Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:The effect of E coli virulence on bacterial translocation and systemic sepsis in the neonatal rabbit model. 205 12

Preterm infants and infants unable to breast feed are particularly susceptible to gut origin sepsis. Many studies have shown the benefits of breast milk in decreasing the incidence of bacterial infections in neonates. Little in vivo work has focused on prevention of neonatal gut origin sepsis with breast milk components. The aim of this study was to determine whether supplementation of a standard neonatal formula with exogenous, luminally administered, human secretory IgA protects against gut origin sepsis in a newborn rabbit model. Sixty New Zealand white rabbit pups were delivered by cesarean section 1 day preterm and divided into two groups--the IgA group (n = 26) and the non-IgA group (n = 34). Animals were gavage-fed a standard artificial formula (KMR) twice daily. The IgA group was supplemented on days 3 and 4 with 6.25 mg/kg of human secretory IgA. The non-IgA group received an equal volume of saline. On the evening of day 3, the animals were orally challenged with Escherichia coli K100. The quantity of bacteria that colonized the cecum was similar in the two groups. The quantity of bacteria that translocated to the mesenteric lymph node, liver, and spleen was significantly lower in the IgA group (P < .05). The incidence of translocation to the organs was also significantly lower in the IgA group (P < .05). The exogenous secretory IgA showed specificity to E coli K100 by ELISA. These data show that neonatal formula supplemented with human secretory IgA decreases the incidence and quantity of bacterial translocation of E coli K100 in a neonatal rabbit model.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The protective role of enteral IgA supplementation in neonatal gut origin sepsis. 773 44