# Finegoldia magna
**Finegoldia magna** is a species of strictly anaerobic, Gram-positive coccus that lives as part of the normal human microbiota of the skin, mouth, gastrointestinal and genitourinary tracts, and that acts as an opportunistic pathogen in soft-tissue, bone and joint, and other deep-seated infections.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) • [2](https://pubmed.ncbi.nlm.nih.gov/17702255/) Formerly known as *Peptostreptococcus magnus* and, before that, *Peptococcus magnus*, it is considered the most pathogenic species among the Gram-positive anaerobic cocci (GPAC) and is the GPAC species most often isolated in pure culture from clinical specimens.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/)
| Key fact | Detail |
|---|---|
| Current name | *Finegoldia magna* (Prévot 1933) Murdoch and Shah 2000; basonym "Diplococcus magnus" Prévot 1933[3](https://www.lpsn.dsmz.de/species/finegoldia-magna) |
| Former names | *Peptococcus magnus* (Approved Lists 1980); *Peptostreptococcus magnus* (Ezaki et al. 1983)[3](https://www.lpsn.dsmz.de/species/finegoldia-magna) • [4](https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=1260&mode=Info) |
| Classification | Bacteria; Bacillota; Tissierellales; Peptoniphilaceae; *Finegoldia*[4](https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=1260&mode=Info) |
| Type strain | ATCC 15794; also CCUG 17636, DSM 20470, GIFU 7629, NCTC 11804[3](https://www.lpsn.dsmz.de/species/finegoldia-magna) |
| Genome | G+C content of 32–33%; complete genome sequence of strain ATCC 29328 available[5](https://academic.oup.com/femsle/article-pdf/210/1/33/19111346/210-1-33.pdf) • [1](https://pubmed.ncbi.nlm.nih.gov/27756620/) |
| Clinical frequency | GPAC account for about 25–30% of isolated anaerobic bacteria from clinical specimens; *F. magna* accounts for 5–12% of all anaerobic isolates and 20–38% of all GPAC[6](https://academic.oup.com/femsre/article/37/4/520/2399123) • [7](https://pmc.ncbi.nlm.nih.gov/articles/PMC10127037/) |
| Risk group | 2 (Canada and Germany); 1 (Switzerland)[3](https://www.lpsn.dsmz.de/species/finegoldia-magna) |
## Taxonomy and nomenclature
The species was first described by A. R. Prévot in 1933 as "Diplococcus magnus", a name that was effectively but not validly published under the [International Code of Nomenclature of Prokaryotes](https://www.edgepedia.org/international-code-of-nomenclature-of-prokaryotes).[4](https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=1260&mode=Info) It was placed in the genus *Peptococcus* because of its cellular arrangement, and its G+C content and DNA-DNA homology data later led Ezaki and colleagues to transfer it to *Peptostreptococcus* in 1983.[8](https://pmc.ncbi.nlm.nih.gov/articles/PMC121377/) In 1999, Murdoch and Shah reclassified *Peptostreptococcus magnus* as *Finegoldia magna* comb. nov., making it the nomenclatural type of the new genus *Finegoldia*; the combination was validated in Validation List No. 75 in 2000.[3](https://www.lpsn.dsmz.de/species/finegoldia-magna) • [4](https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=1260&mode=Info) The genus was named after Sidney M. Finegold, a specialist in anaerobic microbiology.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) The name is on the List of Recommended Names for bacteria of medical importance, and Bartlett and colleagues listed the species as an established human pathogen in 2022.[3](https://www.lpsn.dsmz.de/species/finegoldia-magna)
The reclassification was part of a broader revision of GPAC taxonomy driven by molecular identification methods: when the type species *Peptostreptococcus anaerobius* remained in *Peptostreptococcus*, the remaining species were divided among the new genera *Finegoldia*, *Micromonas* (later *Parvimonas*), *Peptoniphilus*, *Anaerococcus*, and *Gallicola*.[5](https://academic.oup.com/femsle/article-pdf/210/1/33/19111346/210-1-33.pdf)
## Microbiology
*F. magna* cells are strictly anaerobic Gram-positive cocci arranged in pairs, tetrads, and clusters.[2](https://pubmed.ncbi.nlm.nih.gov/17702255/) Its genome has a G+C content of 32–33%, and it is the most common species of GPAC in human clinical specimens.[5](https://academic.oup.com/femsle/article-pdf/210/1/33/19111346/210-1-33.pdf) The genome carries many aminopeptidases and amino acid and oligopeptide transporters, consistent with the use of amino acids as major energy sources, and *F. magna* shows more aminopeptidase activity than other GPAC species.[6](https://academic.oup.com/femsre/article/37/4/520/2399123)
Whole-genome sequencing of clinical isolates has revealed substantial heterogeneity. Two clades show an overall average nucleotide identity of only 90.7%, below the roughly 94% threshold that generally separates bacterial species, suggesting that at least two distinct *Finegoldia* species exist and that both can act as opportunistic pathogens.[9](https://pmc.ncbi.nlm.nih.gov/articles/PMC5654912/)
## Virulence factors
**Adhesion and survival.** Sortase-dependent pili and the *F. magna* adhesion factor (FAF) act at the start of infection, and the peptostreptococcal albumin binding protein (PAB) enhances bacterial survival in the host.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) FAF, the subtilisin-like extracellular serine protease SufA, and the superantigen protein L protect the bacteria from factors of the innate defense system.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) Protein L and FAF are associated with the bacterial surface but can also be released into the environment.[10](https://pmc.ncbi.nlm.nih.gov/articles/PMC7025542/)
**Spread and severity.** SufA, capsule formation, and tissue-destroying enzymes such as collagenase and gelatinase provide deep penetration or spread of infections, and protein L is associated with infection severity.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) • [10](https://pmc.ncbi.nlm.nih.gov/articles/PMC7025542/) Some virulence factors show structural or functional similarities to those of *Streptococcus pyogenes* or *Staphylococcus aureus*.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) The best-described factors are protein L, PAB, SufA, and FAF.[6](https://academic.oup.com/femsre/article/37/4/520/2399123)
**Biofilms.** Biofilm production results in infection chronification, complicated treatment, and persistence of multi-species biofilms.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) In an in vivo polymicrobial wound model, *Pseudomonas aeruginosa* in a monospecies biofilm was 2-fold more susceptible to gentamicin than *P. aeruginosa* in a polymicrobial biofilm containing *S. aureus*, *Enterococcus faecalis*, and *F. magna*.[11](https://academic.oup.com/femsre/article/41/3/276/3089981)
## Clinical role
*F. magna* is a commensal of the skin and mucosal surfaces and one of the most frequent anaerobes isolated from skin.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) [Infection](https://www.edgepedia.org/infection) is associated with host factors such as immunodeficiency, wounds, aging, or the presence of foreign materials and devices.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) Reported infections range from soft-tissue and wound infections and vaginoses to bone and joint infections, septic arthritis, prosthetic valve endocarditis, pleural empyema, endocarditis, prosthetic joint infections, and necrotizing pneumonia.[6](https://academic.oup.com/femsre/article/37/4/520/2399123) • [7](https://pmc.ncbi.nlm.nih.gov/articles/PMC10127037/) It has been the most frequently reported GPAC causing prosthetic joint infections, and in the well-ventilated nasal cavity it was the most common obligate anaerobic species isolated, found in 38.2% of patients in one study.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/)
Although GPAC infections are usually polymicrobial, *F. magna* is often isolated in pure culture.[7](https://pmc.ncbi.nlm.nih.gov/articles/PMC10127037/) In orthopedic infections it is infrequent: a 2025 series of 20 patients found *F. magna* in 15.5% of anaerobic orthopedic infections, with 80% of patients achieving complete clinical recovery after a mean of 2.1 surgical procedures; polymicrobial infections required twice the number of operations and had a failure rate of 36% versus 0% for monomicrobial cases.[12](https://journals.sagepub.com/doi/10.1089/sur.2024.134) In implant-associated infections, most isolates are susceptible to most antibiotics tested, but successful treatment generally requires extraction of the implants.[9](https://pmc.ncbi.nlm.nih.gov/articles/PMC5654912/)
## Antibiotic susceptibility and resistance
Resistance patterns vary by drug class. A 2016 review reported resistance rates to quinolones of 13.0 to 70% and to clindamycin of 0 to 40.0%, with resistance to penicillins below 4%, chloramphenicol 7.0%, and metronidazole below 7%; earlier reviews noted lower resistance rates (10–20%) to clindamycin, metronidazole, and penicillin and higher rates (above 20%) to erythromycin and tetracycline.[1](https://pubmed.ncbi.nlm.nih.gov/27756620/) • [6](https://academic.oup.com/femsre/article/37/4/520/2399123)
A Zurich study of 57 clinical isolates collected between September 2019 and July 2020 tested nine antibiotics by E-test: all strains were susceptible to benzylpenicillin, amoxicillin/clavulanic acid, and metronidazole, while 75% were susceptible to clindamycin.[13](https://pubmed.ncbi.nlm.nih.gov/35391578/) The authors recommended benzylpenicillin, amoxicillin/clavulanic acid, or metronidazole as first-line treatment without prior susceptibility testing, and mandatory testing if cefuroxime, cefepime, levofloxacin, rifampicin, doxycycline, or clindamycin is used.[13](https://pubmed.ncbi.nlm.nih.gov/35391578/) The clinical importance of testing is illustrated by a case in which a periprosthetic joint infection treated with cefepime relapsed because of antibiotic-resistant strains.[13](https://pubmed.ncbi.nlm.nih.gov/35391578/)
## References
1. [Boyanova L, Markovska R, Mitov I (2016). Virulence arsenal of the most pathogenic species among the Gram-positive anaerobic cocci, *Finegoldia magna*. Anaerobe 42:145–151.](https://pubmed.ncbi.nlm.nih.gov/27756620/)
2. [Nonpuerperal breast abscess caused by *Finegoldia magna* (2007). PubMed.](https://pubmed.ncbi.nlm.nih.gov/17702255/)
3. [Species *Finegoldia magna*, LPSN (DSMZ).](https://www.lpsn.dsmz.de/species/finegoldia-magna)
4. [NCBI Taxonomy Browser: *Finegoldia magna* (Taxonomy ID 1260).](https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=1260&mode=Info)
5. [Physical and genetic map of the *Finegoldia magna* (formerly *Peptostreptococcus magnus*) ATCC 29328 genome. FEMS Microbiology Letters.](https://academic.oup.com/femsle/article-pdf/210/1/33/19111346/210-1-33.pdf)
6. [Murphy EC, Frick IM (2013). Gram-positive anaerobic cocci – commensals and opportunistic pathogens. FEMS Microbiology Reviews 37(4):520–553.](https://academic.oup.com/femsre/article/37/4/520/2399123)
7. [Understanding antimicrobial susceptibility profile of *Finegoldia magna*: an insight to an untrodden path (2023). PMC.](https://pmc.ncbi.nlm.nih.gov/articles/PMC10127037/)
8. [Gram-Positive Anaerobic Cocci (1997). PMC.](https://pmc.ncbi.nlm.nih.gov/articles/PMC121377/)
9. [*Finegoldia magna* Isolated from Orthopedic Joint Implant-Associated Infections (2017). PMC.](https://pmc.ncbi.nlm.nih.gov/articles/PMC5654912/)
10. [*Finegoldia magna*, an Anaerobic Gram-Positive Bacterium of the Normal Human Microbiota, Induces Inflammation by Activating Neutrophils (2019). PMC.](https://pmc.ncbi.nlm.nih.gov/articles/PMC7025542/)
11. [Molecular mechanisms of biofilm-based antibiotic resistance and tolerance in pathogenic bacteria. FEMS Microbiology Reviews.](https://academic.oup.com/femsre/article/41/3/276/3089981)
12. [Gabardo S et al. (2025). *Finegoldia magna*: An Infrequent Guest in Orthopedic Infections. Surgical Infections.](https://journals.sagepub.com/doi/10.1089/sur.2024.134)
13. [Walser F et al. (2022). Antimicrobial susceptibility testing is crucial when treating *Finegoldia magna* infections. Eur J Clin Microbiol Infect Dis.](https://pubmed.ncbi.nlm.nih.gov/35391578/)
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*Topic: Encyclopedia › Life and health › Microorganisms and fungi › Bacteria › Medically important pathogenic bacteria*
*Initially written Sep 17, 2026 · Reviewed: Oct 21, 2026 · Edited: Oct 15, 2026; Oct 21, 2026 · Last review: Oct 21, 2026*
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License: Edgepedia Community License 1.0, https://www.edgepedia.org/edgepedia/license