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Home / Equine Research Bank / Infect Immun / Antibody response to Ehrlichia risticii and antibody reactiv...
Infection and immunity1989; 57(10); 2959-2962; doi: 10.1128/iai.57.10.2959-2962.1989

Antibody response to Ehrlichia risticii and antibody reactivity to the component antigens in horses with induced Potomac horse fever.

Abstract: The antibody response and the antibody reactivity to component antigens of Ehrlichia risticii were studied in horses with induced Potomac horse fever. These horses had no detectable antibodies to E. risticii in their preinoculation (PrI) sera by indirect fluorescent-antibody assay and enzyme-linked immunosorbent assay (ELISA). All the horses exhibited typical disease features following experimental infection and responded with specific antibodies, as measured by ELISA and indirect fluorescent-antibody assay. A primary antibody response was detected in 70% of the horses, while a secondary-type antibody response was detected in 30% of the horses by ELISA. In the primary antibody response, a distinct titer was observed at 2 weeks postinoculation (PI), when the immunoglobulin M (IgM)/IgG ratio was 2 to 5, and the overall antibody titer peaked at 6 to 8 weeks PI. The secondary-type antibody response exhibited a characteristic titer at 1 week PI, the IgM and IgG titers were about equal at 2 weeks PI, and the overall antibody titer peaked at 6 weeks PI. A transient depression in the IgG response at 4 weeks PI was observed in both response types. The antibody was maintained at a high titer for over a year in all horses. Western immunoblot reactivity showed that the antisera collected from these infected horses at 4 to 5 weeks PI recognized some or all of the six major E. risticii component antigens (70, 55, 51, 44, 33, and 28 kilodaltons), all of which were apparent surface components. The 6- to 8-week PI antisera recognized up to 16 component antigens, including 9 major antigens (110, 86, 70, 55, 51, 49, 44, 33, and 28 kilodaltons). However, the PrI sera of these horses showed reactivity at various intensities with one to seven of the component antigens. There was no apparent correlation between this reactivity pattern and the subsequent antibody response types.
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Publication Date: 1989-10-01 PubMed ID: 2777369PubMed Central: PMC260755DOI: 10.1128/iai.57.10.2959-2962.1989Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research article investigates the antibody response and antigen reactivity in horses that were artificially infected with Ehrlichia risticii, a bacteria causing Potomac horse fever. The responses were observed over a span of time and compared against pre-inoculation parameters.

Initial Condition of Horses and Induced Infection

  • The study began with horses that showed no trace of antibodies to Ehrlichia risticii in their sera before the experiment. This was confirmed using both indirect fluorescent-antibody assay and enzyme-linked immunosorbent assay (ELISA).
  • The disease was then artificially induced in these horses and they started to exhibit the typical symptoms of Potomac horse fever.

Antibody Response Observation

  • Following the induced infection, specific antibodies rose in the horses’ bodies, noticeable through ELISA and indirect fluorescent-antibody assay.
  • 70% of the horses were found to have a primary antibody response while the remaining 30% showed a secondary-type antibody response.
  • The primary antibody response exhibited a discernible titer at 2 weeks after infection, with a ratio of immunoglobulin M (IgM) and immunoglobulin G (IgG) between 2 and 5. The peak of this response came around 6 to 8 weeks post-infection.
  • The secondary-type response, on the other hand, showed a characteristically different titer at one week post-infection. The IgM and IgG titers reached a roughly equal level at 2 weeks post-infection, and the overall peak came at 6 weeks.
  • Both response types indicated a temporary drop in the IgG response at around 4 weeks after infection. Despite this, the high titer of the antibody was maintained in all horses for over a year.

Antigen Recognition Post-Infection

  • The Western immunoblot test was used to determine the antigens the antibodies recognized. Four to five weeks post-infection, the antisera from the infected horses recognized some or all of the six major E. risticii component antigens.
  • Six to eight weeks post-infection, the antisera recognized up to 16 component antigens.
  • Interestingly, the pre-infection sera showed differing levels of reactivity with one to seven component antigens. There was no apparent link between this pre-infection reactivity pattern and the subsequent types of antibody response.

Cite This Article

APA
Dutta SK, Mattingly BL, Shankarappa B. (1989). Antibody response to Ehrlichia risticii and antibody reactivity to the component antigens in horses with induced Potomac horse fever. Infect Immun, 57(10), 2959-2962. https://doi.org/10.1128/iai.57.10.2959-2962.1989

Publication

Infection and immunity
ISSN: 0019-9567
NlmUniqueID: 0246127
Country: United States
Language: English
Volume: 57
Issue: 10
Pages: 2959-2962

Researcher Affiliations

Dutta, S K
  • Virginia-Maryland Regional College of Veterinary Medicine, University of Maryland, College Park 20742.
Mattingly, B L
    Shankarappa, B

      MeSH Terms

      • Animals
      • Antibodies, Bacterial / biosynthesis
      • Antigens, Bacterial / immunology
      • Blotting, Western
      • Ehrlichia / immunology
      • Horse Diseases / immunology
      • Horses
      • Humans
      • Immunization, Secondary
      • Immunoglobulin G / biosynthesis
      • Immunoglobulin M / biosynthesis
      • Immunosuppression Therapy
      • Rickettsiaceae Infections / immunology
      • Rickettsiaceae Infections / veterinary

      References

      This article includes 11 references
      1. Holland CJ, Ristic M, Cole AI, Johnson P, Baker G, Goetz T. Isolation, experimental transmission, and characterization of causative agent of Potomac horse fever.. Science 1985 Feb 1;227(4686):522-4.
        pubmed: 3880925doi: 10.1126/science.3880925google scholar: lookup
      2. Rikihisa Y, Perry BD. Causative ehrlichial organisms in Potomac horse fever.. Infect Immun 1985 Sep;49(3):513-7.
        pubmed: 4030092doi: 10.1128/iai.49.3.513-517.1985google scholar: lookup
      3. Dutta SK, Myrup AC, Rice RM, Robl MG, Hammond RC. Experimental reproduction of Potomac horse fever in horses with a newly isolated Ehrlichia organism.. J Clin Microbiol 1985 Aug;22(2):265-9.
        pubmed: 4031040doi: 10.1128/jcm.22.2.265-269.1985google scholar: lookup
      4. Ristic M, Holland CJ, Dawson JE, Sessions J, Palmer J. Diagnosis of equine monocytic ehrlichiosis (Potomac horse fever) by indirect immunofluorescence.. J Am Vet Med Assoc 1986 Jul 1;189(1):39-46.
        pubmed: 3525479
      5. Pretzman CI, Rikihisa Y, Ralph D, Gordon JC, Bech-Nielsen S. Enzyme-linked immunosorbent assay for Potomac horse fever disease.. J Clin Microbiol 1987 Jan;25(1):31-6.
        pubmed: 3539995doi: 10.1128/jcm.25.1.31-36.1987google scholar: lookup
      6. Shankarappa B, Dutta SK. Production and characterization of monoclonal antibodies to Ehrlichia risticii.. Am J Vet Res 1989 Jul;50(7):1145-9.
        pubmed: 2774338
      7. Rikihisa Y, Johnson GC, Burger CJ. Reduced immune responsiveness and lymphoid depletion in mice infected with Ehrlichia risticii.. Infect Immun 1987 Sep;55(9):2215-22.
        pubmed: 3497879doi: 10.1128/iai.55.9.2215-2222.1987google scholar: lookup
      8. Champsaur H, Fattal-German M, Arranhado R. Sensitivity and specificity of viral immunoglobulin M determination by indirect enzyme-linked immunosorbent assay.. J Clin Microbiol 1988 Feb;26(2):328-32.
        pubmed: 3125220doi: 10.1128/jcm.26.2.328-332.1988google scholar: lookup
      9. Dutta SK, Penney BE, Myrup AC, Robl MG, Rice RM. Disease features in horses with induced equine monocytic ehrlichiosis (Potomac horse fever).. Am J Vet Res 1988 Oct;49(10):1747-51.
        pubmed: 3189992
      10. Shankarappa B, Dutta SK, Sanusi J, Mattingly BL. Monoclonal antibody-mediated, immunodiagnostic competitive enzyme-linked immunosorbent assay for equine monocytic ehrlichiosis.. J Clin Microbiol 1989 Jan;27(1):24-8.
        pubmed: 2643624doi: 10.1128/jcm.27.1.24-28.1989google scholar: lookup
      11. Dutta SK, Rice RM, Hughes TD, Savage PK, Myrup AC. Detection of serum antibodies against Ehrlichia risticii in Potomac horse fever by enzyme-linked immunosorbent assay.. Vet Immunol Immunopathol 1987 Jan;14(1):85-92.
        pubmed: 3824902doi: 10.1016/0165-2427(87)90077-8google scholar: lookup

      Citations

      This article has been cited 6 times.
      1. Gibson KE, Pastenkos G, Moesta S, Rikihisa Y. Neorickettsia risticii surface-exposed proteins: proteomics identification, recognition by naturally-infected horses, and strain variations. Vet Res 2011 Jun 2;42(1):71.
        doi: 10.1186/1297-9716-42-71pubmed: 21635728google scholar: lookup
      2. Dutta SK, Vemulapalli R, Biswas B. Association of deficiency in antibody response to vaccine and heterogeneity of Ehrlichia risticii strains with Potomac horse fever vaccine failure in horses. J Clin Microbiol 1998 Feb;36(2):506-12.
        doi: 10.1128/JCM.36.2.506-512.1998pubmed: 9466767google scholar: lookup
      3. Kaylor PS, Crawford TB, McElwain TF, Palmer GH. Passive transfer of antibody to Ehrlichia risticii protects mice from ehrlichiosis. Infect Immun 1991 Jun;59(6):2058-62.
        doi: 10.1128/iai.59.6.2058-2062.1991pubmed: 2037365google scholar: lookup
      4. Dutta SK, Shankarappa B, Mattingly-Napier BL. Molecular cloning and analysis of recombinant major antigens of Ehrlichia risticii. Infect Immun 1991 Mar;59(3):1162-9.
        doi: 10.1128/iai.59.3.1162-1169.1991pubmed: 1997417google scholar: lookup
      5. Rikihisa Y. The tribe Ehrlichieae and ehrlichial diseases. Clin Microbiol Rev 1991 Jul;4(3):286-308.
        doi: 10.1128/CMR.4.3.286pubmed: 1889044google scholar: lookup
      6. Shankarappa B, Dutta SK, Mattingly-Napier B. Identification of the protective 44-kilodalton recombinant antigen of Ehrlichia risticii. Infect Immun 1992 Feb;60(2):612-7.
        doi: 10.1128/iai.60.2.612-617.1992pubmed: 1730496google scholar: lookup
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