It’s Not Always Clear

A 47 year old female presented to the ER with abdominal pain and obstructive jaundice. CT and MRI imaging confirmed a 9.7 cm complex pancreatic head and uncinate process mass that encases and obliterates the distal superior mesenteric vein, encases the superior mesenteric artery, abuts the aorta and IVC and extends into the aortocaval space, displacing the aforementioned structures. By definition, the presentation of this mass indicates locally advanced disease. The patient was referred to gastroenterology for a next-day endoscopy and fine needle aspiration of the pancreatic mass with biliary stent placement.

During the procedure, the cytologist made two smears from two separate passes. The two Diff-Quik-stained smears demonstrated scattered isolated atypical cells with vacuoles in the cytoplasm. The cytologist and pathologist agreed that the cells seen were atypical at best and were debating whether they could be lesional cells or macrophages and that it would be better to see a third smear. The third Diff-Quik smear showed the same cells but this time they were forming aggregates or clusters (Images 1-2). The pathology team deemed the third pass suggestive of tumor. The cytologist collected an additional two needle passes to be rinsed in a balanced salt solution for cell block preparation.

Images 1-2: Pancreas, Head, Endoscopic Ultrasound-guided FNA: DQ-stained smear.

The next morning, the cytologist examined the Papanicolaou-stained slides. The same foamy or microvesicular cytoplasmic vacuoles identified on the Diff-Quik smears were also appreciated on the pap-stained slides (Image 3). There was almost a pink hue to the cytoplasm, which made us question a mucinous tumor. The nuclei were small-to-medium in size with irregular nuclear contours and eccentrically placed. Nucleoli were also appreciated within the tumor cells (Image 4). The H&E-stained cell block sections were beautiful, capturing the nesting architecture of the lesional cells identified on smears (Image 5).

Images 3-5: Pancreas, Head, Endoscopic Ultrasound-guided FNA: 3-4: Pap-stained smear; 5: H&E Cell Block section (400X).

The cytologist and pathologist were both confident that this could be a metastatic renal cell carcinoma, clear cell type. However, there was no evidence of a renal mass. Cancer does what cancer wants though, and to rule out renal cell carcinoma, the pathologist ordered PAX-8 and RCC immunohistochemical (IHC) stains. The tumor cells for both stains came back negative. Back to the drawing board. What if this is an odd presentation of a mucinous cystic neoplasm and these vacuoles are just mucin or a serous cystic neoplasm with glycogen vacuoles? Both mucicarmine and PAS (with and without diastase) were negative, ruling out both neoplasms, respectively. The pathologist and cytologist reviewed the clinical history and imaging. It seems like the only evidence of disease is stemming from the pancreatic mass with moderate lymphadenopathy. At this point, our job is to rule out every primary pancreatic tumor and get this woman an accurate diagnosis so she can 1) get peace of mind, 2) move onto surgery and adjuvant therapy, and 3) finally relieve her excruciating pain.

Let the panel ordering commence! We performed IHC stains on paraffin sections of the cell block with proper positive and negative controls. The tumor cells showed positive staining for AE1/AE3, CK19, CD56, synaptophysin (Image 6), chromogranin (weak), and E-cadherin, membranous staining (but no nuclear staining) for beta-catenin, focal staining for CK7, vimentin, and pCEA, very focal staining (rare cells) for CA19.9, and CD10. In addition to PAX-8 and RCC, the tumor cells showed negative staining for PR and S100. Proliferative index by the Ki-67 immunostain was approximately 2%.

Image 6: Pancreas, Head, Endoscopic Ultrasound-guided FNA: Synaptophysin-positive.

Final diagnosis: Low-grade non-functional pancreatic neuroendocrine tumor (pNET/panNET) with clear cell features.

Had the tumor cells been positive for PR and negative for E-cadherin and chromogranin, a solid pseudopapillary neoplasm may have been in the differential. Negative PAS with diastase also helped to eliminate acinar cell carcinoma from the list of primary pancreatic tumors. It is worth mentioning that the clear cell variant of pNET/panNET is very unusual and may be associated with von Hippel-Lindau disease.

The patient underwent an exploratory laparotomy which revealed metastatic disease. As her symptoms progressively worsened over the next year, the patient decided, using a shared decision-making model with her medical oncologist, to pursue adjuvant therapy. CAPTEM (capecitabine and temozolomide) combined therapy was administered in the setting of progressive metastatic disease. Two years after the initial diagnosis and one years after the initiation of CAPTEM therapy, the patient received 2000 cGy of palliative radiation to the pancreatic mass. While this helped to reduce the disease burden within the primary site, extensive metastasis was noted including an obstructive duodenal mass and multiple liver lesions. Forcep biopsies of the duodenum and both FNAs and core biopsies of the liver demonstrated the same clear cell features of the original tumor, however, the Ki-67 proliferation index increased to 5%, which is consistent with an intermediate or grade 2 (G2) pNET. The patient developed uncontrolled bleeding and subsequently severe anemia and went on hospice. Within a matter of weeks after stabilizing her hemoglobin, the patient came off of hospice and began treatment with Lutathera, a radioligand therapy or peptide receptor radionuclide therapy (PRRT) which targets cells with somatostatin receptors. This therapy kept her relatively stable for an additional two years, but imaging demonstrated further progression on PRRT so an mTOR inhibitor was introduced to reduce the disease burden.

The beauty of oncology is that new therapies and advancements are always being developed and released, often improving the patient’s longevity and/or quality of life. The beauty of pathology is that the diagnosis is not always clear, but using the ever-expanding diagnostic and prognostic tools available to us can help us give the patient an answer and guide future treatments.

-Taryn Waraksa-Deutsch, MS, SCT(ASCP)CM, CT(IAC), has worked as a cytotechnologist at Fox Chase Cancer Center, in Philadelphia, Pennsylvania, since earning her master’s degree from Thomas Jefferson University in 2014. She is an ASCP board-certified Specialist in Cytotechnology with an additional certification by the International Academy of Cytology (IAC). She is also a 2020 ASCP 40 Under Forty Honoree.

Microbiology Case Study: A Friend or Foe with No Cell Wall

A 28 year old woman underwent an elective myomectomy for menorrhagia caused by fibroids. Postoperatively, she developed fevers. A CT scan of the abdomen and pelvis showed a complex pelvic fluid collection measuring 5.4 by 4.4 by 7.0 cm. Drainage was attempted by Interventional Radiology without success. She then underwent an exploratory laparotomy with drainage of the collection, evacuation of a hematoma, and removal of an IUD. The abscess fluid was sent to the Microbiology lab for culture.

The Gram stain of the fluid revealed 1+PMN with no organisms. After 48 hours of incubation, there was few to moderate growth of pinpoint clear colonies on blood agar, with characteristic miniscule appearance of a central area of dense growth and peripherally less dense (Figure 1). Upon closeup reviewing of the colonies revealed a “fried egg” appearance (Fig 2).

There was no growth on MacConkey plate. Final identification by MALDI-TOF demonstrated Mycoplasma hominis.

Figure 1. Blood agar plate growing clear small colonies of M. hominis.
Figure 2. Characteristic colonies of organism with peripheral growth and denser central growth with fried-egg appearance.

Discussion

Mycoplasma hominis is a facultative anaerobe of the Mycoplasma genus, which is among the smallest free-living organisms known. They are fastidious and differentiated from other bacteria by their small size and absence of cell walls. Infections with M. hominis predominately involve the urogenital tract of females, causing pelvic inflammatory disease, bacterial vaginosis, and postpartum fever.1 Extragenital manifestations of M. hominis infections are rare but include extragenital abscesses, CNS infections in neonates, and septic arthritis.2 Reports of Mycoplasma hominis infections vary based on demographics (country, age, and number of sexual partners) but have been isolated in 4 to 30% of urogenital infections in females. 1,3

The lack of cell walls confers both diagnostic and clinical challenges. Mycoplasmas is not seen on the routine Gram stain smears. Instead of a cell wall, they have a triple-layered membrane composed of sterol.3 When able to grow in culture, colonies are small and have a ‘fried egg’ appearance on agar.4 Of the Mycoplasma species, M. hominis is the least fastidious and the most common Mycoplasma isolated on conventional culture agar media. 4-6 Non-traditional culture-based diagnosis is often made via molecular testing. 7 It is often detected in coinfections with Trichomonas vaginalis and thought to be a symbiotic relationship. 8-9

Since M. hominis is also found to be colonized in the genital tract of normal healthy individuals, it can be challenging to establish the clinical and diagnostic significance of M. hominis. With evolving molecular diagnostic assays targeting STI agents, it has been a controversial topic for assay manufacturers or labs that develop their own in-house assays whether there is a clinical utility for M. hominis PCR as part of STI multiplex PCR panels.

In contrast to Mycoplasma pneumoniae, M. hominis has intrinsic resistance to macrolides. 10 Preferred treatment regimens for M hominis infections include tetracyclines, clindamycin and fluoroquinolones. 11 However, resistance to members of these antibiotic classes has been reported and differs based on country of origin. 11 The absence of a cell wall explains the inherent resistance of Mycoplasma species to the beta-lactam antibiotic class. Its isolation in coinfections, particularly Trichomonas has been controversial in its contribution to emerging Trichomonas metronidazole resistance. 12

References

  1. Verteramo, R., Pastella, A., Calzolari, E., et al. An epidemiological survey of Mycoplasma hominis and Ureaplasma urealyiticum in gynaecological outpatients, Rome, Italy. Epidemiology & Infection,2013, 141(12), 2650-2657
  2. Zheng X, Olson DA, Tully JG, Watson HL, Cassell Gh, Gustafson DR, Svien KA, Smith TF: Isolation of Mycoplasma hominis from a brain abscess. J Clin Microbiol. 1997, 35: 992-994.
  3. Thomas Prescott Atkinson, Mitchell F. Balish, Ken B. Waites, Epidemiology, clinical manifestations, pathogenesis and laboratory detection of Mycoplasma pneumoniae infections, FEMS Microbiology Reviews, Volume 32, Issue 6, November 2008, Pages 956–973
  4. Razin S. Mycoplasmas. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 37.
  5. Meloni GA, Bertoloni G, Busolo F, Conventi L. Colony morphology, ultrastructure and morphogenesis in Mycoplasma hominis, Acholeplasma laidlawii and Ureaplasma urealyticum. J Gen Microbiol. 1980;116(2):435-443.
  6. Christiansen G, Jensen LT, Boesen T, Emmersen J, Ladefoged SA, Schiotz LK, Birkelund S: Molecular biology of Mycoplasma. Wien Klin Wochenschr. 1997, 109: 557-561
  7. Baczynska, A., Svenstrup, H.F., Fedder, J. et al. Development of real-time PCR for detection of Mycoplasma hominis. BMC Microbiol 4, 35 (2004).
  8. Tine RC, Dia L, Sylla K, Sow D, Lelo S, Ndour CT. Trichomonas vaginalis and Mycoplasma infections among women with vaginal discharge at Fann teaching hospital in Senegal. Trop Parasitol. 2019 Jan-Jun;9(1):45-53.
  9. Vancini, R.G., Benchimol, M. Entry and intracellular location of Mycoplasma hominis in Trichomonas vaginalis . Arch Microbiol 189, 7–18 (2008).
  10. Pereyre S, Gonzalez P, De Barbeyrac B, Darnige A, Renaudin H, Charron A, Raherison S, Bébéar C, Bébéar CM. Mutations in 23S rRNA account for intrinsic resistance to macrolides in Mycoplasma hominis and Mycoplasma fermentans and for acquired resistance to macrolides in M. hominis. Antimicrob Agents Chemother. 2002 Oct;46(10):3142-50.
  11. Krausse R, Schubert S. In-vitro activities of tetracyclines, macrolides, fluoroquinolones and clindamycin against Mycoplasma hominis and Ureaplasma ssp. isolated in Germany over 20 years. Clin Microbiol Infect. 2010;16(11):1649-1655.
  12. Dessì, D., Margarita, V., Cocco, A., Marongiu, A., Fiori, P., & Rappelli, P. (2019). Trichomonas vaginalis and Mycoplasma hominis: New tales of two old friends. Parasitology, 146(9), 1150-1155. doi:10.1017/S0031182018002135

-Dr. Alex Shaffer is a first-year ID fellow (2023-2025) at Montefiore Einstein. Alex is interested in the diagnostic stewardship projects and has been actively involved in various activities with ID and micro lab faculty.

-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.

The Eyes Have It: Clues from Vitreous Humor at Autopsy

When it comes to laboratory testing at autopsy, our options are limited compared to those for living patients. We’ve previously discussed the complexities of postmortem toxicology testing (https://labmedicineblog.com/2023/05/23/toxicology-and-forensic-pathology-more-than-a-numbers-game/) but even basic laboratory studies like a glucose or sodium level cannot be reliably measured from postmortem serum specimens. Upon death, hemolysis and cellular breakdown rapidly set in; as tissue oxygen stores and ATP are depleted, the careful balance of intracellular and extracellular electrolytes is lost, making serum essentially useless as an analyte. This makes potentially lethal conditions which leave only non-specific clues (like diabetic ketoacidosis, dehydration, or hyponatremia) difficult or impossible to prove postmortem. Fortunately at autopsy we can access a unique, relatively protected body fluid which cannot be obtained from living patients- the vitreous humor.

Vitreous humor is the clear, thick fluid which fills the globe of the eye. It is nearly acellular, composed predominantly of water with admixed hyaluronic acid and collagen proteins, and its insulated location provides it relative protection from the effects of decomposition and hemolysis. Vitreous humor is typically collected it at the beginning of an autopsy by inserting a needle into the most lateral aspect of the eye and aspirating the fluid; using this method, one can avoid collecting bits of retina (which interfere with analysis of the sample), and avoid creating any noticeable puncture marks or hemorrhages.

Years of data have shown that vitreous fluid approximates serum levels of major electrolytes, glucose, urea nitrogen (VUN), creatinine, ketones, and ethanol. Vitreous fluid is also valuable in the detection of 6-monoacetylmorphine (6-MAM), a metabolite of heroin which is quickly metabolized to morphine in the blood. Identifying 6-MAM in vitreous fluid allows us to ascertain a decedent used heroin, rather than just morphine.

While vitreous fluid is less affected by decomposition, it is not completely immune. The changes are predictable, though, and learning these patterns prevents misinterpretation of decomposition changes, and allows the pathologist to identify which results are still meaningful.

Vitreous fluid potassium will increase with the postmortem interval – in fact, this electrolyte is often touted (erroneously) as a method to determine time of death. Unfortunately there are many other variables (for example, antemortem potassium levels and rate of decomposition) affecting the rise of vitreous potassium, and this method has not proven to be the “holy grail” many were hoping for.

In contrast, vitreous sodium, chloride, and glucose levels all decrease following death – so while a low level may just be an artifact, a high level can be very meaningful. Even “low” levels should be assessed in the clinical context of the case and the concomitant potassium level. If the potassium is normal or barely elevated, it’s unlikely a “low” value is just decomposition-related.

Vitreous humor poses some challenges in the laboratory, though. Because of the thick, viscous nature of the fluid, it can be challenging to actually run it through the instrument. As decomposition progresses, the eyes can desiccate and make the vitreous humor even thicker. In cases of eye trauma, intraocular hemorrhage can contaminate the vitreous humor as well. Importantly, in situations of suspected head trauma in infants, the recovery of vitreous fluid is deferred until the end of the autopsy. Retinal and optic nerve hemorrhages are usually not identified until the brain is removed, and we need to be sure that any trauma we identify was not created artificially during the autopsy.

In summary, the use of vitreous humor as an analyte is a great illustration of creative problem solving. At autopsy the quality of blood specimens is limited, but we aren’t limited to blood. This lesson can be translated to any area of the laboratory: thinking outside of the proverbial box can lead to unexpected, paradigm-shifting opportunities.

References

Rose KL, Collins KA. Vitreous postmortem chemical analysis. NewsPath. December 2008.

Wyman J, Bultman S. Postmortem distribution of heroin metabolites in femoral blood, liver, cerebrospinal fluid, and vitreous humor. J Anal Toxicol. 2004 May-Jun;28(4):260-3. doi: 10.1093/jat/28.4.260. PMID: 15189677.

-Alison Krywanczyk, MD, FASCP, is currently a Deputy Medical Examiner at the Cuyahoga County Medical Examiner’s Office.

The Impact of ASCPi Certification

The world of medicine relies heavily on the skilled and knowledgeable hands of medical laboratory scientists. However, with globalization and a growing healthcare workforce, ensuring internationally trained scientists can seamlessly integrate into new environments is more critical and challenging than ever.

For laboratory scientists in developing countries, obtaining certification can be a life-changing event. Beyond the simple struggles of daily living, these individuals must overcome the obstacles and difficulties that students in the U.S. rarely (if ever) have to face. Yet still, they seek to prove their knowledge and worthiness by seeking international certification.

ASCP is at the forefront of certifying laboratory scientists in developing countries by offering the ASCPi exam. There are few opportunities for students in second and third-world countries to get the quality training and experience to pass the exam. These students come with diverse life experiences and needs but are still passionate about working in the lab.

I discussed the importance of the ASCPi certification with Marion Carrilo, MS, MLS (ASCP), the visionary founder of Trinity Blood Solutions in Trinidad and Tobago in the West Indies, about the reasons why and the need for certification and how the ASCPi is bridging the gap for international laboratory scientists.

Hi Marion, thanks for talking with me today. First, can you describe your typical student?

The typical individuals pursuing MLS ASCPi certification are experienced medical laboratory technologists/technicians. Many of them have worked in the field for at least five years. They love the profession and want more out of it.

In Trinity’s ASCPi Exam Prep, I get some MLTs who have never done an MLT program but want the theory so they can get up to speed with their colleagues who completed an MLT program. These are not typical individuals and they usually have a degree in biological science and are practicing MLTs.

Why do the students choose to take the ASCPi exam?

Reasons for taking the ASCPi exam will vary according to the region and according to the state of affairs for medical laboratory technologists. In many countries, taking and passing the MLS ASCPi is the first step to migrating to the USA as a medical laboratory tech. People migrate due to poor salaries, bad working conditions, and no or limited opportunities to advance in the profession.

In the Caribbean, taking the MLS ASCPi exam after graduating from an MLT program is not routine. Every country has its criteria for being able to practice in a medical laboratory, and in many cases, it is sufficient to graduate from a local MLT program and/or be registered with a local MLT association or board. ASCP is not yet a household name in the Caribbean, so many who pursue taking the exam do it to migrate. Others take the exam for professional advancement.

Migration to the U.S. or another developed country provides them with better opportunities for professional and personal development. In the U.S., the pathway to professional advancement is sure if you work hard. In developing nations, working hard does not guarantee good success.

Professional advancement can be a promotion to a supervisory role or being able to show the credentials of international certification. In some cases, medical laboratory technologists may have been encouraged to get certified by another colleague who is ASCPi certified.

What are the benefits to the lab of having ASCPi techs?

Whether an individual prepares for the exam on their own or enroll in an exam preparation course, they are exposed to systems and procedures not used in their country. This new exposure encourages those techs to be more conscientious in their practice. Having ASCPi techs helps to maintain laboratory accreditation because the new knowledge now gives them an appreciation for working in quality systems. It also encourages the certified tech to share what they learned through preparation with their colleagues.

What do you think the ACSP should or would like them to do to help international students achieve certification?

Recently, a certified individual told me that making the BOC page more intuitive for international candidates will make ASCPi certification info easier to find and understand.

This never occurred to me because I’ve used it for so long. I agree that the BOC page can be intimidating. An example would be displaying the routes in a table form as opposed to the drop-down menus. Have a dedicated page with only the necessary information for the international candidate. So removing newsletter, BOC eligibility Assistant, Categories of certification etc., U.S certification.

Last month, ASCPi BOC created a new Caribbean Advocacy Team. This team will help to provide ASCP BOC with information about how they can best promote certification in the region. As mentioned before, each region has a specific culture concerning the profession, so having Advocacy Teams in various regions is a great gesture.

I really appreciate you providing your experience with our readers. Do you have any final thoughts you would like to share?

It is a great feeling to know ASCP BOC is providing opportunities for techs to advance globally. Some may say they are contributing to the brain drain of a country, and I’m afraid I have to disagree. Instead, they are providing opportunities for advancement as a tech that are not available in the international candidate’s country.

Migration is an expensive process, so not everyone who becomes certified will leave, although they may have planned to do so initially. Even those who leave may return and help their country or provide assistance to their home country from their new home abroad.

Advancement cannot only be seen as moving up a career ladder; it must be seen holistically. A tech working 12 hours 6 days per week and not being paid enough to provide a reasonable level of comfort for their family stymies the work that tech will do and their mindset about the profession. ASCPi provides a way for these techs to move out of such systems and advance holistically in a profession they love.

The ASCP is doing its part to ensure that there are well-trained medical scientists in the world’s laboratories who can provide accurate and timely results for patient care. Passing the ASCPi exam can be, and has been, a life-changing event for scientists working under the most stressful life conditions worldwide. By bridging the knowledge gap and fostering a culture of excellence, the ASCPi is paving the way for a brighter future in laboratory medicine throughout the world, one well-equipped scientist at a time.

–Darryl Elzie is a Quality Consultant for Inova Blood Donor Services. He has been an ASCP Medical Technologist for over 25 years, performing CAP inspections for 15+ years. He has held the roles of laboratory generalist and chemistry senior technologist. 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.  

Microbiology Case Study: A 53 Year Old Male with Malaise, Bilateral Flank Pain and Decreased Urine Output

Case History

A 53 year old male presented to the emergency department with a one-day history of malaise, bilateral flank pain and decreased urine output. His past medical history was notable for decompensated cirrhosis due to alcohol use disorder complicated by esophageal varices and gastric ulcers, peritoneal ascites, several recent episodes of upper GI bleeding, monoclonal gammopathy of unknown significance, and remote prostate cancer status post prostatectomy. Oral history indicated the patient was actively drinking shortly before presentation and had recently consumed oysters on the half shell, broiled shrimp, and crab meat. While being seen in the emergency department, the patient quickly progressed to septic shock.     

Admission laboratory studies demonstrated severe metabolic acidosis, pancytopenia, and acute renal failure. Initial CT abdomen/pelvis demonstrated cirrhotic liver changes, varices, distal esophageal wall thickening, bilateral perinephric fat stranding extending into the pelvis and perivesical fat. The patient was admitted to the MICU for intubation/mechanical ventilation and administration of multiple pressors, as well as empiric meropenem, vancomycin and micafungin given concern for septic shock.Initial blood cultures drawn in the ED flagged positive with gram negative rods (both aerobic and anaerobic bottles) less than 24 hours after collection.

Laboratory Identification

Blood cultures were processed for culture workup and molecular identification. No identification was able to be established using a commercial multiplex PCR-based molecular panel on the positive blood culture broth. Subsequent growth of the organism on MacConkey agar 18 hours later revealed non-lactose fermenting colonies (Image 1A). The organism was oxidase-negative, positive for catalase and indole (Image 1B) and exhibited hydrogen sulfide production when inoculated on triple sugar iron (TSI) media. The organism was definitively identified as Edwardsiella tarda by MALDI-TOF MS and was broadly susceptible to all antibiotic tested including beta-lactams and fluoroquinolones.

Discussion

Edwardsiella tarda is an infrequently isolated member of the Enterobacterales which is most often associated with gastroenteritis. Reports of additional presentations include peritonitis, intra-abdominal abscess, and wound infections are increasing.1 Bacteremia is rare, and can lead to cholangitis, cholecystitis, and liver abscess via hematogenous spread.     Patients of advanced age (>65 years) and those with hepatobiliary diseases including liver cirrhosis and alcohol abuse and iron storage disorders are at increased risk for extraintestinal disease..2 Colonization of the gastrointestinal tract is believed to be a precipitating even leading to bacteremia. Cases of gastroenteritis are usually self-limiting, although ciprofloxacin or trimethoprim/sulfamethoxazole can be utilized in cases of prolonged duration.5 Prompt and accurate diagnosis of E. tarda bacteremia is important as this presentation is associated with an elevated mortality rate,4 particularly among those with liver disease.     

As members of the Enterobacterales, Edwardsiella sp. share common biochemical features of other members of the order including being catalase-positive and oxidase-negative. Oxidase negativity aids in the distinction between E. tarda and Aeromonas/Plesiomonas, both species which are also associated with aquatic environments and cause gastrointestinal infections.5 E. tarda is non-lactose fermenting and reduces sulfur containing amino acids to hydrogen sulfide. This can result in confusion with members of the genus Salmonella4 as colonies exhibit similar appearances on medias including Hektoen Enteric agar and Xylose-lysine deoxycholate agar formulated for recovery and presumptive identification of Salmonella from gastrointestinal specimens. Importantly, E. tarda is also indole-positive which will biochemically differentiate these two genera.

E. tarda is associated with freshwater or brackish aquatic environments. This organism is a well-known pathogen in aquaculture industries causing serious infections in fish and significant economic loss. As such, vaccines and prophylactic antibiotics are utilized to prevent E. tarda infection among aquatic animals, and diagnostic approaches including specialized multiplex PCRs are available. Human infection is often associated with consumption of contaminated fish and seafood, and diagnosis is almost exclusively dependent on microbiological culture by contrast. Clinical multiplex molecular panels for both gastrointestinal and bloodstream infections lack the ability to detect E. tarda. In this patient’s case, recent consumption of seafood serves as the most likely event leading to E. tarda gastrointestinal colonization and is consistent with previously reported cases of E. tarda bacteremia.3 The patient was treated with meropenem eventually narrowed to piperacillin/tazobactam and blood cultures cleared. He was weaned off pressors and extubated.     Unfortunately, the patient decompensated over the course of three weeks due to worsening shock and acidosis. He was moved to comfort care and expired soon thereafter.

References

  1. Hirai et. al. 2015.  Edwardsiella tarda bacteremia. A rare but fatal water- and foodborne infection: Review of the literature and clinical cases from a single centre. Can. J. Infect. Dis. Med. Microbiol. 26(6): 313-318.
  2. Hasegawa M., and Sanmoto, Y.  2024. Recurrent cholangitis and bacteremia due to Edwardsiella tarda: a case report.     Oxford Med. Case Rep. Volume 2024, Issue 1, January 2024, omad148, https://doi.org/10.1093/omcr/omad148
  3. An et. al.     2023.     Case Report: Disseminated Edwardsiella tarda infection in an immunocompromised patient.     Front. Cell. Infect. Microbiol. 20 November 2023.
  4. Janda, J.M, and Abbott, S.L. 1993. Infections Associated with the genus Edwardsiella: the Role of Edwardsiella tarda in human disease. Clin. Infect. Dis. Oct;17(4):742-8.
  5. Janda, J.M and Abbott, S.L. 1999. Unusual Food-Borne Pathogens: Listeria monocytogenes, Aeromonas, Plesiomonas, and Edwardsiella species. Clin. Lab. Med. 19(3):553-582.

-Andrew Clark, PhD, D(ABMM) is an Assistant Professor at UT Southwestern Medical Center in the Department of Pathology, and Associate Director of the Clements University Hospital microbiology laboratory. He completed a CPEP-accredited postdoctoral fellowship in Medical and Public Health Microbiology at National Institutes of Health, and is interested in antimicrobial susceptibility and anaerobe pathophysiology.

-Francesca Lee, MD, is an associate professor in the Departments of Pathology and Internal Medicine (Infectious Diseases) at UT Southwestern Medical Center

Happy Medical laboratory Professionals Week! A Trip Down Memory Lane

When I think of Lab Week, I think of all the Lab Week celebrations we’ve had in the past: Food, games, from “Guess whose baby picture?” to word searches and coworker trivia, and of course, more food. I’ve seen the same games over and over, but with new coworkers they’re always fun. Probably the most unique game I’ve seen, was “whose sample is this?” Smushed chocolate candy bars were stuffed into sample cups (and looked like you know what) and we had to guess which ‘sample’ came from which candy bar. Lab week also helps us remember the techs we’ve worked with in the past and the good times we’ve had in the lab and outside. And, of course, Lab week always seems to bring up reminiscing, and the question “Remember when?”

As a nod to lab week, I’d like to take you on a little trip down memory lane. Those of us who have been around for a while can laugh and add our own stories. The new techs in the lab, the younger generation will look at us and say “No way!”” or “You’re joking, right?”

I work in a lab that is very fortunate to have a few wonderful techs in their late 60’s and 70’s who still work for us part time. But anyone who has passed through our lab in the past 60 years remembers Irene, who is over 80, and has been here since 1963. That’s before many of us were born! Now Irene doesn’t work every day, or even every month, but she’s there for our students and newly graduated employees when we can use her talents for a few days. She has boxes full of teaching slides and comes in to review WBCs and RBC morphology with them and shares many stories about ‘the old days’ in the lab. Recently she was talking to a new grad and mentioned the old lab and the rabbits they kept in the lab.

“Rabbits?’ he asked.

“Yes, youngster, let me tell you about it.”

Rabbits were used for the first pregnancy tests. The first HCG tests came out in the early 1970’s, but before then, the question “Did the rabbit die?” was associated with a positive pregnancy test. Young rabbits were injected with urine or blood from a woman, and several days later, the animals were dissected to look for enlarged ovaries, a sign that HCG was present in the injected specimen, and a positive pregnancy test. So, in reality the rabbit (or mouse, or frog) always died, whether the woman was pregnant or not.

I fortunately missed the live animals in the lab era. Now that I’m working with techs who are younger than my kids (and not that much older than my grandkids!), when us ‘old timers’ talk about what the lab used to be like, we get incredulous wide-eyed stares.

 “You didn’t wear gloves??”

“They drank coffee in the lab?”

“No computers?”

In my very first job out of college I worked in a hospital lab, and trained in Hematology, Chemistry and Blood Bank. It was the time of the rise in automation, and we had some great ‘new’ analyzers. We had a Coulter S in hematology, the first automated hematology analyzer. The Coulter S offered 7 parameters. In about 1 minute it could analyze and report the WBC, RBC, Hgb, Hct, MCV. MCH and MCHC. Before this we had to prepare samples, lyse RBCs to count WBCs, perform hemoglobin measurement on a spectrophotometer, and calculate the indices! If a physician wanted a differential, we stained slides by hand and counted a 100-cell diff. Platelet count counts fortunately were not ordered on every CBC because those were counted manually!

I remember training in the chemistry department with a lot of instruments which each did only one or 2 tests. Individual tests were done on single test analyzers. Which meant a lot of techs in the lab, and you could be assigned to a bench where you did just Na and K on the flame photometer or just Glucoses and BUNs on single test analyzers all day. We did have a STAT analyzer which did electrolytes, glucose and BUN, and a larger analyzer that did 12 test panels, but they were only used when the full panels were ordered. These multi test analyzers were new and exciting, but in 1980 we were still uncapping and pouring off all our samples by hand. Without gloves!

“What?? No gloves?”

No gloves. We drew blood and worked in the lab with no gloves. Analyzers had glass coils that techs changed with their bare hands, and there were accidents. Techs contracted hepatitis and in the 1980’s the fear of contracting HIV was real. It wasn’t until 1992, when the Occupational Health and Safety Administration (OHSA) published the Bloodborne Pathogens Standard. There was increased awareness of HIV, and OHSA implemented universal precautions to protect workers who may come in contact with bodily fluids. OSHA’s standard required employers to provide personal protective equipment, including disposable gloves.

I once read an article that said that medical technician/technologists were the profession that drinks the most coffee. Now, I don’t know about that because I don’t drink coffee, but what they didn’t mention in the article was that they used to drink it in the lab! Yes, the cup of coffee often sat next to the microscope while doing diffs. And remember, no one wore gloves. I remember a doctor walking through the lab smoking a cigar. And while I don’t remember if I ever saw eating in the lab, I’m pretty sure it happened. These things are so taboo to us now that sometimes we wish we were camels because we often go for hours without a sip of water! We may have been the profession who drinks the most coffee, but today we may be the most dehydrated because the closest ‘clean ‘area to get a drink is way down the hall! And we’re too busy to leave our work and go get a drink!

People often use the term ‘The Good Old Days’ when talking about the past, but in the lab, these times weren’t always ‘good’. Yes, we had good times. But there were also practices that weren’t what we would today consider safe. Besides the lack of gloves, and coffee in the lab, there was also mouth pipetting. Remember spit strings? Techs kept them in their pockets for use in mouth pipetting body fluids (shudder). We washed glassware, even literally rinsing blood out of test tubes and reusing them.

We also love to reminisce about obsolete lab tests. I remember when AST, LDH and CK were used for markers of myocardial infarction. Then we had a new test, the CK-MB, which is now designated antiquated and has been replaced by cardiac troponin I for diagnosing MI. Bleeding times were once widely used as a platelet function test. Today this rather crude test is rarely used and not even offered by many labs. Glass in the lab has been replaced by plastics from vacutainer tubes and blood bags to graduated cylinders and beakers. We no longer count platelets on a hemocytometer because our automated analyzers perform platelet counts. In Urinalysis, we used to do confirmatory tests for glucose, bilirubin and protein in urine. And so many more tests that have been replaced by newer and better testing. What is your favorite or no so favorite ‘obsolete’ lab test?

We’ve certainly come a long way in the last 60 years! Lab Week is a great time to generate new awareness and excitement about the laboratory medicine profession while having some fun with your lab coworkers. Thanks to everyone who is part of the laboratory team for your hard work and dedication. Happy Laboratory professionals Week!

DOWN
1. favorite drink to sip at the microscope while doing diffs
2. standard PPE that wasn’t so standard before 1990
3. standard set of guidelines for prevention of bloodborne pathogens

5. old confirmatory test for urine bilirubin
8. type of pipetting common in the old days
9. you probably won’t use one of these for heating in the lab today
10. historic method for testing for glucose in urine
11. animal kept in lab for pregnancy testing
12. old school test for MI
14. plastic blood collection bags have replaced these

ACROSS
4. used to draw blood before vacutainers
6. carried in your pocket as a pipetting aid
7. used for manual platelet counts
13. obsolete platelet function test
15. dark field microscopy was first test for diagnosis of this STD in 1906

Socha-small

-Becky Socha, MS, MLS(ASCP)CMBBCM 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.

Violence in the Laboratory

The field of laboratory safety is very obviously about the protection and well-being of those who work within the labs. The topics of study within this field typically include chemical hygiene, biohazard safety, and even emergency management. One area of focus that historically has not been discussed under the lab safety umbrella, though, is workplace violence. Unfortunately, this topic definitely needs attention and a place among the other safety subjects.

Teaching laboratory staff how to recognize workplace violence (WVP) is important, and the activities that define acts of such aggression are numerous. The National Institute of Occupational Safety & Health (NIOSH) defines WVP as “any violent act, including physical assaults and threats of assault, directed toward team members at work or on duty and include physical injury, threats, abuse, hostility, harassment, discriminatory language/behavior and other forms of verbal violence that can potentially escalate to physical violence.”

The definition is important so staff can identify it, respond to it, and report it. A higher priority, however, is not only to learn the tools that will help staff recognize when potential threats at work arise, but to also be able to de-escalate a tense situations and mitigate any violence altogether. Teach laboratorians to pay attention signs of aggression such as disruptions, outbursts, throwing objects or threatening gestures.

Employees should be taught to respond to growing violence threats by remaining calm, listening, and by demonstrating empathy. Responding to people by yelling or getting into their personal space will only escalate the situation. Your tone of voice, the volume of your voice, your facial expressions and your posture all give signals to the person who is agitated, and if you respond inappropriately with these non-verbal cues, the situation could get worse. Training staff to de-escalate these situations can go a long way toward preventing certain violent incidents before they occur.

Unfortunately, part of the WVP program must be responding to active shooter threats. The Federal Bureau of Investigation (FBI) offers “Run-Hide-Fight” training that helps employees know how to respond when an active shooter situation arises. * There are details in the response that must be considered ahead of an incident. If you can run to an area of safety without getting hurt, go quickly, but do not try to coerce co-workers or patients to come with you. In these situations, you must first consider only your own safety if you wish to survive. If you are in a situation where you can hide in a safe place, be sure to turn off your phone and other electronic devices. Incoming calls can make noises which can alert the shooter to your position. If you must fight, use whatever you can find as a weapon, and fight to win. Do not give the shooter any opportunity to fire his weapon.

The laboratory may follow a facility WVP plan or it may create its own, but there should be a safety plan in place for such situations. Be sure to establish a strategy to identify and address the factors that contribute to violence throughout the workplace. Allow for and ensure prompt and accurate reporting of all incidents of violence including those that involve no physical injury. Empower leaders and employees with the necessary tools to eliminate violence in their areas.

The faster workplace violence can be detected, the sooner a good response may occur. However, as with personal wellness planning, prevention is always a solid approach. Avoiding violent situations altogether can be a part of the lab culture with regular education and training. Make sure there is a strong Workplace Violence Plan in action in your laboratory.

*https://www.fbi.gov/video-repository/run-hide-fight-092120.mp4/view

–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.

Introduction to Shotgun Wounds

We’ve previously addressed the basics of gunshot wounds (see https://labmedicineblog.com/2023/09/22/the-ins-and-outs-of-gunshot-wounds/) but forensic pathologists need to be familiar with injuries inflicted by a variety of firearms. If you grew up in a rural area (like me) you are probably familiar with shotguns as a typical hunting tool. However, shotguns also have several unique characteristics which are crucial for forensic pathologists to understand.

First, the barrel of a shotgun is most often a “smooth bore” as opposed to the longitudinal spiraling lands and grooves (or “rifling”) found in the barrels of rifles and handguns. This means traditional ballistic “matching” (testing to see if a bullet was fired from a particular weapon) is impossible.

Secondly, shotgun ammunition is constructed differently. Broadly speaking there are three types of shotgun ammunition – birdshot, buckshot, and slugs (from smallest to largest in individual size).

A single shotgun projectile is composed of the ‘shell’, an outer casing of plastic with a metal base. The shell contains primer and gunpowder, “wadding” (fiber or cardboard material), and a plastic “sleeve” which holds the projectile(s) (or “shot”). The individual characteristics can vary depending on the “gauge” (caliber) used, but a single shell will typically contain hundreds of birdshot pellets, tens of buckshot pellets, or one slug. The sleeve initially holds these individual pellets together – but upon leaving the barrel, the plastic flays outward, and the pellets or slug are released. For birdshot and buckshot, this means the individual pellets begin to spread apart and lose speed.

This spread of pellets explains why shotguns are a popular choice for hunting birds – a small, constantly moving target. It also helps us determine the range of fire from the shape of the entrance wound. At a close or contact range, there is minimal opportunity for the pellets to spread, resulting in a single circular wound. As the distance from the target increases to several feet, the wound edges become scalloped and individual pellet wounds are observed around the main entrance wound. At a distant range (approximately ten feet), there are only individual pellets wounds. Importantly, these wound characteristics can only be assessed on the skin surface – not on radiographs, which will only show the pellets in their final location within the body.

The other components of the shell can add to the wound characteristics. At contact range, the plastic sleeve (and even the shell) will enter the body but will likely not be visible by radiograph – these still need to be recovered as evidence. At medium distances, the sleeve and/or shell may strike the skin surface and impart a distinct patterned abrasion, without penetrating the skin.

Fortunately, shotgun wounds are a less common part of day-to-day practice – yet it is still important to be prepared with a basic understanding of how these weapons function and the diverse types of ammunition available.

The petri dish on the left holds a representative sample of birdshot pellets, recovered from a contact-range shotgun wound. The plastic sleeve (right) was also in the wound – note the opened flaps.
This contact-range gunshot wound is large and circular, although there is still some faint scalloping of the edges. The black discoloration to the left is caused by searing of the skin from the hot gas exiting the shotgun barrel.
This intermediate-range shotgun wound has a central main wound with scalloped edges and surrounding satellite entrance wounds caused by the pellets beginning to spread.
At distant range, all the pellets have dispersed. At this range the pellets have lost energy, and the wounds are often superficial; however, depending on the location of the injury on the body, even single pellets can cause lethal trauma.
The dispersal of individual pellets within the body can lead to unexpected findings. In this autopsy, the decedent had a self-inflicted shotgun wound to the chest with birdshot. A few pellets entered the aorta near the arch, and several embolized down the length of the aorta before lodging in the right iliac artery (shown here). This illustrates why the spread of pellets should only be assessed on the skin surface, and not based on radiographs.

References

DiMaio, Vincent J. Gunshot Wounds. 3rd ed., CRC Press, Taylor & Francis Group, 2016.

Dolinak, et al. Forensic Pathology: Principles and Practice. Elsevier Academic Press, 2005.

-Alison Krywanczyk, MD, FASCP, is currently a Deputy Medical Examiner at the Cuyahoga County Medical Examiner’s Office.

Microbiology Case Study: A 72 Year Old Male with Postoperative Fever

Case description

A 72 year-old male with severe aortic stenosis resulting in heart failure underwent aortic valve replacement and became febrile with mild shortness of breath on post-operative day one.  Additional pertinent medical history includes end-stage renal disease secondary to diabetic nephropathy with kidney transplantation seven months prior which was complicated by delayed graft function requiring hemodialysis and immunosuppression. The patient’s presentation was suspicious for either a post-operative fever or a complication of hemodialysis. Physical examination did not suggest infection at either the surgical site or his arteriovenous fistula. A chest CT revealed a moderate, loculated left pleural effusion with left lower lobe atelectasis and nodular consolidations in the right lung, raising concern for pneumonia. A bronchial biopsy was obtained, and histopathological evaluation was consistent with an abscess, but no organisms were visualized. Culture from a left bronchial brushing was also obtained at the same time. Two days later, the patient developed a progressively enlarging forehead lesion (Image 1).

Image 1. Progressively enlarging forehead lesion. Microscopic evaluation following biopsy of the lesion revealed organisms morphologically consistent with Nocardia  species.

Laboratory Identification

Microscopic evaluation of the biopsy of the lesion for culture revealed branching, beaded gram positive filamentous bacteria which stained positive using a modified acid-fast stain, suggestive of Nocardia species. This was corroborated by the bronchial culture, where similar modified acid-fast organisms were visualized and grew chalky white colonies identified as Nocardia sp. by MALDI-TOF MS (Image 2). The isolate was referred to a reference laboratory for definitive speciation and antimicrobial susceptibility testing, and the patient was started empirically on ceftriaxone and trimethoprim/sulfamethoxazole.  Speciation and susceptibility testing subsequently identified the organism as Nocardia brasiliensis with susceptibility to both ceftriaxone and trimethoprim/sulfamethoxazole, and treatment was thereafter continued for 40 days.

Image 2. Modified acid-fast stain of a bronchial culture from the patient showed a branching, modified acid-fast rods consistent with Nocardia.  Cultures of both the lesion and bronchial brushing revealed white, chalky colonies on buffered charcoal yeast extract agar consistent with Nocardia sp.

Discussion

Nocardia is a saprophytic bacterium that is commonly found in soil worldwide. Gram staining of Nocardia sp. usually reveals delicate, weakly or erratically staining, beaded, branching Gram-positive rods. There are currently 130 known species of Nocardia,1 of which more than 50 have been reported to have clinical relevance.2 Disease due to Nocardia is known to occur due to inhalation of the organism from the environment or traumatic inoculation. It is thought to be an opportunistic pathogen most commonly affecting immunocompromised patients3 like the patient in this case.

Manifestations of nocardiosis vary widely depending on the species responsible, with most common presentations being lymphocutaneous, pulmonary, or disseminated disease. Here, we present a patient who displayed both lymphocutaneous and pulmonary forms of Nocardia infection. While prognosis is poorer in immunocompromised patients, with appropriate treatment, recovery rate is high in both lymphocutaneous and pulmonary forms, unlike in disseminated disease, where studies have found mortality rates between 44% to 85%.4

Diagnosis of Nocardia infections is mainly performed through either direct visualization of the organism or through culture. The modified acid-fast stain is commonly performed but has limited sensitivity and should generally be performed in conjunction with the Gram stain.5 Recovery in culture is most reliable from respiratory and/or tissue samples, while blood culture, by contrast, has poorer yield. While some strains, as in this patient, appear within several days in culture, some strains may take up to 2 to 3 weeks to detect5 necessitating extended incubation and consultation with the clinical laboratory.

Treatment requires prolonged courses of antibiotics. Susceptibilities vary by species, making it important to obtain species identification to identify appropriate therapy to guide empiric therapy. Susceptibility testing is performed to allow further tailoring of antibiotic regimens. In this case, the patient was treated with a combination of trimethoprim/sulfamethoxazole and ceftriaxone, both of which cover the majority of clinically relevant Nocardia species, until susceptibility testing revealed that the empiric treatment provided adequate coverage for the Nocardia brasiliensis identified, supporting continuation of the chosen empiric regimen.

References

  1. Genus Nocardia. List of Prokaryotic names with Standing in Nomenclature. https://www.bacterio.net/genus/nocardia (2023).
  2. Hamdi AM, Fida M, Deml SM, Abu Saleh OM, Wengenack NL. Retrospective Analysis of Antimicrobial Susceptibility Profiles of Nocardia Species from a Tertiary Hospital and Reference Laboratory, 2011 to 2017. Antimicrob Agents Chemother. 2020 Feb 21;64(3):e01868-19. doi:10.1128/AAC.01868-19.
  3. McNeil MM, Brown JM. The medically important aerobic actinomycetes: epidemiology and microbiology. Clin Microbiol Rev. 1994 Jul;7(3):357-417. doi:10.1128/CMR.7.3.357.
  4. Traxler RM, Bell ME, Lasker B, Headd B, Shieh WJ, McQuiston JR. Updated Review on Nocardia Species: 2006-2021. Clin Microbiol Rev. 2022 Dec 21;35(4):e0002721. doi: 10.1128/cmr.00027-21.
  5. Saubolle MA, Sussland D. Nocardiosis: review of clinical and laboratory experience. J Clin Microbiol. 2003 Oct;41(10):4497-501. doi: 10.1128/JCM.41.10.4497-4501.2003.

-Albert Budhipramono, MD, PhD, is currently a PGY1 Clinical Pathology Resident at the University of Texas Southwestern Medical Center in Dallas, Texas.


-Clare McCormick-Baw, MD, PhD is an Assistant Professor of Clinical Microbiology at UT Southwestern in Dallas, Texas. She has a passion for teaching about laboratory medicine in general and the best uses of the microbiology lab in particular.

-Andrew Clark, PhD, D(ABMM) is an Assistant Professor at UT Southwestern Medical Center in the Department of Pathology, and Associate Director of the Clements University Hospital microbiology laboratory. He completed a CPEP-accredited postdoctoral fellowship in Medical and Public Health Microbiology at National Institutes of Health, and is interested in antimicrobial susceptibility and anaerobe pathophysiology.

Beam Me Up, Scotty

Wouldn’t it be nice if the samples just magically appeared in the laboratory? Sometimes I wish we had a transporter like in Star Trek that could miraculously produce tubes in the rack already sorted and spun. The reality is, however, that we must rely on others to package and transport samples to the lab. Whether it’s blood, urine, body fluids, or even tissues samples, they make their way from the collection site to the lab.  If you work in a hospital setting, samples are delivered to the lab by one of two methods, a pneumatic tube system (PTS), or an internal courier.

  1. Although very convenient when they work, pneumatic tube systems have a few drawbacks. Tube carriers can quickly become an ergonomic safety concern if staff are not properly trained. It is best to limit the number of samples placed in a single tube as overcrowded tubes can be heavy and cause hand and wrist strains if not properly lifted. Sharps such as syringes or needles should never be transported via the PTS. The person opening the tube may not know they are in there and could easily receive a needlestick exposure. It is not a good idea to transport stool or respiratory samples through the PTS either. Specimen containers could open or break inside the tube carrier and give the recipient a not so nice surprise. Additionally, pneumatic tube carriers are known to aerosolize samples. If a spill were to occur, the pneumatic tube system would have to be cleaned or disinfected immediately. Most maintenance or facilities departments have special carriers designed to disinfect the system in the event of a spill. The hardest part may be getting staff to report the spill and initiating the proper cleanup.

    2. Some laboratory samples are walked down to the lab. Samples must be in a closed primary container and placed in a clean secondary container, usually a sample transport bag. Often, we see staff who are wearing gloves while walking samples to the lab. When asked, they state that they are carrying stool or COVID specimens and don’t want to contaminate themselves. The outside of the secondary container is considered clean, so there should be no need for gloves. Furthermore, if the gloves or outside of the transport bags are truly contaminated, these staff would be bringing contaminated items through the clean hallways of the facility. Then they would open the door to the lab, which is considered clean, with those same contaminated gloves. The Centers for Disease Control (CDC) has guidelines to mitigate the risk of bringing potentially infectious material into clean areas. The Core Infection Prevention and Control Practices for Safe Healthcare Delivery in All Settings document states that staff must “remove and discard PPE upon completing a task before leaving the patient’s room or care area”1. Another thing to consider is what happens if one of the containers leaks during transport. Or even worse, what if a spill were to occur? Small amounts of blood or body fluid can easily be cleaned with an absorbent and disinfectant. A larger spill, say a 24-hour urine jug, or a hazardous material spill like a tissue sample in a large container filled with formalin, would need more attention. Staff should be trained in how to handle large volume spills and transporters should take precautions, such as using a cart and having a spill kit on hand when moving hazardous material like formalin.

    Laboratory staff may not be the ones packaging and shipping samples to the lab, but they are often the recipients and have the responsibility to ensure they themselves and others remain protected. If staff should encounter specimen transport problem situations, be sure they have an effective pathway to communicate and escalate concerns. Often the staff sending specimens are not aware of the risks, so labs should provide that education- they will be thankful for it. Preanalytical processes are at the start of the road toward quality lab results, and everyone involved in each step should keep safe work practices at the forefront.

    1. Centers for Disease Control. CDC’s Core Infection Prevention and Control Practices for Safe Healthcare Delivery in All Settings. (2022). Retrieved from https://www.cdc.gov/infectioncontrol/guidelines/core-practices/index.html

    -Jason P. Nagy, PhD, MLS(ASCP)CM is 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.