Serologic cross-reactions among Ehrlichia equi, Ehrlichia phagocytophila, and human granulocytic Ehrlichia.

1995 ◽  
Vol 33 (5) ◽  
pp. 1098-1103 ◽  
Author(s):  
J S Dumler ◽  
K M Asanovich ◽  
J S Bakken ◽  
P Richter ◽  
R Kimsey ◽  
...  
1997 ◽  
Vol 29 (6) ◽  
pp. 490-492 ◽  
Author(s):  
N. PUSTERLA ◽  
CELESTINE WOLFENSBERGER ◽  
ROSMARIE GERBER-BRETSCHER ◽  
H. LUTZ

2000 ◽  
Vol 68 (9) ◽  
pp. 5277-5283 ◽  
Author(s):  
Patrizio Caturegli ◽  
Kristin M. Asanovich ◽  
Jennifer J. Walls ◽  
Johan S. Bakken ◽  
John E. Madigan ◽  
...  

ABSTRACT Human granulocytic ehrlichiosis (HGE) is a potentially fatal, tick-borne disease caused by a bacterium related or identical toEhrlichia phagocytophila. To identify and characterizeE. phagocytophila group-specific protein antigen genes, we prepared and screened HGE agent and Ehrlichia equi genomic DNA expression libraries using polyclonal equine E. equiantibodies. Two clones, one each from HGE agent and E. equi, that were recognized specifically by antibodies to theE. phagocytophila group ehrlichiae had complete open reading frames of 3,693 and 3,615 nucleotides, respectively. The two clones were 96.6% identical and predicted a protein with at least 11 tandemly repeated ankyrin motifs. Thus, the gene was namedank (for ankyrin). When the encoded protein, named AnkA, was expressed in Escherichia coli, it was recognized by antibodies from rabbits and mice immunized with the HGE agent, sera from humans convalescent from HGE, and sera from horses convalescent from HGE and E. equi infection. Monospecific AnkA antibodies reacted with proteins in HGE agent immunoblots, and AnkA monoclonal antibodies detected cytoplasmic antigen in E. phagocytophila group bacteria and also detected antigen associated with chromatin in infected but not uninfected HL-60 cell cultures. These results suggest that this Ehrlichia protein may influence host cell gene expression.


Author(s):  
Gerhard Dobler

• TBE appears with non-characteristic clinical symptoms, which cannot be distinguished from oth-er forms of viral encephalitis or other diseases. • Cerebrospinal fluid and neuro-imaging may give some evidence of TBE, but ultimately cannot confirm the diagnosis. • Thus, proving the diagnosis “TBE” necessarily requires confirmation of TBEV-infection by detec-tion of the virus or by demonstration of specific antibodies from serum and/or cerebrospinal fluid. • During the phase of clinic symptoms from the CNS, the TBEV can only rarely be detected in the cerebrospinal fluid of patients. • Most routinely used serological tests for diagnosing TBE (ELISA, HI, IFA) show cross reactions resulting from either Infection with other flaviviruses or with other flavivirus vaccines.


TBE appears with non-characteristic clinical symptoms, which cannot be distinguished from other forms of viral encephalitis or other diseases. Cerebrospinal fluid and neuro-imaging may give some evidence of TBE, but ultimately cannot confirm the diagnosis. Thus, proving the diagnosis “TBE” necessarily requires confirmation of TBEV-infection by detection of the virus or by demonstration of specific antibodies from serum and/or cerebrospinal fluid. During the phase of clinic symptoms from the CNS, the TBEV can only rarely be detected in the cerebrospinal fluid of patients. Most routinely used serological tests for diagnosing TBE (ELISA, HI, IFA) show cross reactions resulting from either infection with other flaviviruses or with other flavivirus vaccines.


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