Folliculitis Medication

  • Author: Elizabeth Kline Satter, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Aug 4, 2011
 

Medication Summary

Topical antibiotics can be used as first-line agents in cases of recurrent superficial folliculitis. If the area involved is widespread or persistent or if a deep infection is present, systemic antibiotics may be indicated. The drug of choice must cover penicillin- or methicillin-resistant S aureus in areas of high prevalence or in predisposed patients.

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Antibiotics

Class Summary

For patients who do not respond to standard antimicrobial treatments, therapy should be guided by culture sensitivity.

Erythromycin topical (Erycette)

 

Topical solution (2%). Indicated for infections caused by susceptible strains of microorganisms.

Clindamycin, topical (Cleocin T)

 

Topical solution. Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Mupirocin (Bactroban)

 

DOC for localized disease; inhibits bacterial growth by inhibiting RNA and protein synthesis.

Cephalexin (Keftab)

 

First-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. Has bactericidal activity against rapidly growing organisms. Has primary activity against skin flora; used for skin infections or prophylaxis in minor procedures.

Although cephalosporins have significant staphylococcal coverage in most populations, coverage of Pasteurella species is not as good as amoxicillin and clavulanate.

Dicloxacillin (Dynapen)

 

Treatment of infections caused by penicillinase-producing staphylococci. May use to initiate therapy when staphylococcal infection is suspected.

Erythromycin topical (Ery-Tab, E-Mycin, Eryc)

 

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.

In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be administered q12h. For more severe infections, dose is doubled.

Clindamycin (Cleocin)

 

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest.

Minocycline (Minocin)

 

Not DOC for staphylococcal infection. Treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma species. Was found to be effective in some nontuberculotic mycobacterial infections.

Rifampin (Rifadin)

 

For use in combination with at least 1 other anti-TB drug. Inhibits DNA-dependent bacterial RNA polymerase but not mammalian RNA polymerase. Cross-resistance may occur. Treat for 6-9 mo or until 6 mo have elapsed from conversion to sputum culture negativity.

Ciprofloxacin (Cipro)

 

Inhibits DNA gyrase and topoisomerase IV for bactericidal activity. Use as an alternative for MRSA infection.

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Antifungal agents

Class Summary

Many topical antifungal preparations are available to treat the forms of folliculitis (eg, tinea barbae, Pityrosporum folliculitis) caused by fungus. Topical agents should be active against dermatophytes.

Ketoconazole (Nizoral)

 

Imidazole broad-spectrum antifungal agent. Inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal death.

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Antiviral agents

Class Summary

Inhibitors of DNA polymerase in HSV-1 and HSV-2 strains, inhibiting viral replication.

Famciclovir (Famvir)

 

Prodrug that, when biotransformed into active metabolite penciclovir, may inhibit viral DNA synthesis/replication.

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Contributor Information and Disclosures
Author

Elizabeth Kline Satter, MD, MPH  Chairman, Department of Dermatology, Naval Medical Center San Diego

Elizabeth Kline Satter, MD, MPH is a member of the following medical societies: Alpha Omega Alpha and American Medical Women's Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Daniel J Hogan, MD  Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center

Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, and Canadian Dermatology Association

Disclosure: Nothing to disclose.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Paul Krusinski, MD  Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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A 22-month-old boy with a staphylococcal folliculitis on the buttocks. The lesions have been excoriated. Diaper occlusion may have been related to onset of the rash.
A 30-year-old woman with hot tub folliculitis. She had used a hot tub 2 days prior, wearing a bikini-style bathing suit.
Pseudomonas folliculitis. Courtesy of Hon Pak, MD.
Superficial folliculitis with neutrophils concentrated in the upper aspect of the follicle
Perifolliculitis, showing inflammatory cells surrounding the follicle,
 
 
 
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