Is candida in the urine a true UTI?

Maybe. Likely not.

You may see Candida growing because of a chronic in-dwelling urinary catheter, instrumentation/urologic procedures, contamination, or because of a true UTI or even bloodstream infection.

If the patient has a catheter, remove it and see if the Candida persists. If it cannot be removed, replace it with a new one.

Asymptomatic candiduria should only be treated in high-risk populations: neutropenic patients and those undergoing surgery or urinary tract procedures. Also, if the patient has dysuria, then it should be treated. Most strains are susceptible to fluconazole so this is a first-line agent.

Should I stop vancomycin if my patient has a negative MRSA swab?

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Having the time of his life with a MRSA nasal swab…from the New York Times story “A Bug Rises, and With It a Company” 2008

“If your patient has a negative MRSA nasal swab, and you are using vancomycin to empirically cover hospital-associated pneumonia, you can stop the vanc.”

Yes!!! It turns out this is true. There was a study in 2014 from Arizona that looked at how MRSA nasal swab results correlated with MRSA pneumonia: “The MRSA PCR assay demonstrated 88.0% sensitivity and 90.1% specificity, with a positive predictive value of 35.4% and a negative predictive value of 99.2%.” This means that although a positive MRSA swab doesn’t mean your patient will get MRSA pneumonia, if they are negative for MRSA, there is an excellent chance that they will not have MRSA pneumonia and so empiric vancomycin is not indicated unless there are extenuating circumstances. This was also seen in an earlier study.

What about stopping vancomycin for empiric treatment of other infections, like cellulitis? That is more contentious. There is evidence to suggest that very few cases of MRSA infection would be missed if MRSA-negative patients did not receive vancomycin, but many would argue that it is more important to treat any possible MRSA infection.

Interesting aside: another study looking at rates of MRSA disease found that patients can still develop MRSA infections even if their nasal swab is negative though: “nearly a third of MRSA-infected patients were not nasally colonized, suggesting that nasal colonization need not precede disease and that a negative test for nasal colonization would not rule out MRSA disease in settings of moderate or high prevalence.”

What is the treatment course for HSV meningitis, and when can you switch from IV to PO regimen?

Although there is a pretty standardized regimen for someone with HSV encephalitis–10 mg/kg per dose every eight hours for 14-21 days– the regimen for HSV meningitis is less clear. Specifically, one question: when can you switch over from IV acyclovir to PO valacyclovir (Valtrex)?

PO valacyclovir, although converted through first-pass metabolism into acyclovir, is less able to penetrate the CNS than IV acyclovir. There are no clear guidelines, but a good rule of thumb is that someone with HSV meningitis should receive at least 7 days of IV acyclovir before being evaluated for a PO regimen of valacyclovir or acyclovir.

NB: HSV PCR is the diagnostic test of choice for HSV encephalitis or meningitis. However it may lose its sensitivity after the first week of infection. PCR > viral culture in terms of sensitivity and specificity.

Treating fungemia

The first step, even before starting treatment, is to identify who would be at risk for fungemia. Risk factors include neutropenia, being in the ICU, on TPN, on broad spectrum antibiotics, long-time central-line. Fungus in the sputum or urine may be a red herring, but fungus in the blood is NEVER normal.

Treating fungus depends on what kind it is. The major strains include:

  • Candida albicans
  • C. glabrata
  • C. krusei (which is virtually fluconazole-resistant)

If a patient without risk factors at an institution where <15% are fluconazole resistant, it’s safe to treat with fluconazole. However, if not, then micafungin or even the terrible amphotericin B may be used.

P.S.- patients with fungemia should get a formal ophthalmology consult!

Peaks and troughs and vanc dosing

When do you get a vanc trough? What about a peak? What does it mean, anyway?

Vancomycin is a renally cleared drug used to treat serious infections. A vanc TROUGH is obtained when you expect the patient to be treated for a serious/life-threatening infection, to be treated with other nephrotoxic medications at the same time, or to be treated for >4 days. A trough should be obtained within 30 mins before the 4th dose.

A vanc PEAK is obtained less frequently, when high penetration of a hard-to-reach space is required (osteomyelitis or endocarditis). It should be obtained an hour after vanc finishes infusing.

A RANDOM vanc level should only be obtained in patients on dialysis or with severe renal disease.

How do I use the MIC to determine what antibiotic to use?

Let’s say you order sensitivities for an organism thought to be causing a UTI and you get:

URINE CULTURE:
ESCHERICHIA COLI. 10,000-100,000 ORGANISMS/ML..
Cefazolin interpretative criteria are based on a dosage regimen of 2g every 8h.

SENSITIVITIES: MIC expressed in MCG/ML
AMPICILLIN————=>32 R
AMPICILLIN/SULBACTAM– 16 I
CEFAZOLIN————- <=4 S
CEFEPIME————– <=1 S
CEFTAZIDIME———– <=1 S
CEFTRIAXONE———– <=1 S
CIPROFLOXACIN——— =>4 R
GENTAMICIN———— <=1 S
MEROPENEM————- <=0.25 S
NITROFURANTOIN——– <=16 S
PIPERACILLIN/TAZO—– <=4 S
TETRACYCLINE———- =>16 R
TOBRAMYCIN———— <=1 S
TRIMETHOPRIM/SULFA—- =>16 R
VANCOMYCIN———— 1 S

The MIC (minimum inhibitory concentration) is a measurement of how much antibiotic is required to stop growth of an organism. The smaller the number is, the more effective the antibiotic is. Generally speaking, the smaller the MIC, the more likely it is to treat the infection and prevent resistance from developing.

However, be warned that the drug with the smallest MIC does not always win–this Medscape article explains that MIC is calculated differently for different drugs depending on whether they are concentration or time-dependent, so the MIC for say, Cipro and Zosyn may not be directly comparable. Also, some drugs will not penetrate certain sites–for instance, nitrofurtantoin (Macrobid) is frequently used for uncomplicated UTIs but cannot be used to treat pyelonephritis because of its penentration.

When do you put a patient on “double coverage” for Pseudomonas?

When a patient is really sick or you don’t know exactly what they have, it’s tempting to throw whatever you can at them. It’s terrifying to think that you might not be protecting a patient adequately when you have the chance.

Double coverage for Pseudomonas plays into this fear. It usually refers to the use of an anti-Pseudomonal, such as Zosyn (beta-lactam) PLUS a fluoroquinolone or aminoglycoside or even second beta-lactam, such as meropenem. Sometimes patients with severe sepsis or who are on ventilators are put on double coverage just to “cover all the bases.”

But research doesn’t support the empiric use of double-coverage.  The only situations where “upfront” double coverage is justified is in neutropenic patients or patients on a ventilator at risk for ventilator-associated pneumonia where organism sensitivities are NOT known. If you do decide on double covering a patient, use a beta-lactam and aminoglycoside because that is the only combination there is good evidence for. Once sensitivities return, you should think more about how to practice good antibiotic stewardship and narrow the antibiotics!