FECAL MICROFLORA IN A PATIENT WITH SHORT-BOWEL SYNDROME AND IDENTIFICATION OF DOMINANT LACTOBACILLI

Fecal microflora and lactate concentrations in blood and feces obtaine d from a patient (a 5 year-old boy) with short-bowel syndrome (SBS) we re compared during acidosis to results for the normal condition (no SB S symptoms), The taxonomical position of the lactobacilli found predom inantly in the feces sample obtained 2 days before the fifth attack wa s also studied, The D-lactate level in serum obtained 1 day after the fourth attack was 10-fold higher than that for the normal condition, a lthough there was not a great difference in L-lactate levels, D-Lactat e (3.91 mM) and L-lactate (2.86 mM) were also detected in the feces sa mples collected 2 days before the fifth attack, while no lactate was d etected in the feces sample for the normal condition, The counts of to tal fecal bacteria, especially anaerobic bacteria such as members of t he family Bacteroidaceae, were found to be low, The counts of lactobac illi and the total population of lactobacilli relative to total fecal bacteria in the feces 2 days before the fifth attack (40.4%) were extr emely high, In this case, a majority of the lactobacilli were D-lactat e producers as determined by homolactic fermentation, These lactobacil li were identified as Lactobacillus delbrueckii subsp, lactis, The per centages of bifidobacteria relative to total fecal bacteria in feces s amples obtained both 2 days before the fifth attack (50.9%) and for no rmal condition (61.9%) were also high, although these bacteria were L- lactate producers, In the feces samples for the normal condition, the D-lactate producers decreased to less than 10(9) per g, while the coun ts of L- or DL-lactate producers were 100-fold higher than the numbers in feces samples obtained 2 days before the fifth attack, These resul ts suggested that an increase in the level of D-lactate producers, suc h as L. delbnteckii subsp, lactis, in the colon may be associated with the clinical expression of metabolic acidosis.