Abstract

Human granulocytic anaplasmosis (HGA) is a tick-borne, infectious disease caused by Anaplasma phagocytophilum that generally presents with nonspecific symptoms such as fever, chills, headache, malaise, and myalgia. If not treated immediately, HGA can cause hemophagocytic lymphohistiocytosis (HLH), a well-documented but underrecognized sequela of severe HGA. In this article, we report a case of severe HGA with hyperferritinemia in a 74-year-old male from Central Pennsylvania who initially presented with recurrent fevers, nausea, and malaise to our emergency department and was subsequently discharged home that same day. Ten days later, the patient returned with acute kidney injury, elevated liver transaminases, and profound hyperferritinemia to 5130 ng/mL. Empiric doxycycline was administered for suspected tick-borne disease and serologies eventually came back positive for anti–Anaplasma phagocytophilum antibodies. The patient returned to baseline status 15 days after discharge. Our case shows the challenges in the timely diagnosis of HGA and highlights the role of serum ferritin in aiding this diagnosis. Although our patient did not fulfill the HLH diagnostic criteria, our report demonstrates the importance of recognizing HGA as a reversible cause of HLH.

Highlights

  • Human granulocytic anaplasmosis (HGA) is a tick-borne disease caused by Anaplasma phagocytophilum

  • Incidence of HGA has increased from 348 reported cases in 2000 to approximately 1800 in 2010.19 In the United States of America, HGA mostly occurs in Minnesota, Wisconsin, and New York.[11]

  • Our patient is from Central Pennsylvania with no known travel to endemic areas of HGA

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Summary

Introduction

Human granulocytic anaplasmosis (HGA) is a tick-borne disease caused by Anaplasma phagocytophilum. Initial laboratory evaluation showed a normal leukocyte count of 6.9 × 109 cells/L (normal = 4.0-10.4 × 109 cells/L) and normal liver function with a bilirubin of 0.7 mg/dL (normal = 0.2-1.3 mg/dL), alanine transaminase (ALT) 42 U/L (normal = 13-69 U/L), aspartate aminotransferase (AST) 38 U/L (normal = 15-46 U/L), and alkaline phosphatase 70 U/L (normal = 38-126 U/L). He was discharged home with outpatient follow-up scheduled. Outpatient laboratory values obtained days later demonstrated worsening AKI with creatinine 1.9 mg/dL He had worsening liver function AST 128 U/L, ALT 166 U/L, and total bilirubin of 3.9 mg/dL. Quantitative serum EBV PCR (polymerase chain reaction) demonstrated co-infection with EBV at 851 copies/ mL (normal

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