Lablogatory

Finally Fantastic – The Safety Culture You Waited For

You’ve probably heard that the Fantastic Four are coming back to theaters—again. Marvel is set to release yet another reboot of the beloved superhero team. This will actually be the fifth time this group gets a chance to shine on the big screen (counting the legendary low-budget 1994 Roger Corman version that was never officially released). With each iteration, there’s hope for something better—a truer version, something more polished, more faithful to the source material, and more exciting. That same sense of optimism can and should exist when it comes to giving your laboratory safety program a much-needed reboot. Just like a superhero franchise that never quite landed, a safety program may have launched with good intentions but ended up lost in the noise of daily operations, ineffective habits, or even complete neglect. But a fresh start is always possible.

A reboot doesn’t mean tearing everything down. It means stepping back, taking stock, and relaunching your lab’s safety culture with clear intention and renewed energy. Maybe your program has been around for years. Maybe it started strong but fizzled over time. Maybe people know there are safety policies but couldn’t tell you what they are or why they matter. That’s when you know it’s time to roll out the red carpet and debut the reboot—something finally fantastic.

Start with awareness. Ask your team: what is the current perception of safety in our lab? You might not like the answer, but you need to hear it. If safety is viewed as a burden, an afterthought, or worse—an irrelevant set of rules for someone else—then it’s time to rewrite the script. Meet with staff, leaders, and stakeholders. Ask what concerns them. Ask what they think the safety program is supposed to be doing. Those honest answers are the trailer to the full-length feature you’re about to roll out. Don’t skip this step—if you launch a reboot that no one asked for, you’ll lose your audience faster than an opening weekend box office flop.

Once you know what’s broken—or just stale—it’s time to build your team. A reboot can’t be carried by one star. The best safety programs are ensemble efforts. Designate a safety committee that represents multiple shifts, roles, and experience levels. New staff often bring sharp eyes to longstanding hazards, while seasoned staff can offer insight on what has worked (or what hasn’t) over the years. Empower this group to be a creative force, not just a policy review panel. Let them own a piece of the relaunch. Ask them to think about new ways to communicate, train, and lead safety efforts. Safety doesn’t improve through policy alone; it improves when people care and feel they are part of something that matters.

Part of rebooting a safety program is looking at the training experience. If your safety training looks the same as it did ten years ago—or even last year—it’s time to revamp. Don’t rely solely on slide decks and sign-in sheets. Use interactive content, real-life stories, safety scenarios, and even short quizzes that focus on lab-specific risks. Think of orientation and ongoing education as the origin story—this is where people learn why safety is crucial to their success. Make it relevant, make it relatable, and most importantly, make it stick. A powerful reboot pays off when your audience walks away engaged, not just informed.

Culture doesn’t change overnight. Rebooting a program means creating new rhythms. Consider launching monthly safety themes, having a rotating “safety spotlight” where staff highlight issues or solutions, or using short weekly safety reminders during huddles. Visibility matters. Just like the buzz before a movie release, your reboot needs marketing. Use colorful posters, QR codes linking to safety resources, fun contests, and visible support from leadership. Let the message be clear: safety is not just important, it’s exciting, it’s everyone’s responsibility, and this time, we’re doing it right.

Accountability is the third act in any good reboot. Once you’ve communicated and trained, you need to follow through. That means supervisors modeling safe behaviors, staff speaking up without fear, and leadership reinforcing safety expectations through action, not just words. Set clear goals. Review incident trends. Celebrate progress. And when setbacks happen (and they will), address them directly. A rebooted culture is not afraid of failure. It learns from it and keeps going.

Now, as we await the next big-screen version of the Fantastic Four, think about your own safety origin story. Has your program fizzled out? Does it need better effects, sharper direction, or a whole new cast of champions? Just like a franchise gets another shot to do things better, your lab has the same opportunity. Don’t just relaunch the same tired storyline, build something bold, something that truly reflects who you are and what your team deserves.

This time, make it fantastic.

–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.

The Real Scoop on Formaldehyde

If formaldehyde is so dangerous, then why is it still used in the laboratory today? It is so dangerous, in fact, that the United States Occupational Safety and Hazard Administration (OSHA) has a standard for the chemical, OSHA Formaldehyde standard (29 CFR 1910.1048). However, despite its dangers, formalin is still the best product available with the most tolerable risk for the needs we have in the lab.

Anatomic pathology has faced the great challenge of tissue preservation for hundreds of years. Decomposition, degradation from microbiological contamination, and even optimal hydration have hindered the proper isolation and study of tissue and organs. Early fixatives such as picric acid, osmium tetroxide, and even mercuric chloride were excellent at preserving the samples, but these compounds are extremely toxic and/or volatile. It wasn’t until 1893 when a German physician named Ferdinand Blum discovered the benefits of formaldehyde. Blum concluded that immersion of tissues in a 4% solution of formaldehyde, the 10% neutral buffered formalin widely used today, provided excellent preservation with a much lower risk to the user.

How dangerous is formalin? Keeping formalin off your skin and out of your eyes is crucial since it is a tissue fixative. An even greater risk of working with formalin comes from its respiratory hazards. Formalin off-gases quickly, creating a very dangerous, and unseen hazard. When inhaled, formalin can cause difficulty breathing, coughing, and wheezing. In addition, long-term exposure can cause respiratory issues, skin irritation, and an increased risk of nasopharyngeal cancer, formaldehyde is a known carcinogen.

Baseline exposure monitoring is required by OSHA to demonstrate that employees are not overexposed while working with and around formalin. Badge readings that fall below the time weighted average (TWA) of 0.75 ppm over an eight-hour period or below the short-term exposure limit (SEL) of 2 ppm over a 15-minute period, prove that the lab is a safe environment and additional badge monitoring is not required. However, if the readings exceed the limits, or if changes to the lab or processes are made, subsequent badge monitoring should be performed.

How can the lab control for exposures to the chemical? The best practice is to limit the time staff work with open containers of formalin. Of course, this is not always possible. Therefore, respirators, chemical fume hoods (CFH), grossing hoods, and room ventilation may be necessary. Keeping equipment in good running condition helps to minimize exposure. Therefore, grossing hoods and the CFH should be certified annually, and staff should undergo fit testing for respirators each year as well.

When it comes to hazardous waste, laboratories have several options for removing formalin from the premises. Anatomic pathology labs are required to dispose of both solid and liquid waste, two separate waste streams. Solids can go out as regulated medical waste with proper labeling, but what the liquid waste must be handled differently. Labs can either neutralize the waste onsite or contract with a vendor to have it removed. Organizations can neutralize formalin waste on-site for disposal in their normal sewage system. This does mean, however, that labs need to monitor their neutralization process which includes pH and aldehyde testing of the waste prior to pouring down the drain. It is always recommended to confirm this process with local wastewater treatment centers to ensure the proper steps are being taken prior to disposing of the waste.

Unbuffered formalin can break down quickly, but buffered formalin has a limited shelf life. Therefore, limiting the quantity on hand in the lab not only helps with product quality, it also keeps staff safer. Another good lab practice is to limit the height at which formalin is stored. As with all corrosive chemicals in the department, formalin should be stored below shoulder height. Do you store your formalin in a flammable cabinet? Formaldehyde, the active ingredient in formalin, is a flammable gas. However, only solutions with higher concentrations of formaldehyde are actually listed as flammable. A container of 37% formaldehyde is considered flammable, but 10% NBF is stable under normal conditions and classified as non-flammable.

Chemical spills happen, so departments need to be ready to respond to such an event. A formalin spill in the lab or the operating room cab be dangerous to staff and patients. Knowing how to handle the spill can be the difference between a safe response or an event that causes staff and/or patients harm. As stated, formalin gives off a gas, so placing an absorbent mat or a towel on a spill will only increase the surface area that can generate harmful gases. Therefore, having a neutralizing product available for spills and training staff to use the product is essential. Staff that run through spill drills frequently know the location and contents of their spill kits and respond more effectively. Working with formalin is dangerous, but the more staff know about the product and respect it, the safer their work practices become. Using and keeping formalin in the lab requires some planning and training. The lab is a dynamic environment, so workspaces and procedures should be reviewed often. Train staff on formalin safety and help them to always work safely with formalin.

-Jason P. Nagy, PhD, MLS(ASCP)^CMis a Lab Safety Coordinator for Sentara Healthcare, a hospital system with laboratories throughout Virginia and North Carolina. He is an experienced Technical Specialist with a background in biotechnology, molecular biology, clinical labs, and most recently, a focus in laboratory safety.

Microbiology Case Study: A Middle-Aged Male with Altered Mental Status

Case presentation

A middle-aged male with a history of type 2 diabetes, hypertension, obesity, and alcohol-related cirrhosis presented to the emergency department with altered mental status. He was obtunded, acutely encephalopathic and hypoglycemic. He soon developed emesis and coded during clinical assessment, undergoing emergent intubation. He was found to be profoundly acidotic with labs consistent with disseminated intravascular coagulation and multiorgan failure. The patient was transfused but continued to code multiple times before and during ICU transfer/admission. Despite multiple resuscitation attempts, he expired soon afterwords.

Laboratory workup

Blood cultures drawn in the ED prior to admission became positive with curved gram-negative rods (Image 1A) within 16 hours. An oxidase-positive, indole-positive, beta-hemolytic organism was recovered after 24 hours of incubation. The organism was lactose-fermenting (confirmed by ONPG) and exhibited colorless growth on Thiosulfate Citrate Bile Salts agar suggestive of a lack of sucrose utilization (Image 1B, set up for demonstrative purposes). The organism was definitively identified as Vibrio vulnificus by MALDI-TOF MS. No additional workup was undertaken as the patient had expired prior to the organism being recovered from blood culture.

Image 1. A: Gram stain from a positive blood bottle revealing curve gram-negative rods (100X magnification). Inset demonstrates the morphologically distinct curved appearance. B: Blood and TCBS agars revealing growth of *V. vulnificus*. Lack of yellow colorization on TCBS media indicates lack of sucrose utilization. Biochemical testing revealed oxidase, catalase, and indole positivity also consistent with the MALDI-TOF identification of *V. vulnificius.*

Discussion

Vibrio sp. are marine bacteria that naturally colonize brackish and saltwater aquatic environments. Of the more than 70 currently recognized species, at least 12 are recognized as human pathogens.¹ Human infections are broadly classified as being either cholera (caused by V. cholerae) or vibriosis (caused by other non-V. cholerae Vibrio spp.). Unlike cholera; a severe diarrheal illness usually acquired through ingestion of contaminated food or water, vibriosis represents a group of infections with varied clinical manifestations dependent upon the etiologic agent, route of infection, and host susceptibility.² Non-cholera vibrios are often found in seawater with moderate to high salinity and as clinically important contaminants of raw or undercooked seafood.

V. vulnificus thrives in warmer water and infections follow a seasonality, peaking in the warmer summer months.³ In contrast to V. cholerae and V. parahaemolyticus, V. vulnificus infections generally are associated with patients with underlying conditions, most commonly diabetes, liver disease and iron storage disorders. It is estimated that patients with chronic liver diseases (particularly cirrhosis due to either alcoholism or chronic hepatitis B or C) are 80-fold more likely to develop V. vulnificus-associated primary septicemia than healthy counterparts.² Infections are most common in men aged 45-60 years who make up 85-90% of patients,⁴ consistent with this case. Contaminated food consumption (particularly filter feeding shellfish) can result in gastroenteritis or primary septicemia and disseminated disease.

Non-cholera vibrios are estimated to cause up to 80,000 infections worldwide, with V. parahaemolyicus and V. alginolyticus responsible for most cases. Among this group of organisms, V. vulnificus stands out as being particularly virulent; between 150-200 V. vulnificus infections are reported to the US CDC annually, with 20% being fatal.⁵ This organism oftencauses more than 95% of seafood-related deaths in the United States and the highest case fatality of any foodborne pathogen [2]. V. vulnificus also causes serious skin/soft tissue infections. This can occur either through exposure of a preexisting wound to contaminated seawater, or through injury while handling contaminated seafood. Cutaneous infections can present as cellulitis or bullae, which can progress to necrotizing disease and secondary sepsis is left untreated.⁶

No epidemiological link was able to be established between this patient’s case and either seafood or exposure to seawater, although cases of V. vulnificus infections among patients without classical exposure risk has been documented.⁷ This case of V. vulnificus primary septicemia highlights the acuity of this presentation as well as the importance of including V. vulnificus in differential diagnosis of hosts with associated risk factors and/or epidemiological links. Blood culture remains the gold standard for diagnosis. Importantly, doxycycline in combination with a third-generation cephalosporin constitutes the standard regimen for antibiotic therapy – however, doxycycline is not usually considered a first-line antibiotic for management of patient with gram-negative bloodstream infections, so rapid and accurate identification of V. vulnificus in this setting is essential.

1. Kokashvili, T., et al., Occurrence and Diversity of Clinically Important Vibrio Species in the Aquatic Environment of Georgia. Front Public Health, 2015. 3: p. 232.

2. Baker-Austin, C., et al., Vibrio spp. infections. Nature Reviews Disease Primers, 2018. 4(1): p. 1-19.

3. Hughes, M.J., et al., Notes from the Field: Severe Vibrio vulnificus Infections During Heat Waves – Three Eastern U.S. States, July-August 2023. MMWR Morb Mortal Wkly Rep, 2024. 73(4): p. 84-85.

4. Jones, M.K. and J.D. Oliver, Vibrio vulnificus: disease and pathogenesis. Infect Immun, 2009. 77(5): p. 1723-33.

5. Bharathan, A., et al., Implication of environmental factors on the pathogenicity of Vibrio vulnificus: Insights into gene activation and disease outbreak. Microb Pathog, 2025. 204: p. 107591.

6. Coerdt, K.M. and A. Khachemoune, Vibrio vulnificus: Review of Mild to Life-threatening Skin Infections. Cutis, 2021. 107(2): p. E12-e17.

7. Candelli, M., et al., Vibrio vulnificus—A Review with a Special Focus on Sepsis. Microorganisms, 2025. 13(1): p. 128.

-Rene Bulnes, MD is an Infectious Diseases Clinician and current Medical Microbiology Fellow at the University of Texas Southwestern Medical enter in Dallas, TX.

-Andrew Clark, PhD, D(ABMM) is an Assistant Professor at the Johns Hopkins University School of Medicine in the Department of Pathology, and Director of the Bacteriology Laboratory at the Johns Hopkins Hospital. He completed a CPEP-accredited postdoctoral fellowship in Medical and Public Health Microbiology at National Institutes of Health, and is interested in the molecular mechanisms of antimicrobial resistance, susceptibility testing, and the evaluation of novel technology for the clinical microbiology laboratory.

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!

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

https://www.uptodate.com/contents/tuberculous-meningitis-clinical-manifestations-and-diagnosis
Theorn et al. Scientific Reports. 2014. DOI: 10.1038/srep05658. Accessed. June 19, 2024
Wilhelm Hedin et al., JID, 2023
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)^CMis 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:

Reason, J. (1990). Human Error. Cambridge University Press.
Nickerson, R. S. (1998). Confirmation bias: A ubiquitous phenomenon in many guises. Review of General Psychology, 2(2), 175-220.
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
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.
West, C. P., et al. (2009). Association of resident fatigue and distress with perceived medical errors. JAMA, 302(12), 1294-1300.
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.

Hematology Case Study: Reticulocyte Abnormal Scattergrams

Case 1: Premature newborn with abnormal reticulocyte scattergram, indicated by the * after the parameters. The sample was rerun with a 1:5 dilution to minimize interference. CBC and Retic results shown below.

Table 1. newborn CBC results before and after 1:5 dilution

In this case the dilution was able to minimize interference, so there is no longer an abnormal scattergram flag. After diluting the sample, the HCT was multiplied by the dilution factor. The MCV, Reticulocyte % and Immature Reticulocyte Fraction (IRF) are not multiplied because these are % and fractions or ratios so do not change.

Case 2: 48-year-old woman with sickle cell anemia with abnormal reticulocyte scattergram. The sample was rerun with a 1:3 dilution to minimize interference. CBC and reticulocyte results are shown below.

Table 2. Sickle cell patient results before and after 1:3 dilution

In this case, there is still an * after the reticulocyte % and Immature Reticulocyte Fraction (IRF) indicating that the dilution did not help minimize the interference in the scattergram. In Case 1 a 1:5 dilution was used. In this sickle cell patient, the red blood cell (RBC) count is too low to do a higher dilution. (The raw RBC with the 1:3 dilution was .69. On our analyzer it is important not to dilute a sample so that the RBC would be <0.5 as this suppresses the analyzer flags) This means that reticulocyte results could not be reported from the analyzer, and it was necessary to verify the reticulocyte count with a manual reticulocyte count.

I’ve often said that I really love working in Hematology, especially when these problem specimens come along. About 85% of our CBC’s autovalidate, so it’s easy to say that those aren’t too interesting. It’s the ones that need our attention that that are interesting and give us the opportunities to really use all the theory we learned in school. Some of our most challenging specimens are those with abnormal scattergrams or that have other results that just don’t make sense without further investigation and further work. Yes, they take more time but that’s what we are here for!

I work at a hospital that has a large oncology center where many sickle cell patients are treated. We also have the largest number of babies delivered in the area, and because of that there are many NICU babies. One thing these patients have in common is both populations tend to lean towards spurious reticulocyte counts with reticulocyte abnormal scattergram flags. But why?

The reticulocyte (retic) count is a good marker of erythropoietic activity of the bone marrow. Retic counts, along with the Immature Reticulocyte Fraction (IRF) are useful tools to help diagnose anemia or monitor bone marrow response to therapy. Reticulocytes are a normal stage in the development of RBCs after the nucleus has been extruded but before the cell is mature. Retics still contain RNA which is lost upon cell maturation. On automated hematology analyzers, RBCs are counted using impedance or optical technology. Automated reticulocyte counts are based on identifying young RBCs which have residual nucleic acids after expelling the nucleus. Hematology analyzers stain the RNA in young RBCS with fluorescent or non-fluorescent dyes, and principles of impedance, scatter, fluorescence and flow cytometry are used to measure the immature cells. Reticulocytes have some leftover nucleic acid content, and the youngest reticulocytes, newly out of the bone marrow have even more nucleic acid content. This causes more fluorescence intensity. On analyzers using fluorescence, reticulocytes are separated from mature RBCs by light scatter based on their fluorescence intensity. The total reticulocyte population is separated into 3 fractions of low, medium, and high fluorescence. The percentage of medium plus highly fluorescent reticulocytes represents the youngest of the young RBCs, which is the IRF. These can be visualized on the retic scattergram (figure 1).

Figure 1. Reticulocyte scattergram, Sysmex America

On an extended scattergram, signals with fluorescence intensity between reticulocytes and WBCs represent the upper particle portion (UPP) (figure 2). Interference can be seen on automated reticulocyte scattergrams when there are cells that have more nucleic acid than reticulocytes. Howell-Jolly bodies are DNA remnants seen in Wright-stained RBCs after the nucleus is extruded. These may be found in patients after splenectomy or when splenic function is compromised. They appear as single round dark blue inclusions in RBCs. In patients with Howell-Jolly bodies, interference with the reticulocyte count may be seen, triggering abnormal scattergram flags. Other peripheral blood findings that contain more nucleic acid than mature RBCs and reticulocytes may also cause interference and abnormal scattergrams in the reticulocyte channel. These include shift reticulocytes, basophilic stippling, nucleated RBCs and parasites. In patients with extreme leukocytosis, abnormal numbers of WBCS and WBC fragments may interfere with automated reticulocyte counting.

Figure 2. Extended Reticulocyte Scattergram, Sysmex America

Case 1

Newborns would be expected to have a higher percentage of reticulocytes than adults. Reference ranges for reticulocyte% in newborns is 2-6% compared to 0.5-1.5% for adults. Lower oxygen levels in the womb trigger the increased secretion of erythropoietin, which stimulates red blood cell (RBC) production. Increased production of RBCs results in a higher proportion of reticulocytes circulating in the newborn’s blood. In these cases, the bone marrow will release reticulocytes prematurely into the blood. These young reticulocytes that have more nucleic acid are called shift or stress reticulocytes. Premature infants may have even higher reticulocyte counts and more shift reticulocytes due to their accelerated development needs. As well, in babies with any form of hemolytic disease of the newborn, hemolysis is taking place, and a high reticulocyte count with shift reticulocytes is an indication that there is a compensation by producing more RBCs. In addition, oftentimes in these newborns, nucleated RBCs are present because the constant call for new RBCs leads to even more immature RBCs being released into the peripheral blood. Nucleated RBCs (nRBCs) are another interference factor in reticulocyte scattergrams.

In case 1 the newborn had an MCV of 103.3 which can be attributed to young RBCs known as reticulocytes. Reticulocytes are larger than mature RBCs because RBCs decrease in size with maturity. A high MCV and high reticulocyte(retic) count are therefore normal in newborns. A review of the smear on this baby showed nRBCs, basophilic stippling and slight polychromasia which all may interfere with automated reticulocyte counts. Diluting the samples reduced the interference and give us valid, reportable results.

Case 2

Sickle cell anemia is hemolytic anemia in which the abnormal sickle cells are being destroyed prematurely. Immature red blood cells including reticulocytes and shift reticulocytes are released prematurely from the bone marrow into the bloodstream in response to anemia, indicating the bone marrow’s attempt to compensate for a shortage of red blood cells. Sickle cell patients tend to have high reticulocyte counts, particularly during sickle cell crisis, have shift reticulocytes and often have nucleated RBCs, for the same reasons as premature newborns.

The smear on this patient showed numerous sickle cells, nRBCs, polychromasia, basophilic stippling, and Howell-Jolly bodies. In this case, however, the dilution did not eliminate the interference, and the abnormal reticulocyte flag was still present. A manual reticulocyte count using a Miller ocular was performed and the retic% was 3.2 %, quite a difference from the 12.8% and 9% from our analyzer! This illustrates the importance of resolving the discrepancy before reporting out a spurious count. After all, that’s why we have Medical Laboratory Scientists! Without our careful attention to detail, you’re just guessing.

References

Gaur M, Sehgal T. Reticulocyte count: a simple test but tricky interpretation! Pan Afr Med J. 2021 Sep 2;40:3. doi: 10.11604/pamj.2021.40.3.31316. PMID: 34650653; PMCID: PMC8490160.

Kim A, Park J, Kim M, Lim J, Oh EJ, Kim Y, Park YJ, Han K. Correction of pseudoreticulocytosis in leukocytosis samples using the Sysmex XE-2100 analyzer depends on the type and number of white blood cells. Ann Lab Med. 2012 Nov;32(6):392-8. doi: 10.3343/alm.2012.32.6.392. Epub 2012 Oct 17. PMID: 23130337; PMCID: PMC3486932.

Sysmex Customer Resource Center, Sysmex America, 2025

Uppal, V., Naseem, S., Bihana, I. et al. Reticulocyte count and its parameters: comparison of automated analyzers, flow cytometry, and manual method. J Hematopathol 13, 89–96 (2020). https://doi.org/10.1007/s12308-020-00395-8

-Becky Socha, MS, MLS(ASCP)^CMBB^CM graduated from Merrimack College in N. Andover, Massachusetts with a BS in Medical Technology and completed her MS in Clinical Laboratory Sciences at the University of Massachusetts, Lowell. She has worked as a Medical Technologist for over 40 years and has taught as an adjunct faculty member at Merrimack College, UMass Lowell and Stevenson University for over 20 years. She has worked in all areas of the clinical laboratory, but has a special interest in Hematology and Blood Banking. She currently works at Mercy Medical Center in Baltimore, Md. When she’s not busy being a mad scientist, she can be found outside riding her bicycle.

A long, long time ago on a VHS tape not too far away

Why is storytelling so important? People have been doing it for thousands of years so there must be something behind this practice. Storytelling can be a form of entertainment, such as in plays, operas, and even movies. Passing down stories has been responsible for keeping many cultures alive. Think of a group of early homo sapiens gathered around a campfire, telling the tale of a caveman who ate a smooth, round, red berry and they did not wake up the next day. Stories have also been a part of our advancement as humans, and as a society. Without storytelling, early civilizations may not have been able to farm, build cities, or even navigate the open oceans. When it comes to laboratory safety, stories are also very valuable and should be shared for several reasons. These stories help employees and staff stay safe, but equally as important, they can protect patients. Safety stories not only shed light on the dangers found in the laboratory but can also strengthen the lab’s safety culture by igniting conversations around safety withing the team itself.

So, what kinds of laboratory safety stories can be shared? The most obvious might be stories involving employee injuries or exposures. This type of safety story really has two purposes. First, it can generate discussion around how the injury could have been avoided. If a coworker sustained a hazardous chemical splash to the face, but was wearing safety goggles, staff should conclude that full-face shields must be worn for that process to provide adequate protection. Secondly, the story can make the possibility of an incident more of a reality to others not involved. Have you ever heard someone say, “that could never happen in my lab?” Telling true stories about incidents raises awareness that those types of things can and do happen.

Probability and science demonstrate that almost every possible accident can happen in a lab, it just has yet to occur. Without events occurring over time, employees may become complacent with the biological and chemical risks in the lab. Once this feeling of “immunity to incidents” sets in, employees begin to take short cuts or to pay less attention to tasks, then the chances of an accident increase. Something else could make someone deliberately let their guard down. A person may choose to perform an unsafe act because they do not perceive a risk associated with their actions. If an individual feels that the risk is low or absent, they may not take the necessary precautions (like donning their PPE) before answering a lab phone or pouring xylene into a beaker. Sharing the details around lab accidents will help eliminate any false feelings of security staff may have when working with hazardous substances.

Safety stories do not always have to be centered around negative outcomes, though. Safety stories can also highlight near misses or great catches. It is just as important to discuss (or even celebrate) when bad outcomes are avoided. Talking about events with a positive spin can help motivate staff and boost morale. Some safety stories may not be directly lab-related. It might be just as meaningful to share a story about walking out of the office without your keys and getting locked out of the department.

When is it a good time to share a safety story? Luckily, I work for an organization that believes in starting every meeting with a safety story. Each morning, managers from all hospital locations, along with other key support staff, meet virtually to discuss important items and the status of their labs. Before the team members report out, the person leading the meeting will ask a participant to share a safety story. Of course, injuries and exposures are shared, but other times team members may talk about a successful conversation they had with an outside department. Recently, when an unusual amount of snow fell in the state, many safety stories were shared about how to safely walk on ice and why it might not be a good idea to use hot water to help defrost your car windshield.

It is great that the managers get a chance to share these stories, but it should not stop there. The safety stories have a greater impact in the lab if the lessons learned make it to the staff level. Sharing these stories at a shift change or huddle can be very helpful. Labs with the greatest safety culture are those that routinely discuss safety daily.

One goal of sharing safety stories in the lab is to ultimately avoid unfavorable events. To accomplish this goal, the lab must first understand how the event occurred and what might be missing from the current process that created the opportunity for failure. Like the stories of old that helped keep cultures alive for generations, safety stories are an awesome tool that will maintain your own strong safety culture for years in the laboratory.