Microbial Contamination in Acute Intra-Abdominal Infection with Underlying Acute Nephrosis-Nephritis: An Experimental Study.

Material and methods. 4 groups of 15 white rats: 1st - intact, 2nd - model of nephrosis-nephritis, 3rd - model of intra-abdominal infection, 4th - model of nephrosis-nephritis and intra-abdominal infection. Intra-abdominal infection was simulated by intraabdominal injection of autofaeces mixture. Nephrosis-nephritis was simulated by subcutaneous introduction of 5% sodium nitrite solution. Intra-abdominal infection was simulated 3 months after diabetes simulation. The small and large intestines and peritoneal exudate microflora were studied. The material for examination was taken before the simulation of intra-abdominal infection, in 6, 12, 24, 48 h after. Results. Dysbiosis was found in the 2nd group. In the 3rd group, in 6 h, dysbiosis was found, in the 4th group dysbiosis progressed, with not only quantitative but also qualitative changes in the intestinal microbiocenosis were found, which further progressed. During the development of intra-abdominal infection, permanent changes in the intestinal microbiocenosis and peritoneal exudate microflora were detected. In the 4th group, the changes were more severe. In the 3rd group, in 48 h, microflora’s changes in both intestines and the peritoneal exudate indicate slight regression of pathological processes. In the 4th group, in 48 h, progression of pathological processes was detected. Conclusion. 1. Intestinal dysbiosis was detected in rats 12 h since acute nephrosis-nephritis simulating. 2. Simulating acute intra-abdominal infection in intact rats causes intestinal dysbiosis, a syndrome of excess bacterial colonization of small intestines. 3. Simulation of acute intra-abdominal infection in rats with models of acute nephrosis-nephritis increases intestinal dysbiosis, in 6 h not only quantitative but also qualitative changes in the intestinal microbiocenosis were detected, which further progress. 4. In intact rats, 48 h since acute intra-abdominal infection modeling, signs of dysbiosis regression and a decrease in the number of microorganisms in peritoneal exudate were found, instead in rats with models of acute intra-abdominal infection with underlying acute nephrosis-nephritis, signs of dysbiosis progression and an increase in the number of microorganisms in peritoneal exudate were found.