eMedicine Specialties > Infectious Diseases > Bacterial Infections

Propionibacterium Infections

Author: Sajeev Handa, MB, BCh, BAO, LRCSI, LRCPI, Director, Division of Hospital Medicine, Department of Medicine, Rhode Island Hospital
Contributor Information and Disclosures

Updated: Mar 30, 2009

Introduction

Background

Propionibacterium species are inhabitants of the skin and are usually nonpathogenic. As a result, they are common contaminants of blood and body-fluid cultures. These species are slow-growing, nonsporulating, gram-positive anaerobic bacilli and require at least 6 days for growth in culture.¹

Propionibacterium species belong to the genera of coryneforms and are the best studied because of their association with acne vulgaris. However, Propionibacterium species can cause numerous other types of infections, and these are described briefly in this article.

Propionibacterium acnes is found briefly on the skin of neonates, but true colonization begins during the 1-3 years prior to sexual maturity. During this time, numbers of P acnes rise from fewer than 10/cm² to about 10⁶/cm², chiefly on the face and upper thorax. In the lipid-rich microenvironment of the hair follicle, P acnes produces inflammatory mediators that result in papules, pustules, and later, nodulocystic lesions that are typical of inflammatory acne.

Propionibacterium granulosum is found in the same areas but at numbers about one hundredth of those of P acnes.

Both P acnes and P granulosum may be isolated from the gastrointestinal tract.

Propionibacterium avidum is found in the axilla rather than on exposed areas and increases in numbers at puberty.

Propionibacterium 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.

Frequency

United States

Acne vulgaris is sufficiently common that it may be considered physiologic.

Race

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

Sex

In girls, acne may precede menarche by more than 1 year. The peak of acne activity occurs during the mid-to-late teenaged period, and the incidence subsequently decreases. Acne is more common in males than in females, and it tends to be more severe in males.

Age

Acne vulgaris is a self-limited 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. The condition is often an early manifestation of puberty. In very young individuals, the predominant lesions are comedones, and inflammatory lesions are rare.

Clinical

History

• Acne vulgaris
  • P 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 4 major pathophysiologic features of acne include the following:
    • Hyperkeratinization
    • Sebum production
    • Bacterial proliferation
    • Inflammation
  • Lesions can be described in 3 categories, as follows:
    • Noninflammatory: 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).
      
      

      

      Propionibacterium infection. Nodular-cystic acne.

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      Propionibacterium infection. Nodular-cystic acne.

      
      

      

      Propionibacterium infection. Pustular acne.

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      Propionibacterium infection. Pustular acne.

    • Scars: These appear as punched out pits of varying size and may have multiple openings.
  • 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 oil-containing compounds.
• Other infections
  • In rare cases, Propionibacterium species have been implicated as a cause of brain abscess,² subdural empyema, dental infections, endocarditis (particularly in association with implanted cardiac devices), continuous ambulatory peritoneal dialysis (CAPD), conjunctivitis associated with contact lenses, peritonitis, and breast-implant infections.
  • P 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. P acnes cardiovascular device–related infections typically have a subtle presentation: low grade fever, weight loss, malaise, and myalgias.
  • P 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).
  • P acnes has been implicated in certain spondyloarthropathies associated with florid acne vulgaris, in which it was isolated from bone foci and joints.³
  • P acnes has been implicated in infections following rotator cuff repair, as well as an outbreak of postoperative shoulder infections linked to a ventilation system.¹
  • P acnes has been known to infect internal or external shunts, including Ommaya reservoirs.⁴ In a retrospective analysis of shunt infections in 78 adults, P acnes was isolated in 9% of cases.⁵ P 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. Because P acnes is a low-virulence organism, clinical symptoms may be nonspecific.⁵ Ventriculoperitoneal shunt infections may manifest as peritonitis; ventriculoatrial shunt infections may manifest as fever and bacteremia with the potential to progress to endocarditis. P acnes infection of a distal external shunt typically manifests as a soft-tissue infection.
  • P acnes has been reported as a cause of vision-threatening infectious keratitis when the cornea is compromised. P 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.
  • P 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.⁶
  • In rare cases, P granulosum has been isolated as a cause of endocarditis.⁷
  • P acnes infection has been suggested as a possible trigger for primary biliary cirrhosis.⁸ P granulosum infection has been reported as a potential primer of the immune system prior to the development of sarcoidosis.⁹

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