Corynebacterium striatum is a rod-shaped, Gram-positive bacterium that has emerged as a significant concern in healthcare settings. Historically considered a harmless part of the normal human flora, this organism is now recognized as an opportunistic pathogen capable of causing serious infections. Its increasing relevance stems primarily from its growing prevalence in hospitals and frequent resistance to multiple classes of antibiotics.
Physical Structure and Identification
The physical form of Corynebacterium striatum is distinctive, classifying it as a coryneform bacterium. Under a microscope, it appears as a pleomorphic, or irregularly shaped, Gram-positive rod, often exhibiting a characteristic club-like morphology. These bacilli do not form spores and are typically non-motile.
On a stained smear, the bacteria often arrange themselves in angular clusters or parallel rows, described as a “Chinese letter” or “palisade” arrangement. This visual pattern, along with its ability to grow under both aerobic and facultative anaerobic conditions, aids in preliminary identification. However, colonies on blood agar can appear smooth and glossy, sometimes mimicking less threatening skin microbes like coagulase-negative staphylococci, which complicates initial diagnosis. Accurate identification relies heavily on modern techniques such as Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Mass Spectrometry (MALDI-TOF MS), which analyzes the bacterial protein profile for rapid and specific results.
Infection Context and High-Risk Settings
The transition of C. striatum from a harmless colonizer to an infectious agent is closely linked to healthcare facilities. It is predominantly recognized as a nosocomial pathogen, acquired within hospitals, long-term care facilities, and intensive care units. This environment provides the ideal mix of vulnerable hosts and selective pressures, allowing the bacterium to thrive and cause disease.
Patients with compromised immune systems, including those with underlying conditions like cancer or chronic obstructive pulmonary disease (COPD), are at a substantially greater risk for infection. Prolonged hospitalization is another well-documented risk factor, increasing the patient’s exposure to the hospital environment and potentially resistant strains. The use of invasive medical devices creates a direct pathway for the bacteria to enter the bloodstream or deep tissues. Devices such as central venous catheters, artificial joints, and endotracheal tubes are frequently associated with C. striatum infections.
Prior broad-spectrum antibiotic use selects for C. striatum by eliminating competing, susceptible flora, allowing the inherently resistant bacteria to colonize and initiate infection. The organism exploits breaches in host defenses and medical interventions to become a clinical threat. Its ability to be transmitted person-to-person, even through caregivers, further underscores its potential for causing institutional outbreaks.
Bacterial Factors in Disease Progression
The ability of C. striatum to cause progressive disease stems from factors that allow it to colonize surfaces and evade host defenses. A primary mechanism of pathogenesis is its strong capacity for adhesion to both human tissues and artificial materials. This adherence is often facilitated by surface structures called pili, encoded by operons like SpaDEF, which allow the bacteria to latch onto host epithelial cells and inert surfaces.
Once adhered to a surface, especially indwelling medical devices, C. striatum can form a biofilm—a complex matrix of bacteria encased in a self-produced slime layer. Biofilm formation acts as a protective shield, significantly hindering the penetration of immune cells and antibiotics. This mechanism allows the bacteria to survive in the host environment, leading to long-term or recurrent infections.
While it lacks the potent toxins of some other Corynebacterium species, its persistence and ability to disseminate are sufficient to cause serious, deep-seated infections. Infections commonly manifest as bacteremia (organism in the bloodstream) or as respiratory tract infections, particularly pneumonia in vulnerable patients. The bacterium has also been implicated in severe conditions such as infective endocarditis (infection of the heart valves) and various musculoskeletal infections.
Understanding Multidrug Resistance
The most significant challenge posed by C. striatum is its frequent classification as a multidrug-resistant (MDR) organism. A high percentage of clinical strains demonstrate resistance to three or more distinct classes of antibiotics. This resistance profile is an acquired characteristic, often linked to the selective pressure of widespread antibiotic use in healthcare settings.
The acquisition of resistance genes is a primary driver of MDR. These genes are frequently carried on mobile genetic elements, such as plasmids and transposons, allowing the bacteria to easily transfer resistance traits to other strains or species. For example, resistance to \(\beta\)-lactam antibiotics (including penicillin) is conferred by genes like bla or ampC, which encode \(\beta\)-lactamase enzymes that chemically inactivate the drugs.
Resistance to other major antibiotic groups involves different mechanisms, such as modification of the drug’s target site or the active expulsion of the drug from the cell. Resistance to macrolides, like erythromycin, is often linked to the erm(X) gene, which modifies the ribosomal target. Fluoroquinolone resistance is frequently the result of mutations in the chromosomal gyrA gene, which alters the drug’s target enzyme. This extensive resistance profile severely limits treatment options.
Due to high rates of resistance to common agents, treatment for severe C. striatum infections often relies on last-resort antibiotics. Vancomycin and linezolid are typically the most effective therapeutic choices, as many clinical isolates retain susceptibility to these agents. However, isolated reports of resistance to daptomycin, another alternative, have been documented.