Propionibacterium acnes: Current Researches

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1. Classification

Domain: Bacteria Phylum: Actinobacteria Class: Actinobacteria Order: Actinomycetales Family: propionibacteriaceae Species: propionibacterium acnes

2. Description and significance

Propionibacterium acnes is a non-pathogenic, commensal bacterium that can be found in various locations of the body and in food such as dairy and cheese. P. acnes is a Gram-positive anaerobic bacillus that is slow-growing in nature, requiring a minimum of 6 days of culture growth (2). While P. acnes is most commonly associated with the inflammatory skin infection acne vulgaris, a skin condition commonly known as acne, research studies have demonstrated that it also plays a significant role in many other diseases such as in the lungs and lymph nodes and delayed surgical and implantation infections (3). However, due to its slow growth, P. acnes continues to be an under-recognized cause of diseases other than acne vulgaris and failure to diagnose can lead to serious consequences including mortality (3). Because of P. acnes’ broad association with a variety of disease, treatment options can vary. In most cases, P. acnes is susceptible to antibiotics or through a combination of either antibiotics and/or surgical option (3,4). Although a wide variety of research has been conducted on P. acnes, many questions are unanswered such as its symbiotic relationship in humans, and its antibiotic resistance role. Future research interest includes expanding on treatment options, novel diagnoses criteria specific to P. acnes in relation to different diseases, and its role as a disease-causing agent to further prevent infections and morbidity.

3. Genome structure

P. acnes stores its genetic information in a single circular chromosome. The chromosome encodes for approximately 2333 genes, with a 60% guanine-cytosine nucleotide ratio, containing various enzymes and proteins (6). For instance, P. acnes’ genes code for the Christie-Atkins-Munch-Petersen (CAMP) factors that act as toxins creating pores and allowing entry in the host’s membranes. The CAMP factors, along with enzymes that degrade body tissues, can ultimately lead to tissue inflammation. Moreover, the genome of P. acnes also encodes for proteins such as adhesins, heat shock proteins, and those that contribute in the formation of biofilms (6).

4. Cell structure and Metabolic Processes

P. acnes is a Gram-positive, non-spore forming, bacillus, or rod-like, bacterium. As a bacillus, P. acnes can be found living as individuals or in chains. In addition, as an aerotolerant anaerobic bacterium, the bacterium does not utilize oxygen for electron source, but is able to tolerate the presence of oxygen in the environment (3,4). Since P. acnes is an anaerobic microorganism, it can perform metabolic processes such as Embden-Meyerhof pathway and the pentose phosphate pathway, which allows for metabolization of sugars such as glucose, ribose, and mannose (5). Through the process of fermentation, P. acnes can also utilize lactose to produce propionic acid (4).

6. Ecology and Biofilm

P. acnes is a commensal bacterium found dominantly on the human skin at an optimal temperature of 37°C, particularly within the lipid-rich sebaceous skins and glands (6). These sebaceous sites are located along the neck, head, shoulders, and the armpit areas. P. acnes can also inhabit within the respiratory and intestinal tract as well as the auditory canal (3). Furthermore, along the skins and through the formation of biofilms, P. acnes can be found living in micro-colonies with other cutaneous adhering bacteria such as Staphylococcus, Streptococcus, and Pseudomonas (4). To synthesize biofilms, P. acnes performs quorum sensing to search for nutrient rich surfaces and other skin bacteria before secreting extracellular polysaccharides to form micro-colonies. Through biofilm formation, P. acnes plays a critical role as an opportunistic bacterium in causing implant-associated infections such as orthopedic implants, breast implants, and cerebrovascular and cardiovascular devices (4). In addition to protecting the bacterium from phagocytosis by macrophages, biofilms also allow for horizontal gene transfer, or the transferring of genetic information between different bacterial species, which can lead to increase in antimicrobial agent resistance (3, 6).

7. Pathology

Although P. acnes is considered a low virulent commensal bacterium, there are still some infections associated with the bacterium. Due to horizontal gene transfer inside biofilms, P. acnes can transform from being a commensal bacterium to an opportunistic bacterium. Thus, the pathogenicity of P. acnes as an opportunistic bacterium can be seen in cases such as endocarditis, sarcoidosis, and in joint infections among patients who underwent shoulder surgeries (6). Nevertheless, P. acnes cannot be confirmed as the primary source of inflammation because even when antimicrobial treatments were used to reduce the growth and concentration of P. acnes, recurrence of inflammation was still seen (4).

8. Current Research

P. acnes is most commonly recognized as the bacterial cause of skin acne. Aside from acne, P. acnes is also believed to have a significant pathogenic role in the growth of granulomas in sarcoidosis patients, increasing risks of prostate cancer, and post-surgery, degeneration of intervertebral disks, and implant infections through biofilm formation. In addition, with the increasing antibiotic resistance of P. acnes, more research has focused on alternative treatments such as elimination of P. acnes through photoinactivation of its endogenous porphyrins and drugs that inhibit the Th17 pathway, the pathway that plays a part in the body’s adaptive immunity (12).

Lung and Lymph Nodes: P. acnes is also the most abundant commensal bacterium found in the lungs and lymph nodes (7). Eishi’s study suggests that P. acnes causes sarcoidosis, an inflammatory disease affecting several areas in the body, by forming abnormal masses known as sarcoid granulomas. Using mice as a treatment model, P. acnes’ trigger-factor proteins were found to develop sarcoid granulomas whereas removal of P. acnes through using antibiotics prevented the growth of granulomas. Eishi suggests that prevention of granulomas formation may be possible through the eradication of P. acnes in lymph nodes and lungs (7).

Degenerative Disk Diseases: Through the mechanism of biofilm formation, P. acnes has been found to be associated with the formation of degenerative disk diseases causing herniated disks. Capoor et al. performed on participants undergoing lumbar microdiscectomy, a surgery performed to remove an irritated or inflamed part of a herniated disk, and hypothesized that the ability of P. acnes to form biofilm plays a crucial role in infecting the intervertebral disks. To test their hypothesis, researchers took biopsies from patients with lumbar herniated disk for anaerobic culturing and real-time PCR. However, the result was unclear whether the growth of P. acnes positive was a result of infection or contamination from laboratories, surgeries, skin, or other mediums (8).

Treatment: Although antibiotics are commonly used as medication for P. acnes, there is concern regarding the bacterium’s growing antibiotic resistance. Much research has been done on the mechanisms of antibiotic resistance. In Ross et al.’s study, P. acnes was isolated from patients and characterized genetically and physically to determine whether or not similarities exist in the resistance mechanisms of P. acnes from different regions (9). A total of 73 various strains of antibiotic resistant P. acnes were acquired from different areas including the United Kingdoms, the U.S., Japan, Australia, France, and Germany. These strains were plated onto a medium containing either erythromycin or tetracycline, which are antibiotics used to treat P. acnes. The 16S rRNA and 23S rRNA regions of the bacterium were amplified using polymerase chain reaction to sequence the gene. Ross et al. showed that 58 strains were resistant to erythromycin, 38 strains resistant to tetracycline, and 23 strains resistant to both. A majority of erythromycin resistant strains had point mutations in the 23S rRNA, while a guanine to cytosine transition at E. coli equivalent base 1058 was seen in most tetracycline resistant strains.

The growing antibiotic resistance of P. acnes has led to research of possible alternative treatments. One promising possible new method is the usage of photoinactivation, as performed in Ashkenazi et al.’s study. Repeated exposure of the endogenous porphyrins of P. acnes to intense blue light causes structural damage to P. acnes cell membrane (10). Cultures in test tubes were illuminated horizontally using blue light at 407 to 420 nm with some cultures having to be illuminated two or three times after 24 hours. Viable bacteria were counted to determine extent of inactivation. Ashkenazi indicated that multiple, consecutive illumination periods result in decreasing viability of cultures. Viability was decreased by four orders of magnitude after two periods of illumination and a decrease of five orders of magnitude was seen after three periods of illumination. By also increasing the amounts of coproporphyrin using d-aminolevulinic acid (ALA) in conjunction with photoinactivation, viability was decreased by seven orders of magnitude after illumination. X-ray microanalysis indicated that structural damage of the membranes of P. acnes was caused by illumination; a large decrease in the bacterium’s potassium and phosphorus concentration was noticed when the bacteria were incubated with ALA and illuminated with intense blue light (10).

Another recent study by Verma and Sardana shows that the Th17 pathway, an adaptive immunity pathway, may be a crucial component in acne pathogenesis. This pathway is activated by the adaptive immune system response and triggers the production of various cytokines responsible for the common inflammation found in acne. Evidence to support the significance of the Th17 pathway is seen as cytokines that are components of the Th1/Th17 axis are constantly found in acne lesions. Verma and Sardana proposes that drugs that inhibit or directly interfere with the Th17 pathway could be a potentially better treatment option than antibiotics (11).

9. References

It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.