An aerobic gram positive cocci; forms clusters. Staphylococcus aureus is coagulase positive. Staphylococcus argenteus is a Staphylococcus species closely related to Staphylococcus aureus (Pubmed) but rarely causes disease.
The rest are coagulase negative: S. auricularis, S. capitis, S. caprae, S. cohnii, S. epidermidis, S. haemolyticus, S. intermedius, S. hominis, S. lugdunensis, S. pasteuri, Staphylococcus pseudointermedius, Staphylococcus pettenkoferi, S. saccharolyticus, S. saprophyticus, S. schleiferi, S. simulans, S. warneri, S. xylosus. With a MALDI-TOF you may get to know which one it is.
Being human. Use of needles will increase staph carriage and subsequently the risk of infection. From an ID perspective, there is little difference between a diabetic, a dialysis patient, and a heroin user. Sounds like the start of a joke. A diabetic, a dialysis patient, and a heroin user walk into a bar and the heroin user says...
The nose is way over-rated as a place to find the new colonization of MRSA (see below). It is more likely to be found in the retropharynx (PubMed) or the intestines (PubMed), so a bit of mupirocin in the nose is a waste of time. Besides which, mupirocin resistance is increasing and almost 10% (PubMed).
But if colonized there is a 20x higher risk of bacteremia compared with non-colonized (Pubmed).
MRSA lasts longer than most relationships: "the half-life time (HLT) of MRSA persistence was 549 days, with the duration of persistence dependent on the colonization of different anatomical sites (HLT only wounds 117 days; HLT mouth, throat, bronchial secretions 627 days; HLT nose, wounds and other body sites 801 days; and was prolonged if more than one body site was MRSA-positive (PubMed)." Although another study fourn "found that median duration of colonization was 21 days, and 19.8% of index patients remained colonized at the end of the 6-month study period. Increased age was associated with longer duration of MRSA colonization in index patients. Clindamycin treatment of MRSA SSTI, on the other hand, was associated with earlier clearance of colonization (PubMed)."
As of 2011, it looks like rather than supplanting MSSA, MRSA is adding to the burden of Staphylococcal infections (PubMed). Which is annoying as resistant organisms are supposed to be less fit in an antibiotic free environment. Not so with MRSA
While they may get MRSA bacteremia or infection in the hospital, it is usually from the bug they brought into the hospital from the community (PubMed).
And it can be found in the pork and beef in Georgia, suggesting the people in Georgia don't wash their hands (PubMed). Not you Tim.
S. aureus infections may be more common in the summer. Sweat as a growth factor?
Here is weirdness: exposure to cigarette smoke makes MRSA more virulent (PubMed).
If you have ever wondered with MRSA came from, the genes probably originated in the widespread coagulase negative Staphylococcus sciuri, where "results suggest that it was exposure to β lactams in humancreated environments that has driven evolution of native PBPs towards a resistance determinant." ID is all about applied evolution (PubMed).
Coagulase negative staphylococcus
Part of the human skin. There are different strains on each part of the body. S. lugdunensis, for example, likes to live below the waist (A male bacteria?) especially on the big toe.
- S. intermedius is a zoonosis, mostly from dogs.
- Staphylococcus pseudointermedius is a cause of skin disease in dogs and cats and can be spread to their masters to cause cellulitis (Pubmed).
- Endocarditis. It is the preeminent organism (PubMed). I like that. Preeminent, for both hospital acquired and community acquired disease and as a reason for death. If you don't fear the staph, at least respect the staph.
- Bacteremia. Community acquired S. aureus bacteremia without a focus IS endocarditis. Once in the blood stream it loves loves loves to cause an infection elsewhere. Any pain deserves a radiologic look see. S. aureus in the urine is due to bacteremia (30% probability), not the source of bacteremia; read that sentence again until you get it right. Also, when S. aureus bacteremia seeds the urine, it is often associated with vertebral osteomyelitis (PubMed). It has about a 20-30% chance of seeding prosthetic joints (PubMed). And if the bacteremia persists, it is a bad thing with about a 2.5x mortality (PubMed).
Who needs an ECHO for S. aureus bacteremia? The guidelines say everyone, and preferably a TEE. Seems stupid overkill to me, especially if they have the stigmata of endocarditis. So why even bother being a doctor? But what if they do not have stigmata of endocarditis, a clinically uncomplicated bacteremia? A depressing number of patients will have a vegetation on TEE that will not be clinically evident (PubMed) and a TTE will miss many a vegetation seen by TEE (PubMed).
Like all medicine, ECHO's are best used judiciously. I tend to get ECHO's if I will do something with the result: if I really need to know if I am treating left vrs right sided endocarditis or I am looking for complications. For example, everyone with a pacer or a prosthetic valve with S aureus bacteremia because if the TEE is positive you have to seriously consider taking it all out, not a trivial intervention. And ID docs do use judgement on occasion and not get TEE's (PubMed).
One study suggests that if the patient has NONE of the following (prolonged bacteremia (> 4 days), the presence of a permanent intracardiac device (eg, a prosthetic heart valve, pacemaker, or cardioverter-defibrillator), hemodialysis dependency, spinal infection (eg, vertebral osteomyelitis, epidural, subdural or intraspinal empyema, or abscess), and nonvertebral osteomyelitis) they have low risk of endocarditis (PubMed)(PubMed). Yet, if the patient has any of the preceding, would you let a negative ECHO stop you from treating as if endocarditis? Not me.
And in low risk patients, a TTE is probably enough "A normal TTE ruled out IE in patients without community-acquired SAB, high-risk cardiac conditions, and intravenous drug use (PubMed)." For hospital acquired SAB, a lack of prosthetic intracardiac device, hemodialysis or positive blood cultures for 4 days or more has a very low chance of IE and therefore does not need an ECHO (PubMed).
- Line related bacteremia. There is at least a 20-30% chance that S. aureus from a line will go elsewhere, such as a valve. A TTE will miss 20% of vegetations that are found on subsequent TEE.
Patients with decreased susceptibility to vancomycin (MIC >= 1.5) are more likely to go on to develop (PubMed).
Pay attention here: if the catheter tip is positive for Staphylococcus aureus BUT the blood cultures are negative, 24% of patients will have a subsequent S. aureus bacteremia; if promptly treated the risk of bacteremia is decreased 84% (PubMed)(PubMed). This is not true for other organisms (PubMed).
Peripheral iv's may be the source of hospital staph bacteremias in 7-8% and it is the prior, not current, iv site (Pubmed).
Persisting bacteremia after the line is pulled is a bad thing, more common with methicillin resistance, renal failure, and non-catheter prosthetic devices (PubMed). Sustained bacteremia is the sine qua non of endocarditis.
- Toxic Shock Syndrome. Usually occurs after surgery (often within 48 hours) or with tampon use. Classic is TSS with nasal packing, the tampon equivalent. The wound never looks infected. It still has to be debrided
- Post operative infections of all kinds, especially when prosthetic material is involved. Most of the time it is the patients, not the hospitals, Staph. Pre-op decolonization will decrease the risk of infection.
- Necrotizing infections of all kinds. Soft tissue and lungs predominating; often due to strains that carry the Panton-Valentine leukocidin. The 'nice' thing about serious S. aureus infections is that they can occur in anyone at anytime for no good reason.
When should you worry about MRSA as a cause of CAP?
"MRSA pneumonia was observed more frequently in patients with a previous history of MRSA infection (OR = 6.05; P < 0.001), a PSI score ≥120 (OR = 2.40; P = 0.015), intravenous antibiotic treatment within 30 days of pneumonia (OR = 2.23; P = 0.018) (PubMed)."
If the cultures and nasal swab are negative for MRSA it is reasonable to stop antibiotics (PubMed). This is especially true for VAP.
Coagulase negative Staphylococcus
Infections of prosthetic material of all kinds. Not removing the source in bacteremia increases mortality (PubMed). Community acquired S. lugdunensis is usually endocarditis and a common cause of cellulitis (PubMed), (PubMed). Hospital acquired is more likely to be methicillin resistant with poorer outcomes (Pubmed).
Is the coagulase negative in the blood real? No one ever really know (PubMed). With no intravascular prosthetic material, extremely unlikely, and 1/2 sets usually crap as well. One study suggests it is the real deal if "the patient has at least 3 SIRS criteria or 2 SIRS criteria and a central venous catheter (PubMed)." Other studies suggest that you are only fooling yourself if you think the clinical parameters are of help (PubMed).
In one hospital, S. haemolyticus, S. capitis, S. hominis, and S. lugdunensis in the blood were more often the real deal (PubMed).
- UTI. S. saprophyticus is the #2 cause of outpatient cystitis in women in their child bearing years. I don't think so, I have seen one or two positive cultures in my career, but that's the literature and the board question.
Staphylococcus pseudointermedius: dog bite. Can be mistaken as S.aureus (PubMed).
Important Basic Concepts>
Here are some pearls for that, if taken to heart, may prevent your ID doc from rolling her eyes as she reads the chart AND improve patient care. While rules are made to be be broken, it is just not by you.
Never. Ever. Never. Ever treat S. aureus in the blood culture as a contaminant. That’s a big never with a side of ever. Even if ‘just’ one bottle is positive. For S. aureus there is no ‘just’.
Never. Ever. Never. Ever treat S. aureus bacteremia with oral antibiotics. Note the never here is cleverly combined with the ever to give a sense of an absolute.
Only treat MSSA with anti-staphylococcal beta-lactams. The top 10 options are cefazolin, oxacillin, cefazolin, oxacillin, cefazolin, oxacillin, cefazolin, oxacillin, cefazolin or oxacillin. On rare occasions you can give cefazolin or oxacillin. Cephalexin is the oral option.
If you prefer a 'Never. Ever. Never. Ever'. to an 'only': Never. Ever. Never. Ever use vancomycin, tmp/sulfa, clindamycin, doxycycline or a quinolone for the treatment of MSSA. They lead to markedly inferior outcomes. Allergies notwithstanding of course, although most of the alleged beta-lactam allergies aren’t if you take a careful history.
For MRSA? All options stink on ice. But for bloodstream infections Never. Ever. Never. Ever use tmp/sulfa, clindamycin (the beloved choice of surgical house-staff), doxycycline or a quinolone. Yes I know there is a big ’S’ next to the antibiotic. Sometimes it stands for ‘Sucks’.
Now for the details
This is the classic organisms where in vitro susceptibility may not result in in vivo results. Beware (i.e. know what the hell you are doing). Assuming susceptible, the order for treating S. aureus infections intravenously is nafcillin / oxacillin, OR cefazolin, then anything else. For MSSA bacteremia, treatment with vancomycin has a 35% higher mortality (PubMed). Never, ever use vancomycin for MSSA without a damn good reason.
I was always told that nafcillin was slightly superior to cefazolin based on no data. I was skeptical but followed the wisdom of my elders. Turns out may not be true. Cefazolin was equal to anti-staph penicillins, yet cheaper and fewer side effects (PubMed). This has been confirmed in a meta-analysis (PubMed). And there is one study to suggest decreased mortality (not statistically different) in those who get cefazolin(Pubmed) (PubMed). and cefazolin seems fine for SAB (PubMed).
That being said, I still tend to go with nafcillin for infections where I cannot get good source control. Some S. aureus make beta-lactamses that can kinda sorta degrade cefazolin (PubMed) and clinically there is no way to tell.
As I write this I am uncertain what the best drug is if you cannot use a beta-lactam, but I suspect the order is (NOT based on comparative clinical trials) ceftaroline >= daptomycin = vancomycin > linezolid and I tend to use less linezolid more from its side effects than lack of efficacy. One systematic review gives a cure rate for ceftaroline of 74% (PubMed). A quarter fail. Meh. That's barely better than vancomyin.
For bacteremia, linezolid is probably inferior (PubMed) and I would not use a static drug for bacteremia.
Nothing is better at killing S. aureus than a beta-lactam (if sensitive, duh). Remember, only idiots think vancomycin is 'strong' or 'big gun'. In this era of MRSA is may be best in severe infections to have patients on a beta-lactam AND vancomycin pending sensitivities and then drop the one (PubMed).
And there is this issue of tolerant S. aureus, where the MBC is much higher than the MIC and the organism is nice to the underprivileged. Tolerant staph doesn't die as easy, unlike tolerant ideas (PubMed).
And never ever use rifampin as monotherapy.
And even in 2011 I see the occasional patient put on po vancomycin for some sort of MRSA infection, seriously dude, it you are that clueless, time to pack it in. Vancomycin has zero po absorption, it is only used po for C. difficile.
Vancomycin resistance is still rare, (PubMed) but the MIC to vancomycin is slowly creeping up. It is interesting in that if you treat MSSA bacteremia initially with vancomycin and change to a beta-lactam, you have a higher mortality than if you started with a beta-lactam (PubMed). With real sick patients it MAY be better to start with nafcillin AND vancomycin. while awaiting the susceptibilities.
And to make it even more confusing, patients who get a beta-lactam with their vancomycin for their MRSA bacteremia have better cure rates (PubMed). MRSA ain't simple. But if you really really suspect S. aureus, give a beta-lactam AND vancomycin and stop which every one appropriate when sensitivities return (PubMed).
And curiously, when the MSSA has increased MIC to vancomycin, the patients do worse on a beta-lactam; so there is something about the increase in the vancomycin MIC that makes the bug less easily killed by antibiotics (PubMed).
And to make life annoying you can have a Staph that is mecA by PCR, but be MSSA when tested to antibiotic. It may be that the organism contains only part of the resistance gene, but some can revert to MRSA (PubMed).
Lets talk MRSA (methicillin resistant Staphylococcus aureus. I hate it when people say mursa) for a moment. Pull up a chair and have yourself a beer.
First. If it is MRSA, it is resistant to all beta-lactams, no matter what the in vitro testing says. It is due to a new chunk of DNA.
Second. There are two kinds of MRSA out there.
1) The old hospital strain with the mec A gene resistance gene and the new community USA 300 strain has the mecIV (go speed racer, go) resistance gene. There is also a mecC (Pubmed).
2) The new USA 300 strain that, as of November 2005, is sweeping the world. The USA 300 strain makes the Panton-Valentine leukocidin (maybe not the virulence factor it is cracked up to be) and causes plagues of boils, necrotizing soft tissue infections and hemorrhagic pneumonia. And death (PubMed).
3) MRSA is becoming the most common strain of S. aureus.
4) You can not distinguish soft tissue outpatient MRSA from MSSA on any clinical grounds (PubMed). Or coffee grounds.
5) As the MIC to vancomycin increases, so does the failure rate. Certainly if the MIC is >= 1.5, avoid vancomycin, and for all but the most trivial of MRSA infections (is there such a thing) I use a cutoff of 1.0 (PubMed)
For MRSA soft tissue abscess, and only abscess, not cellulitis, vancomycin AND clinidamycin leads to shorted hospital stays and less readmission (PubMed). It has also been noted that clinidamycin may be better at eradicating MRSA carriage.
Unfortunately ceftaroline was approved for cellulitis and pneumonia. The data that it works for more serious infections like MRSA are usually retrospective not comparative but it appears that "Of these patients, 88.9% (241/271) were infected with methicillin resistant S. aureus (MRSA). Clinically, 88% (426/484) achieved clinical success and hospital mortality was seen in 8% (40/527) (PubMed)".
Depending on the meta-anaylsis, linezolid is probably better than vancomycin (PubMed) (Pubmed) (Pubmed) and the trend suggests linezolid for pneumonia (PubMed) and the better outcomes may be due to suppression of toxins, at least in the mouse model (PubMed).
I am uncertain what the best drug is for MRSA, but I suspect the order is (NOT based on comparative clinical trials) ceftaroline > daptomycin =vancomycin > linezolid and I tend to use less linezolid more from its side effects than efficacy.
Pay attention here. It you are treating MRSA, especially if pneumonia or other serious deep infections, keep the vancomycin trough high, 15 or so, especially if the MRSA has an MIC to Vancomycin of 1 or 2 mcg/ml, which, while 'sensitive' do not do as well (PubMed, PubMed). Problem is, pushing the levels may increase the toxicity. And not all studies demonstrate worse outcomes with increased MIC's (Ref). One retrospective, post hoc, subgroup analysis suggested pushing the vancomycin trough did not improve outcomes, only increased toxicity (PubMed). But if I have learned anything in 30 years, it is that 'retrospective, post hoc, subgroup analysis' is synonymous with crap.
Is linezolid superior to vancomycin for pneumonia? Data keeps going back and forth with a 2010 meta analysis suggesting they are equally a piece of crap (PubMed). As of 2012, the preponderance of data and the best clinical trial (PubMed) point to the Slight superiority of linezolid for MRSA pneumonia with 10% higher cure rate but a similar 60 day mortality. But then a 2014 review suggests they are equal (PubMed). Sigh. The trend suggests linezolid for pneumonia (PubMed) and the better outcomes may be due to suppression of toxins, at least in the mouse model (PubMed). ALthough not supported by data, I tend towards linezolid when the MIC to vancomycin is >= 1.0, but I am hesitant for bacteremic MRSA infections off all sorts. For patients that are STS, I have been giving ceftaroline and either clindamycin or linezolid based on a hope and a prayer, which is something for an atheist.
Treat po with trimethoprim/sulfamethoxazole (give 1-2 DS tid depending on size and gfr (PubMed)
give 2-3 DS po tid although the one study suggests 1 SS bid is not better than 1 DS bid, with a 25% failure rate I'd say both are under-dosed (PubMed)) OR doxycycline (PubMed) or minocycline (which I always forget (PubMed)) or linezolid if they are wealthy. In my neck o' the woods cannot rely on clindamycin or quinolones as too much resistance.
Curiously, giving po cephalexin leads to higher failure rates for outpatient MRSA soft tissue infections (PubMed). That's sarcastic for the sarcasm impaired.
Remember, it is not JUST MRSA that has an increasing MIC to vancomycin, it is occurring in MSSA as well; 5.6% of MSSA will have in increased MIC's to vancomycin (PubMed), and increased MIC to vancomycin can lead to decreased daptomycin efficacy. And higher MICs to vancomycin are associated with increased failure of nafcillin for MSSA. Man, is treating staph a confusing mess or what?
And as the MIC to vancomycin and daptomycin increases, so does the risk for complications (PubMed)
But what do you do if there is failure of vancomycin or the MIC is 2? Maybe ceftaroline(PubMed), but note the last paragraph. Some, with minimal supporting data, are pushing daptomycin to 8-10 mg/kg/d but there are no comparative clinical trials. The best data, and it ain't that great, suggests linezolid PLUS a carbapenems is better than adding rifampin or an aminoglycoside (PubMed).
And here is a wild choice: use daptomycin plus nafcillin for MRSA (PubMed) failing vancomycin. Say what you ask? Per the CID article the combination "(1) restoration of in vitro DAP susceptibility of 1 DAP-R-VISA strain that emerged during therapy in ASBL (nafcillin or oxacillin)-containing media, (2) enhanced killing of this isolate by DAP plus ASBLs, (3) notable increases in DAP membrane binding after organism growth in ASBLs, and (4) reduction in net positive membrane surface charge by ASBLs that was more pronounced in the DAP-R strain, compared with the DAP-susceptible parent (PubMed)" and it worked in patients.
And another curious combination: daptomycin and ceftaroline "In vitro studies showed ceftaroline synergy against MRSA and enhanced MRSA killing by cathelicidin LL-37 and neutrophils. Ceftaroline also induced daptomycin binding in MSSA and MRSA to a comparable degree as nafcillin" (PubMed). Small series suggests efficacy.
Beware the heteroresistant (insert your own non-PC comment, I can't be expected to think of everything, now can I?) MRSA, which occurs in about 6% of MRSA. In heteroresistant strains, subpopulations will be intermediate to vancomycin, with prolonged fevers, bacteremia and worser cure rates (PubMed).
Linezolid is ANTAGONISTIC with vancomycin, gentamicin, and rifampin. Also, the higher the MIC to vancomycin, the more likely there will be daptomycin resistance, so, if you have a persisting staphylococcal bacteremia on vancomycin, recheck the resistance to daptomycin on the most recent isolate, since as you breed vancomycin resistance, you breed daptomycin resistance as well.
Daptomycin resistance can occur on therapy and it may be driven in part by platelet host defense peptides, which can select for resistance even before the beast sees daptomycin (PubMed). So therapy may be doomed before you even start therapy.
So then Clinical Infectious Diseases asks Is It Time to Replace Vancomycin in the Treatment of Methicillin-Resistant Staphylococcus aureus Infections? and they reply "Collectively, the current available data suggest that the optimal therapy for MRSA infections remains unclear", you can see why. I think the answer is mostly yes once the MIC to vancomycin hits 1.0.
Back to MSSA.
For oral therapy, a first generation cephalosporin (e.g. cephalexin) or dicloxacillin can be used. For the obese or when you want to obtain higher blood levels, both cephalexin and dicloxacillin can be given at 1 gram po qid. Never trust levofloxacin or ciprofloxacin, but gatifloxacin or moxifloxacin may have good enough MIC's to work, although misuse has already pissed these antibiotics away.
ALWAYS use a beta-lactam if you can. When MSSA is treated with vancomycin, outcomes are worse. Dialysis patients often get vancomycin for convenience instead of best MSSA therapy to their detriment (PubMed).
I am agnostic on the use of rifampin and its synergy. Certainly for all forms of prosthetic infections it needs to be added to increase cure rates, but for other infections I am not so sure it adds anything to MRSA or MSSA infections unless you are combining with a quinolone. A systematic review suggests it adds little (PubMed). Take that Steve. One exception may be MRSA pneumonia where the MIC is 1 or 2 to vancomycin; I am inclined to add rifampin. The medical literature can be used like a drunk uses a lightpost: for support not illumination. So anothermeta-analysis suggests increased survival for bacteremia with the addition of rifampin (PubMed). Just never ever use rifampin as monotherapy, resistance occurs almost instantly.
There is some data to suggest ceftriaxone works just as well (PubMed) and some data that it does not work as well as anti-staphylococcal beta-lactams. I am hesitant to use third generation cephalosporins unless there has been excellent source control/debridement. I.E. not I.E.
- Bacteremia: once S. aureus it likes to go places and set up infection. The MINIMAL duration of IV therapy for an uncomplicated bacteremia (from a line or cellulitis) is 14 days. If MRSA or any kind of poor host, increase it to 28 days. If it is a primary bacteremia, ie no source, they probably have endocarditis and need at least 28 days (PubMed)(PubMed).
As a rule give it 7 days for the patient to get better before considering a change in therapy; some suggest that should be 3-4 days (PubMed). Since I do such a good job of choosing initial therapy, that is rarely an issue. I kid.
Pay close attention: NEVER NEVER EVER NEVER treat S. aureus bacteremia with oral therapy. Never. Ever. And do NOT treat bacteremia with Clindamycin. Seriously, that is proof positive you are Dunning-Kruger personified. Get some help.
Everyone should get an ECHO, low risk patients ("Characteristics associated with a low risk of endocarditis include absence of a permanent intracardiac device, sterile follow-up blood cultures within 4 days after the initial set, no hemodialysis dependence, nosocomial acquisition of S aureus bacteremia, absence of secondary foci of infection, and no clinical signs of infective endocarditis.") can avoid a TEE (PubMed).
- Furuncle or Carbuncles. I&D, plus antibiotics po, let local susceptibilities by your guide. For MRSA boils, I&D plus trimethoprim/sulfamethoxazole was equal to I&D plus placebo for cure of acute disease, although the antibiotic group had less recurrence (PubMed). So drain. And do not just suck out the pus with a needle, compared to an I&D, 74% of needle aspiration FAILED vrs 20% of open I&D (PubMed). NEJM 2014 review.
Decolonization for recurrent disease:
- 2 weeks of mupirocin to nose and open lesions,
- 2 weeks of Hibiclens baths (PubMed),
- hot water/bleach all reused clothes and sheets, and no scratching after picking your nose usually aborts recurrent disease.
- It maybe necessary to treat family members (decreases infections in family members (PubMed)) or pets; I usually have the entire family Hibiclens, including the dog and cat which can carry MRSA.
- Women (and I suppose men) need to get all new make up, creams and ointments. That can cost far more than antibiotics.
- I have heard up to 20% the weight of an old pillow is made up of dead dust mites, their eggs, feces, and human skin flakes. Or so I have read on the internet. So new pillows for everyone.
- at least in kids, twice week bleach baths do nothing (PubMed).
Mupirocin is of proven benefit only for the dialysis patients, given that MRSA is everywhere, putting a dab in the nose would be expected to be of minimal efficacy. But doing all of the above works in 87% of patients. And there is the start of both mupirocin and hibiclens resistance (PubMed).
MRSA pneumonia: as of this writing (11/17/6) the recommendation is for vancomycin but push the trough to 15 mcg/ml. Whether this is of benefit is questionable (PubMed) and whether one should add rifampin or change to anther agent is unknown.
Is linezolid superior to vancomycin? Data keeps going back and forth with a 2010 meta analysis suggesting they are equally a piece of crap (PubMed). As of 2012, the preponderance of data and the best clinical trial (PubMed) point to the superiority of linezolid for MRSA pneumonia with 10% higher cure rate but a similar 60 day mortality. But then a 2014 review suggests they are equal (PubMed). Sigh.
Whether this is of benefit is questionable (PubMed) and whether one should add rifampin or change to another agent is unknown. Currently I lean towards adding rifampin; especially if the MIC is high (1 or 2 mcg/ml) BUT BUT BUT at the 2007 ICAAC a poster suggested rifampin increases failure rates and bacteremia and complications, so in the one study, it is toxic and antagonistic.
R sided uncomplicated disease, 4 weeks of nafcillin / oxacillin OR two weeks of nafcillin / oxacillin PLUS tobramycin. If MRSA then 4 weeks of vancomycin. Daptomycin (6mg/kg/d) for 4 weeks is non inferior to vancomycin for RIGHT sided endocarditis and bacteremia (PubMed).
Native Left sided disease is 6 weeks intravenous nafcillin/oxacillin, no need to give an aminoglycoside for more than 3 - 5 days. It will alter neither the morbidity or the mortality but they will clear the bacteremia and defervese faster; expect fever and bacteremia for a week after starting therapy. If resistant or intolerant of standard therapy, linezolid may be just as bad (71% success rate) (PubMed).
Aminoglycosides need only be used for first 3 to 5 days where they decrease the number of febrile days but no not decrease mortality or need for valve replacement. Gentamycin toxicity causes CrCr to decrease at a rate of 0.5% per day but does not adversely alter outcome (PubMed). Another study demonstrated that low dose gentamicin tripled the nephrotoxicity rate without altering outcomes (PubMed).
Rifampin probably only adds toxicity (PubMed). Persisting fevers should have a evaluation for myocardial abscess of other metastatic infectious complication (splenic abscess) before changing antibiotics for 'failure.'
Prosthetic valve endocarditis. Surgery probably the best bet (medical therapy has 70% death rate, surgical has 30% death rate), nafcillin / oxacillin (vancomycin ONLY if MRSA or allergy) PLUS gentamicin PLUS rifampin can be tried and will probably fail.
- Line related bacteremia. The minimum duration (pay attention here) of IV therapy is two weeks AFTER pulling the line. Do not try and salvage a line infected with S. aureus. You will fail and each subsequent bacteremia may seed elsewhere. Nafcillin / oxacillin is preferred over vancomycin (ONLY if MRSA or allergy. Listen up. If you use vancomycin for convenience instead of a beta-lactam, your outcomes will me worse.
Vancomycin stinks on ice (PubMed)). If you have MSSA and treat with vancomycin expect a higher failure rate and a slower response (Pubmed) And all beta-lactams that are not nafcillin or cefazolin are INFERIOR (PubMed).
BTW. I know its self serving, but multiple self-serving studies support superior outcomes if an ID consult is obtained (PubMed). Especially if I am the consultant. And, a phone consult isn't good enough (PubMed). And what kind of maroon gives another doc the liability without the chance to not get paid by medicare?
Daptomycin (6mg/kg/d) for 4 weeks is equal to vancomycin for RIGHT sided endocarditis and bacteremia. The problem with daptomycin is resistance develops on therapy in a significant number of patients (PubMed). Four weeks of a quinolone and rifampin is of equal efficacy, I am a tad chicken to do this, as I am to use trimethoprim/sulfamethoxazole despite one retrospective study (PubMed) that show it to be superior to vancomycin, but then, what isn't superior to vancomycin?
If you have to use vancomycin (which only a moron uses for convenience instead of a beta-lactam, or have I mentioned that?) or fevers last > 48 hours after pulling the line, or repeat blood cultures are positive, or patient has a prosthetic valve, or a diabetic, may need to go for 4 to 6 weeks of, lets say it again, intravenous antibiotics. There ain't nothin in infectious diseases that people screw up more than the treatment of line related staph aureus bacteremia.
-Toxic Shock Syndrome. Debride the wound. No matter that it will not look infected. If you don't debride the wound, the patient will die. Nafcillin / oxacillin OR cefazolin OR vancomycin to kill the bug PLUS clindamycin (900 q 8 to interfere with toxin production) PLUS IVIG to bind toxin (an area of controversy, but I am a believer).
- Post operative Infections. If possible debride. Orthopedic devices of all kinds may be salvaged with 6 weeks of IV Nafcillin / oxacillin OR cefazolin OR vancomycin PLUS rifampin followed by 6 months of po (preferably moxifloxacin ) PLUS rifampin.
Coagulase negative Staphylococcus
Positive blood cultures. Is it real? I do not know and neither do you (PubMed). The more blood cultures that are rapidly positive in patients with endovascular material, the more likely it is sigfificant.
Usually resistant to beta-lactams, vancomycin is the treatment of choice if MRSA. However, if beta-lactam susceptible, it is the drug of choice. Linezolid is also reliable BUT you want to really be irritated? Some Staphylococci require linezolid for growth (CDC).
- Infected central catheters. Can frequently be salvaged with declotting the catheter and 2 weeks of vancomycin through the line. I also use an alcohol lock a few times (25% ETOH in the line for 20 minutes).
- Prosthetic Infections of all kinds. If possible debride, orthopedic devices of all kinds may be salvaged with 6 weeks of IV vancomycin PLUS rifampin followed by 6 months of po something (preferably a quinolone) PLUS rifampin.
Staphylococci make dozens of toxins. I am increasingly intrigued with messing with toxin production in necrotizing, staph infections. If I had a patient with necrotizing pneumonia or soft tissue infection I would add clindamycin or doxycycline to the mix of antibiotics. This is a data free piece of advice, but there is a biologic plausibility (aka magical thinking).
One study suggested adding aminoglycosides decreased the odds of S. aureus bacteremia progressing to septic shock.
People really need to quit throwing vancomycin at the 1 out of four positive blood cultures; it is almost never of significance.
I am of the opinion that the world would be a better place if, upon awakening, more people would ask themselves, 'How can I make Mark Crislip's life better?" And it turns out the answer is simple: REPEAT THE DAMN CULTURES BEFORE STARTING VANCOMYCIN FOR GRAM POSITIVES IN THE BLOOD CULTURES. Sorry I metaphorically shouted there. But it gripes my cookies the number of times I am stuck with a 1/2 positive blood cultures for a staph or a strep and the patient is on antibiotics and I cannot repeat the cultures to help determine if it is real. Please. Make my life better. Repeat the cultures. Believe it or not, there is actually a study to show people needed reminding of such a simple concept: A recommendation to perform a blood culture before the administration of intravenous antibiotics increased the detection of Staphylococcus aureus bacteremia (PubMed). Doh.