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Identification of Ascitic Fluid Bacterial Pathogens in Spontaneous Bacterial Peritonitis

Not Applicable
Conditions
Primary Bacterial Peritonitis
Interventions
Other: ascitic fluid culture and microbiological testing
Registration Number
NCT02463721
Lead Sponsor
Tanta University
Brief Summary

Several studies have pointed out changes in the epidemiology of the causative bacteria in SBP and bacterascites and in their susceptibility to antibiotics. In particular, the development of beta-lactamase enzymes, which confer resistance to clavulanate, or extended spectrum beta-lactamases in Escherichia coli. The potential emergence of enterococci, methicillin-resistant S. aureus, or fluoroquinolone-resistant bacteria, following norfloxacin prophylaxis, is also a cause of concern since they may be associated with a higher risk of therapeutic failure.

The microbial etiology of SBP remains relatively constant; however, the antibiotic resistance rate especially for third-generation cephalosporins (including cefotaxime and ceftazidime), ciprofloxacin, and ofloxacin increased dramatically

Detailed Description

Spontaneous bacterial peritonitis (SBP), defined as an infection of ascites in the absence of a contiguous source of infection.

Spontaneous bacterial peritonitis (SBP) is a common and potentially fatal bacterial infection in patients with cirrhosis and ascites, occurring in 10 to 30% of patients, with in-hospital mortality rates ranging from 20 to 30% .

It is secondary to impaired humoral and cellular immune responses that result in indirect intestinal bacterial translocation into the ascitic fluid.

SBP is also associated with a poor long-term prognosis for patients, as mortality rates can reach 50 to 70% at 1 year.

Early diagnosis and early optimal treatment of these infections with appropriate antibiotics and the prevention of hepatorenal syndrome with albumin are required .

Current European and most other international guidelines recommend the use of a third-generation cephalosporin as the first choice, or amoxicillin-clavulanate acid or fluoroquinolones as an alternative choice.

These recommendations are based mainly on clinical trials that were very often conducted a decade or more ago, and on the assumption that E. coli would be involved in nearly half of the cases.

Several studies have pointed out changes in the epidemiology of the causative bacteria in SBP and bacterascites and in their susceptibility to antibiotics. In particular, the development of beta-lactamase enzymes, which confer resistance to clavulanate, or extended spectrum beta-lactamases in Escherichia coli.The potential emergence of enterococci, methicillin-resistant S. aureus, or fluoroquinolone-resistant bacteria, following norfloxacin prophylaxis, is also a cause of concern since they may be associated with a higher risk of therapeutic failure.

Recruitment & Eligibility

Status
UNKNOWN
Sex
All
Target Recruitment
100
Inclusion Criteria
  • Liver cirrhosis with ascites and suspected to have SBP.
  • ascitic fluid PMNL ≥ 250 cells/mm3
Exclusion Criteria
  • ascitic fluid with polymicrobial infections
  • patients started empirical antibiotics without prior culture.

Study & Design

Study Type
INTERVENTIONAL
Study Design
SINGLE_GROUP
Arm && Interventions
GroupInterventionDescription
SBP patientsascitic fluid culture and microbiological testingascitic fluid culture and microbiological testing for 100 patients with liver cirrhosis and ascites with suspicion of SBP
Primary Outcome Measures
NameTimeMethod
identification of SBP bacterial pathogens through gram stain or other specific stains6 months

identification of SBP bacterial pathogens through gram stain or other specific stains

Secondary Outcome Measures
NameTimeMethod

Trial Locations

Locations (1)

Tanta university hospital

🇪🇬

Tanta, Egypt

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