Background
Cutibacterium (formerly known as Propionibacterium) species are nonsporulating, gram-positive anaerobic bacilli that are considered commensal bacteria on the skin. They are usually nonpathogenic and are common contaminants of blood and body fluid cultures. These species are slow-growing and require at least 6 days for growth in culture. [1]
Cutibacterium species belong to the genera of coryneforms (Actinobacteria phylum) and are the best studied because of their association with acne vulgaris. Cutibacterium species, however, can also cause numerous other types of infections, including endocarditis, postoperative shoulder infections, and neurosurgical shunt infections. These are discussed later in the article and are classified as "breast implantation," ”endovascular,” ”orthopedic,” ”neurosurgical,” and ”other” infections.
Cutibacterium acnes (formerly known as Propionibacterium acnes) is found briefly on the skin of neonates, but true colonization begins during the 1 to 3 years prior to sexual maturity. During this time, numbers of C acnes rise from fewer than 10/cm2 to about 106/cm2, chiefly on the face and upper thorax. C acnes grows in the lipid-rich microenvironment of the hair follicle. In acne vulgaris, C acnes produces inflammatory mediators that result in acne papules, pustules, and nodulocystic lesions. C acnes has been classified into types I, IA, IB (C acnes subspecies acnes), IC (C acnes subspecies defendens), and type III (C acnes subspecies elongatum). [2]
Cutibacterium granulosum is found in the same areas but at numbers about one hundredth of those of C acnes.
Both C acnes and C granulosum may be isolated from the gastrointestinal tract.
Cutibacterium avidum is found in the axilla rather than on exposed areas and increases in numbers at puberty.
Cutibacterium propionicus has been implicated as a less-common causative agent of a disease process similar to that of actinomycosis. The most common cause of actinomycosis is Actinomyces israeli infection.
Reclassification
A high-resolution core genome analysis has clarified the phylogeny of the Propionibacteriaceae family in an attempt to better understand how species relate to each other and to unravel adaptive processes behind the transmission and evolutionary adaptation of Propionibacterium acnes to human skin. This work led to the definition of a new genus for cutaneous bacteria, Cutibacterium, which accommodates the former cutaneous species and allows differentiation from other Propionibacterium species, including those present in dairy products and cattle rumen. [3]
Epidemiology
Frequency
United States
Acne vulgaris is sufficiently common that it may be considered physiologic.
There are limited data in the literature quantifying the exact incidence of Cutibacterium endovascular, orthopedic, or neurosurgical shunt infections as frequently their pathogenic potential is overlooked given that it is considered to be of low virulence. The ability of C acnes to adhere to and form a biofilm, particularly on prosthetics, for example, is characteristic of the infections that it may cause.
International
As noted above, data are limited concerning the incidence of Cutibacterium infections for numerous reasons.
Endocarditis
A review performed in 2006 by Clayton et al looked at the world literature available for cases of Cutibacterium endocarditis over the preceding 25 years. [4] In addition to three of their own cases, 36 additional cases were identified. Fourteen cases (42.4%) involved native valves, 16 (48.5%) involved prosthetic valves, and three (9.1%) were associated with intracardiac prosthetic material. Ten of the 14 (71.4%) patients with native valve infection had an underlying cardiac factor predisposing to infection. In this group, the valves most commonly affected were the mitral and aortic valves, whereas those with prosthetic valves were more likely to have aortic valve involvement than mitral valve involvement, partly because of the pattern of the valves replaced. Twenty-nine of the cases were due to P acnes, three were due to C granulosum, and one was an unspecified Propionibacterium species.
Mortality/Morbidity
Cutibacterium endovascular, orthopedic, and neurosurgical infections remain problematic, causing significant morbidity and mortality in affected patients.
Race
Acne appears to be a familial condition and is less common in Japanese people than in the white American population.
Sex
Acne tends to develop at earlier ages in girls than boys. The peak of acne activity occurs during the mid-to-late teenaged period, and the incidence subsequently decreases. Acne is equally common in males and females, but tends to be more severe in males. [5]
Age
Acne vulgaris is a chronic disease that involves the sebaceous follicles, primarily in adolescents. In some cases, it is present at birth, and mild cases of acne vulgaris may be observed in the neonatal period. During puberty, acne typically becomes a common problem. Acne develops in adolescents during adrenarche, when sex hormone levels and subsequent sebaceous gland stimulation occurs. In young individuals, the predominant lesions are comedones, and inflammatory lesions are less common.
Pathophysiology
The three main bacterial genera that reside on the skin’s surface include corynebacteria, cutibacteria, and staphylococci. Interplay of these members is essential for the maintenance of healthy normal skin. While C acnes (predominant in sebaceous sites) is critical in the regulation of skin homeostasis and prevents colonization from harmful pathogens, it may act as an opportunistic pathogen in acne vulgaris. Proliferation of C acnes was once believed to trigger acne, but recent research has instead suggested that a tight equilibrium between members of the skin flora and among C acnes phylotypes may play a role in acne onset. In addition, loss of microbial diversity may lead to chronic inflammation. [3]
C acnes acts as an opportunistic pathogen, causing invasive and chronic implant infections via biofilm growth. A biofilm is defined as a sessile community of microbial cells that are attached to a substratum, an interface, or each other and embedded in a matrix of extracellular polymeric substances. It exhibits an altered phenotype in terms of growth, gene expression, and protein production compared with planktonic bacterial cells. Although C acnes is known to form biofilm on different biomaterials, detailed mechanisms and steps in biofilm formation remain to be fully elucidated. [6]
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Cutibacterium infection. Nodular-cystic acne.
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Cutibacterium infection. Pustular acne.
