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Published on: October 12, 2012
Cytoplasmic, nuclear, and platelet autoantibodies in human granulocytic ehrlichiosis patients
1Wadsworth Center, New York State Department of Health, Albany 12201-2002, USA. wong@wadsworth.org
Serum samples from patients with confirmed human granulocytic ehrlichiosis (HGE) were tested for cytoplasmic, nuclear, and platelet autoantibodies and rheumatoid factor. The indirect fluorescence antinuclear antibody test on Hep-2 cells demonstrated antinuclear titers of > or = 40 and > or = 160 in 44 and 10%, respectively, of serum samples from HGE patients. Two patients (4%) had anticytoplasmic (mitochondrial and spindle apparatus) antibodies with a titer of 80 and two patients (4%) had anticytoplasmic (mitochondrial) antibodies with a titer of 160 or greater. Flow cytometry was used to demonstrate antiplatelet antibodies in 80% of first serum samples from HGE patients. Rheumatoid factor was not detected. Nuclear and cytoplasmic autoantibodies are a major cause of interference when the indirect fluorescence antibody test is used to detect fluorescence of morulae in Ehrlichia-infected equine neutrophils or HL-60 promyelocytes. Antiplatelet antibodies may contribute to the profound thrombocytopenia which is a characteristic laboratory feature during the acute phase of HGE infection. Whether autoantibodies precede infection or are caused by immune activation of HGE deserves further study.
Serum samples from patients with confirmed human granulocytic ehrlichiosis (HGE) were tested for cytoplasmic, nuclear, and platelet autoantibodies and rheumatoid factor. The indirect fluorescence antinuclear antibody test on Hep-2 cells demonstrated antinuclear titers of > or = 40 and > or = 160 in 44 and 10%, respectively, of serum samples from HGE patients. Two patients (4%) had anticytoplasmic (mitochondrial and spindle apparatus) antibodies with a titer of 80 and two patients (4%) had anticytoplasmic (mitochondrial) antibodies with a titer of 160 or greater. Flow cytometry was used to demonstrate antiplatelet antibodies in 80% of first serum samples from HGE patients. Rheumatoid factor was not detected. Nuclear and cytoplasmic autoantibodies are a major cause of interference when the indirect fluorescence antibody test is used to detect fluorescence of morulae in Ehrlichia-infected equine neutrophils or HL-60 promyelocytes. Antiplatelet antibodies may contribute to the profound thrombocytopenia which is a characteristic laboratory feature during the acute phase of HGE infection. Whether autoantibodies precede infection or are caused by immune activation of HGE deserves further study.
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