Category Archives: PATHOGENS

Blood culture contaminants

There are some bacteria out there that usually don’t cause disease. They tend to just hang out and not cause any harm. When we see them in the bloodstream, they often are contaminants, meaning they were introduced during collection of the sample, and are not truly in the bloodstream. Figuring out which ones are contaminants and which ones are not can be tricky. Some are almost always (see * below) contaminants while others are NEVER contaminants. Some can be a contaminant or an infection, like streptococcus viridans group.

*Important to note: any organism can cause an infection in the right context, even those who are usually deemed as contaminants. If you are unsure whether a true infection is present, it’s always best to call an infectious disease specialist to assist with management.

Contaminant =  growth of bacteria in the blood culture bottle that were not present in the patient’s bloodstream and thus introduced during the collection of the sample (Dawson et al.)

USUALLY NOT contaminants:

Staphylococcus aureus
Streptococcus pneumoniae
Group A/B streptococcus
Listeria monocytogenes
Neisseria meningitidis
Fungus (yeast or mold)
…Amongst many other numerous organisms that will take too long to mention in a list

Common blood contaminants:

Coagulase-negative staphylococci
Propionibacterium acnes
Micrococcus spp.
Corynebacterium spp.
Bacillus spp. (*except Bacillus anthracis which causes anthrax!!)

What if multiple bacteria are growing?!

  • multiple growth of bacteria can suggest contamination.
  • however, it again depends on the pathogens involved. If all are skin flora, then probably contaminant. If any of the aforementioned ‘USUALLY NOT CONTAMINANTS’ are present, then it is not a contaminant!

 

Where do contaminants come from:

  1. Patient’s skin
  2. Equipment used to obtain sample and transfer it to culture bottle
  3. Provider’s skin
  4. General environment

 

Factors to consider when deciding whether culture
is contaminant or not:

  1. Patient’s clinical status
    • are there any signs or symptoms to suggest infection with this microbe?
    • Example:
      • You would not expect a patient with pneumonia to grow CoNS in their blood.
      • However, you would take CoNS seriously in a patient with recent valve replacement and fevers.
  1. Microbiology of the species – see above
  2. Time to positivity of blood culture – studies have shown that the average time of positivity of true infections is ~12 hours vs. ~24 hours for contaminants
  3. Inoculum of the isolate – how much growth is there?
    • If only 1 out of 4 blood culture bottles are positive –> MORE LIKELY contaminant
    • If >1 out of 4 blood culture bottles are positive –> true pathogen
  1. Any foreign material? – Contaminants become pathogens when they infect hardware and prosthetic valves/grafts. If those are present and there is a possibility they are infected, would not disregard any pathogen as a contaminant.
  2. Patient’s response to antibiotics and isolate’s susceptibility pattern – clues to whether an isolate is a contaminant or a true infection
    • Contaminant: patient does not respond to antibiotics that treat the blood culture isolate
    • True pathogen: patient DOES respond to antibiotics that treat the blood culture isolate
    • Contaminant: patient responds to antibiotics despite blood culture isolate resistant
    • True pathogen: patient does not respond to antibiotics and isolate is resistant

 

FUN FACT: A retrospective review looked at 626 blood cultures and discovered that by 48 hours, 98% of aerobic gram-positive and gram-negative bloodstream infections were identified.

*This shows that unless there is a high suspicion for anaerobe growth, antibiotics can be de-escalated at 48 hours if there is no growth. (Pardo, J., Klinker, K.P, et al. 2014. Time to positivity of blood cultures supports antibiotic de-escalation at 48 hours. Annals of Pharmacology. 48 (1): 33-40).)

TAKE HOME POINTS:

  • Microbes known to be common contaminants CAN cause disease in certain circumstances
  • Always repeat blood culture when first one is positive for microbes
  • If you’re not sure if it’s a contaminant or not ⇒ call ID
    (it’s always better to double check rather than to miss a true infection)

 

References:

1. Dawson, S. 2014. Blood culture contaminants. Journal of Hospital Infection; 87, 1-10. DOI: 10.1016/j.jhin.2014.02.009
2. Pardo, J., Klinker, K.P, et al. 2014. Time to positivity of blood cultures supports antibiotic de-escalation at 48 hours. Annals of Pharmacology. 48 (1): 33-40).
DOI: 10.1177/1060028013511229
3. Hossain, B., Islam, M.S., et al. 2016. Understanding bacterial isolates in blood culture and approaches used to define bacteria as contaminants: a literature review. Pediatric Infectious Disease Journal. 35(5): S45-51.
DOI: 10.1097/INF.0000000000001106
4. Pien, B.C., Sundaram, P., and et al. 2010. The clinical and prognostic importance of positive blood cultures in adults. American Journal of Medicine. 123 (819-828).
DOI: 10.1016/j.amjmed.2010.03.021

SPICE organisms

First topic at hand is SPICE organisms. These are the organisms that appear to be sensitive to many antibiotics, but once they are exposed to certain antibiotics (ex. 3rd generation cephalosporins), they quickly develop resistance to them.

SPICE stands for:

S: Serratia spp.

P: Providencia

I: “indole-positive” Proteus spp. (this includes: P. vulgaris) *NOT P.mirabilis

C: Citrobacter spp.

E: Enterobacter spp.

*There are other, less known bacteria included in this group (Cronobacter, Edwardsiella, Hafnia, Morganella, Aeromonas)

 

*[Organisms like Pseudomonas and Acinetobacter produce AmpC gene normally – which is why they have intrinsic resistance to 3rd generation cephalosporins and do not technically fall into the AmpC inducer SPICE group.]

 

The SPICE pathogens can be induced to produce an AmpC beta-lactamase gene that encodes an enzyme that cleaves the beta-lactam group in the antibiotic and renders it inactive.

 

This gene may not be detected initially (low level of expression of the gene) but may appear (induced to express higher levels of gene) after a period of exposure to beta-lactam antibiotics.

(Clinical translation: Initially they will appear susceptible to beta-lactams, but eventually will develop resistance to them. *tricky little bastards, aren’t they?)

 

Once beta-lactam is removed, the AmpC gene production is reduced once more and the pathogens will appear sensitive to 3rd generation cephalosporins and penicillins again. .

 

Resistance develops anywhere from 24h to 2-3 weeks.

 

Clinical relevance:

  • If the course of antibiotics is short or if the antibiotic can easily overcome the MIC concentration needed for bacterial killing, then the risk of inducing AmpC gene production is low
    • Clinical examples (~<1 week duration of antibiotics):
      • UTI
      • Pneumonia
  • Short course for intra-abdominal infectionHowever, this becomes an issue in areas where antibiotics have difficulty penetrating (because it is less likely to overcome the MIC concentration needed) or when antibiotics are needed to be given over a longer period of time.
    • Clinical examples:
      • Endocarditis
      • Bacteremia
      • Osteomyelitis
      • Septic arthritis
      • Abscesses

 

Antibiotics to avoid:

  • Penicillin class (including piperacillin-tazobactam)
  • Most cephalosporins (1st, 2nd, and 3rd generation)

 

Antibiotics to use:

  • 4th generation cephalosporins (i.e. cefepime at higher doses, q8h)
  • Carbapenems
  • Aminoglycosides
  • Fluoroquinolones

TAKE-HOME POINTS:

  1. Remember the members of the SPICE group
  2. You may be successful in treating an infection in short courses of therapy or in infections where antibiotic penetration is high. But in patients with bacteremia, bone, joint, or valve infections – strongly consider 4th generation cephalosporin or a carbapenem.

 

 

Have a question, comment, or a suggestion for a future blog post? Post your comment below!

 

 

References:

  • http://m.antimicrobialstewardship.com/clinical_summaries/index.php?page=esbl_and_spice
  • Jacoby, G.A. AmpC beta-lactamases. Clinical Microbiology Review. 2009. 22(1):161-182. doi: 10.1128/CMR.00036-08
  • Harris, P.N.A, and Ferguson, J.K. Antibiotic therapy for inducible AmpC beta-lactamase-producing Gram-negative bacilli: what are the lternatives to carbapenems, quinolones, and aminoglycosides? 2012. International Journal of Antimicrobial Agents, 40: 297-305.