E.coli;

“I go after Streptococcus pneumoniae and many other bacteria causing community-acquired pneumonia with vengeance but lately I have had a hard time keeping up with many gram-negatives, including some E. coli. Who am I?”

FA Manian MD, MPH, , , , , , , , , , , , , , , , , , , , , , , , , , , Leave a comment

Additional hint: “The latest FDA warning against the use of my class of drugs has to do with increased risk of ruptures or tears in the aorta in certain patients, including the elderly and those with hypertension, aortic aneurysm or peripheral vascular disease.” 

Editor’s note: This post is part of the P4P “Talking Therapeutics” series designed to make learning about antibiotics fun. Individual antibiotics give a short description of themselves and you are asked to guess their names. Antimicrobial spectrum, common uses and potential adverse effects follow. Enjoy!

And the answer is…… HERE

Selected antimicrobial spectrum

                Gram-positives: Streptococcus pneumoniae, Staphylococcus aureus                         (some resistance even in MSSA), Enterococcus spp (urine;some resistance)

                Gram-negatives: Enterics (eg, E. coli, Klebsiella spp), Pseudomonas spp,                                 Stenotrophomonas maltophilia, H. influenzae, some ESBLs.

                 AVOID: MRSA, anaerobes

Common clinical uses: community-acquired pneumonia (CAP), healthcare-associated pneumonia (HAP), urinary tract infections (UTIs), legionnaire’s disease, abdominal infection (plus anaerobic coverage)

WATCH OUT! QT prolongation, C. difficile, central nervous system toxicity, seizures, myasthenia gravis, peripheral neuropathy, tendinopathy, drug interactions (eg. warfarin), and most recently aortic aneurysm diagnosis/dissection!

Remember the key features of levofloxacin before you prescribe it!

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Selected references

  1. FDA. FDA warns about increased risk of ruptures or tears in the aorta blood vessel with fluoroquinolone antibiotics in certain patients.  https://www.fda.gov/drugs/drug-safety-and-availability/fda-warns-about-increased-risk-ruptures-or-tears-aorta-blood-vessel-fluoroquinolone-antibiotics. Accessed Nov 26, 2020,.
  2. Marangon FB, Miller D, Muallem MS, et al. Ciprofloxacin and levofloxacin resistance among methicillin-sensitive Staphylococcus aureus isolates from keratitis and conjunctivitis. Am J Ophthal 2004;137:453-58. https://www.ajo.com/article/S0002-9394(03)01287-X/pdf
  3. Yasufuku T, Shigemura K, Shirakawa T, et al. Mechanisms of and risk factors for fluoroquinolone resistance in clinical Enterococcus faecalis from patients with urinary tract infections. J Clin Microbiol 2011;49:3912-16. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209098/
  4.  Rawla P, Helou MLE, Vellipuram AR. Fluoroquinolones and the risk of aortic aneurysm or aortic dissection: A systematic review and meta-analysis. Cardiovasc Hematol Agents Med Chem 2019;17:3-10. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6865049/

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

“I go after Streptococcus pneumoniae and many other bacteria causing community-acquired pneumonia with vengeance but lately I have had a hard time keeping up with many gram-negatives, including some E. coli. Who am I?”

Could my patient with acute dysuria and less than 10,000 E. coli/ml on urine culture still have a urinary tract infection (UTI)?

FA Manian MD, MPH, , , , , , , , Leave a comment

Absolutely! Although historically ≥100,000 bacteria/ml has been used as a criterion for UTI based on studies of women with pyelonephritis in the 1950s,1 several studies have since found that this criterion may not be met in up to 50% of symptomatic patients with UTI. 2-6 A lower criterion of 100-1,000 bacteria/ml of urine increases the sensitivity of urine culture to ~90% or more for diagnosis of UTI (albeit with lower specificity). 2-5

A 1982 NEJM study involving UTIs due to coliforms in acutely dysuric women found that the traditional count of ≥100,000 bacteria/ml in midstream urine missed ~50% of cases based on positive bladder cultures. 2 Similarly a 2013 NEJM study reported that 40% of women with symptomatic UTI would be missed if the ≥100,000 bacteria/ml criterion for midstream urine is used. 3

Among symptomatic men, 32% have been found to have <100,000 bacteria/ml in their midstream urine 4 and a single urine specimen by urethral catheterization growing ≥ 100 bacteria/ml is consistent with bacteriuria for both men and women. 5

Since most of these studies have involved UTI caused by E. coli or other coliforms, more data are needed to find out if the same findings apply to non-coliform urinary pathogens.

Bonus Pearl: Did you know that because quantitative urine culture results are concentration dependent (ie, “per ml”), a dilute urine—as may be found in patients experiencing diuresis—will result in lower numbers of bacteria/ ml. 5

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 References

  1. Kass EH. Asymptomatic infections of the urinary tract. Trans Assoc Am Physicians 1958;69:56-74. https://pubmed.ncbi.nlm.nih.gov/13380946/
  2. Stamm WE, Counts GW, Running KR, et al. Diagnosis of coliform infection in acutely dysuric women. N Engl J Med 1982;307:463-8. https://pubmed.ncbi.nlm.nih.gov/7099208/
  3. Hooten TM, Roberts PL, Cox ME, et al. Voided midstream urine culture and acute cystitis in premenopausal women. N Engl J Med 2013;369:1883-91. https://www.nejm.org/doi/full/10.1056/NEJMoa1302186
  4. Lipsky BA, Ireton RC, Fihn SD, et al. Diagnosis of bacteriuria in men: specimen collection and culture interpretation. J Infect Dis 1987;155:847-54. https://pubmed.ncbi.nlm.nih.gov/3559288/
  5. Nicolle LE, Bradley S, Colgan R, et al. Infectious Diseases Society of America Guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults. Clin Infect Dis 2005;40:643-54. https://pubmed.ncbi.nlm.nih.gov/15714408/
  6. Roberts KB, Wald ER. The diagnosis of UTI: colony count criteria revisited. Pediatrics 2018;141:e20173239. https://doi.org/10.1542/peds.2017-3239

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Could my patient with acute dysuria and less than 10,000 E. coli/ml on urine culture still have a urinary tract infection (UTI)?

My patient with diverticular bleed has now developed signs of bowel ischemia with abdominal pain and sepsis after transcatheter colic artery embolization. Is bowel ischemia common after embolization of lower gastrointestinal (GI) arteries?

FA Manian MD, MPH, , , , , , , , Leave a comment

It may be more common than we think! Reported rates of bowel ischemia following lower GI artery embolization have been as high as 22% (1,2). For this reason, it is prudent to closely monitor for signs of bowel ischemia and infection in patients who undergo embolization to control lower GI bleeding.

In some cases, ischemia of the bowel appears to be mild enough to be treated conservatively, while in other cases bowel infarction with surgical intervention has been necessary (1).  One case report described signs of infection (including fever, abdominal tenderness and leukocytosis) 2 days after arterial embolization in a patient who was treated conservatively (3), while another described “sepsis” 6 days post procedure with bowel wall ischemia requiring surgical resection (1). 

Bowel injury leading to a septic picture following embolization of lower GI arteries should not be surprising given the expected capillary hypoperfusion and risk of tissue hypoxia.  Compared to embolization for upper GI bleed, lower GI embolization may place the patient at higher risk of bowel ischemia bowel ischemia due to lack of a rich collateral blood supply (1).  Older patients may also have mesenteric artery atherosclerotic disease or low cardiac output,  further compromising the collateral blood flow (3).  

At a more molecular level, hypoxia leads to the activation of hypoxia-inducible factor (HIF-1), which plays an important role in inducing gut injury. In fact, deletion of HIF-1a in mice prevented shock-induced intestinal permeability and bacterial translocation that ultimately led to bacteremia (4). 

As for preventing embolization-induced bacteremia, although antibiotics are used for liver and spleen embolization prophylaxis, their role in colic angioembolization is unclear (5).  

Bonus Pearl: Did you know that some of the earliest angioembolizations were performed during the Vietnam War to stop bleeding from bullet injuries? (6)

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References:

  1. Gady, J, Reynolds, H., & Blum, A. Selective arterial embolization for control of lower gastrointestinal bleeding: Recommendations for a clinical management pathway. Current Surg 2003; 60: 344-347. https://www.sciencedirect.com/science/article/abs/pii/S0149794402007493
  2. Rossetti A, Buchs NC, Breguet R, et al. Transarterial embolization in acute colonic bleeding: review of 11 years of experience and long-term results. Int J Colo Dis 2013;28:777-782. https://link.springer.com/article/10.1007/s00384-012-1621-5
  3. Shenoy, S, Satchidanand, S, & Wesp S. Colonic ischemic necrosis following therapeutic embolization. Gastrointest Radiol 1981, 6: 235-237. https://link.springer.com/article/10.1007/BF01890256
  4. Vollmar, B., & Menger, M. Intestinal ischemia/reperfusion: Microcirculatory pathology and functional consequences. Langenbeck Arch Surg 2011; 396: 13-29 https://link.springer.com/article/10.1007%2Fs00423-010-0727-x 
  5. Ryan, J. Mark, Ryan, Barbara M, & Smith, Tony P. Antibiotic prophylaxis in interventional radiology. JVIR 2004; 15: 547-556. https://www.sciencedirect.com/science/article/pii/S1051044307603248
  6. Nolan, T, Phan H, Hardy A, et al. Bullet embolization: Multidisciplinary approach by interventional radiology and surgery. Semin Interven Radiol 2012, 29: 192-6. https://www.ncbi.nlm.nih.gov/pubmed/23997411 

Contributed by Hannah Ananda Bougleux Gomes, Medical Student, Harvard Medical School, Boston, MA.

My patient with diverticular bleed has now developed signs of bowel ischemia with abdominal pain and sepsis after transcatheter colic artery embolization. Is bowel ischemia common after embolization of lower gastrointestinal (GI) arteries?

My previously healthy patient is admitted with a multi-drug resistant E. coli urinary tract infection. Could her urinary tract infection (UTI) be foodborne?

FA Manian MD, MPH, , , , , , , Leave a comment

Yes! Although foodborne infections are often thought to cause infections limited to the GI tract, an increasing number of studies have linked foodborne E.coli to extraintestinal infections in humans, including UTIs.1

Supportive data include frequent genetic similarly between antimicrobial-resistant E. coli from humans and poultry-associated E. coli. 2 In fact, antimicrobial-resistant E. coli isolates from humans may be  genetically more similar to poultry isolates than susceptible commensal E. coli strains in the human GI tract.3

A U.S. study found that 14% of chicken meat products were contaminated with E. coli strains capable of causing extraintestinal disease, 1/3 of which were mutli-drug resistant.4  Another study found that 94% of retail chicken meat samples contained E. coli with ESBL-genes,  of which nearly 40% contained isolates present in humans.5

Among women, UTI caused by antimicrobial-resistant extraintestinal pathogenic E. coli has been linked to high levels of self-reported chicken consumption.6

The plausibility of foodborne transmission of antimicrobial-resistant E. coli to humans is further supported by the finding that drug resistant E coli from chicken carcasses widely contaminate the kitchen during meal preparation and can appear in the intestinal tract of those who prepare such food.2

Bonus Pearl: Did you know that women with multi-drug resistant E. coli UTI are 3.7 times more likely to report frequent consumption of chicken? 6

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References

  1. Manges AR. Escherichia coli and urinary tract infections: the role of poultry-meat. Clin Microbiol Infect 2016;22:122-29. https://www.ncbi.nlm.nih.gov/pubmed/26679924
  2. Manges AR, Johnson JR. Reservoirs of extraintestinal pathogenic Escherichia coli. Microbiol Spectrum 2012;3(5):UTI-0006-2012. https://www.ncbi.nlm.nih.gov/pubmed/26542041
  3. Johnson JR, Menard M, Johsnton B, et al. Epidemic clonal groups of Escherichia coli as a cause of antimicrobial-resistant urinary tract infections in Canada, 2002 to 2004. Antimicrob Agents Chemother 53;2733-2739. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2704706/
  4. Johnson JR, Porter SB, Johnston B, et al. Extraintestinal pathogenic and antimicrobial-resistant Escherichia coli, including sequence type 131 (ST131) from retail chicken breasts in the United States in 2013. Apppl Environ Microbiol 83:e02956-16. https://www.ncbi.nlm.nih.gov/pubmed/28062464
  5. Leverstein-van Hall MA, Dierikx CM, Stuart JC, et al. Dutch patients, retail chicken meat and poultry share the same ESBL genes, plasmids and strains. Clin Microbiol Infect 2011;17:873-880. https://www.ncbi.nlm.nih.gov/pubmed/21463397
  6. Manges AR, Smith SP, Lau BJ, et al. Retail meat consumption and the acquisition of antimicrobial resistant Escherichia coli causing urinary tract infections: a case-control study. Foodborne Path Dis 4:419-431. https://www.ncbi.nlm.nih.gov/pubmed/18041952

 

My previously healthy patient is admitted with a multi-drug resistant E. coli urinary tract infection. Could her urinary tract infection (UTI) be foodborne?

Why has my patient with Clostridium difficile diarrhea developed Klebsiella bacteremia?

FA Manian MD, MPH, , , , , , , , Leave a comment

Although there are many potential sources for Klebsiella sp. bacteremia, C. difficile infection (CDI) itself may be associated with GI translocation of enteric organisms.

A retrospective study of over 1300 patients found an incidence of 1.8% for CDI-associated bacteremia. E. coli, Klebsiella sp. , or Enterococcus sp. accounted for 72% of cases. History of malignancy, neutropenia (at the time of CDAD), and younger age (mean 59 y) were among the risk factors.1 Another study reported over 20 cases of bacteremia caused by C. difficile plus other bacteria often of enteric origin such the aforementioned organisms, Bacteroides sp, Candida sp, and Enterobacter sp.2

CDI is thought to predispose to bacterial translocation through the GI tract by alteration of mucosal indigenous microflora, overgrowth of certain pathogens, and presence of inflammation in the mucosa.3 Interestingly, C. difficile toxin A or B may play an active role in the bacterial adherence and penetration of the intestinal epithelial barrier.4  

Bonus pearl: Did you know that C. difficile may be found in the normal intestinal flora of 3% of healthy adults, 15-30% of hospitalized patients, and up to 50% of neonates? Why neonates seem immune to CDI is another fascinating story!

 

References

  1. Censullo A, Grein J, Madhusudhan M, et al. Bacteremia associated with Clostridium difficile colitis: incidence, risk factors, and outcomes. Open Forum Infectious Diseases, Volume 2, Issue suppl_1, 1 December 2015, 943, https://doi.org/10.1093/ofid/ofv133.659 https://academic.oup.com/ofid/article/2/suppl_1/943/2635179
  2. Kazanji N, Gjeorgjievski M, Yadav S, et al. Monomicrobial vs polymicrobial Clostridum difficile bacteremia: A case report and review of the literature. Am J Med 2015;128:e19-e26. https://www.amjmed.com/article/S0002-9343(15)00458-1/abstract
  3. Naaber P, Mikelsaar RH, Salminen S, et al. Bacterial translocation, intestinal microflora and morphological changes of intestinal mucosa in experimental models of Clostridium difficile infection. J Med Microbiol 1998; 47: 591-8. https://www.ncbi.nlm.nih.gov/pubmed/9839563 
  4. Clostridium difficile toxins may augment bacterial penetration of intestinal epithelium. Arch Surg 1999;134: 1235-1242. https://jamanetwork.com/journals/jamasurgery/fullarticle/390434
Why has my patient with Clostridium difficile diarrhea developed Klebsiella bacteremia?

My patient with pyelonephritis has positive blood cultures for E. coli? Should I order repeat blood cultures to make sure the bacteremia is clearing?

FA Manian MD, MPH, , , , , , , , , Leave a comment

Although a common practice, follow-up blood cultures (FUBCs) may not be necessary in otherwise clinically stable or improving patients with aerobic gram-negative bacteremia. This is probably due to the often-transient nature of gram-negative bloodstream infections  and less propensity of these organisms to cause intravascular infections (eg, endocarditis) compared to gram-positives. 1

A 2017 study addressing the value of FUBCs in gram-negative bacteremia found that repeat positive blood cultures were uncommon with positive results not associated with mortality or higher ICU admissions. 1 Specifically, 17 FUBCs had to be drawn to yield 1 positive result.  Although the numbers of positive FUBCs were too low for in-depth analysis, it was concluded that FUBCs added little value in the management of gram-negative bacteremias.

In contrast, FUBCs are recommended in the following situations: 1-3

  • Staphylocccus aureus bacteremia given the propensity of this organism to cause intravascular (eg, endocarditis) and metastatic infections.
  • Presumed or documented endocarditis or intravascular device infections (eg, intravenous catheters and pacemakers) to document timely clearance of bacteremia
  • Infections involving organisms that may be difficult to clear such as fungemia or multi-drug resistant pathogens.

As with many things in medicine, clinical context is important before ordering tests and blood cultures are no different. The urge to order FUBCs should also be balanced with the possibility of having to deal with  contaminants. 

References

  1. Canzoneri CN, Akhavan BJ, Tosur Z et al. Follow-up blood cultures in gram-negative bacteremia: Are they needed? Clin Infect Dis 2017;65:1776-9. https://www.ncbi.nlm.nih.gov/pubmed/29020307
  2. Tabriz MS, Riederer K, Baran J, et al. Repeating blood cultures during hospital stay: Practice pattern at a teaching hospital and a proposal for guidelines. Clin Microbiol Infect 2004;10:624-27. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1469-0691.2004.00893.x
  3. Mylotte JM, Tayara A. Blood cultures: Clinical aspects and controversies. Eur J Clin Microbiol Infect Dis 200;19:157-63. https://www.ncbi.nlm.nih.gov/pubmed/10795587

 

 

My patient with pyelonephritis has positive blood cultures for E. coli? Should I order repeat blood cultures to make sure the bacteremia is clearing?

200 pearls and counting! Take the Pearls4Peers quiz #2!

FA Manian MD, MPH, , , , , , , , , , , , , , , Leave a comment
Multiple choice (choose 1 answer)
1. Which of the following classes of antibiotics is associated with peripheral neuropathy?
a. Penicillins
b. Cephalosporins
c. Macrolides
d. Quinolones

 

 

2. The best time to test for inherited thrombophilia in a patient with acute deep venous thrombosis is…
a. At least 1 week after stopping anticoagulants and a minimum of 3 months of anticoagulation
b. Just before initiating anticoagulants
c. Once anticoagulation takes full effect
d. Any time, if suspected

 

 

3. All the following is true regarding brain MRI abnormalities following a seizure, except…
a. They are observed following status epilepticus only
b. They are often unilateral
c. They may occasionally be associated with leptomeningeal contrast enhancement
d. Abnormalities may persist for weeks or months

 

 

4. Which of the following is included in the quick SOFA criteria for sepsis?
a. Heart rate
b. Serum lactate
c. Temperature
d. Confusion

 

 

5. All of the following regarding iron replacement and infection is true, except…
a. Many common pathogens such as E.coli and Staphylococcus sp. depend on iron for their growth
b. Association of IV iron replacement and increased risk of infection has not been consistently demonstrated
c. A single randomized-controlled trial of IV iron in patients with active infection failed to show increased infectious complications or mortality with replacement
d. All of the above is true

 

True or false

1. Constipation may precede typical manifestations of Parkinson’s disease by 10 years or more
2. Urine Legionella antigen testing is >90% sensitive in legionnaire’s disease
3. Spontaneous coronary artery dissection should be particularly suspected in males over 50 years of age presenting with acute chest pain
4. Urine dipstick for detection of blood is >90% sensitive in identifying patients with rhabdomyolysis and CK >10,000 U/L
5. Diabetes is an independent risk factor for venous thrombophlebitis

 

 

 

Answer key
Multiple choice questions:1=d; 2=a;3=a;4=d;5=c
True or false questions:1=True; 2,3,4,5=False

 

200 pearls and counting! Take the Pearls4Peers quiz #2!

Is iron therapy contraindicated in my patient with active infection?

FA Manian MD, MPH, , , , , , 1 Comment

In the absence of randomized-controlled trials of iron therapy in patients with active infection, the harmful effects of iron therapy (IT) in this setting remains more theoretical than proven. 1,2

Although many pathogens (eg, E. coli, Klebsiella, Salmonella, Yersinia, and Staphylococcus species) depend on iron for their growth2,3, and iron overload states (eg, hemochromatosis) predispose to a variety of infections, studies evaluating the risk of infection with iron therapy have reported conflicting results.1-4 A 2015 systematic review and meta-analysis of 103 trials comparing IV iron therapy  with several other approaches, including oral iron therapy or placebo, found no increased risk of infections with IV iron.5 In contrast, an earlier systematic review and meta-analysis involving fewer number of trials found an increased risk of infections with IV iron. 6

These varied results are perhaps not surprising since the effects of iron therapy on the risk of infection is likely to be context-specific, depending on the patient’s preexisting iron status, exposure to potential infections and co-infection and genetic background. 4 Of interest, mice with sepsis have worse outcomes when treated with IV iron.7

Perhaps the most prudent approach is to hold off on iron therapy until the active infection is controlled, unless the benefits of urgent iron therapy is thought to outweigh its theoretical harmful effects.

 

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References

  1. Daoud E, Nakhla E, Sharma R. Is iron therapy for anemia harmful in the setting of infection? Clev Clin J Med 2011;78:168-70. http://www.mdedge.com/ccjm/article/95480/hematology/iron-therapy-anemia-harmful-setting-infection
  2. Hain D, Braun M. IV iron: to give or to hold in the presence of infection in adults undergoing hemodialysis. Nephrology Nursing Journal 2015;42:279-83. https://www.ncbi.nlm.nih.gov/pubmed/26207288
  3. Jonker FAM, van Hensbroek MB. Anaemia, iron deficiency and susceptibility of infections. J Infect 204;69:523-27. https://www.ncbi.nlm.nih.gov/pubmed/28397964
  4. Drakesmith H, Prentice AM. Hepcidin and the iron-infection axis. Science 2012;338:768-72. https://www.ncbi.nlm.nih.gov/pubmed/23139325  
  5. Avni T, Bieber A, Grossman A, et al. The safety of intravenous iron preparations: systematic review and meta-analysis. Mayo Clin Proc 2015;90:12-23. http://www.mayoclinicproceedings.org/article/S0025-6196(14)00883-0/pdf
  6. Litton E, Xiao J, Ho KM. Safety and efficacy of intravenous iron therapy in reducing requirement for allogeneic blood transfusion: systematic review and meta-analysis of randomized clinical trials. BMJ 2013;347:f4822. https://www.ncbi.nlm.nih.gov/pubmed/23950195
  7. Javadi P, Buchman TG, Stromberg PE, et al. High dose exogenous iron following cecal ligation and puncture increases mortality rate in mice and is associated with an increase in gut epithelial and splenic apoptosis. Crit Care Med 2004;32:1178-1185. https://www.ncbi.nlm.nih.gov/pubmed/15190970
Is iron therapy contraindicated in my patient with active infection?

Are two sets of blood cultures adequate for evaluation of bacteremia in my febrile patient?

FA Manian MD, MPH, , , , Leave a comment

For great majority of patients, more than 2 sets of blood culture obtained closely apart is not likely to significantly improve the yield of detecting bacteremia. 

Although a 2004 report suggested that 2 sets of blood cultures over 24 h period had a sensitivity of only 80% for bacteremia, several other studies have found much higher sensitivities, ranging from ~90%- 99% 2-3. When broken down by organism, sensitivity of 2 sets of blood cultures may be highest for Staphylococcus aureus (97%), followed by E. coli (91%), and Klebsiella pneumoniae (90%) 2.  The Clinical and Laboratory Standards Institute guidelines recommend paired blood culture sets (each set with 2 bottles, 10 ml of blood in each) to detect about 90-95% of patients with documented bacteremia, and 3 sets for 95-99% detection rate 4.

It seems prudent to strike a balance between drawing more than 2 sets of blood cultures—with its attendant risk of picking up contaminants— and what may be a definite but small incremental increase in the rate of detection of true bacteremia. 

If you are concerned about “continuous” bacteremia (eg, in endocarditis) or a common blood culture contaminant causing true disease (eg, Staphylococcus epidermidis prosthetic valve infection), you may consider a 3rd or 4th set of blood cultures drawn 4-6 hrs after the initial sets.

Whatever you do,  please don’t order only 1 set of blood cultures! Aside from its generally low yield, when positive it may be difficult to distinguish contaminants from true invaders.

 

References

  1. Cockerill FR, Reed GS, Hughes JG, et al. Clinical comparison of BACTEC 9240 Plus Aerobic/F resin bottles and the Isolator aerobic cultures. Clin Infect Dis 2004;38:1724-30. https://www.ncbi.nlm.nih.gov/pubmed/9163464
  2. Lee A, Mirrett S, Reller LB, et al. Detection of bloodstream infections in adults: how many cultures are needed? J Clin Microbiol 2007; 45:3546-48. http://jcm.asm.org/content/45/11/3546
  3. Towns ML, Jarvis WR, Hsueh PR. Guidelines on blood cultures. J Microbiol Immunol Infect 2010;43:347-49. https://www.ncbi.nlm.nih.gov/pubmed/20688297
  4. Weinstein MP, Reller LB, Murphy JR, et al. The clinical significance of positive blood cultures: a comprehensive analysis of 500 episodes of bacteremia and fungemia in adults. I. Laboratory and eipidemiologic observations. Rev Infect Dis 1982;5:35-53. https://www.ncbi.nlm.nih.gov/pubmed/6828811
Are two sets of blood cultures adequate for evaluation of bacteremia in my febrile patient?

My patient with cirrhosis and suspected infection has a normal serum C-reactive protein (CRP). Does cirrhosis affect CRP response to infection?

FA Manian MD, MPH, , , , , , , , Leave a comment

CRP is primarily synthesized by the liver mainly as a response to IL-6 production in inflammatory states1.  Lower CRP production may then be expected in cirrhotic patients with significant infections and several studies support this view2. 

In a particularly convincing study involving E. coli-infected patients with bacteremia, the median CRP level in cirrhotic patients was about 40% that of non-cirrhotic patients (62 mg/L vs 146 mg/L)3.  In another study involving bacteremic patients with or without liver dysfunction, median CRP level was about 60% that of  patients with preserved liver function (81 mg/L vs 139 mg/L)4. 

Some investigators have reported a cut-off CRP value of 9.2 mg/L as a possible screening test for bacterial infections in patients with cirrhosis with a sensitivity and specificity of 88% (AUROC 0.93)5.

Collectively, these data suggest that although CRP response may be diminished in patients with advanced liver disease and acute infection, its synthesis is still maintained.

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 References

  1. Pieri G, Agarwal B, Burroughs AK. C-reactive protein and bacterial infection in cirrhosis. Ann Gastroenterol 2014;27:113-20. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982625/pdf/AnnGastroenterol-27-113.pdf
  2. Ha YE, Kang C-I, Joo E-J, et al. Usefulness of C-reactive protein for evaluating clinical outcomes in cirrhotic patients with bacteremia. Korean J Intern Med 2011;26:195-200. http://pubmedcentralcanada.ca/pmcc/articles/PMC3110852/pdf/kjim-26-195.pdf
  3. Park WB1, Lee KD, Lee CS et al. Production of C-reactive protein in Escherichia coli-infected patients with liver dysfunction due to liver cirrhosis. Diagn Microbiol Infect Dis. 2005 Apr;51(4):227-30. https://www.ncbi.nlm.nih.gov/pubmed/15808312
  4. Mackenzie I, Woodhouse J. C-reactive protein concentrations during bacteraemia: a comparison between patients with and without liver dysfunction. Intensive Care Med 2006;32:1344-51. https://www.ncbi.nlm.nih.gov/pubmed/16799774
  5. Papp M, Vitalis Z, Altorjay I, et al. Acute phase proteins in the diagnosis and prediction of cirrhosis associated bacterial infection. Liver Int 2011;603-11. https://www.ncbi.nlm.nih.gov/pubmed/22145664

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My patient with cirrhosis and suspected infection has a normal serum C-reactive protein (CRP). Does cirrhosis affect CRP response to infection?