Equis ISSN 2398-2977

Intestine: enteropathy - proliferative

Synonym(s): Proliferative enteropathy

Contributor(s): Debbie Archer, Uneeda K Bryant, Catriona Mackenzie

Introduction

  • Cause: Lawsonia intracellularis Lawsonia intracellularis.
  • Signs: ill thrift, diarrhea, fever, anorexia, ventral edema, lethargy, colic, weight loss (non-specific signs).
  • Diagnosis: serology, molecular biology, bacteriology, immunohistochemistry, histopathology, ultrasonography.
  • Treatment: antimicrobials (such as oxytetracycline or erythromycin +/- rifampin, colloids, plasma, intravenous fluids, gastroprotectants.
  • Prognosis: good when the disease is diagnosed early and treated aggressively.

Pathogenesis

Etiology

  • Lawsonia intracellularis Lawsonia intracellularis.
  • Obligate intracellular bacilli.
  • Gram-negative.
  • Curved (comma-shaped), vibrioid or straight with tapered ends.
  • Trilaminar cell wall.
  • Argyrophilic (positive silver staining Warthin-Starry and Steiner's).
  • Requires specialized cell cultures (cell dependent) and media for bacterial growth.
  • Acid-fast by modified Ziehl-Neelson method Staining techniques: Modified Ziehl-Neelson stain.
  • Identifiable in cell cultures with the use of IG4 Lawsonia-specific monoclonal antibody immunostain.

Predisposing factors

General

  • Weaning.
  • Stress, eg shipping/transportation and overcrowding.
  • Immunodeficiency.
  • Introduction of new animals.
  • Endoparasitism.

Pathophysiology

  • L. intracellularis ingested via fecal/oral route → bacteria comes into contact with intestinal surface epithelium → bacteria enters the intestinal cell/enterocyte via endocytosis which forms a vacuole → bacteria within vacuole are released into the apical cytoplasm of enterocytes → bacteria replicate within the cytoplasm of naturally rapid dividing crypt epithelial cells → infected crypt epithelial cells undergo further proliferation and hyperplasia with lack of cellular maturation and microvilli formation →  hyperplastic immature crypt epithelial cells replace mature microvillous containing epithelial cells → resulting in mucosal hypertrophy, malabsorptive diarrhea, and subsequent hyoproteinemia.

Timecourse

  • 2-3 weeks is the incubation period in swine and has been the hypothesized incubation period in horses and other affected species.
  • Peak infection in cell cultures have been reported between 1-5 days after initial infection.

Epidemiology

  • Reports of sporadic cases and outbreaks have been described.
  • Seasonal occurence which varies year to year and by geographical region (typically most frequent between August and late February in the UK and Ireland).
  • Exposure to pigs not commonly reported - the bacterial strain that infects foals differs from the strain that causes disease in pigs.
  • Numerous species can be infected and species specificity of the bacterial strains is thought to play a role in the development of immune responses and clinical disease.
  • A variety of wild species, eg rabbits, foxes and deer, can act as a reservoir for infection.
  • Ingestion of infected fecal material from wild or domestic animals is likely to be the main route of infection in foals.
  • Clinically affected foals can also shed bacteria in their feces and infect other foals.
  • Exposure to the bacteria is very common, however clinical disease tends to only affect individuals or a small number of animals from a group.
  • The individuals immune response (in particular the cell mediate immune response) is very important in preventing clinical disease.
  • L. intracellularis has been shown to survive in the environment for approximately 2 weeks.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Pusterla N & Gebhart C J (2013) Equine proliferative enteropathy - a review of recent developments. Equine Vet J 45 (4), 403-409 PubMed.
  • Allen K J, Pearson G R, Fews D, McOrist S & Brazil T J (2009) Lawsonia intracellularis proliferative enteropathy in a weanling foal, with a tentative histological diagnosis of lymphocytic plasmacytic enteritis. Equine Vet Educ 21 (8), 411-414 VetMedResource.
  • Lavoie J-P & Drolet R (2009) Equine proliferative enteropathy: An emerging disease of foals. Equine Vet Educ 21 (4), 183-185 VetMedResource.
  • Frazer M L (2008) Lawsonia intracellularis infection in horses: 2005-2007. J Vet Intern Med 22 (5), 1243-1248 PubMed.
  • Pusterla N, Higgins J C, Smith P, Mapes S & Gebhart C (2008) Epidemiological survey on rarms with documented occurrence of equine proliferative enteropathy due to Lawsonia intracellularis. Vet Rec 163 (5), 156-158 PubMed.
  • McGurrin M K J, Vengust M, Arroyo L G & Baird J D (2007) An outbreak of Lawsonia intracellularis infection in a Standardbred herd. Can Vet J 49 (9), 927-930 PubMed.
  • Atherton R P & McKenzie III H C (2006) Alternative antimicrobials agents in the treatment of proliferative enteropathy in horses. J Equine Vet Sci 26 (11), 535-541 VetMedResource.
  • Guedes R M C, Gebhart C J, Winkelman N L & Mackie-Nuss R A (2002) A comparative study of an indirect fluorescent antibody test and an immunoperoxidase monolayer assay for the diagnosis of porcine proliferative enteropathy. J Vet Diag Invest 14 (5), 420-423 PubMed.
  • Williams N M, Harrison L R & Gebhart C J (1996) Proliferative enteropathy in a foal caused byLawsonia intracellularis-like bacterium. J Vet Diag Invest 8 (2), 254-256 PubMed.

Other sources of information

  • Smith B P (2009) Large Animal Internal Medicine. 4th edn. pp 728-729.
  • Jubb, Kennedy & Palmer (2007) Pathology of Domestic Animals. 5th edn. Vol. 2. pp 133, 206 & 208.
  • Brenner D J, Krieg N R & Staley J R (2005) Bergeys Manual of Systematic Bacteriology. 2nd edn. Vol. 2. pp 940-943.
  • Reed S M, Bayly W M & Sellon D C (2004) Equine Internal Medicine. 2nd edn. pp 879-880, 882-883, 891-893 & 905.


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