Tag: Infectious Diseases and Antimicrobial Stewardship

ADS – Antifungal Review

This was an imposing topic with lots to cover – it’s great that there weren’t any pictures of Mucor spp. infections – not for the weak of stomach!

In a way, I find mycoses therapeutics to be more straightforward than bacterial infection therapeutics – however, monitoring is more complex with the antifungals, what with therapeutic drug monitoring added to the mix. It was helpful for me to review the risk factors associated with invasive candidiasis, as empiric fluconazole is started on some patients destined for ICU, but it’s always a judgement call whether empiric antifungal coverage is warranted.

Overall, it was a good overview of antifungal susceptibilities and empiric treatment – I had certainly forgotten some of them since undergrad (and I had barely seen any fungal infections during my time on the AMS service).

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ADS – Nephrology

This ADS was a good reminder of the main things that one may encounter in a CKD or ESRD patient dependent on HD or PD. It was a bit of a challenge digging out what I learned during the renal elective in undergrad, and all the antibiotic recommendations for line infections in HD and peritonitis in PD… some take-homes I got:

  • The ferritin target is higher in HD vs non-HD patients (including PD)
  • For MBD: lower the PO4, lower the iPTH, lower the Ca, but DON’T raise the Ca unless the patient is symptomatic.
  • The contraindication of malignancy in patients receiving ESAs depends on the type of malignancy – solid tumours are at higher risk
  • Double-cephalosporin coverage is recommended as first line for peritonitis in PD
  • Fluconazole 100 mg PO daily is recommended as fungal prophylaxis if the patient has had peritonitis in the past, has had exposure to broad spectrum ABX recently, had recent GI surgery, or is immunocompromised
  • Vancomycin +/- gentamicin (if unstable) is recommended for HD catheter-related infections – I assume the vancomycin is preferred over cefazolin because it would cover Enterococcus faecium.

 

Reflections on ID and Antimicrobial Stewardship

I honestly had so much fun on the antimicrobial stewardship service. Apart from learning all about diagnostics, assessing fluid samples, shadowing wound care, attending microbiology rounds, and having a process to assess infection, I think where I grew the most on this rotation was communicating with the medical team. This rotation forced me to be 100% comfortable with my recommendations (at least when it came to antibiotics) and it was valuable for me to be thrown right in and defend those recommendations. Goals and objectives. Did I meet them?

Goal #1: Develop a framework and approach to assessing the patient with a suspected infection. I think I achieved this – for a variety of infections (CNS, SSTI, pulmonary source, endocarditis, GI source, cystitis and pyelonephritis, C diff) I became familiar with how a diagnosis of an infectious process is reached.

Goal #2: Begin to have a framework for correlating clinical presentation to specific microbiological etiologies. Although this is not always possible, in the case of pneumonia or cellulitis, sometimes one can have a higher pre-test probability of a suspected bug based on radiological findings or clinical presentation. See Nuggets of Knowledge for more.

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. Yep. Definitely feel better about this. It was helpful for me to bounce recommendations off Michelle and have her play the physician. What if the response is “my patient got better on antibiotics”, but you feel like the patient does not even have an infection? What if the response is “I’m gonna keep him on vancomycin ‘just in case'”, even though the patient has never swabbed positive for MRSA and doesn’t have any other risk factors?

C3.5 R2: Prepare and deliver educational seminar to pharmacists (#3)

As part of my Antimicrobial Stewardship rotation, I delivered a presentation on aggressive (4.5 g IV q6h) versus non-aggressive (3.375 g IV q6h or 4.5 g IV q8h) dosing of pip/tazo for Pseudomonas infections in adult patients without CF and with good renal function. I decided to focus my presentation on a few sources of infection. This presentation triggered a lot of debate among the pharmacists, which was good to see.

What I thought I did well on this presentation:
– Tackled a topic that had a lot of grey to it! I think I never expected the evidence to be great but it was new for me to draw clinical conclusions based on the level of data I encountered
– I thought I was more prepared with questions from the audience compared to my Medicine presentation, although Michelle and Tien (the ID fellow with us on rotation) had to jump in on occasion.
– My pace was more relaxed, and I did not feel like I was rushing through the presentation

What to work on for next presentation, and BC-wide:
– Need to refine slides to make them more viewer-friendly, especially when going over large amounts of literature
– Need to be more clear on conditions of my recommendations and rationale, i.e. HAP vs VAP, same source, same bugs…therefore same dose!
– Be more economical with what I say, versus what appears on the slides. People need to listen as well as read!

My slides

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

Edit (Nov 3rd, 2017): More pneumonia radiography and clinical pearls:
Anatomically, the right side of the bifurcation from the trachea is superior to the left side…so naturally, bacteria take the path of least resistance and end up in the right lower lobe for the typical consolidation one sees on the CXR
– The CXR will usually lag behind clinical signs and symptoms by a day…so if a patient is a quick presenter to ED, sometimes you can’t visualize the consolidation until you repeat the CXR a day later!
– Depending on local resistance rates, at St Paul’s, levofloxacin covers Pseudomonas, and usually a cipro susceptible strain will be levo susceptible (levofloxacin has the added advantage of covering usual CAP bugs whereas cipro poorly covers Streptococcus pneumoniae).
– The reverse cannot be said – levo susceptible strains are not necessarily cipro susceptible
– Cipro resistant strains may be levo susceptible…but you will need to call your micro lab to get that info.

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