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Home / Equine Research Bank / Vet Res / Evidence of host adaptation in Lawsonia intracellularis infe...
Veterinary research2012; 43(1); 53; doi: 10.1186/1297-9716-43-53

Evidence of host adaptation in Lawsonia intracellularis infections.

Abstract: Lawsonia intracellularis is the causative agent of proliferative enteropathy, an endemic disease in pigs and an emerging concern in horses. Enterocyte hyperplasia is a common lesion in every case but there are differences regarding clinical and pathological presentations among affected species. We hypothesize that host susceptibility to L. intracellularis infection depends on the species of origin of the bacterial isolate. The objective of this study was to evaluate the susceptibilities of pigs and horses to L. intracellularis infection using either a porcine or an equine isolate. Methods: Twelve foals and eighteen pigs were equally divided into three groups and infected with either a porcine or an equine isolate (109L. Intracellularis/challenged animal), and a saline solution (negative control group). The animals were monitored regarding clinical signs, average of daily weight gain, fecal shedding of the bacteria by PCR and humoral serological response. Results: Foals infected with the equine isolate developed moderate to severe clinical signs and maintained a lower average of weight gain compared to control foals. Fecal quantitative PCR in equine isolate-infected foals revealed higher amounts of bacterial DNA associated with longer duration of shedding compared with porcine isolate-infected foals. All four foals infected with the equine isolate demonstrated higher IgG titers in the serum compared with porcine isolate-infected foals. In the pig trial, diarrhea and seroconversion were only observed in animals infected with the porcine isolate. Pathological changes typical of proliferative enteropathy were observed in the necropsied foal infected with equine isolate and in the two necropsied pigs infected with the porcine isolate. Conclusions: Evident clinical signs, longer periods of bacterial shedding and stronger serologic immune responses were observed in animals infected with species-specific isolates. These results show that host susceptibility is driven by the origin of the isolated L. intracellularis strain.
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Publication Date: 2012-06-20 PubMed ID: 22715937PubMed Central: PMC3443049DOI: 10.1186/1297-9716-43-53Google Scholar: Lookup
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Summary

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The research article investigates the host adaptation in Lawsonia intracellularis infections. The study provides evidence that the susceptibility of hosts (specifically pigs and horses) to L. intracellularis infection depends on whether the bacterial isolate comes from the same species.

Research Objective

The researchers aimed to examine the susceptibility of pigs and horses to L. intracellularis, by using either a porcine (pig) or an equine (horse) bacterial isolate. The study wanted to understand whether the species origin of the bacterial isolate influenced the host’s response to infection.

Methodology

  • Twelve horses and eighteen pigs were divided into three groups. Two groups were infected with either a pig or horse isolate of the bacteria, and the third group was administered a saline solution (control group).
  • The research team monitored clinical signs, daily weight gain average, bacteria fecal shedding through PCR testing, and humoral serological response.

Results

  • Horses infected with the horse-specific isolate showed moderate to severe clinical signs, experienced a lower average weight gain compared to control horses, and revealed a higher quantity of bacterial DNA with a longer duration of shedding.
  • All horses infected with the horse-specific isolate demonstrated higher IgG titers (an indication of the immune system’s response to infection) compared to those infected with the pig isolate.
  • For pigs, diarrhea and seroconversion (the time period during which a specific antibody develops and becomes detectable in the blood) occurred only in those animals infected with the pig isolate.
  • Post-mortem examinations showed that lesions typical of proliferative enteropathy (the disease caused by L. intracellularis) were observed only in animals infected with species-specific bacterial isolates.

Conclusions

The study provided evidence that there is a strong correlation between the origin of the bacterial isolate and its corresponding host’s susceptibility. This was demonstrated by more severe clinical signs, increased bacterial shedding duration, and stronger immune response observed in animals infected with species-specific isolates. These findings show that the susceptibilities of pigs and horses to L. intracellularis infection are driven by the species origin of the L. intracellularis strain.

Cite This Article

APA
Vannucci FA, Pusterla N, Mapes SM, Gebhart C. (2012). Evidence of host adaptation in Lawsonia intracellularis infections. Vet Res, 43(1), 53. https://doi.org/10.1186/1297-9716-43-53

Publication

Veterinary research
ISSN: 1297-9716
NlmUniqueID: 9309551
Country: England
Language: English
Volume: 43
Issue: 1
Pages: 53

Researcher Affiliations

Vannucci, Fabio A
  • Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St, Paul, MN, 55108, USA. vannu008@umn.edu.
Pusterla, Nicola
    Mapes, Samantha M
      Gebhart, Connie

        MeSH Terms

        • Animals
        • Bacterial Shedding
        • Desulfovibrionaceae Infections / immunology
        • Desulfovibrionaceae Infections / microbiology
        • Disease Susceptibility / immunology
        • Disease Susceptibility / microbiology
        • Disease Susceptibility / veterinary
        • Feces / microbiology
        • Horse Diseases / immunology
        • Horse Diseases / microbiology
        • Horses
        • Immunoenzyme Techniques / veterinary
        • Immunoglobulin G / blood
        • Intestinal Diseases / immunology
        • Intestinal Diseases / microbiology
        • Intestinal Diseases / veterinary
        • Lawsonia Bacteria / isolation & purification
        • Lawsonia Bacteria / physiology
        • Polymerase Chain Reaction / veterinary
        • Random Allocation
        • Species Specificity
        • Swine
        • Swine Diseases / immunology
        • Swine Diseases / microbiology

        References

        This article includes 34 references
        1. Gebhart CJ, Guedes RMC. Lawsonia intracellularis. Pathogenesis of Bacterial Infections in Animals 2010;pp. 503–509.
        2. Cooper DM, Swanson DL, Gebhart CJ. Diagnosis of proliferative enteritis in frozen and formalin-fixed, paraffin-embedded tissues from a hamster, horse, deer and ostrich using a Lawsonia intracellularis-specific multiplex PCR assay. Vet Microbiol 1997;54:47–62.
          doi: 10.1016/S0378-1135(96)01264-3pubmed: 9050170google scholar: lookup
        3. Lafortune M, Wellehan JF, Jacobson ER, Troutman JM, Gebhart CJ, Thompson MS. Proliferative enteritis associated with Lawsonia intracellularis in a Japanese macaque (Macaca fuscata). J Zoo Wildl Med 2004;35:549–552.
          doi: 10.1638/03-080pubmed: 15732600google scholar: lookup
        4. Lawson GH, Gebhart CJ. Proliferative enteropathy. J Comp Pathol 2000;122:77–100.
          doi: 10.1053/jcpa.1999.0347pubmed: 10684678google scholar: lookup
        5. Stämpfli H, Oliver OE. Chronic diarrhea and weight loss in three horses. Vet Clin N Am Equine Pract 2006;22:e27–e35.
          doi: 10.1016/j.cveq.2005.12.029pubmed: 16627092google scholar: lookup
        6. Frazer ML. Lawsonia intracellularis infection in horses: 2005–2007. J Vet Intern Med 2008;22:1243–1248.
          doi: 10.1111/j.1939-1676.2008.0160.xpubmed: 18681919google scholar: lookup
        7. Guimarães-Ladeira CV, Palhares MS, Oliveira JS, Ramirez MA, Guedes RM. Faecal shedding and serological cross-sectional study of Lawsonia intracellularis in horses in the state of Minas Gerais, Brazil. Equine Vet J 2009;41:593–596.
          doi: 10.2746/042516409X407639pubmed: 19803056google scholar: lookup
        8. Lavoie JP, Drolet R. Equine proliferative enteropathy: an emerging disease of foals. Equine Vet Educ 2009;21:183–185.
          doi: 10.2746/095777309X408858google scholar: lookup
        9. Klein EC, Gebhart CJ, Duhamel GE. Fatal outbreaks of proliferative enteritis caused by Lawsonia intracellularis in young colony-raised rhesus macaques. J Med Primatol 1999;28:11–18.
          doi: 10.1111/j.1600-0684.1999.tb00084.xpubmed: 10372536google scholar: lookup
        10. Jacoby RO. Transmissible ileal hyperplasia of hamsters. I. Histogenesis and immunocytochemistry. Am J Pathol 1978;91:433–450.
          pmc: PMC2018310pubmed: 655259
        11. Guedes RM, Gebhart CJ. Comparison of intestinal mucosa homogenate and pure culture of the homologous Lawsonia intracellularis isolate in reproducing proliferative enteropathy in swine. Vet Microbiol 2003;93:159–166.
          doi: 10.1016/S0378-1135(03)00013-0pubmed: 12637004google scholar: lookup
        12. Pusterla N, Wattanaphansak S, Mapes S, Collier J, Hill J, Difrancesco M, Gebhart C. Oral infection of weanling foals with an equine isolate of Lawsonia intracellularis, agent of equine proliferative enteropathy. J Vet Intern Med 2010;24:622–627.
          doi: 10.1111/j.1939-1676.2010.0482.xpubmed: 20337907google scholar: lookup
        13. Jasni S, McOrist S, Lawson GH. Reproduction of proliferative enteritis in hamsters with a pure culture of porcine ileal symbiont intracellularis. Vet Microbiol 1994;41:1–9.
          doi: 10.1016/0378-1135(94)90130-9pubmed: 7801512google scholar: lookup
        14. Smith DG, Mitchell SC, Nash T, Rhind S. Gamma interferon influences intestinal epithelial hyperplasia caused by Lawsonia intracellularis infection in mice. Infect Immun 2000;68:6737–6743.
          doi: 10.1128/IAI.68.12.6737-6743.2000pmc: PMC97774pubmed: 11083789google scholar: lookup
        15. Vannucci FA, Borges EL, de Oliveira JS, Guedes RM. Intestinal absorption and histomorphometry of Syrian hamsters (Mesocricetus auratus) experimentally infected with Lawsonia intracellularis. Vet Microbiol 2010;145:286–291.
          doi: 10.1016/j.vetmic.2010.03.027pubmed: 20418028google scholar: lookup
        16. Guedes RM, Gebhart CJ. Onset and duration of fecal shedding, cell-mediated and humoral immune responses in pigs after challenge with a pathogenic isolate or attenuated vaccine strain of Lawsonia intracellularis. Vet Microbiol 2003;91:135–145.
          doi: 10.1016/S0378-1135(02)00301-2pubmed: 12458163google scholar: lookup
        17. Wattanaphansak S, Gebhart C, Olin M, Deen J. Measurement of the viability of Lawsonia intracellularis. Can J Vet Res 2005;69:265–271.
          pmc: PMC1250238pubmed: 16479724
        18. Lawson GH, McOrist S, Jasni S, Mackie RA. Intracellular bacteria of porcine proliferative enteropathy: cultivation and maintenance in vitro. J Clin Microbiol 1993;31:1136–1142.
          pmc: PMC262892pubmed: 8501214
        19. Beckler DC, Kapur V, Gebhart CJ. Molecular epidemiologic typing of Lawsonia intracellularis. Proceedings of the Conference of Research Workers in Animal Disease 2004;p. 124.
        20. Pusterla N, Mapes S, Rejmanek D, Gebhart C. Detection of Lawsonia intracellularis by real-time PCR in the feces of free-living animals from equine farms with documented occurrence of equine proliferative enteropathy. J Wildl Dis 2008;44:992–998.
          pubmed: 18957657
        21. Guedes RM, Gebhart CJ, Deen J, Winkelman NL. Validation of an immunoperoxidase monolayer assay as a serologic test for porcine proliferative enteropathy. J Vet Diagn Investig 2002;14:528–530.
          doi: 10.1177/104063870201400618pubmed: 12423042google scholar: lookup
        22. Mapes S, Rhodes DM, Wilson WD, Leutenegger CM, Pusterla N. Comparison of five real-time PCR assays for detecting virulence genes in isolates of Escherichia coli from septicaemic neonatal foals. Vet Rec 2007;161:716–718.
          doi: 10.1136/vr.161.21.716pubmed: 18037693google scholar: lookup
        23. Luna LC. Manual of Histologic Staining. Methods of the Armed Forces Institute of Pathology. 1968;p. 258.
        24. Guedes RM, Gebhart CJ. Preparation and characterization of polyclonal and monoclonal antibodies against Lawsonia intracellularis. J Vet Diagn Investig 2003;15:438–446.
          doi: 10.1177/104063870301500506pubmed: 14535543google scholar: lookup
        25. Jacoby RO, Osbaldiston GW, Jonas AM. Experimental transmission of atypical ileal hyperplasia of hamsters. Lab Anim Sci 1975;25:465–473.
          pubmed: 1097824
        26. Guedes RM, Winkelman NL, Gebhart CJ. Relationship between the severity of porcine proliferative enteropathy and the infectious dose of Lawsonia intracellularis. Vet Rec 2003;153:432–433.
          doi: 10.1136/vr.153.14.432pubmed: 14582733google scholar: lookup
        27. McOrist S, Smith SH, Shearn MF, Carr MM, Miller DJ. Treatment and prevention of porcine proliferative enteropathy with oral tiamulin. Vet Rec 1996;139:615–618.
          pubmed: 9123785
        28. Guedes RM, França SA, Machado GS, Blumer MA, da Costa Cruz EC. Use of tylvalosin-medicated feed to control porcine proliferative enteropathy. Vet Rec 2009;165:342–345.
          doi: 10.1136/vr.165.12.342pubmed: 19767637google scholar: lookup
        29. Murakata K, Sato A, Yoshiya M, Kim S, Watarai M, Omata Y, Furuoka H. Infection of different strains of mice with Lawsonia intracellularis derived from rabbit or porcine proliferative enteropathy. J Comp Pathol 2008;139:8–15.
          doi: 10.1016/j.jcpa.2008.03.001pubmed: 18479698google scholar: lookup
        30. Go YY, Lee JK, Ye JY, Lee JB, Park SY, Song CS, Kim SK, Choi IS. Experimental reproduction of proliferative enteropathy and the role of IFN-gamma in protective immunity against Lawsonia intracellularis in mice. J Vet Sci 2005;6:357–359.
          pubmed: 16294002
        31. Viott A, Vannucci F, Oliveira J, Costa M, Gebhart C, Guedes R. Susceptibility of different mouse strains to Lawsonia intracellularis infection using intestinal mucosa homogenate and pure culture. Proceedings of the 21st Congress of International Pig Veterinary Society 2010.
        32. McOrist S, Morgan J, Veenhuizen MF, Lawrence K, Kroger HW. Oral administration of tylosin phosphate for treatment and prevention of proliferative enteropathy in pigs. Am J Vet Res 1997;58:136–139.
          pubmed: 9028475
        33. Collins AM, Fell S, Pearson H, Toribio JA. Colonisation and shedding of Lawsonia intracellularis in experimentally inoculated rodents and in wild rodents on pig farms. Vet Microbiol 2011;150:384–388.
          doi: 10.1016/j.vetmic.2011.01.020pubmed: 21349664google scholar: lookup
        34. Cooper DM, Swanson DL, Barns SM, Gebhart CJ. Comparison of the 16S ribosomal DNA sequences from the intracellular agents of proliferative enteritis in a hamster, deer, and ostrich with the sequence of a porcine isolate of Lawsonia intracellularis. Int J Syst Bacteriol 1997;47:635–639.
          doi: 10.1099/00207713-47-3-635pubmed: 9226893google scholar: lookup
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