As well as being a cause of eye infections, P. acnes has the potential to cause a
range of other diseases. Some of these are discussed below.
P. acnes in acne vulgaris
Acne vulgaris is the commonest skin disorder amongst the adolescent population and affects around 80% of individuals at some stage in their lives (Dreno & Poli, 2003). It is a multifactorial disorder of the pilosebaceous follicles, and disease mechanisms include sebaceous hyperplasia, follicular hyperkeratinisation, hormone imbalance, bacterial infection and immune hypersensitivity (Gollnick, 2003; Jappe, 2003; Thiboutot, 2000; Webster, 2002). P. acnes is considered to
play a vital role in the pathogenesis of acne vulgaris where it is thought to contribute to the inflammatory phase of the condition (Leyden, 2001). The organism is able to metabolise sebaceous triglycerides, releasing free fatty acids that irritate the follicular wall and surrounding dermis (Coenye et al., 2007). In
addition, P. acnes can also produce exoenzymes and neutrophils chemoattractants
(Kabongo Muamba, 1982; Thiboutot, 2000; Webster, 2002).
Treatment of acne includes keratinolytic and sebosuppressive agents like retinoids (Thiboutot et al., 2008) as well as antibacterial agents. Topical antimicrobial
agents include benzoyl peroxide, clindamycin, erythromycin, tetracycline, azelaic acid and triclosan (Bojar et al., 1994; Dreno, 2004; Krautheim & Gollnick, 2004;
Tan, 2004; Taylor & Shalita, 2004; Webster, 2000). Systemic antibiotics such as tetracycline, doxycycline, minocycline and erythromycin may be indicated in cases where topical treatment is not successful or in patients at risk of scarring and pigmentary changes (Ross et al., 2003).
Shortly after the introduction of topical erythromycin and clindamycin in acne treatment over 40 years ago, resistant strains were detected in the US (Leyden et al., 1983). Since then, reports of resistant P. acnes strains from acne patients have
Ross et al., 2003; Tan et al., 2001). It has been demonstrated that the proportion
of patients carrying resistant bacteria in the UK doubled between 1991 and 1997. Consequently 60% of acne patients were found to carry resistant strains (Eady, 1998). A study carried out in Europe showed that 50% of acne patients were colonised by clindamycin and erythromycin resistant P. acnes and 20% of patients
by tetracycline resistant P. acnes (Ross et al., 2003).
SAPHO and sarcoidosis
In patients suffering from SAPHO syndrome, P. acnes has been recovered from
bone biopsy, synovial fluid and tissue samples (Schaeverbeke et al., 1998). P. acnes has also been isolated from lymph nodes of patients with sarcoidosis, a
systemic granulomatous disease of unknown aetiology (Eishi et al., 2002; Ishige et al., 1999; Yamada et al., 2002). This is not conclusive evidence as recent
findings have shown that P. acnes can normally reside in peripheral lung tissue
and mediastinal lymph nodes. Therefore their presence is not exclusive to sarcoidosis (Ishige et al., 1999).
Prostate disease
P. acnes was isolated from the prostate gland in a substantial portion (35%) of
patients with prostate cancer and an association was demonstrated between positive culture and prostatic inflammation (Cohen et al., 2005). In addition to
this, another study reported P. acnes 16S rRNA gene sequences as the most
common bacterial DNA extracted from prostatic tissue of patients with benign prostatic hyperplasia (BPH) (Alexeyev et al., 2006). Direct visualisation using
multi-colour fluorescence in situ hybridisation (FISH) assay of P. acnes in
prostate tissue has revealed that the organism demonstrated intracellular localisation and stromal biofilm-like aggregates (Alexeyev et al., 2007). It has
therefore been proposed that infection of the prostate gland by P. acnes might be a
contributory factor in developing prostatic inflammation, which in turn might contribute to the development of BPH and prostate cancer through cellular injury and proliferation (Shannon et al., 2006b; Shannon et al., 2008).
Prosthetic joint infections
Prosthetic hip, knee and shoulder-associated infections are common indications for revision arthroplasties (Berthelot et al., 2006; Zeller et al., 2007). P. acnes has
been implicated in up to 22% of revision operations (Tunney et al., 1998). As P. acnes grow predominantly within a biofilm on the surface of the prosthesis, which
renders them more resistant to antibiotics, treatment with systemic antibiotics usually fail. Therefore, removal and replacement of the infected implant is often necessary to eliminate infection (Ramage et al., 2003; Tunney et al., 2007).
Spinal surgery and sciatica
P. acnes is described as a cause of wound contamination during spinal surgery
and immunofluorescence microscopy (IFM) carried out on surgical specimens suggest that P. acnes detected in wounds originates from patient skin (McLorinan et al., 2005). It has also been isolated in cases of spinal osteomyelitis and discitis
(Chia & Nakata, 1996; Esteban et al., 1998; Harris et al., 2005; Kowalski et al.,
2007; Noble & Overman, 1987). Culture of P. acnes from microdiscectomy
material removed for the treatment of sciatica has lead to an association between the organism and sciatica (Stirling et al., 2001). However, others have failed to
culture P. acnes from microdiscectomy material and suggest that these organisms
were contaminants from the skin during the surgical procedure (McLorinan et al.,
2005).
Central nervous system infections
P. acnes is increasingly recognised as a cause of infection after neurosurgical
procedures (Brook, 1988; Brook & Frazier, 1991; Nisbet et al., 2007; Ramos et al., 1995; Skinner et al., 1978). Although it is most frequently isolated from
infected neurosurgical shunts, it has also been described as a pathogen in a wide range of central nervous system (CNS) infections including brain abscess (Barazi
et al., 2003; Berenson & Bia, 1989; Cohle et al., 1981; Maniatis & Vassilouthis,
1980), subdural and epidural empyema (Critchley & Strachan, 1996; Yoshikawa
et al., 1975), and meningitis (Beeler et al., 1976; Everett et al., 1976; Schlesinger
Fatal bacterial granuloma after trauma (FBGT)
P. acnes has recently been identified as the causative agent in FBGT (Gao et al.,
2002). The major clinical presentations of FBGT patients were the development of skin lesions after slight trauma to the face, followed by spreading of dark-red plaques on the skin and frequently death from encephalitis within 5 years.
Endocarditis
P. acnes has been shown to cause infection of prosthetic heart valves (Gunthard et al., 1994; Hinestrosa et al., 2007; Horner et al., 1992; Pan et al., 2005), native
valves (Mohsen et al., 2001) and annuloplasty rings (Vanagt et al., 2004), leading
to endocarditis. Prompt diagnosis and treatment of P. acnes endocarditis are
essential, since the infection tends to follow a very aggressive clinical course resulting in extensive valvular destruction, congestive heart failure, abscess formation, and systemic embolisation (Delahaye et al., 2005; Horner et al., 1992;
Huynh et al., 1995; Lazar & Schulman, 1992; Lewis & Abramson, 1980; Mohsen et al., 2001). Many antibiotics, including penicillin, vancomycin, teicoplanin, and
gentamicin, are considered active in vitro for the treatment of P. acnes infections
and have been reported to be effective in eliminating infection in endocarditis (Horner et al., 1992; Huynh et al., 1995).