Microbiology Case Study: A 58 Year Old Female with Shortness of Breath, Fever, and Chills

Case History

A 58 year old female presented to the emergency department with a chief complaint of shortness of breath, fevers and chills since the previous day. Her past medical history is significant for chronic obstructive pulmonary disease, hypertension, and borderline personality disorder. Vitals signs were significant for an oxygen saturation of 88%. Physical examination of the patient was difficult as the patient became increasingly agitated, however, the patient appeared in no acute distress with moist mucous membranes, anterior lung fields were clear to auscultation, there were no cardiac murmurs, and examination of their skin revealed no rashes or lesions.

Laboratory Findings

Laboratory tests were significant for a lactate level of 2.5 with a white blood cell count and complete metabolic panel within normal limits. Chest x-ray did not show evidence of consolidation or interstitial infiltrates. Urinalysis was within normal limits. One set of blood cultures was also drawn during this initial encounter. The patient became increasingly agitated after initial examination and was discharged with some laboratory tests pending. After incubating for 20 hours, the aerobic blood culture bottle flagged positive for bacterial growth, with gram stain demonstrating a gram negative coccobacillus and a rapid Verigene identification of Acinetobacter. The patient came back to the emergency department the next day with stable vital signs and unremarkable complete blood count and chest x-ray. The patient was started on meropenem which was switched to ciprofloxacin two days later, after bacterial antibiotic susceptibility results showed susceptibility to carbapenems, amikacin, amp/sulbactam, ceftazidime, ciprofloxacin, gentamin and tobramycin.

Image 1. Gram negative coccobacilli characteristic of Acinetobacter on Gram stain.
Image 2. Acinetobacter morphology on MacConkey agar.

Discussion

Acinetobacter is a genus of gram negative bacteria, with some genospecies identified as human pathogens including species in the A. calcoaceticus-A. baumannii complex (ACB) which are difficult to differentiate by phenotypic characteristics. Species in the ACB include genospecies 1 (A. calcoaceticus), genospecies 2 (A. baumannii), genospecies 3, and genospecies 13TU.

In the laboratory, Acinetobacter appear as non-pigmented mucoid, domed colonies with a smooth surface on growth media. Acinetobacter are non-motile, aerobic, catalase positive, oxidase negative, indole negative bacteria. Acinetobacter are also non-glucose fermenters and do not utilize lactose.

Out of the ACB genospecies, A. baumannii is considered the most significant pathogen, causing 80% of nosocomial infection. A. baumannii is an environmental bacteria which inhabits soil and water. In hospital settings, A. baumannii can survive on environmental surfaces for extended periods of time and is resistant to desiccation and cleaning solutions. The most common settings in which A. baumannii infections occur are within intensive care units where there are immunocompromised patients utilizing medical devices such as ventilators or catheters which are surfaces A. baumannii frequently colonizes. Not surprisingly, sites where these medical devices preside are the most common sites of infection for A. baumannii including the respiratory tract (hospital acquired pneumonia), bloodstream infections, and wound infections. Interestingly, A. baumannii wound infection have also been seen at a high prevalence in wartime and disaster victims. A. baumannii has been recovered in 63% of wounds from soldiers in Iraq and Afghanistan and 20% of wounds from victims after a tsunami in 2004.

 Importantly, A. baumannii can be resistant to several classes of antibiotics including fluroquinolones (DNA topoisomerase mutations), aminoglycosides (transposons), beta lactams (AMP C beta lactamase), and carbapenems (OXA carbapenemase), making infections with multidrug resistant organisms challenging to treat. In this case, the microbe had an OXA carbapenemase but was susceptible to carbapenems. In addition, this patient’s relatively benign presentation and normal laboratory results raise the question of whether this bacteria was causing a bloodstream infection or was simply a skin colonizer which grew after being inoculated into the blood culture media. Acinetobacter, in addition to colonizing hospital equipment and surfaces is a common colonizer of the skin as well as respiratory tract of patients on respiratory ventilators. Thus, Acinetobacter can be inadvertently cultured in blood and sputum samples, making correlation of the patient’s clinical symptoms and signs with culture results very important.   

-Liam Donnelly, MD is a 1st year anatomic and clinical pathology resident 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.

Microbiology Case Study: A Male in his Early 20s with Generalized Body Aches

Clinical History

An African American male in his early 20s presented to the emergency department (ED) with complaints of a sore throat, headache, generalized body aches, and fatigue for the past week. He also noted intermittent fever and chills as well as some nausea with a decrease in his appetite. He had been seen multiple times in the ED recently for similar symptoms. His past medical history was non-contributory and he noted no significant travel or exposure history with the exception of attending a local party 10 days ago. His temperature was 100.5°F and vitals were otherwise normal. His physical exam was normal with the exception of dry mucous membranes indicating mild dehydration. Initial laboratory testing showed a leukopenia (white blood cell count of 1.5 TH/cm2) with 39% lymphocytes and rapid antigen testing for group A Streptococcus, influenza, and infectious mononucleosis were negative. The patient was admitted for further work up due to the prolonged nature of his symptoms.   

Laboratory Identification

Results from additional infectious disease testing are in the table below.

This pattern of results is most consistent an acute HIV infection.

Discussion

Human immunodeficiency virus (HIV) is an enveloped, single stranded RNA virus which belongs to the family Retroviridae. HIV is most commonly sexually transmitted via body fluids such as blood, semen, and vaginal secretions directly contacting mucosa membranes. HIV can also be transmitted due to needle stick injuries, blood transfusions, and transplacentally from infected mother to fetus or by breast feeding. Acute HIV illness presents as a mononucleosis-like syndrome with fever, pharyngitis, arthralgias, malaise, and weight loss. During this acute illness, the HIV RNA viral load is extremely high. After a period of clinical latency, which on average is approximately 10 years, there is a deterioration of the immune system, the CD4 count drops, and the patient is at risk for opportunistic infections and neoplastic diseases.

Based on the 2014 CDC/APHL guidelines, the initial screening test for HIV is an antigen-antibody combination assay. These immunoassay based tests detect the p24 antigen and antibodies to HIV-1 and HIV-2 (see image below). By testing for the p24 antigen in addition to HIV antibodies the time to a positive patient result is decreased (window period) as p24 is one of the first viral proteins to appear, even before antibodies are present.    

If the antigen-antibody test is repeatedly positive, the second step in the testing algorithm is an antibody differentiation assay. This test has taken the place of the Western blot and Western blot is no longer recommended in the diagnosis of HIV. If the antibody differentiation test is positive, the diagnosis of HIV-1 or HIV-2 is confirmed. As this step only detects the presence of antibodies, the differentiation test will be negative in an acute HIV infection.

If there is a discrepancy between the first two steps in the testing algorithm or an indeterminate result is obtained, the final step involves nucleic acid amplification testing (NAAT) to detect viral RNA. Viral RNA is the first HIV-1 specific marker to appear following infection. In the case of an acute or untreated long term infection, the viral load can approach levels up to 100 million copies.  

When additional history was obtained from our patient, he said he was sexually active with a new male partner in the past few weeks and did not use protection. He stated he had been treated with Chlamydia in the past. Further testing for CD4 count, other opportunist & sexually transmitted infections, and HIV genotype testing was performed and outpatient HIV care was arranged for the patient. 

-Lisa Stempak, MD, is an Assistant Professor of Pathology at the University of Mississippi Medical Center in Jackson, MS. She is certified by the American Board of Pathology in Anatomic and Clinical Pathology as well as Medical Microbiology. She is the Director of Clinical Pathology as well as the Microbiology and Serology Laboratories. Her interests include infectious disease histology, process and quality improvement, and resident education.

Surgical Pathology Case Study: A 64 Year Old Man with History of Loose Stools and Abdominal Pain

Case History

A 64 year old male presented with a one year history of loose stools, lower abdominal crampy/gassy pain that improved with defection, and an unclear history of melena. A colonoscopy revealed a circumferential, villous, carpet-like lesion extending from 15 cm to the anal verge, with biopsies demonstrating fragments of a villous adenoma. A follow-up CT scan was negative for metastatic disease. The decision was then made to proceed with a low anterior resection with hand-sewn colo-anal anastomosis and diverting loop ileostomy.

Diagnosis

Upon opening the rectum, a 13.8 cm long circumferential, carpet-like lesion is identified, extending to the distal margin (Image 1). Sectioning demonstrated a lesion with a maximum thickness of 1.0 cm, which grossly appears to be confined to the mucosa. Due to the prior biopsy history of a villous adenoma, the entire lesion was completely submitted. This required 116 blocks to be submitted, which were then mapped out to show where each block would have been taken from (Image 2). Although there were many foci of intramucosal carcinoma present, clear cut submucosal invasion was not identified, and the specimen was signed out as a villous adenoma (Image 3).

Image 1. Opened rectum demonstrating the 13.8 cm-long carpet-like lesion.
Image 2. Mapping the lesion to show from where each block is taken.
Image 3. Photomicrograph showing the transition from normal mucosa (black arrow) to villous adenomatous tissue (red arrow).

Discussion

Polyps are an abnormal tissue growth that is a common occurrence within the colon, although they can also be found throughout the small intestine, stomach and esophagus. Polyps can be further classified as being neoplastic or non-neoplastic based on the histological pattern of the cells. The most common types of neoplastic polyps found within the GI tract are colonic adenomas, which are benign polyps that serve as precursors to the majority of colorectal cancers. Nearly half of adults in the Western world will develop adenomas by the age of 50, and there is no gender predilection. It is because of this that it is recommended that all adults get a colonoscopy by the age of 50 (even earlier when there is a family history of developing colorectal cancer).

Most polyps are small, measuring 0.5 cm or less, but can grow to be over 10 cm in size (as seen in this case). When a colonoscopy is performed, these polyps can appear as sessile, meaning flat, or pedunculated, meaning on a stalk. Due to the abnormal epithelial growth of the mucosa, the surface of an adenoma can have a velvety appearance, resembling that of a raspberry. Most patients will not demonstrate any symptoms from their polyps, with the exception of occult bleeding and anemia which are associated with larger polyps.

Dysplasia, which literally means “disordered growth”, occurs when the individual cells lose their uniformity and architecture, often resulting in cells with a hyperchromatic nuclei and a high nuclear to cytoplasmic ratio. The presence of dysplasia contained within the epithelium of a polyp is what classifies the polyp as an adenoma (Image 4). Based on their epithelial growth pattern, adenomas can be classified as either tubular adenomas or villous adenomas. Tubular adenomas tend to be smaller polyps, with a smoother surface and rounded glands on histologic examination. Villous adenomas, in contrast, tend to be larger polyps with long, slender villi noted on histology (Image 5). If an adenoma contains a mixture of tubular and villous elements, they are classified as tubulovillous adenomas. When a dysplastic cell is no longer contained within the epithelium, and instead breaches the basement membrane which separates the epithelium from the underlying tissue, it is termed invasive.

Image 4. Photomicrograph of the villous adenoma, demonstrating the dysplasia that is confined to the mucosa and not extending to the deeper tissue.
Image 5. Photomicrograph of the long, slender villi that are commonly seen in villous adenomas.

What makes this case so interesting is that there is a direct correlation between the size of an adenoma, and the risk of developing colorectal cancer. This is not true with most other cancers, however, as size plays no part in determining whether the tumor is cancerous or not. With colon polyps, the larger the polyp, the greater the chance of developing invasive carcinoma (i.e. cancer). This is why screening colonoscopies are so important. Studies have shown that regular colonoscopies, combined with the removal of the polyps found on the exam, reduce the incidence of colorectal cancer. Why this case is so interesting is that you could assume based on the size of this polypoid lesion, you would find some invasive component. However, after reviewing 116 blocks, not a single focus of invasion could be identified.

It should be stated that although there is a correlation between an adenomas size and the risk of developing cancer, the majority of adenomas will not progress to cancer, and in fact, there are no tools currently available that help to determine why one patient’s adenoma will progress to cancer, while another patient’s adenoma will not.

References

  1. Association of Directors of Anatomic and Surgical Pathology, adapted with permission by the American Cancer Society. Understanding Your Pathology Report: Colon Polyps (Sessile or Traditional Serrated Adenomas). cancer.org. https://www.cancer.org/treatment/understanding-your-diagnosis/tests/understanding-your-pathology-report/colon-pathology/colon-polyps-sessile-or-traditional-serrated-adenomas.html. Accessed February 14, 2019.
  2. Colon Polyps. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/colon-polyps/symptoms-causes/syc-20352875. Accessed February 14, 2019.
  3. Turner JR. Polyps. In: Kumar V, Abbas AK, Fausto N, Aster JC. Robbins and Cotran Pathologic Basis of Disease, 8th edition. Philadelphia, PA: Elsevier, Inc; 2010: 815-820

-Cory Nash is a board certified Pathologists’ Assistant, specializing in surgical and gross pathology. He currently works as a Pathologists’ Assistant at the University of Chicago Medical Center. His job involves the macroscopic examination, dissection and tissue submission of surgical specimens, ranging from biopsies to multi-organ resections. Cory has a special interest in head and neck pathology, as well as bone and soft tissue pathology. Cory can be followed on twitter at @iplaywithorgans.


Hematology Case Study: Symptomatic Anemia in Myelodysplastic Syndrome with Progression to Acute Myelogenous Leukemia

The patient is a 77 year old woman who presented in late Jan 2019 with severe anemia. In Feb 2017 she was diagnosed with myelodysplastic syndrome with no evidence of transformation to acute myelogenous leukemia. A bone marrow biopsy at the time showed 5-7% blasts in the bone marrow. She went through 5 rounds of chemotherapy with Vidaza (azacytidine) over the course of 9 months, with no significant response. She received one unit of RBCs with her 4th round of chemo and was given Aranesp (darbepoetin alfa) injections for anemia support. Aranesp is a man-made erythropoiesis stimulating protein which can be used to treat symptomatic anemia associated with myelodysplastic syndromes (MDS). After the 5th cycle of chemo, because of the lack of response, Vidaza was discontinued. Since then she has received several RBC transfusions to treat anemia and the Aranesp injections have continued.

In Oct 2018, the patient’s CBC showed leukocytosis, anemia, thrombocytopenia and neutrophilia.  See results below:

Patient results 10/2018       reference ranges

WBC  31.6                         4.5-10.5 x 103/μL

RBC  3.0                           3.7-5.3 x 106/μL

Hgb  7.0                            12.0-15.5 g/dl

Hct  23.6                            36.0-46.0 %

MCV  78.4                         80-100 fl

Plt  82                                150-450 x 103/μL

The CBC with automated differential performed at this visit flagged for a smear review. The technologist suspected blasts and the slide was sent for a pathologist’s review. The pathologist’s interpretation was that the differential showed “an aberrant myeloblast population, representing 6% of leukocytes along with an immature appearing monocytic population with phenotypic aberrancies representing 21% of leukocytes.” A leukemia/lymphoma flow cytometry was ordered. Results of the flow cytometry commented that an acute myeloid leukemia could not be excluded, however the differential diagnosis could also include chronic myelomonocytic leukemia. 

By Jan 2018, the patient was receiving blood transfusions every 6-8 weeks. CBC results from this visit shown below:

Patient results 1/2019         reference ranges

WBC  36.5                         4.5-10.5 x 103/μL

RBC  2.7                           3.7-5.3 x 106/μL

Hgb  6.2                            12.0-15.5 g/dL

Plt  65                                150-450 x 103/μL

Unfortunately the differential on this visit showed over 25% myeloblasts, confirmed by pathologist’s review. This sample was sent out for a second leukemia/lymphoma panel. A myeloblast phenotype was detected representing 27% of the leukocytes.

Diagnosis: Acute monoblastic/monocytic leukemia, no remission.

Image 1. Blasts, RBC morphology consistent with severe anemia
Image 2. Blasts seen on slide.

Myelodysplastic syndrome is a disorder of hematopoietic cell production involving clonal proliferation of an abnormal hematopoietic stem cell. It is most commonly diagnosed in patients in their 70s. Failure of the bone marrow to produce mature healthy cells is a gradual process, and therefore MDS is not necessarily a terminal disease. However, pancytopenia is a hallmark of MDS, and when pancytopenia is accompanied by the loss of the body’s ability to fight infections and control bleeding, MDS can be fatal. In addition, patients with MDS have a high risk of conversion to AML. About 30% of patients diagnosed with MDS will progress to acute myeloid leukemia (AML).

This patient was exhibiting pancytopenia, with accompanying anemia and infections, until her WBC began climbing several months ago. This was accompanied by the left shift and blasts seen on the peripheral smear, and prompted the flow cytometry studies.

Acute monoblastic/monocytic leukemia is considered a type of acute myeloid leukemia. In order to fulfill World Health Organization (WHO) criteria for AML-M5, a patient must have greater than 20% blasts in the bone marrow, and of these, greater than 80% must be of the monocytic lineage. AML-M5 can further be classified as M5a or M5b depending on whether the monocytic cells are predominantly monoblasts (>80%) or a mixture of monoblasts and promonocytes (<80% blasts).

The patient’s situation was discussed with the patient and her family. The patient chose more conservative and palliative treatment options over further chemotherapy.

References

https://www.merckmanuals.com/professional/hematology-and-oncology/leukemias/myelodysplastic-syndrome-mds

http://wiki.clinicalflow.com/amol-acute-monoblasticmonocytic-leukemia-m5

-Becky Socha, MS, MLS(ASCP)CM BB CM graduated from Merrimack College in N. Andover, Massachusetts with a BS in Medical Technology and completed her MS in Clinical Laboratory Sciences at the University of Massachusetts, Lowell. She has worked as a Medical Technologist for over 30 years. She’s worked in all areas of the clinical laboratory, but has a special interest in Hematology and Blood Banking. When she’s not busy being a mad scientist, she can be found outside riding her bicycle.

Hematopathology Case Study: A 33 Year Old Man with a Mass Behind the Ear

Case History

A 33 year old man of Japanese ethnicity presents with a 2 month history of a mass behind the right ear. Examination reveals a non-tender local with no other local or generalized adenopathy or hepatosplenomegaly. Laboratory investigations reveal an elevated ESR, serum IgE and peripheral blood eosinophilia. The lesion is excised.

Biopsy Findings

H&E stained sections demonstrate a follicular hyperplasia. The germinal centers demonstrate polarity and tingible body macrophages (A). Focally, follicular centers reveal eosinophilic microabscesses (B, C). Immunohistochemical analysis with an IgE stain reveals deposition in germinal centers (D). A diagnosis of Kimura disease is rendered.

Discussion

Kimura disease, also known as eosinophilic lymphoid follicular hyperplasia is a rare, chronic inflammatory disorder of unknown etiology. While an infectious etiology has been suggested, no pathogen has been identified to be causal, to date. Historically, Kimura disease was considered to be the same as Angiolymphoid Hyperplasia with Eosinophilia (ALHE); however, these entities are not the same.

Generally occurring in Asian males, Kimura disease is most common in the 3rd decade of life and in a head/neck site. It presents as painless, slow-growing adenopathy. An association with nephrotic syndrome has been reported. Peripheral blood eosinophilia, elevated ESR, and serum IgE are common findings. Histologically, nodes reveal hyperplastic follicles with well-formed germinal centers and mantle zones with deposition of IgE and eosinophilic microabscesses, as seen in this case. Perinodal soft tissue may be involved. Necrosis may be present, but is not extensive. Cytologically, FNA material may reveal polymorphous cell population with many eosinophils.

Prognosis is indolent; however, most cases recur after excision and radiation therapy usually yields best outcome.

References:

  1. Zhou P. et al. Kimura disease. Dermatol Online J. 2017 Oct 15;23(10).
  2. García Carretero R et al. Eosinophilia and multiple lymphadenopathy: Kimura disease, a rare, but benign condition. BMJ Case Rep. 2016 Aug 31;2016. pii: bcr2015214211. doi: 10.1136/bcr-2015-214211.
  3. Sun QF et al. Kimura disease: review of the literature. Intern Med J 2008;38:668–72.  

Kamran M. Mirza, MD, PhD, MLS(ASCP)CM is an Assistant Professor of Pathology and Medical Education at Loyola University Health System. A past top 5 honoree in ASCP’s Forty Under 40, Dr. Mirza was named to The Pathologist’s Power List of 2018. Follow him on twitter @kmirza

Whether or Not to Report Cytoplasmic Pattern of ANA IFA

Anti-nuclear antibody (ANA) test is commonly used to screen for systemic rheumatic disease. Indirect immunofluorescence assay using HEp-2 cells as substrate, containing approximately 100-150 autoantigens, is still the gold standard for ANA testing (1). Although the test name refers to only anti-nuclear antibody, there are often cytoplasmic staining patterns overserved in this assay. Cytoplasmic patterns result from antibodies against cytoplasmic components, like Jo-1 or Ribosomal P, and have clinical association with various systemic autoimmune disease, like polymyositis, systemic lupus erythematosus or primary biliary cirrhosis.    

There is no standardized recommendation regarding how to report cytoplasmic pattern on ANA IFA, and laboratories independently decides whether to indicate cytoplasmic pattern in their result.  The International Consensus on ANA Patterns (ICAP) workshop discussed this topic in 2015 and proposed two approaches for reporting ANA cytoplasmic patterns (2). Either to regard cytoplasmic pattern as positive or negative, both approaches recommended to include a statement of cytoplasmic staining.

We encountered cases in our laboratory in which reporting cytoplasmic staining had significant clinical values, and our laboratory started to report cytoplasmic staining as an additional comment in the test result a few years ago. Here is one of these cases:

Case: 35 year old woman with a history of hypertension complained about increasing muscle pain, weakness, and swelling. She had difficulties to raise her arms and had multiple falls, and was admitted to hospital three time for rhabdomyolysis. Her initial laboratory assessment were, CK >11,196 U/L, lactic acid 2.5 mmol/L, ALT 152 U/L, AST 416 U/L, and ALKP 42 U/L. Her ANA IFA test didn’t shown any nuclear staining, but there is very strong cytoplasmic staining observed. The clinician was suspecting inflammatory myositis and ordered myositis autoantibody panel to follow up. This panel detects numerous antibodies that are either specific or associated with inflammatory mycosis.

Her myositis autoantibody test result was positive for antibodies against signal recognition particle (SRP). SRP is an abundant, cytosolic, universally conserved ribonucleoprotein that targets specific proteins to the endoplasmic reticulum in eukaryotes and the plasma membrane in prokaryotes. Antibodies against SRP have been found in 5-8% of adult idiopathic inflammatory myopathies and <1% juvenile myopathies. It is closely associated with necrotizing myositis. Clinically it presents with acute onset, rapidly progressive, severe weakness, with high CK levels and commonly has cardiac and lung involvement. 

Clinically significant antibodies can be present in patients with connective tissue disease that may appear as strong cytoplasmic staining on screening ANA test. It would be helpful to add a comment in these cases to aid the clinician in pursuing further work-up with a strong clinical suspicious of connective tissue disease.

References:

1. Position Statement: Methodology of Testing for Antinuclear. Antibodies American College of Rheumatology. 2009.

2. Damoiseaux J, et al. International consensus on ANA patterns (ICAP): the bumpy road towards a consensus on reporting ANA results. Auto Immun Highlights. 2016 Dec;7(1):1. doi: 10.1007/s13317-016-0075-0. Epub 2016 Jan 30.

Xin-small

-Xin Yi, PhD, DABCC, FACB, is a board-certified clinical chemist, currently serving 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: An 8 Month Old Female with Vomiting and Diarrhea

Clinical History

An 8-month-old female presented to the pediatric emergency department (ED) due to vomiting and diarrhea for the past 10 days.  Per mother, the baby has had a fever and 6-8 episodes of diarrhea & 2-3 episodes of vomiting each day. On the day of admission, the mother noted the diarrhea was like mucous and contained blood and the baby was unable to tolerate anything by mouth. Past medical history was not significant and sick contacts included a sibling with a recent viral illness. In the ED, the baby had a fever of 103.1°F and was tachycardic. On physical exam, the baby was weak & lethargic with dry mucous membranes and a capillary refill of 2-3 seconds. Mom noted the baby did not produce tears when she cried and had decreased urinary output for the past 24 hours, consistent with dehydration. Initial labs revealed an elevated white count of 20.0 TH/cm2 and a C-reactive protein of 6.60 mg/dL, suggestive of an infectious process. Blood, urine, and stool cultures were sent to the microbiology laboratory and the baby was received IV fluids and ceftriaxone. 

Laboratory Identification

Blood culture signaled positive after 36 hours of incubation on the automated instrument and revealed gram negative rods.

Image 1. Whitish gray colonies on sheep blood and MacConkey agars after 48 hours of incubation at 35°C in ambient air.
Image 2. “Bull’s eye” colonies with a pink center and white outer edge on cefsulodin-Irgasan-novobiocin (CIN) agar after 48 hours of incubation at 22°C in ambient air.

MALDI-TOF mass spectrometry identified the isolate as Yersinia enterocolitica. The urinalysis was positive and the urine culture grew >100,000 CFU/ml of Escherichia coli. Stool culture was negative for Salmonella, Shigella, E. coli O157:H7, Aeromonas, and Plesiomonas. Antigens for Shiga toxin and Campylobacter jejuni were both negative. Stool culture for Y. enterocolitica was not ordered. A multiplex PCR panel for gastrointestinal pathogens also identified Y. enterocolitica

Discussion

Yersinia enterocolitica is a member of the Enterobactericeae family and when transferred via the fecal oral route, can cause gastroenteritis, terminal ileitis, and mesenteric lymphadenitis, particularly in young children, the elderly, and immunocompromised patients, who consume raw or undercooked pork, chitterlings, or drink unpasteurized milk products. Because Y. enterocolitica can survive and multiple at refrigerated temperatures, prepackaged lunchmeats and packed red blood cells can be common sources for infection as well. Rarely, septicemia can result from migration of the organisms into the lymph nodes and then the blood.

Stool, blood, and lymph node cultures are often submitted to the microbiology laboratory for the detection of Y. enterocolitica. The organism is a gram-negative rod that can grow well on routine media such as sheep blood, chocolate, and MacConkey agars at 22°C and 35°C in ambient air. When there is a clinical concern for gastroenteritis caused by Y. enterocolitica, a selective media such as cefsulodin-Irgasan-novobiocin (CIN) agar should be added to the stool culture to enhance isolation. Y. enterocolitica grows as “bull’s eye” colonies with a pink center and surrounding clear to white border on CIN agar.

The organism ferments glucose & sucrose, is positive for catalase & urease, and is oxidase negative. Y. enterocolitica is able to be identified by manual and automated biochemical systems, such as API 20E and Vitek as well as MALDI-TOF mass spectrometry. Culture independent multiplex PCR panels for the diagnosis of gastrointestinal syndromes are gaining popularity due to sensitivity & improved turnaround times; however, reimbursement and the necessity for the isolated organism for susceptibility testing and typing the in the case of outbreak investigations continue to be items of concern.

The majority of cases of Y. enterocolitica gastroenteritis do not require antimicrobial treatment. In the case of severe disease and those that are immunocompromised or with systemic disease should receive treatment with a fluorquinolone or trimethoprim sulfamethoxazole. While Y. enterocolitica produces beta lactamases, it is still uniformly susceptible to extended spectrum cephalosporins as well.    

In the case of our patient, she received 8 days of ceftriaxone and was transitioned to oral trimethoprim sulfamethoxazole and discharged home to finish the 21-day course of antibiotics due to bacteremia from Y. enterocolitica. Mother was counseled to fully cook pork products before feeding to the baby.    

-Lisa Stempak, MD, is an Assistant Professor of Pathology at the University of Mississippi Medical Center in Jackson, MS. She is certified by the American Board of Pathology in Anatomic and Clinical Pathology as well as Medical Microbiology. She is the Director of Clinical Pathology as well as the Microbiology and Serology Laboratories. Her interests include infectious disease histology, process and quality improvement, and resident education.