CLOSTRIDIAL PATHOGENICITY IN EXPERIMENTAL NECROTIZING ENTEROCOLITIS IN GNOTOBIOTIC QUAILS AND PROTECTIVE ROLE OF BIFIDOBACTERIA

The pathogenesis of neonatal necrotising enterocolitis (NEC) remains u nclear. Gnotobiotic quails fed a lactose diet have been used to invest igate the role of clostridial strains originating from faecal specimen s of neonates through the intestinal lesions, the changes in microflor a balance and the production of bacterial metabolites, i.e., short-cha in fatty acids and hydrogen. Bifidobacteria are thought to exert vario us beneficial effects on host health, including interaction with the c olonic microflora. Therefore, it was hypothesised that a protective ro le could be exercised through bidifobacterial colonisation. A Clostrid ium butyricum strain (CB 155-3) and a whole faecal flora including thr ee clostridial species (C. butyricum, C. perfringens, C. difficile), e ach from premature infants suffering from NEC, caused caecal lesions i n quails similar to those observed in man, i.e., thickening of the cae cal wall with gas cysts, haemorrhagic ulceration and necrotic areas. C onversely, a whole faecal flora including bifidobacteria (identified a s Bifidobacterium pseudo-catenulatum) and no clostridia, isolated from a healthy premature infant, was unable to produce NEC-like lesions. W hen the two clostridial groups were associated with a Bifidobacterium strain (B. infantis-longum, CUETM 89-215, isolated from a healthy infa nt), bifidobacterial colonisation suppressed all pathological lesions. This study is the first demonstration of a protective role for via C. butyricum bifidobacteria against NEC the inhibition of growth of or t he disappearance of C. perfringens. C. difficile was not found to be r esponsible for the aetiology of the caecal lesions in quails. The main effect of bifidobacteria on lactose fermentation was either a dramati c decrease or a disappearance of butyric acid. The protective role was not associated with changes in H-2 production. Therefore, a new step between colonic colonisation and its relevance to NEC is thought to in volve the fermentation of unabsorbed lactose into butyric acid at the onset of the disease.