346
Notes
Spontaneous Bacterial Peritonitis Caused by Listeria monocytogenes: Two Case Reports and Literature Review A. P o l a n c o 1., C. Giner 1, R. C a n t 6 n 1, A. L e 6 n 1, M. Garcia Gonzalez 2, E B a q u e r o 1, M. M e s e g u e r I
Two new cases of spontaneous bacterial peritonitis (SBP) caused by Listeria monocyto. genes are reported. Listeria monocytogenes was recovered from the ascitic fluid but not from the blood cultures of two adult diabetic inpatients with hepatic cirrhosis and SBP that had been treated empirically with cefotaxime. These two cases add to the 17 cases of Listeria monocytogenes SBP reported previously, stressing the relevance of this microorganism to this clinical condition. The recovery of Listeria monocytogenes from blood has been achieved in only half of the cases reported, suggesting the possibility of a direct translocation mechanism. Combinations of amino- or ureidopenicillins with beta-lactamase inhibitors or carbapenems might be more effective as empiric therapy of SBP in cirrhotic patients.
The syndrome of spontaneous bacterial peritonitis (SBP) is defined as a sudden onset of acute bacterial peritonitis without any apparent external or intraabdominal focus of infection in patients with ascitis caused by liver disease (1). Gram-negative bacteria are recovered most commonly in SBP; Listeria monocytogenes has been considered an exceptional finding in this setting. Listeria monocytogenes is a gram-positive, regular, facultatively anaerobic rod that has been associated with infections in newborns and in adults with impaired cell-mediated immunity (corticosteroid therapy, malignancies or pregnancy). Such infections are manifested primarily as meningitis, bacteremia and endocarditis. We have observed two cases of Listeria monocytogenes SBP, which prompted us to review the
Vol. 1I. No. 4
literature on this subject. A total of 17 cases have been reported previously (2-16). The increasing number of cases of Listeria monocytogenes peritonitis reported during the last few years suggests that this pathogen might not be as uncommon as has been hitherto considered. Materials and Methods, Case no. 1. A 64-yearold diabetic woman previously diagnosed as having non-alcoholic hepatic cirrhosis with hepatoma, oesophageal varices, portal thrombosis and ascitis was admitted to our hospital with low-grade fever, painful abdominal swelling, respiratory distress and Grade I encephaiopathy. Paracentesis yielded seven litres of ascitic fluid containing 2,000 WBC/mm 3 and 2.1 g/dl proteins. No microorganisms were observed on the Gram stain. After 48 h of incubation Listeria monocytogenes type 1 was isolated from blood agar medium. Blood cultures were negative. Serum samples were screened for HBsAg, anti-HBs and anti-HBc by radioimmunoassay and for antibody to hepatitis C virus (anti-HCV) by enzyme immunoassay and found to be positive for anti-HBc and anti-HCM Tests for HIV antibodies were negative. On admission the patient was treated empirically with cefotaxime 1 g q.i.d. She died before the microbiological report was known. Case no. 2. A 74-year-old diabetic man previously diagnosed with non-alcoholic cirrhosis, portal hypertension and chronic renal failure was admitted to the hospital. On physical examination his abdomen was distended with fluid; oedema was observed in both lower extremities. He had no fever, but dyspnea and hepatic encephalopathy Grade II were observed. He was treated empirically with cefotaxime 2 g q.i.d. Two days later the patient's condition worsened and a paracentesis was performed, which yielded a yellowish ascitic fluid containing 300 WBC/mm 3 and 1.9 g/dl proteins. Listeria monocytogenes type 4 was recovered from two blood culture bottles inoculated with the ascitic fluid. No growth was observed on blood agar plates that had been seeded directly with the centrifuged ascitic fluid. Two blood cultures obtained concomitantly yielded no growth. When the microbiological report was available, therapy was changed to ampicillin 2 g t.i.d.; an aminoglycoside was not administered because of renal failure in this patient. Fluid obtained by a further paracentesis was sterile. No improvement was observed and the patient died three weeks after admission.
1Servicio de Microbiologfa, and 2Servicio de Gastroentero-
logfa, Hospital Ram6n y Cajal, Crta. Colmenar Km 9,100, 28034 Madrid, Spain.
Results and Discussion. Four main mechanisms of bacterial colonization of the ascitic fluid in
Vol. 11, 1992
347
Table h Clinical and laboratory data on 21 patients with spontaneous Listeria monocytogenes peritonitis. Author
Age/
Underlying diseases
Ascitic fluid analysis
sex Cirrhosis
Other
Culture
WBC/ mm 3
Proteins (gldl)
Baeteremia
Fever
Encephalopathy
Louria et al. 1967 (2)
64~
no
retieulum cell sarcoma
+
NR
NR
+
yes
NR
Massaehussetts G H 1974 (3)
58/M
no
Hodgkin's disease
+
4,760
NR
+
yes
NR
Rheingold et al.
49/M
yes a
NR
+
1,720
1.2
+
yes
NR
Rheingold et al. 1977 (4)
63/M
yes a
NR
+
1,100
3.4
+
yes
NR
Myers et al. 1983 (5)
71IF
no
CAPD
+
1,288
NR
+
yes
NR
Winslow et al. 1984 (6)
76/M
yes a
peritoneovenous shunt
+
6,150
4.9
+
yes
NR
Bory-Ros et al. 1980 (7)
60/M
no
chronic hepatitis and chronic renal failure
+
1,800
1.7
no
yes
Thomson et al. 1987 (8)
79/F
yes b
NR
+
900
2.0
yes
NR
Rosell et al. 1987 (9)
52/M
yes a
diabetes
+
870
0.02
yes
yes
Rosell et al. 1987 (9)
75/F
yes¢
NR
+
5,400
NR
yes
yes
Soto-Hern~indez et al. 1988 (10)
641M
yes a
NR
+
7,200
1.1
yes
yes
A m a d o r et al. 1988 (11)
46/M
yes c
NR
+
41,000
2
yes
NR
Larson et al. 1988 (12)
32/M
no
renal transplant
a
250
3.9
yes
NR
Castellote et al. 1989 (13)
75fM
yes a
NR
+
300
1.4
yes
yes
L6pez-San Roman et al. 1989 (14)
82/M
yes a
NR
+
950
8.0
yes
NR
AI Wali et al. 1990(15)
53/M
no
CADP
+
800
NR
NR
NR
P6rez-Aguilar et al. 1990 (16)
63/F
yes c
NR
+
2,300
NR
yes
yes
Polaneo et al. 1992
64/F
yes b
diabetes, chronic hepatitis
+
2,000
2.1
yes
yes
Polaneo et aL 1992
74/M
yes c
diabetes
+
300
1.9
yes
yes
1977 (4)
a Ethylic origin. bViral origin. c Origin unknown.
dListeria monocytogenes recovered only from a biopsy specimen from the peritoneal wall. NR = Not reported; C A P D = continuous ambulatory peritoneal dialysis.
-
348
patients with decompensated cirrhosis have been proposed (1, 17): a) translocation of intestinal bacteria facilitated by oedema of villi and degeneration of the basal membrane; b) portal bacteremia with failure of the hepatic reticulo endothelial system (RES) filter due to the development of portal-systemic collateral veins; c) decrease in the RES phagocytic activity and impaired opsonic effect in peritoneal fluid and serum due to the lower Content of proteins and complement; and d) increase in the lymphatic flow through the thoracic duct. Hepatic conditions other than decompensated alcoholic cirrhosis may produce similar effects, and an increasing number of cases of SBP have been reported from patients with non-alcoholic cirrhosis. Translocation is the process by which intestinal microorganisms leave the intestinal lumen and reach extraintestinal sites, causing systemic disease in some cases. It frequently originates in the Peyer's patches (lymphoid follicles) of the small intestine, where microorganisms are ingested by the submucosal macrophages and transported to the mesenteric lymph nodes (18). Listeria monocytogenes can colonize the intestinal tract of healthy people. The production of listeriolysin O allows bacteria to escape from the phagolysosomal compartment of phagocytic cel!s, as our group recently demonstrated (19). Effective translocation and peritoneal colonization is obviously enhanced by the production of this toxin. We have reviewed the literature and have found 17 cases of SBP caused by Listeria monocytogenes (2-16). With the two cases reported here, a total of 19 have now been reported. The main features of Listeria monocytogenes SBP are shown in Table 1. Cirrhosis with decompensated ascitis was the main feature in two-thirds of the patients (13 of 19) and was caused by alcohol in seven cases. Two cases of SBP were associated with viral infections and the pathogenesis was unknown in the remaining patients. In the six non-cirrhotic patients Listeria monocytogenes SBP was associated with continuous ambulatory peritoneal dialysis (CAPD) (2 cases, I patient with a history of likely catheter contamination) (15), immunosuppression (3 cases: Hodgkin's disease, reticulum sarcoma and renal allograft) and chronic renal failure (1 case). Both of our cases were in elderly diabetics suffering from hepatic cirrhosis of unknown origin in one patient and of viral etiology in the other. Both had encephalopathy. There may be an association
Eur. J. Clin. Microbiol. Infect. Dis.
between overgrowth of Listeria monocytogenes and cirrhosis and encephalopathy. It is noteworthy that half of cases of Listeria monocytogenes SBP have been reported by Spanish authors. A more frequent intestinal colonization by listeria in Spain could be related to the dietary habits in our country. Nevertheless, differences in intestinal carriage in healthy populations were not detected by our group in an earlier report (20). Blood cultures were negative in both of our patients, which also suggests a translocation mechanism of Listeria monocytogenes. Blood cultures positive for Listeria monocytogenes were obtained in only half of the patients (9 of 19) in the reviewed series, including one CAPD patient (5) and another with SBP associated with a peritoneal venous shunt (6). A non-bacteremic portal of entry is therefore likely to exist in some cases. We failed to demonstrate the presence of grampositive rods in the Gram-stained direct smear of t h e centrifuged ascitic fluid. Although Listeria monocytogenes was recovered from the centrifuged ascitic fluid in one of our cases, the method of choice is the inoculation of at least 5 ml of ascitic fluid in blood culture bottles (21). The case by Larson et al. (12) is exceptional in that Listeria monocytogenes was isolated only from a biopsy specimen obtained by iaparoscopy of the peritoneal wall but not from blood or ascitic fluid cultures. Most patients in the cases reviewed had an increased protein content and a high WBC count in the ascitic fluid (> 250/mm3). The current empiric therapy of SBP is based on the use of third-generation cephalosporins. Our cases represent good examples of the potential failure of these agents in this clinical setting. We have recently shown that third -generation cephalosporins are inactive against Listeria monocytogenes because of their reduced affinity to the PBP-3 (22). From the results reviewed in this work, it is suggested that combinations of aminopenicillins or ureidopenicillins with betalactamase inhibitors or carbapenems could eventually replace third-generation cephalosporins as the empirical treatment of SBP, particularly in cirrhotic patients.
References
1. HallakA: Spontaneousbacterial peritonitis. American Journal of Gastroenterology 1989, 84: 345-350.
V._.o1.11,1992
2. Louria DB, Hensle I", Armstrong D, Collins H, Blewins A, Krugman D, Buse M: Listeriosis complicating malignant disease. Annals of Internal Medicine 1967, 67: 261-281. 3. Case Records of the Massachussetts General Hospital. New England Journal of Medicine 1974, 291: 516-524. 4. Rheingold OJ, Chiprut RO, Dickinson GM, SchiffER: Spontaneous peritonitis of cirrhosis due to Listeria monocytogenes. Annals of Internal Medicine 1977, 87: 455-456. 5. Myers JP, Peterson G, Rashid A: Peritonitis due to Listeria monocytogenes complicating continuous ambulatory peritoneal dialysis. Journal of Infectious Diseases 1983, 148: 11-30. 6. Winslow DL, Steele ML: Listeria bacteremia and peritonitis associated with a peritoneovenous shunt: successful treatment with sulfamethoxazole and trimethoprim. Journal of Infectious Diseases 1984,149: 820. 7. Bory Ros F, Rigau J: Peritonitis espont~nea por Listeria monocytogenes en la cirrosis hep~itica. Gastroenterologfa y Hepatologla 1980, 3: 157-158. 8. Thomson MM, lnglada Galiana L, Marffnez Avil~s P, de Villalobos E: Peritonitis espontfinea del cirr6tico por Listeria monocytogenes. Revista Clfnica Espafiola 1987, 181: 231. 9. Roseli F, Fornos C, Jan6 X, Boada F, V~izquez D J, Nieto M: Peritonitis espontfinea del cirr6tico por Listeria. Gastroenterologfa y Hepatologfa 1987, 10: 299-301. 10. Soto-Hermindez JL, Nunley D, Guti6rrez CC, Berk SL: Listeria monocytogenes peritonitis, American Journal of Gastroenterology 1988, 83: 180-182. 11. Amador C, Bafiares R, Clemente G, Plasquau F, Guirado A: Peritonitis baeteriana espont~nea por Listeria monocytogenes. Enfermedades Infecciosas y Microbiologfa Clfnica 1988, 6: 361-363. 12. Larson CC, Bathe WB, Ware ALl, Krejs G J: Listeria peritonitis diagnosed by laparoscopy. Gastrointestinal Endoscopy 1988, 34: 352-354. 13. Castellote J, Marffnez Lacasa .I, Xiol X, Sur6s A: Peritonitis bacteriana espontfinea por Listeria monocytogenes. Enfermedades Infecciosas y Microbioiogfa Clfnica 1989, 7: 336. 14. L6pez-San Romfin A, Erdozain JC, B~ircena R, Sdnchez-Ruano J J: Listeria monocytogenes peritonitis. An additional case. American Journal of Gastroenterology 1989, 84: 454--455. 15. Ai-Wali Wi, Bailiod R, Hamilton-Miller JMT, Kyi MS, Brumfitt W: Listeria monocytogenes peritonitis during continuous ambulatory peritoneal dialysis. Postgraduate Medical Journal 1990, 66: 252. 16. P6rez Aguilar F, Candela V, Garcia-Romero E, Berenguer J: Peritonitis bacteriana espont~inea por L&teria monocytogenes. Revista Espafiola de Enfermedades Digestives 1990, 77: 385-386. 17. Wilcox CM, Dismukes WE: Spontaneous bacterial peritonitis. A review of pathogenesis, diagnosis, and treatment. Medicine 1987, 66: 447-456. 18. Wells CL, Maddaus MA, Simmons RL: Proposed mechanism for the translocation of intestinal bacteria. Reviews of Infectious Diseases 1988, 10: 958-979. 19. Cossart P, Vicente MF, Mengaud J, Baquero F, P~rez. Diaz JC, Berche P: Listeriolysin O is essential for virulence of Listeria monocytogenes direct evidence obtained by gene complementation. Infection and Immunity 1989, 57: 3629-3636.
349
20. G6mez Mampaso E, Michaux L, de Rafael L, Carvajai A, Baquero F: Faecal Listeria monoeytogenes carriers and perinatal mortality. In: Woodbine M (ed): Problems of listeriosis. Leicester University Press, Surrey, UK 1975, p. 206-213. 21. Runyon BA, Umland ET, Merlin T: Inoculation of blood culture bottle with ascitic fluid. Improved detection of spontaneous bacterial peritonitis. Archives of Internal Medicine 1987, 147: 73-75. 22. Vicente MF~P~rez-Diaz JC, Baquero F, de Pedro MA, Berenguer J: Penicillin-binding protein 3 of Listeria monocytogenes as the primary lethal target for betalactams. Antimicrobial Agents and Chemotherapy 1990, 34: 539-542.
Isolation of Klebsiella terrigena from Clinical Specimens R. P o d s c h u n * , U . U l l m a n n
In a three-year survey conducted from 1988 to 1990 Klebsiella isolates from human clinical specimens were subjected to additional tests to identify any Klebsieila terrigena strains. Ten strains ofKlebsiella terrigena (0.4 %) were found among 2355 indole-negative Klebsiella isolates. Most of the isolates were recovered from the respiratory tract. In the API 20EC system almost exclusively biotypes no. 1777771 and 1777671 were observed. Serotyping revealed capsule types K2, K5 and K18 in two strains each. In antibiotic susceptibility tests the strains were shown to be comparable in sensitivity to Klebsiella
pneumoniae.
In 1981 a new species of KlebsieUa, Klebsiella terrigena, was described by Izard et al. (1). Klebsiella terrigena closely resembles Klebsiella pneumoniae and can b e serotyped using Klebsiella capsule antisera. T h e two species can be differentiated on the basis of tests for f e r m e n t a t i o n of melezitose, growth at 10 °C and gas production from lactose at 44.5 °C (2). Klebsiella terrigena has b e e n isolated mainly from soil and w a t e r (1, 3), and in the ten years following the first description of this new species no case of isolation f r o m humans was reported. Recently, however, we Department of Medical Microbiology, University of Kiel, Brunswiker Str. 4, D-2300 Kiel, Germany.
Notes
Spontaneous Bacterial Peritonitis Caused by Listeria monocytogenes: Two Case Reports and Literature Review A. P o l a n c o 1., C. Giner 1, R. C a n t 6 n 1, A. L e 6 n 1, M. Garcia Gonzalez 2, E B a q u e r o 1, M. M e s e g u e r I
Two new cases of spontaneous bacterial peritonitis (SBP) caused by Listeria monocyto. genes are reported. Listeria monocytogenes was recovered from the ascitic fluid but not from the blood cultures of two adult diabetic inpatients with hepatic cirrhosis and SBP that had been treated empirically with cefotaxime. These two cases add to the 17 cases of Listeria monocytogenes SBP reported previously, stressing the relevance of this microorganism to this clinical condition. The recovery of Listeria monocytogenes from blood has been achieved in only half of the cases reported, suggesting the possibility of a direct translocation mechanism. Combinations of amino- or ureidopenicillins with beta-lactamase inhibitors or carbapenems might be more effective as empiric therapy of SBP in cirrhotic patients.
The syndrome of spontaneous bacterial peritonitis (SBP) is defined as a sudden onset of acute bacterial peritonitis without any apparent external or intraabdominal focus of infection in patients with ascitis caused by liver disease (1). Gram-negative bacteria are recovered most commonly in SBP; Listeria monocytogenes has been considered an exceptional finding in this setting. Listeria monocytogenes is a gram-positive, regular, facultatively anaerobic rod that has been associated with infections in newborns and in adults with impaired cell-mediated immunity (corticosteroid therapy, malignancies or pregnancy). Such infections are manifested primarily as meningitis, bacteremia and endocarditis. We have observed two cases of Listeria monocytogenes SBP, which prompted us to review the
Vol. 1I. No. 4
literature on this subject. A total of 17 cases have been reported previously (2-16). The increasing number of cases of Listeria monocytogenes peritonitis reported during the last few years suggests that this pathogen might not be as uncommon as has been hitherto considered. Materials and Methods, Case no. 1. A 64-yearold diabetic woman previously diagnosed as having non-alcoholic hepatic cirrhosis with hepatoma, oesophageal varices, portal thrombosis and ascitis was admitted to our hospital with low-grade fever, painful abdominal swelling, respiratory distress and Grade I encephaiopathy. Paracentesis yielded seven litres of ascitic fluid containing 2,000 WBC/mm 3 and 2.1 g/dl proteins. No microorganisms were observed on the Gram stain. After 48 h of incubation Listeria monocytogenes type 1 was isolated from blood agar medium. Blood cultures were negative. Serum samples were screened for HBsAg, anti-HBs and anti-HBc by radioimmunoassay and for antibody to hepatitis C virus (anti-HCV) by enzyme immunoassay and found to be positive for anti-HBc and anti-HCM Tests for HIV antibodies were negative. On admission the patient was treated empirically with cefotaxime 1 g q.i.d. She died before the microbiological report was known. Case no. 2. A 74-year-old diabetic man previously diagnosed with non-alcoholic cirrhosis, portal hypertension and chronic renal failure was admitted to the hospital. On physical examination his abdomen was distended with fluid; oedema was observed in both lower extremities. He had no fever, but dyspnea and hepatic encephalopathy Grade II were observed. He was treated empirically with cefotaxime 2 g q.i.d. Two days later the patient's condition worsened and a paracentesis was performed, which yielded a yellowish ascitic fluid containing 300 WBC/mm 3 and 1.9 g/dl proteins. Listeria monocytogenes type 4 was recovered from two blood culture bottles inoculated with the ascitic fluid. No growth was observed on blood agar plates that had been seeded directly with the centrifuged ascitic fluid. Two blood cultures obtained concomitantly yielded no growth. When the microbiological report was available, therapy was changed to ampicillin 2 g t.i.d.; an aminoglycoside was not administered because of renal failure in this patient. Fluid obtained by a further paracentesis was sterile. No improvement was observed and the patient died three weeks after admission.
1Servicio de Microbiologfa, and 2Servicio de Gastroentero-
logfa, Hospital Ram6n y Cajal, Crta. Colmenar Km 9,100, 28034 Madrid, Spain.
Results and Discussion. Four main mechanisms of bacterial colonization of the ascitic fluid in
Vol. 11, 1992
347
Table h Clinical and laboratory data on 21 patients with spontaneous Listeria monocytogenes peritonitis. Author
Age/
Underlying diseases
Ascitic fluid analysis
sex Cirrhosis
Other
Culture
WBC/ mm 3
Proteins (gldl)
Baeteremia
Fever
Encephalopathy
Louria et al. 1967 (2)
64~
no
retieulum cell sarcoma
+
NR
NR
+
yes
NR
Massaehussetts G H 1974 (3)
58/M
no
Hodgkin's disease
+
4,760
NR
+
yes
NR
Rheingold et al.
49/M
yes a
NR
+
1,720
1.2
+
yes
NR
Rheingold et al. 1977 (4)
63/M
yes a
NR
+
1,100
3.4
+
yes
NR
Myers et al. 1983 (5)
71IF
no
CAPD
+
1,288
NR
+
yes
NR
Winslow et al. 1984 (6)
76/M
yes a
peritoneovenous shunt
+
6,150
4.9
+
yes
NR
Bory-Ros et al. 1980 (7)
60/M
no
chronic hepatitis and chronic renal failure
+
1,800
1.7
no
yes
Thomson et al. 1987 (8)
79/F
yes b
NR
+
900
2.0
yes
NR
Rosell et al. 1987 (9)
52/M
yes a
diabetes
+
870
0.02
yes
yes
Rosell et al. 1987 (9)
75/F
yes¢
NR
+
5,400
NR
yes
yes
Soto-Hern~indez et al. 1988 (10)
641M
yes a
NR
+
7,200
1.1
yes
yes
A m a d o r et al. 1988 (11)
46/M
yes c
NR
+
41,000
2
yes
NR
Larson et al. 1988 (12)
32/M
no
renal transplant
a
250
3.9
yes
NR
Castellote et al. 1989 (13)
75fM
yes a
NR
+
300
1.4
yes
yes
L6pez-San Roman et al. 1989 (14)
82/M
yes a
NR
+
950
8.0
yes
NR
AI Wali et al. 1990(15)
53/M
no
CADP
+
800
NR
NR
NR
P6rez-Aguilar et al. 1990 (16)
63/F
yes c
NR
+
2,300
NR
yes
yes
Polaneo et al. 1992
64/F
yes b
diabetes, chronic hepatitis
+
2,000
2.1
yes
yes
Polaneo et aL 1992
74/M
yes c
diabetes
+
300
1.9
yes
yes
1977 (4)
a Ethylic origin. bViral origin. c Origin unknown.
dListeria monocytogenes recovered only from a biopsy specimen from the peritoneal wall. NR = Not reported; C A P D = continuous ambulatory peritoneal dialysis.
-
348
patients with decompensated cirrhosis have been proposed (1, 17): a) translocation of intestinal bacteria facilitated by oedema of villi and degeneration of the basal membrane; b) portal bacteremia with failure of the hepatic reticulo endothelial system (RES) filter due to the development of portal-systemic collateral veins; c) decrease in the RES phagocytic activity and impaired opsonic effect in peritoneal fluid and serum due to the lower Content of proteins and complement; and d) increase in the lymphatic flow through the thoracic duct. Hepatic conditions other than decompensated alcoholic cirrhosis may produce similar effects, and an increasing number of cases of SBP have been reported from patients with non-alcoholic cirrhosis. Translocation is the process by which intestinal microorganisms leave the intestinal lumen and reach extraintestinal sites, causing systemic disease in some cases. It frequently originates in the Peyer's patches (lymphoid follicles) of the small intestine, where microorganisms are ingested by the submucosal macrophages and transported to the mesenteric lymph nodes (18). Listeria monocytogenes can colonize the intestinal tract of healthy people. The production of listeriolysin O allows bacteria to escape from the phagolysosomal compartment of phagocytic cel!s, as our group recently demonstrated (19). Effective translocation and peritoneal colonization is obviously enhanced by the production of this toxin. We have reviewed the literature and have found 17 cases of SBP caused by Listeria monocytogenes (2-16). With the two cases reported here, a total of 19 have now been reported. The main features of Listeria monocytogenes SBP are shown in Table 1. Cirrhosis with decompensated ascitis was the main feature in two-thirds of the patients (13 of 19) and was caused by alcohol in seven cases. Two cases of SBP were associated with viral infections and the pathogenesis was unknown in the remaining patients. In the six non-cirrhotic patients Listeria monocytogenes SBP was associated with continuous ambulatory peritoneal dialysis (CAPD) (2 cases, I patient with a history of likely catheter contamination) (15), immunosuppression (3 cases: Hodgkin's disease, reticulum sarcoma and renal allograft) and chronic renal failure (1 case). Both of our cases were in elderly diabetics suffering from hepatic cirrhosis of unknown origin in one patient and of viral etiology in the other. Both had encephalopathy. There may be an association
Eur. J. Clin. Microbiol. Infect. Dis.
between overgrowth of Listeria monocytogenes and cirrhosis and encephalopathy. It is noteworthy that half of cases of Listeria monocytogenes SBP have been reported by Spanish authors. A more frequent intestinal colonization by listeria in Spain could be related to the dietary habits in our country. Nevertheless, differences in intestinal carriage in healthy populations were not detected by our group in an earlier report (20). Blood cultures were negative in both of our patients, which also suggests a translocation mechanism of Listeria monocytogenes. Blood cultures positive for Listeria monocytogenes were obtained in only half of the patients (9 of 19) in the reviewed series, including one CAPD patient (5) and another with SBP associated with a peritoneal venous shunt (6). A non-bacteremic portal of entry is therefore likely to exist in some cases. We failed to demonstrate the presence of grampositive rods in the Gram-stained direct smear of t h e centrifuged ascitic fluid. Although Listeria monocytogenes was recovered from the centrifuged ascitic fluid in one of our cases, the method of choice is the inoculation of at least 5 ml of ascitic fluid in blood culture bottles (21). The case by Larson et al. (12) is exceptional in that Listeria monocytogenes was isolated only from a biopsy specimen obtained by iaparoscopy of the peritoneal wall but not from blood or ascitic fluid cultures. Most patients in the cases reviewed had an increased protein content and a high WBC count in the ascitic fluid (> 250/mm3). The current empiric therapy of SBP is based on the use of third-generation cephalosporins. Our cases represent good examples of the potential failure of these agents in this clinical setting. We have recently shown that third -generation cephalosporins are inactive against Listeria monocytogenes because of their reduced affinity to the PBP-3 (22). From the results reviewed in this work, it is suggested that combinations of aminopenicillins or ureidopenicillins with betalactamase inhibitors or carbapenems could eventually replace third-generation cephalosporins as the empirical treatment of SBP, particularly in cirrhotic patients.
References
1. HallakA: Spontaneousbacterial peritonitis. American Journal of Gastroenterology 1989, 84: 345-350.
V._.o1.11,1992
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20. G6mez Mampaso E, Michaux L, de Rafael L, Carvajai A, Baquero F: Faecal Listeria monoeytogenes carriers and perinatal mortality. In: Woodbine M (ed): Problems of listeriosis. Leicester University Press, Surrey, UK 1975, p. 206-213. 21. Runyon BA, Umland ET, Merlin T: Inoculation of blood culture bottle with ascitic fluid. Improved detection of spontaneous bacterial peritonitis. Archives of Internal Medicine 1987, 147: 73-75. 22. Vicente MF~P~rez-Diaz JC, Baquero F, de Pedro MA, Berenguer J: Penicillin-binding protein 3 of Listeria monocytogenes as the primary lethal target for betalactams. Antimicrobial Agents and Chemotherapy 1990, 34: 539-542.
Isolation of Klebsiella terrigena from Clinical Specimens R. P o d s c h u n * , U . U l l m a n n
In a three-year survey conducted from 1988 to 1990 Klebsiella isolates from human clinical specimens were subjected to additional tests to identify any Klebsieila terrigena strains. Ten strains ofKlebsiella terrigena (0.4 %) were found among 2355 indole-negative Klebsiella isolates. Most of the isolates were recovered from the respiratory tract. In the API 20EC system almost exclusively biotypes no. 1777771 and 1777671 were observed. Serotyping revealed capsule types K2, K5 and K18 in two strains each. In antibiotic susceptibility tests the strains were shown to be comparable in sensitivity to Klebsiella
pneumoniae.
In 1981 a new species of KlebsieUa, Klebsiella terrigena, was described by Izard et al. (1). Klebsiella terrigena closely resembles Klebsiella pneumoniae and can b e serotyped using Klebsiella capsule antisera. T h e two species can be differentiated on the basis of tests for f e r m e n t a t i o n of melezitose, growth at 10 °C and gas production from lactose at 44.5 °C (2). Klebsiella terrigena has b e e n isolated mainly from soil and w a t e r (1, 3), and in the ten years following the first description of this new species no case of isolation f r o m humans was reported. Recently, however, we Department of Medical Microbiology, University of Kiel, Brunswiker Str. 4, D-2300 Kiel, Germany.
