Patterns of Antimicrobial Resistance in the Causative Organisms of Spontaneous Bacterial Peritonitis: A Single Centre, Six-Year Experience of 1981 Samples
Background/Aims. Spontaneous bacterial peritonitis (SBP) is one of the leading causes of morbidity and mortality in patients with cirrhosis. This study aims to determine the microbial agents of SBP and the pattern of antibiotic resistance, in a large number of ascitic samples. Methodology. In a cross-sectional, single center, hospital based study, 1981 consecutive ascitic fluid samples were recruited from 2005 to 2011. Samples were dichotomized into three-year periods, in order to assess the trend of resistance to the first-line empirical antibiotics. Results. SBP was found in 482 (24.33%) of samples, of which 314 (65.15%) were culture positive. The most prevalent isolated pathogen was E. coli (33.8%), followed by staphylococcus aureus (8.9%) and Enterococcus (8.6%). No significant changes in the proportion of gram-negative/gram-positive infections occurred during this period. A percentage of resistant strains to cefotaxime (62.5%, 85.7%), ceftazidim (73%, 82.1%), ciprofloxacin (30, 59.8%), ofloxacin (36.8%, 50%), and oxacilin (35%, 51.6%) were significantly increased. E. coli was most sensitive to imipenem, piperacillin-tazobactam, amikacin, ceftizoxime, and gentamicin. Conclusions. The microbial aetiology of SBP remains relatively constant. However, the resistance rate especially to the first-line recommended antibiotics was significantly increased. This pattern must be watched closely and taken into account in empirical antibiotic treatment. 1. Introduction Spontaneous bacterial peritonitis (SBP) is one of the leading causes of morbidity and mortality in patients with cirrhosis [1–3]. Unselected hospitalized cirrhotic patients with ascites were estimated to have 10%–30% risk of developing SBP [2, 3]. Early diagnosis and a prompt antibiotic therapy have considerably decreased the mortality rate associated with an episode of SBP from 80% to approximately 20–30% in the last decade [1, 2, 4–6]. SBP is defined as a monomicrobial infection of the ascitic fluid, which is not accompanied by a definite evidence of a surgically treatable origin [1, 3, 4]. The infection occurs following a translocation or haematogenous dissemination of the intestinal flora. Intestinal bacterial overgrowth can also exacerbate the condition [1, 3]. Studies have indicated that gram-negative Enterobacteriaceae such as Escherichia coli (E. coli) was the most common isolated organisms in SBP [1, 3, 7]. Diagnosis of SBP is established by an elevated ascitic fluid polymorphonuclear leukocyte (PMNL) count (≥250 cells/mm3) [1, 3, 4]. Some studies suggest that the type and the etiology of
References
[1]
European Association for the Study of the Liver, “EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis,” Journal of Hepatology, vol. 53, no. 3, pp. 397–417, 2010.
[2]
S. Ageloni, C. Leboffe, A. Parente et al., “Efficacy of current guidelines for the treatment of spontaneous bacterial peritonitis in the clinical practice,” World Journal of Gastroenterology, vol. 14, no. 17, pp. 2757–2762, 2008.
[3]
J. M. Lee, K.-H. Han, and S. H. Ahn, “Ascites and spontaneous bacterial peritonitis: an Asian perspective,” Journal of Gastroenterology and Hepatology, vol. 24, no. 9, pp. 1494–1503, 2009.
[4]
G. Garcia-Tsao, “Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis,” Gastroenterology, vol. 120, no. 3, pp. 726–748, 2001.
[5]
R. Terg, S. Cobas, E. Fassio et al., “Oral ciprofloxacin after a short course of intravenous ciprofloxacin in the treatment of spontaneous bacterial peritonitis: results of a multicenter, randomized study,” Journal of Hepatology, vol. 33, no. 4, pp. 564–569, 2000.
[6]
N. Singh, M. M. Wagener, and T. Gayowski, “Changing epidemiology and predictors of mortality in patients with spontaneous bacterial peritonitis at a liver transplant unit,” Clinical Microbiology and Infection, vol. 9, no. 6, pp. 531–537, 2003.
[7]
M. K. Park, J. H. Lee, Y. H. Byun et al., “Changes in the profiles of causative agents and antibiotic resistance rate for spontaneous bacterial peritonitis: an analysis of cultured microorganisms in recent 12 years,” The Korean Journal of Hepatology, vol. 13, no. 3, pp. 370–377, 2007.
[8]
J.-H. Lee, J.-H. Yoon, B. H. Kim et al., “Enterococcus: not an innocent bystander in cirrhotic patients with spontaneous bacterial peritonitis,” European Journal of Clinical Microbiology and Infectious Diseases, vol. 28, no. 1, pp. 21–26, 2009.
[9]
A. Alexopoulou, N. Papadopoulos, D. G. Eliopoulos et al., “Increasing frequency of gram-positive cocci and gram-negative multidrug- resistant bacteria in spontaneous bacterial peritonitis,” Liver International, vol. 33, no. 7, pp. 975–981, 2013.
[10]
J. Lata, O. Stiburek, and M. Kopacova, “Spontaneous bacterial peritonitis: a severe complication of liver cirrhosis,” World Journal of Gastroenterology, vol. 15, no. 44, pp. 5505–5510, 2009.
[11]
L. Piroth, A. Pechinot, A. Minello et al., “Bacterial epidemiology and antimicrobial resistance in ascitic fluid: a 2-year retrospective study,” Scandinavian Journal of Infectious Diseases, vol. 41, no. 11-12, pp. 847–851, 2009.
[12]
J. Fernández, M. Navasa, J. Gómez et al., “Bacterial infections in cirrhosis: epidemiological changes with invasive procedures and norfloxacin prophylaxis,” Hepatology, vol. 35, no. 1, pp. 140–148, 2002.
[13]
H. G. Song, H. C. Lee, Y. H. Joo et al., “Clinical and microbiological characteristics of spontaneous bacterial peritonitis (SBP) in a recent five year period,” Taehan Kan Hakhoe Chi, vol. 8, no. 1, pp. 61–70, 2002.
[14]
A. Umgelter, W. Reindl, M. Miedaner, R. M. Schmid, and W. Huber, “Failure of current antibiotic first-line regimens and mortality in hospitalized patients with spontaneous bacterial peritonitis,” Infection, vol. 37, no. 1, pp. 2–8, 2009.
[15]
G. Bhat, K. E. Vandana, S. Bhatia, D. Suvarna, and C. G. Pai, “Spontaneous ascitic fluid infection in liver cirrhosis: bacteriological profile and response toantibi otic therapy,” Indian Journal of Gastroenterology, vol. 32, no. 5, pp. 297–301, 2013.
[16]
P. A. Reuken, M. W. Pletz, M. Baier, W. Pfister, A. Stallmach, and T. Bruns, “Emergence of spontaneous bacterial peritonitis due to enterococci—risk factors and outcome in a 12-year retrospective study,” Alimentary Pharmacology and Therapeutics, vol. 35, no. 10, pp. 1199–1208, 2012.
[17]
T. Yakar, M. Gü？lü, E. Serin, and H. AlI？kan, “A recent evaluation of empirical cephalosporin treatment and antibiotic resistance of changing bacterial profiles in spontaneous bacterial peritonitis,” Digestive Diseases and Sciences, vol. 55, no. 4, pp. 1149–1154, 2010.
[18]
X. Ariza, J. Castellote, J. Lora-Tamayo et al., “Risk factors for resistance to ceftriaxone and its impact on mortality in community, healthcare and nosocomial spontaneous bacterial peritonitis,” Journal of Hepatology, vol. 56, no. 4, pp. 825–832, 2012.
[19]
P. Tandon, A. Delisle, J. E. Topal, and G. Garcia-Tsao, “High prevalence of antibiotic-resistant bacterial infections among patients with cirrhosis at a US liver center,” Clinical Gastroenterology and Hepatology, vol. 10, no. 11, pp. 1291–1298, 2012.
[20]
J. Acevedo, A. Silva, V. Prado, and J. Fernandez, “The new epidemiology of nosocomial bacterial infections in cirrhosis: therapeutical implications,” Hepatology International, vol. 7, no. 1, pp. 72–79, 2013.
