Can I have some tips on how to improve my PowerPoint presentation?

Effective or “high value” PowerPoint presentations take some planning and work. Here are some tips (by no means comprehensive) on how you can improve your PowerPoint presentation,1-4 divided into 4 stages:

Stage I: Planning for your talk

    • “Know your stuff”
    • Prioritize the main objectives of your talk given time  constraints ie, “What would you like your audience to really take away from your talk?”
    • Accept the fact that you will not be able to cover all that you know about the topic during the allotted time
    • Think about how you might keep your audience engaged throughout your talk as you introduce topics and concepts!

Stage II: Preparing your slides

  1. General rules
    • Keep them simple (“Less is more”)
      • Minimize number of slides eg, average no more than 1 slide/min
      • Minimize number of concepts/slide eg,1/slide
      • Minimize clutter 
    • Avoid “apologetic” slides ie, if not easily readable or visible or “too busy”, don’t use them!
    • Practice, practice, practice and edit as needed
  2.  Text
    • Minimize number of words/slide eg, 6×6 rule, maximum 6 words/line, 6 lines/slide
    • Use easily readable font types and sizes
      1. Minimum 24 for small rooms
      2. Minimum 36 for larger rooms
      3. If not readable 10 feet away from monitor, don’t include
    • Check spelling!
    • Choose high contrast colors between background and text eg, black text on white, yellow on dark blue background, not red on green
  3. Tables
    • Avoid reproduction of large tables with tons of data that cannot be read or can easily overwhelm the audience
    • If you use large tables, zero in on a particular section and display a magnified version of that section so that the audience can follow along with you

Stage III: Presenting your talk

  • Remember, you are the presenter, not PowerPoint
  • Engage the audience from the beginning to the end
    • Beginning: Use a “hook” ie, why should the audience be interested in your talk?
    • During
      • Maintain eye contact with the audience
      • Be dynamic/animate
      • Use speech intonations as if you are having a conversation with the audience
      • Do not read slides word-by-word
    • End: Highlight your take-home points eg, “if you don’t remember anything else…”

Stage IV: Post-Presentation

  • Ask for feedback from colleagues, audience, coordinators, etc… 
  • Self-reflect ie, what went well, what didn’t go so well?
  • Apply lessons learned to your next PowerPoint presentation!

Five take-home points for this pearl

  • Less is more, keep your presentation clear and simple
  • Time is limited; prioritize your message
  • Keep your audience engaged throughout the talk
  • Conclude with take-home points
  • Practice, practice, practice

Bonus Pearl: Did you know that people generally remember 20% of what they hear, 30% of what they see, and 50% of what they see and hear? 2

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References

  1. Collins J, et al. Evaluation of speakers at a national radiology continuing medical education course. Med Educ Online 2002;7:17 https://pubmed.ncbi.nlm.nih.gov/28253766/ 
  2. Collins J. Education techniques for lifelong learning. RadioGraphics 2004;24:1177-83. https://pubmed.ncbi.nlm.nih.gov/15256637/ 
  3. Harolds JA. Tips for giving a memorable presentation, Part IV. Using and composing PowerPoint slides. Current Nuclear Medicine 2012;37:977-80. https://pubmed.ncbi.nlm.nih.gov/22899205/ 
  4. Grech V. WASP (write a scientific paper):Optimization of PowerPoint presentations and skills. Early Human Development 2018;125:53-56.https://pubmed.ncbi.nlm.nih.gov/29929910/ 

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, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their 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!

Can I have some tips on how to improve my PowerPoint presentation?

Why doesn’t my patient with lactic acidosis have hyperkalemia?

Although hyperkalemia may be observed in a variety of conditions associated with metabolic acidosis, it is less likely to be seen in conditions associated with excess organic acids (eg, in lactic acidosis or diabetic ketoacidosis). A likely explanation for this finding revolves around the amazing organic anion transporter (OAT) and its attendant role in counteracting hyperkalemia by bringing potassium (K+) back into the cells.1-5 See details of impact of extracellular and intracellular pH on K+ homeostasis in Figure.1 

Recall that in metabolic acidosis the increased concentration of hydrogen ion (H+) outside the cell reduces sodium (Na+) influx into cells through the Na+-H+ exchange channel resulting in a drop in the intracellular Na+.  Since the Na+K+ATPase ion channel depends on the intracellular Na+ for bringing K+ into the cells, the end-result is higher K+ concentrations in the extracellular space, potentially resulting in hyperkalemia.  This is what is often seen in conditions of mineral (non-organic) acid excess (eg, in respiratory acidosis or poor renal function).

In the case of organic acidosis, however, the OAT also plays an important factor in K+ homeostasis (Figure)1.  As the name suggests, this transporter allows  organic acids such as lactic acid or ketones to enter the cell. As the H+ concentration increases intracellularly, there is more Na+-H+ exchange and more influx of Na+ into the cell.  More available Na+ intracellularly means more Na+ is pumped out by Na+K+ATPase, and more K+ is brought into the cell,1-5 mitigating the impact of metabolic acidosis on K+ efflux into the  extracellular space and potentially even causing hypokalemia! 

Concurrent hyperkalemia and lactic acidosis or diabetic ketoacidosis may of course still occur.  However, in such cases, hyperkalemia is often due to an epiphenomenon related to complicating factors.  In the case of lactic acidosis, this may be related to concurrent renal dysfunction,3 while in diabetic ketoacidosis it may be related to hyperosmolarity or insulin deficiency.1

So next time you see a patient who has hyperkalemia and lactic acidosis, ask yourself  “What else am I missing that can explain the hyperkalemia?“.

Bonus Pearl

Did you know that lactic acid in human blood was first discovered by the German physician–chemist, Johann Joseph Sherer, who sampled post-mortem blood from 2 women who died of puerperal fever in 1843? 6

Contributed by Nabi Chaudhri-Martinez MD, Mercy Hospital-St. Louis, St. Louis, Missouri

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References:

  1. Aronson PS, Giebisch G. Effects of pH on potassium: new explanations for old observations. J Am Soc Nephrol. 2011 Nov;22(11):1981-9. doi: 10.1681/ASN.2011040414. Epub 2011 Oct 6. PMID: 21980112; PMCID: PMC3231780. https://jasn.asnjournals.org/content/22/11/1981.long
  2. Orringer CE, Eustace JC, Wunsch CD, Gardner LB. Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated with hyperkalemia. N Engl J Med. 1977 Oct 13;297(15):796-9. doi: 10.1056/NEJM197710132971502. PMID: 19702. https://www.nejm.org/doi/10.1056/NEJM197710132971502?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
  3. Fulop M. Serum potassium in lactic acidosis and ketoacidosis. N Engl J Med. 1979 May 10;300(19):1087-9. doi: 10.1056/NEJM197905103001905. PMID: 34793. https://www.nejm.org/doi/10.1056/NEJM197905103001905?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub 0pubmed
  4. Adrogué HJ, Madias NE. Changes in plasma potassium concentration during acute acid-base disturbances. Am J Med. 1981 Sep;71(3):456-67. doi: 10.1016/0002-9343(81)90182-0. PMID: 7025622. https://www.amjmed.com/article/0002-9343(81)90182-0/pdf
  5. Nigam SK, Bush KT, Martovetsky G, et al. The organic anion transporter (OAT) family: A systems biology perspective. Physiol Rev 2015;95:83:123. The Organic Anion Transporter (OAT) Family: A Systems Biology Perspective (physiology.org)
  6. Kompanje EJ, Jansen TC, van der Hoven B, Bakker J. The first demonstration of lactic acid in human blood in shock by Johann Joseph Scherer (1814-1869) in January 1843. Intensive Care Med. 2007;33(11):1967-1971. doi:10.1007/s00134-007-0788-7 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040486/

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, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their 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!

Why doesn’t my patient with lactic acidosis have hyperkalemia?

Does my patient testing positive for hepatitis A IgM really have acute hepatitis A infection even though he is completely asymptomatic?

Not necessarily! A positive hepatitis A (HA) IgM in a patient without any symptoms could indicate a few different things: 1. Asymptomatic infection; 2. Prior HA infection with prolonged IgM presence; 3. False positive results due to cross-reacting antibodies; and 4. Commercial kits with a falsely low cutoff value.1

A 2013 retrospective study found that of patients testing positive for HA IgM antibody, only 11% could be confirmed to have acute HA infection; 57% had recent and/or resolved hepatitis and 29% had reasons to have elevated hepatic enzymes other than HA infection, at least some likely to be false-positive.1

Other viral illnesses and autoimmune conditions have been associated with false positive HA-IgM.1-3  One case report described a patient with malaise, fever, jaundice, and elevated liver enzymes who tested positive for HA-IgM but ultimately was found to be infected with Epstein-Barr virus (EBV)2. In another case report, a patient was described as having a drug-induced liver injury in the setting of infliximab usage. False positive Hep A IgM was suspected to be due to a polyclonal B-cell autoimmune-mediated response stimulated by the infliximab.3

So, even a positive HA-IgM should always be interpreted in the context of the patient’s history and likelihood of active HA infection based on epidemiological factors.1

Bonus Pearl: Did you know that modes of transmission of HA include person-to-person via saliva or sex, consuming raw/undercooked shellfish, or drinking contaminated drinking water?4

Contributed by Joseph Kinsella, Medical Student, A.T. Still Osteopathic Medical School,  Kirksville, Missouri

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References

  1. Alatoom A., Ansari M. Q, Cuthbert J. (2013). Multiple factors contribute to positive results for hepatitis a virus immunoglobulin M antibody. Arch Pathol Lab Med 2013;137:90–95. https://doi.org/10.5858/arpa.2011-0693-oa
  2. Valota M, Thienemann F, Misselwitz B. False-positive serologies for acute hepatitis A and autoimmune hepatitis in a patient with acute Epstein–Barr virus infection. BMJ Case Reports CP 2019;12: e228356.
  3. Tennant E, Post JJ. Production of false-positive immunoglobulin m antibodies to hepatitis a virus in autoimmune events. J Infect Dis 2016;213: 324–325. https://doi.org/10.1093/infdis/jiv417
  4. Mayo Foundation for Medical Education and Research. (2020, August 28). Hepatitis A. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/hepatitis-a/symptoms-causes/syc-20367007.

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, Mass General Hospital, Harvard Medical School or its affiliated institutions. 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!

Does my patient testing positive for hepatitis A IgM really have acute hepatitis A infection even though he is completely asymptomatic?

What’s the evidence that immunocompromised patients need a 3rd booster mRNA Covid vaccine shot?

At this time, the Centers for Disease Control and Prevention (CDC) recommendation for a booster shot of an mRNA vaccine in patients with moderate to severe immunocompromised state (1,2) is based primarily on the concern for waning immunity following the initial series—including a decline in neutralizing antibodies— in this patient population, and the finding that at least some immunocompromised patients may have a significant improvement in certain laboratory measurements of immunity following their booster shot. 

Although there are no randomized-controlled trials of the efficacy of the 3rd shot in protecting against Covid-19 in immunocompromised patients, the recent surge in the highly transmissible SARS-CoV-2 variants in many parts of the world (including the U.S.)  as well as immunocompromised patient population accounting for nearly one-half of all breakthrough Covid-19 cases requiring hospitalization (1) make it urgent to adopt these recommendations. 

A randomized trial involving 120 solid organ transplant patients (median age 67 y) found higher neutralizing antibody levels and SARS CoV-2 specific T-cell counts after the mRNA-1273 (Moderna) vaccine booster dose compared to placebo (3).

In another study involving 101 solid organ transplant patients, of 59 subjects who were seronegative before the 3rd dose, 44% became seropositive 4 weeks after the 3rd vaccine dose ( BNT162b2-Pfizer vaccine administered 2 months after the second dose). Patients who did not have an antibody response were older, had higher degree of immunosuppression and had a lower estimated glomerular filtration rate than those with antibody response (4).

A “spectacular increase” in anti-spike antibodies with levels close to the general population has also been reported among hemodialysis patients receiving a third dose of Pfizer mRNA vaccine (5). 

Until further data from larger studies become available,  these studies support administration of a 3rd dose booster mRNA vaccine in moderate to severely immunosuppressed individuals.

Bonus Pearl: Did you know that although immunocompromised patients have significantly worse influenza outcome, the data on the impact of immunocompromised status on the outcome of Covid-19 is less clear with published evidence that both supports and refutes this association (6)?  

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References

  1. CDC. Data and clinical considerations for additional doses in immunocompromised people: ACIP Meeting, July 22, 2021. ACIP Data and Clinical Considerations for Additional Doses in Immunocompromised People (cdc.gov)
  2. CDC. Interim clinical considerations for use of Covid-19 vaccines currently authorized in the United States. August 13, 2021. Interim Clinical Considerations for Use of COVID-19 Vaccines | CDC
  3. Hall VG, Ferreira VH, Ku T, et al. Randomized trial of a third dose of mRNA-1273 vaccine recipients. N Engl J Med 2021, Aug 11. Randomized Trial of a Third Dose of mRNA-1273 Vaccine in Transplant Recipients | NEJM
  4. Kamar N, Abravanel F, Marion O. Three doses of an mRNA Covid-19 vaccine in solid-organ transplant recipient. N Engl J Med 2021, Aug 12.Three Doses of an mRNA Covid-19 Vaccine in Solid-Organ Transplant Recipients | NEJM
  5. Frantzen L, Thibeaut S, Moussi-Frances J, et al. Covid-19 vaccination in haemodialysis patients: Good things come in threes… Neph Dial Transplant, 20 July 2023. COVID-19 Vaccination in Haemodialysis Patients: Good things come in threes… – PubMed (nih.gov)
  6. Parisi C. An opportunity to better understand the impact of coronavirus on immunocompromised patients. J Infect Dis 2021;224:372-3. Opportunity to Better Understand the Impact of Coronaviruses on Immunocompromised Patients | The Journal of Infectious Diseases | Oxford Academic (oup.com)

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate 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!

What’s the evidence that immunocompromised patients need a 3rd booster mRNA Covid vaccine shot?

What’s the connection between severe hypoglycemia and hypothermia?

The association of severe hypoglycemia and low body temperatures has been well documented at least since 1960s.  Hypothermia is thought to be caused by low blood glucose in the brain (neuroglucopenia) which may serve as a protective mechanism for decreasing energy demand during glucose deprivation.1-2

A 2012 retrospective study involving mostly patients with diabetes mellitus with severe hypoglycemia (majority with serum glucose 18-54 mg/dl) found that 23% of patients had hypothermia (defined as body temperature < 95◦F or 35◦C). The incidence of hypothermia was not affected by age, diabetes, season or time of day.  Two patients had extremely low temperatures (<90◦F).  There was an association between hypothermia and severity of hypoglycemia.1

An older experimental study (1974) involving 36 recumbent nude men in thermoneutral environment found that that insulin-induced hypoglycemia was associated with rectal temperatures below 96.2◦F (36◦C) in 33%.  Cooling was attributed to reduction in heat production and to secretion of sweat, peripheral vasodilatation and hyperventilation.2

But before you attribute hypothermia to hypoglycemia, make sure other causes of hypothermia such as sepsis, hypoadrenalism, hypothyroidism, alcohol and stroke are ruled out.3  

Bonus Pearl: Did you know that heat production is accomplished by shivering, which can increase the normal basal metabolic rate by 2-5 times as well as via non-shivering thermogenesis through increased levels of thyroxine and epinephrine?3

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References

  1. Tran C, Gariani K, Hermann FR, et al. Hypothermia is a frequent sign of severe hypoglycaemia in patients with diabetes. Diab Metab 2012;38:370-72. https://www.sciencedirect.com/science/article/abs/pii/S1262363612000535?via%3Dihub
  2. Strauch BS, Felig P, Baxter JD, et al. Hypothermia in hypoglycemia. JAMA 1969;210:345-46. https://jamanetwork.com/journals/jama/article-abstract/349081
  3. McCullough L, Arora S. Diagnosis and treatment of hypothermia. Am Fam Physician 2004;70:2325-2332. https://www.aafp.org/afp/2004/1215/p2325.html

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, Mass General Hospital, Harvard Medical School or its affiliated institutions. 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!

What’s the connection between severe hypoglycemia and hypothermia?

“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?”

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?”

How effective are face masks in reducing transmission of Covid-19?

Overall, review of data to date suggests that face masks are quite effective in reducing the transmission of coronaviruses, including SARS-CoV-2, the cause of Covid-19. A Lancet 2020 meta-analysis involving over 12,000 subjects, found that transmission of coronaviruses (SARS-CoV-2, SARS and MERS) was reduced with face masks by 85% (adjusted O.R. 0.15, 95%CI 0.07-0.34).1

More specific to Covid-19, a study from Mass General Brigham hospitals found a significant drop in healthcare worker (HCW) SARS-CoV-2 PCR positivity rate from 21.3% to 11.5% following adoption of universal masking of HCWs and patients.2

An U.S. epidemiologic survey of 2,930 unique counties plus New York City found mandating face mask use in public was associated with a significant decline in the daily Covid-19 growth rate. 3 It was estimated that more than 200,000 Covid-19 cases were averted by May 22, 2020 as a result of the implementation of these mandates.

Another 2020 meta-analysis involving 21 studies reported an overall efficacy of masks (including surgical and N-95 masks) of 80% in healthcare workers and 47% in non-healthcare workers for respiratory virus transmission (including SARS, SARS-CoV-2 and influenza).4

A criticism of above reports has been their primarily retrospective nature. A randomized-controlled Danish study found a statistically insignificant 20% reduction in incident SARS-CoV-2 infection among mask wearers (5,6).    Despite its randomized-controlled design, this study had several limitations, including relatively low transmission rate in the community and lack of universal mask wearing in public during the study period. In addition, less than one-half of participants in the mask group reported adherence to wearing masks, and there was no assurance that masks were worn correctly when they did wear them. 

At most, this study suggests that it’s not enough for the uninfected to wear masks; the infected—often with little or no symptoms— should also wear them to help curb the pandemic.

So please do your part and tell your friends and family members to do the same by masking up while we are at war with Covid-19!

Bonus Pearl: Did you know that universal wearing of masks in the public in response to a respiratory virus pandemic is nothing new?  It was adopted as far back as 100 years ago during the 1918 Spanish influenza pandemic!

References

  1. Chu DK, Akl EA, Duda S, et al. Physical distancing, face masks, and eye protection to prevent person-to-person transmission of SARS-CoV-2 and COVID-19: a systematic review and meta-analysis. Lancet 2020;395: 1973-87. https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(20)31142-9.pdf
  2. Wang X, Ferro EG, Zhou G, et al. Association between universal masking in a health care system and SARS-CoV-2 positivity among health care workers. JAMA 2020;324:703-4. https://jamanetwork.com/journals/jama/fullarticle/2768533
  3. Lyu W, Wehby GL. Community use of face masks and COVID-19: evidence from a natural experiment of state mandates in the US. Health Affairs 2020;39: July 16. https://www.healthaffairs.org/doi/full/10.1377/hlthaff.2020.00818
  4. Liang M, Gao L, Cheng Ce, et al. Efficacy of face mask in preventing respiratory virus transmission: A systematic review and meta-analysis. Travel Med Infect Dis 2020;36:1-8. https://pubmed.ncbi.nlm.nih.gov/32473312/ 
  5. Bundgaard H, Bundgaard JS, Tadeusz DE, et al. Effectiveness of adding a mask recommendation to other public health measures to prevent SARS-CoV-2 infection in Danish mask wearers. Ann Intern Med 2020; November 18. https://pubmed.ncbi.nlm.nih.gov/33205991/
  6. Frieden TR Cash-Goldwasser S. Of masks and methods. Ann Intern Med 2020; November 18. https://www.acpjournals.org/doi/10.7326/m20-7499

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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!

How effective are face masks in reducing transmission of Covid-19?

How does iron overload increase the risk of infection?

Iron overload, either primary (eg, hereditary hemochromatosis) or secondary (eg, hemolysis/frequent transfusion states), may increase the risk of infections through at least 2 mechanisms: 1. Enhancement of the virulence of the pathogen; and 2. Interference with the body’s normal defense system.1-7

Excess iron has been reported to enhance the growth of numerous organisms, ranging from bacteria (eg, Yersinia, Shigella, Vibrio, Listeria, Legionella, Ehrlichia, many other Gram-negative bacteria, staphylococci, streptococci), mycobacteria, fungi (eg, Aspergillus, Rhizopus/Mucor, Cryptococcus, Pneumocystis), protozoa (eg, Entamaeba, Plasmodium, Toxoplasma) and viruses (HIV, hepatitis B/C, cytomegalovirus, parvovirus). 1-7

In addition to enhancing the growth of many pathogens, excess iron may also inhibit macrophage and lymphocyte function and neutrophil chemotaxis .1,2 Iron loading of macrophages results in the inhibition of interferon-gamma mediated pathways and loss of their ability to kill intracellular pathogens such as Legionella, Listeria and Ehrlichia. 2

Not surprisingly, there are numerous reports in the literature of infections in hemochromatosis, including Listeria monocytogenes meningitis, E. Coli septic shock, Yersinia enterocolitica sepsis/liver abscess, Vibrio vulnificus shock (attributed to ingestion of raw oysters) and mucormycosis causing periorbital cellulitis. 2

Bonus pearl: Did you know that the ascitic fluid of patients with cirrhosis has low transferrin levels compared to those with malignancy, potentially enhancing bacterial growth and increasing their susceptibility to spontaneous bacterial peritonitis? 8

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 References

  1. Weinberg ED, Weinberg GA. The role of iron in infection. Curr Opin Infect Dis 1995;8:164-69. https://journals.lww.com/co-infectiousdiseases/abstract/1995/06000/the_role_of_iron_in_infection.4.aspx
  2. Khan FA, Fisher MA, Khakoo RA. Association of hemochromatosis with infectious diseases: expanding spectrum. Intern J Infect Dis 2007;11:482-87. https://www.sciencedirect.com/science/article/pii/S1201971207000811
  3. Thwaites PA, Woods ML. Sepsis and siderosis, Yersinia enterocolitica and hereditary haemochromatosis. BMJ Case Rep 2017. Doi:10.11336/bvr-206-218185. https://casereports.bmj.com/content/2017/bcr-2016-218185
  4. Weinberg ED. Iron loading and disease surveillance. Emerg Infect Dis 1999;5:346-52. https://wwwnc.cdc.gov/eid/article/5/3/99-0305-t3
  5. Matthaiou EI, Sass G, Stevens DA, et al. Iron: an essential nutrient for Aspergillus fumigatus and a fulcrum for pathogenesis. Curr Opin Infect Dis 2018;31:506-11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6579532/
  6. Alexander J, Limaye AP, Ko CW, et al. Association of hepatic iron overload with invasive fungal infection in liver transplant recipients. Liver Transpl 12:1799-1804. https://aasldpubs.onlinelibrary.wiley.com/doi/full/10.1002/lt.20827
  7. Schmidt SM. The role of iron in viral infections. Front Biosci (Landmark Ed) 2020;25:893-911. https://pubmed.ncbi.nlm.nih.gov/31585922/
  8. Romero A, Perez-Aurellao JL, Gonzalez-Villaron L et al. Effect of transferrin concentration on bacterial growth in human ascetic fluid from cirrhotic and neoplastic patients. J Clin Invest 1993;23:699-705. https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1365-2362.1993.tb01289.x

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!

How does iron overload increase the risk of infection?

Can I use fist bump when I greet my patients or coworkers in the hospital?

Fist bump may be a safer practice than handshake with respect to transfer of potential pathogens but should not be considered a “safe”’ alternative. Studies to date have demonstrated transfer of bacteria even with fist bump, albeit often at lower counts. 1-3

In an experimental study involving healthcare workers in a hospital,1 fist bump was still associated with bacterial colonization, albeit at levels 4 times less than that of palmar surfaces following handshakes. Smaller contact surface area and reduced total contact time were thought to contribute to lower risk of bacterial transfer via fist bump.

In another experiment involving E. coli, fist bump was associated with ~75% less transfer of bacteria relative to “moderate handshake”.2

Interestingly, in a 2020 study of 50 methicillin-resistant Staphylococcus aureus (MRSA)-colonized patients,3 the rate of MRSA isolated from the fist after a fist bump was not significantly lower than that of the dorsal surface of the hand after a handshake (16% vs 22%, P=0.6).  

In contrast, “cruise tap”, defined as contact between 2 knuckles alone, may be safer than fist bump. In the MRSA study above, cruise tap was associated with significantly lower rate of bacterial transfer compared to handshakes (8% vs 22%, P=0.02).3

Even a safer alternative is to avoid skin-to-skin contact altogether by using elbow bump, or no “bump” at all, particularly in the Covid-19 era!

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References

  1. Ghareeb PA, Bourlai T, Dutton W, et al. Reducing pathogen transmission in a hospital setting. Handshake verses fist bump: a pilot study. https://pubmed.ncbi.nlm.nih.gov/24144553/
  2. Mela S, Withworth DE. The fist bump: A more hygienic alternative to the handshake. Am J Infect Control 2014;42:916-7. http://www.apic.org/Resource_/TinyMceFileManager/Fist_bump_article_AJIC_August_2014.pdf
  3. Pinto-Herrera NC, Jones LD, Ha W, et al. Transfer of methicillin-resistant Staphylococcus aureus by first bump versus handshake. Infect Control Hospital Epidemiology 2020;41:962-64. https://pubmed.ncbi.nlm.nih.gov/32456719/

 

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!

Can I use fist bump when I greet my patients or coworkers in the hospital?

How often is Covid-19 in hospitalized patients complicated by bacterial infection?

Despite frequent use of empiric antibiotics in hospitalized patients with Covid-19,current data suggests a low rate of documented bacterial co-infection (BCI) in such patients. In fact, the overall reported rate of BCI in hospitalized patients with Covid-19 is generally no greater than 10%.1-3   It’s quite likely that most patients with Covid-19 and chest radiograph changes solely have a coronavirus (SARS-CoV-2) lung infection,4 particularly early in the course of the disease.  

A meta-analysis involving 30 studies (primarily retrospective) found that overall 7% of hospitalized Covid-19 patients had a laboratory-confirmed BCI with higher proportion among ICU patients (14%).Mycoplasma pneumoniae was the most common (42% of BCIs), followed by Pseudomonas aeruginosa and H. influenzae.  Notably, diagnosis of M. pneumoniae infection was based on antibody testing for IgM, which has been associated with false-positive results. Other caveats include lack of a uniform definition of respiratory tract infection among studies and potential impact of concurrent or prior antibiotic therapy on the yield of bacteriologic cultures. 5,6

A low prevalence of BCI was also found in a UK study involving 836 hospitalized Covid-19 patients: 3.2% for early BCI (0-5 days after admission) and 6.1% throughout hospitalization, including hospital-acquired infections.Staphylococcus aureus was the most common respiratory isolate among community-acquired cases, while Pseudomonas spp. was the predominant healthcare associated respiratory isolate.  Similarly, S. aureus. and Streptococcus pneumoniae were the most commonly isolated organisms from blind bronchoalveolar lavage of critically ill patients with Covid-19 during their first 5 days of admission, while gram-negative bacilli became dominant later during the hospitalization.8

The discordance between high rates of antibiotic treatment and confirmed bacterial co-infection in Covid-19 patients is likely a reflection of the difficulty in distinguishing Covid-19 pneumonia from bacterial pneumonia based on clinical or radiographic findings alone.

We need better tests to help distinguish bacterial vs Covid-19 pneumonia. Some have suggested using a low serum procalcitonin to help guide the withholding of or early discontinuation of antibiotics, especially in less severe Covid-19 cases. Formal studies of the accuracy of procalcitonin in Covid-19 are needed to test this hypothesis, given its suboptimal sensitivity in bacterial community-acquired pneumonia. 

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Reference

  1. Stevens RW, Jensen K, O’Horo JC, et al. Antimicrobial prescribing practices at a tertiary-care center in patients diagnosed with COVID-19 across the continuum of care. Infect Control Hosp Epidemiology 2020. https://reference.medscape.com/medline/abstract/32703323
  2. Lansbury L, Lim B, Baskaran V, et al. Co-infections in people with COVID-19: a systematic review and meta-analysis. J Infect 2020;81:266-75. https://pubmed.ncbi.nlm.nih.gov/32473235/
  3. Rawson TM, Moore LSP, Zhu N. Bacterial and fungal co-infection in individuals with coronavirus: A rapid review to support COVID-19 antimicrobial prescribing. Clin Infect Dis 2020 (Manuscrpit published online ahead of print 2 June ). Doi:10.1093/cid/ciaa530.https://pubmed.ncbi.nlm.nih.gov/32358954/
  4. Metlay JP, Waterer GW. Treatment of community-acquired pneumonia during the coronavirus 2019 (COVID-19) pandemic. Ann Intern Med 2020; 173:304-305. https://pubmed.ncbi.nlm.nih.gov/32379883/
  5. Chang CY, Chan KG. Underestimation of co-infections in COVID-19 due to non-discriminatory use of antibiotics. J Infect 2020;81:e29-30. https://pubmed.ncbi.nlm.nih.gov/32628960/
  6. Rawson TM, Moore LSP, Zhu N, et al. Bacterial pneumonia in COVID-19 critically ill patients: A case series. Reply letter. Clin Infect Dis 2020. https://academic.oup.com/cid/advance-
  7. Hughes S, Troise O, Donaldson H, et al. Bacterial and fungal coinfection among hospitalized patients with COVID-19: a retrospective cohort study in a UK secondary-care setting. Clin Microbiol Infect 2020. https://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(20)30369-4/fulltext
  8. Dudoignon E, Camelena F, Deniau B, et al. Bacterial pneumonia in COVID-19 critically ill patients: A case series. Clin Infect Dis 2020. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7337703/

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!

How often is Covid-19 in hospitalized patients complicated by bacterial infection?