• G P Bongaerts, J J Tolboom, A H Naber, W J Sperl, R S Severijnen, J A Bakkeren, and J L Willems.
• Department of Medical Microbiology, University Hospital Nijmegen Sint Radboud, The Netherlands.
• Microb. Pathog. 1997 May 1;22(5):285-93.

AbstractPreviously, we have demonstrated that short bowel syndrome (SBS) patients suffer daily from D-lactic acidemia; in these patients rather high amounts of (bacterial) D-lactate emerge in blood and urine with a circadian rhythm. The aim of this study was to establish the microbial basis of D-lactic acidemia in SBS. Therefore, faecal flora of (young and adult) SBS-patients was analysed qualitatively and quantitatively, and compared to that of controls. The isolated bacterial species were screened for massive D- and/or L-lactate production after in vitro growth. After introduction of oral feeding in SBS-infants shortly after the resection, lactobacilli increased from < or = 1% up to 60 +/- 5% of the faecal flora within 2-3 weeks. In the faeces of patients with oral feeding the lactate producers Lactobacillus acidophilus and Lactobacillus fermentum were the major resident bacteria (each with 10(10)-10(12) cfu/g faeces). During active growth in vitro these lactobacilli produced massive amounts of D- and L-lactic acid from glucose. Use of oral antibiotics in two SBS-children did not reduce the total numbers of lactobacilli, but caused shifts within the intestinal populations of at least lactobacilli. It is concluded that the strongly reduced intestinal capacity for carbohydrate absorption and the oral consumption of easily fermentable carbohydrates form the physiological basis for D-lactic acidemia in SBS, and that the fermentative D-lactate production by intestinal bacteria, especially the abundant, resident lactobacilli, forms its microbial basis. In these patients the antimicrobial and therapeutic effects of antibiotics are unpredictable.

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