Looking through the positive blood cultures in the morning, the Microbiology Registrar noticed a set positive for Staphylococcus lugdenensis. There were no clinical details on the request form but checking the patient’s blood tests showed a high white blood cell count and C-reactive protein. There was clearly something going on so the registrar gave the ward team a call. The team said the patient was being treated for pyelonephritis with Gentamicin but further questioning revealed that they also had a prosthetic aortic valve. The registrar wondered whether the patient might have infective endocarditis but the team weren’t convinced at first. The registrar explained the risks and suggested repeating the blood cultures as well as asking the Cardiologists for an opinion about the possible diagnosis.
What is S. lugdenensis?
S. lugdenensis, first identified in 1988, is a catalase-positive Gram-positive coccus. It is in the same group as other coagulase negative staphylococci (CoNS) such as S. epidermidis (because it is tube coagulase negative) however it in fact has more in common with the more virulent S. aureus than the CoNS organisms (see previous blog). Like S. aureus, S. lugdenensis is both slide coagulase positive due to the presence of “clumping factor” and also produces proteins that allow it to acquire iron from haemoglobin, which increases its virulence.
S. lugdenensis is a classic microbiology FRCPath Part 2 exam organism because inexperienced examinees can be caught out by assuming it is not pathogenic because it is not S. aureus.
S. lugdenensis has a particular ability to stick to heart valves and blood vessels walls by attaching to von Willebrand factor; a blood protein whose specific function is to bind other proteins together e.g. it plays a major role in blood coagulation and is important in platelet adhesion to wound sites. Von Willebrand factor also binds to collagen in damaged endothelial cells of blood vessel walls and heart valves and then binds to platelets forming clots, hence the association between S. lugdenensis and infective endocarditis.
How does infection with S. lugdenensis present?
As one of the CoNS S. lugdenensis is most commonly seen as a skin contaminant in blood cultures however it has been described as causing infections in bones and joints, IV devices, urinary catheters and also infective endocarditis (IE). Only 1-2% of all IE is caused by S. lugdenensis but the mortality from untreated IE is 100% so it is important not to miss the diagnosis or this causative pathogen.
Watch out for it…the classic FRCPath Part 2 exam question is a patient with S. lugdenensis in their blood culture who turns out to have IE.
How many patients with S. lugdenensis in their blood have IE?
If patients have a single blood culture positive for S. lugdenensis (bacteraemia) then 15% have IE. Compare this to S. aureus where the rate of IE in patients with a single positive blood culture is about 11-13%. Having positive blood cultures with either of these bacteria essentially carries the same risk for IE! If they have two separate blood cultures positive with S. lugdenensis then the rate increases to 25%! That’s a huge percentage in microbiology terms, so I’m left questioning why don’t I routinely request echocardiography for S. lugdenensis bacteraemia?!?
The modified Duke’s criteria for the diagnosis of infective endocarditis are made up of major and minor criteria. The microbiological major criterion is a typical microorganism from 2 or more sets of blood cultures, ideally more than 12 hours apart. The typical microorganisms referred to are: viridans streptococci, S. aureus, Streptococcus gallolyticus (formerly known as S. bovis) and HACEK bacteria (see blog). Yep, there is no mention of S. lugdenensis and yet this is as likely to cause IE as S. aureus! So maybe the “modified” Duke’s criteria need modifying again?
How is S. lugdenensis IE treated?
In contrast to many of the CoNS which are resistant to antibiotics, S. lugdenensis is almost always sensitive to the beta-lactams. In the UK we tend to follow the British Society for Antimicrobial Chemotherapy (BSAC) guidelines:
S. lugdenensis, first identified in 1988, is a catalase-positive Gram-positive coccus. It is in the same group as other coagulase negative staphylococci (CoNS) such as S. epidermidis (because it is tube coagulase negative) however it in fact has more in common with the more virulent S. aureus than the CoNS organisms (see previous blog). Like S. aureus, S. lugdenensis is both slide coagulase positive due to the presence of “clumping factor” and also produces proteins that allow it to acquire iron from haemoglobin, which increases its virulence.
S. lugdenensis is a classic microbiology FRCPath Part 2 exam organism because inexperienced examinees can be caught out by assuming it is not pathogenic because it is not S. aureus.
S. lugdenensis has a particular ability to stick to heart valves and blood vessels walls by attaching to von Willebrand factor; a blood protein whose specific function is to bind other proteins together e.g. it plays a major role in blood coagulation and is important in platelet adhesion to wound sites. Von Willebrand factor also binds to collagen in damaged endothelial cells of blood vessel walls and heart valves and then binds to platelets forming clots, hence the association between S. lugdenensis and infective endocarditis.
How does infection with S. lugdenensis present?
As one of the CoNS S. lugdenensis is most commonly seen as a skin contaminant in blood cultures however it has been described as causing infections in bones and joints, IV devices, urinary catheters and also infective endocarditis (IE). Only 1-2% of all IE is caused by S. lugdenensis but the mortality from untreated IE is 100% so it is important not to miss the diagnosis or this causative pathogen.
Watch out for it…the classic FRCPath Part 2 exam question is a patient with S. lugdenensis in their blood culture who turns out to have IE.
How many patients with S. lugdenensis in their blood have IE?
If patients have a single blood culture positive for S. lugdenensis (bacteraemia) then 15% have IE. Compare this to S. aureus where the rate of IE in patients with a single positive blood culture is about 11-13%. Having positive blood cultures with either of these bacteria essentially carries the same risk for IE! If they have two separate blood cultures positive with S. lugdenensis then the rate increases to 25%! That’s a huge percentage in microbiology terms, so I’m left questioning why don’t I routinely request echocardiography for S. lugdenensis bacteraemia?!?
The modified Duke’s criteria for the diagnosis of infective endocarditis are made up of major and minor criteria. The microbiological major criterion is a typical microorganism from 2 or more sets of blood cultures, ideally more than 12 hours apart. The typical microorganisms referred to are: viridans streptococci, S. aureus, Streptococcus gallolyticus (formerly known as S. bovis) and HACEK bacteria (see blog). Yep, there is no mention of S. lugdenensis and yet this is as likely to cause IE as S. aureus! So maybe the “modified” Duke’s criteria need modifying again?
How is S. lugdenensis IE treated?
In contrast to many of the CoNS which are resistant to antibiotics, S. lugdenensis is almost always sensitive to the beta-lactams. In the UK we tend to follow the British Society for Antimicrobial Chemotherapy (BSAC) guidelines:
Initial Therapy |
Antibiotic |
Native valve |
IV Flucloxacillin 2g QDS (6 x per day if weight >85kg) |
Prosthetic valve |
IV Flucloxacillin 2g QDS (6 x per day if weight >85kg) PLUS PO Rifampicin 300-600mg BD PLUS IV Gentamicin 1mg/kg BD |
Duration of treatment: 4 weeks for native valves and 6 weeks for prosthetic valves.
It is important to get the treatment of S. lugdenensis IE right as even with adequate antibiotics the mortality is approximately 35-40%. Guess what? That’s about the same as S. aureus again… S. lugdenensis really does need to be added to those typical microorganisms in Duke’s criteria!
So what should we recommend for these patients?
I think we should make the same recommendations for patients with S. lugdenensis bacteraemia as we do for S. aureus. ALL PATIENTS should have a second set of blood cultures taken, ideally without giving antibiotics (as antibiotics will make the subsequent blood cultures negative). Patients should be discussed with a Cardiologist and consideration should be given as to the likelihood of IE and whether echocardiography to look for vegetations is indicated.
If IE is confirmed or is clinically very likely (e.g. presence of a prosthetic valve) then antibiotic treatment should be started according to the BSAC guidelines.
The Microbiology Registrar continued to follow up the patient. The patient did get repeat blood cultures taken but as they were already on antibiotics these did not grow any bacteria! However, the patient was referred to the Cardiologists who performed a transthoracic echocardiogram the next day which showed the presence of a large vegetation on the prosthetic aortic valve confirming infective endocarditis. The patient was started on appropriate antibiotics but unfortunately developed heart failure and had to undergo replacement of her heart valve. She did eventually make a full recovery but was in hospital for several months.
It is important to get the treatment of S. lugdenensis IE right as even with adequate antibiotics the mortality is approximately 35-40%. Guess what? That’s about the same as S. aureus again… S. lugdenensis really does need to be added to those typical microorganisms in Duke’s criteria!
So what should we recommend for these patients?
I think we should make the same recommendations for patients with S. lugdenensis bacteraemia as we do for S. aureus. ALL PATIENTS should have a second set of blood cultures taken, ideally without giving antibiotics (as antibiotics will make the subsequent blood cultures negative). Patients should be discussed with a Cardiologist and consideration should be given as to the likelihood of IE and whether echocardiography to look for vegetations is indicated.
If IE is confirmed or is clinically very likely (e.g. presence of a prosthetic valve) then antibiotic treatment should be started according to the BSAC guidelines.
The Microbiology Registrar continued to follow up the patient. The patient did get repeat blood cultures taken but as they were already on antibiotics these did not grow any bacteria! However, the patient was referred to the Cardiologists who performed a transthoracic echocardiogram the next day which showed the presence of a large vegetation on the prosthetic aortic valve confirming infective endocarditis. The patient was started on appropriate antibiotics but unfortunately developed heart failure and had to undergo replacement of her heart valve. She did eventually make a full recovery but was in hospital for several months.
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