing, and over 50% of ulcers become infected.
  • Diagnosing infection - determining which wounds are infected can be challenging since classic signs of infection may be absent in the setting of significant peripheral vascular disease and neuropathy. The IDSA guidelines state that the presence of ≥ 2 of the following establishes infection: (1) redness, (2) local swelling or induration, (3) local tenderness or pain, (4) local warmth, (5) purulent discharge (thick, opaque to white or sanguineous secretion). Other signs of infection include nonpurulent secretions, friable or discolored granulation tissue, undermining of wound edges, and foul odor.
  • Wound cultures - only infected wounds should be cultured. Cultures should be from deep tissue, obtained by biopsy or curettage, and after the wound has been cleansed and debrided. Specimens from nondebrided wounds or wound drainage should be avoided because they provide less accurate results.
  • Imaging - all new diabetic foot ulcers should have a plain film X-ray to look for bony abnormalities (deformity, destruction), soft tissue gas, and radio-opaque foreign bodies. If signs of osteomyelitis or deep tissue abscess are present, an MRI should be obtained. Bone scans may also be used to diagnose osteomyelitis if MRI is not available.
  • Treatment - wounds with necrotic tissue or surrounding callus should be debrided. Pressure should be redistributed off the wound. Patients with systemic signs of infection (e.g. fever, leukocytosis), deeper infections, inadequate home care, and/or failed outpatient treatment should be admitted to the hospital. Skin equivalents, growth factors, granulocyte colony-stimulating factors, hyperbaric oxygen therapy, and negative pressure wound therapy have not been proven to expedite wound healing. With proper treatment, up to 77% of ulcers heal within 1 year. Unfortunately, recurrence is common with 40% of patients having ulcer return within 1 year and 65% within 5 years. [5,38]

Treatment (IDSA 2014)

Diabetic foot ulcer, empiric outpatient treatment for mild infections
  • Mild infections - no systemic symptoms; only skin and superficial subcutaneous tissue involved; erythema ≤ 2 cm
  • Duration: duration of therapy for mild infections should be 1 - 2 weeks given that clinical signs of infection have resolved
Clindamycin was not listed under MRSA coverage, but it was noted to be "usually active against community-associated MRSA"
Diabetic foot ulcer, empiric outpatient treatment for moderate infections
  • Moderate infections - no systemic symptoms; may involve structures deeper than skin and subcutaneous tissue; erythema ≥ 2 cm
  • Duration: duration of therapy for moderate infections should be 2 - 3 weeks given that clinical signs of infection have resolved
    • Non-MRSA
    • MRSA coverage
      • Linezolid 400 - 600 mg twice daily for 7 - 14 days ($$)
Clindamycin was not listed under MRSA coverage, but it was noted to be "usually active against community-associated MRSA"

Herpes labialis | Fever blisters | Cold sores

Overview

  • Epidemiology - herpes labialis is caused by the herpes simplex virus type 1 (HSV-1). HSV-1 infection is ubiquitous, with up to 90% of the world's population being seropositive for HSV-1 by the age of 35 years. HSV-1 infection usually occurs in childhood between the ages of 6 months and 5 years. Affected individuals may be asymptomatic, or they may present with high fever, irritability, and painful oral ulcers (herpetic gingivostomatitis) that resolve over the course of 2 - 3 weeks. After the primary infection, approximately a third of patients will go on to have recurrent episodes of herpes labialis throughout life.
  • Diagnosis - herpes labialis typically presents with prodromal symptoms of itching and burning followed by clusters of vesicles that form along the border of the lip and adjacent skin. The vesicles rupture, ulcerate, and crust over within 24 - 48 hours. Complete resolution usually occurs within 7 - 10 days. Outbreaks may be triggered by stress, systemic illness, trauma, and ultraviolet light.
  • Treatment - oral antiviral agents decrease healing time and speed resolution by about 1 - 2 days on average. They are most effective when initiated promptly, preferably during the prodromal phase. Topical treatments have not been studied extensively, and their effects are unknown. Suppressive therapy can reduce outbreaks in patients with recurrent disease. [32,39,40]

Treatment

Acute episode
Suppressive therapy
Topical treatment
  • Acyclovir cream - apply 5 times a day for 4 days. Approved for ≥ 12 years. Indicated for recurrent episodes. ($$$$)
  • Xerese cream - apply 5 times a day for 5 days. Approved for ≥ 6 years. Indicated for recurrent episodes. ($$$$)

Herpes zoster | Varicella zoster | Shingles

Overview

  • Epidemiology - herpes zoster is caused by the varicella zoster virus (VZV). VZV infection typically occurs in childhood (chickenpox), and it's estimated that 95% of the world's population has been infected. For patients infected with varicella, the lifetime risk of shingles is 10 - 20%. For patients who live to be 85 years, the lifetime risk is 50%.
  • Symptoms - herpes zoster typically starts with pain, itching, and/or tingling in an area of skin on one side of the body. Over the course of 1 - 3 days, a blistering rash appears that is confined to an area of skin innervated by a single nerve (dermatome). Fever, headache, malaise, and lymphadenopathy are common. The blisters eventually become pustular and crust over (herpes zoster images). The chest, neck, forehead, and lumbosacral areas are most commonly affected. In most immunocompetent patients, the condition resolves in 2 - 4 weeks.
  • Postherpetic neuralgia (PHN) - postherpetic neuralgia is a syndrome where the pain from herpes zoster persists for ≥ 90 days after the onset of rash. It occurs in 10 - 50% of affected patients, and the risk increases with age.
  • Vaccines - there are two shingles vaccines - Shingrix and Zostavax. Shingrix cuts the risk of shingles by roughly 90% for at least 4 years. Zostavax cuts the risk by about 50%. The vaccines also reduce the risk of postherpetic neuralgia should shingles occur. Shingrix is a dead vaccine, and Zostavax is a live vaccine. Shingrix is recommended for all adults ≥ 50 years and is preferred over Zostavax. See screening and immunization recommendations for more.
  • Treatment - antivirals decrease pain and speed resolution of rash, but they have not been proven to decrease PHN risk. Steroids may reduce acute pain, but they also have not been proven to reduce PHN risk. Treatment should be started as soon as possible. Most zoster trials have excluded patients with symptoms > 72 hours, but a benefit beyond this timeframe cannot be excluded. Patients with visual symptoms should be referred to ophthalmology.
  • Recurrence - the lifetime risk of recurrent shingles in immunocompetent individuals is 5% [13,14,28]

Treatment regimens (IDSA 2007)

Antivirals - most patients
  • Acyclovir 800 mg five times a day for 7 - 10 days ($)
  • Famciclovir 500 mg three times a day for 7 days ($-$$)
  • Valacyclovir 1000 mg three times a day for 7 days ($)
Corticosteroids - select patients
  • Prednisone 60 mg a day for 7 days, then 30 mg a day for 7 days, then 15 mg a day for 7 days, then discontinue (IDSA regimen, others may suffice) ($)
Pain control

Hidradenitis suppurativa

Overview

  • Epidemiology - in population studies, the prevalence of hidradenitis suppurativa (HS) has ranged from 1 - 4%. Risk factors include family history, female sex (3:1), smoking, Crohn's disease, and obesity. The condition typically develops in the early twenties, and in some people, it may resolve or abate with age.
  • Diagnosis - HS is characterized by recurrent painful, pruritic nodules in the apocrine-gland regions of the body. Over time, the nodules form scars that exhibit chronic purulent discharge and sinus formation. The axillary (armpits) and inguinal (groin) areas are most commonly affected (hidradenitis suppurativa images). A delay in diagnosis is common as lesions may initially be treated as recurrent abscesses or boils.
  • Pathology - the pathology of HS involves perifollicular lymphocyte infiltration of the hair follicles followed by sebaceous gland loss. As HS progresses, local increases in interleukin (IL)-1, tumor necrosis factor (TNF), IL-17, S100A8 protein, S100A9 protein, caspase-1, and IL-10 lead to the migration of neutrophils, monocytes, and mast cells into the affected tissue. Chronic inflammation causes tissue destruction and scarring.
  • Treatment - no consensus guidelines for HS management have been published, and treatments range from medications to surgical excision of affected skin. Adalimumab (Humira®) is the only FDA-approved treatment. [16,17,29]

Treatment


Impetigo

Overview

  • Epidemiology - nonbullous impetigo can occur at any age, but it is most common in children aged 2 - 5 years; bullous impetigo occurs mainly in infants. Impetigo cases peak during the summer and fall, and it is most prevalent in hot, humid climates.
  • Pathology - impetigo is an infection of the superficial layers of the epidermis. Nonbullous impetigo is caused by Staphylococcus aureus (80%), Group A β-hemolytic Streptococcus (Strep pyogenes) (10%), or a combination of the two (10%). Bullous impetigo is caused by Staphylococcus aureus. Bacteria infect the skin through barrier disruptions (e.g. cuts, bites, dermatitis, cheilitis) or direct invasion. The face is frequently affected, and self inoculation to other sites is common. Impetigo is spread through skin contact and is highly contagious.
  • Symptoms - nonbullous impetigo (70% of cases) presents as pustules or vesicles that coalesce and rupture, producing the golden-crusted erosions that are characteristic of the disease. Bullous impetigo (30% of cases) begins as vesicles that progress to flaccid, fluid-filled bullae that eventually rupture, leaving a rim of crusted skin. The intertriginous regions and trunk are most commonly affected (impetigo images).
  • Treatment - untreated impetigo usually resolves in 14 - 21 days. Antibiotics speed resolution and may help to prevent rare complications (e.g. glomerulonephritis). Topical antibiotics are preferred for smaller lesions. Oral antibiotics are recommended for extensive lesions, and if MRSA is suspected, doxycycline, clindamycin, or sulfamethoxazole-trimethoprim (SMX-TMP) should be prescribed (see cellulitis for more). Lesions typically heal without scarring. Frequent hand washing and covering lesions can help prevent spread among children. Infected children can return to school after 48 hours of antibiotic therapy. [41,42]

Treatment regimens

Pediatric (IDSA 2014)
  • Amoxicillin-clavulanate 25 mg/kg/day (max 1750 mg/day) of the amoxicillin component given in 2 divided doses for 7 days ($)
  • Cephalexin 25 - 50 mg/kg/day (max 1000 mg/day) given in 3–4 divided doses for 7 days ($)
  • Clindamycin 20 mg/kg/day (max 1600 mg/day) given in 3 divided doses for 7 days ($-$$)
  • Erythromycin 40 mg/kg/day (max 1000 mg/day) given in 3–4 divided doses for 7 days ($$$$)
  • Mupirocin - apply ointment twice a day for 5 days ($)
  • Retapamulin - apply ointment twice a day for 5 days ($$$-$$$$)
Pediatric (other)
  • Benzathine penicillin G (Bicillin L-A®)
    • ≤ 6 kg: 225 mg (300,000 units) IM given as a one time dose
    • 6.1 - 10 kg: 337.5 mg (450,000 units) IM given as a one time dose
    • 10.1 - 15 kg: 450 mg (600,000 units) IM given as a one time dose
    • 15.1 - 20 kg: 675 mg (900,000 units) IM given as a one time dose
    • > 20 kg: 900 mg (1,200,000 units) IM given as a one time dose ($$-$$$)
  • Sulfamethoxazole-trimethoprim
    • Once daily: 8 mg/kg/day (trimethoprim component) (max 320 mg/day) given once daily for 5 days
    • Twice daily: 8 mg/kg/day (trimethoprim component) (max 320 mg/day) given in two divided doses for 3 days ($)
Adults (IDSA 2014)

Intertrigo

Overview

  • Epidemiology - intertrigo is a common skin condition that most often occurs in warm and humid environments. Patients with obesity, diabetes, incontinence, and immobility are at greatest risk.
  • Pathology - intertrigo occurs in overlapping skin folds where trapped moisture, friction, and decreased airflow lead to breakdown of the stratum corneum and maceration. Fungus and bacteria are able to gain access to the superficial epidermis, and infection occurs. Candida species are the most common fungal pathogen, and Staph aureus, Group A strep, and Pseudomonas are possible bacterial pathogens.
  • Symptoms - intertrigo causes a red, well-circumscribed rash in areas of overlapping skin. Maceration with fissures and ulceration may be present. Patients often report burning, itching, pain, and discomfort in the affected area. Intertrigo can occur anywhere that skin overlaps (e.g. neck, armpit, under the breasts, abdominal folds, between the buttocks, groin, finger and toe webs). (Candida intertrigo images)
  • Diagnosis - the presence of the characteristic rash is usually enough to make a diagnosis. Satellite lesions are a sign of secondary Candida infection, and a foul odor may indicate bacterial infection. KOH staining of skin scrapings, Wood lamp examination, and cultures may be performed but are rarely necessary. Unresponsive cases may require a skin biopsy.
  • Treatment - recommendations for treating secondary fungal infections are presented below. If a bacterial infection is suspected, topical agents (e.g. mupirocin) can be used for small areas and oral therapies (e.g. cephalexin) for larger ones. Itching and discomfort may be relieved with low-potency steroids (e.g. hydrocortisone). Preventive therapies are key to helping resolve active infections and preventing recurrences.
  • Prevention - efforts should be made to keep areas of overlapping skin dry and clean. Other preventive measures are listed below (see prevention below). [48,49]

Treatment

Candida infection
  • First-line
    • Nystatin cream - apply twice daily for 2 - 4 weeks ($)
    • Topical azoles (e.g. clotrimazole, miconazole) - apply twice daily for 2 - 4 weeks ($)
  • Extensive and/or resistant cases

Bacterial infection
Discomfort / itching

Prevention

The following may help to prevent intertrigo
  • Measures to prevent sweating and promote drying such as wearing loose clothing, changing or removing sweaty clothing, and drying sweaty skin
  • Barrier agents to prevent skin breakdown (e.g. zinc oxide ointment (Desitin®), petrolatum, dimethicone)
  • Separating skin surfaces with absorbent products (e.g. gauze pads)
  • Drying powders (e.g. Gold Bond®)
  • Antifungal powders (e.g. miconazole)

Lice

Overview

  • Epidemiology - head lice (Pediculus humanus capitis) are parasites that must remain on human hosts to survive. The prevalence of head lice in developed nations is 1 - 3%, and the incidence is highest in children between the ages of 2 - 11 years. Girls are affected more than boys, and blacks are affected less than other races.
  • Pathology - after reaching a host, lice lay eggs at the base of the hair shaft. The eggs hatch after 7 days, and a nymph is released. The nymph goes through 3 transformations over the course of a week before becoming an adult. In order to survive, the adult must suck blood from the scalp several times a day. Females lay about 8 eggs per day, and the cycle repeats itself. Lice can live for about 30 days on the scalp and die within 1 - 2 days off of it.
  • Transmission - lice are primarily passed through direct head-to-head contact; transmission through fomites (e.g. combs, hats, sheets) is much less common. Lice can only crawl; they do not hop or jump. Pets do not transmit lice.
  • Symptoms - the most common symptom of lice is scalp itching. Itching is secondary to a hypersensitivity reaction to lice saliva, and it may not develop for weeks after infestation.
  • Diagnosis - a diagnosis of lice is made by the direct observation of lice or eggs. The adult louse is about the size of a sesame seed and is usually tan to grayish-white in color. Lice are commonly found behind the ears and on the back of the neck. Eggs are found 1 cm from the scalp and are pigmented to match the color of the hair. Empty egg casings called nits are white and can be found throughout the hair. Nits are often confused with dandruff, and the two can be differentiated by the fact that nits are firmly affixed to the hair shaft where dandruff is not. Nits may remain in the hair for months after successful treatment, so their presence does not indicate an active infection.
  • Treatment - children with head lice do not need to be removed from school. After treatment is initiated, they can return to class with precautions to avoid head-to-head contact. Family members of infested patients should be examined and treated if live lice are found. Since lice cannot survive for more than 2 days off of the scalp, only items that have been in contact with the infected person's head 24 - 48 hours before treatment should be considered for cleaning. Washing or drying items at ≥ 130° F should be sufficient. Furniture and carpeting can be vacuumed. See the CDC lice treatment guidelines for more. Treatment of pubic lice is similar to head lice [12, 21]

Topical treatment

Over-the-counter (OTC)
  • Permethrin 1% lotion (Nix®) - apply to damp hair and scalp. Leave on for 10 minutes then rinse with water. Repeat in 7 days if necessary. Approved for patients ≥ 2 months. ($)
  • Pyrethrins 0.3% / piperonyl butoxide 4% shampoo (Rid®) - apply to dry hair and scalp. Leave on for 10 minutes then wash with water and shampoo. Repeat in 7 - 10 days. Approved for patients ≥ 2 years. ($)
Prescription
  • Benzyl alcohol 5% lotion (Ulesfia®) - apply to dry hair to completely saturate the scalp and hair; leave on for 10 minutes, then thoroughly rinse off with water. Repeat application after 7 days. The Ulesfia® PI gives recommendations for the number of bottles needed depending on hair length - Ulesfia® PI. Approved for children ≥ 6 months. ($$-$$$$)
  • Malathion 0.5% lotion (Ovide®) - apply lotion on dry hair in amount just sufficient to thoroughly wet the hair and scalp. Allow hair to dry naturally. After 8 - 12 hours, shampoo hair. Rinse and use fine tooth comb. Repeat in 7 - 9 days if necessary. Not approved for infants. ($$-$$$)
  • Spinosad 0.9% (Natroba®) - apply to dry scalp and hair. Leave on for 10 minutes then rinse with warm water. May repeat in 7 days. Approved for patients ≥ 4 years. ($$$-$$$$)
  • Ivermectin lotion (Sklice®) - apply to dry hair and scalp. Leave on for 10 minutes then rinse with water. Approved for patients ≥ 6 months. ($$$$)

Systemic treatment


Onychomycosis (nail fungus)

Overview

  • Epidemiology - onychomycosis is a fungal infection of the fingernails or toenails prevalent in about 10% of the general population. Age is a significant risk factor, and the prevalence climbs to 20% in people older than 60 years and 50% in those older than 70. Other risk factors for onychomycosis include nail trauma, excessive sweating, tinea pedis, psoriasis, diabetes, HIV, and peripheral artery disease.
  • Pathology - dark, moist environments such as sweaty shoes promote fungal growth, and microtrauma to the nail causes breaks in the seal between the distal nail and underlying epidermis that allow dermatophytes to gain access to the nailbed. From there, dermatophytes invade the overlying nail, causing subungual hyperkeratosis (excessive proliferation and scaling of the skin under the nail), onycholysis (detachment of nail plate from its bed), nail thickening and crumbling, and yellow and/or white discoloration. Trichophyton rubrum and Trichophyton mentagrophytes are the two most common dermatophytes in the U.S..
  • Diagnosis - onychomycosis is the most common cause of nail dystrophies, but other etiologies (e.g. psoriasis, lichen planus, dermatitis) are present in 50% of cases, so it is important to confirm the diagnosis before starting treatment. KOH staining of nail scrapings is simple and cheap but only has a sensitivity of 50 - 60%. Nail clippings that have been stained with periodic acid-Schiff (PAS) have sensitivities around 80%. Nail cultures can take weeks to come back and have a sensitivity around 50 - 60%.
  • Treatment - in most cases, treatment of onychomycosis is for cosmetic reasons, but severe cases can cause pain and difficulty walking. It can take > 12 months for treatment to have its full effect. Topical treatments should be reserved for cases where < 50% of the nail is involved, ≤ 4 nails are affected, and thickness is < 3 mm. Treatment success rates are provided in the table below.
  • Recurrence - recurrence occurs in about 25 - 30% of patients [9,25,26,43]

  • Mycological cure - negative culture and negative KOH
  • Normal nail - mycological cure and completely normal-appearing nail
  • Reference - Manufacturer PI
Onychomycosis treatment success rates
Treatment Mycological cure Normal nail
Terbinafine 70% 38%
Itraconazole 54% 14%
Ciclopirox 36% 9%
Efinaconazole 55% 18%
Tavaborole 31% 7%

Treatment regimens

Systemic therapy
  • Toenails
    • Terbinafine (Lamisil®) 250 mg once daily for 12 weeks ($)
    • Itraconazole (Sporanox®) 200 mg once daily for 12 weeks; OR 200 mg twice daily for 1 week a month for 3 consecutive months ($)
    • Griseofulvin
      • Griseofulvin microsize 500 mg once daily for 6 months ($$)
      • Griseofulvin ultramicrosize 375 mg twice daily for 6 months ($$$)
  • Fingernails
Topical
  • Ciclopirox 8% (Penlac®) - Apply once daily at bedtime to affected nail(s) for 48 weeks. Cover entire nail and under the tip. FDA-approved for toenails and fingernails. One 6.6 ml bottle ($)
  • Efinaconazole 10% (Jublia®) - Apply once daily to affected nail(s) for 48 weeks. When applying, ensure that the toenail, the toenail folds, toenail bed, hyponychium, and the undersurface of the toenail plate, are completely covered. FDA-approved for toenails only. ($$$$)
  • Tavaborole 5% (Kerydin®) - Apply once daily to affected nail(s) for 48 weeks. Cover entire nail and under the tip. FDA-approved for toenails only. ($$$$)

Pseudofolliculitis barbae

Overview

  • Epidemiology - pseudofolliculitis barbae (PB) is an inflammatory skin condition that primarily affects black people. In black men who shave regularly, the prevalence of PB has been as high as 85% in some studies.
  • Pathology - PB occurs when tight curly hairs are shaved close to the skin. As the hairs regrow, they curl inwards back into the skin, eventually penetrating it. This produces an inflammatory reaction that causes painful, itchy pustules and papules to form. Over time, infection, scarring, hyperpigmentation, and keloids can develop. (PB image) In men, the anterior neck, cheeks, and chin are most commonly affected. Women can develop lesions in areas of frequent shaving, such as the axilla and pubic region. A condition similar to PB called acne keloidalis nuchae occurs on the occipital scalp (back of the head). (acne keloidalis nuchae image)
  • Treatment - there are very few randomized trials involving PB treatments, and no consensus guidelines have been published. Patients with acutely inflamed lesions should stop shaving. Adjusting shaving techniques and topical therapies may be helpful. Laser hair removal is the only definitive therapy. [19,44]

Treatment

  • Discontinue shaving if possible
  • Shaving technique - use electric shaver with length set to 0.5 - 3 mm; shave in direction of hair growth; do not pull skin taut while shaving; avoid dry shaving; if a razor is used, shave frequently to prevent hairs from growing to a length that can penetrate skin
  • Avoid plucking hairs
  • Keratolytics - daily applications of retinoids, salicylic acid, or alpha hydroxy acids
  • Apply mild-to-medium potency topical steroids after shaving
  • Benzoyl peroxide + clindamycin twice daily [Based on PMID 15228130]
  • Topical retinoids
  • Laser hair removal [19,44]

Scabies

Overview

  • Epidemiology - scabies is caused by the Sarcoptes scabiei variety hominis mite. Scabies affects > 300 million people annually and is found in all parts of the world.
  • Transmission - scabies is mainly passed through direct skin-to-skin contact. Passage through fomites (e.g. linens, clothing) is uncommon. Scabies can infect livestock and pets, but they are not considered a significant source of human transmission. Scabies mites can live for up to 3 days off of human skin.
  • Pathology - once a female mite reaches the skin, she burrows into the epidermis and begins to lay 2 - 4 eggs per day. The eggs hatch in 3 - 4 days, releasing larvae that migrate to the skin and form new burrows in the stratum corneum. Adult mites emerge about 10 - 14 days later. Male mites explore the skin looking for unfertilized females; they are about half the size of females and are rarely seen. Female mites can live for 4 - 6 weeks on a human host.
  • Symptoms - when a person is infected for the first time, symptoms develop 2 - 6 weeks after infestation. Patients with a prior history of scabies develop symptoms within days because of previous sensitization to scabies proteins and feces. Symptoms include generalized itching that is worse at night, red papules at sites of infection, and wavy lines where the mite burrows. Common sites of infection are the interdigital space of the fingers and toes, under watches and jewelry, the elbows and armpits, the groin, and other skin folds. Infants can develop lesions over the entire body (scabies images). The size of female mites (0.3 - 0.5 mm) is at the limit of human visibility, and most infected persons do not observe mites. Severe infection in immunocompromised patients can result in a condition known as crusted (Norwegian) scabies that is characterized by exfoliating scales of skin containing thousands of mites. This form of scabies is highly contagious.
  • Diagnosis - most cases are diagnosed clinically when a person has symptoms and skin findings consistent with the disease. Skin scrapings of burrows contain mites, eggs, and mite fecal matter that can be observed under a microscope; in practice, scrapings are rarely performed.
  • Treatment - household members, sexual contacts, and persons who had close skin-to-skin contact with an infected individual should be treated. It is important to consider that most patients are asymptomatic for 2 - 6 weeks after infection, but they can still spread the disease during this time. Bedding, clothes, and towels that an exposed person used within 3 days before treatment should be washed in hot water and dried in a hot dryer. Shoes and other nonwashable items can be sealed in an airtight plastic bag for 72 hours. In the first few days after initiating therapy, itching may worsen and/or persist; this is not a sign of treatment failure. One treatment is generally sufficient; retreatment is rarely necessary. See CDC scabies treatment recommendations for more. [10,11,31]

Treatment regimens

First-line
  • Permethrin 5% cream (Elimite®) - thoroughly massage cream into the skin from the head to the soles of the feet. Leave on for 8 - 14 hours (preferably overnight), then wash. Infants should be treated on the scalp, temple, and forehead. May repeat in 8 - 15 days if necessary. ($)
Other
  • Sulfur ointment 5 - 10% - In studies, has been applied for 3 days to 3 weeks. Ointment is applied over entire body, washed off after 24 hours, and then reapplied for another 24 hours. Available OTC in a number of products. [PMID 29018829, PMID 26342502, PMID 27027929]
  • Ivermectin (Stromectol®) 200 mcg/kg/dose given one time and then repeated in 8 - 15 days (NOTE: 1000 mcg = 1 mg). Take with food. ($)

NOTE: Ivermectin is approved for patients ≥ 5 years but has been used in trials in patients ≥ 2 years who weigh at least 15 kg (see lice above)
Body weight (kg) Number of 3 mg ivermectin tablets
15 - 24 1
25 - 35 2
36 - 50 3
51 - 65 4
66 - 79 5
≥ 80 200 mcg/kg


Tinea capitis (scalp fungus)

Overview

  • Epidemiology - tinea capitis is a scalp dermatophyte infection that primarily affects children between 3 - 7 years old. The prevalence varies between regions and ethnicities, with school-aged black boys having the highest prevalence (up to 13% in some studies).
  • Pathology - tinea capitis occurs when dermatophytes invade hair follicles and infect the surrounding structures. In the U.S., 90 percent of cases are caused by Trichophyton tonsurans, and Microsporum species accounts for less than 5 percent. Children are more susceptible to infection than adults because their skin contains less sebum, a lipid-rich substance that resists infection.
  • Symptoms - tinea capitis can vary in presentation depending on the dermatophyte involved. The Trichophyton species most common in the U.S. often presents with scaly, oval patches that may or may not exhibit hair loss; this appearance may cause it to be misdiagnosed as seborrheic dermatitis. Itching, broken-off hairs that look like black dots, and cervical/occipital lymphadenopathy are often present. In severe cases, inflamed, puss-filled nodules called kerions can develop that may lead to scarring alopecia.
  • Transmission - tinea capitis is primarily spread through person-to-person contact. Dermatophytes can live for months off of human skin, making animals and fomites (e.g. hats, brushes, towels, couches, pillows) other potential sources.
  • Treatment - topical treatments are not effective. Terbinafine is not effective against Microsporum species, while griseofulvin and azoles are. Lab monitoring during griseofulvin treatment and terbinafine therapy of < 6 weeks duration is likely unnecessary in healthy patients. [6,7,22]

Treatment

Pediatric (Infants)
Pediatric (≥ 1 year)
  • Terbinafine tablets
  • NOTE: Tablet dosing based on one small study [PMID 12195561]
    • Weight 10 - 20 kg: 62.5 mg daily for 4 weeks
    • Weight 20 - 40 kg: 125 mg daily for 4 weeks
    • Weight > 40 kg: 250 mg daily for 4 weeks ($)
  • Terbinafine granules
  • NOTE: Terbinafine granules are FDA-approved for children ≥ 4 years old
    • Weight < 25 kg: 125 mg daily for 6 weeks
    • Weight 25 - 35 kg: 187.5 mg daily for 6 weeks
    • Weight > 35 kg: 250 mg daily for 6 weeks
  • Griseofulvin microsize
    • 20 - 25 mg/kg once daily for 6 - 8 weeks ($)
  • Griseofulvin ultramicrosize
    • 10 - 15 mg/kg once daily for 6 - 8 weeks ($$)
  • Itraconazole
    • 5 mg/kg once daily for 2 - 4 weeks ($-$$$)
    • Alternative:
      • Weight < 20 kg: 50 mg once daily for 4 weeks
      • Weight > 20 kg: 100 mg once daily for 4 weeks
      • [Based on PMID 11069511]
  • Fluconazole
    • 6 mg/kg once daily for 2 - 3 weeks ($-$$)
    • [Based on PMID 10468805]
    • Alternative:
      • 8 mg/kg once weekly for 8 - 12 weeks ($-$$)
      • [Based on PMID 10809856]
Adults

Tinea corporis / pedis / cruris / barbae / manuum

Overview

  • Epidemiology - tinea corporis infections are fungal infections of the superficial skin that affect 10 - 20% of the population over a lifetime. Children and young adults have the highest incidence, and the infections are more prevalent in warm, humid environments.
  • Terminology - tinea corporis infections are often referred to by different names depending on the area of the body they affect
    • Tinea corporis (ringworm) - anywhere on the body
    • Tinea pedis (athlete's foot) - feet
    • Tinea cruris (jock itch) - groin
    • Tinea barbae - beard area
    • Tinea manuum - hands
    • Tinea faciei - face
  • Pathology - Trichophyton species are the most common cause of tinea infections. The fungus is spread through direct person-to-person contact, contact with infected animals (e.g. dogs, cats, farm animals), and fomites (e.g. towels, clothing). Once it reaches the skin, the fungus invades the keratinized, non-living layer of the skin and spreads outwardly. Self-inoculation to other parts of the body is common. Tinea barbae differs from the other infections in that it is mostly spread by farm animals.
  • Symptoms - the incubation period for tinea infections is 1 - 3 weeks, after which a rash develops that is pruritic and erythematous with a scaly, raised edge that may contain pustules or vesicles. The rash spreads centrifugally and results in annular patches of varying sizes (tinea corporis images). The center part of the lesions may clear, resulting in a ring shape that gives it the name "ringworm." Other findings that are specific for tinea subtypes include the following:
    • Tinea pedis can cause macerated red erosions in the interdigital spaces (tinea pedis images)
    • Tinea manuum is typically unilateral and presents as a dry, scaly rash covering the palms (tinea manuum images)
    • Tinea cruris usually starts in the inguinal fold and spreads to involve the adjacent thigh (tinea cruris images)
    • Tinea barbae may present with typical tinea lesions in the beard area, or it may be inflammatory and cause kerions (tinea barbae images)
  • Diagnosis - tinea infections are usually a clinical diagnosis. KOH preparations of skin scrapings from the lesion border may be performed to look for septate hyphae. Fungal cultures are available but can take weeks to grow.
  • Treatment - when lesions are confined to a small area, topical medications are preferred. Topical treatments should be applied for 2 - 4 weeks. If lesions fail to respond, other etiologies should be explored (e.g. nummular eczema, pityriasis rosea). Tinea cruris and tinea pedis often occur together, and both should be treated, or recurrence is likely. Tinea barbae usually requires oral therapy, and longer courses of treatment (4 - 6 weeks) may be required. Keeping the skin dry and avoiding sources of infection can help to prevent recurrences. Antifungal powders may also be effective. [7,8,45,46]

Treatment

Pediatric
  • First-line
    • Terbinafine (Lamisil®) - topical terbinafine 1% applied once or twice daily ($)
    • Topical azoles (e.g. clotrimazole, miconazole) - apply twice daily ($)
  • Extensive and/or resistant cases
    • Terbinafine tablets
    • NOTE: Dosing based on study in children ≥ 2 years with tinea capitis [PMID 12195561]
      • Weight 10 - 20 kg: 62.5 mg daily for 2 - 4 weeks
      • Weight 20 - 40 kg: 125 mg daily for 2 - 4 weeks
      • Weight > 40 kg: 250 mg daily for 2 - 4 weeks ($)
    • Fluconazole (Diflucan®) 6 mg/kg (max 150 mg) once weekly for 2 - 4 weeks ($)
    • Griseofulvin
      • Griseofulvin microsize 10 mg/kg once daily (max 500 mg/day) for 2 - 4 weeks. Tinea pedis should be treated for 4 - 8 weeks. ($)
      • Griseofulvin ultramicrosize 7.25 mg/kg once daily (max 375 mg/day) for 2 - 4 weeks. Tinea pedis should be treated for 4 - 8 weeks. ($$)
Adults
  • First-line
    • Terbinafine (Lamisil®) - topical terbinafine 1% applied once or twice daily ($)
    • Topical azole (e.g. clotrimazole, miconazole) - apply twice daily ($)
  • Extensive and/or resistant cases
    • Terbinafine (Lamisil®) 250 mg once daily for 2 - 6 weeks ($)
    • Itraconazole (Sporanox®) 200 mg once daily for 7 days ($)
    • Fluconazole (Diflucan®) 150 - 200 mg once weekly for 2 - 6 weeks ($)
    • Griseofulvin
      • Griseofulvin microsize 500 mg once daily for 2 - 4 weeks. Tinea pedis should be treated for 4 - 8 weeks. ($-$$)
      • Griseofulvin ultramicrosize 375 mg once daily for 2 - 4 weeks, Tinea pedis should be treated for 4 - 8 weeks. ($$)

Tinea versicolor (pityriasis versicolor)

Overview

  • Epidemiology - tinea versicolor, also called pityriasis versicolor, is a superficial fungal infection of the skin that occurs primarily in warm, moist environments. The prevalence of tinea versicolor is as high as 50% in some tropical countries and as low as 1% in colder regions.
  • Pathology - tinea versicolor is caused by Malassezia, a fungus that is part of the normal skin flora. Malassezia causes the characteristic rash of tinea versicolor when factors are present that favor its filamentous form (e.g. moisture, heat, oily skin). Since Malassezia is part of the normal skin flora, tinea versicolor is not contagious.
  • Symptoms - tinea versicolor is marked by irregularly shaped, scaly patches of hypo- or hyperpigmented skin. The rash most commonly affects the back, chest, upper arms, neck, and face (tinea versicolor images). Lesions may be asymptomatic or slightly pruritic.
  • Diagnosis - tinea versicolor is usually diagnosed based on the presence of the characteristic rash. An ultraviolet black light (Wood lamp) may show coppery-orange fluorescence when shown across the rash. KOH preparations of skin scrapings can be performed to look for hyphae.
  • Treatment - topical therapies are preferred. Extensive and/or severe cases may require oral therapy. Topical terbinafine (Lamisil®) is effective, but oral terbinafine is not.
  • Recurrence - recurrence after treatment is common (80% at 2 years) [8,23,47]

Treatment

Topical
  • Selenium sulfide 2.5% lotion - apply to affected area and lather with a small amount of water. Leave on skin for 10 minutes then rinse off. Perform once daily for 7 days, then on the first and third day of the month for 6 months (2.5% strength is prescription-only) ($)
  • Ketoconazole 2% shampoo (Nizoral®) - Apply the shampoo to the damp skin of the affected area and a wide margin surrounding this area. Lather, leave in place for 5 minutes, and then rinse off with water. Perform once daily for up to 3 days. (2% strength is prescription-only) ($)
  • Zinc pyrithione shampoo (Head and Shoulders®, etc.) - Apply to affected area and leave in place for 5 minutes. Perform daily for 2 weeks. ($)
  • Terbinafine (Lamisil®) - topical terbinafine applied twice daily for one week ($) NOTE: Oral terbinafine is not effective [23]
Systemic (oral) therapy



Pricing legend
  • $ = 0 - $50
  • $$ = $51 - $100
  • $$$ = $101 - $150
  • $$$$ = > $151
  • Pricing based on one month of therapy at standard dosing in an adult
  • Pricing based on information from GoodRX.com®
  • Pricing may vary by region and availability