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Journal of Clinical Microbiology, March 2002, p. 1121, Vol. 40, No. 3
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.3.1121.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

LETTER TO THE EDITOR

Helicobacter Infection and Spontaneous Bacterial Peritonitis


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LETTER
 
Spontaneous bacterial peritonitis (SBP) is defined as an ascitic fluid infection without an evident intra-abdominal surgically treatable source; it primarily occurs in patients with advanced cirrhosis (1). The diagnosis is established by a positive ascitic fluid bacterial culture and an elevated absolute polymorphonuclear leukocyte count (>=250 cells/ml). The disease is responsible for increased mortality, but with appropriate antibiotic treatment of the infection, SBP-related mortality approaches zero. Most cases of SBP are due to gut bacteria such as Escherichia coli and Klebsiella, but SBP can also occur in cases of streptococcal and, infrequently, staphylococcal infection (5). However, a variant of SBP is characterized by a culture-negative neutrocytic ascites (4). The demonstration that several Helicobacter spp. are able to colonize the intestine of several animals (3, 6) prompted us to investigate the potential role of Helicobacter species infection in cases of SBP in patients with cirrhosis of the liver. Consecutive patients with cirrhosis and SBP (documented by paracentesis), admitted to the Department of Internal Medicine, University of Sassari, Sassari, Italy were enrolled in the study. Patients who had been treated with any antibiotic regimen during the previous 30 days were excluded from the study. In each patient, the Helicobacter pylori infection was established by 13C urea breath testing. Ascitic fluid was collected from the cirrhotic patients by paracentesis performed at the time of diagnosis. Samples were stored in brucella broth with 20% glycerol at -80°C until processed. Selective brain heart infusion-agar plates (Difco Laboratories, Detroit, Mich.), containing 7% defibrinated horse blood (Cocalico Biologicals, Reamstown, Pa.) as well as vancomycin (Sigma), nalidixic acid (Sigma), amphotericin B (Sigma), and trimethoprim (Sigma), were inoculated with 100 µl of brucella broth containing the ascitic fluid. Plates were incubated at 37°C under 12% CO2 and 95 to 99% relative humidity and observed daily for up to 3 weeks for H. pylori-like colonies. Ascitic fluid samples utilized for culture were further examined by PCR analysis for Helicobacter spp. and H. pylori sequences. Genomic DNA was extracted using the QIAmp tissue kit (QIAGEN, Chatsworth, Calif.) following the manufacturer's instructions. Sequence data on Helicobacter-specific 16S rRNA gene and on the H. pylori vacA m1/m2 middle region were used to select two oligonucleotide primers for PCR as previously reported (2). Brucella broth inoculated with known numbers of H. pylori (NCTC 11637) served as positive control. Over a time period of 6 months, a total of 10 patients (mean age, 64 years; range, 55 to 78 years; 7 men) was enrolled. All of the patients had decompensated cirrhosis; four of them had associated hepatocellular carcinoma. A positive 13C urea breath test result was obtained for 6 cirrhotic patients. PCR amplifications of DNA extracted from the ascitic fluid of all of these patients were negative for the Helicobacter 16S rRNA gene and for the H. pylori vacA region. We were not able to isolate H. pylori organisms from any sample cultured.

Our results suggest that an association of Helicobacter spp. and H. pylori infection with SBP seems to be unlikely and that other infections could be responsible for this complication in patients with cirrhosis of the liver.


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REFERENCES
 
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  1. Akriviadis, E. A., and B. A. Runyon. 1990. Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis. Gastroenterology 98:127-133.[Medline]
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  2. Dore, M. P., A. R. Sepulveda, H. El-Zimaity, Y. Yamaoka, M. S. Osato, K. Mototsugu, A. M. Nieddu, G. Realdi, and D. Y. Graham. 2001. Isolation of Helicobacter pylori from sheep—implications for transmission to humans. Am. J. Gastroenterol. 96:1396-1401.[Medline]
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  3. Foltz, C. J., J. G. Fox, R. Cahill, J. C. Murphy, L. Yan, B. Shames, and D. B. Schauer. 1998. Spontaneous inflammatory bowel disease in multiple mutant mouse lines: association with colonization by Helicobacter hepaticus. Helicobacter 3:69-78.[CrossRef][Medline]
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  4. Guarner, C., and B. A. Runyon. 1995. Spontaneous bacterial peritonitis: pathogenesis, diagnosis, and management. Gastroenterologist 3:311-328.[Medline]
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  5. Runyon, B. A., J. G. McHutchison, M. R. Antillon, E. A. Akriviadis, and A. A. Montano. 1991. Short-course versus long-course antibiotic treatment of spontaneous bacterial peritonitis. A randomized controlled study of 100 patients. Gastroenterology 100:1737-1742.[Medline]
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  6. Saunders, K. E., Z. Shen, F. E. Dewhirst, B. J. Paster, C. A. Dangler, and J. G. Fox 1999. Novel intestinal Helicobacter species isolated from cotton-top tamarins (Saguinus oedipus) with chronic colitis. J. Clin. Microbiol. 37:146-151.[Abstract/Free Full Text]
Maria P. Dore*
Michele Casu
Giuseppe Realdi
Institute of Internal Medicine
University of Sassari
Viale San Pietro, 8
Sassari 07100, Italy

Andrea Piana
Ida Mura
Institute of Hygiene and   Preventive Medicine
University of Sassari
Sassari, Italy

* Phone: 39 079 229886
Fax: 39 079 228207
E-mail: mpdore{at}uniss.it

Journal of Clinical Microbiology, March 2002, p. 1121, Vol. 40, No. 3
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.3.1121.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




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