Food Safety has always been a very significant public health issue but its global importance has begun to be realized only in the last two or three decades. Not only has epidemiological surveillance shown a constant increase in the prevalence of foodborne illness, there have also been some large devastating outbreaks of diseases such as cholera, salmonellosis, enterohaemorrhagic Escherichia coli infections and hepatitis A in both developed and developing countries. Furthermore, cholera and other diarrhoeal diseases that were traditionally considered to be spread by water or person-person contact have been shown to be largely foodborne. During the early decades of the 21st century, foodborne diseases can be expected to increase further, especially, but not exclusively, in developing countries. The reasons being a number of environmental and demographic changes which are taking place now and will continue well into the next century. They vary from climatic changes, changes in microbial and other ecological systems, shrinking water supplies, increased age of human populations to globalization of food and feed trade and mass tourism. Meeting the huge challenge of food safety in the 21st century will be a major task of the public health community. It will require the application of new methods of identifying, monitoring and assessing of foodborne hazards, including the wide application of the hazard analysis and critical control point system. Both traditional and new technologies for assuring food safety should be improved and fully exploited. This needs to be done through legislative measures where suitable but much greater reliance will have to be placed on voluntary compliance and on education of consumers and other food-handlers. Indeed, this will be an important task of the Primary Health Care System aiming at “Health for all.”
Guar gum is widely used in the food industry as a thickening agent. Guar and other galactomannans are ingested as a normal part of the human diet. Guar is completely degraded in the large intestine. Often large amounts of gas are produced. The objective of the study was to determine which species are responsible for the degradation of guar in the GI tract. It was observed that only a limited number of species is able to degrade and ferment guar. Guar degrading strains could be isolated from faecal samples of all volunteers and in 90% of the saliva of volunteers. The main species isolated from humans were Bifidobacterium dentium and Clostridium butyricum. From several samples of animal faeces Streptococcus bovis could be isolated. In addition some strains of Bacteroides ovatus were able to degrade guar to a limited extent. Fermentation resulted in the production of short-chain fatty acids and, when Cl. butyricum was present, in a large gas production. Competition experiments showed that Cl. butyricum degrades guar faster than both other species under simulated physiological conditions. It was concluded that Cl. butyricum is the main guar degrading species and the causative agent of the gas formation after guar intake.
The effect of a culture powder of Propionibacterium freudenreichii ET-3 cells containing a bifidogenic growth stimulator (BGS) on fecal flora was studied in twelve healthy subjects with a mean age of 42.6 (range, 27-56 years). One gram of BGS powder containing 17.4 U of BGS activity was administered for 14 days, three times a day after meals. A significantly higher number of bifidobacteria in fecal samples was observed during the intake period of the BGS powder. The frequency of occurrence of the bifidobacteria also increased from 92% to 100%. These results indicate that the BGS acts in the intestine as a growth stimulator of bifidobacteria when the BGS powder is administered.
Glutamine formation was observed by coupling the reaction of bacterial glutamine synthetase with the sugar fermentation system of Bifidobacterium pseudolongum c. About 5 mM glutamine was formed in 1 hr of incubation at 37°C with 15 mM glutamate, 15 mM NH4Cl, 30 mM potassium phosphate buffer (pH 7.0), 10 mM glucose, 3.4 mg/ml toluol-treated B. pseudolongum c cells and 50 units/ml glutamine synthetase. The reaction proceeded in autoclaved swine feces without the addition of NH4Cl. In the toluol-treated fresh feces of a breast-fed infant where bifidobacterial growth occurred preferentially, glutamine formation proceeded without the addition of bifidobacterial cells, NH4Cl, or phosphate, however glutamate was necessary. Based on these results, ammonia detoxification in the intestine by bifidobacteria was discussed.
In order to know the accumulation of menaquinones produced by intestinal bacteria in new born animals, phylloquinone (K) and menaquinone (MK-n) concentrations were determined in the feces, milk, plasma and vernix caseosa of beagle dams and in the feces, liver and plasma of pups 1 through 60 days old. K and menaquinones (MK-4-MK-13) were detected in dams' feces, where MK-10, -11 and -12 were predominant. K was detected in the feces of pups 3 days after birth, and menaquinones appeared after 7 days. The highest concentration of menaquinones in the pups' feces was found on day 14 and the concentration gradually decreased thereafter. K and MK-4 were detected in the liver of pups on the first day after birth, and menaquinones, especially MK-7, were detected after 3 days. Long-chain menaquinones (MK-9-MK-13) appeared after 7 to 14 days and their concentrations increased thereafter. The total menaquinone concentration in pups' liver at 1, 3, 7, 14, 28 and 60 days was 1.89, 8.39, 9.67, 11.91, 11.43 and 55.12 pmol/g, respectively. K, MK-4, MK-6, MK-7 and MK-8 were detected in the dams' plasma and milk. The concentration of MK-4 in milk was about 60-fold higher, the K concentration was almost twice as high, and the MK-7 and -8 concentrations were lower than those in plasma. Except for MK-4, the concentration of K and menaquinones in the pups' plasma were lower on the first day after birth but increased after 3 days, and their concentrations were comparable with those in the dams' plasma. K, MK-4 and MK-6-MK-10 were detected in the vernix caseosa. MK-4 was present at a concentration of about 200 pmol/g, MK-6 and MK-7 at about 25 pmol/g, and K at approximately 7 pmol/g. These data showed a pattern of menaquinone accumulation, especially in the liver, after birth and revealed that a certain menaquinone (MK-7) appeared in the liver as early as 3 days after birth in beagle pups.
The detoxification ability and toxin binding properties (ability and strength) of aflatoxin B1 by six strains of probiotic bacteria were studied. The detoxification ability of the organisms ranged between 20-50%. About 60-80% of the bound aflatoxin was removed when washed with water, and only 10-40% of the toxin was strongly bound to the bacterial cells. Among the organisms studied, Bifidobacterium infantis 1912 demonstrated a significantly higher aflatoxin binding ability than the other strains, while Bifidobacterium pseudolongum 20099 showed the least aflatoxin binding ability of about 10% of the added 50 ng of aflatoxin B1. Bifidobacterium bifidum 1 showed the least aflatoxin B1 binding strength during the 180 min treatment.
The effects of ingested fructooligosaccharides (FOS) (3 g/day) and placebo on stool frequency and stool condition were investigated in healthy female volunteers. According to stratification analysis, the stool frequency during the period of FOS intake was: 1) higher than that during the period of non-intake comparing subjects with an inherent (non-intake period) stool frequency of ≤ 3 times/week; 2) higher than that during the period of placebo intake comparing those subjects with an inherent frequency of > 3 to le; 5 times/week; and 3) not higher or lower, with no significant differences observed between the three periods, comparing those subjects with an inherent frequency of > 5 times/week. Three statistical methods were applied in the analyses, and comparisons revealed that the non-parametric Wilcoxon signed rank-sum test was suitable in this study.