Lawsonia intracellularis infection and proliferative enteropathy in foals

Nicola Pusterla, Connie Gebhart

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Equine proliferative enteropathy (EPE) is a disease of foals caused by the obligate intracellular organism Lawsonia intracellularis. This organism is unique in that it causes proliferation of infected enterocytes, resulting in thickening of the intestinal epithelium, most often the small intestine. This disease affects mainly weanling foals and causes fever, lethargy, peripheral edema, diarrhea, colic and weight loss. The diagnosis of EPE may be challenging and relies on the presence of hypoproteinemia, thickening of segments of the small intestinal wall observed on abdominal ultrasonography, positive serology and molecular detection of L. intracellularis in feces. The epidemiology and genetic basis for pathogenesis for this disease is beginning to be elucidated. Phenotypic traits, genomic features, and gene expression profiles during L. intracellularis infection in vitro and in vivo are presented. In addition, this article reviews the epidemiology, pathological and clinicopathological findings, diagnosis, and control of EPE.

Original languageEnglish (US)
Pages (from-to)34-41
Number of pages8
JournalVeterinary Microbiology
Volume167
Issue number1-2
DOIs
StatePublished - Nov 29 2013

Fingerprint

Desulfovibrionaceae Infections
Lawsonia Bacteria
Lawsonia intracellularis
digestive system diseases
foals
Horses
horses
epidemiology
infection
Hypoproteinemia
Lethargy
Colic
Molecular Epidemiology
Enterocytes
colic
enterocytes
organisms
Serology
Intestinal Mucosa
intestinal mucosa

Keywords

  • Epidemiology
  • Equine proliferative enteropathy
  • Horse
  • Lawsonia intracellularis
  • Real-time PCR
  • Serology

ASJC Scopus subject areas

  • Microbiology
  • veterinary(all)

Cite this

Lawsonia intracellularis infection and proliferative enteropathy in foals. / Pusterla, Nicola; Gebhart, Connie.

In: Veterinary Microbiology, Vol. 167, No. 1-2, 29.11.2013, p. 34-41.

Research output: Contribution to journalArticle

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