How long should I treat my patient with urinary tract infection and E. Coli bacteremia?

Although traditionally 7 to 14 days of antibiotic therapy has been recommended for Gram-negative bacteremia, more recent studies suggest that shorter antibiotic treatment courses are as effective as longer treatments for a variety of infections, particuarly those due to Enterobacteriaceae (eg, E. Coli, Klebsiella sp) in patients with low severity illness (1). 

Keep in mind that short course therapy may not apply to all patients with UTI and bacteremia, such as those with prostatitis (not included in the most recent study [1,2]), which requires longer course of antibiotics (3)

 
A 2019 randomized-controlled study involving primarily patients with bacteremia caused by E. Coli or Klebsiella sp. (~75%) with most cases associated with UTI (~70%) found that 7 days was as effective as 14 days of treatment in hemodynamically stable patients who are afebrile for at least 48 hours without an ongoing focus of infection (1). More specifically, there was no significant difference between the 2 groups in the rates of relapse of bacteremia or mortality at 14 or 28 days.

 
An accompanying editorial concluded that “7 days of treatment may be sufficient for hospitalized, non-critically ill patients with Gram-negative bacteremia and with signs of early response to treatment” (4)  Again, the accent should be on hemodynamically stable patients who respond rapidly to treatment. 

 
Bonus Pearl: While on the subject of shorter course antibiotic therapy, a 2016 “mantra” article nicely summarizes more recent suggestions for common infectious disease conditions (5). Obviously, clinical judgment should be exercised in all cases.
• Community-acquired pneumonia                               3-5 days (vs 7-10 days)
• Nosocomial pneumonia                                                 8 days or less (vs 10-15 days)
• Pyelonephritis                                                                  5-7 days (vs 10-14 days)
• Intraabdominal infection                                             4 days (vs 10 days)
• COPD acute exacerbation                                             5 days or less (vs >6 days)
• Acute bacterial sinusitis                                               5 days (vs 10 days)
• Cellulitis                                                                            5-6 days (vs 10 days)

 

 

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References
1. Yahav D, Franceschini E, Koppel F, et al. Seven versus 14 days of antibiotic therapy for uncomplicated Gram-negative bacteremia: A noninferiority randomized controlled trial. Clin Infect Dis 2019; 69:1091-8. https://academic.oup.com/cid/article/69/7/1091/5237874       2. Yahav D, Mussini C, Leibovici L, et al. Reply to “Should we treat bacteremic prostatitis for 7 days”.  Clin Infect Dis 2010;70:751-3. DOI:10:1093/cid/ciz393.

3.  De Greef J, Doyen L, Hnrard S, et al. Should we treat bacteremic prostatitis for 7 days? Clin Infect Dis 2020;70:351https://academic.oup.com/cid/article-abstract/70/2/351/5488067?redirectedFrom=fulltext
4. Daneman D, Fowler RA. Shortening antibiotic treatment durations for bacteremia. Clin Infect Dis 2019;69:1099-1100. https://academic.oup.com/cid/article-abstract/69/7/1099/5237877?redirectedFrom=fulltext
5. Spellberg B. The new antibiotic mantra: “ Shorter is better”. JAMA Intern Med 2016;176:1254-55. https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2536180

How long should I treat my patient with urinary tract infection and E. Coli bacteremia?

My patient with history of intravenous drug use has noticed excessive growth of thick hair at the site of a previous abscess on her arm. Is there a connection between skin and soft tissue infections and localized hypertrichosis?

Localized hypertrichosis after infectious rash or “HAIR”, has been reported following a variety of skin and soft tissue infections (SSTIs), including sites of previous septic thrombophlebitis, cellulitis and olecranon bursitis. 1,2  A similar phenomenon has also been described in infants with recent chicken pox, as well non-infectious skin conditions arising from repeated irritation, friction, burns, excoriated insect bites, and fractures with cast application.1,2

Although heat and hyperemia have been implicated as growth stimulants for the hair follicle, 3 the exact mechanism of this intriguing phenomenon is unclear. It is possible that the sustained inflammatory process associated with chronic or more severe SSTIs leads to protracted stimulation of certain growth receptors in the human hair follicles (eg, transient vanilloid receptor-1) through heat and inflammation, as observed in mice in vivo.4

Aside from its possibly undesirable esthetic effects, localized HAIR appears to have no adverse health consequences, is reversible, and should require no further evaluation.

Note: 2 of the publications cited were written by the author of this post.

References

  1. Manian, FA. Localized hypertrichosis after infectious rash in adults. JAAD Case Reports 2015; 1:106-7. https://www.jaadcasereports.org/article/S2352-5126(15)00051-X/pdf
  2. Manian, FA. Localized hypertrichosis after infectious rash (“HAIR”) in adults: a report of 5 cases. Open Forum Infect Dis 2014;1 (Suppl 1):S195-S195. http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC5782143&blobtype=pdf
  3. Leung AK, Kiefer GN. Localized acquired hypertrichosis associated with fracture and cast application. J Natl Med Assoc 1989;81:65-7. https://www.ncbi.nlm.nih.gov/pubmed/2724357
  4. Bodo E, Biro T, Telek A, et al. A hot new twist to hair biology; involvement of vanilloid receptor-1 (VR1/TRPV1) signaling in human hair growth control. Am J Pathol 1005;166:985-8. https://www.sciencedirect.com/science/article/pii/S0002944010623206

 

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My patient with history of intravenous drug use has noticed excessive growth of thick hair at the site of a previous abscess on her arm. Is there a connection between skin and soft tissue infections and localized hypertrichosis?

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

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)?

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?

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?