Staphylococcus lugdunensis: Not Your Father’s (or Mother’s) Coagulase-Negative Staphylococcus

Special Feature

By Ellen Jo Baron, PhD, D(ABMM)

Staphylococcus lugdunensis, in contrast to the other skin and mucus membrane-colonizing coagulase-negative staphylococci, has virulence factors that closely resemble those of Staphylococcus aureus and consequently causes similar aggressively destructive infections. Because diagnostic microbiology laboratories are only just beginning to recognize the importance of this species, some clinically important isolates may go unrecognized.

Lugdunum is Latin for Lyon, France, where the organism was first characterized in 1989.1 Recent discoveries from French scientists have further differentiated the species.

In one event, a seemingly innocent change in a surgical technique, in which the incision was placed in the shaved pubic area for esthetic concealment, resulted in a dramatic increase in postoperative wound infections due to S lugdunensis. The resulting investigation revealed that 22% of incoming surgical patients carried the organism on the skin of the inguinal area.2 van der Mee-Marquet and associates reviewed previous case reports and found that a preponderance of S lugdunensis soft-tissue infections occurred below the waist (73% of all infections). Another recent study showed 69% of a series of S lugdunensis infections occurred in the pelvic girdle, all pointing to a perineal, pelvic girdle, or inguinal cutaneous source for the organism.3 In fact, there appears to be an association between perineal or inguinal skin breaks (vasectomy, femoral arterial catheterization, prostatic cancer) and subsequent development of S lugdunensis endocarditis.4,5 Endocarditis is one of several more serious types of infections, including brain abscess, osteomyelitis, peritonitis, and toxic shock syndrome, caused by this organism.6,7 The bulk of reports, however, associate S lugdunensis with skin and soft-tissue infections, such as breast abscess, furuncles, and others.

Endocarditis due to S lugdunensis resembles that caused by S aureus, with associated abscess formation and rapid progression. Most cases are community-acquired, which fits with predisposing factors, including vasectomy or other perineal or pelvic girdle site infection.4,7,8 A recent Stanford case and another report describe endocarditis following angiography.9,10 These case reports and studies emphasize the need for antimicrobial prophylaxis for "clean" perineal procedures, as several authors have suggested. Only one-fourth of endocarditis patients have prosthetic valves, again more similar to endocarditis caused by S aureus than that due to other coagulase negative staphylococci. Three-fourths of patients, however, have pre-existing cardiac abnormalities. Again, unlike endocarditis due to S epidermidis and more similar to that due to S aureus, symptoms typically present acutely within the first 2-3 weeks, with 50% of patients presenting with hemodynamic instability on admission and 25% of cases showing valvular destruction.4 The overall mortality rate associated with S lugdunensis endocarditis, despite appropriate antibiotics and surgical intervention as needed, is high, with estimates from 50% to 73% in the literature. One key difference between S aureus and S lugdunensis is the latter’s relative susceptibility to penicillins. Most strains are actually penicillin susceptible, in which case of course, penicillin is the drug of choice. Oxacillin (methicillin) resistance is so rare that it motivated a case report (the first to describe infection with a MRSL) when such an isolate caused a bloodstream infection in a neonate in Singapore.11 Of 59 clinical isolates evaluated in one study, all were susceptible to oxacillin, cephalothin, gentamicin, rifampicin, and vancomycin. Seventy-six percent of isolates were beta-lactamase negative, with penicillin G MICs < 0.13 microgram/mL.12

Both S lugdunensis and S aureus may harbor similar virulence factors such as an accessory gene regulator (agr) and ability to bind extra-cellular matrix protein.13,14 S lugdunensis is also similar to S aureus in that it is infrequently recovered as colonizer or contaminant.12 S lugdunensis is most commonly recovered from skin and skin structure infections followed by blood and vascular catheter infections.

Because S lugdunensis are typically slide-coagulase (clumping-factor) positive, they may be confused with S aureus on initial screening of colonies. Another coagulase-negative staphylococcus, S schleiferi, is also typically slide-coagulase positive. The tube coagulase tests for both S lugdunensis and S schleiferi, however, are negative. Laboratories should have a heightened suspicion for this species from serious infectious sites and sterile body fluids, and should use special tests, such as the pyrrolidonyl peptidase (PYR) test, which is positive, to differentiate this species from S aureus.15 Importantly, if staphylococci are placed immediately into liquid coagulase test tubes, this species may be misidentified as a conventional "coagulase-negative staphylococcus." Physicians may wish to check that their laboratories are aware of detecting this species and have appropriate methods in place.

As laboratories improve their ability to recognize S lugdunensis, we are becoming more aware of its role in serious infections and the need for aggressive early medical and surgical intervention.

Dr. Baron is Director of the Clinical Microbiology/Virology Laboratory and Professor of Pathology at Stanford University Medical School. She is an Editor of the Manual of Clinical Microbiology.

References

1. Freney J, et al. Int J Syst Bacteriol. 1988;38:168-172.

2. van der Mee-Marquet N, et al. Staphylococcus lugdunensis infections: High frequency of inguinal area carriage. J Clin Microbiol. 2003;41:1404-1409.

3. Bellamy R, Barkham T. Staphylococcus lugdunensis infection sites: Predominance of abscesses in the pelvic girdle region. Clin Infect Dis. 2002;35:E32-34.

4. Vandenesch F, et al. Endocarditis due to Staphyloccocus lugdunensis: Report of 11 cases and review. Clin Infect Dis. 1993;17:871-876.

5. Seenivasan MH, Yu VL. Staphylococcus lugdunensis endocarditis—the hidden peril of coagulase-negative staphylococcus in blood cultures. Eur J Clin Microbiol Infect Dis. 2003;22:489-491.

6. Paterson DL, Nuttall N. Serious infections due to Staphylococcus lugdunensis. Aust N Z J Med. 1997;27:591.

7. Fervenza FC, et al. Staphylococcus lugdunensis endocarditis: A complication of vasectomy? Mayo Clin Proc. 1999;74:1227-1230.

8. Lessing MP, et al. Native-valve endocarditis caused by Staphylococcus lugdunensis. QJM. 1996;89:855-858.

9. Poutanen S, et al. Clin Microbiol Newsletter. 2002.

10. Polenakovik H, et al. Staphylococcus lugdunensis endocarditis after angiography. Mayo Clin Proc. 2000;75:656-657.

11. Tee WS, et al. Staphylococcus lugdunensis carrying the mecA gene causes catheter-associated bloodstream infection in premature neonate. J Clin Microbiol. 2003;41:519-520.

12. Herchline TE, et al. Penicillinase production and in vitro susceptibilities of Staphylococcus lugdunensis. Antimicrob Agents Chemother. 1990;34:2434-2435.

13. Vandenesch F, et al. Agr-related sequences in Staphylococcus lugdunensis. FEMS Microbiol Lett. 1993;111:115-122.

14. Paulsson M, et al. Serum and tissue protein binding and cell surface properties of Staphylococcus lugdunensis. J Med Microbiol. 1993;38:96-102.

15. De Paulis AN, et al. Five-test simple scheme for species-level identification of clinically significant coagulase-negative staphylococci. J Clin Microbiol. 2003;41:1219-1224.