Microbiology Case Study: A 50 Year Old Male with Fever and Diarrhea

Case History

A 50 year old male initially presented with cold symptoms. He was seen and evaluated at urgent care, with suspicion for bronchitis, but with no improvement with albuterol. Physical exam raised a suspicion for bacterial sinusitis. The patient was treated with amoxicillin/clavulanic acid with little improvement, and he was admitted to the hospital a week later for fever and diarrhea. Blood cultures were obtained. He was initially treated with cefepime prior to the speciation of the culture, and then switched to erythromycin for a 7 day course.

Laboratory Identification

Blood cultures were positive for gram negative curved/spiral rods. Gram stain and colony morphology were consistent with Campylobacter which was confirmed as C. jejuni by MALDI-TOF.

campy1

Image 1. Gram stain showing gram negative curved/spiral rods.

Discussion

C. jejuni are gram negative curved or spiral rods. Campy CVA agar is used for stool cultures because it is selective for Campylobacter and contains cefoperazone, vancomycin, and amphotericin B (CVA) which inhibit normal fecal flora. The media is incubated at 42°C under microaerophilic conditions, supporting the growth of Campylobacter jejuni and C. coli. C. jejuni is thermophilic, with growth on blood agar at 37°C and 42°C. Growth does not occur at 25°C. The colonies on blood agar are non-hemolytic, gray and smooth. Our isolate grew, albeit not happily, on blood and chocolate at 37°C with 5-10% CO2.

Infection is often transmitted by contaminated foods such as undercooked chicken. C. jejuni are most commonly associated with human infections however, C. coli have also been implicated. Guillain-Barre syndrome has been associated with patients following an infection with C. jejuni. It is not known how our patient was exposed. Macrolides are effective treatment modalities for C. jejuni, as well as fluoroquinolones, however, resistance to fluoroquinolones is increasing.

 

-Mustafa Mohammad, MD is a 3rd year anatomic and clinical pathology resident at the University of Vermont Medical Center.

Wojewoda-small

-Christi Wojewoda, MD, is the Director of Clinical Microbiology at the University of Vermont Medical Center and an Assistant Professor at the University of Vermont.

Safety Success in the Anatomic Pathology Laboratory

The pathologist walked into the histology laboratory every morning to say hello to the staff. As he did so, he drank from his cup of coffee.

The gross room was very small, and the eyewash station was placed on the faucet in the only sink in the room. One foot above the sink were the sharp ends of all of the cutting tools that hung on the wall. That was also the hand washing sink.

The morgue was the only space in the hospital where chemical waste could be stored before being picked up. The waste containers were not dated, and a funnel was left in the opening of one of them.

It can be difficult to oversee safety for a clinical laboratory, but often the people responsible for it have a clinical lab background, so the understanding of the regulations is clear. However, if you are responsible for the anatomic pathology (AP) areas as well, you may need to broaden the scope of your safety learning. Each of the lab safety situations mentioned above are real, and detecting and resolving those and other issues is important. Knowing the regulations for histology, cytology, and the morgue settings is a good place to start. Next, spend some time in those areas, and learn the processes that occur every day. Ask questions and look at procedures.

Bio-safety regulations in the AP lab are no different than for clinical laboratory staff. Many specimens, body parts and cadavers may be handled, and Standard Precautions should be used. That includes the use of gloves, lab coats, and face protection.

Chemical hygiene is also important in the AP lab, and since these areas tend to utilize many more chemicals than others, the management of them can seem daunting. Be sure to keep an updated chemical inventory which designates carcinogens, reproductive toxins and acute toxins. Ensure all staff have access to Safety Data Sheets (SDS) and that they have been trained to properly store chemicals. That means strong acids and bases should be stored near the floor, and they should never be stored together. Other incompatible chemicals should be separated as well. Ensure that proper spill supplies are available, and that staff can clean up various types of chemical spills. Conducting spill drills is a great way to keep staff ready for the real event.

Exposure monitoring should occur depending on what chemicals are used in the area. Managing chemical safety also includes ensuring proper labeling of all chemical containers. Primary container should have current Globally Harmonized System (GHS) compliant labels, and secondary containers also need adequate labeling. Secondary containers may be labeled using a GHS format or NFPA and HMIS conventions may be used.

Chemical or Hazardous waste handling must also be monitored closely in AP areas. If chemical waste is stored in the lab in a Satellite Accumulation Area, the containers should not be dated, and they should be stored at or near the point of waste generation. Central Accumulation Areas are areas where waste is stored before it is removed from the site. In these areas, containers must be dated, and a log should be kept for weekly checks of the areas. Weekly checks include looking for container leaks, dates on containers, and making sure containers remain closed. All chemical waste containers must remain closed unless someone is actively working with them. Never leave an open hazardous waste container open or with a funnel in it while unattended.

Special safety consideration should be given to tissue cutting in the histology area. Microtome and cryostat use presents specific sharps dangers because of the large sharp blades in use. If a blade guard is included with the equipment, train staff to always engage it before placing hands near the blade. Use magnet-tipped implements to remove the blades and rubber-tipped forceps to install new ones. Follow manufacturer guidelines for cryostat decontamination, but avoid using formaldehyde fumes for that purpose.

If laboratory staff is exposed to formaldehyde concentrations greater than 0.1 parts per million in their routine work, there is a safety training program that is required by OSHA. This formaldehyde training needs to be administered at the time of initial job assignment and whenever a new exposure to formaldehyde is introduced into the work area. The training must also be repeated annually.

As a lab safety officer, I learned over time how to work with and coach pathologists for safety. There is no more coffee consumed in the lab. The cramped gross room was remodeled to improve safety. Understanding the issues and reporting them was the key to getting this done. It took a difficult inspection by the EPA to teach me how to properly handle chemical waste. Today the representative from the state is my best reference, and she is willing to come to the labs and help us with waste regulation compliance. If your background is clinical, don’t ignore the special considerations in the anatomic pathology areas. Use your resources to learn what happens there, and understand the regulations so that employees in every area of the lab can work safely.

 

Scungio 1

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

Microbiology Case Study: An 18 Year Old with Vaginal Discharge

Case Presentation

An 18 year old girl presents to her pediatrician with her mother for her pre-college check-up. She has no past medical history. After her mother leaves the room for the social history component, the girl admits to having sex with her boyfriend for the first time two weeks ago and complains of a yellow green malodorous vaginal discharge that started a week ago. She endorses mild pelvic pain. A pelvic exam is performed and mild cervical tenderness is noted. The cervix is pink, nulliparous, inflamed and is covered by small red punctate spots. A thin yellow green frothy discharge of fishy odor is also detected. A wet prep is made and reveals squamous cells and numerous motile organisms.

trich1
Figure 1.  Trichomonas vaginalis in a Pap test. The protozoa are often found next to squamous cells. (ThinPrep)

trich2
Figure 2.  Collection of Trichomonas vaginalis parasites eating at a squamous cell in a Pap (ThinPrep)

Discussion

Our patient was diagnosed with Trichomonas vaginalis (TV). TV is a flagellated parasitic protozoan for which humans are the only known host. It is 10-20 um long and 2-14 um wide with multiple flagella projecting from the anterior and posterior sides. It has a single trophozoite stage and does not survive well outside of its host. TV is a predatory obligate parasite that eats bacteria, vaginal epithelial cells, and red blood cells. It uses fermentative metabolism to produce the carbohydrates needed for fuel. TV is a sexually transmitted disease; however, because it is not reportable to local health departments, the true epidemiologic incidence rate is unknown. Its prevalence is highly variable by population and location. For example, some studies cite a prevalence of 3.1% of American pre-menopausal women (2.3% of adolescents) [1], while in certain high-risk populations the rate might be as high as 47% [2]. Most affected patients are asymptomatic; about a third of females become symptomatic within six months of infection. Symptoms for females include vulvar and vaginal irritation and itching, pain with urination and a diffuse, malodorous, yellow-green vaginal discharge. The cervix becomes reddened in a punctuated fashion causing the well-known strawberry cervix seen on colposcopy. In males, urethritis can develop. TV is often diagnosed via wet mount microscopy, where the protozoa can be seen moving around (Video 1). However, the sensitivity is relatively low, especially among males. Detection by nucleic acid probe from urine, endocervical, and vaginal swabs are considered more sensitive. TV can also be incidentally discovered on Pap tests (Figures 1 and 2). Treatment typically consists of a single dose of metronidazole [1,2]. It is critical that partners be treated as well, because otherwise reinfection may occur.

 

References

  1. Kissinger P. Trichomonas vaginalis: a review of epidemiologic, clinical and treatment issues. BMC Infectious Diseases. 2015; 15(307): 1-8.
  2. Meites E et al. A review of evidence-based care of symptomatic trichomoniasis and asymptomatic Trichomonas vaginalis infections. Clinical Infectious Diseases. 2015; 61(S8): S837-48.

 

AM

-Amanda Strickland, MD, is a 2nd year Anatomic and Clinical Pathology Resident at UT Southwestern Medical Center.

Erin McElvania TeKippe, PhD, D(ABMM), is the Director of Clinical Microbiology at Children’s Medical Center in Dallas Texas and an Assistant Professor of Pathology and Pediatrics at University of Texas Southwestern Medical Center.

 

Chemistry Case Study: Unexplained Metabolic Acidosis

Case Workup

A 24-year-old female at 34 weeks of gestation was transferred from an outside hospital with history of nephrolithiasis and right side pyelonephritis, for which she underwent stent placement 2 weeks ago. She started experiencing severe pain and muscle spasms in her hip and was unable to move her leg due to the pain. She had decreased appetite and also noted vomiting. Her bilirubin and aminotransferases were found to be elevated. Additionally, her blood gas analysis showed a bicarbonate of 9 mEq/L, pH of 7.2 with 99% SpO2. Our clinical chemistry team was consulted on her low pH.

Patient’s laboratory workup is shown in the table below. We first ruled out some common causes of metabolic acidosis, including lactic acidosis and diabetic ketoacidosis. Ingestion of toxic alcohols was ruled out based on normal osmolality and osmolar gap. Normal BUN, creatinine, and their ratio ruled out renal failure.

Positive urinary ketones were noted, with an elevated anion gap. Serum beta-hydroxybutyrate was therefore measured and a result of 3.0 mmol/L (ref: <0.4 mmol/L) confirmed ketoacidosis. Patient had no history of diabetes and no recent alcohol consumption. On the basis of excluding other causes, and also considering her decreased appetite and recurrent vomiting, it is believed that ketoacidosis was caused by “starvation.”

Test Result Ref * Test Result Ref *
Albumin 2.0 3.5 – 5.0 g/dL pH 7.24 7.32-7.42
ALK 139 35 – 104 U/L pCO2 (V) 21 45-51 mmHg
ALT 177 5 – 50 U/L pO2 (V) 46 25-40 mmHg
AST 159 10 – 35 U/L O2 Sat (V) 72 40 – 70 %
Total Bili 2.0 0.0 – 1.2 mg/dL Glucose 74 65-99 mg/dL
Direct Bili 1.5 0.0 – 0.3 mg/dL Urine ketones 2+ Negative
Lactic acid 0.9 0.5 – 2.2 mmol/L Urine protein 2+ Negative
Protein 6.0 6.3 – 8.3 g/dL Chloride 104 98-112 mEq/L
Sodium 138 135-148 mEq/L CO2 9 24-31 mEq/L
Potassium 4.6 3.5-5.0 mEq/L Anion gap 25 7-15 mEq/L
Creatinine 0.6 0.5 – 0.9 mg/dL eGFR >90  >90 mL/min/1.73 m2
BUN 8 6 – 20 mg/dL Osmolality 286 275 – 295 mOsm/kg

* Reference ranges are for normal adults, not for pregnant women.

Discussion

With optimal glucose level and sufficient insulin secretion, glucose is converted by glycolysis to pyruvate, which is then converted into acetyl-CoA and subsequently into the citric acid cycle to release chemical energy in the form of ATP. When glucose availability becomes limited, fatty acid is used as an alternative fuel source to generate acetyl-CoA. Ketone bodies are generated in this process, and their accumulation result in metabolic acidosis. In healthy individual, fasting is seldom suspected to be the cause of metabolic acidosis. Sufficient insulin secretion prevents significant free fatty acid accumulation. However, under certain conditions when there is a relatively large glucose requirement or with physiologic stress, 12 to 14 hour fast could lead to significant ketone bodies formation, resulting in overt ketoacidosis (1-3).

Ketoacidosis is most commonly seen in patients with diabetic ketoacidosis. Similar metabolic changes are seen with poor dietary intake or prolonged fasting and resulting acidosis is referred to as “starvation ketoacidosis” (2). During pregnancy, especially in late pregnancy, there is an increased risk for starvation ketoacidosis, due to reduced peripheral insulin sensitivity, enhanced lipolysis, and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis (1-2, 4). Other cases described with starvation ketoacidosis include patients on strict low-carbohydrate diet (5-6), young infants after fasting (7), and patients with prolonged fasting before surgery (3).

Although starvation ketoacidosis is rare, healthcare provider should be aware of this entity especially in pregnant patients, because late recognition and delay in treatment are associated with a greater risk for impaired neurodevelopment and fetal loss (2). Moreover, given the popularity of low-carbohydrate diet nowadays, starvation ketoacidosis should be considered when assessing patient’s acid-base imbalance in conjunction with their dietary lifestyles.

References

  1. Frise CJ,Mackillop L, Joash K, Williamson C. Starvation ketoacidosis in pregnancy. Eur J Obstet Gynecol Reprod Biol. 2013 Mar;167(1):1-7.
  2. Sinha N,Venkatram S, Diaz-Fuentes G. Starvation ketoacidosis: a cause of severe anion gap metabolic acidosis in pregnancy. Case Rep Crit Care. 2014;2014:906283.
  3. Mostert M, Bonavia A. Starvation Ketoacidosis as a Cause of Unexplained Metabolic Acidosis in the Perioperative Period. Am J Case Rep. 2016; 17: 755–758.
  4. Mahoney CA. Extreme gestational starvation ketoacidosis: case report and review of pathophysiology. Am J Kidney Dis. 1992 Sep;20(3):276-80.
  5. Shah P,Isley WL. Ketoacidosis during a low-carbohydrate diet. N Engl J Med. 2006 Jan 5;354(1):97-8.
  6. Chalasani S, Fischer J. South Beach Diet associated ketoacidosis: a case report. J Med Case Rep. 2008;2:45. Epub 2008 Feb 11.
  7. Toth HL, Greenbaum LA. Severe acidosis caused by starvation and stress. Am J Kidney Dis. 2003;42(5):E16.

 

Xin-small

-Xin Yi, PhD, DABCC, FACB is a board-certified clinical chemist. She currently serves as the Co-director of Clinical Chemistry at Houston Methodist Hospital in Houston, TX and an Assistant Professor of Clinical Pathology and Laboratory Medicine at Weill Cornell Medical College.

Microbiology Case Study: A 58 Year Old Female with Lung Nodules

Case History

A 58 year old female with past medical history significant for Type II diabetes, hypertension, hyperlipidemia, chronic diastolic heart failure, and hypothyroidism was hospitalized for following a fall and was found to have compression fractures. The hospitalization was complicated by flash pulmonary edema requiring intubation. CT chest obtained during this hospitalization demonstrated lung nodules, which were biopsied and cultured.

Laboratory Identification

The bacterial and mycobacterial cultures grew gram positive bacilli which were positive on Modified Kinyoun stain. They were negative for Auramine/Rhodamine. The organism grew on several media, including 7H11, Chocolate, and Buffered Charcoal Yeast Extract (BCYE). They formed chalky, white-pink colonies. The organism was confirmed as Nocardia nova by a reference laboratory.

nocard1

Image 1. Modified acid fast bacilli on Modified Kinyoun stain.

nocard2

Image 2. Chalky white-pink colonies on BCYE agar.

Discussion

Nocardia nova is a weakly acid fast, aerobic filamentous, beaded, gram positive bacilli with right-angled branching. It is identified by a Modified Kinyoun stain. Nocardia grows best on BCYE agar; however it also can grow within 3-5 days on blood and chocolate agar. It forms chalky white-pink colonies. Molecular testing is performed to speciate Nocardia, primarily 16S ribosomal RNA gene sequencing, as well as mass spectrometry. Most infections can be treated with sulfonamides for 6-12 months, however, the CDC recommends performing speciation and susceptibility testing on every isolate due to specific susceptibility profiles and drug resistant strains. Our patient was treated with high dose sulfamethoxazole/trimethoprim and meropenem.

Nocardia nova is commonly found in soil and is one of several pathogenic Nocardia species. Nocardia is often inhaled and presents as a chronic pulmonary infection with cough, shortness of breath, and fever. Nocardia can also cause pleural effusions, empyema, pericarditis, abscesses, or dissemination to deep organs, especially the brain. Nocardia can also be contracted though trauma, causing cutaneous diseases such as a mycetoma or cellulitis. Because of its low virulence, Nocardia generally affects immunocompromised patients, however those with preexisting pulmonary disease can also be susceptible to infection.

 

-Mustafa Mohammad, MD is a 3rd year anatomic and clinical pathology resident at the University of Vermont Medical Center.

Wojewoda-small

-Christi Wojewoda, MD, is the Director of Clinical Microbiology at the University of Vermont Medical Center and an Assistant Professor at the University of Vermont.

Hematopathology Case Study: A 69 Year Old Female with Persistent Monocytosis

Case History

A 69 year old female with a past medical history significant for endometrial adenocarcinoma, traumatic brain injury, atrial fibrillation, hypertension, hyperlipidemia, and persistent monocytosis (absolute monocyte count ranging from 1.6-3.7 K/uL) who had an indeterminate lesion identified in the T5 vertebra, read as “hemangioma, although surrounding edema is worrisome for malignancy” upon staging imaging for history of endometrial carcinoma.

CBC at the time was: WBC 9.8; HGB 12.9; HCT 37.6; PLT 154; MCV 92 fL; MCH 31.7.

Automated differential showed: 43.0 Neutrophils; 34.8 Lymphocytes; 20.0 Monocytes; 1.4 Eosinophils; 0.2 Basophils; 0.6 Immature granulocytes.

Absolute monocyte count was 1.95 K/uL.

This lesion was biopsied and given the findings, a subsequent bone marrow biopsy was performed on 5/4/2017. The bone marrow core biopsy contained multiple compact aggregates of spindle shaped cells with hypogranular cytoplasm, morphologically compatible with atypical mast cells. Within these aggregates, numerous eosinophils are present. By immunohistochemistry, the mast cells are brightly positive for CD117 and mast cell tryptase. Concurrent bone marrow aspirate flow cytometry demonstrated a small population of mast cells that co-expressed CD2 and CD25.

Of note, the patient was found to have a persistent absolute monocytosis. Flow cytometry revealed an abnormal population of monocytes that displayed aberrant phenotypic expression of CD2 and CD56 (subset).

Next-generation sequencing revealed two truncation mutations in the TET2 gene (K988* in 34.6% of the reads and Q1138* in 36.4% of the reads). Cytogenetic analysis revealed a normal female karyotype (46,XX).

myelomono1

myelomono2

myelomono3

Overall, an immunophenotypically abnormal population of mast cells and monocytes are present in the context of a long-standing absolute monocytosis and the presence of two TET2 truncating mutations, supporting a diagnosis of systemic mastocytosis with an associated hematologic non-mast cell lineage disorder (best classified as chronic myelomonocytic leukemia).

Discussion

A diagnosis of systemic mastocytosis is a combination of clinical, morphologic, immunophenotypic, and molecular analyses, as required by the World Health Organization (WHO 2008). By current consensus guidelines, SM variants are partly distinguished by clinicopathologic criteria referred collectively as B and C findings. B findings include: >30% of bone marrow mast cells (MC) on biopsy and/or serum tryptase levels >200 ng/mL; increased marrow cellularity/dysplasia without meeting diagnostic criteria for another myeloid neoplasm; or enlargement of liver, spleen, or lymph nodes without evidence of organ damage. C findings include: evidence of organ damage caused by a local MC infiltrate, such as abnormal liver function and/or ascites, hypersplenism, cytopenias, large osteolytic lesions/fractures, and malabsorption with weight loss caused by MC infiltrate in the gastrointestinal tract.

Systemic mastocytosis commonly occurs in two types with different clinical courses based upon the aforementioned findings. Indolent SM (ISM) is defined by the absence of C findings. Smoldering SM is a subtype of ISM that displays 2 or more B findings. ISM may become more aggressive and a descriptive term of advanced SM refers to a category including aggressive SM (ASM), mast cell leukemia (MCL), and “SM with an associated myeloid neoplasm.” The latter entity comprises more than 90% of cases that have previously been referred to as SM with an associated hematologic non-mast cell lineage disorder (SH-AHNMD).

ASM and MCL are characterized by organ damage and histologic characteristics. ASM often exhibits multifocal bone marrow infiltration of atypical mast cells that are often spindled in shape with hypogranular or immature morphology. Marked fibrosis often accompanies the infiltrate as well as a KIT D816V mutation. MCL is codified by more than 20% of the marrow aspirate nucleated cells represent by mast cells and on core biopsy, a compact infiltrate is often identified with usually low level fibrosis. In MCL, circulating mast cells are greater than 10% of nucleated cells but according to Gotlib et al., the aleukemic MCL (less than 10% circulating mast cells) is more common.

In the context of our patient, myeloid neoplasms associated with SM are often represented by MDS, MPN, or MDS/MPN overlap disorders, and occasionally AML.

Associated lymphoid or plasma cell neoplasms have been described, but in a much lower frequency.

In accordance with the diagnostic implications, KIT D816V mutational analysis is important therapeutically. Most patients with SM harbor the KIT D816V mutation (>80% in one clinical series; 90-100% in research studies using purified MCs), which is a considered imatinib-resistant mutation. Midostaurin (a second generation TKI) may provide some disease response while nilotinib or dasatinib are usually less likely to lead to a durable response. The rare patients who have a juxtamembrane domain KIT mutation are much more likely to respond to imatinib or masitinib.

For disease response, criteria were first published in 2003 by Valent, et al. In a reiterated version published in 2007, the evaluation of clinical evidence of organ damage (C findings), was the foundation for determining appropriate response. Another facet to determining response was in relation to BM MC burden, serum tryptase level, and organomegaly, which further subcategorized the levels of major response (MR). MR was defined as normalization of 1 or more C findings. In turn, MR was divided into 3 categories:

  1. Complete remission (resolution of MC infiltrates in organs, serum tryptase less than 20 ng/mL, and disappearance of SM-associated organomegaly)
  2. Incomplete remission (decrease in MC infiltrates in organs and/or serum tryptase levels and/or visible regression of organomegaly by >50%)
  3. Pure clinical response (without decrease in MC infiltrates, serum tryptase levels, or organomegaly)

Partial response (PR) is defined as incomplete regression of 1 or more C findings and include good partial response (GPR; >50% regression of 1 or more C findings) and minor response (<50% regression).

Lastly, the Mayo Clinic published revised response criteria in 2010 which established minimal baseline laboratory abnormalities for organ damage to be evaluated in order to allow for more accurate assessment of response to therapy that is clinically more relevant.

Overall, systemic mastocytosis is a rare entity that displays a range of presentations that can be described as indolent up to an aggressive (advanced) phenotype. The hallmarks for diagnosis include histologic, immunophenotypic, molecular, and clinical findings.

 

References

  1. Gotlib, J et al. “International Working Group-Myeloproliferative Neoplasms Research and Treatment (IWG-MRT) & European Competence Network on Mastocytosis (ECNM) consensus response criteria in advanced systemic mastocytosis,” Blood, 2012.
  2. Horny HP et al. “Mastocytosis,” In: Swerdlow S et al. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. Lyon: IARC Press; 2008:53-63
  3. Valent P et al. “Aggressive systemic mastocytosis and related mast cell disorders: current treatment options and proposed response criteria.” Leuk Res. 2003;27(7):635-641.
  4. Pardanani A, et al. “A critical reappraisal of treatment response criteria in systemic mastocytosis and a proposal for revisions. Eur J Haematol. 2010;84(5):371-378.

 

PhillipBlogPic-small

-Phillip Michaels, MD is a board certified anatomic and clinical pathologist who is a current hematopathology fellow at Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA. His research interests include molecular profiling of diffuse large B-cell lymphoma as well as pathology resident education, especially in hematopathology and molecular genetic pathology.

Applying the Flipped Classroom to Medical Laboratory Science

Our Medical Laboratory Science (MLS) program curricular model applies the “reverse-lecture-homework-paradigm” (more commonly known as “flipping the classroom”) to the majority of our didactic courses. For our MLS program, this model works best for those MLS courses that we are able to provide strong hands-on laboratory lessons in our classroom setting. For those courses that are not amenable to this (like clinical chemistry where the laboratory procedures are highly automated), we provide the learning content in a traditional lecture-based format with supplemental laboratory lessons. This combination of approaches to instruction and learning—whereby we provide both traditionally designed courses (live, synchronous, “face-to-face” learning) and online courses (virtual, asynchronous, distance learning)—ends up supporting all of our students’ varied learning styles.

As an example, in our course in bacteriology, we can teach hands-on laboratory lessons using manual procedures for identifying bacteria that can be readily instituted in our program classroom/teaching laboratory. Because we can easily reproduce these techniques for our students, we use the flipped-classroom approach in this course and provide all of the lecture material as online learning lessons that our students complete as homework before the next day’s laboratory session. By having our students complete the lecture material as homework, we can dedicate more classroom time to learning laboratory techniques that are more closely anchored in what our students are going to do for a living.

From the standpoint of education theory and Bloom’s cognitive domain of learning, lesson content that requires basic recall of information (knowledge and comprehension) is presented as homework in the online lesson. In the hands-on laboratories, more of the higher level cognitive domains of interpretation and problem solving are applied, and the lab techniques are performed in the presence of the instructor, allowing for greater instructor-student interaction, questions, and joint problem solving.

The instructor role radically changes in this model, and he/she is no longer put in the position of “expert at the lecture podium,” allowing for greater opportunity to partner with the students in the classroom as a facilitator or guide in their learning. The literature commonly refers to the redefining of the instructor’s role in educating the student as moving away from being the “sage on stage” to that of facilitator or “guide on the side.” Our instructors have more time to help the students hone their laboratory techniques and apply the learning material in context and also answer questions.

Our instructors have found the experience rewarding, and they have been very successful using this format. They are able to partner with our students more collaboratively, and they can assume more of a mentorship role. It should be noted that there is a substantial amount of front-end time required to build the courses. Each lesson plan includes learning objectives, an online lesson, a hands-on lab, and a self-assessment. Our courses also include online discussion boards, homework assignments, and study guides for exam preparation (both written tests and laboratory practicals). Once an online course is built, however, we have found that it is easier to update and maintain versus a lecture-based course that may need redevelopment when instructors change.

The students’ role in the classroom also changes. When they are presented with the lecture material as online homework, they gain a newfound control over the material that doesn’t exist in a face-to-face traditional lecture format. They have control over when they study the learning content and the length of time they study. They can go in and out of the online lecture content as often as they want. The lesson material can include links to additional resources that they can delve further into if they desire. This format places each student in the “driver’s seat,” and the student moves from being a passive learner to active.

As for our students, they consistently come to class prepared for each hands-on activity, ask questions, and perform well on their written and practical examinations. Our students tend to form study groups outside of the classroom, and they review and process the online content with their peers, which results in a classroom environment that is collegial, team-oriented, and mutually supportive.

Reference

Bloom, Benjamin S., (Ed.), Taxonomy of Education Objectives: Handbook I: Cognitive Domain, N.Y., David McKay Company, Inc. 1956.

 

Lehman_small

-Susan M. Lehman, MA, MT(ASCP)SM graduated from the University of Wisconsin-Madison in 1983 with a BS in medical technology. She is program director for the Medical Laboratory Science Program and course director for Clinical Microbiology I and II; her areas of interest include distance education and education methodology.