What’s the connection between lemon juice and disseminated candidiasis in my patient with illicit IV drug use?

Lemon juice is often used by IV drug users to help dissolve poorly water soluble street drugs, such as brown heroin or crack-cocaine, and may serve as a vehicle for Candida albicans infection. 1-3

Contamination of lemon juice (either from wild lemons or from the plastic containers) is thought to occur from either the skin and/or oropharynx of the user.1  Other fruit juices such as orange juice as well as raspberry syrup have been implicated as a source of disseminated candidiasis in IV drug users.4

Experimental inoculation of lemons with small numbers of C. albicans has demonstrated rapid growth of the organism at room temperature resulting in inadvertent injection of a large inoculum size. 2 Once inoculated directly into the blood stream, C. albicans disseminates and can present in many ways, including skin lesions, ocular lesions/endophthalmitis, and osteoarticular infections (eg, costochondral, hip joint, and vertebral infections).1  

So it is advisable to not only ask about what recreational drug is being injected but also what it is injected with!

Bonus Pearl: Did you know that although lemon juice is an excellent growth medium for C. albicans, it has bactericidal properties against Staphylococcus aureus and Pseudomonas aeruginosa? 1

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References

  1. Bisbe J, Miro JM, Latorre X, et al. Disseminated candidiasis in addicts who use brown heroin: report of 83 cases and review. Clin Infect Dis 1992;15:910-23. https://www.ncbi.nlm.nih.gov/pubmed/1457662
  2. Newton-John HGF, Wise K, Looke DFM. Role of the lemon in disseminated candidiasis of heroin abusers. Med j Aust 1984;140:780-81. https://onlinelibrary.wiley.com/doi/abs/10.5694/j.1326-5377.1984.tb132597.x?sid=nlm%3Apubmed
  3. Shankland GS, Richardson MD. Source of infection in candida endophthalmitis in drug addicts. Br J Ophthalmol 1986;292:1106-7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1954783/pdf/702.pdf
  4. Scheidegger C, Pietrzak J, Frei R. Methadone diluted with contaminated orange juice or raspberry syrup as a potential source of disseminated candidiasis in drug abusers. Eur J Clin Microbiol Infect Dis 1993;12:229-31. https://link.springer.com/article/10.1007/BF01967124
What’s the connection between lemon juice and disseminated candidiasis in my patient with illicit IV drug use?

When should I consider Pseudomonas aeruginosa as a cause of respiratory tract infection in my hospitalized patient with COPD exacerbation?

The most consistent risk factor for isolation of P. aeruginosa from sputum of adults with COPD is the presence of more advanced pulmonary disease (eg, FEV-1 <35%-50% of predicted value) or functional impairment (1-5).

 

Chronic corticosteroid use is also frequently cited as an important predictor of respiratory tract colonization/infection due to P. aeruginosa in patients with COPD, while the data on antibiotic use during the previous months have been conflicting (2,4). Other risk factors may include prior isolation of P. aeruginosa and hospital admission during the previous year (1).
A prospective study of patients hospitalized for COPD exacerbation found P. aeruginosa to be the most frequently isolated organism, growing from 26% of validated sputum samples at initial admission, followed by Streptococcus pneumoniae and Hemophilus influenzae. In the same study, bronchiectasis (present in up to 50% of patients with COPD) was not shown to be independently associated with the isolation of P. aeruginosa (1).
Of interest, compared to the patients without P. aeruginosa, patients hospitalized for acute exacerbation of COPD and isolation of P. aeruginosa from sputum have significantly higher mortality: 33% at 1 year, 48% at 2 years and 59% at 3 years (5).

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References
1. Garcia-Vidal C, Almagro P, Romani V, et al. Pseudomonas aeruginosa in patients hospitalized for COPD exacerbation: a prospective study. Eur Respir J 2009;34:1072-78. https://www.ncbi.nlm.nih.gov/pubmed/19386694
2. Murphy TF. Pseudomonas aeruginosa in adults with chronic obstructive pulmonary disease. Curr Opin Pulm Med 2009;15:138-42. https://www.ncbi.nlm.nih.gov/pubmed/19532029
3. Miravitlles M, Espinosa C, Fernandez-Laso E, et al. Relationship between bacterial flora in sputum and functional impairment in patients with acute exacerbations of COPD. Chest 1999;116:40-6. https://www.ncbi.nlm.nih.gov/pubmed/10424501
4. Murphy TF, Brauer AL, Eschberger K, et al. Pseudomonas aeruginosa in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2008;177:853-60. https://www.ncbi.nlm.nih.gov/pubmed/18202344
5. Almagro P, Silvado M, Garcia-Vidal C, et al. Pseudomonas aeruginosa and mortality after hospital admission for chronic obstructive pulmonary disease. Respiration 2012;84:36-43. https://www.karger.com/Article/FullText/331224

 

 

When should I consider Pseudomonas aeruginosa as a cause of respiratory tract infection in my hospitalized patient with COPD exacerbation?

How does azithromycin (AZ) benefit patients with severe COPD or cystic fibrosis (CF)?

AZ is a macrolide antibiotic which interferes with bacterial protein synthesis by binding to the 50S ribosomal subunit. It is often used to treat acute respiratory tract infections due to Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, as well as Mycoplasma, Chlamydia, and Legionella sp1. Although it has no in vitro activity against many aerobic gram-negative bacilli such as Pseudomonas aeruginosa, its chronic use has often been associated with a significant reduction in the frequency of disease exacerbations in patients with chronic bronchiectasis and colonization due to this organism, including patients with COPD or CF1-3.

Because P. aeruginosa is invariably macrolide-resistant, the beneficial effect of AZ in chronically infected or colonized patients must be due to factors other than its direct effect on bacterial replication.  Several mechanisms have been invoked including: 1. Inhibition of quorum-sensing dependent virulence factor and biofilm production 2.Blunting of host inflammatory response (eg, ↑IL-10, and ↓ IL-1ß, IL-6, IL-8, TNF-α, and ↓ chemotaxis); and 3. Enhanced antiviral response1.

The latter finding is quite unexpected but AZ appears to augment interferon response to rhinovirus in bronchial cells of COPD patients3.  With respiratory viruses (including rhinoviruses) causing 20-55% of all COPD exacerbations, perhaps this is another way AZ may help the host! Who would have thought!!

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References

  1. Vos R, Vanaudenaerde BM, Verleden SE, et al. Anti-inflammatory and immunomodulatory properties of azithromycin involved in treatment and prevention of chronic lung allograft rejection. Transplantation 2012;94:101-109.
  2. Cochrane review. Treatment with macrolide antibiotics for people with cystic fibrosis and chronic chest infection. Nov 14, 2012. http://www.cochrane.org/CD002203/CF_treatment-with-macrolide-antibiotics-for-people-with-cystic-fibrosis-and-chronic-chest-infection
  3. Menzel M, Akbarshahi H, Bjermer L, et al. Azithromycin induces anti-viral effects in cultured bronchial epithelial cells from COPD. Scientific Reports 2016; 6:28698. DOI:10.1038/srep 28698.

 

 

How does azithromycin (AZ) benefit patients with severe COPD or cystic fibrosis (CF)?

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?

In most situations, you will most likely choose an antibiotic based on the laboratory reporting of “Susceptible” (vs “Resistant”), not the actual MIC value of the drug and that’s fine.  

However, there may be a few instances when you may need to pay more attention to the actual MICs. Many experts recommend caution when “high” MICs within a susceptible range are observed in the following situations:   

  1. Vancomycin MIC >1 ug/ml in Staphylococcal aureus (methicillin-sensitive or –resistant) infections because of its possible association with clinical failure and, at times, increased mortality1,2.
  2. Ciprofloxacin or levofloxacin MIC>0.25 ug/ml in bacteremia caused by Gram-negative bacilli (including Enterobacteriacae as well as Pseudomonas aeruginosa) because of its association with an adverse outcome (eg, longer average hospital stay post-culture and duration of infection) but not necessarily mortality3-5.
  3. Levofloxacin MIC ≥ 1.0 ug/ml in Streptococcus pneumoniae infections, because of its association with an adverse clinical outcome based on drug pharmacodynamics and anecdotal reports of treatment failure6,7.

 

References

  1. Jacob JT, DiazGranados CA. High vancomycin minimum inhibitory concentration and clinical outomces in adults with methicillin-resistant Staphylococcus aureus infections: a meta-analysis. Int J Infect Dis 2013;17:e93-e100.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3780595/
  2. Kalil AC, Van Schooneveld TC, Fey PD, et al. Association between vancomycin minimum inhibitory concentration and mortality among patients with Staphylococcus aureus bloodstream infections: A systematic review and meta-analysis. JAMA 2014;312:1552-1564. https://www.ncbi.nlm.nih.gov/pubmed/25321910
  3. DeFife R, Scheetz MH, Feinglass J, et al. Effect of differences in MIC values on clinical outcomes in patients with bloodstream infections caused by Gram-negative organisms treated with levofloxacin. Antimicrob Agents Chemother 2009;53:1074-79. http://aac.asm.org/content/53/3/1074.full
  4. Falagas ME, Tansarli GS, Rafailidis PI, et al. Impact of antibiotic MIC on infection outcome in patients with susceptible Gram-negative bacteria a systematic review and meta-analysis. Antimicrob Agents Chemother 2012;56:4214-22. https://www.ncbi.nlm.nih.gov/pubmed/22615292
  5. Zelenitsky SA, Harding GKM, Sun S, et al. Treatment and outcome of Pseudomonas aeruginosa bacteremia: an antibiotic pharmacodynamics analysis. J Antimicrob Chemother 2003;52:668-674. https://www.ncbi.nlm.nih.gov/pubmed/12951354
  6. Davidson R, Cavalcanti R, Brunton JL, et al. Resistance to levofloxacin and failure of treatment of pneumococcal pneumonia. N Engl J Med 2002;346:. 2002;346:747-50. https://www.ncbi.nlm.nih.gov/pubmed/11882730
  7. De Cueto M, Rodriguez JM, Soriano MJ, et al. Fatal levofloxacin failure in treatment of a bacteremic patient infected with Streptococcus pneumoniae with a preexisting parC mutation. J Clin Microbiol 2008;46:1558-1560.  http://jcm.asm.org/content/46/4/1558.full

Contributed in part by Nick Van Hise, Pharm.D., BCPS, Infectious Diseases Clinical Pharmacist, Edward-Elmhurst Hospitals, Naperville, Illinois.

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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?

How should patients with hospital-associated pneumonia (HAP) be empirically treated under the 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society?

Although empiric selection of antibiotics should be based on the local distribution of pathogens associated with HAP and their antimicrobial susceptibilities, routine coverage of Staphylococcus aureus (not necessarily methicillin-resistant S. aureus [MRSA]) and Pseudomonas aeruginosa or other gram-negative bacilli is recommended1.

In patients not at high risk of mortality (including ventilatory support and septic shock) or risk for MRSA (i.e.prior IV antibiotic use within 90 days, hospitalization in a unit where >20% of S. aureus isolates are MRSA or the prevalence of MRSA is unknown), piperacillin-tazobactam, cefepime, levofloxacin, imipenem or meropenem alone is suggested.

In patients not at high risk of mortality but with factors that increase the likelihood of MRSA, piperacillin-tazobactam, cefepime/ceftazidime, ciprofloxacin/levofloxacin, imipenem/meropenem, or aztreonam, plus vancomycin or linezolid should be considered.

In patients at high risk of mortality or receipt of IV antibiotics during the prior 90 days vancomycin or linezolid plus 2 of the following should be used: piperacillin-tazobactam, cefepime/ceftazidime, ciprofloxacin/levofloxacin, imipenem/meropenem, amikacin/gentamicin/tobramycin, or aztreonam are recommended (avoid double β-lactams).

In patients with structural lung disease increasing the risk of gram-negative infections (ie, bronchiectasis or cystic fibrosis), double anti-pseudomonal coverage is recommended.

 

Reference

  1. Kalil AC, Metersky ML, Klompas M, et al. Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis, Advance Access published July 14, 2016.
How should patients with hospital-associated pneumonia (HAP) be empirically treated under the 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society?

What are some of the major changes in the 2016 Infectious Diseases Society of America and the American Thoracic Society guidelines on pneumonia in hospitalized patients?

The most noticeable change is the elimination of the concept of health-care associated pneumonia (HCAP) altogether1. This action is in part related to the fact that many patients with HCAP were not at high risk for multi-drug resistant organisms (MDROs) , and that individual patient risk factors, not mere exposure to healthcare facilities, were better determinant of  the need for broader spectrum antimicrobials.

Other noteworthy points in the guidelines include:

  • Although hospital-associated pneumonia (HAP) is still defined as a pneumonia not incubating at the time of admission and occurring 48 hrs or more following hospitalization, it now only refers to non-VAP cases; VAP cases are considered a separate category.
  • Emphasis is placed on each hospital generating antibiograms to guide providers with respect to the optimal choice of antibiotics.
  • Despite lack of supportive evidence, the guidelines recommend obtaining respiratory samples for culture in patients with HAP.
  • Prior intravenous antibiotic use within 90 days is cited as the only consistent risk factor for MDROs, including methicillin-resistant Staphylococcus aureus (MRSA) and Pseudomonas sp.

 

Reference

  1. Kalil AC, Metersky ML, Klompas M, et al. Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis 2016 ;63:e61-e111.  Advance Access published July 14, 2016. https://www.ncbi.nlm.nih.gov/pubmed/27418577
What are some of the major changes in the 2016 Infectious Diseases Society of America and the American Thoracic Society guidelines on pneumonia in hospitalized patients?