Effect of Bacterial Enterotoxins on the Gastrointestinal Tract

Banwell, John G.; Sherr, Howard P.

doi:10.1016/s0016-5085(19)33080-x

Cited by 97 publications

(46 citation statements)

References 197 publications

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“…Although no control data are available to compare with the results of colonic perfusion in Case 24, the data are compatible with a normal functioning colon-that is water, sodium, and chloride were absorbed, potassium was secreted into the lumen, and rectal PD was normal; rectal PD was increased in Case 1. These observations suggest that in these 2 patients the diarrhoea resulted from small intestinal secretion of fluid and electrolytes overwhelming the reabsorptive capacity of a normal colon, as occurs in patients with cholera. 26 The mechanisms underlying small intestinal secretion have been under intense investigation in recent years and there is now evidence that the 2 mucosal enzymes, adenylate cyclase and (Na+-K+)-ATPase are fundamental in the regulation of fluid and solute transport across the small intestine, and in the pathogenesis of various diarrhoeal states.27-28 Adenylate cyclase participates in secretion of water and electrolytes, whereas (Na+-K+)-ATPase is concerned with active sodiumcoupled absorption of monosaccharides and aminoacids which creates osmotic gradients for passive water absorption. Since adenylate cyclase and (Na+-K+)-ATPase regulate opposing transport systems, increased activity of the former or reduced activity of the latter will result in a net secretory state.…”

Section: Discussionmentioning

confidence: 99%

Lethal familial protracted diarrhoea

Candy¹,

Larcher²,

Cameron³

et al. 1981

Archives of Disease in Childhood

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SUMMARY 24 children with severe protracted diarrhoea from 10 families, in which at least one sibling was affected, are reported. In two families the siblings were from 1st-cousin marriages, in one family both parents had unaffected children from previous marriages, and in another family the mother had a normal daughter from an earlier marriage. The onset of the diarrhoea was on the first day of life in 12 infants, some time during the first 17 days in 10, and at 13 weeks and 1 year 6 days in the remaining two. In each case the diarrhoea was 'cholera-like'. Investigations failed to show any of the established causes of protracted diarrhoea and 21 (87 5 %) infants died after an illness that had lasted between 12 days and 6 years 38 weeks, despite periods of prolonged intravenous feeding and the administration of a wide variety of pharmacological agents. The 2 patients who recovered appeared to do so spontaneously. 14 (58 %) had associated extra-gastrointestinal or gastrointestinal-related anomalies. Steady-state perfusion studies were performed in the proximal jejunum of 2 patients, and in the colon of one. In both cases the jejunum was in a net secretory state with respect to water, glucose absorption was markedly reduced, and the transmural potential difference was also depressed; in one of these patients fructose absorption was also reduced, and in the other colonic function appeared to be normal. These studies suggest that the diarrhoea resulted from small intestinal secretion overwhelming the reabsorptive capacity of a normally-functioning colon. Although this series of lethal protracted diarrhoea does not represent a single disease entity, the familial pattern suggests an autosomal recessive mode of inheritance for at least one of the conditions.We have previously reported a series of 82 cases of protracted diarrhoea in infancy and briefly described 6 patients in whom diarrhoea dated from the newborn period;1 of these 6 patients, 2 were siblings and 2 others had similarly affected siblings. Four of the 6 patients died, giving a mortality rate for the series of 5 %.We now report 24 cases (including the 4 patients we described earlier), from 10 families in which at least one sibling also had severe protracted diarrhoea. Each patient has presented to one of three hospitals* during the last 14 years, and 22 of them have been reported in abstract form.2 PatientsThe clinical details of the patients and unaffected siblings are shown in Table 1. The siblings in families 2 and 7 were from 1st-cousin marriages, both

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Section: Discussionmentioning

confidence: 99%

Lethal familial protracted diarrhoea

Candy¹,

Larcher²,

Cameron³

et al. 1981

Archives of Disease in Childhood

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“…In view of the current interest in the effect of bacterial toxins upon intestinal absorption (Low-Beer and Read, 1971;Banwell and Sherr, 1973;Sladen, 1973), we decided to study the action of staphylococcal enterotoxin upon the intestinal absorption of water and electrolytes in dogs. Enterotoxins A and C were used, enterotoxin A being the one most often isolated from staphylococcal-induced food poisoning in humans (Casman et al, 1967).…”

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confidence: 99%

Influence of staphylococcal enterotoxin on water and electrolyte transport in the small intestine.

Elias¹,

Shields²

1976

Gut

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SUMMARY The direct and indirect effects of staphylococcal enterotoxins A and C on the flux of water, sodium, and potassium have been studied in paired Thiry Vella fistulae in dogs. Administration of toxin resulted in a significant decrease in absorption, both in the loop to which the toxin had been administered and its pair. This decrease in absorption was associated with a decrease in movement out of the lumen, movement into the lumen remaining relatively unchanged. The mechanism of action of staphylococcal enterotoxins is discussed, and comparisons made with other enterotoxins.Staphylococcal enterotoxin has been implicated in two types of gastroenteritis-staphylococcal food poisoning, after the ingestion of preformed toxin, and staphylococcal enterocolitis in which the bowel is colonised by the organism, the toxin being produced locally.Enterotoxin, whose existence was postulated in 1912 (Barber, 1912) was first demonstrated in 1929 (hDack et al., 1930) and purified in the 1960s. Five types of enterotoxin, designated A, B, C, D, and E, have been described and classified according to their precipitin reactions with specific antitoxins (Casman et al., 1963;Bergdoll et al., 1965;Casman et al., 1967;Bergdoll et al., 1971). These are simple protein molecules (with a molecular weight around 30000) which show serological specificity and lack of cross-neutralization, although one strain of Staphylococcus aureus can produce more than one type of enterotoxin.The clinical effect of staphylococcal enterotoxin is diarrhoea, which may on occasion be so profuse as to produce a clinical picture like cholera (British Medical Journal, 1971). In view of the current interest in the effect of bacterial toxins upon intestinal absorption (Low-Beer and Read, 1971;Banwell and Sherr, 1973;Sladen, 1973), we decided to study the action of staphylococcal enterotoxin upon the intestinal absorption of water and electrolytes in dogs. Enterotoxins A and C were used, enterotoxin A being the one most often isolated from staphylococcal-induced food poisoning in humans (Casman et al., 1967).Received for publication 7 April 1976 Methods Paired Thiry Vella fistulae of eitherjejunum (approximately 16 cm long) or ileum (approximately 22 cm long) were prepared in healthy beagle dogs weighing 7-16 kg and freed from intestinal parasites. Continuity of the intestine was restored by end-to-end anastomosis, and the ends of the loops were exteriorised on the abdominal wall. The dimensions of each fistula were such as to obtain a serosal surface of approximately 100 cm2.Tests were conducted under general anaesthesia, using intravenous pentobarbitone (30 mg per kg body weight), to minimise variations induced by extraneous or emotional factors. Pentobarbitone has been shown not to affect rates of absorption of water and electrolytes (Code et al., 1960).The rates of absorption and secretion of water, sodium, and potassium were then measured in these loops using the technique described by Shields et al. (1966). In brief, a multiperforate catheter was inser...

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“…Collectively these attributes are called "virulence factors." These include the ability to (0) elaborate enterotoxins that alter intestinal salt and water transport mechanisms (8,11,(51)(52)(53)(54), (b) adhere to and thus colonize the mucosal surface (5 4--69), and (c) invade and penetrate the intestinal mucosa (60--63). The ability of coliform organisms to elaborate enterotoxins and to adhere to the mucosa is genetically determined by extrachromosomal ele ments or plasmids that are transmissible to related organisms.…”

Section: Bacterial Factorsmentioning

confidence: 99%

“…The mechanisms by which the cytotoxins cause diarrhea are uncertain. All bacterial enterotoxins thus far purified have proved to be proteins and all appear to act primarily on the small intestine (8,11,(51)(52)(53)(54).…”

Section: Bacterial Factorsmentioning

confidence: 99%

“…Strains of bacteria that elaborate enterotoxins are V. cholerae, nonchol era vibrios, V. parahemolyticus, Y. enterocolitica, E. coli, Klebsiella sp., Enterobacter sp., Citrobacter sp., Serratia sp., A. hydrophilia, Shigella sp., Salmonella sp., C peifringens, s. aureus, and B. cereus (8,11,(51)(52)(53)(54). Other bacteria may also elaborate enterotoxins but these are less certain at present.…”

Section: Bacterial Factorsmentioning

confidence: 99%

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Pathogenesis of Acute Bacterial Diarrheal Disorders

Giannella¹

1981

Annu. Rev. Med.

104

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Acute bacterial diarrheal disease is a worldwide problem of enormous magnitude. In recent years a number of bacteria have been added to the list of recognized etiologic agents causing acute diarrheal disease. This was made possible by our increased understanding of the mechanisms by which such bacteria cause diarrhea and by the development of methods to detect these bacterial enteropathogens. We are now able to define an etiologic agent in 50-80% of cases of acute diarrhea, depending on the particular population. The bacterial agents recently incriminated as important causes of diarrhea include E coli Y. enterocolitica, B. cereus, C. fetus, V. parahemolyticus, and many other coliform organisms. Establishment of an enteric infection depends upon a complex interplay between host defense mechanisms and bacterial virulence factors adapted to overcome these defenses. Bacterial enteropathogens cause diarrhea primarily by elaborating enterotoxins (which also requires the organisms to adhere to the surface of the intestinal cell) and by invading the intestinal mucosa. The number of known bacterial enterotoxins has rapidly increased. Enterotoxins cause intestinal secretion and diarrhea by stimulating the adenyl cyclase system or the guanyl cyclase system and by other mechanisms yet to be defined. The ability of enterotoxigenic bacteria to adhere to the intestine involves a specific binding interaction between bacterial structures called pili or fimbriae and specific receptors on the surface of intestinal cells. Both bacterial pili and the intestinal receptors are under genetic control. A variety of other bacteria, Salmonellae, Shigellae, Y. enterocolitica etc, must invade the mucosa to cause diarrheal disease. The ability to invade is essential to the pathogenesis of disease and requires particular surface characteristics of the bacterium as well as the active participation of both the bacterium and the host cell. The bacteria probably elaborate substances that signal the host cell to initiate the invasive process, i.e. endocytosis. The mechanism by which invasive bacteria evoke intestinal secretion is uncertain but is probably a multifactorial process involving products elaborated by the mucosal acute inflammatory reaction and enterotoxins elaborated by the bacteria.

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Effect of Bacterial Enterotoxins on the Gastrointestinal Tract

Cited by 97 publications

References 197 publications

Lethal familial protracted diarrhoea

Lethal familial protracted diarrhoea

Influence of staphylococcal enterotoxin on water and electrolyte transport in the small intestine.

Pathogenesis of Acute Bacterial Diarrheal Disorders

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