Spontaneous bacterial peritonitis

Koulaouzidis, Anastasios; Bhat, Shivaram; Saeed, Athar A.

doi:10.3748/wjg.15.1042

Cited by 112 publications

(94 citation statements)

References 87 publications

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“…Common Gram-negative bacteria such as Escherichia coli and other coliforms such as Klebsiella spp. have been reported to be causative agents in at least 50% of cases [6][7][8][9][10]. Other causative organisms reported have included pneumococci, streptococci and miscellaneous Gram-positive and other Gram-negative organisms [6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Characterisation of bacteria in ascites—reporting the potential of culture-independent, molecular analysis

Rogers

Russell

Preston

et al. 2010

Eur J Clin Microbiol Infect Dis

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Spontaneous bacterial peritonitis (SBP) is a severe complication of liver disease. A significant proportion of patients have culture-negative ascites, despite having similar signs, symptoms and mortality to those with SBP. Therefore, empirical antibiotic treatment for infection is often started without knowledge of the causative organisms. Here, we investigated the potential of molecular techniques to provide rapid and accurate characterisation of the bacteria present in ascitic fluid. Ascites samples were obtained from 29 cirrhotic patients undergoing clinically indicated therapeutic paracentesis. Bacterial content was determined by terminal restriction fragment length polymorphism (T-RFLP) analysis, quantitative polymerase chain reaction (PCR) and 16S ribosomal clone sequence analysis. Bacterial signal was detected in all samples, compared to three out of ten using standard methods. Bacterial loads ranged from 5.5 × 10 2 to 5.4 × 10 7 cfu/ml, with a mean value of 1.9 × 10 6 cfu/ml (standard deviation± 9.6 × 10 6 cfu/ml). In all but one instance, bacterial species identified by culture were also confirmed by molecular analyses. Preliminary data presented here suggests that culture-independent, molecular analyses could provide rapid characterisation of the bacterial content of ascites fluid, providing a basis for the investigation of SBP development and allowing early and targeted antibiotic intervention.

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Section: Introductionmentioning

confidence: 99%

Characterisation of bacteria in ascites—reporting the potential of culture-independent, molecular analysis

Rogers

Russell

Preston

et al. 2010

Eur J Clin Microbiol Infect Dis

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“…Spontaneous bacterial peritonitis is a frequent and severe complication of decompensated cirrhosis [98]. Bacterial translocation is the key mechanism in its pathogenesis and the common causative microorganisms are gram-negative bacteria such as Escherichia coli and Klebsiella pneumoniae [99]. The clinical manifestations of spontaneous bacterial peritonitis are subtle and require a high index of suspicion and almost always occur in a large volume of ascites in patients with liver cirrhosis.…”

Section: Ascites: the Portal Hypertensive Peritoneummentioning

confidence: 99%

“…On the contrary, "bacteriascites" is the term used to describe the colonization of ascitic fluid by bacteria in the absence of a local inflammatory reaction, which suggests the concurrent failure of defensive mechanisms [99].…”

Section: Ascites: the Portal Hypertensive Peritoneummentioning

confidence: 99%

“…Abdominal pain can be continuous and is different from tense ascites. Ascitic polymorphonuclear leukocyte cell count is essential for diagnosis and management [98,99]. However, by means of a polymerase chain reaction (PCR)-based method and automated nucleotide sequencing is possible to detect and identify the presence of fragments of bacterial DNA in patients with culture-negative, non-neutrocytic ascites, indicating the existence of bacterial DNA translocation [100].…”

Section: Ascites: the Portal Hypertensive Peritoneummentioning

confidence: 99%

“…However, by means of a polymerase chain reaction (PCR)-based method and automated nucleotide sequencing is possible to detect and identify the presence of fragments of bacterial DNA in patients with culture-negative, non-neutrocytic ascites, indicating the existence of bacterial DNA translocation [100]. Paralysis ileus, hypotension and hypothermia are seen in advanced illness, where prognosis may be death and one third of patients will develop renal failure [90,99].…”

Section: Ascites: the Portal Hypertensive Peritoneummentioning

confidence: 99%

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Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Aller¹,

Arias²,

Prieto³

et al. 2012

ABB

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Prehepatic portal hypertension induces a splanchnic low-grade inflammatory response that could switch to high-grade inflammation with the development of severe and life-threatening complications when associated with chronic liver disease. The extraembryonic origin of the portal system maybe determines the regression to an extraembryonic phenotype, i.e., vitellogenic and amniotic, during the evolution of both types of portal hypertension. Thus, prehepatic portal hypertension, or compensated hypertension by portal vein ligation in the rat, is associated with molecular mechanisms related to vitellogenesis, where hepatic steatosis and splanchnic angiogenesis stand out. In turn, extrahepatic cholestasis in the rat induces intrahepatic portal hypertension, or decompensated hypertension, with ascites and hepatorenal syndrome. The splanchnic interstitium, the mesenteric lymphatic system, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of ascites. The hypothetical comparison between the ascitic and the amniotic fluid also allows for translational investtigation. The induced regression of the splanchnic system to extraembryonic functions by portal hypertension highlights the great relevance of the extraembryonic structures even during post-natal life.

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Etiology and mortality of spontaneous bacterial peritonitis in liver transplant recipients: A cohort study

et al. 2014

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Spontaneous bacterial peritonitis (SBP) in liver transplantation (LT) recipients who progress to cirrhosis has received little attention. We investigated the adequacy of empirical treatment with third-generation cephalosporins for SBP in this population and the impact of transplantation on the evolution of the infection. We performed a cohort study with 138 SBP episodes: 19 in LT patients and 119 in non-LT patients. The etiology of SBP was identified for 73.7% of the episodes in LT patients and for 38.7% of the episodes in non-LT patients (P 5 0.004). The main microorganisms in recipients were Escherichia coli (35.7%) and Streptococcus pneumoniae (21.4%). The etiologies did not differ in non-LT patients. The cephalosporin sensitivity was similar in the 2 groups (85.7% versus 78.4%, P 5 0.7). LT recipients developed renal failure (57.9% versus 25.2%, P 5 0.004) and encephalopathy (42.1% versus 22%, P 5 0.08) more often than non-LT patients, and the mortality rates during episodes (52.6% versus 13.4%, P < 0.001) and at 6 months (70.6% versus 34.7%, P 5 0.005) were higher. According to a multivariate analysis, the mortality-associated risk factors at diagnosis were a Model for End-Stage Liver Disease (MELD) score > 18 odds ratio (OR) 5 6.1 and being an LT recipient (OR 5 4.45). At 6 months, the risk factors for mortality were a MELD score > 18 (OR 5 3.08), being an LT recipient (OR 5 3.47), a known etiology (OR 5 2.08), and the presence of hepatocellular carcinoma (OR 5 3.73). Liver Transpl 20:856-863, 2014. V C 2014 AASLD.Received January 14, 2014; accepted April 3, 2014.The treatment of choice for end-stage cirrhosis is liver transplantation (LT). Nonetheless, the recurrence of the primary disease, the development of liver cirrhosis (especially in patients with hepatitis C virus, in whom reinfection almost always occurs), and associated complications are common causes of late graft loss and have an impact on morbidity and mortality. [1][2][3][4] It is well recognized that spontaneous bacterial peritonitis (SBP) is associated with a high mortality rate (approximately 20%) in patients with cirrhosis, 5-7 and the first SBP episode predicts a significant decrease in survival, even in the short term, with 1-year survival rates ranging from 28.5% to 93%. [8][9][10][11][12][13] Nonantipseudomonal third-generation cephalosporins (3CP) are the treatment of choice for SBP, 5,6,10 but several recent studies have reported that bacterial resistance to 3CP has reached a disturbing level of 43%. 6,14 Nosocomial and health care-related infections are often associated with multidrug-resistant microorganisms such as Enterobacteriaceae producing extended-spectrum beta-

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Spontaneous bacterial peritonitis

Cited by 112 publications

References 87 publications

Characterisation of bacteria in ascites—reporting the potential of culture-independent, molecular analysis

Characterisation of bacteria in ascites—reporting the potential of culture-independent, molecular analysis

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Etiology and mortality of spontaneous bacterial peritonitis in liver transplant recipients: A cohort study

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