The optimal modeling method of specific tuberculosis peritonitis (experimental research)

The objective: to create a reproducible model of chronic tuberculosis peritonitis to study pathophysiological mechanisms of its progression and to develop pathogenetically based therapy.Subjects and Methods. The study was performed using 10 male rabbits of the Chinchilla breed. The animals were administered intraperitoneal culture of Mycobacterium tuberculosis, tuberculosis peritonitis modeling was performed according to the proposed method.Results. In the course of the experiment, it was proved that all animals developed tuberculous peritonitis with lesions of the large omentum and serous integuments of internal organs. Molecular genetic tests of fragments of the omentum and peritoneum detected DNA of Mycobacterium tuberculosis.

Pathogenetic role of tumor necrosis factor (TNF-α) for the development of peritoneal tuberculosis in an experiment

Currently tuberculosis is considered as a group of diseases united by one etiological factor. The pathogenesis of certain localizations of tuberculous inflammation, in particular peritoneum tuberculosis, hasn’t been sufficiently studied. The role of cytokine mechanisms in the development of the disease and the elaboration of non-sterile immunity requires further experimental studies, in particular the creation of a reproducible model on laboratory animals.The aim: to study the effect of TNF-α on the development of tuberculosis of the serous coat of the abdominal cavity, as well as to evaluate the possibility of modeling tuberculous peritonitis in laboratory animals using infliximab.Materials and methods. The studies were conducted on 18 male rabbits, which were simulated peritoneal tuberculosis by intra-abdominal administration of a suspension of Mycobacterium tuberculosis. 10 rabbits of the experimental group were intravenously injected with an infliximab solution and an iron (III) hydroxide sucrose complex intraperitoneally a day before infection.Results. In the control group of animals, tuberculosis either didn’t develop, or in a third of cases it affected only the pulmonary parenchyma, while proliferative processes prevailed. On the contrary, in animals with inactivated TNF-α, in 100 % of observations, tuberculous peritonitis was detected with associated lung damage and the predominance of alterative caseous processes.Conclusion. The created model of tuberculous peritonitis shows the leading role of TNF-α in the activation of macrophages, as well as in attracting cells to the site of infection. This is the primary signal necessary for the formation and stability of granulomas since the neutralization of this cytokine leads to a loss of control over the infection and the destruction of the granuloma with the development of destructive tuberculosis in the serous coat of the abdominal cavity.

A Rare Case: Tuberculous Peritonitis, Encapsulating Peritoneal Sclerosis, and Incisional Hernia in Continuous Ambulatory Peritoneal Dialysis Patient

BACKGROUND: Peritonitis is the most common infectious complication of peritoneal dialysis (PD) with an estimated ratio of 1:20–30 patients per month. In addition, less than 3% cases are due to Mycobacteria, although not all are caused by Mycobacteria tuberculosis. Therefore, specific examinations are needed for proper diagnosis. Encapsulating peritoneal sclerosis (EPS), another rare complication of PD, accounts for 0.7–13.6 per 1000 patients per year. CASE REPORT: A 37-year-old man undergoing PD, with complaints of intermittent abdominal pain and cloudy fluid, followed by nausea, vomiting, and constipation. Furthermore, visible protrusion was observed on the abdominal wall due to the wound from the Tenckhoff catheter insertion surgery. This is clearly comprehended as the patient sits or stands but disappears on lying down. Along with the condition, continuous ambulatory PD (CAPD) ultrafiltration ability decreases, rough defecation occurs, with a hard sensation on the lower right abdomen. Moreover, the patient had earlier suffered peritonitis for the 3rd time. The results of the dialysate fluid analysis showed a cloudy liquid coloration, as the number of cells 278, polymorphonuclear 87, mononuclear 13, Ziehl–Neelsen +1 and acid-resistant bacteria +3 staining, including GeneXpert MTB/RIF, were positive. Furthermore, abdominal computed tomography (CT) scan revealed a thick peritoneum, partly with calcification, air-filled intestinal, dilated colon with wall thickening. Furthermore, the mesentery lining the liver and intestine were observed to be dense with multiple calcifications to support an EPS. Definitive diagnosis is confirmed by laparotomy and/or laparoscopy, but CT scan provides an alternative. Subsequently, CAPD utilization is discontinued and switched to renal replacement therapy to hemodialysis twice a week due to several complications associated with PD, ranging from recurrent peritonitis, tuberculous peritonitis, EPS, and incisional hernias responsible for an ineffective PD ultrafiltration. CONCLUSION: At present, the combination of clinical symptoms, radiology, and medical pathology remains the key to diagnosing tuberculous peritonitis and EPS. Consequently, prompt and precise analysis determines a good prognosis.

Features of the pathogenetic mechanisms of tuberculous peritonitis in an experiment

The prevalence of tuberculous peritonitis that has been observed in the recent decades is the result of lymphohematogenous spread of Mycobacterium tuberculosis (MBT) from lungs and other extrapulmonary sources. It is still unclear why certain organs and anatomical regions get involved in the inflammatory process during generalization of the tuberculosis infection. Why do some cases develop into peritoneal tuberculosis and other into kidney tuberculosis? Thus study aimed to investigate the pathogenesis of tuberculous peritonitis in a reproducible biological model. Tuberculous peritonitis was modeled in 18 rabbits (10 in the test group, 8 in control) by intraperitoneal inoculation of the MBT suspension. In order to suppress peritoneal macrophages and major cytokines, test group rabbits were injected with the TNFα inhibitor and iron (III) hydroxide sucrose complex before being infected, while control group rabbits received no immunosuppressive drugs. Autopsy of the control group animals revealed changes characteristic of pulmonary tuberculosis in 37.5% of cases, with no damage to other organs and systems registered. Conversely, test group rabbits had the signs of tuberculous peritonitis in their abdominal cavities. The results of this study suggest that it is the local immunity of an anatomical area that largely determines whether a secondary focus of extrapulmonary tuberculosis infection will develop there or not. For the peritoneum, a smaller pool of peritoneal macrophages and weaker cytokine production is a necessary and sufficient condition to have tuberculous peritonitis developing therein.