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Veterinary immunology and immunopathology1998; 59(3-4); 239-251; doi: 10.1016/s0165-2427(97)00074-3

Serum and mucosal antibody isotype responses to M-like protein (SeM) of Streptococcus equi in convalescent and vaccinated horses.

Abstract: Equine strangles, caused by the clonal pathogen Streptococcus equi, is a source of serious economic loss despite the widespread use of commercial vaccines. The anti-phagocytic 58 kDa M-like protein (SeM) is an important protective antigen. The objective of this study was to define differences, if any, between SeM-specific convalescent serum and mucosal IgA and IgG subisotypes and those induced by vaccination with commercial strangles vaccine. SeM-specific opsonophagocytic IgGb was the predominant serum antibody in horses intramuscularly vaccinated or recently recovered from infection. Infection also induced high levels of specific opsonophagocytic serum IgGa during and shortly after S. equi infection whereas vaccination stimulated only low levels of serum IgGa. Specific serum IgGc and opsonophagocytic IgA were present at very low levels following infection or vaccination. A strong specific mucosal antibody response occurred during the acute and convalescent phases of infection whereas vaccinated horses made no mucosal response. Specific IgGb was generally predominant in nasopharyngeal washings during the acute phase but was replaced by specific IgA during convalescence. SeM-specific mucosal IgGa and IgG(T) but not IgGc were detected only during the acute and early convalescent phase. The results therefore indicate that vaccination, although inducing SeM-specific serum isotype responses qualitatively and quantitatively similar to those seen in convalescence, did not induce mucosal responses. This suggests that mucosal immunity may be important in acquired resistance to strangles.
Publication Date: 1998-02-27 PubMed ID: 9477475DOI: 10.1016/s0165-2427(97)00074-3Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't
  • Research Support
  • U.S. Gov't
  • Non-P.H.S.

Summary

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The research article focuses on comparing the antibody response against equine strangles in horses that have recovered from infection and those vaccinated against it. The study finds that while the commercial vaccine stimulates similar serum antibody responses, it does not trigger a mucosal response, suggesting the importance of mucosal immunity in resistance against the disease.

Objective

The primary objective of this study was to understand the various differences between the Streptococcus equi-specific antibody responses in convalescent, or recovered, horses and those vaccinated with a commercial strangles vaccine.

Methodology

  • The researchers focused on the M-like protein (SeM) of Streptococcus equi. The protein is anti-phagocytic and serves as an important protective antigen.
  • The researchers assessed the presence and levels of IgA and IgG sub-antibodies in the serum and mucosal samples from both vaccinated and convalescent horses. They were particularly interested in specific serum IgGc and opsonophagocytic IgA levels.

Results

  • The results indicated that specific opsonophagocytic IgGb was the predominant antibody in horses vaccinated intramuscularly and those recently recovered from infection.
  • The infections also triggered high levels of specific opsonophagocytic serum IgGa during and shortly after infection, while vaccination stimulated only low-level serum IgGa.
  • Very low levels of specific serum IgGc and opsonophagocytic IgA were present post-infection or vaccination.
  • Interestingly, during the acute and convalescent phases of infection, a significant mucosal antibody response was noted. This was not practiced in vaccinated horses.
  • IgGb was generally predominant in the nasopharyngeal washings during the acute phase but was replaced by specific IgA during convalescence.

Conclusion

In a nutshell, the findings revealed that while vaccination induces SeM-specific serum isotype responses similar to those seen in convalescence, it failed to stimulate mucosal responses. This observation is significant as it indicates the potentially essential role of mucosal immunity in the acquired resistance to equine strangles, a disease that continues to cause significant economic losses in the equine industry, despite the availability of commercial vaccines.

Cite This Article

APA
Sheoran AS, Sponseller BT, Holmes MA, Timoney JF. (1998). Serum and mucosal antibody isotype responses to M-like protein (SeM) of Streptococcus equi in convalescent and vaccinated horses. Vet Immunol Immunopathol, 59(3-4), 239-251. https://doi.org/10.1016/s0165-2427(97)00074-3

Publication

ISSN: 0165-2427
NlmUniqueID: 8002006
Country: Netherlands
Language: English
Volume: 59
Issue: 3-4
Pages: 239-251

Researcher Affiliations

Sheoran, A S
  • Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington 40546-0099, USA.
Sponseller, B T
    Holmes, M A
      Timoney, J F

        MeSH Terms

        • Animals
        • Antibodies, Bacterial / biosynthesis
        • Bacterial Vaccines / administration & dosage
        • Convalescence
        • Horse Diseases / immunology
        • Horse Diseases / microbiology
        • Horses
        • Immunity, Mucosal
        • Immunoglobulin A / biosynthesis
        • Immunoglobulin G / biosynthesis
        • Immunoglobulin Isotypes / immunology
        • Nasal Mucosa / immunology
        • Opsonin Proteins / immunology
        • Phagocytosis
        • Streptococcal Infections / immunology
        • Streptococcal Infections / veterinary
        • Streptococcus equi / immunology

        Citations

        This article has been cited 11 times.
        1. Delph KM, Beard LA, Trimble AC, Sutter ME, Timoney JF, Morrow JK. Strangles, convalescent Streptococcus equi subspecies equi M antibody titers, and presence of complications.. J Vet Intern Med 2019 Jan;33(1):275-279.
          doi: 10.1111/jvim.15388pubmed: 30520521google scholar: lookup
        2. Wimer CL, Schnabel CL, Perkins G, Babasyan S, Freer H, Stout AE, Rollins A, Osterrieder N, Goodman LB, Glaser A, Wagner B. The deletion of the ORF1 and ORF71 genes reduces virulence of the neuropathogenic EHV-1 strain Ab4 without compromising host immunity in horses.. PLoS One 2018;13(11):e0206679.
          doi: 10.1371/journal.pone.0206679pubmed: 30440016google scholar: lookup
        3. Boyle AG, Timoney JF, Newton JR, Hines MT, Waller AS, Buchanan BR. Streptococcus equi Infections in Horses: Guidelines for Treatment, Control, and Prevention of Strangles-Revised Consensus Statement.. J Vet Intern Med 2018 Mar;32(2):633-647.
          doi: 10.1111/jvim.15043pubmed: 29424487google scholar: lookup
        4. Velineni S, Timoney JF. Characterization and protective immunogenicity of the SzM protein of Streptococcus zooepidemicus NC78 from a clonal outbreak of equine respiratory disease.. Clin Vaccine Immunol 2013 Aug;20(8):1181-8.
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        5. Fulde M, Rohde M, Polok A, Preissner KT, Chhatwal GS, Bergmann S. Cooperative plasminogen recruitment to the surface of Streptococcus canis via M protein and enolase enhances bacterial survival.. mBio 2013 Mar 12;4(2):e00629-12.
          doi: 10.1128/mBio.00629-12pubmed: 23481605google scholar: lookup
        6. Lewis MJ, Wagner B, Irvine RM, Woof JM. IgA in the horse: cloning of equine polymeric Ig receptor and J chain and characterization of recombinant forms of equine IgA.. Mucosal Immunol 2010 Nov;3(6):610-21.
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        9. Morton HC, Pleass RJ, Storset AK, Brandtzaeg P, Woof JM. Cloning and characterization of equine CD89 and identification of the CD89 gene in chimpanzees and rhesus macaques.. Immunology 2005 May;115(1):74-84.
        10. Flock M, Jacobsson K, Frykberg L, Hirst TR, Franklin A, Guss B, Flock JI. Recombinant Streptococcus equi proteins protect mice in challenge experiments and induce immune response in horses.. Infect Immun 2004 Jun;72(6):3228-36.
        11. Hooper-McGrevy KE, Wilkie BN, Prescott JF. Immunoglobulin G subisotype responses of pneumonic and healthy, exposed foals and adult horses to Rhodococcus equi virulence-associated proteins.. Clin Diagn Lab Immunol 2003 May;10(3):345-51.