Month: April 2025

Microbiology Case Study: Diarrhea in a Patient with Renal Transplant

Case History

            A-58-year-old female with past medical history of breast cancer in remission, renal transplant 8 years ago on tacrolimus, now presenting with inability to tolerate oral intake, dyspnea on exertion and gastrointestinal symptoms such as profuse foul-smelling, non-bloody diarrhea, and vomiting. She denied exposure to sick contacts, recent travel, or changes in diet. She had other co-morbidities including hypertension, atrial arrhythmia, hyperlipidemia, and past C. difficile infection. On the physical exam, she was afebrile, normotensive, with a normal heart rate and rhythm, and her abdomen is soft and non-distended, with tenderness to palpation. Cardiology was consulted due to new onset paroxysmal atrial fibrillation on telemetry, and the renal transplant team was contacted for admission in concern for her rising creatinine. Upon admission to the floor, the patient had 2 more loose stools which were collected for stool culture and multiplex, syndromic gastrointestinal PCR panel, which tested positive for norovirus. She was kept on contact precautions.

Discussion

            Norovirus is a single stranded positive-sense RNA virus belonging to the Calciciviridae family. Noroviruses are divided into 10 genogroups based on the amino acid sequence of VP1, the norovirus capsid protein. Genogroups GI and GII account for 90% of reported infections including outbreaks, with the GII.4 genotype being the cause of most severe disease, and it is more frequently implicated in outbreaks than other genotypes (1).

            The median incubation period for norovirus infections is 1.2 days, with most symptomatic patients presenting with diarrhea and vomiting. Asymptomatic shedding of norovirus is common, mainly in the pediatric population, where 11.6 – 49.2% of stool samples were found to contain norovirus in random recruitment studies globally. Most patients with norovirus infection have spontaneous resolution of symptoms by the third day of illness. Elderly, young, and immunocompromised patients face greater risk of severe and prolonged symptoms from norovirus infection. Chronic infection with norovirus may occur in immunocompromised hosts, with associated symptoms lasting up to weeks or months in these patients (2).

            Transmission of norovirus occurs through oral-oral and fecal-oral routes, and transmission can occur directly via exposure to human emesis or feces, or through contamination of food, water, or fomites with such samples. Median viral titers have been recorded at 3.9 x 104 copies/mL in emesis samples from patients with norovirus GII, with aerosolization of viral particles possible due to projectile vomiting and toilet flushing (de Graaf). Once inoculated, norovirus particles primarily infect macrophages and dendritic cells in the gastrointestinal tract, with current reports suggesting that particles enter these cells via attachment to blood group antigens, or HGBAs, and Toll-like receptors (3). VP1, the capsid protein of norovirus, has been found to induce expression of aquaporin-1 in human intestinal cell culture. This leads to small molecule permeability at the intestinal barrier, which likely leads to the watery diarrhea seen in norovirus infection (4).

            Norovirus is implicated as the cause of 19% of all acute gastroenteritis cases globally, with virtually every country reporting norovirus cases (5). These infections frequently occur in the form of outbreaks, with the highest rates of infection recorded in the winter months (Figure 1). Crowded and closed environments, including daycare centers, cruise ships, and restaurants, are known facilitators of outbreaks. More than half of all norovirus outbreaks are reported in healthcare settings, such as hospitals and long-term care facilities (6).  

Figure 1. Increase in norovirus outbreaks was reported in 2025. (Data adapted from CDC: Norovirus Outbreaks Reported by State Health Departments. https://www.cdc.gov/norovirus/php/reporting/norostat-data-table.html)

Immunological assays (e.g., antigen detection) and transmission electron microscopy can be used for detection of gastrointestinal viruses, but these methods have limited sensitivity and specificity and not recommended for clinical diagnosis (7). Laboratory detection by molecular methods is the preferred method for norovirus diagnosis. Testing of stool specimens may be performed on single plex or FDA-approved, commercially available, multiplex syndromic PCR panels. While PCR is the most sensitive approach, false-positives have been reported (8). Five regions of the genome (A,B,C,D, and E) of the norovirus genome have been used for genotyping while viral capsid gene (encoded by regions C, D, and E) is typically used given the viral capsid being involved in host-receptor interactions and immune response (9). In certain instances, sequencing and detection of the ORF1 and ORF2 genes may help identify strains after antigenic drift events (10).

            Oral or intravenous rehydration is the mainstay of norovirus treatment in all patients. In immunocompetent patients, norovirus is expected to resolve spontaneously (11). Chronic symptomatic infection with norovirus in immunocompromised patients poses a significant clinical challenge, especially when reduction in immunosuppressants is not feasible. In such patients, case reports have suggested that nitazoxanide may achieve resolution of symptoms, and one retrospective study proposed that addition of metronidazole led to resolution of norovirus symptoms in nitazoxanide-refractory cases (12-14). However, no randomized controlled trials have demonstrated the efficacy of nitazoxanide or metronidazole in chronic norovirus infection. Norovirus vaccines are currently in development, but challenges include high genetic diversity of circulating strains, lack of understanding regarding herd immunity and correlates of immune response, and the lack of standardized testing approaches such as cell cultures or animal models for efficacy studies.

References

1. Carlson KB, Dilley A, O’Grady T, Johnson JA, Lopman B, Viscidi E. A narrative review of norovirus epidemiology, biology, and challenges to vaccine development. NPJ Vaccines. 2024;9(1):94. Published 2024 May 29. doi:10.1038/s41541-024-00884-2

2. Robilotti E, Deresinski S, Pinsky BA. Norovirus. Clin Microbiol Rev. 2015;28(1):134-164. doi:10.1128/CMR.00075-14

3. Chen J, Cheng Z, Chen J, Qian L, Wang H, Liu Y. Advances in human norovirus research: Vaccines, genotype distribution and antiviral strategies. Virus Res. 2024;350:199486. doi:10.1016/j.virusres.2024.199486

4. Zhang M, Zhang B, Chen R, et al. Human Norovirus Induces Aquaporin 1 Production by Activating NF-κB Signaling Pathway. Viruses. 2022;14(4):842. Published 2022 Apr 18. doi:10.3390/v14040842

5. Zhang P, Hao C, Di X, et al. Global prevalence of norovirus gastroenteritis after emergence of the GII.4 Sydney 2012 variant: a systematic review and meta-analysis. Front Public Health. 2024;12:1373322. Published 2024 Jun 27. doi:10.3389/fpubh.2024.1373322

6. Tsai H, Yune P, Rao M. Norovirus disease among older adults. Ther Adv Infect Dis. 2022;9:20499361221136760. Published 2022 Nov 14. doi:10.1177/20499361221136760

7. Rabenau HF, Stürmer M, Buxbaum S, Walczok A, Preiser W, Doerr HW. Laboratory diagnosis of norovirus: which method is the best? Intervirology. 2003;46(4):232-8. doi: 10.1159/000072433.

8. Caza M, Kuchinski K, Locher K, Gubbay J, Harms M, Goldfarb DM, Floyd R, Kenmuir E, Kalhor M, Charles M, Prystajecky N, Wilmer A. Investigation of suspected false positive norovirus results on a syndromic gastrointestinal multiplex molecular panel. J Clin Virol. 2024 Dec;175:105732. doi: 10.1016/j.jcv.2024.105732. Epub 2024 Sep 30. 

9. Mattison K, Grudeski E, Auk B, Brassard J, Charest H, Dust K, Gubbay J, Hatchette TF, Houde A, Jean J, Jones T, Lee BE, Mamiya H, McDonald R, Mykytczuk O, Pang X, Petrich A, Plante D, Ritchie G, Wong J, Booth TF. Analytical performance of norovirus real-time RT-PCR detection protocols in Canadian laboratories. J Clin Virol. 2011 Feb;50(2):109-13. doi: 10.1016/j.jcv.2010.10.008. Epub 2010 Nov 10.

10. Mattison K, Grudeski E, Auk B, Charest H, Drews SJ, Fritzinger A, Gregoricus N, Hayward S, Houde A, Lee BE, Pang XL, Wong J, Booth TF, Vinjé J. Multicenter comparison of two norovirus ORF2-based genotyping protocols. J Clin Microbiol. 2009 Dec;47(12):3927-32. doi: 10.1128/JCM.00497-09. Epub 2009 Oct 21.

11. Mirza S, Hall A. Norovirus | CDC Yellow Book 2024. wwwnc.cdc.gov. Published May 1, 2023. https://wwwnc.cdc.gov/travel/yellowbook/2024/infections-diseases/norovirus

12. Haubrich K, Gantt S, Blydt-Hansen T. Successful treatment of chronic norovirus gastroenteritis with nitazoxanide in a pediatric kidney transplant recipient. Pediatr Transplant. 2018;22(4):e13186. doi:10.1111/petr.13186

13. Siddiq DM, Koo HL, Adachi JA, Viola GM. Norovirus gastroenteritis successfully treated with nitazoxanide. J Infect. 2011;63(5):394-397. doi:10.1016/j.jinf.2011.08.002

14. Soneji M, Newman AM, Toia J, Muller WJ. Metronidazole for treatment of norovirus in pediatric transplant recipients. Pediatr Transplant. 2022;26(8):e14390. doi:10.1111/petr.14390

-Brendan Sweeney is a third-year medical student at the George Washington University School of Medicine and Health Sciences. His research interests include infectious diseases, hematopathology, and point of care diagnostics.

-Rebecca Yee, PhD, D(ABMM), M(ASCP)CM is the Chief of Microbiology, Director of Clinical Microbiology and Molecular Microbiology Laboratory at the George Washington University Hospital. Her interests include bacteriology, antimicrobial resistance, and development of infectious disease diagnostics.

Primary Biliary Cholangitis: Insights into Diagnosis, Symptoms, and Treatment

Introduction

Primary Biliary Cholangitis (PBC), formerly known as Primary Biliary Cirrhosis, is a chronic autoimmune disorder that gradually destroys the small bile ducts of the liver. This progressive destruction results in inflammation and cholestasis. Prolonged hepatic cholestasis results in fibrosis and cirrhosis and, if left unmanaged, ultimately, liver failure. This article aims to provide key insights into this rare condition.

Overview

Primary biliary cholangitis is considered an autoimmune disease in that liver injury is sustained by the presence of self-directed anti-mitochondrial antibodies (AMA) that target the bile duct cells.1 While PBC remains elusive, studies suggest that the combination of environmental triggers and genetic factors elicit PBC. Environmental triggers may include exposure to toxic chemicals, smoking cigarettes, and infections such as urinary tract infections.2 The inflammation that occurs in PBC is thought to result from a direct insult of environmental factors and toxins.3 Sex and age may also increase the risk of PBC, as it is more common among women worldwide and generally diagnosed between the ages of 30-60.2 Prognosis may be dependent on early detection and response to treatment.

Presentation

In the early stages, most patients may be asymptomatic, as up to 60% of patients do not exhibit signs or symptoms at diagnosis.4 Common early symptoms may include fatigue and itchy skin. Later signs and symptoms of PBC may include jaundice, ascites, upper right quadrant abdominal pain, splenomegaly, bone, muscle, and joint pain, steatorrhea, osteoporosis, dry eyes and mouth, xanthomas, hyperpigmentation, and hypothyroidism.2 These symptoms may affect people to varying degrees; they can occur earlier or later in the disease course and may appear mild to severe at any stage.5 Incidentally, asymptomatic patients may be diagnosed when blood tests are ordered for other reasons, such as routine testing.2

Image courtesy of Ipsen Biopharmaceuticals4

Lab Findings

Tests to diagnose PBC may include imaging tests, blood tests, and liver biopsy. The diagnostic criteria for PBC include an absence of any other liver disease, no signs of extrahepatic biliary obstruction on imaging tests, and at least 2 out of 3 of the following:

•           Elevation of alkaline phosphatase (ALP) at least 1.5 times the upper limit of normal

•           The presence of anti-mitochondrial antibody (AMA) with a titer of 1:40 or higher

•           Histopathological evidence of primary biliary cirrhosis.3

Those patients who are asymptomatic with abnormal liver chemistry, specifically abnormal ALP, should be evaluated for PBC. Also, patients experiencing nonspecific right upper quadrant pain, unexplained itching, fatigue, jaundice, hyperpigmentation, or unintentional weight loss should be assessed for PBC.3 In cases of atypical disease presentation with elevated ALP but normal AMA, alternative diagnoses should be explored, and a liver biopsy may be necessary for confirmation.3 However, it is important to note that liver biopsy is not required for diagnosis; instead, it is helpful in disease prognosis and staging. Patients with primary biliary cholangitis may develop iron deficiency anemia secondary to chronic blood loss caused by portal hypertensive gastropathy. In addition to anemia, patients who have already developed cirrhosis may have an elevated prothrombin time (PT), thrombocytopenia, and leukopenia.3

Treatment and Management

The key aim of therapy for primary biliary cholangitis is to halt disease progression while addressing the symptoms and complications associated with chronic cholestasis. Medications approved by the Food and Drug Administration (FDA) are currently available to help slow disease progression. Among FDA-approved treatments, Ursodeoxycholic acid (UDCA) is the most commonly prescribed and typically used as the first line of therapy. While UDCA does not cure primary biliary cholangitis (PBC), it aids in bile flow through the liver and has been shown to improve liver function and slow the progression of liver scarring.² However, additional therapies are often needed to manage symptoms such as fatigue, itching, dry eyes and mouth, and other complications associated with PBC.

Conclusion

Primary biliary cholangitis (PBC) is a rare but significant autoimmune disorder that progressively damages the liver, leading to cholestasis, fibrosis, and potentially liver failure if untreated. Early detection and intervention are crucial in mitigating disease progression and managing associated symptoms. Diagnostic criteria, including the presence of AMA and elevated ALP, play a pivotal role in identifying PBC, even in asymptomatic patients. Effective therapies like ursodeoxycholic acid (UDCA) have demonstrated their ability to slow progression and improve patient outcomes, though addressing symptoms and complications remains a critical component of care. By understanding the pathophysiology, presentation, and treatment of PBC, healthcare providers can better support patients with this challenging condition.

References

1Lenci I, Carnì P, Milana M, Bicaj A, Signorello A, Baiocchi L. Sequence of events leading to primary biliary cholangitis. World J Gastroenterol. 2023 Oct 7;29(37):5305-5312. doi: 10.3748/wjg.v29.i37.5305. PMID: 37899786; PMCID: PMC10600805.

2Mayo Clinic [Internet]. Rochester (MN): Mayo Foundation for Medical Education and Research; c1998-2025. Primary biliary cholangitis: symptoms and causes; [updated 2023 Sep 20; cited 2025 Jan 21]; [about 3 p.]. Available from: https://www.mayoclinic.org/diseases-conditions/primary-biliary-cholangitis/symptoms-causes/syc-20376874

3Pandit S, Samant H. Primary Biliary Cholangitis. [Updated 2023 Feb 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459209/

4Ipsen Biopharmaceuticals [Internet]. Map PBC; [updated 2024 Aug; cited 2025 Jan 21]; [about 2 p.]. Available from: https://www.mappbc.com/?gclsrc=aw.ds&gad_source=1&gclid=EAIaIQobChMIreWL_pWgigMV7Ub_AR2q_ygQEAAYBCAAEgL83vD_BwE 

5Cleveland Clinic [Internet]. Primary Biliary Cholangitis (PBC): Overview; [updated 2023; cited 2025 Jan 21]; [about 3 p.]. Available from: https://my.clevelandclinic.org/health/diseases/17715-primary-biliary-cholangitis-pbc#overview

-Kaysi Bujniewicz, MLS(ASCP)CM graduated Magna Cum Laude from University of North Dakota School of Medicine with a Bachelor of Science in Medical Laboratory Science. She has worked in clinical laboratories for over eight years as a certified and licensed Medical Laboratory Technician and a Medical Laboratory Scientist. Although her true callings are in Immunohematology and Clinical Microbiology, she currently works as a Generalist.

Safety Super Villains and Origin Stories

In Marvel’s latest Captain America movie, I knew I was going to be treated to seeing two villains, and I wondered if they would be handled well. If you know me, you know I want the movies to stick to the source material and not wander too far away. I was happily surprised. The villains were handled well, and it was fun watching the origin of one of them unfold as the movie progressed. All heroes and villains have an origin story.  Sometimes its worthwhile to know them so you can understand the character motivations as their stories progress.

As a laboratory safety consultant, I have billed myself as “the Superhero of Lab Safety.” I did that in part because I have been reading and collecting comic books for many years, and I wanted to insert my hobby into my work where possible. Superheroes are exciting, but they wouldn’t have much to do without super villains to battle. If I was truly a superhero for lab safety, I had been wondering in the last few years, who or what is the super villain? What creates a lab safety super villain?

Like many of the heroes I love to read about, I had an origin story. Terry Jo Gile, “the Safety Lady” was a renowned lab safety expert who took me, a new safety officer, under her wing and trained me. She taught me how to write, how to speak and present, how to seek out and fix safety issues, and how to run a business using these skills. We both wore capes the first time we presented together. Now she is retired from her work, and I fly around training up a sidekick of my own.

When I read my favorite comics, I noticed that many super villains were scientists, and they were created in a lab setting. Lex Luthor became a villain as a result of a chemical exposure that caused him to lose his hair. Dr. Doom was involved in a laboratory fire that burned him so badly he had to wear an iron mask and a suit of armor to hide his features. Scientist Norman Osborn exposed himself to an untested mixture which empowered him but drove him insane, turning him into the Green Goblin. The man who would become the Joker slipped on a gantry and tripped into a vat of acid which eventually drove him mad.

So, what unsafe environment allowed these villain origins to occur? What allows safety super villainy to occur in your labs? Is it the unsafe laboratory environment? Is it the technologist who refuses to put down his cell phone or wear PPE? Is it the co-worker who sees this bad behavior and refuses to coach him? Is it the laboratory leader who does not adequately support safety? Or maybe it is a combination of some or all of these factors.

Chemical safety, fire safety, exposure control, and physical safety played a role in the creation of these villains. In real life, however, unsafe practices and surroundings can result in consequences that are not as simple as becoming a villain. They can lead to time away from work, an end to a career, costs to the department, and even loss of life. Teaching laboratorians about these types of consequences is both informational and motivating.

Train laboratorians in the safe management of chemicals and biologicals in the department. Show them the location of fire safety equipment and provide regular training on how to use it. Enforce good safety practices like using PPE, washing hands, and utilizing protective engineering controls properly. Conduct regular inspection of the lab physical environment to make sure hazards are mitigated before an employee can be injured or exposed. This ongoing complete management of the lab safety program can prevent the origin story of an unwanted and pesky lab super villain.

To stop a super villain, a hero needs to shut down the environment where the villain can be created. Work around potential bumps in the road by outsmarting the villain. Manage up when necessary, and model the safety change you want to see. Lastly, a safety superhero never gives up. They keep pushing forward until they have that final victory. If pieces of a villain’s origin story are sneaking around your laboratory, put on your cape and get to work! A safety superhero’s job is never done!

–Dan Scungio, MT(ASCP), SLS, CQA (ASQ) has over 25 years experience as a certified medical technologist. Today he is the Laboratory Safety Officer for Sentara Healthcare, a system of seven hospitals and over 20 laboratories and draw sites in the Tidewater area of Virginia. He is also known as Dan the Lab Safety Man, a lab safety consultant, educator, and trainer.

Microbiology case study: Not so-cording MTB in a case of pediatric TB meningitis

Case History

An 11-year-old girl was brought by her mother to the Emergency Room because of altered mental status, described as abnormal movements and staring with a period unresponsiveness lasting 15 minutes.

One week previously, she had returned from a 6 week trip to Ghana with her family to visit other family members there.  Malaria prophylaxis had been prescribed but was not taken during the trip.  Since coming back, she had constant frontal and bilateral headaches with retro-orbital pain, accompanied by nausea, poor appetite, and several episodes of vomiting.  She did not have cough, congestion, earaches, or fever. Past medical history was unremarkable.  Nobody else in the family was sick.  She had some mostquito bites while in Ghana, but no fever or illness.Confusion, fever, and neck stiffness were noted on physical exam.

A spinal tap was done, with the following results: wbc 46 per mm3 (lymphocytes 98%, monocytes 2%), rbc 25 per mm3, glu 41 mg/dL, pro 72 mg/dL, no organisms on Gram stain and Kinyoun stains, meningitis/encephalitis PCR panel negative, and PCR for Mycobacterium tuberculosis negative. The bacterial culture had no growth after 5 days of incubation.

A CT scan of the head done without contrast was normal. An MRI of the brain done with contrast showed focal contrast enhancement in the left corona radiata and several other small foci of contrast enhancement, including within the right occipital lobe and cerebellum, alsong with possible leptomeningeal contrast enhancement along several sulci.

After 4 weeks, growth was observed in the Mycobacterial Growth Indicator Tube (MGIT) culture.  A Kinyoun stain of the growth is shown in Figure 1, and colony morphology is shown in Figure 2. The organism was subcultured on the Middlebrook 7H10 (the growth shown in Figure 2) and identified by MALDI-ToF (Matrix assisted laser desorption ionization Time of Flight) as Mycobacterium tuberculosis complex (MTBc). The antimicrobial susceptibility test was performed at the department of health, which reported out susceptible to all first-line agents, except resistance to INH.

Fig 1 (A): Acid-fast bacilli from Kinyon stain of positive MGIT culture.
Fig 1(B and C): Close up images of Fig1-A.
Fig 2: Dry Crusty scaly morphology of Mycobacteria subcultured from positive MGIT.

Discussion

Tuberculous (TB) meningitis is a severe form of extrapulmonary tuberculosis caused by Mycobacterium tuberculosis (Mtb). It typically presents with a subacute onset of constitutional symptoms, including malaise, fever, headache, and altered mental status, which can progress to stupor, coma, and death if untreated. Clinical features often include headache, vomiting, meningeal signs, focal neurological deficits, cranial nerve palsies (our case has cranial nerve 6 palsy), and raised intracranial pressure.

The diagnosis of TB meningitis is generally based on clinical suspicion, CSF analysis, and neuroimaging. CSF analysis is typically non-specific and shows lymphocytic pleocytosis, elevated protein, and low glucose levels. Confirmatory tests include CSF smear, culture, and nucleic acid amplification tests for Mtb. While mycobacterial culture is still a gold-standard method for the definitive diagnosis, it usually takes long for growth detection and the downstream diagnostic methods, such as MALDI-ToF (Matrix Assisted Laser Desorption Ionization Time of Flight). Since laboratories are reliant on (MALDI-ToF) after the discontinuation of Hologic GenProbe products, subculturing the organism from the liquid growth for MALDI-ToF results in additional delay in identification.

The cording characteristics of MTB from culture growth was a classic tell-tale sign for preliminary laboratory identification. While the presence of “cord factor” denotes the virulence of mycobacterial species (particularly MTBc) and was thought to be unique to MTBC, it was later demonstrated to be present in non-tuberculous mycobacterial (NTM) species. Therefore, care should be taken, and the time of growth should be considered when interpreting the Kinyon stain of positive cultures.

On the other hand, Xpert MTB/RIF is FDA-approved only on sputum samples, although studies show off-label utilization on CSF. The sensitivity of this test in CSF is mediocre due to the paucibacillary nature of the infection. Neuroimaging, such as MRI or CT, can reveal meningeal enhancement and hydrocephalus, which are suggestive of TB meningitis; however, clinicians still rely heavily on microbiologic results for definitive diagnosis.

As TB meningitis is a fatal disease and the confirmed diagnosis may take a long time, treatment should be initiated promptly based on clinical suspicions. Treatment includes anti-tuberculous medications with steroids for 2 months. Then NIH and RIF for an additional 7-10 months. It is noteworthy to mention that susceptibility is important as some MTB strains are drug-resistant, as is the case for our patient, whose isolate is resistant to INH.

References

  1. https://www.uptodate.com/contents/tuberculous-meningitis-clinical-manifestations-and-diagnosis
  2. Theorn et al. Scientific Reports. 2014. DOI: 10.1038/srep05658. Accessed. June 19, 2024
  3. Wilhelm Hedin et al., JID, 2023
  4. Lablogatory – a cording too cording by Richard Davis

-Dr. Mahmoud Ali, MD, is a pediatric infectious disease fellow at Montefiore Medical Center and Albert Einstein College of Medicine, Bronx, NY.

-Phyu Thwe, Ph.D, D(ABMM), MLS(ASCP)CM is Associate Director of Infectious Disease Testing Laboratory at Montefiore Medical Center, Bronx, NY. She completed her medical and public health microbiology fellowship in University of Texas Medical Branch (UTMB), Galveston, TX. Her interests includes appropriate test utilization, diagnostic stewardship, development of molecular infectious disease testing, and extrapulmonary tuberculosis.

Lab Errors and Human Factors: A Psychological Perspective

In the world of clinical laboratories, we often focus on metrics, SOPs, and compliance checklists to reduce errors. But as any seasoned laboratorian or quality professional knows, mistakes still happen—sometimes even when all the systems are in place. Why? Because at the center of every lab process is a human being. And humans, for all their training and dedication, are not robots.  (Even though it seems admin sometimes thinks we are.)

As a regulatory affairs manager and laboratorian with a background in psychology, I’ve spent years navigating the intersection between compliance and cognition. Understanding how people think, react, and sometimes err has helped me see lab operations through a different lens. In this post, I want to explore the concept of human factors and how they play a role in lab errors—not to assign blame but to foster a culture of safety, empathy, and improvement.

The Cognitive Load We Carry

Laboratorians are tasked with high-stakes responsibilities: matching blood types, identifying critical values, and interpreting complex diagnostic results. Add in interruptions, multitasking, and staffing shortages, and the mental bandwidth gets stretched thin.

Cognitive overload can lead to slips and lapses. A mislabeled specimen, for example, might result not from negligence but from working memory overload.1 When we acknowledge this, we can begin to design systems that support mental function instead of taxing it.

The Role of Confirmation Bias

Confirmation bias—the tendency to favor information confirming our beliefs—can creep into lab work. If a pathologist or a technologist “expects” to see a result or a specific pattern, they may inadvertently interpret ambiguous data to match their expectation.2,3 This is not a character flaw but a function of how our brains process information. Peer review, second reads, and built-in verification steps can guard against this type of error.

Fatigue, Stress, and Emotional Load

We often underestimate the impact of emotional and physical fatigue on performance. Long shifts, personal stressors, or the emotional toll of working in healthcare environments can impair judgment and focus.4,5

Labs prioritizing wellness—through break policies, mental health support, or manageable scheduling—not only show compassion but can contribute to improved performance and fewer mistakes.

Designing with Humans in Mind

So, how can labs address human factors without compromising accountability? Start by shifting the narrative. Instead of asking, “Who made the mistake?” ask, “What in the system allowed this to happen?” 6 (As a side note, this is the true purpose of a root cause analysis.)

Incorporate human factors thinking into root cause analysis. Provide human-centric training that acknowledges common cognitive pitfalls. And most importantly, build a culture where speaking up about near misses is welcomed, not punished.

Last Thought

Human error isn’t a moral failing; it’s a predictable part of being human. When labs take a psychologically informed approach to error prevention, they open the door to safer practices, stronger teams, and more resilient systems.

Understanding human factors doesn’t weaken quality systems—it strengthens them. And perhaps more importantly, it reminds us that the people behind the results matter just as much as the results themselves.

References:

  1. Reason, J. (1990). Human Error. Cambridge University Press.
  2. Nickerson, R. S. (1998). Confirmation bias: A ubiquitous phenomenon in many guises. Review of General Psychology, 2(2), 175-220.
  3. Michel, M., Peters, M.A.K. Confirmation bias without rhyme or reason. Synthese 199, 2757–2772 (2021). https://doi.org/10.1007/s11229-020-02910-x
  4. Lockley, S. W., et al. (2007). Effects of health care provider work hours and sleep deprivation on safety and performance. The Joint Commission Journal on Quality and Patient Safety, 33(11 Suppl), 7-18.
  5. West, C. P., et al. (2009). Association of resident fatigue and distress with perceived medical errors. JAMA, 302(12), 1294-1300.
  6. Dekker, S. (2014). The Field Guide to Understanding ‘Human Error’. Ashgate Publishing.

-Darryl Elzie, PsyD, MHA, MLS(ASCP)CM, CQA(ASQ), is the Regulatory Affairs Manager Inova Blood Donor Services. He has been an ASCP Medical Laboratory Scientist for over 25 years, performing CAP inspections for two decades. He has held the roles of laboratory generalist, chemistry senior technologist, and quality consultant. He has a Master’s in Healthcare Administration from Ashford University, a Doctorate of Psychology from The University of the Rockies, and is a Certified Quality Auditor (ASQ). Inova Blood Donor Services is the largest hospital-based blood center in the nation. Dr. Elzie is also a Counselor and Life Coach at issueslifecoaching.com.