Updated: Jun 18, 2009
Pseudomonas folliculitis is a community-acquired skin infection, which results from the bacterial colonization of hair follicles after exposure to contained, contaminated water (eg, whirlpools,1,2,3,4,5,6 swimming pools,7 water slides, bathtubs). First reported in 1975 in association with whirlpool contamination, Pseudomonas folliculitis is caused by strains of Pseudomonas aeruginosa that are acquired secondary to skin contamination.
The rash of Pseudomonas folliculitis has also been described following the use of diving suits in both seawater and fresh water immersion,8,9 and, less commonly, following the use of contaminated bathing objects (eg, synthetic and natural sponges).10,11,12 Pseudomonas folliculitis has occurred after skin depilation and with no obvious recreational exposure.
Pseudomonas folliculitis also rarely occurs as a perioral acneiform eruption in patients on long-term antibiotic (eg, tetracycline) therapy for acne.13
The ubiquitous gram-negative bacterial organism, P aeruginosa, found in soil and fresh water, gains entry through hair follicles or via breaks in the skin. Bacterial serotype O:11 is the most commonly reported isolate for water-associated Pseudomonas folliculitis, but other serotypes that have been reported include O:1, O:3, O:4, O:6, O:7, O:9, O:10, and O:16. Serotype O:11 is possibly more invasive or better adapted to survive in halogenated water.
Minor trauma from wax depilation or vigorous rubbing with sponges may facilitate the entry of organisms into the skin.10,11 Hot water, high pH (>7.8), and low chlorine level (<0.5 mg/L) all predispose to infection.
The actual incidence of Pseudomonas folliculitis is difficult to assess because of the transient nature of the bather population.
Most cases of Pseudomonas folliculitis resolve without any adverse reactions.
No racial differences in incidence are known for Pseudomonas folliculitis.
No sexual differences in incidence are known for Pseudomonas folliculitis.
Pseudomonas folliculitis is characterized by a rash, described as a dermatitis or a folliculitis.
The predominant manifestation of Pseudomonas folliculitis is dermatitis (79%).
Contact Dermatitis, Irritant
Acne
Bromide sensitivity
Staphylococcal folliculitis
Gram-negative folliculitis
Standard hematoxylin and eosin preparation displays a severe follicular epithelial inflammatory response, which may result in follicular distention and rupture. The pilar canal is filled with a dense polymorphonuclear leukocytic infiltrate, often accompanied by a brisk perifollicular lymphocytic infiltration. Both the epidermis and the infected apocrine glands remain intact.
P aeruginosa is usually a self-limited infection, clearing in 2-10 days. Despite the discomfort caused by the Pseudomonas folliculitis rash, no treatment is necessary. Systemic spread is typically not observed.
Systemic antibacterials for uncomplicated Pseudomonas folliculitis infections have shown no benefit. Persistent infections may benefit from a standard 7- to 10-day course of ciprofloxacin.
Bactericidal antibacterials inhibit bacterial growth and proliferation.
Member of fluoroquinolone family of synthetic, broad-spectrum antibacterials. Contains piperazine moiety responsible for antipseudomonal activity. Interferes with DNA gyrase normally needed for synthesis of bacterial DNA.
Severe infection: 750 mg PO bid for 7-14 d
Mild-to-moderate infection: 500 mg PO q12h for 7-14 d
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT); food delays absorption, resulting in peak concentrations closer to 2 h after dosing rather than 1 h; however, overall absorption is not substantially affected; dairy products (eg, milk, yogurt) reduce absorption (avoid concurrent use)
Antidiabetic agents, antiarrhythmic agents, CYP1A2 metabolized drugs, methotrexate, and metoprolol
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy; phototoxicity may occur with exposure to sunlight
Fluoroquinolones are associated with an increased risk of tendinitis and tendon rupture in persons of all ages; risk is further increased in older patients (usually >60 y), those taking corticosteroids, and those with kidney, heart, or lung transplants
Gregory DW, Schaffner W. Pseudomonas infections associated with hot tubs and other environments. Infect Dis Clin North Am. Sep 1987;1(3):635-48. [Medline].
Highsmith AK, Le PN, Khabbaz RF, Munn VP. Characteristics of Pseudomonas aeruginosa isolated from whirlpools and bathers. Infect Control. Oct 1985;6(10):407-12. [Medline].
McCausland WJ. Pseudomonas aeruginosa rash associated with whirlpool. JAMA. Nov 29 1976;236(22):2490-1. [Medline].
Price D, Ahearn DG. Incidence and persistence of Pseudomonas aeruginosa in whirlpools. J Clin Microbiol. Sep 1988;26(9):1650-4. [Medline].
Ratnam S, Hogan K, March SB, Butler RW. Whirlpool-associated folliculitis caused by Pseudomonas aeruginosa: report of an outbreak and review. J Clin Microbiol. Mar 1986;23(3):655-9. [Medline].
Rose HD, Franson TR, Sheth NK, Chusid MJ, Macher AM, Zeirdt CH. Pseudomonas pneumonia associated with use of a home whirlpool spa. JAMA. Oct 21 1983;250(15):2027-9. [Medline].
Jacobson JA. Pool-associated Pseudomonas aeruginosa dermatitis and other bathing-associated infections. Infect Control. Oct 1985;6(10):398-401. [Medline].
Lacour JP, el Baze P, Castanet J, Dubois D, Poudenx M, Ortonne JP. Diving suit dermatitis caused by Pseudomonas aeruginosa: two cases. J Am Acad Dermatol. Dec 1994;31(6):1055-6. [Medline].
Saltzer KR, Schutzer PJ, Weinberg JM, Tangoren IA, Spiers EM. Diving suit dermatitis: a manifestation of Pseudomonas folliculitis. Cutis. May 1997;59(5):245-6. [Medline].
Bottone EJ, Perez AA 2nd, Oeser JL. Loofah sponges as reservoirs and vehicles in the transmission of potentially pathogenic bacterial species to human skin. J Clin Microbiol. Feb 1994;32(2):469-72. [Medline].
Frenkel LM. Pseudomonas folliculitis from sponges promoted as beauty aids. J Clin Microbiol. Oct 1993;31(10):2838. [Medline].
Maniatis AN, Karkavitsas C, Maniatis NA, Tsiftsakis E, Genimata V, Legakis NJ. Pseudomonas aeruginosa folliculitis due to non-O:11 serogroups: acquisition through use of contaminated synthetic sponges. Clin Infect Dis. Aug 1995;21(2):437-9. [Medline].
Böni R, Nehrhoff B. Treatment of gram-negative folliculitis in patients with acne. Am J Clin Dermatol. 2003;4(4):273-6. [Medline].
Berger RS, Seifert MR. Whirlpool folliculitis: a review of its cause, treatment, and prevention. Cutis. Feb 1990;45(2):97-8. [Medline].
Agger WA, Mardan A. Pseudomonas aeruginosa infections of intact skin. Clin Infect Dis. Feb 1995;20(2):302-8. [Medline].
Ratnam S, Hogan K, March SB, Butler RW. Whirlpool-associated folliculitis caused by Pseudomonas aeruginosa: report of an outbreak and review. J Clin Microbiol. Mar 1986;23(3):655-9. [Medline].
Evans MR, Wilkinson EJ, Jones R, Mathias K, Lenartowicz P. Presumed Pseudomonas folliculitis outbreak in children following an outdoor games event. Commun Dis Public Health. Apr 2003;6(1):18-21. [Medline].
Fox AB, Hambrick GW Jr. Recreationally associated Pseudomonas aeruginosa folliculitis. Report of an epidemic. Arch Dermatol. Oct 1984;120(10):1304-7. [Medline].
Yu Y, Cheng AS, Wang L, Dunne WM, Bayliss SJ. Hot tub folliculitis or hot hand-foot syndrome caused by Pseudomonas aeruginosa. J Am Acad Dermatol. Oct 2007;57(4):596-600. [Medline].
Gustafson TL, Band JD, Hutcheson RH Jr, Schaffner W. Pseudomonas folliculitis: an outbreak and review. Rev Infect Dis. Jan-Feb 1983;5(1):1-8. [Medline].
Malterud K, Thesen J. [Whirlpool and pseudomonas infection--a local outbreak]. Tidsskr Nor Laegeforen. Jun 28 2007;127(13):1779-81. [Medline].
MMWR. An outbreak of Pseudomonas folliculitis associated with a waterslide--Utah. MMWR Morb Mortal Wkly Rep. Aug 19 1983;32(32):425-7. [Medline].
Tate D, Mawer S, Newton A. Outbreak of Pseudomonas aeruginosa folliculitis associated with a swimming pool inflatable. Epidemiol Infect. Apr 2003;130(2):187-92. [Medline].
Chiller K, Selkin BA, Murakawa GJ. Skin microflora and bacterial infections of the skin. J Investig Dermatol Symp Proc. Dec 2001;6(3):170-4. [Medline].
Pseudomonas folliculitis, pseudomonal folliculitis Pseudomonas aeruginosa folliculitis, whirlpool folliculitis, spa pool folliculitis, hot tub folliculitis, gram-negative folliculitis
Charles B Toner, MD, Assistant Professor, Department of Dermatology, Uniformed Services University of the Health Sciences; Mohs Micrographic Surgeon, Consultant, Charles County Dermatology, Maryland, and Georgia Dermatology & Skin Cancer Center
Charles B Toner, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Medical Association, American Society for Dermatologic Surgery, Association of Military Dermatologists, and Association of Military Surgeons of the US
Disclosure: Nothing to disclose.
Stephen J Krivda, MD, Assistant Professor of Dermatology, Uniformed Services University of the Health Sciences; Chief of the Integrated Department of Dermatology, Chief of Dermatology Service, Director of Dermatopathology, Staff Dermatopathologist, Walter Reed Army Medical Center; Head, Department of Dermatology, Staff Dermatologist and Dermatopathologist, National Naval Medical
Stephen J Krivda, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Leonard Sperling, MD, Chair, Professor, Department of Dermatology, Uniformed Services University of the Health Sciences
Leonard Sperling, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
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.
Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.
Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
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