Gastroenterologia Japonica Copyright 9 1992 by The Japanese Society of Gastroenterology
Vol. 27, No. 5 Printed in Japan
Spontaneous bacterial peritonitis due to Clostridium perfringens in a patient with liver cirrhosis and pure red cell aplasia Hisashi TSURUMI 1'2, Kenzaburo TANI 1, Kenji TAJIKA 1, Seiji IRIE 1, Yukio KOBAYASHI 1, Arinobu TOJO 1, Shin-ichiro OKAMOTO 1, Keiya OZAWA1, Hisataka MORIWAKI 2, Yasutoshi MUTO 2, and Shigetaka ASANO 1 1Department of Internal Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan; and eFirst Department of Internal Medicine, Gifu University School of Medicine, Gifu, Japan Summary: A 63-year-old man with decompensated liver cirrhosis and pure red cell aplasia complained of pyrexia, abdominal distention and abdominal pain. A diagnosis of spontaneous bacterial peritonitis (SBP), Conn's syndrome, was made upon the isolation of an anaerobe Clostridium perfringens from both ascitic fluid and peripheral blood. The bacteria were found to be susceptible to piperacillin, and administration of the antimicrobial agent markedly improved his SBP. The anaerobes should be kept in mind as one of the possible pathogens of SBP, although anaerobic infection has been reported to be quite rare in the disease. Gastroenterol Jpn 1992;27:662-667. Key words: anaerobic bacteria; Clostridium perfringens; Conn's syndrome; spontaneous bacterial peritonitis.
Introduction Spontaneous bacterial peritonitis (SBP), Conn's syndrome, is one of well d o c u m e n t e d complications of decompensated liver cirrhosis and other non-cirrhotic diseases accompanying ascites 1-4. It is of characteristic that SBP occurs without any apparent external or intra-abdominal focus of infection. It is reported that enteric Gram-negative rods including Escherichia coli and Klebsiella pneumoniae, and Streptococcus pneumoniae are c o m m o n , while anaerobic bacteria are very rare as pathogens of SBP 5. Here we report SBP due to an anaerobe Clostridium perfringens infection in a cirrhotic patient with concomitant pure red cell aplasia (PRCA).
Case Report A 63-year-old m a n was admitted to our hospital with chief complaints of abdominal fullness and
disturbed consciousness on 15 March, 1991. At the age of 23, he had a blood transfusion because of a right femur fracture. At the age of 57, he was referred to our hospital because of anemia. His peripheral blood examinations showed a red blood cell count of 1.48• 106/~d, hemoglobin 5.8 g/dl, and hematocrit 16.4%. The nucleated cell count of the bone marrow was 5.2 • 104/~1, with only 0.8% erythroid cells (Figure 1). A diagnosis of PRCA was made, and treatment with prednisolone and methotrexate was commenced. Subsequently, methotrexate was discontinued and the dose of prednisolone was decreased because of the appearance of liver dysfunction and glucose intolerance. Thereafter, he received 400 ml of packed red blood cells every m o n t h and 10 mg ofprednisolone everyday. Two m o n t h s prior to admission, he had started feeling abdominal fullness and general malaise. His consciousness disturbance appeared 2 days before admission. Physical examinations on arrival revealed a
Received February 6, 1992. Accepted April 17, 1992. Address for correspondence: Hisashi Tsurumi, M.D., First Department of Internal Medicine, Gifu University School of Medicine, 40 Tsukasamachi, Gifu-shi, Gifu, 500, Japan.
October 1992
Clostridial spontaneous peritonitis
663
Figure 1. The bone marrow aspiration revealed normal cellularity (nucleated cell count; 5.2 x 104/p.I) with marked decrease of erythroid cell (0.8%). Myeloid maturation was normal. (May-Giemsa stain, x 400).
Figure 2. Abdominal computed tomography showed massive ascites and nodular liver.
semicomatous (grade IV) lean patient with anemia and abdominal distention without rebound tenderness. Flapping tremor was observed without any neurological focal signs. Laboratory examinations were as follows: hemoglobin, 7.0 g/ dl; white blood cells, 3,000/~1 (neutrophils 2,300/ ~tl); platelets, 8 x 104/~d; reticulocytes, 0.050/0;AST, 64 IU/I; ALT, 106 IU/1; LDH, 487 IU/1; total pro-
tein, 5.0 g/dl; albumin, 2.9 g/dl; total bilirubin, 1.4 mg/dl; prothrombin time, 34%; hepaplastin test, 42%; a-fetoprotein, 43.6 ng/ml; blood sugar, 533 mg/dl and ammonia, 181 ~g/dl. HBs antigen, anti-HBc(IgG) antibody and anti-HCV antibody were negative. Plasma amino acid composition was as follows: valine, lll.9nmol/ml; leucine, 45.6 nmol/ml; isoleucine, 21.7 nmol/ml; tyrosine, 87.3 nmol/ml; phenylalanine, 91.8 nmol/ml and methionine, 137.4 nmol/ml (Fischer's ratio 1.0). Urinalysis revealed glucosuria (2 g/dl) without ketone body. Ultrasonography and computed tomography (Figure 2) showed nodular liver, splenomegaly and massive ascites. According to his past history, physical examinations and the laboratory data, his consciousness disturbance was considered to originate from the combination of hepatic encephalopathy due to cirrhosis and non-ketotic diabetic coma. The cirrhosis was considered to be caused by blood transfusion. Intravenous administration of branched chain amino acid-rich solution (Aminoleban| insulin and diuretics was commenced soon after the admission and his consciousness became clear 12 hours after the infusion. On the following day, he suddenly developed fever and abdominal pain.
664
Vol. 27, No. 5
H. Tsurumi et aL
I I
40rag
l
Aminoleban t000ml . .J 9 "
"
I ..... 2oC ....
I
coma grade
p.o. 20rag i.v.
splronolactone lOOmg
furosemide
500ml
~ ......
,
p.o.
i.v.
3
intermediate insulin
130ur
piparaci,in 6g i.v.
s,~.
I
flapping tremor In -
+)
II-
flapping(_)tremor
I0
(~ temp.
blood culture .Cl. perfringens(
39 t
+)
C R P 2.6mE/all
CRP
0.1mg/dl
37 abdominal distension grade
fasting blood
sugar
~
. .......
puncture/culture Cl. perfringens ( + )
[
Figure 3. Clinical course of a case, 63 years old, male, spontaneous bacterial peritonitis, Conn's syndrome, p.o.; per os, i.v.; intravenous injection, c.i.v.; continuous i.v., s.c.; subcutaneous injection.
'1~ascites
CI. perfringens
(--)
I
Ot
total protein,
~1,~,~ 20%
albumin
blood transfusion
hemoglobin
5Oral
_
--
~
400ml
(g/d0 it
1
0
,'o
2'o
3b day of hospitalization
The ascites obtained by test puncture showed the following: specific gravity, 1.012; protein, 0.7 g/dl; albumin, 0.5 g/dl; leukocyte, 800/~1 (neutrophils, 640/[.d) and LDH, 77 IU/1. Bacteriological studies demonstrated the Gram-positive rod Clostridium perfringens in the culture of both the ascitic fluid and the peripheral blood. Antimicrobial susceptibility studies were as follows; piperacillin (+ + +), ampicillin ( + + + ) , cefuroxime ( + + + ) , imipenem/cilastatin (+ +), erythromycin (+ +), aztreoham ( - ) , ofloxacin (+ + +). Since a diagnosis of SBP was made from the typical clinical findings,
the administration of piperacillin, (2g/8 hrs.), was continued for 14 days. His general condition gradually improved and he was discharged on day 62 (Figure 3). Discussion Recent advances in anaerobic bacteriology have elucidated that anaerobes account for more than 99% of all intestinal flora6. However, SBP is known to be associated with aerobic bacteria despite the proximity of the peritoneal cavity to the intestine.
October 1992
Table
665
Clostridial spontaneous peritonitis
1. Clinical characteristics of reported SBP (spontaneous bacterial peritonitis) cases due to anaerobic infection (a) Clinical symptoms Age
Sex
Diagnosis
Precipitating events or complications
1 2
63 60
M F
PRCA, steroid, diabetes mellitus small bowel biopsy
3
33
M
4
54
F
cirrhosis cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol)
Case
5
NC
6
NC
7
63
M
8 9
42 57
F F
10
63
M
11
59
M
12
33
NC
13
53
NC
14
53
NC
15
58
F
cirrhosis cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol)
portacaval shunt incision, wound l e a k a g e esophageal, gastric bleeding, diabetes
Reference Fever
Abdominal pain
Coma
+
+
+
Present case
--
+
+
(7)
+
-
+
(7)
+
-
-
(8)
mellitus
NC
NC
(9)
NC
NC
(9)
+
+
+
(10)
+ +
+
+ +
(11) (12, 13)
+
+
-
(12)
+
+
+
(14)
intraarterial catheter
-
-
+
(15)
umbilical hernia leakage, splenorenal shunt
+
+
-
(15)
(-)
+
-
+
(15)
-
+
+
(16)
pneumoperitoneum, cholelithiasis, gastric ulcer, renal failure, hemodialysis
(-) gastroduodenal intraarterial vasopressin therapy superior mesenteric intraarterial vasopressin
(-)
upper gastrointestinal bleeding, repeat SBP
NC: not clarified
There have been only 15 reported SBP cases due to anaerobic or microaerophilic bacteria 7-16 (Table 1), and there has been no reported case of anaerobic SBP in the Japanese literature. The rarity of anaerobic SBP appears to be due to the poor growth of anaerobic bacteria in ascites which has relatively high oxygen content 7'17 and/or inadequate culture techniques. Clinical features in anaerobic SBP were reported to be indistinguishable from those associated with aerobic bacteria 7-16. In only 4 (cases 4, 12, 14 and the present case) of the above-mentioned 15 cases, were anaerobic bacteria actually detected in cultures of both the ascitic fluid and the blood. Although the exact pathogenesis of SBP remains unknown, two possible infectious routes
for SBP have been postulated; transmural migration of enteric bacteria is or hematogenous spread of enteric bacteria by intrahepatic and/or extrahepatic shunt of portal blood flow. The latter route may induce SBP by increasing systemic bacteremia owing to decreased clearance of enteric bacteria by the liver5:8. In our case, the hematogenous route was considered to be more important because of the presence of systemic bacteremia as well as bacterial ascites. Both impaired reticuloendothelial system (RES) in cirrhosis 5'19 and the immunocompromised state indicated by glucose intolerance, steroid treatment and severe anemia seemed to contribute to the SBP in t h e case. Although the direct relationship of anaerobic SBP with PRCA is unclear, it is possible that the severe
666
Vol. 27, No. 5
H. Tsurumi et al.
Table 1. Clinical characteristics of reported SBP (spontaneous bacterial peritonitis) cases due to anaerobic infection (b) Peripheral blood Case
WBC (/[.tl)
Bil (mg/dl)
Ascites
LDH AIb (IU/I) (g/dl)
PT WBC (neut) (sec.) (/~tl)
Protein (g/dl)
Culture Blood/Ascites
0.7
CI. perfringens/CI, perfringens
piperacillin
NC
(-)/Bacteroides fragilis, E. coli, Strep. group D (-)/ CI. perfringens CI. perfringens/ CI. perfringens (-)/ Bacteroides fragilis (-)/ CI. perfringens NC/CI. perfringens
clindamycin, died, gentamycin not septic penicillin (PCG) survived
1
3000
1.4
487
2.9
16.9
2
17300
1.1
352
2.2
14
800 (640) 400
3
19200
5.2
250
3.2
15
many
3.0
4
13400
5.0
NC
3.3
15.7
NC
5
NC
4366 (4362) NC
6
NC
NC
7
17000
NC
NC
NC
NC
NC
8
9400
33
NC
1.8
23
9
17900
2.8
NC
2.4
NC
10
8000
NC
NC
NC
NC
11
17400
3.3
195
2.4
16
numerous
1.1
12
20300
44.5
NC
2.4
NC
1600
1.0
13
8600
17.5
NS
2.3
NC
1400
1.2
14
NC
4.2
NC
2.2
NC
4100
2.0
15
16900
6.9
NC
3.2
14.6
4200 (3570)
NC
4500 (4230) 4000 (3840)
NC
NC/CI.tertium
NC
400 (200)
NC
Citrobacter/Bacteroides, E. coli, P, Morganii, Citrobacter, gram-positive rod (-)/Bacteroides fragilis, Peptostrep., Strep., Staph. epidermidis, Diphtheroids (-)/ Campylobacter fetus Anaerobic diphtheroids/ Diphtheroids (-)/Peptococci, Peptostreptococcus anaerobius Bacteroides/Bacteroides, a-Streptococcus (-)/ CI. cadaveris
Antibiotics
Outcome survived
PCG
survived NC
NC
NC
NC
broad-spectrum, died, antibiotics septic cefoxitin survived cephaloridine, kanamycin
died, septic
clindamycin
survived
clindamycin, gentamycin NC
died, not septic NC
NC
NC
NC
NC
aztreonam, PCG died, not imipenem septic NC: not clarified
anemia due to PRCA induced hypoxemia, reduced the oxygen content in the ascitic fluid, and thus caused anaerobic SBP. However, it seems to be likely that repeated blood transfusions in this patient with PRCA caused post-transfusion liver cirrhosis, which was later decompensated, accompanied with ascites, and provided the site of anaerobic infection. Since SBP is one of the important prognostic factors for liver cirrhosis 2~ the prevention of SBP is of practical importance 21'22. Careful bacteriological examinations should be performed to detect not only aerobic bacteria but also anaerobic bacteria in a cirrhotic patient with fever and ascites. In order to prevent a fatal outcome of SBP, the
immediate administration of effective antibiotics is essential. References 1. Gribbin JC, Cox CJ. Spontaneous bacterial peritonitis in a healthy adult male. Aust N Z J Surg 1990;60:723-725. 2. Thomas FB, Fromkes JJ. Spontaneous bacterial peritonitis with acute viral hepatitis. J Clin Gastroenterol 1981;4:259-262. 3. Isner J, Macdonald JS, Schein PS. Spontaneous streptococcus pneumonia peritonitis in a patient with metastatic gastric cancer. Cancer 1977;39:2306-2309. 4. Lipsky PE, Hardin JA, Schour L, et al. Spontaneous peritonitis and systemic lupus erythematosus. JAMA 1975;232:929-931. 5. Hallak A. Spontaneous bacterial peritonitis. Am J Gastroenterol 1989;84:345-350. 6. Hill M J, Draser BS. The normal colonic bacterial flora. Gut 1975;16:318-323.
October 1992
Clostridial spontaneous peritonitis
7. Targan SR, Chow AW, Guze LB. Role of anaerobic bacteria in spontaneous peritonitis of cirrhosis. Am J Med 1977;62:397-403. 8. Brown RL, Peter G. Clostridial spontaneous peritonitis. JAMA 1976;236:2095-2096. 9. Weinstein MP, Iannini PB, Stratton CW, et al. Spontaneous bacterial peritonitis. A Review of 28 cases with emphasis on improved survival and factors influencing prognosis. Am J Med 1978;64: 592-598. 10. Woelfel GF, Hansbrough JE Spontaneous bacterial peritonitis and pneumoperitoneum. JAMA 1983;249:921-922. 11. Butler T, Pitt S. Spontaneous bacterial peritonitis due to Clostridium tertium. Gastroenterology 1982;82:133-134. 12. Bar-Meir S, Conn HO. Spontaneous bacterial peritonitis induced by intraarterial vasopressin. Gastroenterology 1976;70:418-421. 13. Conn HO, Fessel JM. Spontaneous bacterial peritonitis in cirrhosis: variation on a theme. Medicine 1971;50:161-197. 14. Targan SR, Chow AW, Guze LB. Spontaneous peritonitis of cirrhosis due to Campylobacter fetus. Gastroenterology 1976;71: 311-313.
667
15. Correia JP, Conn HO. Spontaneous bacterial peritonitis in cirrhosis: Endemic or epidemic? Med Clin North Am 1975;59:963-981. 16. Herman R, Goldman IS, Bronzo R, et al. Clostridium cadaveris: An unusual cause of spontaneous bacterial peritonitis. Am J Gastroenterol 1992;87:140-142. 17. Sheckman P, Onderdonk AB, Bartlett JG. Anaerobes in Spontaneous peritonitis. Lancet 1977;2:1223. 18. Hoefs JC, Runyon BA. Spontaneous bacterial peritonitis. Dis Mon 1985;31:1-48. 19. Lahnborg G, Friman L, Bergham L. Reticuloendothelial function in patients with alcoholic liver cirrhosis. Scand J Gastroenterol 1981;16:481-489. 20. Crossley IR, Williams R. Spontaneous bacterial peritonitis. Gut 1985;26:325-331. 21. Soriano G, Guarner C, Teixido M, et al. Selectiveintestinaldecontamination prevents spontaneous bacterial peritonitis. Gastroenterology 1991;100:477-481. 22. Hoefs JC. Spontaneous bacterialperitonitis: Prevention andtherapy. Hepatology 1990;12:776-781.
Vol. 27, No. 5 Printed in Japan
Spontaneous bacterial peritonitis due to Clostridium perfringens in a patient with liver cirrhosis and pure red cell aplasia Hisashi TSURUMI 1'2, Kenzaburo TANI 1, Kenji TAJIKA 1, Seiji IRIE 1, Yukio KOBAYASHI 1, Arinobu TOJO 1, Shin-ichiro OKAMOTO 1, Keiya OZAWA1, Hisataka MORIWAKI 2, Yasutoshi MUTO 2, and Shigetaka ASANO 1 1Department of Internal Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan; and eFirst Department of Internal Medicine, Gifu University School of Medicine, Gifu, Japan Summary: A 63-year-old man with decompensated liver cirrhosis and pure red cell aplasia complained of pyrexia, abdominal distention and abdominal pain. A diagnosis of spontaneous bacterial peritonitis (SBP), Conn's syndrome, was made upon the isolation of an anaerobe Clostridium perfringens from both ascitic fluid and peripheral blood. The bacteria were found to be susceptible to piperacillin, and administration of the antimicrobial agent markedly improved his SBP. The anaerobes should be kept in mind as one of the possible pathogens of SBP, although anaerobic infection has been reported to be quite rare in the disease. Gastroenterol Jpn 1992;27:662-667. Key words: anaerobic bacteria; Clostridium perfringens; Conn's syndrome; spontaneous bacterial peritonitis.
Introduction Spontaneous bacterial peritonitis (SBP), Conn's syndrome, is one of well d o c u m e n t e d complications of decompensated liver cirrhosis and other non-cirrhotic diseases accompanying ascites 1-4. It is of characteristic that SBP occurs without any apparent external or intra-abdominal focus of infection. It is reported that enteric Gram-negative rods including Escherichia coli and Klebsiella pneumoniae, and Streptococcus pneumoniae are c o m m o n , while anaerobic bacteria are very rare as pathogens of SBP 5. Here we report SBP due to an anaerobe Clostridium perfringens infection in a cirrhotic patient with concomitant pure red cell aplasia (PRCA).
Case Report A 63-year-old m a n was admitted to our hospital with chief complaints of abdominal fullness and
disturbed consciousness on 15 March, 1991. At the age of 23, he had a blood transfusion because of a right femur fracture. At the age of 57, he was referred to our hospital because of anemia. His peripheral blood examinations showed a red blood cell count of 1.48• 106/~d, hemoglobin 5.8 g/dl, and hematocrit 16.4%. The nucleated cell count of the bone marrow was 5.2 • 104/~1, with only 0.8% erythroid cells (Figure 1). A diagnosis of PRCA was made, and treatment with prednisolone and methotrexate was commenced. Subsequently, methotrexate was discontinued and the dose of prednisolone was decreased because of the appearance of liver dysfunction and glucose intolerance. Thereafter, he received 400 ml of packed red blood cells every m o n t h and 10 mg ofprednisolone everyday. Two m o n t h s prior to admission, he had started feeling abdominal fullness and general malaise. His consciousness disturbance appeared 2 days before admission. Physical examinations on arrival revealed a
Received February 6, 1992. Accepted April 17, 1992. Address for correspondence: Hisashi Tsurumi, M.D., First Department of Internal Medicine, Gifu University School of Medicine, 40 Tsukasamachi, Gifu-shi, Gifu, 500, Japan.
October 1992
Clostridial spontaneous peritonitis
663
Figure 1. The bone marrow aspiration revealed normal cellularity (nucleated cell count; 5.2 x 104/p.I) with marked decrease of erythroid cell (0.8%). Myeloid maturation was normal. (May-Giemsa stain, x 400).
Figure 2. Abdominal computed tomography showed massive ascites and nodular liver.
semicomatous (grade IV) lean patient with anemia and abdominal distention without rebound tenderness. Flapping tremor was observed without any neurological focal signs. Laboratory examinations were as follows: hemoglobin, 7.0 g/ dl; white blood cells, 3,000/~1 (neutrophils 2,300/ ~tl); platelets, 8 x 104/~d; reticulocytes, 0.050/0;AST, 64 IU/I; ALT, 106 IU/1; LDH, 487 IU/1; total pro-
tein, 5.0 g/dl; albumin, 2.9 g/dl; total bilirubin, 1.4 mg/dl; prothrombin time, 34%; hepaplastin test, 42%; a-fetoprotein, 43.6 ng/ml; blood sugar, 533 mg/dl and ammonia, 181 ~g/dl. HBs antigen, anti-HBc(IgG) antibody and anti-HCV antibody were negative. Plasma amino acid composition was as follows: valine, lll.9nmol/ml; leucine, 45.6 nmol/ml; isoleucine, 21.7 nmol/ml; tyrosine, 87.3 nmol/ml; phenylalanine, 91.8 nmol/ml and methionine, 137.4 nmol/ml (Fischer's ratio 1.0). Urinalysis revealed glucosuria (2 g/dl) without ketone body. Ultrasonography and computed tomography (Figure 2) showed nodular liver, splenomegaly and massive ascites. According to his past history, physical examinations and the laboratory data, his consciousness disturbance was considered to originate from the combination of hepatic encephalopathy due to cirrhosis and non-ketotic diabetic coma. The cirrhosis was considered to be caused by blood transfusion. Intravenous administration of branched chain amino acid-rich solution (Aminoleban| insulin and diuretics was commenced soon after the admission and his consciousness became clear 12 hours after the infusion. On the following day, he suddenly developed fever and abdominal pain.
664
Vol. 27, No. 5
H. Tsurumi et aL
I I
40rag
l
Aminoleban t000ml . .J 9 "
"
I ..... 2oC ....
I
coma grade
p.o. 20rag i.v.
splronolactone lOOmg
furosemide
500ml
~ ......
,
p.o.
i.v.
3
intermediate insulin
130ur
piparaci,in 6g i.v.
s,~.
I
flapping tremor In -
+)
II-
flapping(_)tremor
I0
(~ temp.
blood culture .Cl. perfringens(
39 t
+)
C R P 2.6mE/all
CRP
0.1mg/dl
37 abdominal distension grade
fasting blood
sugar
~
. .......
puncture/culture Cl. perfringens ( + )
[
Figure 3. Clinical course of a case, 63 years old, male, spontaneous bacterial peritonitis, Conn's syndrome, p.o.; per os, i.v.; intravenous injection, c.i.v.; continuous i.v., s.c.; subcutaneous injection.
'1~ascites
CI. perfringens
(--)
I
Ot
total protein,
~1,~,~ 20%
albumin
blood transfusion
hemoglobin
5Oral
_
--
~
400ml
(g/d0 it
1
0
,'o
2'o
3b day of hospitalization
The ascites obtained by test puncture showed the following: specific gravity, 1.012; protein, 0.7 g/dl; albumin, 0.5 g/dl; leukocyte, 800/~1 (neutrophils, 640/[.d) and LDH, 77 IU/1. Bacteriological studies demonstrated the Gram-positive rod Clostridium perfringens in the culture of both the ascitic fluid and the peripheral blood. Antimicrobial susceptibility studies were as follows; piperacillin (+ + +), ampicillin ( + + + ) , cefuroxime ( + + + ) , imipenem/cilastatin (+ +), erythromycin (+ +), aztreoham ( - ) , ofloxacin (+ + +). Since a diagnosis of SBP was made from the typical clinical findings,
the administration of piperacillin, (2g/8 hrs.), was continued for 14 days. His general condition gradually improved and he was discharged on day 62 (Figure 3). Discussion Recent advances in anaerobic bacteriology have elucidated that anaerobes account for more than 99% of all intestinal flora6. However, SBP is known to be associated with aerobic bacteria despite the proximity of the peritoneal cavity to the intestine.
October 1992
Table
665
Clostridial spontaneous peritonitis
1. Clinical characteristics of reported SBP (spontaneous bacterial peritonitis) cases due to anaerobic infection (a) Clinical symptoms Age
Sex
Diagnosis
Precipitating events or complications
1 2
63 60
M F
PRCA, steroid, diabetes mellitus small bowel biopsy
3
33
M
4
54
F
cirrhosis cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol)
Case
5
NC
6
NC
7
63
M
8 9
42 57
F F
10
63
M
11
59
M
12
33
NC
13
53
NC
14
53
NC
15
58
F
cirrhosis cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol) cirrhosis (alcohol)
portacaval shunt incision, wound l e a k a g e esophageal, gastric bleeding, diabetes
Reference Fever
Abdominal pain
Coma
+
+
+
Present case
--
+
+
(7)
+
-
+
(7)
+
-
-
(8)
mellitus
NC
NC
(9)
NC
NC
(9)
+
+
+
(10)
+ +
+
+ +
(11) (12, 13)
+
+
-
(12)
+
+
+
(14)
intraarterial catheter
-
-
+
(15)
umbilical hernia leakage, splenorenal shunt
+
+
-
(15)
(-)
+
-
+
(15)
-
+
+
(16)
pneumoperitoneum, cholelithiasis, gastric ulcer, renal failure, hemodialysis
(-) gastroduodenal intraarterial vasopressin therapy superior mesenteric intraarterial vasopressin
(-)
upper gastrointestinal bleeding, repeat SBP
NC: not clarified
There have been only 15 reported SBP cases due to anaerobic or microaerophilic bacteria 7-16 (Table 1), and there has been no reported case of anaerobic SBP in the Japanese literature. The rarity of anaerobic SBP appears to be due to the poor growth of anaerobic bacteria in ascites which has relatively high oxygen content 7'17 and/or inadequate culture techniques. Clinical features in anaerobic SBP were reported to be indistinguishable from those associated with aerobic bacteria 7-16. In only 4 (cases 4, 12, 14 and the present case) of the above-mentioned 15 cases, were anaerobic bacteria actually detected in cultures of both the ascitic fluid and the blood. Although the exact pathogenesis of SBP remains unknown, two possible infectious routes
for SBP have been postulated; transmural migration of enteric bacteria is or hematogenous spread of enteric bacteria by intrahepatic and/or extrahepatic shunt of portal blood flow. The latter route may induce SBP by increasing systemic bacteremia owing to decreased clearance of enteric bacteria by the liver5:8. In our case, the hematogenous route was considered to be more important because of the presence of systemic bacteremia as well as bacterial ascites. Both impaired reticuloendothelial system (RES) in cirrhosis 5'19 and the immunocompromised state indicated by glucose intolerance, steroid treatment and severe anemia seemed to contribute to the SBP in t h e case. Although the direct relationship of anaerobic SBP with PRCA is unclear, it is possible that the severe
666
Vol. 27, No. 5
H. Tsurumi et al.
Table 1. Clinical characteristics of reported SBP (spontaneous bacterial peritonitis) cases due to anaerobic infection (b) Peripheral blood Case
WBC (/[.tl)
Bil (mg/dl)
Ascites
LDH AIb (IU/I) (g/dl)
PT WBC (neut) (sec.) (/~tl)
Protein (g/dl)
Culture Blood/Ascites
0.7
CI. perfringens/CI, perfringens
piperacillin
NC
(-)/Bacteroides fragilis, E. coli, Strep. group D (-)/ CI. perfringens CI. perfringens/ CI. perfringens (-)/ Bacteroides fragilis (-)/ CI. perfringens NC/CI. perfringens
clindamycin, died, gentamycin not septic penicillin (PCG) survived
1
3000
1.4
487
2.9
16.9
2
17300
1.1
352
2.2
14
800 (640) 400
3
19200
5.2
250
3.2
15
many
3.0
4
13400
5.0
NC
3.3
15.7
NC
5
NC
4366 (4362) NC
6
NC
NC
7
17000
NC
NC
NC
NC
NC
8
9400
33
NC
1.8
23
9
17900
2.8
NC
2.4
NC
10
8000
NC
NC
NC
NC
11
17400
3.3
195
2.4
16
numerous
1.1
12
20300
44.5
NC
2.4
NC
1600
1.0
13
8600
17.5
NS
2.3
NC
1400
1.2
14
NC
4.2
NC
2.2
NC
4100
2.0
15
16900
6.9
NC
3.2
14.6
4200 (3570)
NC
4500 (4230) 4000 (3840)
NC
NC/CI.tertium
NC
400 (200)
NC
Citrobacter/Bacteroides, E. coli, P, Morganii, Citrobacter, gram-positive rod (-)/Bacteroides fragilis, Peptostrep., Strep., Staph. epidermidis, Diphtheroids (-)/ Campylobacter fetus Anaerobic diphtheroids/ Diphtheroids (-)/Peptococci, Peptostreptococcus anaerobius Bacteroides/Bacteroides, a-Streptococcus (-)/ CI. cadaveris
Antibiotics
Outcome survived
PCG
survived NC
NC
NC
NC
broad-spectrum, died, antibiotics septic cefoxitin survived cephaloridine, kanamycin
died, septic
clindamycin
survived
clindamycin, gentamycin NC
died, not septic NC
NC
NC
NC
NC
aztreonam, PCG died, not imipenem septic NC: not clarified
anemia due to PRCA induced hypoxemia, reduced the oxygen content in the ascitic fluid, and thus caused anaerobic SBP. However, it seems to be likely that repeated blood transfusions in this patient with PRCA caused post-transfusion liver cirrhosis, which was later decompensated, accompanied with ascites, and provided the site of anaerobic infection. Since SBP is one of the important prognostic factors for liver cirrhosis 2~ the prevention of SBP is of practical importance 21'22. Careful bacteriological examinations should be performed to detect not only aerobic bacteria but also anaerobic bacteria in a cirrhotic patient with fever and ascites. In order to prevent a fatal outcome of SBP, the
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October 1992
Clostridial spontaneous peritonitis
7. Targan SR, Chow AW, Guze LB. Role of anaerobic bacteria in spontaneous peritonitis of cirrhosis. Am J Med 1977;62:397-403. 8. Brown RL, Peter G. Clostridial spontaneous peritonitis. JAMA 1976;236:2095-2096. 9. Weinstein MP, Iannini PB, Stratton CW, et al. Spontaneous bacterial peritonitis. A Review of 28 cases with emphasis on improved survival and factors influencing prognosis. Am J Med 1978;64: 592-598. 10. Woelfel GF, Hansbrough JE Spontaneous bacterial peritonitis and pneumoperitoneum. JAMA 1983;249:921-922. 11. Butler T, Pitt S. Spontaneous bacterial peritonitis due to Clostridium tertium. Gastroenterology 1982;82:133-134. 12. Bar-Meir S, Conn HO. Spontaneous bacterial peritonitis induced by intraarterial vasopressin. Gastroenterology 1976;70:418-421. 13. Conn HO, Fessel JM. Spontaneous bacterial peritonitis in cirrhosis: variation on a theme. Medicine 1971;50:161-197. 14. Targan SR, Chow AW, Guze LB. Spontaneous peritonitis of cirrhosis due to Campylobacter fetus. Gastroenterology 1976;71: 311-313.
667
15. Correia JP, Conn HO. Spontaneous bacterial peritonitis in cirrhosis: Endemic or epidemic? Med Clin North Am 1975;59:963-981. 16. Herman R, Goldman IS, Bronzo R, et al. Clostridium cadaveris: An unusual cause of spontaneous bacterial peritonitis. Am J Gastroenterol 1992;87:140-142. 17. Sheckman P, Onderdonk AB, Bartlett JG. Anaerobes in Spontaneous peritonitis. Lancet 1977;2:1223. 18. Hoefs JC, Runyon BA. Spontaneous bacterial peritonitis. Dis Mon 1985;31:1-48. 19. Lahnborg G, Friman L, Bergham L. Reticuloendothelial function in patients with alcoholic liver cirrhosis. Scand J Gastroenterol 1981;16:481-489. 20. Crossley IR, Williams R. Spontaneous bacterial peritonitis. Gut 1985;26:325-331. 21. Soriano G, Guarner C, Teixido M, et al. Selectiveintestinaldecontamination prevents spontaneous bacterial peritonitis. Gastroenterology 1991;100:477-481. 22. Hoefs JC. Spontaneous bacterialperitonitis: Prevention andtherapy. Hepatology 1990;12:776-781.
