Changes in etiologic and antibiotic resistance profiles of bacteria causing spontaneous peritonitis in Egyptian patients with liver cirrhosis

ABSTRACT

To evaluate the recent changes in bacteria causing spontaneous bacterial peritonitis [SBP] in cirrhotic patients and its clinical significance on treatment, we compared the etiologic agents and their antibiotic resistance profiles over a four year period. In the prospective period of the study, 150 ascitic fluid [AF] samples obtained from SBP patients admitted consecutively to the Hepatology Department of Theodor Bilharz Research Institute during 2006-2007 were examined for polymorphnuclear leukocytes [PMLs] by blood cell counter and by a bedside dipstick test [Multistix SG10, Bayer]. Blood and AF cultures were performed using BACTEC blood culture bottles and purified bacterial isolates were identified with a BBL Crystal Id System and software. Antibiotic sensitivity testing and extended-spectrum beta-lactamase [ESBL]- production were determined by disk diffusion and modified double disk synergy tests [MDDST] respectively. Genes encoding ESBLs were detected by PCR and typed by DNA sequencing. In the retrospective period of the study [2004-2005], the laboratory records of 140 episodes of SBP were examined for the culture positive rate, causes of SBP and their antibiotic resistance patterns recorded. Results showed that the overall culture positivity rate was significantly higher in prospective study period [32%] versus retrospective period [16.4 %] p<0.05 and the main bacterial isolates were E.coli, 47.8% and Klebsiella pneumoniae, 28.1% with no differences in the two study periods. Gram positive bacteria [GPB] were isolated more frequently in the prospective than retrospective period [25% versus 13%]. Two opportunistic bacterial species [Staphylococcus haemolyticus and Pantoea agglomerans] were detected as a cause of SBP in the prospective period. Species identification of Pantoea isolate was confirmed by DNA extraction, sequencing of ribosomal RNA and phylogenetic analysis. ESBLs were detected among 17.6% of E. coli and Klebsiella isolates of the prospective period and all were of the CTX-M15 type. The rate of resistance to cefotaxime significantly increased from 45% to 72 % and to ciprofloxacin from 25% to 47% and treatment failure rate was 65% in recent years. No resistance was detected to imipenem over the entire study period. For the GPB, 50% were resistant to ampicilin/sulbactam, cefotaxime and gentamicin and one S. haemolyticus isolate was methicillin resistant. In conclusion the emergence of multidrug resistant opportunistic pathogens and ESBL-producing E. coli and Klebsiellae as causal agents of SBP, together with an increase in resistance to antibiotics commonly used for the empiric treatment of bacterial peritonitis have serious implications on patient management in our region. Rapid diagnosis of SBP by a bedside dipstick test and identification of the causative organism by culture using blood culture bottles and direct sensitivity testing to establish an effective antibiotic therapy is recommended