Abstract.: We report a patient with pancreatic pseudocysts that were superinfected with Streptococcus pneumoniae. The literature on the prevalence of superinfection of pancreatic tissue by S. pneumoniae, as well as on its prophylaxis and treatment, is reviewed. In addition, a possible pathophysiologic pathway is discusse

Bauerfeind, P.

Gubler, C.

Ossola, N.

Zinkernagel, A.

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Infection 31 · 2003 · No. 4 © URBAN & VOGEL 251Streptococcus pneumoniae as an Uncommon Causeof Superinfected Pancreatic PseudocystsC. Gubler, A. Zinkernagel, N. Ossola, P. BauerfeindAbstractWe report a patient with pancreatic pseudocysts that weresuperinfected with Streptococcus pneumoniae. The literatureon the prevalence of superinfection of pancreatic tissue byS. pneumoniae, as well as on its prophylaxis and treatment,is reviewed. In addition, a possible pathophysiologicpathway is discussed.Infection 2003; 31: 251–253DOI 10.1007/s15010-003-4019-zIntroductionSuperinfection of necrotic pancreatic tissue, peripancreaticfluid and pseudocysts is well known to cause serious com-plications in both acute and chronic pancreatitis. It resultsin significant morbidity and mortality. Predominantly, gram-negative aerobic bacteria, such as Echerischia coli,Pseudomonas ssp., Proteus and Klebsiella ssp., are found ascausative organisms. Uncommonly, gram-positive bacteria,such as Staphylococcus aureus, Enterococcus faecalis andfungi, can be isolated [1]. Since 40 to 50% of the patients suf-fering from necrotizing pancreatitis develop bacterial su-perinfection [2], prophylactic administration of antibioticsis recommended [3]. If superinfection of pancreatic pseudo-cysts is suspected, microbiologic sampling should be at-tempted [4, 5] to establish an appropriate antibiotic therapy.Case ReportA 45-year-old Caucasian man, with a history of alcohol abuse, pre-sented to our tertiary hospital because of upper abdominal painwhich had worsened over a period of 5 weeks. Three weeks priorto admission, he observed jaundice of the eyes, darkening of theurine and pale watery stools. A weight loss of 8 kg over the last 2months was reported. His medical history revealed no signs of gas-trointestinal bleeding, hepatic cirrhosis, diabetes mellitus and nohistory of pancreatitis. Physical examination was unremarkable,except for pain in the upper abdominal quadrants on deep palpa-tion, without signs of peritonitis.Laboratory test showed an elevated pancreatic amylase(206 U/l), a slight leukocytosis (9.8  103 µl) and a C-reactive pro-tein (CRP) of 9 mg/l (reference value < 5mg/l).An acute viral hep-atitis caused by hepatitis viruses A, B or C was excluded.Both the computed tomography (CT) and ultrasound of theabdomen showed the head of the pancreas to be enlarged, withmultiple calcifications. The whole pancreatic duct was irregularlydilated. The peripancreatic fat was homogeneously infiltrated asfar as the abdominal wall . Three small pseudocysts were present,the largest of which measured 3.5  2 cm (Figure 1). An acuteepisode of a chronic alcoholic pancreatitis with pseudocysts wasdiagnosed .The patient’s situation improved within the next 4 dayswhile fasting. Pancreatic amylase returned to normal values.After1 week, having resumed oral alimentation, the abdominal pain in-creased, as did the CRP and the leukocytes. We suspected a sec-ondary infection of the pseudocysts and therefore performed anultrasound-guided puncture of the most accessible cyst; pus wasInfection Case ReportC. Gubler, P. Bauerfeind (corresponding author)Dept. of Gastroenterology and Hepatology, University Hospital of Zurich,CH-8091 Zurich; Switzerland; Phone: (+41/1) 255-1111 , Fax: -4503,e-mail: peter.bauerfeind@usz.ch A. ZinkernagelDept. of Infectious Disease, University Hospital of Zurich, SwitzerlandN. OssolaDept. of Internal Medicine, University Hospital of Zurich, SwitzerlandC. Gubler and A. Zinkernagel contributed equally to this workReceived: February 12, 2003 • Revision accepted: May 5, 2003Figure 1. Pancreatic pseudocysts demonstrated by ultrasound.aspirated and gram-positive diplococci were visualized. Culturerevealed penicillin-sensitive Streptococcus pneumoniae.Intravenous antibiotic therapy with amoxicillin and metro-nidazole was initiated, the patient improved and nutrition couldbe established without pain. Metronidazole was stopped after an-aerobic organisms were excluded and amoxicillin was continuedfor a total of 3 weeks. Therapy was not switched to penicillin Gconsidering the ease of administration and the possibility to treatthe patient in an ambulatory setting.DiscussionIn Western countries, alcohol abuse is the predominant eti-ology of chronic pancreatitis. In about 20% of patients withcalcifications of the pancreatic tissue, there is no history ofabdominal pain or of acute pancreatitis [6]. The discrimi-nation between chronic and acute pancreatitis is crucial be-cause of the different mortality rates. In acute pancreatitis,mortality rises from 1% to 15% if necrosis develops and to35% if a superinfection occurs [7]. The latter will developafter the first 10 to 14 days in about 60% of all patients [8].Early antibiotic prophylaxis should be part of standardtreatment in severe pancreatitis and reduces the infectionrate to about 30% [9]. In 1998, a meta-analysis of eightprospective trials showed a significant reduction of mor-tality by routine administration of broad-spectrum antibi-otics, such as imipenem, in cases with necrosis [3, 10]. As aconsequence of this policy, there has been a shift fromgram-negative to gram-positive microorganisms and fungi[10, 11]. Standard treatment for an infected necrosis issurgery or drainage [12].Pancreatic pseudocysts represent a different entitycompared to infected necroses with or without abscess [13].The policy concerning when and how to drain noninfectedpseudocysts is discussed elsewhere [14]. If an infectionwithin the pseudocyst is assumed, microbiological analysisby puncture of the cyst should be attempted, either percu-taneously or by ultrasound-guided endoscopy. Cultureshould guide antimicrobial therapy, since the microbiologicspectrum can be broad.In this case, the Gram stain revealed gram-positivecocci that were subsequently identified as S. pneumoniae.In view of the literature on case reports and laboratoryanalyses, this finding was not altogether surprising.Although rare, involvement of S. pneumoniae in pan-creatic disease has been described previously [15] and wasalways associated with alcoholism. To date, S. pneumoniaewas identified as the causative microorganism of pancre-atic disease in one case report [16] and in a group of ninepatients from Hungary [17]. The route of infection of thepancreatic lesions remains unclear.An explanation may befound by studying the high prevalence of S. pneumoniaebacteremia in alcoholics [18, 19].A well-defined mechanism causing pneumonia andbloodstream infections is aspiration during periods of highserum alcohol levels. In addition, malnutrition and poor hy-giene, especially neglected dental status, contribute to ahigher incidence of bloodstream infections. Once the bac-teria have entered the bloodstream, they should be con-trolled by the immune system. However, chemokine pro-duction is impaired in patients with high alcohol levels.Thisresults in insufficient recruitment of macrophages and,therefore, a much higher probability of bacteremia [18, 19].Necrotic tissue and pseudocysts are found in noninfectiouspancreatitis.They offer ideal cultural growth conditions forbacteria arriving via the bloodstream. This could explainwhy superinfection of pancreatic tissue with S. pneumoniaeis most frequently found in alcoholics.Considering the literature and the probable patho-physiologic mechanisms, prophylaxis should be part of thestandard treatment for severe pancreatitis to reduce the in-fection rate. If an infection within the pseudocyst is as-sumed, microbiological analysis by puncture of the cyst andearly antibiotic treatment should be attempted if no pro-phylaxis had been given.References1. Garg PK, Khanna S, Bohidar P, Kapil A, Tandon RK: Incidence,spectrum and antibiotic sensitivity pattern of bacterial infec-tions among patients with acute pancreatitis. J GastroenterolHepatol 2001; 16: 1055–1059.2. Beger HG, Bittner R, Block S, Buchler M: Bacterial contaminationof pancreatic necrosis. A prospective clinical study. Gastroen-terology 1986; 91: 433–438.3. Golub R, Siddiqi F, Pohl D: Role of antibiotics in acute pancreati-tis; a meta-analysis. J Gastrointest Surg 1998; 2; 496–503.4. Yousaf M, McCallion K, Diamond T: Management of severe acutepancreatitis. Br J Surg 2003; 90: 407–420.5. Rau B, Pralle U, Mayer M, Beger HG: Role of ultrasonographicallyguided fine-neddle aspiration cytology in the diagnosis of in-fected pancreatic necrosis. Br J Surg 1998; 85: 179–184.6. Layer P, Yamamoto H, Kalthoff L, Clain JE, Bakken LJ, DiMagno EP:The different courses of early and late onset idiopathic and alco-holic chronic pancreatitis. Gastroenterology 1994; 107:1481–1487.7. Vesentini S, Bassi C, Talamini G, Cavallini G, Campedelli A, Peder-zoli P: Prospective comparison of C-reactive protein level, Ran-son score and contrast-enhanced computed tomography in theprediction of septic complications of acute pancreatitis. Br JSurg 1993; 80: 755–757.8. Gerzof SG, Banks PA, Robbins AH, Johnson WC, Spechler SJ, Wet-zner SM, Snider JM, Langevin RE, Jay ME: Early diagnosis of pan-creatic infection by computed tomography-guided aspiration.Gastroenterology 1987; 93; 1315–1320.9. Gloor B, Müller C, Worni M, Stahel PF, Redaelli C, Uhl W, BuchlerMW: Pancreatic infection in severe pancreatitis. Arch Surg 2001;136; 592–596.10. Bassi C, Falconi M, Talamini G, Uomo G, Papaccio G, Dervenis C,Salvia R, Minelli EB, Pederzoli P: Controlled clinical trial of pe-floxacin versus imipenem in severe acute pancreatitis. Gas-troenterology 1998; 115: 1513–1517.11. Büchler MW, Gloor B, Müller C, Friess H, Seiler CA, Uhl W: Acutenecrotizing pancreatitis: treatment strategy according to thestatus of infection. Ann Surg 2000; 232: 619–626.12. Schmid SW, Uhl W, Friess H: Review: the role of infection inacute pancreatitis. Gut 1999; 45: 311–316.C. Gubler et al. S. pneumoniae and Superinfected Pancreatic Pseudocysts252 Infection 31 · 2003 · No. 4 © URBAN & VOGEL13. Fedorak IJ, Ko TC, Djuricin G, McMahon M, Thompson K, Prinz RA:Secondary pancreatic infections: are they distinct clinical enti-ties? Surgery 1992; 112: 824–830.14. Seifert H, Binmoeller KF, Sohendra N: Pancreatic pseudocysts:how and when should they be drained? Bildgebung 1995; 62(suppl 1): 12–18.15. Taylor S, Sander C: Unusual manifestations of invasive pneumo-coccal infection. Am J Med 1999; 107; 12–27.16. Denis F, Mounier M, Descottes B, Cubertafond P, Catanzano G:Abdominal infections caused by Streptococcus pneumoniae. EurJ Clin Microbiol 1984; 3: 443.17. Thege M, Pulay I, Balla E, Tihanyi T: Streptococcus pneumoniae asan etiologic agent in infectious complications of pancreatic dis-ease. Microb Drug Resist 2002; 8: 73–76.18. Stanford TJ, Danforth J: Ethanol feeding inhibits proinflamma-tory cytokine expression from murine alveolar macrophages exvivo. Alcohol Clin Exp Res 1997; 21: 1212–1217.19. Boé DM, Nelson S, Zhang P, Bagby GJ: Acute ethanol intoxicationsuppresses lung chemokine production following infection withS. pneumoniae. J Inf Dis 2001; 184: 1134–1142.C. Gubler et al. S. pneumoniae and Superinfected Pancreatic PseudocystsInfection 31 · 2003 · No. 4 © URBAN & VOGEL 253Editor’s NoteThe case report of C. Gubler et al. above will be the last contribution to the series Clinical Quiz for the time being.The correct answer to Quiz Case Infection 3/2003 is Streptococcus pneumoniae.The editor would like to thank all those who have contributed to this section.

Streptococcus pneumoniae as an UncommonCause of Superinfected Pancreatic Pseudocysts

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Streptococcus pneumoniae as an UncommonCause of Superinfected Pancreatic Pseudocysts

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