In this editorial, we comment on the article by Liakina V: "Antibiotic resistance in patients with liver cirrhosis: Prevalence and current approach to tackle" (World J Clin Cases 2023, 11: 7530-7542). In this excellent review, Liakina presents current data on bacterial complications in patients with cirrhosis. Bacterial infections are the most common complication in patients with liver cirrhosis. We focus specifically on spontaneous bacterial peritonitis (SBP) which is the most representative infectious complication. Liakina V suggested starting empirically, in all patients with suspected SBP, third-generation cephalosporins when the number of polymorphonuclear leukocytes (PMNs) in ascites is greater than 250/mm3. This statement creates some doubts in our clinical practice so we discuss on the unsolved pitfalls of diagnosis and treatment that are often encountered in patients with ascitic fluid infections, especially on bacterascites that is defined as ascitic bacterial growth with PMNs below 250/mm3. The severity of liver disease and overall prognosis are highly comparable for patients with bacterascites and SBP in some recent well-conducted studies. Furthermore, we present a brief analysis of the prevalence of antibiotic-resistant isolates with an introduction of currently approved antibiotic drug options to treat ascitic fluid infections avoiding antibiotic resistance. In light of the most recent epidemiological data, third-generation cephalosporins should not be considered as an empirical antibiotic treatment of choice for ascitic fluid infections.

Third-generation cephalosporins (3rd GCs) have recently become controversial as the first-line strategy for empirical spontaneous bacterial peritonitis (SBP) treatment. This study aimed to identify SBP treatment efficacy predictors of 3rd GCs.

In this retrospective cohort study, 279 cirrhosis patients with SBP who received 3rd GC monotherapy for initial empirical treatment from 2013 to 2019 were included. Nonresponse was defined as a decreased ascites polymorphonuclear (PMN) count < 25% from baseline after 48 hours of antibacterial treatment. Multivariate regression analysis was used to identify efficacy predictors of 3rd GCs in treating SBP. Kaplan-Meier analysis was used to evaluate survival data.

The nonresponder group included 120 patients with no response, and the responder group included 159 patients with responses. The response rate to 3rd GCs was 57.0% among all patients. The common pathogens were Escherichia coli (40.6%), Staphylococcus (15.6%), Klebsiella pneumonia (12.5%), and Streptococcus (12.5%) in 32 ascites culture isolates. Nosocomial SBP (NSBP) (odds ratio [OR]: 2.371, 95% confidence interval [CI]: 1.323-4.249, P = .004), pneumonia (OR: 11.561, 95% CI: 1.876-71.257, P = .008), recurrent SBP (OR: 3.386, 95% CI: 1.804-6.357, P < .001), platelet count (≥113.5 × 109/L) (OR: 3.515, 95% CI: 1.973-6.263, P < .001), and ascites PMN count (≤0.760 × 109/L) (OR: 4.967, 95% CI: 2.553-9.663, P < .001) were independent predictors of nonresponse to 3rd GCs against SBP. Survival plot analysis at 30 days showed worse survival for the nonresponders (P = .003).

NSBP, pneumonia, recurrent SBP, increased platelet count, and lower ascites PMN count were independent predictors of nonresponse to 3rd GC in treating SBP. Nonresponse to initial antibiotic treatment was associated with worse survival.

Carbapenem antibiotics were first introduced in the 1980s and have long been considered the most active agents for the treatment of multidrug-resistant gram-negative bacteria. Over the last decade, carbapenem-resistant Enterobacteriaceae (CRE) have emerged as organisms causing spontaneous bacterial peritonitis. Infections caused by CRE have shown a higher mortality rate than those caused by bacteria sensitive to carbapenem antibiotics. Current antibiotic guidelines for the treatment of spontaneous bacterial peritonitis are insufficient, and rapid de-escalation of empiric antibiotic treatment is not widely recognized. This review summarizes the molecular characteristics, epidemiology and possible treatment of spontaneous bacterial peritonitis caused by CRE.

Introduction: Spontaneous bacterial peritonitis (SBP) is a main infectious complication in end-stage liver disease (ESLD) patients. The increasing trend of bacterial resistance in ESLD patients with SBP has been associated with low treatment efficacy of traditional therapy. Cephalosporin use has been restricted to community-acquired infections and in areas/health care settings with low rates of multidrug-resistant (MDR) bacteria. To date, several changes are necessary with regard to empiric therapy recommendations in areas/health care settings with high rates of MDR bacteria. Areas covered: An overview of the epidemiology and antimicrobial treatments of SBP caused by Gram-negative bacteria. Expert opinion: Broad-spectrum antibiotics have been recommended as empiric therapy for suspected SBP in areas/health care settings with high rates of MDR bacteria and secondary treatment, with newer antibiotics, for SBP caused by MDR-Gram-negative bacteria (i.e. new beta-lactam/beta-lactamase inhibitor combinations, cefiderocol, plazomicin, and eravacycline) either alone or in combination.

The Chinese Society of Hepatology developed the current guidelines for the Management of Ascites and Its Related Complications in Cirrhosis based on the published evidences and the panelists' consensus. The guidelines provided recommendations for the diagnosis and management of cirrhotic ascites emphasizing a step-wise approach with the first-, second-, and third-line therapy. For refractory ascites, vasoconstrictors and albumin are recommended for splanchnic vasodilation and selective vasopressin (V2) receptor antagonists for moderate-to-severe hyponatremia. For spontaneous bacterial peritonitis, empirical anti-infection treatment was recommended based on the local microbiological examination of community- or hospital-acquired infections. For hepatorenal syndrome, the administration of vasopressor terlipressin and albumin is recommended.

Spontaneous bacterial peritonitis (SBP) is the most common infection in end-stage liver disease patients. SBP is defined as an ascitic fluid infection with a polymorphonuclear leucocyte count ≥ 250/mm3 without an evident intra-abdominal surgically treatable source. Several mechanisms contribute to SBP occurrence, including translocation of gut bacteria and their products, reduced intestinal motility provoking bacterial overgrowth, alteration of the gut's barrier function and local immune responses. Historically, Gram-negative enteric bacteria have been the main causative agents of SBP, thereby guiding the empirical therapeutic choice. However, over the last decade, a worryingly increasing prevalence of Gram-positive and multi-drug resistant (MDR) SBP has been seen. Recently, the microbiological spectrum of SBP seems to have changed in Europe due to a high prevalence of Gram-positive bacteria (48%-62%). The overall proportion of MDR bacteria is up to 22%-73% of cases. Consequently, empirical therapy based on third-generation cephalosporins or amoxicillin/clavulanic acid, can no longer be considered the standard of care, as these drugs are associated with poor outcomes. The aim of this review is to describe, with an epidemiological focus, the evidence behind this rise in Gram-positive and MDR SBP from 2000 to present, and illustrate potential targeted therapeutic strategies. An appropriate treatment protocol should include daptomycin plus ceftaroline and meropenem, with prompt stepdown to a narrower spectrum when cultures and sensitivity data are available in order to reduce both cost and potential antibiotic resistance development.

To systematically review literature upon aetiology of nosocomial spontaneous bacterial peritonitis (N-SBP) given the rising importance of multidrug-resistant (MDR) bacteria.

A literature search was performed on MEDLINE and Google Scholar databases from 2000 to 15th of November 2016, using the following search strategy: "spontaneous" AND "peritonitis".

The initial search through electronic databases retrieved 2556 records. After removing duplicates, 1958 records remained. One thousand seven hundred and thirty-five of them were excluded on the basis of the screening of titles and abstract, and the ensuing number of remaining articles was 223. Of these records, after careful evaluation, only 9 were included in the qualitative analysis. The overall proportion of MDR bacteria turned out to be from 22% to 73% of cases across the studies.

N-SBP is caused, in a remarkable proportion, by MDR pathogens. This should prompt a careful re-assessment of guidelines addressing the treatment of this clinical entity.