Please Don’t Tell Me I Died of Cardiac Arrest

Ask any forensic pathologist what their professional pet peeve is and many of them will likely say “bad death certificates” (right after needing to scratch one’s nose in the middle of an autopsy). Despite the importance of death certificates to public health statistics, studies repeatedly demonstrate an unacceptably high error rate. Death certification isn’t taught in medical schools, and physicians usually learn on the fly. The media often perpetuates these errors, which is why you’ll see news headlines declaring a celebrity died of “cardiac arrest.” However, death certification is a relatively simple concept which can be easily grasped with a little instruction.

Cause of death is “that which in a continuous sequence, unbroken by an efficient intervening cause, results in death and without which death would not have occurred”. Put more simply, it is the etiologically specific disease or injury which triggers the chain of events leading to death. There’s no time limit; a cause can take years (as in breast cancer) or seconds (as in a gunshot wound). Conversely, mechanism of death describes the biochemical and biophysical processes by which the cause exerts its lethal effects. Mechanisms are non-specific and often happen in everyone who is dying (for example, hypoxia, metabolic acidosis, kidney failure). It’s easy to see why doctors list mechanisms on the death certificate—usually in a critically ill patient we’re focused on treating these mechanisms, by providing oxygen, replenishing electrolytes, and performing dialysis until kidney function has returned.

The most common example of this is “cardiac arrest.” Everyone who is dead is in cardiac arrest, by definition—what caused the cardiac arrest is what we really need to know. Putting only a mechanism on a death certificate doesn’t help families understand why their loved one died or inform them of their own potential medical risks, and it provides no useful information to public health prevention efforts.

Finally, manner of death describes the circumstances surrounding death. There are typically five options – natural, accidental, suicidal, homicidal, or undetermined. The most common manner of death error is ignoring fall-related injuries in the elderly or debilitated. A ground-level fall with femoral neck fracture can lead to death in a susceptible individual by blood loss, deconditioning, pneumonia, decubitus ulcers, or thromboembolism. Falls are not a “natural” event – they are potentially preventable, and especially in a vulnerable population may be a warning sign for neglect or abuse. For this reason, we categorize these deaths as accidental.

The nuances around death certification demonstrate one of my favorite roles as a forensic pathologist—public health informaticist. Accurate categorization of deaths allows us to track mortality data and intervene (for example, by notifying communities of a new potent fentanyl analog, or identifying trends in suicide). A death certificate of “cardiac arrest” is therefore frustratingly vague, and our patients and their families deserve a better answer. An academic autopsy program may find it worthwhile to do a quality assurance review of hospital death certificates to identify systemic errors or deficiencies. The CDC offers a free online tutorial (at, which is an excellent resource for physicians or family members who want to learn more about this process.

Causes of DeathMechanisms of Death
Atherosclerotic cardiovascular diseaseCardiac ischemia
Type II Diabetes MellitusAcute renal failure
Blunt force injuriesExsanguination
Aspiration pneumonia due to cerebral infarctSepsis

Causes vs Mechanisms of Death: Notice that the causes are all etiologically specific diseases or injuries. The mechanisms are non-specific and lead the reader to ask “…due to what?”. For example, cardiac ischemia can be due to atherosclerosis, vasospasm, or blood loss from trauma.

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

Microbiology Case Report: Left Upper Quadrant Abdominal Pain in a 39 Year Old Male

A 39 year old male presented to a hospital in Dallas, TX with left upper quadrant abdominal pain, nausea, decreased appetite, and a feeling of bloating. The abdominal pain was described as a gradual onset of pain over the course of 2 to 3 weeks. He had no known weight loss, night sweats, chills, diarrhea, or recent trauma. The patient was afebrile on exam with unremarkable vital signs and reported tenderness in the left upper quadrant on palpation of the abdomen. Of note, he was admitted to the hospital 6 weeks prior with abdominal discomfort and was found to have a splenic abscess on computed tomography (CT) scan of the abdomen. There was no surgical drainage of the abscess at that time, and he was treated with two weeks of antibiotics with initial improvement in symptoms. The patient had a past medical history of 3 previous episodes of acute sigmoid diverticulitis that were each treated with bowel rest and 14 days of empiric antibiotics. After the second episode of diverticulitis, the patient had a colonoscopy with findings of colitis and 2 polyps were removed that were negative for malignancy. Following the third episode of diverticulitis, the patient had a sigmoid and partial descending colectomy about 2 years prior to the current presentation.

On admission, a CT scan of the abdomen and pelvis revealed a 3.5 x 1.9 cm air and fluid collection of the inferior border of the spleen and 5.2 x 1.6 cm fluid collection of lateral spleen. The collections were noted to be increased compared to the prior imaging 6 weeks before. Blood cultures were without growth at 5 days. A transthoracic echocardiogram showed no significant valvular abnormalities or vegetations. On hospital day 5, the patient was taken to the operating room for a laparoscopic splenectomy and left diaphragm repair. Surgical findings included a large spleen with omental adhesions and a thick rind along the spleen, which was closely adherent to the diaphragm. A portion of the colon closely adherent to the spleen was also noted. Histopathologic examination showed multifocal splenic abscesses with surrounding fibrosis on hematoxylin and eosin (H&E) stain and granules with surrounding Splendore-Hoeppli material on higher magnification (Figure 1). On Grocott-Gomori methenamine silver (GMS) stain, the granule was seen to be composed of mixed bacterial morphologies with a predominance of filamentous rods typical of Actinomyces (Figure 2). Based on histopathological examination, a diagnosis of splenic actinomycosis was rendered.

Figure 1. Granule with surrounding Splendore-Hoeppli material (H&E 400x magnification).
Figure 2. Granule with mixed bacterial morphologies (GMS 100x magnification).


Actinomycosis is a slowly progressive infection characterized by fibrotic mass-like lesions, abscesses, granules, progression across tissue planes, and the development of sinus tracts. The incidence of actinomycosis has declined in the U.S., which is thought to be due to better oral hygiene and the organism’s susceptibility to a wide range of antibiotics.4 The clinical manifestation of actinomycosis is classified by the anatomical site of infection. This includes oral-cervicofacial, thoracic, abdominopelvic, central nervous system, musculoskeletal, and disseminated forms of disease. Oral-cervicofacial disease is the most common form and classically develops with fevers and perimandibular soft tissue swelling that may have a firm or “woody” consistency on palpation.4 Abdominopelvic disease occurs in about 20% of cases with intra-abdominal manifestations usually due to appendicitis, inciting trauma, or previous surgical procedure and pelvic disease most often due to intra-uterine contraceptive devices.1 The clinical manifestations of actinomycosis are often difficult to correctly diagnose, and the presentation and imaging findings often mimic malignancy further complicating the assessment. Diagnosis relies on consideration of the disease process and diagnostic sampling for histopathology and microbiologic studies.

Although most actinomycotic lesions are polymicrobial, species of the genus Actinomyces are the predominant etiologic agents.2 Actinomyces are a group of gram positive filamentous facultatively anaerobic or microaerophilic bacteria that are normal flora of the gastrointestinal and genitourinary tracts. The organisms typically have true branching and may appear beaded due to irregular Gram staining. Importantly, Actinomyces spp. will be negative with modified acid-fast staining, which can be used to differentiate it from Nocardia spp. The bacteria are relatively slow growing on primary culture and mature colonies may have a variety of morphologies. The classic “molar tooth” appearance is characteristic of A. israelii.3 On histopathology, actinomycotic lesions have a surrounding area of fibrosis and central suppurative inflammation with granules. The granules consist of accumulations of organisms with club-shaped ends and filamentous rods seen on special staining.4 Optimal diagnosis would consist of visualization of these features on histopathology or other direct method. Isolation of the organism can be useful but should be taken in the context of the clinical picture as the mere isolation of Actinomyces in culture does not always imply actinomycosis.

Splenic involvement of actinomycosis is an uncommon cause of the intra-abdominal disease process. In our case, the most likely etiology for splenic actinomycosis was due to the recurrent episodes of acute sigmoid diverticulitis with breaches in the mucosal barrier and direct invasion into the spleen. The surgical management in this case was splenectomy to avoid splenic rupture. Medical management involves antibiotic therapy with high-dose penicillin as first-line therapy. The treatment duration has historically been to treat with parenteral penicillin for 2 to 6 weeks and then transition to oral penicillin or amoxicillin up to a year based on clinical response.


  1. Bennhoff D: Actinomycosis: diagnostic and therapeutic considerations and a review of 32 cases. Laryngoscope 1984; 94: pp. 1198-1217.
  2. Blaser MJ, Dolin R, Bennett JE. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. Ninth edition. Elsevier; 2020.
  3. Pfaller, M. A., Carroll, K. C., & Jorgensen, J. H. (2015). Manual of clinical microbiology (11th edition.). ASM Press.

-Zane Conrad, MD is a medical microbiology fellow at UT Southwestern Medical Center.

-Dominick Cavuoti, DO is a professor at UT Southwestern and practices Infectious disease pathology, medical microbiology and cytology.

-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.

-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.

Microbiology Case Study: A 28 Year Old with Unilateral Groin Pain

Case History

A 28 year old male reported to the ED with complaints of right groin pain, nausea, and vomiting for the past five days. The patient was not taking any active home medications and reported no chronic medical conditions at the time of presentation. He reported that he and his fiancée have a 5 month old kitten but denied any scratches or bites. Physical exam showed a tender right inguinal region covering a hard, non-reducible mass with no overlying erythema or fluctuance. Due to fever and tachycardia (temperature: 38.3 ˚C/ pulse: 136 beats/min), patient met criteria for sepsis without shock. CT of the abdominal pelvis showed enlarged right inguinal lymph nodes with suspected lymphadenitis and no inguinal hernia. Patient was started on ampicillin/sulbactam, ceftriaxone to cover possible STD, and azithromycin to cover possible cat-scratch disease. STI testing was negative for trichomonas, syphilis, chlamydia, and gonorrhea. Due to suspected azithromycin allergy, doxycycline was administered instead for empiric cat scratch disease treatment. Serology studies for Bartonella henselae in addition to right inguinal lymph node biopsy (Images 1 and 2). Lymph node biopsy revealed multiple cores displaying reactive lymphoid tissue with microabscesses surrounded by palisading histiocytes concerning for cat scratch disease lymphadenitis. Serology results showed elevated IgG and IgM titers for Bartonella henselae and PCR testing for Bartonella henselae performed on the lymphoid tissue confirmed the diagnosis. Patient was discharged on doxycycline and pain management medications.

Images 1 (left) and 2 (right). Lymph node biopsy showing necrotizing stellate   granulomas with neutrophilic infiltration and necrosis.


The majority of cat scratch disease infections are caused by Bartonella henselae, a facultative, intracellular gram negative bacillus.1,2 Bartonella henselae is usually acquired through a cat flea (Ctenocephalides felis) vector or transferred from a cat scratch or bite.1 Culture and polymerase chain reaction (PCR) have demonstrated Bartonella presence in cat saliva, gingiva, blood, claws, skin, and feces.3 Due to its fastidious nature, it is difficult to culture Bartonella henselae from samples taken from the human lymph node.4 In the past, Warthin-Starry or Steiner stains have been used to identify Bartonella henselae microscopically. 5,6,7 However, these silver stains are historically expensive, bulky, and difficult to interpret. Therefore, diagnosis typically relies on the combination of a variety of factors, including clinical, epidemiological, serological, and histological.4 PCR and serology or immunofluorescence have proven to be effective in detection of Bartonella henselae and are commonly used in the clinical setting for confirmation of diagnosis.4,8 Necrotizing stellate granulomas with neutrophil infiltration are the characteristic findings on histology (Images 1 and 2). Early histological findings are more likely to show histiocytes, follicular hyperplasia, and microabscesses bordering a thickened lymph node capsule.9

Cat scratch disease is most frequently characterized by self-limiting lymphadenopathy.1 The lymphadenopathy is usually close to the location of the cat scratch or bite and develops 1-2 weeks after exposure, although nearly a quarter of patients with cat scratch disease do not report close contact with cats.1 A papule or wheal may develop at the site of infection prior to lymphadenopathy.1 Cat scratch disease has not been documented to be transmitted between individuals.1 Fever, malaise, arthralgia and headache are other commonly reported symptoms.1 While most symptoms will resolve spontaneously, lymphadenopathy may last for weeks to months.1, Nonclassical presentations of cat scratch disease are reported in 10-15% of cases. Less common presentations that have been reported include, but are not limited to endocarditis, ophthalmic disease, central nervous system disease, hepatitis, splenitis, osteomyelitis, musculoskeletal arthropathy, and pulmonary disease. Immunocompromised patients infected with Bartonella henselae may present with widespread disease or with other diseases associated with Bartonella, including bacillary angiomatosis. While the majority of cases will resolve spontaneously, antimicrobial therapy including azithromycin can be used for treatment.1 In patients allergic to macrolides, doxycycline has proven to be effective. Pharmacologic pain management is also indicated when necessary.1


  1. Zangwill, K. M. (2021). Cat Scratch disease and Bartonellaceae: the known, the unknown and the curious. The Pediatric Infectious Disease Journal40(5S), S11-S15.
  2. Welch, D. F., Hensel, D. M., Pickett, D. A., San Joaquin, V. H., Robinson, A., & Slater, L. N. (1993). Bacteremia due to Rochalimaea henselae in a child: practical identification of isolates in the clinical laboratory. Journal of Clinical Microbiology31(9), 2381-2386.
  3. Lappin MR, Hawley J. Presence of Bartonella species and Rickettsia species DNA in the blood, oral cavity, skin and claw beds of cats in the United States. Vet Dermatol. 2009 Oct;20(5-6):509-14. doi: 10.1111/j.1365-3164.2009.00800.x. PMID: 20178489.
  4. Hansmann Y, DeMartino S, Piémont Y, Meyer N, Mariet P, Heller R, Christmann D, Jaulhac B. Diagnosis of cat scratch disease with detection of Bartonella henselae by PCR: a study of patients with lymph node enlargement. J Clin Microbiol. 2005 Aug;43(8):3800-6. doi: 10.1128/JCM.43.8.3800-3806.2005. PMID: 16081914; PMCID: PMC1233974.
  5. Cotter B, Maurer R, Hedinger C. Cat scratch disease: evidence for a bacterial etiology. A retrospective analysis using the Warthin-Starry stain. Virchows Arch A Pathol Anat Histopathol. 1986;410(2):103-6. doi: 10.1007/BF00713512. PMID: 2432720.

-Grant Whitebloom is a second-year medical student at the Medical College of Georgia. He is interested in Internal Medicine and its subspecialties.

-Hasan Samra, MD, is the Director of Clinical Microbiology at Augusta University and an Assistant Professor at the Medical College of Georgia.

Microbiology Case: Immunocompromised Patient with Altered Mental Status

Case Presentation

Patient is a 45 year old Vietnamese male who presented initially to the Emergency Room with altered mental status at home. Patient presented with hypotension and hypothermia and was admitted to the ICU. Past medical history is significant for HIV although the patient has not be on antiretroviral therapy (ART), syphilis, and active Pneumocystis infection. His CD4 count was 15 on arrival, and he was placed on multiple prophylactics for prevention of opportunistic infections. Blood and cerebrospinal fluid (CSF) were submitted for cultures. Encapsulated yeast were seen on the CSF which was positive for Cryptococcus neoformans on a rapid multiplex-PCR panel (BioFire Film Array Meningitis/Encephalitis panel) followed by isolation of the yeast in culture and identification using the MALDI-TOF. Yeast was also found in the blood cultures, also identified as Cryptococcus using a rapid blood culture identification panel (BioFire Film Array Blood Culture Identification Panel 2.0) which subsequently grew out C. neoformans, also identified using MALDI-TOF.


Cryptococcus species areencapsulated yeast cells with a natural habitat in the soil. Promotion of organism replication happens in alkaline pH environments with higher nitrogen concentrations. For example, soil contaminated with turkey, chicken, bat, or pigeon droppings can contribute to this growing environment. Yeast cells can become airborne with soil disruption, and contribute to increased risk of infection to immunocompromised hosts with certain activities. Aside from pulmonary infections, meningoencephalitis is another common manifestation of infection.1 Patients may have neurological deficits and increased intracranial pressure. A wide spectrum of symptoms have been reported including fever, malaise, headache, neck stiffness, photophobia, nausea, vomiting and sometimes rarely a cough, dyspnea, and skin rashes. Generally speaking, Cryptococcus neoformans is usually associated with infections in immunocompromised patients while Cryptococcus gatti is associated with infections in immunocompetent patients.2 Positive blood cultures with Cryptococcus is typically representative of disseminated infection.

The major virulence factor is the capsule which plays a role in preventing phagocytosis and providing an adherence mechanism to mucosal linings. Not all strains produce capsules, but the colony on growth medium could be mucoid (image 1). The capsules of Cryptococcus may group to one another, almost forming a ‘honeycomb’ matrix with the polysaccharide capsule separating the forms from each other. Additionally, Cryptococcus produce a melanin pigment, which is considered a virulence factor because it protects the yeast from oxidant-induced stressors. As such, the Fontana-Masson stain used in histopathology will be positive due to the melanin production of the organism. Cryptococcus neoformans is responsible for most human infections, and Cryptocococcal infections are considered to be opportunistic, with immunocompromised populations being at highest risk.3

Image 1. Visible capsule stained with Giemsa on the CSF specimen is highly indicative of Cryptococcus (top left). Budding yeast stained with Gram-stain observed in blood cultures (top right). Mucoid colony growth of Cryptococcus neoformans on Chocolate agar, Sheep Blood agar, and cream-white colonies on Sabouraud dextrose agar (bottom).

Microscopically, Cryptococcus is an irregularly sized (4-10µm), round, encapsulated yeast. It can also appear as a budding yeast.3 Direct staining of the CSF specimen can be done using India ink which will form a “halo” around the yeast cells as the ink stains the capsule. Cream-colored, sometimes mucoid, colonies will appear in agar plates in 3-7 days. Aside from PCR and MALDI-TOF, differentiation between Cryptococcal neoformans and Cryptococcal gatti can be possible using canavanine, glycine, bromothymol blue agar. Growth of Cryptococcus gatti will turn the agar blue. Detection of cryptococcal antigen through immunodiagnostic tests of the serum and the cerebrospinal fluid can also provide a diagnosis of the infection. CSF parameters of infected individuals typically show low white blood cell count, low glucose, and elevated protein but up to 30% of the cases have also reported normal CSF parameters.4 Histopathology staining using mucicarmine is specific for the presence of Cryptococcus. Radiograph imaging of the brain have also been shown to be helpful.

Rapid detection of Cryptococcal infections and other opportunistic infections are imperative to improving patient outcomes. Mortality from cryptococcal meningitis in the “meningitis belt” of Sub-Saharan Africa approaches 75%, with an 89% incidence rate.5 A combination of factors including higher HIV carriage rate, lack of available preventative care, and dry seasons with dry winds and cold nights lend to this region’s higher incidence rates. Moreover, lack of cheaper and reliable testing methods for detection and possible initiation of prophylactic medications are contributors of higher mortality rate. Recent studies investigate how the efficacy of rapid antigen assays like lateral flow assays might have a role in filling some of these care gaps in an efficient and cost-effective way, but further study is required.5 Mainstays of treatment for cryptococcal infections include amphotericin B, flucytosine, and fluconazole.2 Monitoring intracranial pressure and keeping it under check plays an important role in reducing the mortality associated with cryptococcal meningitis.6 Lumbar puncture is the recommended option for management of intracranial pressure and either a ventricular drain or ventricular peritoneal shunt is used in patients who require frequent lumbar punctures.


  1. Park BJ, Wannemuehler KA, Marston BJ, Govender N, Pappas PG, Chiller TM. Estimation of the current global burden of cryptococcal meningitis among persons living with HIV/AIDS. AIDS. 2009 Feb 20;23(4):525-30.
  2. Cox, Gary M, Perfect, John R. Cryptococcus neoformans meningoencephalitis in patients with HIV: Treatment and prevention. June 9, 2021, UptoDate. Accessed 10/7/2022
  3. Winn, Washington C. Jr. et al. Koneman’s Color Atlas and Textbook of Diagnostic Microbiology, 6th Edition. 2006. Lippincott Williams and Wilkins.
  4. Garlipp CR, Rossi CL, Bottini PV. Cerebrospinal fluid profiles in acquired immunodeficiency syndrome with and without neurocryptococcosis. Rev Inst Med Trop Sao Paulo. 1997 Nov-Dec;39(6):323-5.
  5. Okolie CE, Essien UC. Optimizing Laboratory Diagnostic Services for Infectious Meningitis in the Meningitis Belt of sub-Saharan Africa. ACS Infect Dis. 2019 Dec 13;5(12):1980-1986. doi: 10.1021/acsinfecdis.9b00340. Epub 2019 Nov 18. PMID: 31738509.
  6. Rolfes MA, Hullsiek KH, Rhein J, Nabeta HW, Taseera K, Schutz C, Musubire A, Rajasingham R, Williams DA, Thienemann F, Muzoora C, Meintjes G, Meya DB, Boulware DR. The effect of therapeutic lumbar punctures on acute mortality from cryptococcal meningitis. Clin Infect Dis. 2014 Dec 01;59(11):1607-14.

-Dr. Katelyn Swanson is a currently a PGY-1 pathology resident at George Washington University. She completed a clinical laboratory science program at Franciscan Health in Indianapolis, IN, and received her MLS (ASCP) certification before attending and graduating medical school from Lake Erie College of Osteopathic Medicine at Seton Hill. She completed a transitional year internship at Walter Reed National Military Medical Center and one General Medical Officer billet with the Navy before starting pathology residency. She is still exploring her research interests.

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

Forensic Pathology: Getting to the Heart of the Matter

When I was about to complete residency in anatomic and clinical pathology, I was speaking with a colleague and mentioned I was pursuing dual fellowships in forensic and cardiovascular pathology. He furrowed his brow and asked, “What are you going to do with that?”

I was slightly surprised by this response, but he’s not the only person who would react that way. Many people (even pathologists) think of forensic pathology as gunshot wounds and motor vehicle accidents. While those deaths do come to our office, the majority of autopsies performed in the forensic setting are still due to natural causes, with heart disease making up a significant proportion. My interest in cardiovascular pathology was piqued when, as a medical student, I observed an autopsy on a healthy adolescent athlete who collapsed during a cross country race. The pathologist identified a congenital anomaly in his coronary arteries, in which the left coronary artery arose from the opposite cusp and traveled between the aortic and pulmonary arteries. This meant the coronary artery was susceptible to compression by the two surrounding, larger arteries, leading to ischemia and potential lethal arrhythmia whenever his heart rate became elevated. In another case, a relatively healthy young man had suddenly collapsed shortly after taking his first dose of prescribed azithromycin for a sinus infection. While the autopsy was macroscopically unremarkable, postmortem genetic testing revealed a likely pathogenic variant in a gene associated with long QT syndrome. In the context of the azithromycin (a drug known to prolong the QT interval), a lethal arrhythmia was triggered. His family was unaware of this heritable channelopathy, and they were urged to see a cardiologist themselves for a risk assessment.

These experiences made me see how our ability to detect and identify subtle cardiac disease at autopsy could have profound impacts on the emotional and physical well-being of families. It’s not news that pathology is facing a shortage of recruits, and both forensics and cardiovascular pathology are particularly feeling the squeeze. Unsurprisingly, these are both fields to which residents have very little exposure. Many residents don’t rotate through forensics until their 3rd year (after they’ve already chosen a specialty) and few academic centers have a specialized cardiovascular pathology service. The required number of autopsies to complete residency has now been decreased from 50 to 30, meaning residents see even less cardiovascular pathology during training. I can anecdotally add that myself and several other forensic pathologists I’ve met were occasionally discouraged from entering the field by academic mentors, who considered it a waste of potential. As a profession, we need to recognize the public health impact and academic worth of forensic autopsies and encourage residents’ exposure to the field. Not only is a well-trained forensic pathologist needed to accurately interpret injuries at autopsy, they are the front line in recognizing natural diseases that went undiagnosed prior to death. Additional cardiovascular training helps us to recognize potentially heritable cardiovascular disease; this not only helps families understand why and how their loved one died, but it also affords them the opportunity to obtain screening and interventional measures. It isn’t just natural deaths, either; people who died from any cause could have early signs of heritable disease, and overlooking them could mean disastrous consequences for the family. I would strongly encourage any pathology trainee with an interest in public and preventative health, molecular pathology, and non-neoplastic disease to consider combined training in forensics and cardiovascular pathology. The National Association of Medical Examiners offers free membership to trainees, and the Society for Cardiovascular Pathology offers a one-on-one mentorship program to introduce new members to the field – you will be a welcome addition to either or both groups! If you have specific questions you’d like to ask, I’m available at

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

Hematology Case Study: 75 Year Old Man with Leukopenia

A 75 year old male first presented earlier this year with abnormal CBC results. The patient has a history of Type 2 diabetes, high blood pressure and atrial fibrillation. He was diagnosed with non-small-cell lung cancer (NSCLC) 6 years ago. His stage II NSCLC was completely removed with surgery. Surgery was followed up with adjuvant cisplatin-based chemotherapy to reduce the chance that the cancer would return. In June, he was referred to the hematology oncology department following consecutive CBCs that revealed leukopenia and thrombocytopenia. The CBC results from these specimens are shown below in Table 1.

Table 1. CBC results from a 75 year old male.

The peripheral blood sample from June was sent for flow cytometry. A leukemia/lymphoma phenotype was performed. Result comments noted proportionately decreased granulocytes with a left shift and 4% blasts. The blasts were CD34+, CD117+, HLA-DR+, CD13+ and CD33+ and were identified as myeloblasts. There were proportionately increased atypical monocytes with CD23 expression. Lymphocytes were also proportionately increased and included an increased population of CD57+, CD3+ T cells consistent with T-cell large granular (LGL) expansion. Immunophenotypic findings raised a concern for a myelodysplastic process. The hematologist discussed the findings with the patient and the patient was scheduled for a bone marrow biopsy. The procedure was performed 3 weeks later. CBC results on the day of the procedure are shown below in Table 2.

Table 2. CBC results day of bone marrow procedure. Pre-op diagnosis: Anemia, Leukopenia.

Bone marrow aspirate showed markedly increased myeloblasts (55%), consistent with acute myeloid leukemia (AML), nonacute promyelocytic leukemia (APL) type. The phenotype of the blasts was CD13+, CD33+, CD117+ and HLA-DR+. Blasts were negative for CD34. Several genomic variations were found in the specimen. These included variations in IDH2, SRSF2, STAG2 and ASXL1. Diagnosis: Increase in myeloblasts consistent with AML, nonAPL type.

In July, 20 days after the bone marrow procedure and AML diagnosis, the patient was scheduled to begin his first cycle of Azacitidine (Vidaza). Based on his critical hemoglobin, the patient received 1 unit of packed RBCs followed by his first Vidaza injections. This Cycle 1, Day 1 chemotherapy was well tolerated, and he returned home. The following day he returned for his second treatment. His CBC showed good response to the previous day’s transfusion and his Cycle 1, Day 2 Vidaza was administered without incident. However, that evening the patient presented to the ER with nausea, vomiting and nose bleeds. The patient was admitted to the hospital and received another RBC transfusion. For the next several days the patient continued to do poorly, requiring additional RBC transfusions, and the Vidaza treatments were deferred, then discontinued. The patient had several ER visits and hospital admissions with transfusions over the next 2 weeks. During this time, we saw his blast% on his differential peak at over 60%. The patient was transferred to the palliative care team with care and comfort measures. CBC results from Cycle 1, Day 1 and subsequent CBC results are shown below. Note the sharp increase in blasts over a 2-week period.

Table 3. CBC results after chemotherapy initiated, then discontinued
Image 1. Cells classified as blasts on CellaVision

AML is the most common acute leukemia in adults. In AML with minimal differentiation, evidence of bone marrow failure is characterized by anemia, neutropenia, and thrombocytopenia. The median age for patients with AML in the US is 66-67, and those who are older than 55-65 at diagnosis often have challenges and lower odds for long term survival. These older patients tend to have poor tolerance to traditional aggressive chemotherapy because of other health issues. This patient was likely not a good candidate for strong chemotherapy because of his age and health history. In these more fragile patients, Vidaza may be used. Vidaza is a class of drug called a hypomethylating agent that works by switching off DNA methyltransferase. This switches on genes that stop the cancer cells growing and dividing. The goal is to reduce the number of abnormal blood cells and to control cell growth.

As you can see from the CBC results, the onset of this patient’s AML was very abrupt, and the disease progressed rapidly. He has several risk factors that made him more likely to be diagnosed with AML. Older age is a risk factor for AML, and AML is more common in males than females. He has a history of smoking which is a behavioral risk factor associated with AML. Additionally, patients with cancer who are treated with certain chemotherapy drugs are more likely to develop AML in the years following treatment. This patient was treated with cisplatin following lung cancer surgery. Cisplatin is an alkylating agent which has been linked to an increased risk of AML.

Also interesting is the note on the peripheral blood phenotype interpretation that a T-cell large granular lymphocyte (LGL) expansion was present. These are an increased population of CD57+, CD3+ T cells. LGL clones have been described in AML and a hallmark of this association is cytopenia, as is observed in this patient. The patient’s poor prognosis can partly be attributed to the p.Gly646TrfsTer12 alteration in the ASXL1 gene, identified in the bone marrow interpretation. This alteration is associated with decreased overall survival and poor prognosis which was observed in this patient.

I work in a hospital with a large hematology/oncology practice, and we see a lot of adult leukemia patients. Many of the patients we see regularly have Chronic Lymphocytic Leukemia (CLL). We feel like we get to know these patients, because even though we never see them, we see their CBCs every week, sometimes for many years. This was an interesting case because it reminded me of the sudden onset and rapid progression of AML. It was amazing to see the differentials change so dramatically in a matter of weeks. This patient is currently receiving care and comfort end of life measures.


Fattizzo, B, Bellani, V, et al. Large Granular Lymphocyte Expansion in Myeloid Diseases and Bone Marrow Failure Syndromes: Whoever Seeks Finds. Front. Oncol., Sec. Cancer Immunity and Immunotherapy. 01 October 2021.

Pratcorona M, Abbas S, Sanders MA, Koenders JE, et al.Acquired mutations in ASXL1 in acute myeloid leukemia: prevalence and prognostic value. Haematologica. 2012 Mar;97(3):388-92. doi: 10.3324/haematol.2011.051532. Epub 2011 Nov 4. PMID: 22058207; PMCID: PMC3291593.

Thomas XG, Dmoszynska A, Wierzbowska, et al. Results from a randomized phase III trial of decitabine versus supportive care or low-dose cytarabine for the treatment of older patients with newly diagnosed AML. Journal of Clinical Oncology 29:2011

Turgeon, Mary Louis. Clinical Hematology Theory and Procedures, 6th ed, Jones and Bartlett Learning, 2017.


-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.

Tumor on the Brain

Back in my Master’s program at Jefferson, I fondly remember the week we covered central nervous system (CNS) tumors. I was fascinated by the mnemonic tools we would use to identify different CNS tumors, such as “fried eggs” for oligodendrogliomas, perivascular pseudorosettes in ependymomas, and the whorling associated with meningiomas. Fortunately, for our patients, and unfortunately, for our diagnostic curiosity, we rarely see CNS tumors at my institution. Brain lesions resulting from metastatic carcinomas are typically well-identified via imaging and treated appropriately by the surgical, medical, and radiation oncology teams, but cytologists are available to screen cerebrospinal fluids (CSFs) for CNS involvement. For primary CNS tumors, however, we’re left recollecting the core memory of the second semester of our didactic phase. When a metastatic CNS tumor made its way into our lab, our cytology team swooned with excitement. (Yes, I know, but please introduce me to a lab professional who doesn’t embrace their quirks.) A 27-year-old male patient presented to radiation oncology three years after surgical debulking of a brain tumor at an outside institution. The patient, who was referred to radiation oncology at to treat the residual tumor at the original institution, did not follow up and developed an 8 centimeter recurrence a year after the initial resection. At this point, the patient experienced complete vision loss and underwent a biparietal-occipital craniectomy. A repeat brain MRI was performed a year later, and once again, a large enhancing extra-axial mass was identified along with multiple smaller masses also increasing in size. The patient received radiation after worsening difficulty with ambulation. After almost completing the planned fractions of radiation, the patient elected to stop their radiation therapy due to worsening seizures. A left neck mass was identified six months prior, and while the mass had not grown or caused pain, the patient was referred to head and neck surgical oncology for evaluation. Surveillance imaging demonstrated an enlarged left level 5A lymph node, suggestive of metastatic disease. Multiple ultrasound-guided fine needle aspiration biopsies were obtained from the lymph node, and ROSE was performed. The Diff-Quik-stained and concurrent Pap-stained smears demonstrated lesional tissue, although everything from epithelioid histiocytes to spindle cell melanoma to a renal primary were considered as a differential. Based on the location, a salivary gland primary was also a possibility for this case. The streaked cytoplasm and pseudoinclusions in both smears were concerning for a metastasis of the patient’s primary CNS tumor, but we were still hesitating to make the call.

Images 1-4. Lymph Node, Neck, Left, Level 5A, US-guided FNA. 1-2: Diff-Quik-stained smears, 3-4: Pap-stained smears.

The following morning, the H&E-stained FFPE cell block sections demonstrated the characteristic whorls expected for the patient’s primary, although the idea of metastasis was uncanny.

Images 5-6. Lymph Node, Neck, Left, Level 5A, US-guided FNA. H&E sections (6: 100x, 7: 400x).

We then used immunohistochemical studies to confirm our morphologic diagnosis. Immunostains performed on the cell block slides with adequate controls show that the tumor cells are positive for vimentin and PR (focal), while negative for AE1/AE3, EMA, CK7, CK20, TTF-1, Napsin A, p40, Pax8, synaptophysin, and S-100. The Ki-67 proliferation index fell at 18%, which is consistent with intermediate aggressive disease in a WHO Grade 2 atypical meningioma.

Images 7-8. Lymph Node, Neck, Left, Level 5A, US-guided FNA. Cell block section immunohistochemistry. 7: Vimentin-positive; 8: focally PR-positive.

The patient had next gen sequencing performed on his tissue, which demonstrated an NF-2 mutation, indicating he may benefit from MTOR inhibitors, but he elected not to pursue systemic therapy.

Where meningiomas account for 36% of primary brain tumors, atypical meningiomas comprise only 5-15% of all meningiomas (Cai et al., 202. Extracranial metastasis of atypical meningioma is a rare event, with only a few cases documented in the literature. While meningioma metastases are uncommon, a thorough collaboration between clinical impression and pathologic interpretation is necessary to ensure the possibility is not entirely excluded.


Cai C., Kresak J.L., Yachnis A.T. (2021) Atypical meningioma. Pathology Outlines. Retrieved October 11th, 2022, from

P.S. I’d like to take this opportunity for a shameless plug. My Doctor of Health Science (DHSc) research survey is live now through November 23rd, 2022. If you’re a medical laboratory professional or pathologist, please consider contributing to our field of laboratory medicine! Click the following link to read the consent form and take the one-time anonymous survey. Thank you for your time!

-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: What’s with the Rash?

Case presentation

A 79 year old female with a past medical history of COPD, hypertension, diabetes, and eczema presented to the emergency department with a localized rash on the right knee (Figure 1). The rash began after gardening and persisted for three weeks.

The patient reported some itching, warmth, and tenderness but denied nausea, vomiting, fever, and diarrhea. Her vital signs were BP 175/76| Pulse 91 | Temp 98.5 °F (36.9 °C) (Oral) | Resp 20 | SpO2 96%. The remainder of her physical exam was notable: right knee skin rash. There was no induration or fluctuance or drainage. She exhibited a full range of knee motion; there was no palpable knee joint effusion (Figure 1).

Lab CBC results were unremarkable. X-Ray knee AP and lateral – right showed soft tissue prominence anterior to the patella, which suggests prepatellar edema and a fluid collection. Lyme antibody screening was negative. Two sets of blood culture bottles were sent to the microbiology laboratory. After 24 hours of incubation, aerobic bottles were positive with the organism shown in: Gram stain (Figure 2), culture growth showing alpha-hemolytic colonies (Figure 3), H2S production on the TSA agar slant (Figure 4). 

Identification by Matrix-assisted laser desorption ionization Time of flight (MALDI-ToF) revealed Erysipelothrix rusiopathiae at a score above 2.0. 


Erysipelothrix is a non-spore-forming, catalase-negative, facultative gram positive bacillus. It is not acid-fast or motile. It is distributed worldwide and is primarily considered an animal pathogen responsible for causing erysipelas that may affect a wide range of animals. Erysipelothrix is ubiquitous in soil, food scraps, and water contaminated by infected animals.1 It can survive in the soil for several weeks. In pig feces, the survival period of this bacterium ranges from 1 to 5 months.

Erysipelothrix can also cause zoonotic infections in humans, called erysipeloid. Most human infections are acquired through occupational exposure, such as fish handlers, veterinarians, and butchers, via direct injection of the organism through abrasion or injuries. Notably, the human disease of “erysipelas” is not caused by Erysipelothrix but by Streptococcus. 

Erysipeloid typically develops at the site of infection between 2 and 7 days after exposure. E. rusiopathiae infection can be categorized as 1) localized cutaneous erythematous 2) generalized cutaneous form due to traumatic injury and skin penetration of the organism, and 3) septicemic form.2 Skin infection can sometimes progress to bacteremia, most commonly associated with endocarditis3. The implication of endocarditis in the setting of E. rusipathiae infection is associated with increased mortality rate.2,3 

E. rusiopathiae can easily be grown on routine media, including blood and chocolate agar plates, in a clinical microbiology laboratory.1 The colonies appear as small alpha-hemolytic and can resemble alpha Streptococcus species. It can also be confused with Corynebacterium species due to the similarity in Gram stain characteristics. E. rusipathiae produces H2S on the triple iron sugar media (Figure 4), which is one of the distinguishing morphologies from other Gram-positive rods, such as Listeria or Bacillus species.1 It can be identified by Matrix-assisted laser desorption ionization Time of Flight (MALDI-ToF) directly from the positive blood culture broth (using Sepsityper Kit with Bruker MALDI-Biotyper (MBT)) or from isolated colonies. 

E. rusiopathiae is generally sensitive to penicillin. It is intrinsically resistant to vancomycin and aminoglycosides.4 CLSI (Clinical Laboratory of Standard Institution) M45 ED3 recommended ampicillin or penicillin for primary testing agents.4 While antimicrobial susceptibility testing is not warranted for every case of E. rusiopathiae, it is imperative that the organism be identified due to the critical nature of infection resulting in endocarditis. Since vancomycin is typically used for broad-spectrum coverage of gram positive organisms,4 early identification of this organism and notification of clinicians is helpful for appropriate antimicrobial management.


  1. Jorgensen, Chapter 27. Manual of Clinical Microbiology. 11th Edition.

2. Principe L, Bracco S, Mauri C, Tonolo S, Pini B, Luzzaro F. Erysipelothrix Rhusiopathiae Bacteremia without Endocarditis: Rapid Identification from Positive Blood Culture by MALDI-TOF Mass Spectrometry. A Case Report and Literature Review. Infect Dis Rep. 2016 Mar 21;8(1):6368. doi: 10.4081/idr.2016.6368. PMID: 27103974; PMCID: PMC4815943.

3. Wang T, Khan D, Mobarakai N. Erysipelothrix rhusiopathiae endocarditis. IDCases. 2020 Sep 9;22:e00958. doi: 10.1016/j.idcr.2020.e00958. PMID: 32995274; PMCID: PMC7508995.

4. CLSI. Methods for Antimicrobial Dilution and Disk Susceptibility Testing of Infrequently Isolated or Fastidious Bacteria. 3rd ed. CLSI guideline M45. Wayne, PA: Clinical and Laboratory Standards Institute; 2016.

-Azal Al-Ani, MD is a third-year AP/CP pathology resident at Montefiore Medical Center, Bronx, NY. She completed her medical school at Al-Anbar Medical College, Iraq. Her interest includes hematopathology and dermatopathology

-Phyu M. Thwe, PhD, D(ABMM), MLS(ASCP)CM is Associate Director of Infectious disease testing laboratory at Montefiore Medical Center, Bronx, NY. She completed her CPEP microbiology fellowship at the University of Texas Medical Branch in Galveston, TX. Her interest includes appropriate test utilization and extra-pulmonary tuberculosis.

Into the Badlands of Safety

During a recent trip to South Dakota, I was able to visit Badlands National Park. I am not a hiker or a camper, so I was not sure I would enjoy the park very much, but it turned out to be the highlight of our vacation. The vastness of the landscape and the unusual beauty of the rock formations cannot be captured in pictures. It is truly something that should be see in person at least once in a lifetime. While walking the trails of the park, it looked and felt like walking in an alien world. It looks strange, and there are hidden dangers- rattlesnakes, potential high heat, and crumbly walkways with sudden drop-offs.

The experience reminded me of how the laboratory must seem to visitors or workers who need to come into the department to perform various duties. The laboratory must seem like a foreign world, and indeed, there are many hidden dangers within. If I had walked blindly into Badlands National Park and not read the warning signs, would I have been bitten by a snake or could I have walked off a cliff? Of course. Do the signs in your lab adequately warn visitors of the dangers? Do visitors pay attention?

The lab staff reported a plugged floor drain under the hematology analyzer, so the facilities plumber arrived to repair it. He asked the staff if the analyzer was running, and because they were not processing any samples, they said it was not. When the plumber bent down to look at the drain, the analyzer cycled waste through the drain line which quickly splashed into the eyes and mouth of the plumber.

Warning signs are required in many labs for many reasons, but they are not sufficient for protection from the hazards in the department. Those who enter the “badlands” of the lab need to be told about the dangers, and they need as much information as possible. If someone is coming in to work on equipment, offer proper personal protective equipment. If someone will be on the floor of a biohazard lab, make sure a lab coat and gloves are in use, and lay a pad on the floor if possible. Make sure people understand proper terminology. An analyzer may not be actively running samples, but it is still “on,” and there are still potential hazards present.

It should not be assumed that people who come to work in the lab department will have general knowledge of the laboratory or of lab safety practices. It is a good practice to use a safety training checklist for vendors or others who enter the department and to go over that checklist at least annually. Couriers can be harmed by pathogens, chemicals, or dry ice. Phlebotomists who are expected to process samples should be trained in centrifuge operations, spill clean up and more. Environmental service workers and biomedical engineering staff need to understand the chemical and biohazards in the department.

Instrument service representatives have training, but not typically much of that training is focused on lab safety. Some representatives keep a reusable lab coat with them, and wear it from lab to lab, washing it at home when visibly dirty. There are some OSHA violations in those behaviors. PPE that is used on a lab cannot be removed from that lab (except for professional laundering). Lab coats used in a laboratory cannot be laundered at home. These are unsafe (and illegal) practices, but until someone notifies the representatives about them, the behaviors will continue.

When someone works in the lab “badlands” every day, it is easy to become complacent about the hazards within, or they may be well-trained and no longer consciously think about the tools they use to mitigate those hazards. That is not true for someone who may enter, someone who does not have the same background, experience, and training. Laboratorians are responsible for their safety as well, and educating those visitors about the potential dangers can keep them safe so they can go into more familiar climates with their health fully intact. 

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: A 67 Year Old with Foot Pain

Case description

A 67 year old male presented at the clinic with a primary complaint of foot pain; she has a previous medical history of M. tuberculosis infection of her prosthetic joint, osteoarthritis, and leukopenia. The patient described joint pains during the check-up and mentioned that she also started to have periumbilical pain two weeks ago, along with worm-like objects in her stool. The patient was in Ethiopia for 8 months in the past year and was very active. He has had some weight loss but no change in appetite; he denies any diarrhea, skin rashes, fever, or chills. The patient consumed undercooked meat products during the time she visited Ethiopia. No abnormal neurological symptoms presented at the time of the visit.

Orders were placed for H. Pylori antigen, fecal bacteria pathogen PCR, Giardia and Cryptosporidium antigen, and Ova & Parasite exam for the patient’s GI symptoms. The Ova & Parasite exam detected the objects in Image 1.

Image 1. Patient stool sample wet mount preparation.


The Ova & Parasite exam was reported as Taenia species. The eggs had a diameter of around 37um. An infectious disease consult was ordered and a single dose of 600mg praziquantel was prescribed for the treatment. Repeat Ova & Parasite exams are ordered for 3 days post-treatment looking for dying parasites and 1 month post-treatment to confirm the cure (no eggs).

Taenia in the Taeniidae family of tapeworms (BioLib, n.d.). Three species are commonly found and most clinically important in human infection: Taenia saginata, Taenia solium, and Taenia asiatica; most Taeniasis is asymptomatic or has mild symptoms (Centers for, 2020b).

Taenia solium, or pork tapeworm often found in pork, is the most dangerous species to humans for two reasons. First, this is the only species that can cause the neurologic symptoms by cysticercosis in brain tissue; second, this species can take humans as intermediate hosts, which means it can cause human to human transmission within the household (Schmidt et al., 2009).

Taenia asiatica also lives in pigs, primarily in the liver instead of muscle. This species has a very similar genetic, morphology, and immunology to T. saginata. It is frequently found in Asia (Schmidt et al., 2009).

Taenia saginata, or beef tapeworm, is what our patient was assumed to have in this case. The life cycle is shown below in Figure 2. The patient presented because his ankle pain started to impact his walking significantly; however, he was not seeking help for his worm-like objects in the clinic, probably due to the mildness of the symptoms. The parasite infection was brought into sight because of his travel history and stool observation. Per CDC, Eastern Europe, Russia, eastern Africa, and Latin America are the highest risk areas (Centers for, 2020a). The patient stayed for 8 months in Ethiopia in eastern Africa. Ethiopia has a relatively poor sanitation status and a high prevalence of taeniasis (Jorga, 2020). The major contributors for our infectious disease clinicians to assume this patient has T. saginata infection but not T. solium infection are: there are no neurological symptoms, and there is no pork exposure due to his religion. Visualization of the tapeworm eggs or segments is important for identification the species. In this case, many eggs were found on the wet mount slide from the patient’s stool sample.

Treatment of taeniasis is with Praziquantel. Praziquantel removes the tapeworms from the human body by detaching the worm suckers from vessel walls. The medication is safe to give to ≥1year old patients (UpToDate, 2022).

Image 2. Taeniasis life cycle. Alive Taenia eggs or gravid proglottids in the environment get ingested by farm or wild animals. Oncospheres develop in the GI tract, then hatch to the intestine wall and penetrate the wall to migrate to muscle tissue. In the muscle tissue, oncospheres develop into cysticerci (cysticercosis happens at this step). After the meat products (generally animal muscle) get ingested by humans, the cysticerci grow into adult worms in humans. Some segments/worms/eggs will be released into the environment through feces to complete the life cycle (which allows detection and diagnosis of human infections).


BioLib: Biological library. Taenia | (n.d.). Retrieved from

Centers for Disease Control and Prevention. (2020a, September 18). CDC – taeniasis – general information . Epidemiology & Risk Factors. Retrieved from

Centers for Disease Control and Prevention. (2020b, September 18). CDC – taeniasis – general information . frequently asked questions. Retrieved from

Jorga, E., Van Damme, I., Mideksa, B. et al. Identification of risk areas and practices for Taenia saginata taeniosis/cysticercosis in Ethiopia: a systematic review and meta-analysis. Parasites Vectors 13, 375 (2020).

Schmidt, G. D., & Roberts, L. S. (2009). Chapter 21 Tapeworms. In Foundations of Parasitology, eighth edition (pp. 346–351). essay, McGraw-Hill Higher Education.

UpToDate. (2022). Praziquantel: Drug information. UpToDate. Retrieved from

-Sherry Xu is a Masters student in the department of Pathology and Laboratory Medicine at the University of Vermont Medical Center.

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