Povidone-iodine in peritonitis. I. Adverse effects of local instillation in experimental E, coli peritonitis.

Lethal quantities of undiluted povidone-iodine solution ip appear to cause mortality by inducing a chemical peritonitis with resulting hypovolemic shock. Sublethal doses of polyvinyl-pyrrolidone-iodine (PVP-I) given synchronously with Escherichia coli increased the mortality of E. coli or E. coli-hemoglobin peritonitis. Pretreatment of the peritoneal cavity with dilute PVP-I reduced the mortality of E. coli peritonitis, but this appears to be a nonspecific effect, since PVP-I in sublethal quantities is rapidly neutralized within the peritoneal cavity. Our single attempt at operative lavage with dilute PVP-I increased the mortality of E. coli peritonitis induced 1 hr earlier.     

Bile peritonitis in acute cholecystitis.

In a series of 20 patients with bile peritonitis seen during a 15-year period, 15 were men and 5 women, with an average of 72 years. They represented 1.8% of 1123 patients with acute cholecystitis admitted during the same period. Three patients were not operated upon and all died, while 5 of 17 operated patients died. The high mortality rate is due to a delay in diagnosis and treatment. Early operative treatment of acute cholecystitis should be resorted to whenever possible.     

Factors influencing the outcome of E. coli peritonitis in rats

Substances that may influence the course and outcome of intra-abdominal sepsis were investigated in an experimental model of Escherichia coli peritonitis in rats. All rats received an intraperitoneal injection of E. coli. In the first set of experiments, substances commonly contaminating the abdominal cavity after trauma were intraperitoneally injected, and the following mortality rates were found: saline solution (controls) 27%, hemoglobin solution 80% (p less than 0.01), whole blood 20% (p greater than 0.05), whole blood together with bile 93% (p less than 0.001) and bile 87% (p less than 0.01). In the second set of experiments, intravenous injection of commonly used solutions gave mortality rates of 20% (controls) for saline solution, 80% for dextran (p less than 0.01) and 47% for Intralipid (p greater than 0.05). E. coli peritonitis in rats thus was aggravated by intraperitoneal hemoglobin, bile or whole blood plus bile, and also by intravenous dextran.     

Bile peritonitis in acute cholecystitis

A review of all patients treated for acute cholecystitis (n = 5848) during an 18-year period (1969-1986) at two hospitals (one practising early surgery in patients with acute cholecystitis and the other not) disclosed that 104 (1.8%) had bile within the abdominal cavity at surgery; 71 with a visible perforation of the gallbladder and 33 without. The bile was infected in 82% of performed cultures (most commonly with Escherichia coli). Mortality was 7.7% (8/104 patients), being 20% (4/20) in the hospital practising delayed surgery and 5% (4/84) in the hospital practising early surgery (p less than 0.10). Infectious complications were responsible for the deaths by leading to multiple organ failure with pulmonary or renal insufficiency or gastro-intestinal bleeding. The timing of surgery was the only factor that had prognostic significance, i.e. the longer the hospital delay before surgery the higher the mortality, although elderly patients or patients with perforation tended to have a worse prognosis. In conclusion, the results of this study indicated that early surgery is important in patients with acute cholecystitis as a means of lowering mortality in bile peritonitis in this condition.     

Determination of mouse bladder inflammatory response to E. coli lipopolysaccharide

Evaluation of the severity of histologic changes associated with cystitis is often subjective and inconsistent from one sample to the next. The objective of this study was to establish a consistent, reproducible method to quantify histologic changes in a mouse model of lipopolysaccharide (LPS)-induced cystitis. Either LPS (n=8) or pyrogen-free saline (n=8) was instilled intravesically into the bladders of female C57bk-6 J mice. Twenty-four hours later, mice in these groups as well as eight untreated controls were sacrificed and bladders were removed, fixed in formalin, and stained with hematoxylin and eosin (H&E). A bladder inflammatory index (BII) was described by reviewing tissues for edema, leukocyte infiltration, and hemorrhage. Cross-sections were evaluated by a single pathologist in a blinded manner based on the objective BII described. The BII method for objectively analyzing bladder inflammation was effective and reproducible. Bladders instilled with LPS had significantly increased inflammation scores for edema, leukocyte infiltration, and hemorrhage compared with those instilled with saline or untreated controls (n=8, P < 0.05). These results demonstrate that LPS causes bladder inflammation when instilled intravesically and that inflammation of mouse bladders can be objectively quantified using the histological method described. Received: 22 October 1999 / Accepted: 14 March 2000     

Virulence of wild-type E. coli uroisolates in experimental pyelonephritis

This study was designed to analyze the colonizing and invasive properties of wild-type bacteriuric E. coli possessing a variety of phenotypic characteristics in experimental nonobstructive pyelonephritis (P and Type 1 [T] fimbriae, hemolysin [Hly], presence of K capsules, flagella [H], serotype, biotype, human and mouse serumcidal resistance). Special emphasis was on the role of Gal-Gal adhesin (P fimbriae) of non-genetically engineered uroisolates. It was shown that organisms that are P+ or T+ or Hly+ are more likely to colonize bladders than strains negative for those parameters (P less than 0.001). Additionally, P+ strains were more often associated with kidney histopathology than P- E. coli (P less than 0.05). However, the data also indicated that fimbriae (P and Type 1) were not sole determinants of virulence since two strains devoid of fimbriae, hemolysin, K capsules and sensitive to human serumcidal activity caused incipient and acute pyelonephritis. Even among identical serotypes and biotypes, the presence/absence of fimbriae did not appear to be the critical factor in urovirulence, nor did the presence of several positive characteristics (hemolysin, K capsule, flagella, serum resistance) in a given strain enhance uropathogenicity. Therefore, these properties do not need to work together to render an E. coli urovirulent. These phenotypic characters may simply represent associated or serologic markers with the host serving as the dominant determinant of susceptibility to urinary infection. The findings emphasize the inherent limitations in relating and extrapolating colonizing and invasive properties of genetically engineered strains to those of naturally occurring, wild-type E. coli human uroisolates causing pyelonephritis.     

Bile acids in experimental colorectal cancer.

Cogent epidemiological and experimental data implicate bile acids as endogenous co-carcinogens in colorectal cancer. A series of experiments was designed to test the ability of sodium deoxycholate (SDC) to promote intestinal hyperplasia and neoplasia in rats (n = 265). The intermediary role of faecal anaerobes was explored in animals receiving oral metronidazole. Intrarectal instillation of SDC trebled tumour yield in functioning large bowel and increased both crypt depth and crypt cell production rate. Metronidazole reduced this tumour promotion without affecting SDC-induced hyperplasia. By contrast, SDC was totally inactive in colon isolated as a Thiry-Vella fistula. Bile acids probably promote colorectal carcinogenesis by stimulating mucosal hyperplasia but only in the presence of faeces.     

Persistence of E. coli O- and K-antigens in experimental pyelonephritis

Summary Experimental chronic pyelonephritis was produced in guinea pigs by ligation of a ureter and injection of various strains of E. coli. Using direct and indirect immunofluorescence the localisation and persistence of E. coli somatic O-antigen and capsular K-antigen was demonstrated in sterile kidneys. The possible pathogenetic role of persistent antigen as the cause of renal inflammation is discussed.     

Bile peritonitis after the use of latex rubber T-tubes.

Three cases of biliary peritonitis following the removal of a latex rubber T-tube from the common duct in the second postoperative week are reported. This is a well-recognized complication following the use of polyvinyl chloride T-tubes in biliary duct surgery, but its occurrence with latex rubber T-tubes is extremely uncommon.     

Serum prognostic indicators in experimental Bacteroides peritonitis.

Serum lysozyme and hemolytic complement (CH100) levels were measured in dogs with experimental Bacteroides peritonitis. The CH100 levels showed little change in surviving animals. Nonsurvivors showed a moderate decrease in complement levels shortly after contamination. Both surviving and nonsurviving animals showed a slight initial decrease in lysozyme levels shortly after contamination. In surviving dogs this was followed by an increase to normal levels. In nonsurvivors, levels continued to increase, reaching a threefold magnification just prior to death. As a result of antibiotic therapy, CH100 levels exhibited no major changes; however, dogs deprived of antibiotic showed noticeable and persistent increases in lysozyme levels while treated animals showed only a mild elevation in lysozyme levels. The changes in the level of serum lysozyme may be a good indicator of antibiotic efficacy and approaching death from Bacteroides peritonitis.     

The effect of noxytiolin in experimental peritonitis.

The evidence for the value of noxytiolin (Noxyflex) in peritonitis is contradictory. In a controlled trial of the effect of noxytiolin in pertonitis in rabbits we have found a significant increase in mortality in the trial group compared with a control group, but no significant difference when a dose equivalent to the recommended human dose is used. The postoperative course is adversely affected in the animals receiving noxytiolin.     

The effect of splenectomy on antibody response to lipopolysaccharide (E. coli) immunization

The influence of splenectomy on the antibody response to lipopolysaccharide (LPS: E. coli 0128:B12) was investigated in mice. Splenectomy had little effect on the primary response to the LPS. However, the level of IgG anti-LPS antibodies of splenectomized mice was significantly lower than that of sham-operated mice when the mice were immunized 1, 3, and 7 days after the operation and reimmunized 7 days after the first immunization. There was no significant difference in those immunized 30 days after the operation and reimmunized 7 days later. In mice immunized before splenectomy and reimmunized 30 days after splenectomy, the level of IgG anti-LPS antibodies was low, even in the mice splenectomized 30 days after primary immunization. Our results indicate that splenectomy impairs the antibody response to lipopolysaccharides.     

Influence of dextran on blood clearance and organ distribution of radiolabelled E. coli and on survival in experimental E. coli septicemia

Previous reports indicated impaired function of the reticuloendothelial system following administration of dextran. In the present experimental study, intravenous injection of Escherichia coli resulted in four deaths among 15 rats pretreated with i.v. dextran 70, but none in 15 controls (p less than 0.05). To evaluate the influence of dextran on bacterial clearance from blood and distribution in organs, 125I-labelled, heat-killed E. coli was injected 1 or 24 hours following i.v. injection of 1.0 ml sterile saline solution or 1.0 ml dextran 70. After both of these intervals, dextran resulted in significant (p less than 0.05) decrease of blood clearance compared with the controls. The organ distribution in counts/minute (cpm)/g tissue was compared in liver, spleen and lungs. Splenic uptake was reduced at both times following dextran administration, while there was increase in pulmonary uptake at 1 hour and in hepatic uptake at 24 hours post-dextran (p less than 0.005 and p less than 0.02, respectively). Evaluation of cpm/total organ weight showed no change after dextran injection, except for increased (p less than 0.05) pulmonary uptake after 1 hour.     

Mechanism of the adjuvant effect of hemoglobin in experimental peritonitis. IX: The infection-potentiating effect of hemoglobin in Escherichia coli peritonitis is strain specific

Hemoglobin solutions have been said to consistently increase the lethality of otherwise nonlethal bacterial inocula in experimental models of Escherichia coli peritonitis. We tested the capacity of stroma-free hemoglobin to potentiate the lethality of each of 26 separate clinical isolates of E. coli. The LD50 of each strain with and without stroma-free hemoglobin was then correlated with the ability of that strain to express putative "virulence characteristics": the expression of 0 (lipopolysaccharide) and K (capsular) antigens, the ability to produce colicin V, the capacity to hemagglutinate mammalian red cells in the presence of 1% mannose, and the ability to secrete alpha-hemolysin. No perfect correlations were found. The LD50 of only four of the 26 strains of E. coli was affected by hemoglobin. Each of these four strains could hemagglutinate red cells and secreted alpha-hemolysin. Many other strains whose lethality was not increased by hemoglobin also had these virulence properties. We must conclude that the infection-potentiating effect of hemoglobin cannot be shown for most clinical isolates of E. coli and that the mechanism cannot be correlated with the usual "virulence characteristics" of E. coli.