Antacid, sucralfate, and prostaglandin E2 effects on the growth and potential for translocation of Pseudomonas aeruginosa, Escherichia coli, and Staphylococcus aureus in an in vitro gastric simulation

M. P. Goeger, G. K. Dupuis, David Herndon, M. C. Robson, J. P. Heggers

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Viable bacteria in the gut of thermally injured patients may be translocated through the gut mucosa, causing widespread infection. Increased flora from optimization of bacterial growth by pH elevation, coupled with the decreased intestinal motility common among patients whose mucosal integrity has been compromised, may increase the incidence of translocation. Gastric pH in these patients is monitored and maintained around pH 6 by various agents to reduce susceptibility to stress ulceration. Whole milk, given as a nutrient source, also raises pH. An in vitro trial simulating gastric fluid under conditions found in patients with burns was conducted to evaluate the growth of commonly ingested bacteria. Bicarbonate buffer containing pepsin and adjusted to pH 2, 4, or 7 with HCl was dosed with magnesium and aluminum hydroxide antacid (Maalox) (10 ml), sucralfate (Carafate) (0.4 gm), or prostaglandin E2 (PGE2) (10 ng) before inoculation with Escherichia coli (3 x 102 organisms), Pseudomonas aeruginosa (3 x 102 organisms), or Staphylococcus aureus (2 x 101 organisms). Bacterial growth and pH were determined periodically over the 24-hour trial. Milk was added at intervals in half the samples to simulate patient feeding. Maalox increased pH in all samples containing milk (initially pH 2, 4, or 7) to over 7.0 in 2 hours, and increased pH more slowly without milk. Carafate had a moderating effect, increasing pH 2 and pH 4 and decreasing pH 7, with a narrower pH range found in the milk groups. PGE2 treatments combined with milk also increased pH 2 and pH 4, but slightly elevated pH 7 within 24 hours. Without milk, PGE2 did not alter pH from initial values. Bacterial growth did not occur during the first 4 hours. At 24 hours, Maalox and Carafate groups without milk still showed no response, whereas bacteria in PGE2-treated groups had multiplied except in pH 2. Overall, groups with milk were capable of supporting growth, likely a result of both higher pH values and presence of substrate. Both S. aureus and P. aeruginosa responses were limited by Maalox and milk alone and enhanced by Carafate and PGE2. E. coli, however, grew in all treatments. This observation confirms that seen in cases of translocation, where most bacteria found systemically outside the gut are E. coli.

Original languageEnglish (US)
Pages (from-to)7-12
Number of pages6
JournalJournal of Burn Care and Rehabilitation
Volume12
Issue number1
StatePublished - 1991

Fingerprint

Sucralfate
Antacids
Dinoprostone
Pseudomonas aeruginosa
Staphylococcus aureus
Stomach
Escherichia coli
Growth
Milk
In Vitro Techniques
Bacteria

ASJC Scopus subject areas

  • Rehabilitation
  • Surgery
  • Nursing(all)
  • Health Professions(all)
  • Emergency Medicine

Cite this

Antacid, sucralfate, and prostaglandin E2 effects on the growth and potential for translocation of Pseudomonas aeruginosa, Escherichia coli, and Staphylococcus aureus in an in vitro gastric simulation. / Goeger, M. P.; Dupuis, G. K.; Herndon, David; Robson, M. C.; Heggers, J. P.

In: Journal of Burn Care and Rehabilitation, Vol. 12, No. 1, 1991, p. 7-12.

Research output: Contribution to journalArticle

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abstract = "Viable bacteria in the gut of thermally injured patients may be translocated through the gut mucosa, causing widespread infection. Increased flora from optimization of bacterial growth by pH elevation, coupled with the decreased intestinal motility common among patients whose mucosal integrity has been compromised, may increase the incidence of translocation. Gastric pH in these patients is monitored and maintained around pH 6 by various agents to reduce susceptibility to stress ulceration. Whole milk, given as a nutrient source, also raises pH. An in vitro trial simulating gastric fluid under conditions found in patients with burns was conducted to evaluate the growth of commonly ingested bacteria. Bicarbonate buffer containing pepsin and adjusted to pH 2, 4, or 7 with HCl was dosed with magnesium and aluminum hydroxide antacid (Maalox) (10 ml), sucralfate (Carafate) (0.4 gm), or prostaglandin E2 (PGE2) (10 ng) before inoculation with Escherichia coli (3 x 102 organisms), Pseudomonas aeruginosa (3 x 102 organisms), or Staphylococcus aureus (2 x 101 organisms). Bacterial growth and pH were determined periodically over the 24-hour trial. Milk was added at intervals in half the samples to simulate patient feeding. Maalox increased pH in all samples containing milk (initially pH 2, 4, or 7) to over 7.0 in 2 hours, and increased pH more slowly without milk. Carafate had a moderating effect, increasing pH 2 and pH 4 and decreasing pH 7, with a narrower pH range found in the milk groups. PGE2 treatments combined with milk also increased pH 2 and pH 4, but slightly elevated pH 7 within 24 hours. Without milk, PGE2 did not alter pH from initial values. Bacterial growth did not occur during the first 4 hours. At 24 hours, Maalox and Carafate groups without milk still showed no response, whereas bacteria in PGE2-treated groups had multiplied except in pH 2. Overall, groups with milk were capable of supporting growth, likely a result of both higher pH values and presence of substrate. Both S. aureus and P. aeruginosa responses were limited by Maalox and milk alone and enhanced by Carafate and PGE2. E. coli, however, grew in all treatments. This observation confirms that seen in cases of translocation, where most bacteria found systemically outside the gut are E. coli.",
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