Histoplasma capsulatum in New England: A Case Study

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Histoplasma capsulatum in New England: A Case Study

LORI-ANN CAMARA, KATERINA MIRAGLIA, SUSAN J. LECLAIR

ABBREVIATIONS: COPD ? Chronic Obstructive Pulmonary Disease, CBC ? Complete Blood Count, BUN ? Blood Urea Nitrogen, EBV ? Epstein Barr Virus, CMV ? Cytomegalovirus, AIDS ? Autoimmune Deficiency Syndrome

INDEX TERMS: Histoplasma capsulatum, Mould microscopic morphology, Biphasic fungal infections, Fungal pneumonia

Clin Lab Sci 2014;27(1):6

Lori-Ann Camara, MLS(ASCP)CM, St. Luke's Hospital, New Bedford, MA 02740

Katerina Miraglia, D.C., MLS(ASCP)CM, Department of Medical Laboratory Science, University of Massachusetts, Dartmouth, MA 02747-2300

Susan J. Leclair, Ph.D., Department of Medical Laboratory Science, University of Massachusetts , 285 Old Westport Road, Dartmouth, MA

Address for Correspondence: Susan J. Leclair, Ph.D., Department of Medical Laboratory Science, University of Massachusetts , 285 Old Westport Road, Dartmouth, MA 02747-2300, 508-999-8786, sleclair@umassd.edu

Overview: A healthy adult experienced a necrotic lesion on her back. She developed a reduced appetite, profound weakness, and fever. Routine x-rays and CAT scans demonstrated bilateral hilar adenopathy and patchy infiltrates. During bronchoscopy, biopsies and cultures for bacteria and fungi were taken.

Patient History: A 24-year-old female was admitted to the hospital after treatment by her primary care physician for a necrotic skin lesion on her back. She is a social worker in a large urban area in the Northeast quadrant of the country and recently returned from a

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vacation in Honduras where she experienced a "bite" on her back. Approximately 10 days after her return, she experienced generalized weakness, night sweats, chills and headaches. She also states that she has experienced a significant drop in appetite. She did not complain of any chest pain but commented about heaviness behind her sternum. Medical imaging confirmed the presence of abdominal and inguinal adenopathy. The only relevant family history included a parent with COPD due to smoking and a paternal uncle with sarcoidosis. Given the continued presence of a now necrotic lesion, her primary care physician initiated a course of doxycycline for a suspected rickettsial infection. The necrotic lesion resolved but the systemic symptoms persisted and, together with the imagining results, a bronchoscopy was justified.

Relevant Medical History: The patient has been healthy although her childhood medical history includes bouts of asthma that diminished over time. She stated that she has not have an instance of asthma for at least 10 years. Initial potential diagnoses included lymphoma, tuberculosis, disseminated bacterial, fungal or parasitic disease and sarcoidosis. Biopsies and cultures were taken from the sites of adenopathy and immunologic studies were ordered for Lyme Disease, Rickettsia spp., and Erlichia spp.

Her admission CBC in Table 1 showed a decreased white cell count with neutropenia, eosinophilia, and monocytosis suggesting an acute inflammation with high antigenic stimulation which is also reflected in the increased erythrocyte sedimentation rate. The common metabolic panel seen in Table 2 revealed hypoalbuminenia that could account for the decreased anion gap.1 Hypoalbuminemia is associated with poor diet which correlated well with her history. The decreased BUN/Creatinine ratio was not considered significant due to the BUN value which was explained by her lack of appetite and, specifically, a lack of high protein foods in recent days. With both values within

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reference intervals, follow up with a nutritionist was suggested.

Table 1. Report of relevant hematology laboratory testing at time of admission

Test

Patient Result

WBC

3.8x109/L

RBC

3.8x1012/L

Hgb

13.3 g/dL

HCT

38.5%

MCV

83.9fL

MCH

29.0pg

MCHC

34.5 g/dl

RDW

12.5%

PLT

194x109/L

MPV

6.8%

NE%

50.3%

LY%

28.1%

MO%

15.1% HIGH

EO%

5.7% HIGH

BA%

0.5%

NE Intermediate Form 3.0%

NE #

1.9x109/L

LY #

0.6x109/L

MO #

0.6x109/L

EO #

0.2x109/L

BA #

0.0x109/L

ESR

40mm/hr HIGH

Reference Intervals 4.5 ? 11.0 4.2 ? 4.6 12.8 ? 15.2 38 ? 45 80 - 94 27 - 32 32 - 36 11.0 ? 14.5 150 - 450 6.8 - 10 45 - 78 16 - 45 3 - 12 0 - 5 0 - 2 0 2.0 ? 7.7 1.0 ? 4.8 0.0- 0.8 0.0 ? 0.5 0.0 ? 0.2 0 - 15

Table 2. Report of relevant chemistry laboratory testing at time of admission

Test Sodium Potassium Chloride Carbon Dioxide Anion gap BUN Creatinine BUN/creatinine ratio Total Protein Albumin

Patient Result

138 mEq/L

4.3 mEq/L

102 mEq/L

32 mmol/L

4 mEq/L LOW

8mg/dL

1.1mg/dL

8.9

LOW

6.1

3.3

LOW

Reference Intervals 135 ? 144 3.3 ? 5.1 98 - 109 23 - 32 7 - 16 5 - 25 0.8 ? 1.4 12.0 ? 20.0 6.0 to 8.3 3.6 ? 4.9

Differential Diagnosis Initial pathologic examination of the lymph nodes showed multiple granulomas. Granulomas can form when macrophages ingest but do not completely degrade or eliminate foreign material.2 Initiating events of granuloma formation include the presence of nonliving material such as particulate air pollutants, autoimmune disorders such as sarcoidosis, and living

substances such as bacteria, fungi and parasites. Granulomas are characterized by a combination of lymphocytes, neutrophils, eosinophils, multinucleated giant cells, fibroblasts and collagen (fibrosis). The relative number of cells can be a clue to the cause of the granuloma. For example, granulomas with numerous eosinophils may signify coccidioidomycosis or allergic bronchopulmonary fungal disease, while granulomas with numerous neutrophils might reflect blastomycosis or cat-scratch disease.3

Histological examination of the lymph nodes demonstrated no malignant cells or architectural distortion due to a malignancy, eliminating the potential for either Hodgkin or Non-Hodgkin Lymphoma. With potential malignant disorders eliminated, the investigation focused on sarcoidosis due to the family history and infections characterized by pulmonary granulomas such as tuberculosis, histoplasmosis, coccidioidomycosis or common viral disorders.

The cause of sarcoidosis is unknown with infections, autoimmune disease and genetic mutations having been implicated.4 A common disease, sarcoidosis has no specific age, race or gender predilections. It commonly occurs in adults from 20 ? 24 years of age. The current assumption is an interaction between a genetic risk and a triggering event. While tissue biopsy is a significant test to assess the potential for a diagnosis of sarcoidosis, other laboratory tests are helpful. These include increased values for angiotensin-converting enzyme (ASCE) assay and liver function studies to include Albumin, Alanine Transaminase, Alkaline Phosphatase, Aspartate Transaminase, Bilirubin, and Lactate Ddehyrogenase.5 In this situation, however, all of these tests, save the albumin, were within reference intervals.

The preliminary bacteriological reports of the biopsies showed no bacterial growth with Gram stain and acidfast stain. Additional samples from both the bronchoscopy and the hilar node biopsies were submitted for fungal culture. Tuberculosis was eliminated as the cause for the negative acid-fast stain and correlated with the negative T-cell interferon release skin test.6

Serological tests for Brucella, Coccidioides, Dengue fever, rickettsia, spotted fever, CMV, EBV, Q fever, and

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Table 3. Report of relevant immunology laboratory testing

Test Brucella IgG Antibody Brucella IgM Antibody Brucella Ab Interpretation

Coccidiodes Ab (CF) Coccidioides IgG Antibody Coccidioides IgM Antibody CMV IgM antibody CMV DNA Quant PCR CMV DNA PCR copies/mL Dengue Fever IgG Antibody Dengue Fever IgM Antibody EBV capsid antigen ? IgG antibody EBV capsid antigen ? IgM antibody EBV nuclear antigen Antibody

Patient Result Negative Negative Recommend repeat in 14-21 days if recent infection is suspected 1:4 Negative Negative Negative None detected None detected 0.2 0.52 Negative Negative Positive

EBV DNA Quant PCR EBV 95% Conf Intervals

EBV interpretation

Malaria smear

Q Fever Phase I IgG Antibody Q Fever Phase I IgM Antibody Q Fever Phase II IgG Antibody Q Fever Phase II IgM Antibody

Spotted Fever Group IgG Spotted Fever Group IgM

Rickettsia IgG Antibody Rickettsia IgM Antibody Ricketsia typhii IgG Rickettsia typhii IgM Beta-2 glucan assay

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