Eikenella corrodens is a Gram-negative, facultative anaerobic bacillus, meaning it can survive with or without oxygen, which contributes to its ability to cause deep-seated infections. It presents a challenge in clinical settings due to growing antibiotic resistance. This organism is a member of the HACEK group, a collection of fastidious bacteria known primarily for causing infective endocarditis. As a natural part of the human oral and upper respiratory tract flora, E. corrodens is typically a harmless commensal organism that coexists with its host. It becomes an opportunistic pathogen when a break in the mucosal barrier allows it to invade sterile body sites.
Clinical Manifestations of Infection
The most recognized clinical presentation involves trauma related to its oral habitat, particularly human bite wounds. These are often referred to as “clenched-fist injuries” or “fight bites,” where the bacteria are forcefully inoculated into deep tissue spaces like joints, tendons, and bones. Because the injury is often small and the infection is slow-growing, or “indolent,” diagnosis and treatment can be delayed, leading to significant tissue destruction.
Head and neck infections are also common, including dental abscesses, periodontitis, and deep neck space infections originating from poor oral hygiene or dental procedures. In immunocompromised patients or those with underlying conditions like malignancy, E. corrodens can cause serious, invasive disease in distant sites such as the lungs (aspiration pneumonia or lung abscesses) and the abdomen. Furthermore, the organism is a known cause of infective endocarditis, which is a destructive, slow-onset infection of the heart valves.
E. corrodens rarely acts alone in these infections, frequently being isolated as part of a polymicrobial collection. It is often found alongside other mouth-dwelling bacteria, such as Streptococcus species and various anaerobes, which complicates the selection of appropriate initial antibiotic therapy. Treatment must cover all potential pathogens present in the wound or abscess.
Mechanisms of Antibiotic Evasion
The most clinically significant mechanism of antibiotic evasion in E. corrodens is the production of beta-lactamase enzymes. This enzyme acts by hydrolyzing the beta-lactam ring structure common to antibiotics like penicillin, ampicillin, and amoxicillin, rendering the drug inactive. While the majority of strains were historically susceptible to penicillin, the prevalence of beta-lactamase-producing strains is increasing, undermining the efficacy of standard penicillin-based treatments.
The genes responsible for this resistance are often carried on mobile genetic elements, such as plasmids, allowing them to be transferred between bacteria. This ability to acquire and share resistance genes is a major driver of therapeutic failure when relying on antibiotics without an accompanying beta-lactamase inhibitor. The presence of these enzymes necessitates the use of specialized drug combinations to protect the antibiotic from destruction.
Beyond acquired resistance, E. corrodens possesses intrinsic resistance to several commonly used antibiotics. The organism is uniformly resistant to both metronidazole and clindamycin, two drugs frequently used to treat mixed anaerobic infections originating from the oral cavity. This fixed resistance pattern makes their empirical use in suspected E. corrodens infections a therapeutic trap.
Standard and Alternative Treatment Protocols
The primary treatment strategy for confirmed E. corrodens infection involves using beta-lactam antibiotics that are either resistant to the organism’s beta-lactamase or are combined with an inhibitor. Amoxicillin-clavulanate is often the preferred choice for empirical therapy in human bite wounds because the clavulanate component successfully neutralizes the beta-lactamase enzyme. For more severe or invasive infections, such as endocarditis, third-generation cephalosporins like ceftriaxone are highly effective and considered the preferred first-line treatment.
Alternative protocols are necessary for patients with severe penicillin allergies or for strains confirmed to be resistant to first-line agents. Fluoroquinolones, such as ciprofloxacin, have demonstrated good activity against E. corrodens and can serve as a viable alternative. Ampicillin-sulbactam is also effective against beta-lactamase-producing strains and is often used for parenteral (intravenous) treatment of deep infections.
Treatment decisions should be guided by laboratory susceptibility testing, especially when initial therapy is failing or the infection is deep-seated. Susceptibility testing helps confirm the strain’s sensitivity to various agents, ensuring the chosen antibiotic is active against the specific isolate. Furthermore, surgical intervention, such as incision and drainage, is frequently required for managing deep abscesses or localized collections of pus, as antibiotics alone cannot effectively penetrate and sterilize these sites.
Laboratory Identification
Accurate diagnosis of E. corrodens requires recognizing its unique growth requirements and colonial characteristics. It is a fastidious organism with complex nutritional needs, and it grows slowly, often requiring at least 48 hours of incubation before colonies become visible. Optimal growth is achieved in an atmosphere enriched with carbon dioxide, classifying it as a capnophile.
The species name, corrodens, meaning “to corrode,” refers to its ability to pit or create small depressions in the agar surface as it grows. Although this pitting is a classic sign, its absence does not rule out the organism, as only about half of all isolates exhibit this characteristic. Another strong identifier is the faint, characteristic odor of bleach, or hypochlorite, that some colonies produce on the culture plate. Identifying these specific traits is important because the slow growth rate can lead to the organism being overlooked or outgrown by other bacteria in a mixed-culture sample.