Cutibacterium (Propionibacterium) Infections 

Updated: Oct 19, 2021
Author: Amro Elshereye, MBBS; Chief Editor: John L Brusch, MD, FACP 



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.


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]



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.


As noted above, data are limited concerning the incidence of Cutibacterium infections for numerous reasons.


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.


Cutibacterium endovascular, orthopedic, and neurosurgical infections remain problematic, causing significant morbidity and mortality in affected patients.


Acne appears to be a familial condition and is less common in Japanese people than in the white American population.


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]


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.


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]




Acne vulgaris

C acnes plays an important role in the pathogenesis of inflammatory acne–producing proinflammatory mediators, including lipases, neuraminidases, phosphatases, and proteases.

Acne usually affects the face and, to a lesser degree, the back, chest, and shoulders. On the trunk, lesions tend to be near the midline.

The four major pathophysiologic features of acne include the following:

  • Hyperkeratinization

  • Sebum production

  • Bacterial proliferation

  • Inflammation

Lesions can be described in three categories, as follows:

  • Comedonal: Comedones are either open (blackheads) or closed (whiteheads). The open comedo appears as a flat or slightly raised lesion with a central dark-colored follicular impaction of keratin and lipid. The closed comedo is a pale, slightly elevated, small papule without a visible orifice and is a potential precursor for the larger inflammatory lesions.

  • Inflammatory: Inflammatory lesions vary from small papules with an inflammatory areola to pustules (papulopustular) to large, tender, fluctuant nodules (nodular).

    Cutibacterium infection. Nodular-cystic acne. Cutibacterium infection. Nodular-cystic acne.
    Cutibacterium infection. Pustular acne. Cutibacterium infection. Pustular acne.
  • Scars: These appear as depressed or hypertrophic papules of varying sizes and shapes.

Exacerbations of acne vulgaris may follow the ingestion of numerous types of drugs, such as iodides, bromides, glucocorticoids, and lithium, as well as the application of occlusive compounds that can block follicles.

Breast implantation

A known local complication of breast implantation is capsular contracture, reported in 5.2% to 30% of cases. C acnes, along with coagulase-negative staphylococci and Corynebacterium species, has a well-established role in subclinical infection in capsular contracture.[6]


Cutibacterium species are an underrecognized cause of endocarditis and, as noted above, have been associated with both native and prosthetic valves, but most often develp on valve prostheses. The indolent nature of the organism results in cases typically associated with a relatively long history with minimal clinical signs of infection at initial presentation.

Risk factors for cutibacterium endocarditis are male gender and prosthetic valves. In one series of 51 cases of cutibacterium prosthetic valve endocarditis, 50 patients were male [7] . The mean onset of infection was 3 years after surgery. 

In the review performed by Clayton et al, fever was the most common presenting complaint (81.8%), followed by lethargy and malaise (42.4%), and sweats and chills (27.2%). There was a paucity of examination findings, limited to a murmur reported in 45.4% of cases, and only 12.1% of the cases had the classical stigmata of infective endocarditis (eg, Osler nodes, Janeway lesions, splinter hemorrhages, macular hemorrhages).

Complications may be serious, with the development of intracardiac abscesses[4] and CNS emboli, congestive cardiac failure, cardiac abscesses, and valve dehiscence.[8]

C acnes cardiovascular device–related infections typically have a subtle presentation that can include low-grade fever, weight loss, malaise, and myalgias.


C acnes is frequently implicated in anaerobic arthritis in association with prosthetic joints. In rare cases, it has also been found to be responsible for osteomyelitis and prosthetic vascular graft infections.

Spinal osteomyelitis is an infection of the vertebral body and/or the intervertebral space and can be associated with indwelling hardware. It may present acutely, with delayed onset, or, most frequently, late (years), following spinal surgery. The rate of C acnes infection following spinal surgery is generally low but increases to up to 12% of all infections when instrumentation is used.[6]

C acnes has been isolated from involved joints in rare cases of rheumatoid arthritis and chronic juvenile arthritis, presumably as a result of bacterial inoculation, usually during infiltration (injection).

C acnes has been implicated in certain spondyloarthropathies associated with florid acne vulgaris, in which it was isolated from bone foci and joints.[9]

C acnes is an important cause of shoulder prosthetic joint infections (PJI). The shoulder appears to have a propensity for C acnes, and the bacterium should not always be considered a contaminant.[1] In a review performed by Millett et al on 10 patients presenting with pain (average age, 57 y) with Cacnes following shoulder surgery, it was found that at the time of confirmation of the diagnosis, clinical signs of infection were absent. C-reactive protein and the erythrocyte sedimentation rates were inconsistently elevated. Cultures took an average of 7 days to confirm growth. Of note, the average time from surgery to diagnosis was 1.8 years. All the patients ended up undergoing irrigation and debridement and received antibiotic treatment for 6 weeks.[10]

C acnes has been implicated as the leading cause of shoulder PJI with more than 40% of shoulders undergoing revision being culture positive. New research suggests that there is a discordance between the rates of positive culture (40%) and infection (5%) of shoulder joints by C acnes. The role of positive C acnes cultures in shoulder joint needs to be further investigated. [11]


C acnes has been known to infect internal or external shunts, including Ommaya reservoirs.[12]

In a retrospective analysis of shunt infections by Conen et al in adults aged 12 years or older, out of 78 episodes, C acnes was isolated in 9% of cases, ranking third. The most common organisms were coagulase-negative staphylococci, followed by Staphylococcus aureus.[13]

C acnes shunt infections characteristically present with a paucity of symptoms. When present, they are related to obstruction and/or shunt malfunction, with signs of raised intracranial pressure (ie, headache, nausea, vomiting, lethargy, and/or mental status changes). Fever and meningeal symptoms may or may not be present. Ventriculoperitoneal shunt infections may manifest as peritonitis; ventriculoatrial shunt infections may manifest as fever and bacteremia, with the potential to progress to endocarditis. C acnes infection of a distal external shunt typically manifests as a soft-tissue infection.

In rare cases, Cutibacterium species have been implicated as a cause of brain abscess[14] and subdural empyema. A case report describes a patient who developed C acnes cerebral abscess as a consequence of severe chronic sinus disease.[15]

Other infections

C acnes has been reported as a cause of vision-threatening infectious keratitis when the cornea is compromised. C acnes has also been implicated in chronic pseudophakic-related endophthalmitis following cataract surgery and placement of an artificial intraocular lens. The presentation is characterized by low-grade intraocular inflammation, possibly chronic, and may be misdiagnosed as noninfectious iritis.

In rare cases, Cutibacterium species have been implicated as a cause of dental infections, conjunctivitis associated with contact lenses, peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD), and breast-implant infections.

C acnes has been isolated in cases of transfusion-transmitted bacterial infection, which typically manifests as fever and chills with or without tachycardia and hypotension during or after transfusion of blood or blood products.[16]

C acnes infection has been suggested as a possible trigger for primary biliary cirrhosis.[17]

C granulosum infection has been reported as a potential primer of the immune system prior to the development of sarcoidosis.[18] Latent infection with C acnes has been implicated as a cause of sarcoidosis since it is the only microorganism that has been isolated from sarcoid lesions by bacterial culture.[19]

C avidum has been implicated in causing a splenic abscess post cardiac catheterization.[20]


The prognosis of acne vulgaris is usually favorable, and the only sequela is scarring, which can be minimized. In patients with scarring, cosmetic options include dermabrasion, excision, subcision, punch grafting, and laser resurfacing.

Complications for other infections are described in the Clinical section.

Isotretinoin is contraindicated in pregnancy. A pregnancy test should be performed prior to commencing treatment, and patients should be warned about the drug's teratogenic effects. Patients must sign written consent forms and be enrolled into the iPledge program. Female patients of childbearing potential must be on two forms of birth control.

Although Cutibacterium species are frequently nonpathogenic, the presence of Cutibacterium species in a sterile body fluid culture should never be automatically assumed as contamination until a thorough history and physical examination and assessment is completed.



Diagnostic Considerations

Comedones are not unique to acne vulgaris. Senile comedones (ie, Favre Racouchot syndrome) are common, particularly in the periorbital area of elderly persons. In addition, radiation therapy may result in comedones.

Acnelike lesions may develop in individuals with Behçet disease and in immunocompromised hosts.

Disseminated cryptococcosis may present as an acneiform eruption.

Differential Diagnoses



Approach Considerations

C acne infections pose a diagnostic challenge since it is difficult to determine if isolation from a clinical specimen is contamination or true infection [21] . If c acne infection is suspected then prolonged specimen incubation should be requested to avoid false negative results. 

Laboratory Studies

Acne vulgaris

A hormonal workup may be appropriate in adult female acne patients with signs of androgen excess, such as virilization. Hormonal workup may also be appropriate in preadolescent patients presenting with acne to evaluate for precocious puberty.

In some high-risk patients, Cutibacterium species are capable of causing significant infections, and efforts should be made to obtain specimens free of contamination by the normal flora of the mucous membranes and skin, where they reside. In addition, strict anaerobic technique should be followed to ensure isolation in suspected cases of Cutibacterium infection. The generation time of C acnes is 5.1 hours compared with the approximate 24-minute generation time of Staphylococcus aureus.[22]

Implant-associated infections

In order to successfully diagnose implant-associated infections, multiple conventional tissue cultures, sonification of the removed implant or its mobile parts, and/or synovial fluid aspiration is recommended. Sonification is a method whereby bacteria are dislodged from the surface of an implant and biofilm clumps are broken into a suspension of single cells. The sonification fluid is then plated onto aerobic and anaerobic sheep agar plates and inoculated into a thioglycolate broth. This is then incubated for 7 days and the CFU/mL is calculated.[6]

In prosthetic joint infections, prolonged incubation beyond 13 days of aspirates and or of blood cultures is recommended to optimize the recovery of C acnes.[22]

CNS shunt infections require evaluation of cerebrospinal fluid (CSF) and blood cultures, particularly in cases of suspected ventriculoatrial shunt infections, in which case the yield may be higher. In the review performed by Conen et al, infection was defined by the first positive culture of CSF, wound swab, or shunt tip specimen; the initiation of an appropriate antimicrobial treatment for shunt-associated infection; or surgery at the site of the shunt (whichever occurred first).[13]

Other infections

In cases of C acnes infectious keratitis, cultures were positive for C acnes using thioglycolate broth. None became positive before 7 days of growth, and the recommendation is to monitor the culture for at least 10 days to ensure isolation of this fastidious organism.[23]

In chronic pseudophakic-related endophthalmitis, culture of a vitreous biopsy sample may be positive for C acnes. If the artificial lens is removed, Gram stain and electron microscopy of the capsule may demonstrate gram-positive rods.

In transfusion-transmitted bacterial infection, blood should be collected from the opposite arm; aside from appropriate hematologic tests, this blood should be sent for culture. Following reporting, the blood-product bag should be sent to the microbiology laboratory for Gram stain and culture.

Imaging Studies

Implant-associated infections

In cardiovascular device–related infections, C acnes can be difficult to recover in cultures of clinical specimens unless anaerobic cultures are obtained and held for extended periods. CT scanning, ultrasonography, and MRI are useful in demonstrating fluid collection around a device, which can suggest infection. Percutaneous aspirate of the fluid with ultrasound or CT guidance may confirm device infection. Transesophageal echocardiography is required to visualize a vegetation in prosthetic valve endocarditis.[24]

In CNS shunt infections, neuroimaging studies may be used to look for evidence of ventriculitis or CSF obstruction. CT scanning or ultrasonography may be helpful in evaluating loculations at the distal end of a ventriculoperitoneal shunt.



Approach Considerations

The approach to treatment of cutibacterium infections should be guided by antimicrobial susceptiblity. The duration of treatment and choice of antimicrobials will depend on the site of infection. The cutibacterium isolates are generally susceptible to penicillns, cephalosporins, carbapenems, and clindamycin.[25]  

Medical Care

Acne vulgaris

Topical and oral agents act at various stages in the evolution of an acne lesion and may be used alone or in combination to enhance efficacy. Most cases of acne vulgaris are controlled with combinations of oral or topical vitamin A derivatives, topical benzoyl peroxide, oral or topical antibiotics, and topical beta-hydroxy acids such as salicylic acid. Topical agents should be applied to the entire affected area to treat existing lesions and to prevent the development of new ones. Topical steroid creams should not be used to treat acne because their long term use is associated with the development of acne-like lesions. Photodynamic therapy is another promising therapy that is being further evaluated.

CNS shunt infections

Device removal is indicated for CNS shunt infections (see Surgical Care), and antibiotic treatment should be focused once results of Gram staining and culture are available.[26] Empiric initial coverage with vancomycin plus ceftazidime, cefepime, or meropenem would be appropriate.

Other infections

Determination of the clinical significance of an isolate of Cutibacterium species must be made with caution because this will influence the need to direct therapy against that isolate.

Transfusion-transmitted bacterial infection

This requires stoppage of the blood transfusion, resuscitation of the patient, and, if suspicion is high, administration of empiric broad-spectrum antibiotics until results are available. A typical combination would be intravenous vancomycin and gentamicin.

Surgical Care

Acne vulgaris

Surgical care involves manual removal of comedones and drainage of pustules and cysts. When performed correctly, acne surgery speeds resolution and rapidly enhances cosmetic appearance. Scar revision via dermabrasion, excision, subcision, or laser therapy may be performed. Inflamed papules and cysts may be injected with intralesional steroids. Risks include hypopigmentation and skin atrophy.

General recommendations for implant-associated infections

Owing to the variable clinical presentation of C acnes implant-associated infections, there is no general consensus on best treatment. Surgical recommendations, however, should not differ dramatically from infections caused by other microorganisms. Implant-associated infections require surgical removal of the infected implant and debridement of any infected tissue and dead bone. As C acnes infection typically has a delayed presentation following implant surgery, extensive and aggressive debridement of all infected tissue with removal of the implant is recommended. Surgical therapy needs to be accompanied by prolonged antibiotic treatment in order to ensure eradication of remaining bacteria. For most prosthetic joint infections, a 3- to 6-month course of antibiotic treatment is suggested, including 2 to 6 weeks of intravenous treatment with a beta-lactam, depending on implant size.[6]

Cardiovascular device–related infections

Removal of the device is usually recommended.[27] Bacteremia without a clear source may warrant an aggressive course of intravenous antibiotic therapy.

CNS shunt infections

Device removal, external drainage, and subsequent shunt replacement should be performed once the CSF is sterile.[26]

Chronic pseudophakic-related endophthalmitis

This may require vitrectomy,[28] intravitreal vancomycin therapy, and replacement of the intraocular lens to ensure cure.[29]


Acne vulgaris

The goals of therapy in acne vulgaris include reduction of comedonal and inflammatory lesions, improvement of psychosocial symptoms, and avoidance of scarring. The duration of therapeutic intervention for acne vulgaris should be at least 8 weeks to assess effectiveness, unless the patient has an allergy or experiences intolerable adverse effects. If the patient shows inadequate improvement after sequential interventions, referral to a dermatologist is recommended.[30]

Other infections

Isolation of Cutibacterium species in the settings described above may require the assistance of an infectious diseases specialist for interpretation.


Acne vulgaris

In cases of acne vulgaris, there may be a correlation between foods with a high glycemic index and development of acne. Consumption of a diet with low glycemic index foods may be reasonable if the patient feels that diet is aggravating the condition. In addition, avoidance of dairy, including skim milk, is recommended, as it may reduce the number of skin lesions.[30]



Medication Summary

The following information primarily pertains to the treatment of Cutibacterium acne vulgaris.

Antibiotics used to treat anaerobic infections usually suffice for other types of Cutibacterium infections. C acnes is generally highly susceptible to a wide range of antibiotics. These include the penicillins, carbapenems, and clindamycin. In addition, vancomycin and teicoplanin have been used. However, resistance is beginning to emerge. Some of these antibiotics are discussed after the treatment of acne vulgaris. Daptomycin has been used for the treatment of Cutibacterium osteomyelitis.[31]

Retinoid-like Agents

Class Summary

These agents stimulate cellular retinoid receptors and help normalize keratinocyte differentiation and are comedolytic. In addition, they have anti-inflammatory properties. Oral isotretinoin also reduces sebum production in the skin. Retinoids are classified into 3 generations. The first comprises topical tretinoin and systemic isotretinoin. Acitretin is a second-generation retinoid used to treat psoriasis. The third-generation retinoids include topical adapalene and tazarotene.

Topical tretinoin (Retin-A Micro, Atralin, Avita, Altreno)

Inhibits microcomedo formation. Decreases cohesiveness of keratinocytes in sebaceous follicles, which allows for easy removal. Anti-inflammatory properties. Available as creams, gels, and lotions.

Adapalene (Differin)

Inhibits microcomedo formation. Decreases cohesiveness of keratinocytes in sebaceous follicles, which allows for easy removal. Has anti-inflammatory properties. Available as creams, lotions, and gels.

Tazarotene (Tazorac, Fabior)

Inhibits microcomedo formation. Decreases cohesiveness of keratinocytes in sebaceous follicles, which allows for easy removal. Has anti-inflammatory properties. Available as creams, foams, and gels.

Isotretinoin (Claravis, Amnesteem, Absorica, Myorisan, Zenatene)

Oral retinoid indicated for recalcitrant, nodulocystic acne. Addresses all four pathogenic factors involved in the development of acne, including follicular hyperkeratinization, inflammation, sebum production, and C acnes growth. Treatment is weight-based, usually dosed initially 0.5 mg/kg and increased to 1 mg/kg in 2 divided doses for 15-20 weeks. Once-daily dosing is not recommended. May adjust dose to administer up to 2 mg/kg/day. Patients must be registered into government regulated iPledge program in order to receive the medication.

Antibiotics, Other

Class Summary

Oral antibiotics are useful in inflammatory acne, and improvement is usually seen after several weeks of use. Antibiotic monotherapy is discouraged owing to the risk of resistant bacteria development.

Females should be warned about the development of Candida albicans vaginitis. A rare complication of long-term oral antibiotic use is the development of gram-negative folliculitis. Tetracycline class antibiotics can cause sun sensitivity. Doxycycline is associated with GERD and should be taken at least 30 minutes prior to sleep. Minocycline is rarely associated with a lupuslike syndrome, minocycline-induced hyperpigmentation, and pseudotumor cerebri.

Topical antibiotics are used in almost all patients treated for acne. Monotherapy should be avoided to reduce risk of antibiotic resistance. Concurrent use of benzoyl peroxide eliminates the risk of resistance development. Topical antibiotics are available as monotherapy or in fixed-dose combination products, along with benzoyl peroxide or retinoids. Topical antibiotics used include clindamycin and erythromycin, although resistance to erythromycin favors the use of clindamycin.


Inhibits bacterial protein synthesis by binding with 30S and, possibly, 50S ribosomal subunit(s). Tetracycline has anti-inflammatory activity. May administer 250-500 mg PO bid.

Minocycline (Solodyn, Minocin, Ximino, CoreMino, Minolira)

Treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma species. The brand name Solodyn is an extended-release formulation indicated for acne and prescribed at 1 mg/kg dose per day. The minocycline dose should be lowered in patients with renal impairment.

Erythromycin topical (Ery, Erygel)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Commonly prescribed for acne as a topical gel in combination with benzoyl peroxide. Use limited owing to resistant C acnes strains. Apply bid after washing the skin and drying it.

Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS)

Antibiotic with activity against many gram-positive and gram-negative organisms. Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Available as 80 mg trimethoprim and 400 mg sulfamethoxazole or as 160 mg trimethoprim and 800 mg sulfamethoxazole (double strength).

Clindamycin (Cleocin)

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Commonly used topically, but can be given orally. Oral monotherapy administration should be avoided to reduce risk of antibiotic resistance. May administer 75-300 mg/day in divided doses.

Clindamycin topical (ClindaGel, Cleocin-T, Evoclin)

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Commonly used topically but can be given orally. Apply thin film twice daily except for the gel form. Apply gel form once daily.

Daptomycin (Cubicin, Cubicin RF)

Daptomycin binds to bacterial membranes and causes rapid membrane potential depolarization, thereby inhibiting protein, DNA, and RNA synthesis, ultimately causing cell death. It is indicated to treat complicated skin and skin-structure infections caused by S aureus (including methicillin-resistant strains), S pyogenes, S agalactiae, S dysgalactiae, and E faecalis (Vancomycin-susceptible strains only). Daptomycin has been used for the treatment of Cutibacterium osteomyelitis.

Doxycycline (Doryx, Doxy 100, Avidoxy, Vibramycin, Oracea)

Broad-spectrum, synthetically derived bacteriostatic antibiotic in the tetracycline class. Almost completely absorbed, concentrates in bile, and is excreted in urine and feces as a biologically active metabolite in high concentrations.

Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. May block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.


Used in prophylaxis. Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or have resistant staphylococcal infections. For abdominal penetrating injuries, it is combined with an agent active against enteric flora and/or anaerobes.

To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 hours prior to next dosing. Use creatinine clearance to adjust dose in patients diagnosed with renal impairment.

Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing gastrointestinal or genitourinary procedures.

Meropenem (Merrem)

Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria.

Has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci compared to imipenem.

Cefepime (Maxipime)

Fourth-generation cephalosporin. Gram-negative coverage comparable to ceftazidime but has better gram-positive coverage (comparable to ceftriaxone). Cefepime is a zwitter ion; rapidly penetrates gram-negative cells. Best beta-lactam for IM administration. Poor capacity to cross blood-brain barrier precludes use for treatment of meningitis.


Aminoglycoside antibiotic for gram-negative coverage bacteria including Pseudomonas species. Synergistic with beta-lactamase against enterococci. Interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits.

Dosing regimens are numerous and are adjusted based on CrCl and changes in volume of distribution, as well as body space into which agent needs to distribute. Dose of gentamicin may be given IV/IM. Each regimen must be followed by at least trough level drawn on third or fourth dose, 0.5 hours before dosing; may draw peak level 0.5 h after 30-min infusion.

Sarecycline (Seysara)

Tetracycline derivative that inhibits protein synthesis by binding to ribosomal subunits 30S and possibly 50S of susceptible bacteria.

Aldosterone Antagonists, Selective

Class Summary

Aldosterone antagonist may reduce free testosterone levels and compete with androgens binding at the sebaceous gland.

Spironolactone (Aldactone, CaroSpir)

Aldosterone antagonist that competes with testosterone and dihydrotestosterone binding at the receptor in the sebaceous gland. It also reduces free testosterone levels, as more is bound by the increased quantity of SHBG. To treat acne in women may administer 25-200 mg once daily.


Class Summary

Hormonal therapies can be used in females with acne, especially those with premenstrual acne flares, who have failed other therapies. Patients may also have signs of hyperandrogenism (eg, hirsutism, irregular menses, menstrual dysfunction). Serum androgen levels may or may not be elevated.

Available options include combination estrogen-progestin oral contraceptive pills, which suppress ovarian androgen production as well as androgen receptor blockers that block the effect of androgens peripherally at the sebaceous gland.

Ethinyl estradiol, drospirenone, and levomefolate (Beyaz, Rajani)

Combination of estrogen and progestin treats acne in adult women. Suppresses ovarian production of androgens.

Ethinyl estradiol and norethindrone (Estrostep Fe, Tilia Fe, Tri-Legest Fe)

Combination of estrogen and progestin treats acne in adult women. Suppresses ovarian production of androgens.

Ethinyl estradiol and norgestimate (Ortho Tri-Cyclen, Tri-Estarylla, TriNessa, Tri-Previfem, Tri-Sprintec)

Combination of estrogen and progestin treats acne in adult women. Suppresses ovarian production of androgens.

Ethinyl estradiol and drospirenone (Yaz, Gianvi, Loryna, Nikki, Vestura)

Combination of estrogen and progestin treats acne in adult women. Suppresses ovarian production of androgens.

Acne Products

Class Summary

Acne products are used for the treatment of mild to moderate acne vulgaris. These agents may have antibacterial and comedolytic properties. In severe cases, the agents may be used as an adjunct in the therapeutic regimens.

Erythromycin and benzoyl peroxide (Benzamycin, Aktipak)

Contains erythromycin, which is a macrolide antibiotic, as well as benzoyl peroxide. Benzoyl peroxide, in addition to being an antibacterial agent, is a keratolytic and desquamative agent. With benzoyl peroxide, free-radical oxygen is released upon administration, oxidizing bacterial proteins in sebaceous follicles and decreasing the number of anaerobic, bacterial, and irritating free fatty acids. Has keratolytic and comedolytic effects.

Erythromycin is indicated for infections caused by susceptible strains of microorganisms.

The combination drug may be applied topically twice daily.

Clindamycin and tretinoin (Ziana, Veltin)

Contains the topical antibiotic clindamycin 1.2% as well as tretinoin 0.025%. Clindamycin reduces C acnes levels and is anti-inflammatory. Tretinoin normalizes differentiation of keratinocytes and is anti-inflammatory. Apply daily to affected areas.

Clindamycin and benzoyl peroxide (Acanya, Duac, BenzaClin, Neuac, Onexton)

Contains the topical antibiotic clindamycin as well as benzoyl peroxide. Clindamycin reduces C acnes levels and is anti-inflammatory. Benzoyl peroxide is an antibacterial agent, comedolytic, and anti-inflammatory. Benzoyl peroxide reduces risk of development of bacterial resistance to clindamycin. Acanya gel contains 2.5% benzoyl peroxide and Duac CS and BenzaClin contain 5% benzoyl peroxide. Apply Acanya and Duac CS once daily. BenzaClin is applied twice daily.

Azelaic acid (Azelex, Finacea)

Has been shown to help reduce inflammation and may aid in treatment of postinflammatory hyperpigmentation. Apply twice daily. Improvement may be seen within 4 weeks.

Benzoyl peroxide (BenzePro, PanOxyl, Neutrogena Clear Pore, Benziq, Clearskin)

Benzoyl peroxide is an oxidizing agent that possesses antibacterial properties and is comedolytic. The antibacterial activity results from the release of active or free-radical oxygen that can oxidize bacterial proteins. Benzoyl peroxide is oxidized into benzoic acid upon skin contact. It is available OTC and by prescription.


Questions & Answers


What are Cutibacterium (Propionibacterium) infections?

How are Cutibacterium (Propionibacterium) classified?

What is the US prevalence of Cutibacterium (Propionibacterium) infections?

What is the global prevalence of Cutibacterium (Propionibacterium) infections?

What is the prevalence of Cutibacterium (Propionibacterium) infections in patients with endocarditis?

What is the morbidity and mortality associated with Cutibacterium (Propionibacterium) infections?

What are the racial predilections of Cutibacterium (Propionibacterium) infections?

What are the sexual predilections of Cutibacterium (Propionibacterium) infections?

Which age groups have the highest prevalence of Cutibacterium (Propionibacterium) infections?

What is the pathophysiology of Cutibacterium (Propionibacterium) infections?


Which clinical history findings are characteristic of Cutibacterium acnes infection?

Which Cutibacterium (Propionibacterium) infections are associated with breast implants?

Which Cutibacterium (Propionibacterium) infections cause endocarditis?

Which Cutibacterium (Propionibacterium) infections are associated with orthopedic conditions?

Which clinical history findings are characteristic of Cutibacterium (Propionibacterium) infection following neurosurgery?

Which conditions may be caused by Cutibacterium (Propionibacterium) infection?

What are the possible complications of Cutibacterium (Propionibacterium) infection?


Which condition are included in the differential diagnoses of Cutibacterium (Propionibacterium) infection?

What are the differential diagnoses for Cutibacterium (Propionibacterium) Infections?


What is included in the workup of Cutibacterium (Propionibacterium) acne vulgaris?

How are implant-associated Cutibacterium (Propionibacterium) infections diagnosed?

How is Cutibacterium acnes infectious keratitis diagnosed?

How is chronic pseudophakic-related endophthalmitis diagnosed?

How transfusion-transmitted Cutibacterium (Propionibacterium) infections diagnosed?

What is the role of imaging in the workup of implant-associated Cutibacterium (Propionibacterium) infections?


How is acne vulgaris treated?

How are CNS shunt infection treated?

What is the approach to the treatment of Cutibacterium (Propionibacterium) infections?

How are transfusion-transmitted Cutibacterium (Propionibacterium) infections treated?

What is the role of surgery in the treatment of acne vulgaris?

What is the role of surgery in the treatment of implant-associated Cutibacterium (Propionibacterium) infections?

What is the role of surgery in the treatment of cardiovascular device related Cutibacterium (Propionibacterium) infections?

What is the role of surgery in the treatment of CNS shunt infection?

What is the role of surgery in the treatment of chronic pseudophakic-related endophthalmitis?

What are the goals of treatment for acne vulgaris?

Which specialist consultations are beneficial to patients with Cutibacterium (Propionibacterium) infections?

Which dietary modifications are used in the treatment of Cutibacterium (Propionibacterium) infections?


Which medications are used in the treatment of Cutibacterium (Propionibacterium) infections?

Which medications in the drug class Acne Products are used in the treatment of Cutibacterium (Propionibacterium) Infections?

Which medications in the drug class Estrogens/Progestins are used in the treatment of Cutibacterium (Propionibacterium) Infections?

Which medications in the drug class Aldosterone Antagonists, Selective are used in the treatment of Cutibacterium (Propionibacterium) Infections?

Which medications in the drug class Antibiotics, Other are used in the treatment of Cutibacterium (Propionibacterium) Infections?

Which medications in the drug class Retinoid-like Agents are used in the treatment of Cutibacterium (Propionibacterium) Infections?