George H. Bornside

Stability of human fecal flora.

Recent experimental studies show that neither increased dietary fiber nor its absence alters the numbers and major groups of fecal bacteria. Although the total number of bacteria per gram of feces remains constant, the daily fecal mass doubles with added dietary fiber and is halved in its absence. Thus, the total output of fecal bacteria is related to dietary fiber.

The normal microbial flora: comparative bacterial flora of animals and man.

SummaryIn a qualitative and quantitative study of bacteria, the mid small intestine and colon of rabbits and dogs, and the upper jejunum and terminal ileum of surgical patients were sampled at laparotomy.The small intestine of rabbits, dogs, and humans was not sterile. The bacterial groups found most frequently were also those present in the greatest numbers. In rabbits and dogs the small intestine contained varied and quantitatively large flora. In man, the small intestine contained only slight median numbers of coliforms and streptococci. These findings support the view that the small intestine of man contains sparse, transient, bacterial flora.

Absolute barrier isolation and antibiotics in the treatment of experimental burn wound sepsis

Abstract 1. 1. A model for studying the effect of absolute barrier isolation on mortality from burn wound sepsis is described. 2. 2. Systemic polymyxin alone did not increase survival in this model. 3. 3. Topical mafenide with or without systemic polymyxin markedly improved survival from experimental burn wound sepsis. 4. 4. The mortality of animals treated with systemic and oral polymyxin, topical mafenide, and absolute barrier (germfree) isolation was the same as the mortality of similarly treated animals without isolation. 5. 5. In this model, absolute barrier isolation was of no value in the treatment of experimentally contaminated burn wounds.

CLOSTRIDIUM SORDELLI TOXIN IN STRANGULATION OBSTRUCTION: FURTHER STUDIES OF SERIAL CHANGES OF INTESTINAL CONTENTS.

Summary Gas gangrene antitoxin neutralized lethal doses (LD 50 ) of soluble preformed heat-labile toxin in loop fluid of dogs with experimental strangulation obstruction. A reconstruction experiment was employed to demonstrate that C. sordelli toxin was the only lethal agent in supernatant fractions of strangulation fluids from dogs and rabbits. Peritoneal fluid was not as heavily laden with bacteria as loop contents from the same animals. The viable bacterial content of strangulation fluids was greatly diminished after being frozen or refrigerated. Clostridial toxins, viable bacteria and endotoxins may each play a role in the toxicity of strangulation obstruction. Preformed clostridial exotoxins have now been demonstrated in strangulation obstruction in the rabbit, rat, guinea pig and dog.

Enhanced Bacterial Virulence in Fluids Produced in Strangulation Intestinal Obstruction.

Summary Sterile, non-lethal ultrafiltrates of strangulation fluids from humans, dogs, and rats promoted a rapid, lethal E. coli infection in healthy mice by fewer bacteria than was possible with saline suspensions of the same organisms. Cl. welchii and Cl. sordelli, similarly suspended, killed only a small proportion of test mice. Sublethal dosages of several substances that might contribute to the virulence-enhancing activity of strangulation fluids were also studied: E. coli endotoxin enhanced the virulence of Cl. sordelli and E. coli; Cl. welchii exotoxin enhanced only E. coli; bile and mucin enhanced all 3 test microorganisms. Synergism between bacteria of one species and products of another may contribute to the severity of mixed bacterial infections. The identity of the factor in strangulation fluids is unknown. There is as yet no evidence of a role for a bacterial virulence-enhancing factor in the pathophysiology of strangulation intestinal obstruction.

Imbalance of the normal microbial flora: influence of strangulation obstruction upon the bacterial ecology of the small intestine.

SummaryBacteria are present to varying degrees in the normal small intestine of dogs, rabbits, guinea pigs, rats, and man. After strangulation obstruction of the small bowel, there is a marked increase in the bacterial population of the small bowel in all species studied.Different flora are normally present in the different species; following strangulation, similarities appear, particularly the uniform presence of clostridia as a dominant organism.Near-maximal bacterial counts were reached 6 hr. after strangulation.These studies have emphasized the importance of the intestinal flora in determining the outcome in strangulation obstruction.

Bactericidal effect of hyperbaric oxygen determined by direct exposure.

Summary Exposure of small inocula of microorganisms on the surface of blood agar medium to high pressure oxygen (HPO; 100% O2 at 3 atmospheres absolute) has provided a simple direct method for quantitating its antibacterial effect upon 102 strains from among 20 microbial species. The bactericidal effect was dependent upon the duration and intensity of exposure to HPO, and was independent of common taxonomical characteristics such as cellular morphology, gramstaining reaction, and a strict or facultative growth requirement for normobaric oxygen.

Exposure of Pseudomonas aeruginosa to hyperbaric oxygen: inhibited growth and enhanced activity of polymyxin B.

Summary The growth of Pseudomonas aeruginosa was studied in stationary broth cultures (11 mm deep) exposed to 100% oxygen at 3 atmospheres absolute (3 ATA). During exposure, growth was greatly inhibited. Cultures transferred to air after high pressure oxygen (HPO) resumed logarithmic growth at rates similar to unexposed cultures, but lag periods increased. The minimal inhibitory concentration (MIC) of polymyxin B was determined for 6 strains of P. aeruginosa after exposure to HPO for 3, 6 and 12 hours. The longer the exposure, the lower the MIC. Regardless of the strain, after 3 hours exposure to HPO about 75% of the amount of antibiotic required for the MIC of unexposed cultures was needed; after 6 hours exposure, about 50%; and after 12 hours exposure, about 30%. This suggests that it may be possible to increase the therapeutic effectiveness of an antibiotic administered at its maximum dosage if exposure of the patient to HPO can also bathe the infecting microorganisms with oxygen.

The abnormal pigment in strangulation obstruction.

Summary o 1. Spectrophotometric absorption curveswere plotted for peritoneal fluids or intestinal contents from seven patients with strangulation obstruction, one patient with acute hemorrhagic pancreatitis, and the following experimental animals: 31 dogs with strangulation obstruction, 4 dogs with hemorrhagic pancreatitis, 6 dogs with bile peritonitis and 2 pools of peritoneal fluid from 54 rabbits with strangulation obstruction. 2. Essentially normal hemoglobin was found in most specimens. Several contained hemochromogen-like substances. An abnormal pigment similar to the hemin pigment described in 1949 was found in only one specimen. This specimen was a terminal peritoneal fluid from a dog with experimental strangulation obstruction. Peritoneal fluid from a companion dog operated upon at the same time served as a control for subsequent studies. 3. The quantitative bacteriology of theperitoneal fluid containing the abnormal pigment and that of the control peritoneal fluid were similar. Each peritoneal fluid was lethal for mice and dogs when injected intraperitoneally. The presence of the pigment was not related to either bacterial flora or lethality, and is not explained.

Partial reversal by sodium ascorbate of hyperoxia-induced damage to HEp-2 cell cultures.

SummaryHyperoxia induced cellular damage was used as an experimental model system for examining the ameliorative role of antioxidants. Multiplication of HEp-2 cells in monolayer culture was inhibited after exposure to 100% O2 either hyperbarically at 3 atm absolute (atma) or normobarically at 1 atma for periods from 15 s to 4 h. The inhibition was characterized by a slower rate of replication for a period from 1 to 3 d after exposure than in unexposed cultures, and then massive cellular death. Less killing followed exposure to normobaric O2 than to hyperbaric O2, and the shorter the period of exposure to hyperoxia the less killing. Addition of 100 μg/ml of sodiuml-ascorbate to unexposed cultures enhanced growth (cell number at 6 d) almost twofold. When added ascorbate was present only during hyperoxic exposure (but not afterward), subsequent growth in air was enhanced 1.6-fold. However, when cells were exposed without added ascorbate, there was from 2 to 12-fold greater growth in air in the presence of the added ascorbate (as compared to exposed controls). This greater growth was always only a partial reversal of the lethal effect resulting from hyperoxia. Addition of 25 μg/ml catalase did not affect control or exposed cultures. Addition of ascorbate plus catalase was not as effective as ascorbate alone in promoting growth; the catalase moiety antagonized some of the growth enhancing influence of ascorbate. This suggests that extracellular H2O2 was not a factor in the lethal effect resulting from hyperoxia.