PMID- 10896393
OWN - NLM
STAT- MEDLINE
DCOM- 20001205
LR  - 20170214
IS  - 0300-9858 (Print)
IS  - 0300-9858 (Linking)
VI  - 37
IP  - 4
DP  - 2000 Jul
TI  - Vascular ultrastructure and DNA fragmentation in swine infected with Shiga 
      toxin-producing Escherichia coli.
PG  - 318-27
AB  - Shiga toxins (Stx) produced by Escherichia coli cause systemic vascular damage 
      that manifests as edema disease in swine and hemolytic uremic syndrome in humans. 
      In vitro, Stx inhibit protein synthesis and, depending on circumstances, induce 
      necrosis, apoptosis, or both. The mechanism of in vivo Stx-mediated vascular 
      damage is not known. The ability of Stx to cause apoptosis of vasculature in vivo 
      was studied in pigs with edema disease that was produced by oral inoculation with 
      Stx-producing E. coli. Arterioles of ileum and brain were evaluated by terminal 
      dUTP nick-end labeling (TUNEL) assay for DNA fragmentation in myocytes (10 
      infected pigs, 5 control pigs) and by transmission electron microscopy for 
      ultrastructural changes characteristic of apoptosis (17 infected pigs, 8 control 
      pigs). In comparison with controls, increased numbers of TUNEL-positive 
      arterioles were detected in 6/10 (60%) subclinically affected pigs 14-15 days 
      after inoculation. Ultrastructurally, lesions in myocytes consisted of lysis 
      (necrosis), with cytoplasmic debris and nuclear fragments contained between 
      intact basement membranes. Endothelial cell changes ranged from acute swelling to 
      necrosis and detachment from basement membrane. Subclinically affected pigs (n = 
      14) tended to have changes predominantly in myocytes, whereas pigs with clinical 
      illness (n = 3) more commonly had changes in endothelial cells. The arteriolar 
      lesions and clinical signs of edema disease are attributed to the effects of Stx 
      on vasculature. Therefore, our findings suggest that the Stx-induced arteriolar 
      lesions seen in this study were primarily necrotic, not apoptotic. We suspect 
      that necrosis was the principal cause of the DNA fragmentation detected.
FAU - Matise, I
AU  - Matise I
AD  - Veterinary Medical Research Institute, Iowa State University, Ames 50011, USA.
FAU - Sirinarumitr, T
AU  - Sirinarumitr T
FAU - Bosworth, B T
AU  - Bosworth BT
FAU - Moon, H W
AU  - Moon HW
LA  - eng
GR  - AI41328/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Vet Pathol
JT  - Veterinary pathology
JID - 0312020
RN  - 75757-64-1 (Shiga Toxin)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Arterioles/pathology
MH  - Blood Vessels/*pathology
MH  - *DNA Fragmentation
MH  - Edema/pathology/*veterinary
MH  - Escherichia coli Infections/pathology/*veterinary
MH  - In Situ Nick-End Labeling/veterinary
MH  - Microscopy, Electron/veterinary
MH  - *Shiga Toxin
MH  - Swine
MH  - Swine Diseases/*genetics/microbiology/*pathology
MH  - Vascular Diseases/pathology/*veterinary
EDAT- 2000/07/15 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/07/15 11:00
PHST- 2000/07/15 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/07/15 11:00 [entrez]
AID - 10.1354/vp.37-4-318 [doi]
PST - ppublish
SO  - Vet Pathol. 2000 Jul;37(4):318-27. doi: 10.1354/vp.37-4-318.