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Biomedical subjects

N F Pierce

Publications and source records attributed to N F Pierce.

At least 73 records · Page 4Linked to original sources
PubMed1973

Differential inhibitory effects of cholera toxoids and ganglioside on the enterotoxins of Vibrio cholerae and Escherichia coli.

Natural cholera toxoid appears to act as a competitive inhibitor of cholera enterotoxin and is thus a useful tool for studying the interaction of cholera enterotoxin with cell membranes. Cholera enterotoxin binds to gut mucosa more rapidly than does its natural toxoid. Once binding occurs, however, it appears to be prolonged for both materials. Formalinized cholera toxoid has no inhibitory effect upon cholera enterotoxin. Enterotoxic activity, ability to bind to gut mucosa, and antitoxigenicity appear to be independent properties of cholera enterotoxin. Natural cholera toxoid does not inhibit Escherichia coli enterotoxin, indicating that although the two enterotoxins activate the same mucosal secretory mechanism they occupy different binding sites in the mucosa. Ganglioside, which may be the mucosal receptor of cholera enterotoxin, is highly efficient in deactivating cholera enterotoxin. By contrast, ganglioside is relatively inefficient in deactivating heat-labile E. coli enterotoxin and is without effect upon the heat-stable component of E. coli enterotoxin. These findings suggest that ganglioside is not likely to be the mucosal receptor for E. coli enterotoxin. Differences in cellular binding of E. coli and cholera enterotoxins may explain, at least in part, the marked differences in the time of onset and duration of their effects upon gut secretion.

Animals↗
PubMed1973

Differences in the response of rabbit small intestine to heat-labile and heat-stable enterotoxins of Escherichia coli.

The response of adult rabbit small intestine to the heat-stable (ST) and heat-labile (LT) enterotoxins of Escherichia coli has been investigated by employing the ligated loop technique. Fluid accumulation was determined in relation to enterotoxin dose and duration of gut exposure. The individual responses to ST and LT differed in a characteristic manner. Onset of net fluid accumulation in response to ST appeared to be immediate even at the lowest dose tested. Onset of net fluid accumulation in response to LT was rapid at high doses but delayed at low doses. Maximum volume per length ratios elicited by ST occurred between 4 and 6 h after injection of loops over the entire range of doses tested. However, maximum ratios elicited by LT occurred no less than 10 h after injection even at low doses. Fluid accumulation elicited by LT increased in duration with increasing dose; high doses of LT producing a response which was sustained for at least 18 h. The net effect of these differences in reaction characteristics is a sharp increase in the proportion of the cumulative net secretory response attributable to LT with time. Therefore, a 6-h assay time is appropriate for the titration of ST, whereas an 18-h assay is not. The 18-h assay was found more appropriate for toxin-antitoxin neutralization studies since only LT was neutralized by anti-enterotoxin serum. LT of E. coli (swine) strain P-263 and (human) strain 334 was neutralized by antibody stimulated by enterotoxin from E. coli (human) strain H-10407. LT was labile to mild acid conditions, whereas ST was not.

Animals↗
PubMed1973

Effect of Escherichia coli on fluid transport across canine small bowel. Mechanism and time-course with enterotoxin and whole bacterial cells.

An Escherichia coli strain isolated from a patient with severe cholera-like diarrhea elaborates a partly heat-labile enterotoxin shown to cause prompt adenyl cyclase stimulation and isotonic fluid secretion by canine jejunum. Both responses disappear upon removal of the enterotoxin. The duration of action of a submaximal dose of this E. coli enterotoxin was brief, despite sustained exposure to the jejunum, suggesting inactivation of the enterotoxin by its interaction with the mucosa. Inoculation of whole bacterial cultures of this E. coli strain into canine duodenum was followed by bacterial survival and induction of net secretion after 4-7 h. The onset of fluid production was associated with increasing gut mucosal adenyl cyclase activity. Washed bacterial cells could also produce fluid secretion. In vivo multiplication of this enterotoxin-producing E. coli was demonstrated 6-12 h after intraduodenal inoculation of approximately 10(6) organisms. This was associated with fluid secretion. Intestinal fluid production occurred without microscopic pathology in the mucosa.

Adenylyl Cyclases↗
PubMed1972

The use of Ringer's lactate in the treatment of children with cholera and acute noncholera diarrhoea.

Two regimens of fluid and electrolyte therapy were studied in children with severe cholera and noncholera diarrhoea. In one, lactated Ringer's solution was the sole intravenous fluid, additional water, glucose, and potassium being given by mouth. In the other, three different intravenous solutions were employed to meet all fluid and electrolyte requirements. The response to therapy was satisfactory with each regimen. Because of prolonged stupor or vomiting about 15% of children treated by the first regimen were unable to ingest a sufficient quantity of glucose solution by mouth, and intravenous supplementation with a hypotonic glucose-saline solution was necessary. It is concluded that lactated Ringer's solution is suitable as the sole intravenous solution for children with acute cholera and noncholera diarrhoea provided oral supplementation, as described, is possible. The study also provides useful observations on the means of evaluating fluid requirements in such children and specific guidelines for such therapy.

Administration, Oral↗
PubMed1972

Gastric acidity in cholera and noncholera diarrhoea.

Gastric acid production, unstimulated and following stimulation with betazole hydrochloride, was measured in Indian men with cholera or acute vibrio-negative diarrhoea-Measurements were made during acute illness and after different periods of convalescence. Men from the same socioeconomic group and from a higher one served as controls. Stimulated acid production was severely reduced during diarrhoea caused by V. cholerae and related vibrios but not during acute vibrio-negative diarrhoea. Acid production returned to stable convalescent values 1-3 days after cessation of diarrhoea. Stimulated acid production was significantly lower in controls from the lower socioeconomic group than in those from the higher socioeconomic group. Achlorhydria that did not respond to betazole administration occurred in 32% of the convalescent cholera patients but in none of the controls or convalescent vibrio-negative diarrhoea patients. It is concluded from these results that diarrhoea produced by V. cholerae and related vibrios is accompanied by transient inhibition of gastric acid secretion, that cholera occurs largely in a population with impaired acid secretion, and that preexisting achlorhydria may predispose to infection with V. cholerae.

Acute Disease↗
PubMed1971

Acute undifferentiated human diarrhea in the tropics. II. Alterations in intestinal fluid and electrolyte movements.

The nature and magnitude of fluid and electrolyte loss into the small intestine were defined by the marker perfusion technique in patients with acute undifferentiated diarrhea (AUD) in the tropics. The patients were divided into two groups according to their small bowel bacteriologic findings, namely those with a predominant Escherichia coli flora and those with a mixed flora. 11 normal subjects served as controls. Net jejunal fluid secretion occurred into the lumen in four of seven patients with E. coli flora and three of seven with a mixed flora. The magnitude of secretion in the jejunum was greater in the E. coli flora patients than in those with a mixed flora. Four E. coli patients and one mixed flora patient had net fluid secretion in the ileum, although the magnitude of secretion in this area was less than in the jejunum. Intestinal fluid had higher bicarbonate concentration in the ileum than in the jejunum but was isotonic in both regions. It resembled in composition fluid from the same region of intestine in normal individuals. Recovery of normal fluid and electrolyte absorptive function was usually complete in both jejunum and ileum by 6-8 days after onset of the disease. Increase in unidirectional flux rates for H(3)O and (24)Na occurred in acute E. coli flora diarrhea and returned to normal levels in recovery: increase in J(beta) (plasma to lumen flux) primarily accounted for the increase in fluid loss. Intestinal biopsy revealed no alterations in villous architecture.A relationship between small bowel fluid production and the presence of toxigenic strains of E. coli within the small bowel has been found for E. coli flora patients. In many respects this disease resembles acute cholera. The mixed flora group represents a less defined entity which requires further study.

Adolescent↗