Table 2.

Summary of the changes in microbial resident population observed in the different pathologic conditions and the underlying pathogenetic mechanisms.

	Change in microbial populations	Pathogenetic mechanisms involved
BPD	Decreased abundance of Lactobacillus, reduction in the bacterial community turnover with increasing time from birth, decreased colonization by Staphylococcus in the first days after birth, increased colonization by Ureaplasma	A decreased abundance of protective species allows a relative overgrowth of potentially pathogen microbial populations; moreover, Ureaplasma-colonized newborns present peripheral blood leukocytosis and less severe RDS but early radiographic and histologic changes typical of BPD
EUGR	Low diversity, persistent dominance of Enterobacteriaceae, and a paucity of strictly anaerobic taxa including Veillonella compared to infants with appropriate growth. Relative abundance of Klebsiella and Staphylococcus. Increased rate of Parabacteroides.	Nutritional efficacy is dramatically affected by infant dysbiosis. In particular, Parabacteroides produce acetic and propionic acid that reach the blood circulation, affecting the storage of sugar in muscle, liver, and fat; acetic acid is also involved in reduced food intake due to loss of appetite.
LOS	Decreased bacterial diversity with a predominance of Proteobacteria and Firmicutes, whereas Bifidobacteria are usually found in healthy controls. A strong relation with Fusobacteria and Tenericutes has also been described.	Gut microbiota can translocate across a dysfunctional or immature intestinal barrier, overwhelm neonatal immune system and cause sepsis; moreover, intestinal dysbiosis is supposed to alter local and systemic immune function. Natural prebiotics, such as raffinose, inhibit the growth of potentially pathogenic bacteria and promote proliferation of Bifidobacterium.
NEC	Decreased bacterial diversity with increased rate of Clostridia, Enterobacteriaceae, and Staphylococcus are frequently observed; a predominance of Proteobacteria (such as Escherichia coli and Klebsiella) is considered strictly associated with the pathogenesis of the disease.	Antibiotics pressure and enteral feeding generate changes in gut microbiota which may lead to an overgrowth of potential pathogens; moreover, LPS of Gram Negative activates TLR-4 and premature gut reacts with an exaggerated cytokine mediated inflammatory response, which may be due to a deficient expression of inhibitors of the NFkB pathway.

BPD, Bronchopulmonary Dysplasia; EUGR, Extra-Uterine Growth Restriction; LOS, Late-Onset sepsis; NEC, Necrotising Enterocolitis.