Staphylococcus lugdunensis

Staphylococcus lugdunensis. It is a coagulase-negative species of the genus Staphylococcus first described in 1988 by a team led by Jean Fréney from samples isolated in Lyon, France. Unlike many of its less virulent coagulase-negative relatives, it is notable for causing aggressive, abscess-forming infections that can mimic those of Staphylococcus aureus. Its clinical recognition is crucial as it exhibits unique antibiotic susceptibility patterns and possesses a distinct arsenal of virulence factors.

Microbiology and identification

This bacterium is a gram-positive, coccus-shaped organism that grows in clusters and tests negative for the enzyme coagulase, a key test that traditionally distinguishes it from Staphylococcus aureus. It is often identified in clinical laboratories using automated systems like VITEK or MALDI-TOF, but it can be preliminarily recognized by several phenotypic traits. These include a positive pyrrolidonyl arylamidase (PYR) test, which it shares with Staphylococcus aureus and Enterococcus species, and the production of a characteristic "clumping factor" that can cause slide coagulase tests to be falsely positive. Colonies on blood agar typically exhibit a strong, sweet odor and may display a narrow zone of beta-hemolysis, resembling the hemolysis of Streptococcus pyogenes.

Clinical significance

Despite being part of the normal skin flora, particularly in the inguinal and perineal regions, it is an emerging and aggressive pathogen. It is most infamous for causing severe infective endocarditis, which carries a high mortality rate and often requires urgent surgical intervention, similar to cases caused by Staphylococcus aureus. Beyond cardiac infections, it is frequently isolated from skin and soft tissue infections such as abscesses, cellulitis, and wound infections. It has also been implicated in osteomyelitis, septic arthritis, and vascular catheter-related bacteremia, demonstrating a broad pathogenic potential that challenges its historical classification as a mere contaminant.

Virulence factors

The pathogenicity is mediated by a collection of potent virulence determinants. A key factor is the lugdunin operon, which encodes a novel, non-ribosomally synthesized cyclic peptide antibiotic called lugdunin that also functions as a virulence factor, promoting colonization and competition. It produces a fibrinogen-binding adhesin similar to the clumping factor of Staphylococcus aureus, facilitating attachment to host tissues and medical devices like prosthetic heart valves. The organism also secretes a broad-spectrum bacteriocin and several hydrolytic enzymes, including a DNase and a lipase, which contribute to tissue invasion and abscess formation. Unlike Staphylococcus epidermidis, it generally does not produce slime or a prominent biofilm on polystyrene.

Epidemiology

It is a commensal inhabitant of human skin, with colonization rates highest in the inguinal and perineal areas, and lower on the anterior nares compared to Staphylococcus aureus. Infections are typically community-acquired or associated with healthcare settings, often following breaches in the skin barrier from surgery, intravenous catheters, or trauma. There are no known large-scale outbreaks linked to this organism; infections are generally sporadic. Its true incidence is likely underestimated due to frequent misidentification in clinical laboratories as other species like Staphylococcus aureus or Staphylococcus haemolyticus.

Treatment and antimicrobial resistance

Fortunately, it remains largely susceptible to a wide range of antibiotics, which distinguishes it from many other coagulase-negative staphylococci like Staphylococcus epidermidis. Most isolates are susceptible to penicillin-derivatives such as oxacillin, anti-staphylococcal penicillins, and glycopeptide antibiotics like vancomycin. Resistance to methicillin, mediated by the mecA gene, is rare but has been documented in isolates from locations like Taiwan and the United States. First-line therapy for serious infections like endocarditis often involves a beta-lactam antibiotic such as nafcillin or cefazolin, sometimes combined with an aminoglycoside like gentamicin for synergy.