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There are two aspects about the presence of Candidain the human orointestinal tract: (i) it is a part of normal human flora and (ii) it is a risk factor for immunocompromised patients. The orointestinal tract can be considered a reservoir for Candidaspecies, several of which are from the oral cavity, stomach, duodenal juice and faeces. Their germ counts in normal small and large bowel do not exceed 104cfu/ml resp. g. The input of Candidato a well-developed faecal flora system under continuous flow culture conditions did not lead to a multiplication of the yeast. The take in of faecal flora into a Candidacontinuous flow culture diminish Candidagerm counts. If, however, the faecal flora was destroyed, e.g. by antibiotics, we found the yeasts multiplying, with the formation of germ tubes and mycelial structures. Colonization by Candidahas to be seen as a starting-point of the development of subsequent candidosis in immunosuppressed or intensive care patients. The best protection against Candidacolonization in the gut is the existence of a normal bacterial flora. Lactulose, which promotes the Gram-positive potential of faecal flora, may protect indirectly by supporting the indigenous flora.

In continuous-flow culture, long generation times and high bacterial counts favour survival of bacteria. A chemotherapeutic agent that achieves a bactericidal effect under these circumstances can therefore be seen as highly effective. In our continuous-flow culture we obtained bactericidal effects with ciprofloxacin 1-2 mg/L, cefotaxime 4 mg/L and mezlocillin 32 mg/L. These effects were seen irrespective of whether conditions were aerobic or anaerobic. There were no significant differences between monocultures and mixed cultures simulating faecal flora with the various Escherichia coli strains tested. Cefotaxime had an initial effect but an increase in counts was then observed as a result of regrowth of E. coli survivor strains in aerobic monoculture and mixed cultures. Mezlocillin was completely bactericidal in monocultures, but regrowth occurred in mixed cultures under anaerobic conditions. Neither the bacterial composition of this culture nor the resistance pattern explained this regrowth. These results were observed in long-term experiments followed for up to 7 days. We conclude that the antibiotics tested are highly effective against E. coli under unfavourable conditions simulating in-vivo situations.

Summary Microecological problems have escalated recently in clinical medicine. We studied the microecology of the upper small bowel. Duodenal flora was examined, displaying microbial growth in 90.8% of the 400 patients examined. The microflora was classified according to germ quality into definite types of colonization. Frequency of microbial colonization is normally 36.7% and 63.3% by overgrowth, indicating differing dysbioses. Simulation of microbial overgrowth in the duodenum is possible with a continuous-flow culture, demonstrating a biocenosis of several groups of micro-organisms with great metabolic activity. Continuous culture technique suggests possibilities for future studies of human gastrointestinal microecology.

Summary Dysbiosis does not necessarily mean disease. Typical clinical picture of disease caused by metabolic activity of dysbiotic microflora is the microbial over-growth syndrome. We studied case histories of 434 patients without consideration of their basic illnesses and correlated them with types of dysbioses of duodenal juice. 55% of 314 patients with gastrointestinal disorders revealed a dysbiosis. A dysbiosis could also be found in up to 64% of pancreatic diseases, whereas intestinal dysfunctions and chronic inflammatory diseases usually show normal colonization. These cases express alteration of milieu conditions and disturbed interorganic connections. We only treated cases with objective pathological findings, obtaining best results with chemotherapeutic treatment of dysbioses with only one species.

Summary: Fungal resistance is caused by an acquisition of intrinsically resistant species, by selection of resistant strains from a population or by mutation of an initially susceptible strain. According to different classes of antimycotics there are different resistance mechanisms: differences in the uptake mechanisms, drug target alterations, mostly the ergosterolbiosynthesis pathway, and the efflux or pumping mechanisms to the outside.