Cutibacterium avidum

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Classification

Higher order taxa

Bacteria (Domain); Actinobacteria (Phylum); Actinomycetia (Class); Propionibacteriales (Order); Propionibacteriaceae (Family); Cutibacterium (Genus) [1].

Species

Cutibacterium avidum

Description and significance

Cutibacterium avidum, formerly classified as Propionibacterium avidum, is a bacterium in the Actinomycota that was first identified in the early 20th century in a patient with acne vulgaris [2]. C. avidum typically colonizes the human skin microbiome and can cause acne. Treatments of acne and other skin conditions typically target C. avidum and other Cutibacterium species [3]. Other infections by C. avidum have been noted following surgical complications [3]. Postsurgical complications caused by C. avidum pose substantial threats to the patient and current research aims to determine how to prevent and treat C. avidum infection throughout surgical operations [3].

Genome structure

C. avidum has a circular chromosome with 2,526,138 nucleotide base pairs, 2,242 protein-coding genes, and 55 RNA coding genes [4]. C. avidum, C. acnes, and C. granulosum share approximately 1,400 protein-coding genes that mostly correspond to the propionate production pathway, cell respiration, and fatty acid metabolism [3]. Other regions of note on the C. avidum chromosome include regions coding for exopolysaccharide synthesis, and prophage regions [5].

C. avidum has a genomic island that encodes exopolysaccharides and 30 other genes, 19 of which encode glycosyltransferases and enzymes involved in monosaccharide and polysaccharide posttranscriptional modification [5]. The various genes encoding for exopolysaccharides are likely involved in biofilm formation and evasion of phagocytosis [5].

Other remarkable genetic factors in C. avidum include CRISPR loci which increase resistance to horizontal gene transfer and uptake of free or viral DNA [4][6].

C. avidum was originally classified within the Propionibacterium genus, but it and other species, like Cutibacterium acnes and Cutibacterium granulosum, were eventually reclassified into the Cutibacterium genus due to genomic G+C content and peptidoglycan compositional differences [2].

Cell structure and Metabolic Processes

C. avidum is a Gram-positive anaerobe that colonizes the sebaceous follicles in human skin [3]. C. avidum cell walls consist of peptidoglycan and other polysaccharides including galactose, glucose, mannose, and 2,3-diamino-2,3-dideoxyglucuronic acid [3]. C. avidum does not form pili, unlike C. granulosum [3].

Similar to other species in the Cutibacterium genus, C. avidum ferments lactose to propionic acid in its anaerobic environment [7][8]. Propionic acid produced by Cutibacterium species regulates pH in the human skin environment and contributes to pathogenesis in patients with acne [9].

Other proteins produced by C. avidum include hyaluronidase, lecithinase, gelatinase, hydrolyzed casein, alpha-galactosidase, alpha-glucosidase, beta-glucosidase, arginine arylamidase, proline arylamidase, phenylalanine arylamidase, leucine arylamidase, tyrosine arylamidase, glycine arylamidase, and glutamyl glutamic acid arylamidase [3]. Hyaluronidase contributes to acne pathogenesis as hyaluronic acid availability within the skin’s epidermal tissue is necessary for skin health [3]. C. avidum does not produce indole, nitrate reductase, beta-galactosidase, or histidine arylamidase [3]. Other metabolic activity generated by C. avidum includes hydrolysis of gelatin and esculin, fermentation of glucose, ribose, maltose and sucrose [3].

Ecology

C. avidum is found in human sebaceous follicles and regions of the skin containing eccrine sweat glands (11). C. avidum, C. acnes, and C. granulosum’ are the most common bacterial species within the sebaceous follicle and sweat gland environments (3). In comparison to other Cutibacterium species, such as C. granulosum or C. acnes, C. avidum requires more water rather than lipids and other nutrients; this metabolism is linked to differences in pathogenesis caused by different Cutibacterium species (3, 12). C. avidum has also been found in hen intestines and has been observed to colonize tissue such as the abdomen, breast, and prostate following human surgical procedures (3, 6, 13, 14, 15).

Pathology

C. avidum is known to cause acne vulgaris in its human hosts but is less associated with acne and other skin disorders in comparison to its counterparts, C. acnes and C. granulosum (11, 16, 17). C. avidum-produced hyaluronidase and neuraminidase degrade hyaluronic acid and sialic acid, respectively, in part leading to the pathogenesis of acne vulgaris (18). Hyaluronidase hydrolyzes the extracellular matrix of eukaryotes, yet it is unclear what role it plays in C. avidum pathogenesis (3). C. avidum also causes acne via triacylglycerol lipase, which hydrolyzes the triglycerides in sebum; the following release of free fatty acids within pilosebaceous follicles causes an inflammatory response in the skin, leading to acne vulgaris (3). The release of free fatty acids via triacylglycerol lipase is also responsible for bad odor, specifically in the axilla region (19, 20).

C. avidum has also been observed to caused postsurgical complications, infecting the bone, breast, prostate, abdomen, spleen, and has caused infective endocarditis and skin abscesses (6, 13, 14, 15). Tetracycline and benzoyl peroxide are both common treatments for acne vulgaris and are both effective on acne caused by C. avidum; tetracycline has a slight effect on the extracellular lipase in C. avidum, thus benefiting the prognosis of acne patients (21, 22, 23). C. avidum is resistant to erythromycin treatment (24).

Immunomodifier abilities have also been observed in environments colonized by C. avidum. Nearby cells have been stimulated to gain nonspecific antibacterial, antiviral, or antitumor abilities when in proximity to C. avidum (19, 25, 26).

Current Research

Antitumor activity

C. avidum has been observed to stimulate the immune system in multiple in vivo studies. Studies have shown that anaerobic coryneforms used as antitumor agents as they were observed to stimulate cells in the reticuloendothelial system (26). C. avidum, in particular, was observed to be more effective than other Cutibacterium species in inhibiting tumor growth. Other studies attribute these effects to the bacteria’s increased resistance to macrophage degradation correlated with reticuloendothelial stimulation (27).

Further research has expanded on these findings to reveal that C. avidum could prevent metastatic tumor growth in the lungs and liver (28). These findings suggest that further research into the antitumor activity of C. avidum could discover new treatments for patients with cancer or those with genetic or environmental risk factors for cancer.

References

1. Schoch CL, et al. NCBI Taxonomy: a comprehensive update on curation, resources and tools. Database (Oxford). 2020: baaa062. PubMed: 32761142 PMC: PMC7408187.

2. Scholz CFP, Kilian M. 2016. The natural history of cutaneous propionibacteria, and reclassification of selected species within the genus Propionibacterium to the proposed novel genera Acidipropionibacterium gen. nov., Cutibacterium gen. nov. and Pseudopropionibacterium gen. nov. Int J Syst Evol Microbiol 66:4422–4432.

3. Corvec, S. (2018). Clinical and Biological Features of Cutibacterium (Formerly Propionibacterium) avidum, an Underrecognized Microorganism. Clinical Microbiology Reviews, 31(3). https://doi.org/10.1128/CMR.00064-17.

4. Ördögh, L., Hunyadkürti, J., Vörös, A., Horváth, B., Szűcs, A., Urbán, E., Kereszt, A., Kondorosi, É., & Nagy, I. (2013). Complete Genome Sequence of Propionibacterium avidum Strain 44067, Isolated from a Human Skin Abscess. Genome Announcements, 1(3). https://doi.org/10.1128/genomeA.00337-13.

5. Wildeman P, Brüggemann H, Scholz CFP, Leimbach A, Söderquist B. 2016. Propionibacterium avidum as an etiological agent of prosthetic hip joint infection. PLoS One 11:e0158164.

6. Brüggemann H, Lomholt HB, Tettelin H, Kilian M. 2012. CRISPR/cas loci of type II Propionibacterium acnes confer immunity against acquisition of mobile elements present in type I P. acnes. PLoS One 7:e34171.

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