Bacterial toxins, resistance

Endotoxin. A heat-stable bacterial toxin not freely liberated into the surrounding medium. Endotoxins are released only when the integrity of the cell wall is disturbed, are less potent than most exotoxins, are less specific, and do not form toxoids. When injected in large quantities, endotoxins produce hemorrhagic shock and severe diarrhea. Smaller amounts cause fever, altered resistance to bacterial infections, leukopenia followed by leukocytosis, and numerous other biological effects. 

The enzymatic specificity of diphtheria toxin deserves special comment. The toxin ADP-ribosylates EF-2 in all eukaryotic cells in vitro whether or not they are sensitive to the toxin in vivo, but it does not modify any other protein, including the bacterial counterpart of EF-2. This narrow enzymatic specificity has called attention to an unusual posttranslational derivative of histidine, diphthamide, that occurs in EF-2 at the site of ADP-ribosylation (see fig. 1). Although the unique occurrence of diphthamide in EF-2 explains the specificity of the toxin, it raises questions about the functional significance of this modification in translocation. Interestingly, some mutants of eukaryotic cells selected for toxin resistance lack one of several enzymes necessary for the posttranslational synthesis of diphthamide in EF-2 that is necessary for toxin recognition, but these cells seem perfectly competent in protein synthesis. Thus, the raison d etre of diphthamide, as well as the biological origin of the toxin that modifies it, remains a mystery. 

Food may be contaminated with toxins produced by bacteria, such as botulinum toxin. This is produced by the bacterium Clostridium botulinum and is one of the two most potent toxins known to humans (the other being ricin). As little as one hundred-millionth of a gram (1 X 10-8 g) of the toxin would be lethal for a human. Fortunately, the toxin is destroyed by heat so that cooked food is unlikely to be contaminated (although the bacterial spores are quite resistant). The bacteria grow in the absence of air (they are anaerobic), and consequently, the foodstuffs most likely to be contaminated are those that are bottled or canned and eaten without cooking, for example, raw or lightly cooked fish. 

Bacterial Cultures. Bacterial cultures were obtained from the Kansas State University (KSU) stock culture collection and were stored using the Protected Bead storage system. The following cultures were used for the Salmonella specimen S. lille (UGA), S. montevideo (UGA), S. typhimurium (UGA), S. agona (KSU 05 from CDC outbreak isolate), and S. newport (KSU 06 CDC outbreak isolate). The following cultures were used for the Escherichia coli specimen E. coli 0157 H7 (CDC 01,03), E. coli 0157 H7 (USDA-FSIS 011-82 Rif resistant 100 ppm), E. coli 0157 H7 (ATCC 43895 HUS associated Type I II toxins Rif. Res.) and E. coli ATCC 23740 (Genotype K-12 prototrophic lambda). 

Benzene also affects functional immune responses, as indicated by decreased resistance to infectious agents. Pre-exposure to benzene at >30 ppm for 5-12 days increased the bacterial counts in mice on day 4 of infection with Listeria monocytogenes (Rosenthal and Snyder 1985). Recovery of the immune system was noted on day 7. The effects did not occur at 10 ppm. In addition, a concentration-dependent statistically significant depression was noted in T- and B-lymphocyte populations from day 1 through day 7 at 30 ppm and above. B-cells were more sensitive to benzene than were T-cells on a percentage-of-control basis. This indicates a benzene-induced delay in immune response to L. monocytogenes. Concentrations of 200 or 400 ppm for 4-5 weeks (5 days per week) suppressed the primary antibody response to tetanus toxin in mice, but there was no effect at 50 ppm (Stoner et al. 1981). In another intermediate-duration exposure study, no changes were noted in the numbers of splenic B-cells, T-cells, or... 

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