Tag: Infectious Diseases and Antimicrobial Stewardship

Nuggets of Knowledge: When to treat a urinary candidiasis or a catheter tip-isolated positive Candida culture, and osteomyelitis tidbits

I have a patient who, after a bout in ICU and after 3 weeks of hospitalization, had Candida albicans growing in the urine (with no flank pain, or urinary urgency or discomfort), and also on her central venous catheter tip (only growing in 1 of 2 bottles). She has a Foley in and suffers from urinary incontinence. She also presents with symptoms of an URTI (query HAP query COPDE) However, blood cultures are negative in all bottles. Do you treat with fluconazole?
Risk factors for candiduria: elderly, female, indwelling urinary device, on broad-spectrum ABX, diabetes.
IDSA says: if blood cultures are positive, then definitely treat. However, asymptomatic candiduria is NOT treatable unless neutropenic, an infant, or will undergo urologic surgery. In other patients, treatment does NOT affect mortality. Definitely try and pull the Foley!
Data is lacking regarding negative blood cultures and positive cath tip cultures: data from this paper would seem to indicate that you would NOT treat just a positive cath tip culture. Given that this patient also does not present with symptoms of a UTI (she has urinary incontinence at baseline), it would seem that fluconazole treatment is NOT warranted.
UPDATE (Oct 21): so I found out that it is “common practice” to treat for 2 weeks after central catheter removal with an echinocandin (if you don’t know it’s an azole-susceptible Candida sp.) or fluconazole (if indeed Candida albicans). I guess it is playing it safe – catheter tip in the blood…treat AS IF it is a candidemia.

Osteomyelitis XR and CT “language”
– “Periosteal reaction” = usually means new bone is growing from destructed old bone due to either injury or infection
– “Osteolysis” = can be from inflammatory etiology or malignancy
– “Subperiosteal abscess” or “subcutaneous gas” = anaerobic involvement

In diabetic patients only, a probe to bone of an infected wound automatically means that the patient has osteomyelitis. No imaging is necessary.

Also learned that wound care nurses can be your best friend on an ID or AMS service…look for the “wet ones” to be infected, and “dry eschar” or the like to be infection mimics! Of course though, always correlate with clinical status and imaging.


Nuggets of Knowledge: CAP radiography, beta-lactams, 5th generation cephalosporins,and atypical coverage

Few things learned today…

Causative organisms and imaging
– Staphylococcus aureus 
is not a common cause of CAP, but one is at higher risk if a patient had influenza prior to developing a pneumonia
– S. aureus pneumonia can be correlated with cavitations (indicating an abscess) on a CXR…but then again, cavitations could also reflect group A strep or S. pneumoniae pneumonia.
– Combined with risk factors of course, Pseudomonas aeruginosa pneumonia could be gathered by bronchiectasis on the CXR

Atypical coverage is only warranted if one feels that the host immune system will not be able to overcome such an infection, such as in the case of immunocompromised patients, or those with structural lung disease.

Beta-lactams and coverage of a CAP
– High-dose amoxicillin (1 g PO TID) is only recommended if intermediate Strep is suspected…and local resistance rates indicate that it is not a worry here
– Risk factors for a beta-lactam resistant Strep pneumo: patient <2 or >65 yo, beta-lactam therapy within last 3 months, alcoholism, medical comorbids, immunosuppressed, exposure to child in daycare centre.
– For outpatients only: amoxicillin, amoxi/clav, cefuroxime are all acceptable alternatives. IDSA guidelines recommend adding a macrolide or doxycycline for atypical coverage, but practically, only if immunocompromised or structural lung disease is present.
– For inpatients: cefotaxime, ceftriaxone, ampicillin. Respiratory FQs ONLY USED FOR TRUE BETA-LACTAM ALLERGY.

Haemophilus influenzae can produce beta-lactamases. Which cephalosporins and penicillins overcome these enzymes?
Cefuroxime is more active than cefazolin to H. influenzae and M. catarrhalis that produce beta-lactamases
– 3rd generation cephalosporins are distinguished by stability against beta-lactamases of Gram-negative bacilli

Ceftaroline is a 5th gen cephalosporin with activity against MRSA, VISA, and S. pnuemoniae resistant to penicillin or CTX. It does NOT cover ESBL, Pseudomonas aeruginosa, Acinetobacter baumanii, or B. fragilis

Goals and Objectives: Infectious Diseases and Antimicrobial Stewardship rotation

Goal #1: Develop a framework and approach to assessing the patient with a suspected infection. Objectives to meet this goal:
– Develop a head to toe approach to evaluating whether the patient actually has an infection or not
– Know the common clinical and radiographical presentations for pneumonia, cellulitis, infective endocarditis, sepsis, UTI, septic arthritis, and osteomyelitis.
– Develop a monitoring plan to assess drug therapy for each intervention made during my time on the AMS service.

Goal #2: Begin to have a framework for correlating clinical presentation to specific microbiological etiologies. Objectives to meet this goal:
– For each infectious syndrome, where it is possible, acquire knowledge on distinguishing factors on radiography or clinical presentation that would differentiate between different causative pathogens.
– Attempt to interpret dictations from 1-2 X-rays or CT scans, i.e. “pulmonary infiltrates”, “ground glass lesions”, per day.

Goal #3: Develop a convincing yet professional approach to communicating interventions from Antimicrobial Stewardship to physicians and other health professionals who are most responsible for the patient.
– Practice, practice, practice. Become involved in that aspect of the service.
– Incorporate pharmaceutical teaching into interventions.

Nuggets of Knowledge: Upper GI bleeds, splenic infarcts and abscesses

Upper GI bleeds (UGIB) – I always thought that the colour of the stool is a good indicator of whether it is an UGIB or lower GIB (LGIB). However, I learned that it wasn’t a sensitive indicator, although it can aid in the diagnosis. General management for a non-variceal bleed is as follows:

Non-variceal bleed:
– IV PPI (increases gastric pH –> stabilizes blood clots –> improves survival). Is intermittent dosing better, or continuous infusion better? This meta-analysis seems to say that there is a 28% RRR (2.64% ARR) for re-bleed within 7 days for intermittent dosing, although the results were pooled from a variety of intermittent regimens.
– Prokinetics: only warranted if endoscopy is needed to rule in or rule out UGIB. Erythromycin 3 mg/kg IV over 20-30 mins, 30-90 mins pre-procedure.
– Somatostatin and octreotide: clinical efficacy proven, but PPIs and prokinetics (with endoscopy) are much cheaper and there is more clinical experience.

Splenic infarcts and abscesses: when are antibiotics indicated?
Splenic INFARCTS: due to a whole bunch of different diseases, such as underlying cancer, embolic disease (such as A-fib or IE), splenomegaly, trauma. Treat the underlying cause.
Splenic ABSCESS: usually results from an endocarditis. May be accompanied by left-sided pleural effusion. This requires drainage + antibiotics +/- splenectomy. Usually the abscess is polymicrobial – usually E coli, Streptococcus spp, Enterococcus spp, and anaerobes.

Nuggets of Knowledge – when is Pneumocystis pneumonia prophylaxis warranted in a non-HIV infected patient?

I notice that quite a few of the patients I have encountered so far in Clinical Orientation and my 1st patient on my Oncology rotation are on SMX/TMP for PCP prophylaxis. It begged the question: when is it warranted? According to this meta-analysis, if the risk is >6%, you give prophylaxis. Which conditions warrant this type of risk? Should all cancer patients receive it?

– Cancer patients who SHOULD receive PCP prophylaxis: HL, NHL, brain tumours, myelodysplasia, ALL, lymphoproliferative dz, or myeloma, relapsed dz, “high-dose” corticosteroids, or R-CHOP-14 regimen
– Treatment with 20 or more mg prednisone equivalent for 1 month or more
– Alemtuzumab or temozolomide recipients
– Allogenic and select autologous (w/purine analogue conditioning Tx) HCT recipients
– Solid organ transplant recipients

There are a few SMX/TMP regimens… DS tab daily, DS tab qMWF, SS tab daily… there isn’t much direction to choose one. There was an RCT in HIV-infected patients that wasn’t statistically significant for daily SMX/TMP, but there was roughly 2x more discontinuation due to ADRs from the daily group.

I’ve personally seen DS tab qMWF most but it all depends on patient-specific factors such as adherence and recent lab work!

Nuggets of Knowledge – July 31st hodge podge: warfarin bridging, lumbar puncture findings, and ID tidbits

When to NOT bridge warfarin with LMWH following a procedure (low risk)
– Laprascopic surgery
– Dermatologic procedures
– Ophthalmologic procedures
– Colonoscopies
– Bone marrow aspirate and biopsy, lumbar punctures
– Thoracentesis

CSF findings that would raise suspicion of viral encephalitis (not meningitis)
– Increased WBC but <250/mL
– Increased protein but <150 mg/dL
– Normal glucose (decreased with herpes simplex)
– RBC usually absent, but positive in HSV-1 or if contaminants present

Gram-negative bacilli may be divided into fermenters and non-fermenters.
Fermenters can be found in GI/GU: 
E. coli, Proteus mirabilis, Klebsiella spp.
Non-fermenters (skin, resp, GU): Pseudomonas aeruginosa, Acinetobacter spp., Legionella pneumophila

Acinetobacter susceptibilities follow Pseudomonas susceptibilities closely!

And while I’m at it..
Gram-negative cocci
– Neisseria gonorrhoeae
– Neisseria meningitidis
– Moraxella catarrhalis
– Haemophilus influenzae

Nuggets of Knowledge – Intro to Infectious Diseases

Few tidbits from the ADS on ID.

  • Presence of polymorphonuclear cells (PMNs) indicates inflammation
  • Beware of epithelial cell contamination in a sample
  • Coagulase-negative Staphylococcus spp is often a contaminant of blood cultures
  • A C&S will NEVER have PO susceptibility data due to concerns with bioavailability. Consult microbiology if you need direction.
  • Eosinophilia increases suspicion of allergic reactions or parasitic infections
  • Lymphocytosis increases suspicion of malignancy or bacterial infections
  • Acute phase reactants are non-specific but add to the overall picture
  • Pearl: cellulitis treated with ABX will appear to worsen for 2-3 days due to killing of bacteria and subsequent release of endotoxins
  • Some antibiotics perform poorly in acidic environments, so therefore will not penetrate and treat an abscess.
  • When do you consult microbiology?
    • Need more specific identification on an organism
    • Need additional susceptibility or MIC data
    • Need guidance on which test to use to identify a bug

And of course, this fun gem:


Vancomycin tapering for C. difficile

I found this one to be interesting, and involved some digging into EMR. The patient was in for C. difficile associated diarrhea (CDAD), and was the first instance that I could see on Meditech (since 2010 at least), and was on vancomycin 125 mg PO QID since the 28th (closing in on one week). The order read as follows:

vancomycin 125 mg PO TID x 2 days (starting Jul 5th) then
vancomycin 125 mg PO BID x 3 days then
vancomycin 125 mg PO daily x 2 days then stop.

Immediately I thought that I better look into it as I was unfamiliar with taper regimens for PO vancomycin. What I found was that there really is not that much evidence to support taper regimens despite it appearing on UpToDate and some clinical guidelines, and taper regimens are only recommended under guidelines for the 2nd recurrence. In addition, it was the patient’s first bout with C. difficile as far as we knew; in that case what is recommended is either metronidazole 500 mg PO TID or vancomycin 125 mg PO QID x 14 days, if severe (see the paper above for more details). I decided to write it in the clinical book that the pharmacy had, describing my concerns so that the clinical pharmacist could reassess and follow up. It was a good opportunity to delve a bit deeper into an order and try and make an intervention from the dispensary.

QTc prolongation + Torsades de Pointes risk stratification and management

For this Nugget of Knowledge, I put several tags on it because I think I will be referring to it on multiple rotations…I just picked the ones that I suspect it will come in most handy.

Probably not the first thing that comes to mind when one thinks about drug distribution, but always a thing to keep in mind on a dispensary shift if a patient is on a bunch of QT prolonging drugs – how do you know who is at higher risk than another? Today I attended a CSHP webinar on this very topic; here are some pearls I picked up:

FDA and Health Canada definition of a prolonged QTc
>500 ms OR >60 ms above baseline

Beware of the hypos – K, Mg, and Ca

Risk stratification tool #1 – Tisdale et al – validated in cardiac critical care units
– Assigns varying point values to different risk factors
– Offending DRUGS are given more weight than say, hypokalemia
– Great positive predictive value for high risk individuals
– They did not routinely measure magnesium levels
– However, only predicts risk of prolonged QT, NOT TdP or any hard outcomes such as mortality.

Risk stratification tool #2 – Haugaa et al with the Mayo Clinic – not validated, but had patients across the board: peds, medicine, cardiology, ICU, you name it
– EQUAL weighing of risk factors
– Hard outcome: mortality
– Good predictive value of mortality for scores 4 or above
– ONLY valid for baseline QTc of 500 ms or greater

These tools are great for stratifying patients according to risk and will help me prioritize interventions. As always I would perform NESA on each offending drug (or each option to treat a condition) to see if it is worth the risk. Also, downloaded the CredibleMeds app onto my phone – a great tool to quickly look up rough risk levels for various medications to prolong the QT interval.