Aberrant Ex Vivo Clot Characteristics in a Swine Model of E coli Sepsis-Induced Coagulopathy

Sunday, March 22, 2026

2:30 PM - 3:30 PM Central Time

Location: Connections Central - RST 12

LG

Luis A. Gardea, BS (he/him/his)

Baylor College of Medicine

Disclosure(s): No relevant financial relationship(s) to disclose.
AS

Arun Saini, MD, MS, FCCM

Baylor College of Medicine at Texas Childrens Hospital

Disclosure(s): No relevant financial relationship(s) to disclose.
RF

Ryan Fleischmann, BS

Associate Laboratory Director
Bayor College of Medicine

Disclosure information not submitted.
JC

Justin Courson, PhD

Instructor
Baylor College of Medicine

Disclosure information not submitted.
SR

Stefanie Rivera, BS

Research Technician
Baylor College of Medicine

Disclosure information not submitted.
BS

Brooks Scull, PhD

Laboratory Director
Baylor College of Medicine

Disclosure information not submitted.
MM

Marina Martinez-vargas, PhD

Instructor
Baylor College of Medicine

Disclosure information not submitted.
VV

Vinod Vijayan, PhD

Associate Professor
Baylor College of Medicine

Disclosure information not submitted.
KT

Katri Typpo, Select Member MD (she/her/hers)

Baylor College of Medicine

Disclosure information not submitted.
CA

Carl Allen, MD PhD

Professor
Baylor College of Medicine

Disclosure information not submitted.
MC

Miguel Cruz, PhD

Professor
Baylor College of Medicine

Disclosure information not submitted.
TN

Trung Nguyen, MD

Associate Professor
Baylor College of Medicine Texas Children's Hospital

Disclosure information not submitted.

Introduction: Sepsis-induced coagulopathy (SIC) increases morbidity and mortality, with no specific therapies available beyond supportive care. Developing large animal pediatric models is crucial for understanding mechanisms and testing new treatments. We present data on a pediatric swine model of SIC induced by Escherichia coli (E. coli). We hypothesize that piglets with SIC post-E. coli inoculation will show abnormal ex- vivo clot characteristics compared to their pre-sepsis state.

Methods: Eight 4-week-old piglets were implanted with jugular and carotid catheters and a telemetry device in a femoral artery for continuous hemodynamic monitoring. Four days later, each piglet was injected with human pathogenic E. coli in 8 different doses, ranging from 0.5e5 to 3e8 CFU/kg I.V. We measured fibrin polymerization (FP) using a turbidity assay and clot structure via confocal and electron microscopy in platelet-poor plasma obtained at pre-, and 48 or 70h post-E. coli inoculation or when criteria for early euthanasia were met.

Results: Out of 8 piglets, 2 piglets met early euthanasia criteria at 48 and 60h, and 6 piglets were analyzed through 70h. We found increased maximum FP (mean absorbance (405 nm) of 0.27+/- 0.07 vs. 0.17 +/- 0.04, n=8, p < 0.0001, paired t-test) and decrease in platelet count (492X10^3 per mm +/- 70 vs. 334X10^3/mm, n =8, p =0.01, paired t-test) post sepsis compared to pre-sepsis baseline. Two piglets who received the highest dosing, 0.5e8 and 3e8 CFU/kg E. coli, developed SIC, whereas the others did not. In the piglet with SIC (3e8 CFU/kg dose), electron microscopy revealed a denser fibrin mesh with irregular fibrin fibers, contrasting with the pre-sepsis baseline, where the mesh was less dense and the fibrin fibers were smoother. Moreover, tissue histopathologic evaluation showed disseminated microvascular thrombi and necrosis of the renal and hepatic parenchyma.

Conclusions: In our swine E. coli SIC model, we demonstrated aberrant ex vivo clot characteristics, including increased clot formation and dense clot structure with histopathological evidence of microvascular thrombi and necrosis in the liver and kidneys. This swine model will help elucidate the mechanisms of SIC, differences in host-pathogen (gram -ve vs. +ve bacteria) interaction, and response to novel therapeutic interventions.