JPC SYSTEMIC PATHOLOGY
DIGESTIVE SYSTEM
August 2018
D-B13

SIGNALMENT (JPC #1782684): 2-day-old piglet

HISTORY:  This animal had diarrhea.  There was 100% morbidity and 90% mortality in affected litters.

HISTOPATHOLOGIC DESCRIPTION:  Small intestine (multiple sections): Multifocally, intestinal villi are moderately blunted with sloughed and/or eroded enterocytes that are swollen and vacuolated (degenerate) or shrunken, with a scant amount of hypereosinophilic cytoplasm and a pyknotic nucleus (necrosis).  Subjacent to the mucosa within the lamina propria there are low to moderate numbers of neutrophils, fewer lymphocytes, hemorrhage, fibrin, and edema.  Small caliber vessels are expanded up to two times normal (congestion).  Multifocally crypts are expanded by necrotic cellular debris and few neutrophils (crypt abscesses) with mild crypt hyperplasia.  There are scattered aggregates of basophilic, 1x2 um bacilli on the surface of villar enterocytes.  There are variables amounts of amorphous, eosinophilic granular cellular and proteinaceous debris within the intestinal lumen.  Focally expanding the submucosa of the ileum are hypertrophic lymphoid follicles with germinal centers, upward of 2mm, which contain numerous tingible body macrophages (hyperplasia). Multifocally moderate numbers of neutrophils transmigrate the mucosal epithelium.  

MORPHOLOGIC DIAGNOSIS:  Small intestine: Enteritis, neutrophilic, acute, multifocal, moderate, with superficial bacilli, crypt abscesses, mild villar blunting, and lymphoid hyperplasia, porcine.

ETIOLOGIC DIAGNOSIS: Enteric colibacillosis

CAUSE:  Enterotoxigenic Escherichia coli

CONDITION: Enterotoxigenic colibacillosis

SYNONYMS:  ETEC, white scours, neonatal diarrhea, baby pig diarrhea, coliform scours, enterotoxigenic E. coli (ETEC)

GENERAL DISCUSSION:

PATHOGENESIS:

TYPICAL CLINICAL FINDINGS:

TYPICAL GROSS FINDINGS: 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

ULTRASTRUCTURAL FINDINGS:

DIFFERENTIAL DIAGNOSIS:

COMPARATIVE PATHOLOGY:

References:

  1. Fairbrother JM, Gyles CL. Escherichia coli In: Zimmerman JJ, Karriker LA, Ramirez A, Schwartz KJ, Stevenson GW, eds., eds. Diseases of Swine. 10th ed. Ames, IA: Blackwell Publishing; 2012:723-729.
  2. Gelberg HB. Alimentary system and the peritoneum, omentum, mesentery, and peritoneal cavity. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2017:333,376-377.
  3. Gyles C, Boerlin P. Horizontally transferred genetic elements and their role in pathogenesis of bacterial disease. Vet Pathol. 2014;51(2):328-340.
  4. Fulton RM, Boulianne M, et al. Bacterial diseases.  In: Boulianne M, ed.  Avian Disease Manual. 7th ed.  Jacksonville, FL: American Association of Avian Pathologists, Inc; 2013:87-89.
  5. Koenig A. Gram-negative bacterial infections. In: Greene CE, ed. Infectious Diseases of the Dog and Cat. 4th ed. St Louis, MO: W.B. Saunders Company; 2012:351-352.
  6. Radostits OM, Gay CC, Hinchcliff KW, Constable PD. Diseases caused by bacteria. In: Radostits OM, Gay CC, Blood DC, Constable PD. Veterinary Medicine, A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. 10th ed. Philadelphia, PA: W.B. Saunders Company Ltd; 2007:847-896.
  7. Uzal FA, Plattner BL, Hostetter JM. Alimentary system. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 2. 6th ed. Philadelphia, PA: Elsevier Saunders; 2016:112, 158-167.
  8. Zachary JF. Mechanisms of microbial infections. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2017:158-159.

 

E. coli subtypes Virulence Factors Examples

Attaching and effacing / enteropathogenic

 (AEEC, EPEC)

· Osmotic diarrhea

· Acute inflammatory response

· Structural cellular alterations; does NOT invade enterocytes

· Gross: granular and rough mucosa; hemorrhage and fibrin

· Ultrastructure: pedestal formation beneath attachment

· Locus for enterocyte effacement: pathogenicity island that controls attaching-effacing trait

· Fimbriae: P and S

·EPEC adherence factor

· Esp A/B/D- bacterial proteins exported via type III secretion system into the host cell; Esp-b & -D create pore in host membrane to introduce Tir (translocated-intimin-receptor protein)

·Tir “focuses” actinà forming “pedestal

· Intimin (bacterial outer membrane protein) binding to Tir (in host membrane) = Intimate Attachment

· Post weaning

· Diarrhea in rabbits, calves, pigs, lambs, dogs and humans

· Most often seen in calves with other enteropathogens such as Cryptosporidium parvum, ETEC, coronavirus, BVD, coccidian

·

Enterohemorrhagic (EHEC, VTEC: verotoxin-producing, STEC: Shiga toxin-producing)

· Acute inflammatory response

· Structural cellular alterations; invades enterocytes

· Targets colon

· Gross: granular and rough mucosa; hemorrhage and fibrin

· Ultrastructure: pedestal formation beneath attachment

· Shiga toxin or Shiga-like toxins

· Bind the host cell receptor globotriaosylceramide (Gb3)à inhibition of protein synthesis with subsequent necrosis

· Primarily affects intestinal epithelium and vascular endothelium, due to the presence of Gb3 receptors in these tissues

· Mucosal loss à lamina propria exposure à endotoxin (LPS) uptake

·Post weaning

· Lab animals, cattle, pigs, humans

· Fibrinohemorrhagic enterocolitis in calves (under 4-weeks old)

·Hemolytic uremic syndrome

· Greyhound: cutaneous/renal glomerular vasculopathy – associated with 0157:H7

· Edema disease: pigs few weeks after weaning; (F18ab fimbriae)à vasculitis & edema

Enterotoxigenic (ETEC)

·Secretory diarrhea

·Non-inflammatory

·Non-structural cellular alterations;  does NOT invade enterocytes

·No gross lesions

·Fimbriae:

· Heat-labile toxins: LTIà similar to cholera toxin; LTIIà cAMP pathwayà irreversible secretion of electrolytes (Cl- esp)/H2O in gutà secretory diarrhea

· Heat-stable toxins: STaà inhibition of Na/Cl co-transport and H2O absorption via ↑ in cGMP; STb (primarily associated with ETEC in pigs)à promotes secretion by stimulating prostaglandin E2 and 5-hydroxytrypamine

·<4 days old

· Secretory diarrhea in neonatal pigs, calves, lambs, and humans

· Common in pigs few hours to 1 week old

Enteroinvasive (EIEC)

·Enterocyte internalization à sepsis

·Invade intestinal enterocytes and disseminate throughout body

· Poorly documented in domestic animals

· Only confirmed experimentally in neonatal swine

· Results in septicemia with fibrinous arthritis, ophthalmitis, serositis, meningitis, white-spotted kidneys (cortical abscesses)

Edema disease, enterotoxemic colibacillosis (EDEC)

·Adhesion involved in diffuse adherence (AIDA) with F18

·Enteric colonization with Shiga-toxin ( or verotoxin 2e; Stx2e) producing E. coli and classic enterotoxemia à targets vascular endothelium

·Pigs: few weeks after weaning

· Endothelial injury of arterioles and arteries -> edema; neurologic signs due to brain edema, edema also in eyelids, gastric sub mucosa, gallbladder, and mesentery of spiral colon

Postweaning E. coli enteritis

·Gross: deep red gastric venous infarcts; congested flaccid small intestine

·  

· Possibly caused by classic enterotoxigenic F4 (K88) or hemolytic E. coli

·Piglets: First 1-2 weeks of weaning

Septicemic colibacillosis

· Generalized septicemia: enters via navel, upper respiratory tract, tonsil, intestine

·Enteritis not always present

·Colicin V (plasmid): encodes aerobactin: siderophore that helps survive in low iron environments, outer membrane protein to combat bactericidial components of serum, capsule to impede phagocytosis

·Calves; less common in others species

· Neonates most commonly affected

·Multisystemic disease in poultry


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