Propionibacterium acnes

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Propionibacterium acnes is a commensal, non-sporulating bacilliform (rod-shaped), gram-positive bacterium found in a variety of locations on the human body including the skin, mouth, urinary tract and areas of the large intestine. P. acnes is most commonly associated with its implicated role as the predominant cause of the common inflammatory skin condition Acne vulgaris. It is primarily anaerobic and has an optimal growing temperature of 37°C.

Taxonomic Classification

Higher Order Taxa:

Bacteria; Actinobacteria; Actinobacteridae; Actinomycetales; Propionibacterineae; Propionibacteriaceae; Propionibacterium

Alternative Nomenclature:

  • Corynebacterium acnes
  • Bacillus acnes
  • Corynebacterium acnes (Gilchrist 1900 and Eberson 1918)
  • Bacillus acnes (Gilchrist 1900)


Genomic Structure

The genome of P. acnes has been sequenced in its entirety and has been shown to consists of a single 2.56026 Mbp circular DNA plasmid containing 2351 putative genes coding for 2297 known protein products and constituing a 60% G-C (guanine-cytosine) content.


Cell Structure and Metabolism

P. acnes’ genome codes for a wide variety of metabolic products. Metabolic analysis has shown that P. acnes has the ability to live in anaerobic as well as “microaerobic” conditions. It has the key metabolic requirements to carry out oxidative phosphorylation, Krebs cycle, Embden-Meyerhof pathway and the pentose phosphate pathway. Under in vitro anaerobic conditions, P. acnes can grows permissively on media such as glucose, glycerol, ribose, fructose, mannose and N-acetylglucosamine. In vivo, the bacteria produce various lipases to digest excess skin oil and sebum in the pilosebaceous units (regions that contains the hair follicle and sebaceous gland) of adolescent and adult human skin. For energy P. acnes can employ a fermentative process yielding biproducts like short-chain fatty acids and propionic acid from which it gets its name. In addition to fermatation, P. acnes can utilize various other anaerobic pathways deriving energy with the help of enzymes such as nitrate reductase, dimethyl sulfoxide reductase and fumarate reductase.


P. acnes shares its environment with a variety of different bacteria including Pityrosporum ovale, Staphylococcus areus, Corynebacterium aenes, and Staphylococcus epidermidis among others. These bacteria share some metabolic similarities with P. acnes and some of which have been studied as possible contributors to the various human pathologies.


The role of P. acnes in human pathology is complex. It has been associated with a wealth of human pathologies including pulmonary angitis, endocarditis, sarcoidosis, corneal ulcers, hyperostosis, cholesterol gallstones, allergic alveolitis and synovitis, pustulosis and most commonly acne vulgaris. Acne vulgaris is the most widely studied of these associated illnesses and it is thought that degradative enzymes like the lipases utilized by P. acnes damage host tissue and surface proteins or more specifically heat shock proteins stimulate immune infiltration. Research in this area is ongoing, however, and it is still not completely understood why P. acnes colonies are found in both inflammed acne lesions and normal sebaceous tissue.

Applications to Biotechnology

P. acnes' production of a fatty acid isomerase has been investigated as possible canidadate for use in a dietary enrichment program which would help produce large quantities of supposed beneficial conjugated linoleic acids (CLAs) which might be theraputic applications in the treatment of cancer, obesity and diabetes.

Current Research

1. Research in to bacteriophages that infect P. acnes are under investigation with the hope of leading to potential bacteriophage therapy to treat acne thus sidestepping potential problems associated with long-term antibiotic treatments and the rising threat of bacterial resistant strains of P. acnes.[3] 2. Use of P. acnes in conjugated linoleic acid biosynthesis for the treatment of cancer, obesity and diabetes.[6] 3. Attempt to characterize and Investigation of the effects of theraputic methods on different biotypes of P. acnes for treatment of acne vulgaris.[4]


1. Allison, Clive et al. Dissimilatory Nitrate Reduction by Propionibacterium acnes. Applied and Environmental Microbiology. 1989. Vol. 55 (11): 2899-2903.

2. Brüggemann, Holger et al. The Complete Genome Sequence of Propionibacterium Acnes, a Commensal of Human Skin. Science. 2005. 305: p. 671-672.

3. Farrar, Mark D. et al. Genome Sequence and Analysis of a Propionibacterium acnes Bacteriophage, Journal of Bacteriology.2007. Vol. 189 (11) p. 4161–4167.

4. Higaki, Shuichi et al. Propionibacterium acnes Biotypes and Susceptibility to Minocycline and Keigai-rengyo-to. International Journal of Dermatology. 2004. 43: p. 103–107.

5. Ingham, Eileen The Immunology of Propionibacterium acnes and Acne. Current Opinion in Infectious Diseases. 1999. Vol. 12(3): p. 191-197.

6. Liavonchanka, Alena et al. Structure and Mechanism of the Propionibacterium acnes Polyunsaturated Fatty Acid Isomerase. PNAS. 2006. Vol. 103 (8): p. 2581.

7. Moore, W.E.C. et al. Validity of Propionibacterium acnes (Gilchrist) Douglas and Gunter Comb. Nov. Journal of Bacteriology. 1962. p. 870-874.

8. Oprica, Cristina et al. Clinical and Microbiological Comparisons of Isotretinoin vs. Tetracycline in Acne Vulgaris. Acta Derm Venereol. 2007. Vol. 87: p. 246–254.

9. Rosenberg, E. William Bacteriology of Acne. Annual Reviews. 1969. Vol. 20: p. 201-206.

This page was created by Christopher B. Smith under the supervision of Professors Rachel Larson and Kit Pogliano at the University of California, San Diego.