Eikenella corrodens in periodontitis and beyond

In the bustling newsroom of periodontal disease, the red complex pathogens, such as like Porphyromonas gingivalis (Pg), dominate the front-page headlines, while the orange complex reliably grabs a byline. Meanwhile, a quieter character from the green complex lingers in the footnotes, politely raising its hand for attention. That overlooked contributor is Eikenella corrodens (Ec), a facultatively anaerobic, nonmotile, Gram-negative rod.

While it’s a common and usually harmless resident of the mouth, upper airways, gut, and genitourinary tract, trouble starts when the mucosal barrier is broken, or the host’s immune system is weakened. Then the ordinarily polite commensal Ec can become a serious opportunistic pathogen.¹ Clinically, Ec appears in settings familiar to dentists and physicians.

Ec in periodontitis and systemic infections

In the mouth, it’s associated with periodontitis, often as part of a mixed community. Its reach extends beyond the oral cavity; however, reports link Ec to infections of the upper respiratory tract, pleura and lungs, abdomen, joints, and bones. It’s also well known in wound infections, particularly the classic “fight bite” injury, where saliva introduces the organism into skin and soft tissues and those infections may progress to cellulitis.²

A big concern is the relationship between Ec and infective endocarditis, which shows the ability to enter the bloodstream and persist in low-oxygen environments.³ The shift from commensal to pathogen is often triggered by specific host factors.⁴ Poor oral hygiene permits overgrowth in dental plaque, driving tissue destruction and abscess formation. Dental extractions and invasive procedures provide direct access to the bloodstream, sometimes resulting in infective endocarditis, especially in patients with pre-existing heart valve disease.⁵

Virulence factors of Ec in oral disease

Ec uses multiple virulence mechanisms. Biofilm formation is central, particularly in oral and prosthetic infections, protecting the organism from host defenses and antibiotics.⁶ The bacterium expresses adhesins that enable coaggregation with other microbes, strengthening its role in multispecies biofilms.

In peri-implantitis, Ec adheres firmly to titanium surfaces and stabilizes biofilm communities.⁷ Like other Gram-negative bacteria, Ec possesses lipopolysaccharide (LPS) in its outer membrane. LPS and outer-membrane vesicles provoke inflammation, recruiting immune cells and causing local tissue damage.

In periodontal lesions, this activity contributes to gingival breakdown and bone loss; in abscesses, it can drive necrosis and expansion of infection. Certain conditions increase Ec’s pathogenic potential, such as poor oral hygiene, systemic immunosuppression (e.g., diabetes, leukemia, cancer, rheumatoid arthritis), intravenous drug use, and structural or prosthetic heart valves.

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Diagnosing Ec infections in dentistry and medicine

Diagnosis is often difficult because clinical features are nonspecific. Patients may present with fever, malaise, or new heart murmurs in the setting of endocarditis. Suspicion should be heightened in those with recent dental or urologic procedures, intravenous drug use, or human bite wounds.

It offers another advantage of shared medical and dental records. If a patient’s salivary diagnostics reveal elevated levels of Ec, providing that information to their medical team could offer valuable clinical insight. In the lab, Ec is known for its slow growth, its ability to pit or corrode agar surfaces, and its distinctive bleach-like odor. Biochemically, it is oxidase-positive, catalase-negative, and a poor fermenter.

Treatment options and antibiotic resistance in Ec

Management depends on the site of infection. Abscesses and severe bite injuries typically require surgical drainage or debridement. Ec is usually susceptible to penicillin, third-generation cephalosporins, and fluoroquinolones.⁸ However, it’s intrinsically resistant to clindamycin and metronidazole, which are often used for other anaerobic infections.^9,10

Beta-lactamase production, while uncommon, has been documented, conferring penicillin resistance in some strains.¹¹ There’s thought that prophylaxis with antibiotics is warranted in at-risk patients undergoing invasive dental or surgical procedures, especially those with heart valve disease or immunosuppression. However, the concern for antibiotic stewardship is always top of mind.

Ultimately, Ec may never make the bold headlines like Pg or the rest of the red complex but ignoring it would be a mistake. This quiet footnote in the microbial cast has the potential to step into the spotlight when conditions change—when oral hygiene falters, barriers are breached, or host defenses are compromised.

Its ability to form biofilms, coaggregate with fellow microbes, and provoke damaging inflammation makes it far more than a passive bystander. For clinicians, it’s essential to recognize Ec’s dual identity—harmless commensal one moment, opportunistic pathogen the next. In the story of periodontal disease and systemic infection, Ec reminds us that even supporting characters can change the plot.

References

1. Brook I. The role of anaerobic bacteria in bacteremia. Anaerobe. 2010;16(3):183-189. doi:10.1016/j.anaerobe.2009.12.001
2. Liang ZC, Ouyang H, Song XJ, et al. Eikenella corrodens isolated from pleural effusion: a case report. World J Clin Cases. 2024;12(18):3596-3602. doi:10.12998/wjcc.v12.i18.3596
3. Watkin RW, Baker N, Lang S, Ment J. Eikenella corrodens infective endocarditis in a previously healthy non-drug user. Eur J Clin Microbiol Infect Dis. 2002;21(12):890-891. doi:10.1007/s10096-002-0846-6
4. Suwanagool S, Rothkopf MM, Smith SM, LeBlanc D, Eng R. Pathogenicity of Eikenella corrodens in humans. Arch Intern Med. 1983;143(12):2265-2268.
5. Thornhill MH, Crum A, Rex S, et al. Infective endocarditis following invasive dental procedures: IDEA case-crossover study. Health Technol Assess. 2022;26(28):1-86. doi:10.3310/NEZW6709
6. Karim MM, Nagao A, Mansur FJ, et al. The periodontopathogenic bacterium Eikenella corrodens produces an autoinducer-2-inactivating enzyme. Biosci Biotechnol Biochem. 2013;77(5):1080-1085. doi:10.1271/bbb.130047
7. Renvert S, Roos-Jansåker AM, Lindahl C, Renvert H, Persson GR. Infection at titanium implants with or without a clinical diagnosis of inflammation. Clin Oral Implants Res. 2007;18(4):509-516. doi:10.1111/j.1600-0501.2007.01378.x
8. Li L, Shi YB, Weng XB. Eikenella corrodens infections in human: Reports of six cases and review of literatures. J Clin Lab Anal. 2022;36(2):e24230. doi:10.1002/jcla.24230
9. Cercenado E, Cercenado S, Bouza E. In vitro activities of tigecycline (GAR-936) and 12 other antimicrobial agents against 90 Eikenella corrodens clinical isolates. Antimicrob Agents Chemother. 2003;47(8):2644-2645. doi:10.1128/AAC.47.8.2644-2645.2003
10. Goldstein EJ, Citron DM, Merriam CV, Warren YA, Tyrrell KL, Fernandez H. In vitro activities of a new des-fluoroquinolone, BMS 284756, and seven other antimicrobial agents against 151 isolates of Eikenella corrodens. Antimicrob Agents Chemother. 2002;46(4):1141-1143. doi:10.1128/AAC.46.4.1141-1143.2002
11. Lacroix JM, Walker C. Characterization of a beta-lactamase found in Eikenella corrodens. Antimicrob Agents Chemother. 1991;35(5):886-891. doi:10.1128/AAC.35.5.886