Susceptibility of cattle to Ehrlichia risticii, the causative agent of Potomac horse fever

2001 ◽  
Vol 148 (3) ◽  
pp. 86-87 ◽  
Author(s):  
N. Pusterla ◽  
J. Berger Pusterla ◽  
E. DeRock ◽  
J. E. Madigan
1987 ◽  
Vol 121 (10) ◽  
pp. 232-232 ◽  
Author(s):  
J. Dawson ◽  
M. Ristic ◽  
C. Holland ◽  
R. Whitlock ◽  
J. Sessions

2000 ◽  
Vol 38 (3) ◽  
pp. 1293-1297 ◽  
Author(s):  
Nicola Pusterla ◽  
John E. Madigan ◽  
Joon-Seok Chae ◽  
Elfriede DeRock ◽  
Eileen Johnson ◽  
...  

We report successful helminthic transmission of Ehrlichia risticii, the causative agent of Potomac horse fever, using trematode stages collected from Juga yrekaensis snails. The ehrlichial agent was isolated from the blood of experimentally infected horses by culture in murine monocytic cells and identified as E. risticii ultrastructurally and by characterization of three different genes.


2000 ◽  
Vol 92 (2) ◽  
pp. 151-156 ◽  
Author(s):  
Nicola Pusterla ◽  
Eileen Johnson ◽  
Joon-seok Chae ◽  
Jeannine Berger Pusterla ◽  
Elfriede DeRock ◽  
...  

2009 ◽  
Vol 37 (18) ◽  
pp. 6076-6091 ◽  
Author(s):  
Mingqun Lin ◽  
Chunbin Zhang ◽  
Kathryn Gibson ◽  
Yasuko Rikihisa

1998 ◽  
Vol 64 (8) ◽  
pp. 2888-2893 ◽  
Author(s):  
Jeffrey E. Barlough ◽  
Gerhard H. Reubel ◽  
John E. Madigan ◽  
Larisa K. Vredevoe ◽  
Paul E. Miller ◽  
...  

ABSTRACT Ehrlichia DNA was identified by nested PCR in operculate snails (Pleuroceridae: Juga spp.) collected from stream water in a northern California pasture in which Potomac horse fever (PHF) is enzootic. Sequencing of PCR-amplified DNA from a suite of genes (the 16S rRNA, groESL heat shock operon, 51-kDa major antigen genes) indicated that the source organism closely resembledEhrlichia risticii, the causative agent of PHF. The minimum percentage of Juga spp. harboring the organism in the population studied was 3.5% (2 of 57 snails). No ehrlichia DNA was found in tissues of 123 lymnaeid, physid, and planorbid snails collected at the same site. These data suggest that pleurocerid stream snails may play a role in the life cycle of E. risticii in northern California.


2000 ◽  
Vol 32 (4) ◽  
pp. 275-279 ◽  
Author(s):  
J. E. Madigan ◽  
N. Pusterla ◽  
E. Johnson ◽  
J.-S. Chae ◽  
J. Berger Pusterla ◽  
...  

1998 ◽  
Vol 36 (6) ◽  
pp. 1501-1511 ◽  
Author(s):  
Gerhard H. Reubel ◽  
Jeffrey E. Barlough ◽  
John E. Madigan

We report on the production and characterization of Ehrlichia risticii, the agent of Potomac horse fever (PHF), from snails (Pleuroceridae: Juga spp.) maintained in aquarium culture and compare it genetically to equine strains. Snails were collected from stream waters on a pasture in Siskiyou County, Calif., where PHF is enzootic and were maintained for several weeks in freshwater aquaria in the laboratory. Upon exposure to temperatures above 22°C the snails released trematode cercariae tentatively identified as virgulate cercariae. Fragments of three different genes (genes for 16S rRNA, thegroESL heat shock operon, and the 51-kDa major antigen) were amplified from cercaria lysates by PCR and sequenced. Genetic information was also obtained from E. risticii strains from horses with PHF. The PCR positivity of snail secretions was associated with the presence of trematode cercariae. Sequence analysis of the three genes indicated that the source organism closely resembledE. risticii, and the sequences of all three genes were virtually identical to those of the genes of an equine E. risticii strain from a property near the snail collection site. Phylogenetic analyses of the three genes indicated the presence of geographical E. risticii strain clusters.


1998 ◽  
Vol 36 (2) ◽  
pp. 506-512 ◽  
Author(s):  
Sukanta K. Dutta ◽  
Ramesh Vemulapalli ◽  
Biswajit Biswas

Ehrlichia risticii is the causative agent of Potomac horse fever (PHF), which continues to be an important disease of horses. Commercial inactivated whole-cell vaccines are regularly used for immunization of horses against the disease. However, PHF is occurring in large numbers of horses in spite of vaccination. In a limited study, 43 confirmed cases of PHF occurred between the 1994 and 1996 seasons; of these, 38 (89%) were in horses that had been vaccinated for the respective season, thereby clearly indicating vaccine failure. A field study of horses vaccinated with two PHF vaccines indicated a poor antibody response, as determined by immunofluorescence assay (IFA) titers. In a majority of horses, the final antibody titer ranged between 40 and 1,280, in spite of repeated vaccinations. None of the vaccinated horses developed in vitro neutralizing antibody in their sera. Similarly, one horse experimentally vaccinated three times with one of the vaccines showed a poor antibody response, with final IFA titers between 80 and 160. The horse did not develop in vitro neutralizing antibody or antibody against the 50/85-kDa strain-specific antigen (SSA), which is the protective antigen of the original strain, 25-D, and the variant strain of our laboratory, strain 90-12. Upon challenge infection with the 90-12 strain, the horse showed clinical signs of the disease. The horse developed neutralizing antibody and antibody to the 50/85-kDa SSA following the infection. Studies of the new E. risticiiisolates from the field cases indicated that they were heterogeneous among themselves and showed differences from the 25-D and 90-12 strains as determined by IFA reactivity pattern, DNA amplification finger printing profile, and in vitro neutralization activity. Most importantly, the molecular sizes of the SSA of these isolates varied, ranging from 48 to 85 kDa. These studies suggest that the deficiency in the antibody response to the PHF vaccines and the heterogeneity ofE. risticii isolates may be associated with the vaccine failure.


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