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The effect of E coli virulence on bacterial translocation and systemic sepsis in the neonatal rabbit model
R J Jackson1, S D Smith, R M Wadowsky
1University of Pittsburgh School of Medicine, PA.
Insights
Bacterial colonization in newborns can lead to gut translocation. However, only virulent E. coli strains caused systemic sepsis, highlighting bacterial virulence and host responses in neonatal infection development.
Area of Science:
- Neonatal surgery
- Infectious disease
- Gastroenterology
Background:
- Bacterial translocation and systemic infection in surgical neonates stem from gut colonization, weakened defenses, and barrier disruption.
- The newborn rabbit model mimics human development, including early gut closure to macromolecules and adaptable nutrition.
Purpose of the Study:
- To investigate bacterial translocation and systemic sepsis following colonization with virulent (K1) and avirulent (K100) Escherichia coli strains in newborn rabbits.
Main Methods:
- New Zealand white rabbit pups (2-5 days old) were colonized with K1 E. coli, K100 E. coli, or left uninoculated (controls).
- Mesenteric lymph nodes, liver, spleen, and colon were cultured 72 hours post-inoculation to assess bacterial translocation and systemic sepsis.
Main Results:
- Both K1 and K100 E. coli significantly increased translocation to the mesenteric lymph node (MLN) compared to controls.
- Only the virulent K1 E. coli strain significantly increased translocation to the liver and spleen, indicating systemic sepsis (67% vs. 0% for K100 and controls).
- Colonization alone did not result in systemic sepsis; progression depended on bacterial virulence and/or neonatal host responses.
Conclusions:
- Escherichia coli colonization in newborns promotes mesenteric lymph node translocation.
- Systemic sepsis development is contingent upon specific bacterial characteristics and/or the neonatal host's immune response.
- The newborn rabbit model is suitable for studying factors influencing bacterial translocation and sepsis in neonates.
Abstract:
In the surgical neonate, three factors that promote bacterial translocation and systemic infection are: (1) intestinal bacterial colonization and overgrowth; (2) compromised host defenses; and (3) disruption of the mucosal epithelial barrier. The newborn rabbit provides an excellent model to study these factors. Like the human, there is early closure of the gut mucosa to macromolecules, and nutrition can be maintained by breast or formula feeding. This study examines translocation and systemic sepsis after colonization with virulent K1 and avirulent K100 strains of Escherichia coli. New Zealand white rabbit pups (2 to 5 days old) were studied. The gastrointestinal tracts of 12 were colonized with K1 E coli; 14 were colonized with K100 E coli; 12 control animals were not inoculated. Mesenteric lymph node (MLN), liver, spleen, and colon homogenate were cultured 72 hours postinoculation. No bacteria were isolated from the colons of all but one control animal. Translocation or systemic sepsis did not occur. Translocation to the MLN was significantly increased (P less than .03) in K1 (50%) and K100 (36%) groups compared with controls (0%). Translocation to liver and spleen (systemic sepsis) was significantly increased (P less than .03) in K1 animals (67%) compared with K100 (0%) or controls (0%). Colonization by both strains of E coli led to translocation to the MLN, but only K1 E coli caused systemic sepsis. This suggests that although colonization by E coli in the newborn leads to translocation to the MLN, progression to systemic sepsis is the result of characteristics of the bacteria and/or neonatal host responses.