Propionibacterium acnes

Authors: Itzhak Brook, MD, MSc


Propionibacteria are pleomorphic, sometimes branching bacilli. Propionibacterium acnes is the most commonly isolated species and is often a contaminant in blood cultures along with other Propionibacterium spp.


Propionibacterium spp. are part of the normal flora of the skin (38), conjunctiva (4), external ear canal (6), mouth, and upper respiratory tract, and, occasionally, intestine, urethra, and vagina (38).

Clinical Manifestations

Propionibacterium acnes is associated with the inflammatory process in acne lesions (2). Uncommonly, Propionibacterium spp. have been identified with or without other aerobic or anaerobic bacteria as causes of infections, including brain abscesses, subdural empyema, parotid and dental infections, conjunctivitis associated with contact lens, pulmonary infections, peritonitis, and osteomyelitis (3-58). The organisms have been identified in device-related infections include those of joint prostheses, shunts and prosthetic heart valves.  It has also been recovered from specimens obtained from patients with endocarditis, with artificial or native valves, with central nervous system shunt infections, intravenous catheters, and with septic arthritis, especially in prosthetic joints and from other serious infections (3-5891830).

P. acnes may play a role in other conditions, including inflammation of the prostate leading to cancer, SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome, sarcoidosis and sciatica. (30,31)

Laboratory Diagnosis

The organisms are common contaminants of cultures of blood and body fluids and have traditionally been considered nonpathogenic for humans (818). Therefore, interpretation of the significance of an isolate must be undertaken with caution. Propionibacteria are the most commonly isolated anaerobic gram-positive non-sporulating bacilli, accounting for 15% to 20% of all anaerobes isolated in some studies (9,18).

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P. acnes secretes several proinflammatory products, which play an important role in the development of acne inflammation. These include lipases, proteases, hyaluronidases, and chemotactic factors. Immune response to P. acnes includes humoral and cell-mediated immunity as well as complement activation. Recent results indicate that keratinocytes and sebocytes, as major components of pilosebaceous unit, may act as immune cells and may be activated by P. acnes via toll-like receptors (TLRs) and CD14, and through CD1 molecules may recognize altered lipid content in sebum, followed by the production of inflammatory cytokines (26).

Propionibacterium spp. possess immunostimulatory mechanisms that have been extensively studied (103940). These include activation of complement (40), stimulation of lysosomal enzyme release from human neutrophils (40), and production of serum-independent neutrophil chemotactic factors (40). These organisms can be differentiated phenotypically according to their metabolic end products by the use of gas liquid chromatography (25). Propionibacterium spp. typically produce large amounts of propionic acid and all Propionibacterium spp. are indole positive. The pathogenicity and potential for synergy with aerobic bacteria was studied in a subcutaneous abscess model in mice (7). Single and mixed infections with 11 clinical isolates of Propionibacterium acnes and three facultative bacteria (Staphylococcus aureus,Escherichia coli, and Klebsiella pneumoniae) were studied. Abscesses were induced by pure cultures of six of 11 strains of P. acnes and by the three facultative bacteria. The abscesses produced by each of the six virulent P. acnes isolated mixed with S. aureusE. coli, or K. pneumoniae were larger than those induced by the single organisms in 16 of the 18 combinations. There was a significant increase in the numbers of the six P. acnes strains in 13 of the 18 bacterial mixtures and in the numbers of the facultative bacteria in 17 of the 18 combinations. These data illustrate the potential virulence of some P. acnes strains and their synergic capacity with facultative bacteria.

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The susceptibility of P. acnes needs to be monitored to verify current susceptibility. Incases of serious infections, susceptibility tests of P. acnes isolates should be performed, to assure the proper use of antimicrobials (32).

Single Drugs

P. acnes, as well as most other Propionibacterium .spp. are generally (but not universally) susceptible to penicillin-G, amoxicillin, ticarcillin, ticarcillin/sulbactam, piperacillin/tazobactam, cefazolin, cefoxitin, cefotetan, third-generation cephalosporins (e.g., ceftriaxone, cefotaxime), chloramphenicol, clindamycin, erythromycin, imipenem, meropenem, tetracycline, vancomycin, rifampin, fluoroquinolones (e.g., ciprofloxacin, ofloxacin, levofloxacin, gatifloxacin, moxifloxacin, trovafloxacin) and the combinations of penicillins and β-lactamase inhibitors (1111314151617192022333637).  Propionibacterium spp. are generally resistant to the 5-nitroimidazole agents, including metronidazole, tinidazole, and ornidazole (MIC90 > 16 µg/mL) and the aminoglycosides (91022232432,).

Resistant strains have developed to erythromycin, especially in individuals who used this agent for topical therapy of acne (3334). Most erythromycin-resistant isolates (MIC90 51 2 µg/mL) were cross-resistant to clindamycin and B-type streptogramins. Tetracycline resistant strains have also been recovered from patients with acne who attended dermatology clinics (3334). Tetracycline-resistant isolates displayed varying degrees of cross-resistance to doxycycline and minocycline.

The overall incidence of P. acnes antibiotic resistance among isolates recovered from patients with acnes vulgaris has increased from 20% in 1978 to 62% in 1996 (28). Resistance to specific antibiotics varied and was most commonly reported with erythromycin, clindamycin, tetracycline, doxycycline, and trimethoprim. Resistance to minocycline is rare. Repeated use of topical clindamycin was associated with increased resistance to clindamycin (28). Topical clindamycin phosphate and nadifloxacin were bacteriostatic against P. acnes in a mouse burn model (27). However, emergence of resistance occurred with the organisms when they were passaged in vitro.

Recent susceptibility testing of P .acnes isolates recovered from patients with acnes illustrated in-vitro resistance to  erythromycin ( 12.5-35%), azithromycin (82%), clindamycin ( 7.5-30%), tetracycline (8%), minocycline  (1%), doxycycline  (9%), and trimethoprim-sulfamethoxazole ( 26-46%) (2129, 35).

Combinations of Drugs

No known synergistic combination is thought to benefit treatment of Propionibacterium spp. infection (27).

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Penicillin-G in a dose ranging from 1.2 million units to as high as 20 million units per day in adults and 100 to 250,000 units/kg/d every four hours in children is the treatment of choice for serious infections, including bacteremia, central nervous system, and soft tissue infections. In cases of penicillin allergy or concern about resistance, other antibiotics should be considered. All isolates of serious infections should be tested for in vitro efficacy because of the possible recovery of resistant strains. Alternative treatments to penicillin are listed in Table 1.

In clinical situations that involve polymicrobial infections, coverage against the other potential pathogens, aerobic and anaerobic, should be included. This can be achieved by choosing single therapy with an antimicrobial that possesses wider coverage (e.g., imipenem) or by additional agents that cover other organisms (e.g., aminoglycoside or fluoroquinolone for Enterobacteriaceae, or a penicillinase-resistant penicillin for Staphylococcus aureus). Treatment of central nervous system infection requires the use of antimicrobials with good penetration through the blood-brain barrier (8).


Improvements and resolution of the infections are determined through a variety of clinical and laboratory tests. In the case of bacteremia, the lack of recovery of organisms from the blood is an important endpoint. The reduction in the number of white blood cells are important signs of improvement. Improvement in intraabdominal, biliary tract, genital and pulmonary infections can be judged through clinical and radiographic resolution of the infection-returns the gastrointestinal and pulmonary system to normal function, and disappearance of purulence. Central nervous system infection can be followed by repeated lumbar punctures and radiography. In the case of subcutaneous tissue infection, return of the tissue to normal color and blood perfusion and resolution of the purulent inflammation are desired.


Currently, there are no vaccines available.


Removal of foreign bodies, surgery and debridements when indicated, and fluid management are important and integral components to any therapy of Propionibacterium spp. infection.

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1. Bansal MB, Chuah SK, Thadepalli H. Susceptibility of intestinal anaerobes to new beta-lactam antibiotics. Chemotherapy 1984;30:237-243. [PubMed]

2. Beylot C, Auffret N, Poli F, Claudel JP, Leccia MT, Del Giudice P, Dreno B. Propionibacterium acnes: an update on its role in the pathogenesis of acne. J Eur Acad Dermatol Venereol. 2014 ;28:271-8.[PubMed]

3. Brook I, Frazier EH. Infections caused by Propionibacterium species. Rev Infect Dis 1991;13:819-822. [PubMed]

4. Brook I, Petit TH, Martin WJ, Finegold SM.  Aerobic and anaerobic bacteriology of acute conjunctivitis. Ann Ophthalmol 1978;11:13-16. [PubMed]

5. Brook I. Infection caused by Propionibacterium in children. Clin Pediatr (Phila) 1994;33:485-490. [PubMed]

6.  Brook I. Microbiological studies of the bacterial flora of the external auditory canal in children. Acta Otolaryngol (Stockh) 1981;91:284-287. [PubMed]

7. Brook I. Pathogenicity of Propionibacterium acnes in mixed infections with facultative bacteria. J Med Microbiol 1991;34:249-252. [PubMed]

8. Brook, I.:Anaerobic Infections Diagnosis and Management.  A Textbook.  Informa Healthcare USA, Inc. New York. 2007.

9. Brook I. Recovery of anaerobic bacteria from clinical specimens in 12 years at two military hospitals. J Clin Microbiol 1988;26:1181-1188. [PubMed]

10. Burkhart CG, Burkhart CN, Lehmann PF. Acne: a review of immunologic and microbiologic factors. Postgrad Med J. 1999 ;75(884):328-31. [PubMed]

11. Chow AW, Bednorz D. Comparative in vitro activity of newer cephalosporins against anaerobic bacteria. Antimicrob Agents Chemother 1978;14:668-671. [PubMed]

12. Cooper AJ. Systematic review of Propionibacterium acnes resistance to systemic antibiotics. Med J Aust 1998;169:259-261. [PubMed]

13. Credito KL, Jacobs MR, Appelbaum PC. Anti-anaerobic activity of levofloxacin alone and combined with clindamycin and metronidazole. Diagn Microbiol Infect Dis 2000;38:181-183. [PubMed]

14. Denys GA, Jerris RC, Swenson JM, Thornsberry C. Susceptibility of Propionibacterium acnes clinical isolates to 22 antimicrobial agents. Antimicrob Agents Chemother 1983;23:335-337. [PubMed]

15. Drulak MW, Chow AW. Comparative in vitro activity of ceftizoxime, cefoperazone, and cefoxitin against anaerobic bacteria. Antimicrob Agents Chemother 1981;20:683-685. [PubMed]

16. Ednie LM, Jacobs MR, Appelbaum PC. Activities of gatifloxacin compared to those of seven other agents against anaerobic organisms. Antimicrob Agents Chemother 1998;42:2459-2462. [PubMed]

 17. Ednie LM, Spangler SK, Jacobs MR, Appelbaum PC. Antianaerobic activity of the ketolide RU 64004 compared to activities of four macrolides, five β-lactams, clindamycin, and metronidazole. Antimicrob Agents Chemother 1997;41:1037-1041. [PubMed]

 18. Finegold SM. Anaerobic Bacteria in Human Disease. New York: Academic Press; 1977.

19. Goldstein EJ, Citron DM. Comparative activity of ciprofloxacin, ofloxacin, sparfloxacin, temafloxacin, CI-960, CI-990, and WIN 57273 against anaerobic bacteria. Antimicrob Agents Chemother 1992;36:1158-1162. [PubMed]

20. Goldstein EJ, Sutter VL, Finegold SM. Comparative susceptibilities of anaerobic bacteria to metronidazole, ornidazole, and SC-28538. Antimicrob Agents Chemother 1978;14:609-613. [PubMed]

21. González R1, Welsh O, Ocampo J, Hinojosa-Robles RM, Vera-Cabrera L, Delaney ML, Gómez M.  In vitro antimicrobial susceptibility of Propionibacterium acnes isolated from acne patients in northern Mexico. Int J Dermatol. 2010;49:1003-7.  [PubMed]

22. Henderson DK, Chow AW, Guze LB. Comparative susceptibility of anaerobic bacteria to ticarcillin, cefoxitin, metronidazole, and related antimicrobial agents. Antimicrob Agents Chemother 1977;11:679-682.[PubMed]

23. Höffler U, Niederau W, Pulverer G. Susceptibility of cutaneous propionibacteria to newer antibiotics. Chemotherapy 1980;26:7-11.  [PubMed]

24. Humphrey S. Antibiotic resistance in acne treatment. Skin Therapy Lett. 2012;17:1-3. [PubMed]  

25. Jousimies-Somer HR, Summanen P, Baron EJ, Citron DM, Wexler HM, Finegold SM. 2002.Wadsworth-KTL anaerobic bacteriology manual. 6th ed. Belmont, CA: Star Publishing.

26. Knor T. The pathogenesis of acne. Acta Dermatovenerol Croat. 2005;13:44-9. [PubMed]  

27. Komagata Y, Komiyama K, Nomura S. Fundamental studies on antibacterial activity of clindamycin against Propionibacterium acnes. Jpn J Antibiot 1998;51:130-136. [PubMed]

28. Leyden J, Levy S. The development of antibiotic resistance in Propionibacterium acnes. Cutis 2001;67(2 Suppl):21-24. [PubMed]

29.  Moon SH1, Roh HS, Kim YH, Kim JE, Ko JY, Ro YS. Antibiotic resistance of microbial strains isolated from Korean acne patients. J Dermatol. 2012;39:833-7. [PubMed]

30.  Perry A, Lambert P. Propionibacterium acnes: infection beyond the skin. Expert Rev Anti Infect Ther. 2011;9:1149-56.  [PubMed]

31. Levy PY, Fenollar F, Stein A, Borrione F, Cohen E, Lebail B, Raoult D. Propionibacterium acnes Postoperative Shoulder Arthritis: An Emerging Clinical Entity. Clin Infect Dis 2008;46:1884–1886. [PubMed]

32. Rasmussen BA, Bush K, Tally FP. Antimicrobial resistance in anaerobes. Clin Infect Dis 1997;24(Suppl 1):S110-S120. [PubMed]

33. Ross JI, Eady EA, Cove JH, Jones CE, Ratyal AH, Miller YW, Vyakrnam S, Cunliffe WJ. Clinical resistance to erythromycin and clindamycin in cutaneous propionibacteria isolated from acne patients is associated with mutations in 23S rRNA. Antimicrob Agents Chemother 1997;41:1162-1165. [PubMed]

34.  Ross JI, Snelling AM, Eady EA, Cove JH, Cunliffe WJ, Leyden JJ, Collignon P, Dreno B, Reynaud A, Fluhr J, Oshima S. Phenotypic and genotypic characterization of antibiotic-resistant Propionibacteriumacnes isolated from acne patients attending dermatology clinics in Europe, the USA, Japan, and Australia. Br J Dermatol 2001;144:339-346. [PubMed]

35. Schafer F1, Fich F, Lam M, Gárate C, Wozniak A, Garcia P. Antimicrobial susceptibility and genetic characteristics of Propionibacterium acnes isolated from patients with acne. Int J Dermatol. 2013;52:418-25. [PubMed]

36. Shore KP. Susceptibility of anaerobic bacteria in Auckland: 1991-1996. NZ Med J 1999;112:424-426. [PubMed]

37. Smith MA, Alperstein P, France K, Vellozzi EM, Isenberg HD. Susceptibility testing of Propionibacterium acnes comparing agar dilution with E-test. J Clin Microbiol 1996;34:1024-1026. [PubMed]

38. Socransky SS, Manganiello SD. The oral microbiota of man from birth to senility. J Periodontol 1971;42:285:294. [PubMed]

39. Webster GF, Leyden JJ, Tsai CC, Baehni P, McArthur WP. Polymorphoneuclear leukocyte lysosomal release in response to Propionibacterium acnes in vitro and its enhancement by sera from inflammatory acne patients. J Invest Dermatol 1980;74:398-401. [PubMed]

40.  Webster GF, Leyden JJ. Characterization of serum-independent polymorphonuclear leukocyte chemotactic factors produced by Propionibacterium acnes. Inflammation 1980;4:261-269. [PubMed]

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Table 1. Antimicrobials for the Treatments of Probionibacteria Infections

Agent Dose Route Comment
 Penicillin *  1.2 to 20 million units per day (100,000 to 250,000 units/kg/d for children) every 4 to 6 hours   oral, intravenous  First-line therapy for propionibacteria infection
Ampicillin/amoxicillin 2 to 3 g/d (40 to 80 mg/kg/d for children) every 8 hours oral, intravenous (ampicillin)   
Chloramphenicol 12.5 to 25 mg/kg/d every 6 hours oral, intravenous, intramuscular maximum daily dose for adults is 4 g 
Clindamycin 150 to 450 mg every 6 hours (25 to 40 mg/kg/d every 6 to 8 hours for children)  oral, intravenous, intramuscular  
Tetracycline 250 to 500 mg every 6 hours (15 to 20 mg/kg/d intravenous or 25 to 50 mg/kg/d oral every 6 hours for children)  oral, intravenous maximum daily dose for adults is 2 g; do not use for children younger than 9 years
Erythromycin 250 to 500 mg every 6 hours (10 mg/kg every 6 hours for children)  oral, intravenous  
Vancomycin 15 mg/kg every 12 hours or 6 to 8 mg/kg every 6 hours (10 mg/kg every 6 hours for children)  intravenous  
Imipenem 0.5 to 1 g every 6 to 8 hours(15 to 24 mg/kg every 6 to 8 hours for children)  intravenous or intramuscular maximum daily dose for adults is 2 g
Meropenem 0.5 to 1 g every 8 hours (40 mg/kg/d every 8 hours for children)  intravenous  
Gatifloxacin 400 mg daily  oral or intravenous not approved for use in children
Moxifloxacin 400 mg daily oral not approved for use in children

* = drug of choice

What's New

Ghosh M, Talwani R, et al. Propionibacterium skull osteomyelitis treated with daptomycin. Clin Neurol Neurosurg. 2009 May 16. [Epub ahead of print]

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