A rare case of delayed anaplasma phagocytophilum-induced pancytopenia: A diagnostic conundrum. (March 2022) - Song, David
Abstract: Introduction: Human granulocytic anaplasmosis (HGA) is a potentially fatal tick-borne disease caused by the obligate intracellular bacterium Anaplasma phagocytophilum. It is most commonly found in the Northeastern and Midwestern parts of the United States especially during spring and summer months. The clinical picture of anaplasmosis is varied ranging from common symptoms such as fever, headache and myalgia to rarer presentations such as pancytopenia. Case presentation: We present a case of a 62 year old male who presented with watery diarrhea, fever, and pancytopenia. Although there is a broad differential for pancytopenia, a thorough history provides clues regarding the diagnosis. In our patient, a recent history of camping in Upstate New York was suggestive of an infectious etiology from a tick borne illness. Clinical discussion: A tick-borne panel guided us to identify the diagnosis of HGA. Although the exact underlying pathogenesis of tick-borne illnesses leading to pancytopenia is still unknown, the pancytopenia is postulated to be due to a multi-nodal mechanism involving immune and non immune platelet destruction, global bone marrow suppression, hemophagocytic lymphohistiocytosis and myelosuppressive chemokines release. Conclusion: We hope that this case report elucidates the importance of obtaining a meticulous history in guiding clinicians towards prompt diagnosis, even in instances where there may be an evolving clinical picture. Highlights: Human granulocytic anaplasmosis (HGA) is a potentially fatal tick-borne disease caused by the obligate intracellular bacterium Anaplasma phagocytophilum . A prompt diagnosis and management will facilitate an early recovery and prevent any fatal complications such as pancytopenia. HGA causing pancytopenia is likely due to a multi-modal mechanism involving immune and non-immune platelet destruction, global bone marrow suppression, hemophagocytic lymphohistiocytosis, and myelosuppressive chemokines release.