Month: October 2015

Should we treat asymptomatic candiduria?

FA Manian MD, MPH, Leave a comment

This is a common scenario among our hospitalized patients with indwelling catheters, prior antibiotic therapy or diabetes mellitus who seem to have no clinical signs of infection. Fortunately, candidemia from urinary sources appears uncommon to rare, with up to nearly ½ of patients clearing their candiduria with removal of the indwelling catheter alone (1). The Infectious Diseases Society of America guidelines do not recommended treatment of asymptomatic candiduria unless the patient belongs to a group at high risk of dissemination, such as severely immunosuppressed or neutropenic patients, infants with low birth weight, and patients who will undergo urologic manipulation (2).  Supporting such recommendation is a retrospective long-term follow-up of patients with candiduria demonstrating no significant improvement in rates of recurrences of candiduria or candidemia with treatment (3).  Fluconazole is usually considered the first-line agent of choice when treatment is indicated.  

1. Kauffman CA. Candiduria. Clin Infect Dis 2005;41:S371-6.

2. Pappas PG, Kauffman CA, Andes D, et al. Clinical Practice Guidelines for the Management of Candidiasis: 2009 Update by the Infectious Diseases Society of America. Clin Infect Dis 2009; 48:503–35.

3. Revankar SG, Hasan MS, Revankar VS, et al. Long-term follow-up of patients with candiduria. Eur J Clin Microbiol Infect Dis 2011;30:137-140.

Should we treat asymptomatic candiduria?

Should we routinely use broad spectrum empiric antibiotic therapy in our diabetic patients with cellulitis of the lower extremities?

FA Manian MD, MPH, , Leave a comment

The short answer is “No”!

The myth that diabetics with acute bacterial skin and skin structure infections should be routinely placed on antibiotics against gram-positives as well as gram-negatives and/or anaerobes probably originates from the extrapolation of data revolving around the frequent polymicrobial nature of diabetic foot infections.  These infections often originate from chronic ulcers and are complicated by deep tissue infection or gangrene (1), which is often not the case in our diabetic patients with cellulitis alone.  

In a recent study of the microbiology of cellulitis or cutaneous abscess in hospitalized patients, Staphylococcus and Streptococcus sp. accounted for 90% of cultured organisms in  diabetic patients, not significantly different than that of non-diabetics (1).

These finding support national guidelines which do not recommend routine use of broader spectrum antibiotics in diabetics with cellulitis or cutaneous abscess (2).  

References

1. Jenkins TC, Knepper BC, Moore SJ, et al. Comparison of the microbiology and antibiotic treatment among diabetic and nondiabetic patients hospitalized for cellulitis or cutaneous abscess. J Hosp Med 2014;9:788-794. https://www.ncbi.nlm.nih.gov/pubmed/25266293

2. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections. Clin Infect Dis 2014;59:e10-e52. https://www.ncbi.nlm.nih.gov/pubmed/24973422

Should we routinely use broad spectrum empiric antibiotic therapy in our diabetic patients with cellulitis of the lower extremities?

Is there any utility in screening for methicillin-resistant Staphylococcus aureus (MRSA) colonization when selecting empiric antibiotic therapy for skin and soft tissue infections (SSTIs)?

FA Manian MD, MPH, , Leave a comment

The reported rates of MRSA colonization in patients with community-associated MRSA SSTI have been surprisingly low, ranging from 7% to 41% (55% among hospitalized patients) (1), making it difficult to exclude MRSA as a causative pathogen based on a negative screening test alone.

The concordance between what grows from the nares and what is isolated from the SSTI site is also far from ideal.  Among patients with methicillin-sensitive S. aureus (MSSA) SSTI , 12% may be colonized with MRSA and of those with MRSA SSTI, 32% may be colonized with MSSA (1). 

In the absence of a reliable screening test to help us select an empiric antibiotic regimen in patients with SSTI, we should pay special attention to the clinical features of the SSTI.  Empiric MRSA antibiotic coverage should be considered for patients with purulent SSTIs, deep tissue infections, or those with systemic toxicity( 2), irrespective of colonization status.  

References

1. Ellis MW, Schlett CD, Millar EV, et al. Prevalence of nasal colonization and strain concordance in patients with community-associated Staphylococcus aureus skin and soft tissue infections. Infect Control Hosp Epidemiol 2014;35:1251-6. https://www.ncbi.nlm.nih.gov/pubmed/25203178  

2. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011;52:e18-55.2. https://www.ncbi.nlm.nih.gov/pubmed/21208910 

 

Is there any utility in screening for methicillin-resistant Staphylococcus aureus (MRSA) colonization when selecting empiric antibiotic therapy for skin and soft tissue infections (SSTIs)?

Should we routinely cover for methicillin-resistant Staphylococcus aureus (MRSA) when treating patients for cellulitis?

FA Manian MD, MPH, , , Leave a comment

No! Despite the MRSA epidemic, β-hemolytic streptococci (BHS) are still considered the primary cause of non-purulent cellulitis (e.g. without abscesses, or infections involving deep soft tissues, wounds, or ulcer).

In a prospective study of patients admitted to the hospital for “diffuse,  non-culturable “(i.e. many of our patients), most had serological evidence of acute  BHS, and >95% responded to a β-lactam antibiotic treatment (1) . 

The current Infectious Diseases Society of America guidelines do not endorse empiric coverage of  MRSA for non-purulent cellulitis,  unless there is systemic toxicity or poor response to  β-lactam  monotherapy (2). More specifically, the guidelines recommend a  β-lactam antibiotic for treatment of non-purulent cellulitis in hospitalized patients with modification to MRSA coverage if no clinical response.

One advantage to β-lactam monotherapy is the ease of switch to an equivalent oral antibiotic (e.g. cephalexin) when transitioning from parenteral antibiotic therapy.  

References

1. Jeng A, Beheshti M, Li J, et al. The role of beta-hemolytic streptococci in causing diffuse nonculturable cellulitis: a prospective investigation. Medicine (Baltimore) 2010;89:217-26. https://www.ncbi.nlm.nih.gov/pubmed/20616661

2. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011;52:e18-55. https://www.ncbi.nlm.nih.gov/pubmed/21208910

 

Should we routinely cover for methicillin-resistant Staphylococcus aureus (MRSA) when treating patients for cellulitis?

Besides malignancy, what other causes of cachexia should we usually consider in our hospitalized patients?

FA Manian MD, MPH, , , Leave a comment

Although cachexia , a loss of >5% body weight over 12 months,  has been reported in about 30% of patients with cancer, many other chronic conditions  commonly encountered in our hospitalized patients may also be a culprit.  In fact, cachexia is not infrequent in CHF (20%), COPD (20%), kidney failure (40%), or rheumatoid arthritis (10%) (1,2).  We also shouldn’t overlook HIV and tuberculosis as a cause.

Cachexia is a multifactorial disease which does not fully reverse with nutritional support.  Numerous mediators have been implicated, including cytokines such as tumor-necrosis factor-α, and interleukin [IL]-1 and -6, as well as transforming growth factors such as myostatin and activin A (2). 

In patients with CHF, angiotensin II appears to be a key mediator, associated with insulin resistance, depletion of  ATP in skeletal muscles, poor appetite, reduction in insulin-like growth factor-1 (IGF-1), and an increase in glucocorticoid and IL-6 levels.  All these factors contribute to “cardiac cachexia” through muscle wasting, reduced food intake and lower muscle regeneration. 

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References

  1. Morely JE, Thomas DR, Wilson M-M G. Cachexia: pathophysiology and clinical relevance. Am J Clin Nutr 2006;83:735-43. https://www.ncbi.nlm.nih.gov/pubmed/16600922
  2. Yoshida T, Delafontaine P. Mechanisms of cachexia in chronic disease states. Am J Med Sci 2015;35:250-256. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4587350/
Besides malignancy, what other causes of cachexia should we usually consider in our hospitalized patients?

Should corticosteroids (CS) be routinely considered in the treatment of hospitalized patients with community-acquired pneumonia (CAP)?

FA Manian MD, MPH, , Leave a comment

A recent systematic review on the subject concluded that for hospitalized adults with CAP, systemic CS may reduce mortality by about ~3% (primarily in severe CAP), mechanical ventilation need by ~5%, and hospital stay by ~1 day (1). But determining who might benefit the most and at what CS dosage regimen without undue risk of side effects (e.g. hyperglycemia) may be tricky.  

A randomized control trial of patients with CAP on prednisone 50 mg daily x 7d (vs placebo) showed a significant shorter time to clinical stability (3 vs 4.4 d) and higher in-hospital hyperglycemia in the CS group (2).; this study was not powered to detect significant difference in mortality, however.  Less treatment failure with adjunctive CS but without impact on mortality was recently reported in a small study involving patients with serum CRP >150 mg/L (i.e. high inflammatory state) (3).

Fortunately, a multicenter trial (ESCAPe, Extended Steroid in CAP) is currently underway. In the meantime, before considering CS, we need to be confident of the diagnosis and severity of CAP, its potential adverse effects in individual patients, and the appropriateness of the antibiotic (s) on board.

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References

1. Siemieniuk RAC, Meade MO, Alonso-Coello P, et al. Corticosteroid therapy for patients hospitalized with community-acquired pneumonia: a systematic review and meta-analysis. Ann Intern Med 2015;165:519-528. https://www.ncbi.nlm.nih.gov/pubmed/26258555

2. Blum CA, Nigro N, Briel M. Adjunct prednisone therapy for patients with community-acquired pneumonia: a multi-centre, double-blind randomized, placebo-controlled trial. Lancet 2015;385:1511-1518. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(14)62447-8/abstract

3. Torres A, Sibila O, Ferrer M, et al. Effect of corticosteroids on treatment failure among hospitalized patients with severe community-acquired pneumonia and high inflammatory response: a randomized clinical trial. JAMA 2015;313:677-86. https://www.ncbi.nlm.nih.gov/pubmed/25688779

 

Should corticosteroids (CS) be routinely considered in the treatment of hospitalized patients with community-acquired pneumonia (CAP)?

How should minimum inhibitory concentrations (MICs) reported by the microbiology lab be interpreted?

FA Manian MD, MPHLeave a comment

MIC is the minimum inhibitory concentration of an antibiotic (AB) that inhibits an organism invitro, By itself, MIC does NOT take into account the pharmacokinetics (PKs) or pharmacodynamics (PDs) of an AB which ultimately determine its susceptibility cut-offs.

“Susceptible” implies that the isolate is inhibited by the usually achievable concentrations of the AB when recommended dosage is followed for the specific site of infection. “Intermediate” suggests that the MIC approaches usually attainable blood and tissue levels but at less- than-desirable expected clinical response rates, and generally should be avoided when an alternative AB exists. “Resistant” refers to isolates that are not inhibited by the usually achievable AB concentrations. In the absence of PK/PD data, comparing MICs can be misleading (i.e. lower MIC does not necessarily suggest a more potent AB).

Short answer: you can generally skip the MIC data and make antibiotic selection based on susceptibility report alone.

Please also see a related pearl on P4P at https://pearls4peers.com/2016/12/19/when-should-i-pay-attention-to-the-minimum-inhibitory-concentration-mic-of-an-antibiotic-despite-the-lab-reporting-it-to-be-in-the-susceptible-range/

 

Reference

Turnridge J, Paterson DL. Setting and revising antibacterial susceptibility breakpoints. Clin Microbiol Rev 2007;20:391-408. https://www.ncbi.nlm.nih.gov/pubmed/17630331  

How should minimum inhibitory concentrations (MICs) reported by the microbiology lab be interpreted?