Finegoldia magna is a serious opportunistic pathogen and a highly virulent member of the Gram-positive anaerobic cocci (GPAC) group. Capable of causing deep-seated and life-threatening infections, it was historically often dismissed as a contaminant. Modern diagnostic techniques have confirmed its role in a broad spectrum of human illness. It was formerly known as Peptostreptococcus magnus before being reclassified into its own genus, reflecting its unique pathogenic potential.
Defining the Organism
Finegoldia magna is a Gram-positive coccus, appearing microscopically as small, non-spore-forming, spherical bacteria. Its name, derived from the Latin word magna meaning “large,” refers to its relatively larger size compared to other anaerobic cocci. The organism is a strict obligate anaerobe, meaning it cannot grow or thrive in the presence of oxygen and relies on fermentation for energy.
This bacterium is a common member of the normal human microbiota, colonizing non-sterile body surfaces like the skin, oral cavity, and the gastrointestinal and genitourinary tracts. This colonization explains its role as an opportunistic pathogen. Any break in the skin or mucosal barrier allows it to enter normally sterile tissues, where it can initiate an infection.
F. magna is consistently identified as the most pathogenic species among the Gram-positive anaerobic cocci. Its prevalence is notable, often constituting a significant percentage of all anaerobic isolates recovered from human infections.
Virulence Factors and Mechanisms of Pathogenicity
The capacity of F. magna to cause infection is due to surface proteins and secreted enzymes that allow it to adhere to host tissues and evade the immune system. Protein L, a surface factor, binds to the kappa light chains of human immunoglobulins (antibodies). By binding antibodies without activating the immune response, the bacterium effectively masks itself from host defenses.
The F. magna Adhesion Factor (FAF) facilitates initial attachment to host cells. FAF also aids immune evasion by binding to and neutralizing antimicrobial peptides (AMPs), such as LL-37. The bacterium produces SufA, a subtilisin-like extracellular serine protease, which cleaves and releases FAF from the bacterial surface.
SufA is also a tissue-destroying enzyme, degrading human proteins like collagen and fibrinogen, essential components of tissue structure and blood clotting. This degradation contributes to the deep penetration and spread of infection, often resulting in tissue damage. Additionally, the Peptostreptococcal Albumin Binding protein (PAB) enhances bacterial survival by binding to albumin, which provides a selective advantage and increases the organism’s growth rate during infection.
F. magna infections are difficult to treat due to the organism’s strong ability to form complex biofilms, especially on medical devices and implants. Biofilms are protective structures that shield bacterial communities from antibiotic penetration and the host’s immune cells, contributing to chronic infection. In polymicrobial infections, F. magna utilizes enzymes like collagenase and gelatinase to break down tissue barriers, allowing co-infecting pathogens to spread more easily.
Clinical Spectrum of Infections
Finegoldia magna is implicated in a wide range of infections, typically tied to a breach in the skin or mucosal barrier. The most frequent infections involve the skin and soft tissues, including deep-seated abscesses, surgical site infections, and chronic, non-healing lesions such as diabetic foot ulcers.
The organism also causes serious bone and joint infections, including septic arthritis and chronic osteomyelitis. Its ability to form biofilms makes it a notable pathogen in prosthetic joint infections (PJI), where it colonizes artificial implants, making eradication challenging. These orthopedic infections range from aggressive, early postoperative cases to more subtle, late-onset presentations.
Beyond localized infections, F. magna can cause severe systemic disease when it enters the bloodstream, leading to bacteremia and life-threatening conditions. These include infective endocarditis, where bacteria colonize the heart valves, and necrotizing pneumonia.
Patient risk factors for developing invasive infections involve underlying health conditions, recent trauma, or surgical procedures. Individuals with chronic diseases like diabetes are at a higher risk, especially when poor circulation leads to chronic ulcers that serve as an entry point. The implantation of a foreign body, such as a prosthetic joint, also elevates the risk of deep-seated infection.
Antibiotic Resistance and Treatment Strategies
Treating infections caused by F. magna requires careful consideration of its susceptibility profile. The bacterium is generally responsive to anti-anaerobic agents like metronidazole and beta-lactam antibiotics, such as penicillin and amoxicillin/clavulanic acid. These agents are often considered first-line options for empirical therapy.
The clinical challenge is the organism’s variable resistance to certain commonly used antibiotics, especially clindamycin and macrolides like erythromycin. Resistance to clindamycin varies significantly by region, sometimes exceeding 25% of tested strains. This variability means clindamycin cannot be reliably used as a stand-alone empirical treatment without local resistance data.
Due to these unpredictable resistance patterns, Antimicrobial Susceptibility Testing (AST) is necessary for clinical management. AST is mandatory when considering antibiotics such as clindamycin, cephalosporins, or fluoroquinolones, as resistance can lead to treatment failure. For severe or device-related infections, agents like carbapenems or linezolid may be required, often combined with surgical removal or debridement of infected tissue.