Abnormal colonization of the GI tract, or an unfavorable
balance between commensal and pathogenic bacteria,
dysbiosis (an inappropriate composition of gut microflora),
are perhaps the most important triggers in the pathogenesis
of NEC. Preterm VLBW neonates may be particularly susceptible
to dysbiosis; studies have shown that preterm
neonates are at greater risk of developing an abnormal
intestinal colonization, secondary to contact with nosocomial
flora and frequent exposure to antibiotics in the
NICU.22 That fact that dysbiosis induces NEC was further
supported by studies on the inhibition of gastric acid by H2-
blockers which allows pathogenic bacteria to proliferate in
the GI tract, leading to neonatal NEC.