The Staphylococcus genus of bacteria is commonly found in the environment and on the human body. These organisms are traditionally grouped based on the presence of a single enzyme. The primary differentiator used in the laboratory is the coagulase test, which determines an organism’s ability to produce the coagulase enzyme. This enzyme causes blood plasma to clot, a characteristic strongly associated with the highly virulent species Staphylococcus aureus. Coagulase Negative Staphylococcus (CoNS) is a large, diverse group of species that do not produce this clotting enzyme. CoNS species are a prominent part of the normal human flora and are recognized as a major cause of opportunistic infections in medical settings.
Identifying Coagulase Negative Staphylococcus
The CoNS group encompasses more than 40 distinct species, many of which are indigenous to humans. These bacteria primarily colonize the skin and mucous membranes, thriving in moist environments like the armpits, groin, and nasal passages. Staphylococcus epidermidis is the most frequently isolated species, accounting for a significant portion of the staphylococci found on healthy human skin. Other clinically relevant species include Staphylococcus saprophyticus, a known cause of urinary tract infections, and Staphylococcus lugdunensis, which can cause severe, S. aureus-like infections.
Because CoNS species are so prevalent on the skin, their presence in a laboratory culture can present a challenge for clinicians. Isolating CoNS from a blood sample or other sterile site may simply indicate contamination from the patient’s own skin flora during the collection process. A true infection is usually confirmed by finding the bacteria in multiple, sequential cultures or by a high concentration of the organism, correlated with clinical symptoms.
CoNS as Opportunistic Pathogens
Coagulase Negative Staphylococcus are considered opportunistic pathogens, meaning they only cause disease when the host’s normal defenses are weakened or when the bacteria gain access to a body site they do not typically inhabit. This shift from harmless colonizer to infectious agent is strongly linked to modern medical practices, particularly the increased use of indwelling devices. These bacteria are now among the leading causes of hospital-acquired bloodstream infections, especially among patients in intensive care units.
The patient population most susceptible includes those with compromised immune systems, such as individuals undergoing chemotherapy or those with chronic diseases. Premature infants are also at high risk. The presence of foreign material in the body creates a surface for the bacteria to colonize, making patients with implanted medical devices highly vulnerable. CoNS species, particularly S. epidermidis, are responsible for a large percentage of infections associated with devices like central venous catheters, prosthetic joints, shunts, or artificial heart valves.
How CoNS Causes Infection
The primary mechanism by which CoNS causes device-related infection is the production of a biofilm, a complex, protective matrix that shields the bacteria from the host’s immune system and antibiotics. Biofilm formation is a multi-stage process that begins when free-floating bacterial cells initiate adherence to a surface. This initial attachment is often non-specific and is mediated by bacterial surface proteins binding to host proteins coating the device.
Following initial adherence, the cells begin the accumulation phase, where they proliferate and form multilayered microcolonies. During this time, the bacteria secrete a slimy, extracellular polymeric substance (EPS), which acts as the “glue” for the community. For many CoNS strains, this matrix is largely composed of polysaccharide intercellular adhesin (PIA), which facilitates cell-to-cell binding and creates a robust physical barrier.
The final stage is maturation, where the biofilm develops into a structured, three-dimensional architecture. Bacteria encased within this mature matrix exhibit significantly reduced metabolic activity and are shielded from immune cells like phagocytes, making the infection extremely difficult to eradicate. This protective structure is the reason why CoNS infections linked to devices are so persistent and challenging to treat.
Management and Treatment of CoNS Infections
A major challenge in treating CoNS infections is the widespread prevalence of antibiotic resistance within the species. Most CoNS strains associated with healthcare settings are resistant to methicillin and other penicillin-related antibiotics. This methicillin resistance is similar to that found in MRSA (S. aureus), often leading to the term MRSE when referring to methicillin-resistant S. epidermidis.
Because of this high rate of resistance, the primary treatment for serious CoNS infections is often the intravenous antibiotic vancomycin. Alternative agents for resistant strains or for patients who cannot tolerate vancomycin include linezolid and daptomycin. However, the bacteria’s ability to form a biofilm means that antibiotics alone frequently fail to clear the infection completely.
The physical removal of the infected foreign material is often necessary to achieve a full cure, particularly in cases involving prosthetic joints or cardiac devices. Without source control, the bacteria within the biofilm can continue to shed, causing persistent infection despite prolonged antibiotic courses. For less severe infections, a combination of antibiotics and specialized antibiotic lock therapy may be attempted.