Epidemiology, clinical relevance and prognosis of staphylococci in hospital-acquired postoperative intra-abdominal infections: an observational study in intensive care unit.

The pathogenic role of staphylococci in hospital-acquired postoperative intra-abdominal infections (HAIs) has never been evaluated. In a tertiary care university hospital, we assessed the clinical characteristics and outcomes of patients admitted to the intensive care unit for HAIs according to the presence of staphylococci (S-HAI) or their absence (nS-HAI) in peritoneal cultures. Patients with S-HAIs were compared to nS-HAIs patients. Overall, 380 patients were analyzed, including 87 (23%) S-HAI patients [29 Staphylococcus aureus (Sa-HAIs) and 58 coagulase-negative staphylococci (CoNS-HAIs)]. The clinical characteristics did not differ between the S-HAI and nS-HAI patients. Adequacy of empirical anti-infective therapy was achieved less frequently in the staphylococci group (54 vs 72%, respectively, p < 0.01). The 90-day (primary endpoint) and one-year mortality rates did not differ between these groups. The S-HAI patients had decreased rates of postoperative complication (p < 0.05). The adjusted analysis of the clinical outcomes reported a decreased frequency of surgical complications in the staphylococci group (OR 0.43, 95% CI [0.20-0.93], p = 0.03). While the trends toward decreased morbidity criteria were observed in S-HAI patients, the clinical outcomes were not different between the CoNS-HAI and Sa-HAI patients. In summary, our data are not substantial enough to conclude that staphylococci exhibit no pathogenicity in HAIs.

Protective Effects of Baicalin on Peritoneal Tight Junctions in Piglets Challenged with Glaesserella parasuis.

Glaesserella parasuis (G. parasuis) causes inflammation and damage to piglets. Whether polyserositis caused by G. parasuis is due to tight junctions damage and the protective effect of baicalin on it have not been examined. Therefore, this study aims to investigate the effects of baicalin on peritoneal tight junctions of piglets challenged with G. parasuis and its underlying molecular mechanisms. Piglets were challenged with G. parasuis and treated with or without baicalin. RT-PCR was performed to examine the expression of peritoneal tight junctions genes. Immunofluorescence was carried out to detect the distribution patterns of tight junctions proteins. Western blot assays were carried out to determine the involved signaling pathways. Our data showed that G. parasuis infection can down-regulate the tight junctions expression and disrupt the distribution of tight junctions proteins. Baicalin can alleviate the down-regulation of tight junctions mRNA in peritoneum, prevent the abnormalities and maintain the continuous organization of tight junctions. Our results provide novel evidence to support that baicalin has the capacity to protect peritoneal tight junctions from G. parasuis-induced inflammation. The protective mechanisms of baicalin could be associated with inhibition of the activation of PKC and MLCK/MLC signaling pathway. Taken together, these data demonstrated that baicalin is a promising natural agent for the prevention and treatment of G. parasuis infection.

An Acquired and Endogenous Glycocalyx Forms a Bidirectional "Don't Eat" and "Don't Eat Me" Barrier to Phagocytosis.

Macrophages continuously survey their environment in search of pathogens or apoptotic corpses or debris. Targets intended for clearance expose ligands that initiate their phagocytosis ("eat me" signals), while others avoid phagocytosis by displaying inhibitory ligands ("don't eat me" signals). We report that such ligands can be obscured by the glycosaminoglycans and glycoproteins that coat pathogenic as well as malignant phagocytic targets. In addition, a reciprocal barrier of self-synthesized or acquired glycocalyx components on the macrophage surface shrouds phagocytic receptors, curtailing their ability to engage particles. The coating layers of macrophages and their targets hinder phagocytosis by both steric and electrostatic means. Their removal by enzymatic means is shown to markedly enhance phagocytic efficiency. In particular, we show that the removal of mucins, which are overexpressed in cancer cells, facilitates their clearance. These results shed light on the physical barriers that modulate phagocytosis, which have been heretofore underappreciated. VIDEO ABSTRACT.

[Tuberculous abdominal cocoon as a rare variant of peritonitis]. / Osumkovyvayushchii tuberkuleznyi perivistserit kak redkii variant peritonita.

OBJECTIVE: To study and systematize clinical symptoms of tuberculous perivisceritis, to clarify diagnostic value of laboratory and instrumental survey in these patients and to identify the features of surgical treatment. MATERIAL AND METHODS: There were 8 patients with tuberculous perivisceritis. Examination included computed tomography of the abdominal cavity and chest, ultrasound, laparoscopy. All patients underwent surgical treatment with histological, cytological, microbiological and molecular genetic analysis of peritoneal exudate and biopsy of peritoneal specimens. RESULTS: Clinical picture of tuberculous perivisceritis is variable and non-specific. Periods of exacerbation are replaced by periods of prolonged remission. The complex of radiological survey used in verification of perivisceritis does not allow accurate determining the nature of disease. However, peritoneal tuberculosis may be suspected as a rule considering signs of thickening of the peritoneum. Objective confirmation of perivisceritis is possible only during surgical intervention. In this case, etiological factor can be established only after a thorough histological examination of resected fibrous capsule. CONCLUSION: Clinical picture of tuberculous perivisceritis does not have specific symptoms. The disease is characterized by prolonged and undulating course. Acute peritonitis and acute intestinal obstruction may be suspected during exacerbation of the pathological process. Laparotomy followed by complete excision of fibrous capsule and adhesiolysis is preferred.

Use of adenosine deaminase (ADA) to diagnose suspected peritoneal tuberculosis in Rwanda: a cross-sectional study.

BACKGROUND: Peritoneal tuberculosis is the most common cause of low albumin gradient ascites in developing countries, but it can be easily confused with other causes of ascites. Peritoneal tuberculosis requires early recognition of symptoms and signs in order to make a quick diagnosis for appropriate treatment. Measurement of adenosine deaminase (ADA) level > 39 in ascites fluid is an established test to diagnose peritoneal tuberculosis. Many low-income countries do not currently test for adenosine deaminase in ascites fluid, including Rwanda. METHOD: Cross-sectional, descriptive study conducted through the Internal Medicine Department of three university teaching hospitals in Rwanda. Participants were patients older than 16 years presenting to tertiary referral hospitals with ascites of unknown cause. RESULTS: Of 103 ascites fluid samples collected, 52 of them (50.5%) had an elevated ADA, consistent with a presumptive diagnosis of peritoneal TB. Among those 52 subjects diagnosed with peritoneal TB, 39 out of 52 (75%) did not receive anti-TB medications. Among the 17 subjects who were treated with anti-TB medications, 4 of 17 (23.6%) did not have peritoneal TB based on ADA level. Samples with low-albumin gradient ascites were more likely to have high ADA ≥39 IU/L (p = 0.039). CONCLUSION: Our findings suggest that 3out of 4 patients with PTB in Rwanda are not getting TB treatment and 1 in 4 patients who are taking TB medications do not need it. Even if the true number of Rwandans who are being undertreated and overtreated is less than our study suggests, these results should prompt a larger study of peritoneal tuberculosis. Adding adenosine deaminase (ADA) to the diagnostic tools available to clinicians could help achieve the goal of correctly putting every Rwandan with tuberculosis on treatment, while avoiding unnecessary tuberculosis medications in those who do not have the disease.

Effect of (-)-α-Bisabolol on the Inflammatory Response in Systemic Infection Experimental Model in C57BL/6 Mice.

(-)-α-Bisabolol (BISA) is an unsaturated monocyclic sesquiterpenes compound, mainly found in the essential oil of chamomile (Matricaria chamomilla). It has been reported that this compound has several biological activities, but there are few studies evaluating the activity of this compound in the systemic inflammatory response in infectious processes. The aim of this study was to evaluate the effect of BISA on the inflammatory response and survival rate in a systemic infection model, and in vitro neutrophils phagocytic activity. BISA at concentration of 3, 10, 30, and 90 µg/ml did not presented in vitro cytotoxicity in MTT assay, and at concentrations of 1 and 3 µg/ml the BISA treatment increased in vitro phagocytic neutrophil activity. For the inflammatory response study, we verified the BISA treatment effect in a cecal ligation and puncture (CLP)-induced systemic infection model in mice; in this model, we demonstrate that BISA at dose of 100 mg/kg reduced the leukocyte recruitment in peritoneal cavity; at dose of 200 mg/kg, the NO concentration was increased in the peritoneal cavity. The bacteria CFU number was reduced in mice blood in the BISA treatment, at doses of 100 and 200 mg/kg. The BISA treatment at doses of 50 and 100 mg/kg increased the myeloperoxidase activity and reduction NO production in lung tissue of mice in CLP model. At dose of 100 mg/kg, the BISA treatment was able to reduce the mortality rate of mice submitted to CLP-induced sepsis and observed for 7 days. The results suggest an effect of BISA on inflammatory response, with activity on leukocyte chemotactic and NO production, in addition to increasing the survival rate of animals submitted to CLP model.

Impact of colibacillosis on production in laying hens associated with interference of the phosphotransfer network and oxidative stress.

The objective of this study was to evaluate the productive impact of colibacillosis on laying hens and to investigate whether energetic metabolism and oxidative stress were involved in the pathogenesis of the disease. An experimental shed containing 270 laying hens of the Hy-Line lineage (32 weeks old) presented approximately 40% daily laying, and many birds presented with diarrhea and apathy followed by death. Necropsy revealed macroscopic lesions compatible with colibacillosis and infectious agent Escherichia coli was isolated from fecal samples of all birds in the infected group, as well as from tissue (ovary, liver and peritoneum). Sixteen chickens were selected for this study, divided into two groups: Control (animals without clinical alterations) and infected (with diarrhea and apathetic). E. coli isolates were subjected to the antimicrobial susceptibility testing according to the methodology approved by CLSI, 2018. This testing showed sensitivity to gentamicin, amoxicillin, norfloxacin and colistin. It was then determined that laying hens would be treated with norfloxacin (15 mg/kg) diluted in water offered at will to the birds for three days. Blood collections were performed via brachial vein after the diagnosis of E. coli (before starting treatment) and seven days after treatment. Three debilitated chickens died on the second day after initiating therapy. Before treatment, birds with clinical signs had higher levels of lipoperoxidation (LPO) and activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx) than in the control group (asymptomatic animals). After treatment, LPO levels remained higher in birds that had clinical disease (infected group), whereas the activity of SOD and GPx enzymes did not differ between groups. Activity levels of creatine kinase (CK) and pyruvate kinase (PK) were higher in the group of chickens with clinical disease before treatment. Post-treatment, no differences were observed between groups in terms of CK; however, PK activity remained high in these animals. In the hens that died, there were lesions characteristic of avian colibacillosis, with ovary involvement, explaining the low laying activity of the birds at their peak of production. For 10 days after starting treatment, the percentage of laying increased to 90%. Therefore, we conclude that colibacillosis interferes with the phosphotransfer network by stimulating ATP production, in addition to causing oxidative stress of the birds during laying, that negatively affects health and productive efficiency.

Mansoura simple scoring system for prediction of spontaneous bacterial peritonitis: lesson learnt.

BACKGROUND AND OBJECTIVE: Spontaneous bacterial peritonitis (SBP) is a common bacterial infection with life-threatening sequelae in cirrhotic ascites. The purpose of this retrospective cohort study was to recognize the predictors of SBP to build up a noninvasive system to exclude or establish an episode of SBP. PATIENTS AND METHODS: Of 1194 consecutive patients with cirrhotic ascites, only 966 patients were enrolled in this study. SBP was diagnosed once polymorphonuclear count was at least 250 cells/mm and/or there was a positive ascitic fluid culture result. Biochemical and clinical parameters were evaluated as predictors of SBP. A scoring system was established in the training group of 682 and validated in a second group of 284 participants. RESULTS: The incidence of SBP was 12.3 and 12% in the training and validation groups, respectively. Age of at least 55 years, mean platelet volume (MPV) of at least 8.5 fl, neutrophil-to-lymphocyte ratio (NLR) of at least 2.5, and C-reactive protein (CRP) of at least 40 mg/l were identified as independent predictors of SBP. A scoring system including these four variables (age, MPV, and NLR with 1 point each, whereas CRP with 2 points) achieves a specificity of 98.2% with a positive predictive value for the diagnosis of SBP of 88.1% (score≥4). At a threshold of 1 point, the negative predictive value is 97.5% with a sensitivity of 92.9%. SBP is not associated with a high Model for End-stage Liver Disease score (P=0.135). CONCLUSION: The combination of age, MPV, NLR, and CRP in a simple scoring system, Mansoura simple scoring system, supports quick and accurate exclusion or diagnosis of SBP.

[Tuberculous peritonitis. 'Forgotten' disease]. / Tuberkuleznyi peritonit. 'Zabytaia' bolezn'.

AIM: To analyze diagnosis and treatment of patients with tuberculous peritonitis, to develop the algorithms for instrumental examination and differential diagnosis. MATERIAL AND METHODS: There were 48 patients with tuberculous peritonitis. The examination included radiography, abdominal and thoracic computed tomography, ultrasound, and laparoscopy. All patients underwent histological, cytological, microbiological and molecular-genetic analysis of abdominal exudate and peritoneal biopsy. Exclusion criterion was signs of secondary peritonitis. RESULTS: Clinical picture of tuberculous peritonitis was accompanied by nonspecific symptoms. Previously identified pulmonary tuberculosis and HIV-infection were present in 93.8 and 70.8% of patients. Diagnostic laparoscopy of abdominal cavity as the main method of instrumental diagnosis together with cytological, molecular-genetic and microbiological research of peritoneal exudate and tissue specimens were useful to determine diagnosis in 87.2-95.8% of cases. CONCLUSION: Tuberculous peritonitis may be assumed in patients with previous tuberculosis of lungs or other localizations, HIV-infection. Computed tomography is the most informative method to diagnose tuberculous peritonitis. Diagnostic laparoscopy is indicated for suspected tuberculous peritonitis. This procedure is supplemented by peritoneal biopsy, cytological, molecular-genetic and microbiological examination of peritoneal exudate and tissue specimens.

Clinical features and outcomes of abdominal tuberculosis in southeastern Korea: 12 years of experience.

BACKGROUND: Abdominal tuberculosis (TB) is an uncommon form of infection with Mycobacterium tuberculosis in Korea. In this study, we aimed to highlight the clinical features, diagnostic methods, and outcomes of abdominal TB over 12 years in Southeastern Korea. METHODS: A total of 139 patients diagnosed as having abdominal TB who received anti-TB medication from January 2005 to June 2016 were reviewed. Among them, 69 patients (49.6%) had luminal TB, 28 (20.1%) had peritoneal TB, 7 (5.0%) had nodal TB, 23 (16.5%) had visceral TB, and 12 (8.6%) had mixed TB. RESULTS: The most frequent symptoms were abdominal pain (34.5%) and abdominal distension (21.0%). Diagnosis of abdominal TB was confirmed using microbiologic and/or histologic methods in 76 patients (confirmed diagnosis), while the remaining 63 patients were diagnosed based on clinical presentation and radiologic imaging (clinical diagnosis). According to diagnostic method, frequency of clinical diagnosis was highest in patients with luminal (50.7%) or peritoneal (64.3%) TB, while frequency of microscopic diagnosis was highest in patients with visceral TB (68.2%), and frequency of histologic diagnosis was highest in patients with nodal TB (85.2%). Interestingly, most patients, except those with nodal TB, showed a good response to anti-TB agents, with 84.2% showing a complete response. The mortality rate was only 1.4% in the present study. CONCLUSIONS: Most patients responded very well to anti-TB therapy, and surgery was required in only a minority of cases of suspected abdominal TB.

Galectin-3 aggravates experimental polymicrobial sepsis by impairing neutrophil recruitment to the infectious focus.

Sepsis is an overwhelming systemic inflammation resulting from an uncontrolled infection that causes extensive tissue damage, organ dysfunction and eventually death. A growing body of evidence indicates that impaired neutrophil migration to the site of infection is associated with poor outcome in sepsis. Here we show that galectin-3 (Gal-3), an endogenous glycan-binding protein, plays a critical role in sepsis outcome. We found that serum Gal-3 concentration increased in patients with septic shock and mice undergoing sepsis induced by cecal ligation and puncture (CLP). Mice deficient in Gal-3 (Gal-3 KO) are more resistant to sepsis induced by CLP, showing lower levels of biochemical markers and neutrophil infiltration for organ injury/dysfunction than those observed in wild-type mice (WT). Furthermore, Gal-3 KO mice show an increased number of neutrophils in the primary focus of infection and reduced bacterial loads in the peritoneal cavity, blood, and lungs. Mechanistically, blood neutrophils from septic mice show higher levels of surface-bound Gal-3 than neutrophils from naive mice. The deficiency of Gal-3 was associated with increased rolling and adhesion of these cells in mesenteric venules. Our results indicate that Gal-3, secreted during sepsis, inhibits neutrophil migration into the infectious focus, which promotes the bacterial spread and worsens the outcome of sepsis.

Early cellular responses of germ-free and specific-pathogen-free mice to Francisella tularensis infection.

Bacteria that are highly virulent, expressing high infectivity, and able to survive nebulization, pose great risk to the human population. One of these is Francisella tularensis, the etiological agent of tularemia. F. tularensis is a subject of intense scientific interest due to the fact that vaccines for its immunoprophylaxis in humans are not yet routinely available. One of the substantial obstacles in developing such vaccines is our insufficient knowledge of processes that initiate and regulate the expression of effective protective immunity against intracellular bacteria. Here, we present data documenting the different pattern of cellular behavior occurring in an environment unaffected by microbiota using the model of germ-free mice mono-associated with F. tularensis subsp. holarctica strain LVS in comparison with a classic specific-pathogen-free murine model during early stages of infection.

Tissue macrophages as mediators of a healthy relationship with gut commensal microbiota.

Mammals and microorganisms have evolved a complex and tightly controlled mutual relationship. This interaction grants protection and energy source for the microorganisms, and on the other hand, provides several immunologic, metabolic and physiological advantages for the host. The gastrointestinal tract (GI) harbors the largest bacteria diversity within the body and complex mechanisms control microbiota community under homeostasis. However, once disrupted, microbiota imbalance can lead to overt growth of resident and invasive populations, with potential risk for lethal diseases. In these cases, bacteria might also escape from the intestines and reach different organs through the blood and lymphatic circulation. To control these unwanted conditions, all body tissues are populated with resident macrophages that have the ability to capture and eliminate pathogens, avoiding their dissemination. Here we discuss the different routes for bacterial translocation from the intestinal tract, and how macrophages act in the removal of these microorganisms to prevent systemic infections and restore the homeostasis.

Rat strain differences in peritoneal immune cell response to selected gut microbiota: A crossroad between tolerance and autoimmunity?

AIMS: Some gut commensals can be protective, whereas others are implicated as necessary for development of inflammatory/autoimmune diseases. Peritoneal immune cells may play an important role in promoting autoimmunity in response to gut microbiota. This study investigated the phenotype and the function of peritoneal immune cells in the autoimmunity-resistant Albino Oxford (AO), and the autoimmunity-prone Dark Agouti (DA) rat strains upon stimulation with their own colonic E. coli or Enterococcus. MAIN METHODS: Rats were intraperitoneally injected with their own E. coli or Enterococcus. Peritoneal cells isolated two days later were tested for nitric oxide (NO) and cytokine production, and for arginase and myeloperoxidase (MPO) activity. The phenotype of cells was determined using flow cytometry. KEY FINDINGS: While the Enterococcus injection did not affect the composition of peritoneal cells in AO rats, the E. coli treatment increased the percentages of activated CD11bintHIS48hi neutrophils, and decreased the proportion of resident (CD11bhiHIS48int/low, CD163 + CD86+) and anti-inflammatory CD68 + CD206+ macrophages. E. coli increased the production of NO and urea, but preserved their ratio in cells from AO rats. Conversely, both E. coli and Enterococcus diminished the proportion of resident and anti-inflammatory macrophages, increased the proportion of activated neutrophils, and induced inflammatory polarization of peritoneal cells in DA rats. However, injection of E. coli maintained the ratio of typical CD11bintHIS48int neutrophils in DA rats, which correlated with the sustained MPO activity. SIGNIFICANCE: The rat strain differences in peritoneal cell response to own commensal microbiota may contribute to differential susceptibility to inflammatory/autoimmune diseases.

Peritonitis with Listeria monocytogenes in a patient on automated peritoneal dialysis.

We present a case where Listeria monocytogenesserotype 1/2a was determined to be the causative agent of peritonitis in a patient on automated peritoneal dialysis. The patient, a 53-year-old Caucasian woman from the Faroe Islands was admitted to the National Hospital reporting of constant abdominal pain and a fever. Peritoneal cultures were positive for growth of L. monocytogenes. The patient was successfully treated with oral amoxicillin for 2 weeks and intraperitoneal vancomycin for 3 weeks. To date, the patient has not been readmitted due to peritonitis. The Faroese salmon was the suspected source of infection with L. monocytogenes.

Inflammatory response and peritoneal contamination after transrectal natural orifice specimen extraction (NOSE) versus mini-laparotomy: a porcine in vivo study.

BACKGROUND: Transrectal natural orifice specimen extraction (NOSE) avoids abdominal organ retrieval during laparoscopic procedures and may reduce surgical trauma. However, this has not been proven clinically and transrectal peritoneal contamination is feared to cause infectious complications. This experimental study was designed to evaluate inflammatory response and peritoneal contamination after transrectal NOSE versus mini-laparotomy. METHODS: 24 German Landrace pigs underwent transrectal NOSE (N = 12) or mini-laparotomy (N = 12) for standardized extraction of water-instilled balloon. Blood samples were taken for analysis of leucocytes, CRP, IL-6, IL-10, and TNFα at 6, 12, 24, 48, 72 h as well as 7 and 14 days postoperatively. After 14 days laparoscopy was performed to inspect the abdomen and for microbiological swab sampling. RESULTS: Leucocytes were higher in the NOSE group at 72 h (19.3 ± 3.9/nl vs. 15.8 ± 4.2/nl, p = 0.046). IL-6 was lower in the NOSE group at day 7 (165 ± 100/nl vs. 306 ± 70/nl, p = 0.030). No difference was found comparing inflammatory parameters at all other time points. No difference was found regarding peritoneal contamination, which was 58.3% (7/12) in the NOSE group and 41.7% (5/12) in the MiniLap group (p = 0.414). CONCLUSIONS: The results suggest a pronounced acute inflammatory response after transrectal NOSE compared to mini-laparotomy, while late cytokine response seems to be less after transrectal NOSE, which may reflect less intense wound healing process. Using standardized rectal decontamination and endolumenal colon occlusion transrectal NOSE seems to be safe and comparable to mini-laparotomy with regard to peritoneal contamination. Clinical evidence is needed now to weight transrectal NOSE against mini-laparotomy during laparoscopic surgery.