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Peritonitis caused by Campylobacter jejuni and serologically confirmed in a patient being treated with continuous ambulatory peritoneal dialysis
Journal of Infection (I99o)
2 I , 71-75
CASE REPORT P e r i t o n i t i s c a u s e d b y Campylobacter jejuni a n d s e r o l o g i c a l l y c o n f i r m e d in a p a t i e n t b e i n g t r e a t e d w i t h c o n t i n u o u s ambulatory peritoneal dialysis David J. G o o d m a n and Keith A. Wise* Austin Hospital, Heidelberg, Victoria 3084, Australia Accepted for publication 26 January I99O
Summary A case of Campylobacter jejuni peritonitis in a patient being treated with continuous ambulatory peritoneal dialysis is described. The significance of the organism isolated from our patient was initially doubtful because of a rapid defervescence of symptoms with minimal specific antibiotic therapy, lack of a preceding diarrhoeal illness and the time taken to isolate and identify the organism. Serial serum IgM, IgA and IgG antibody estimations clearly showed an acute seroconversion confirming that the strain of C. jejuni isolated was the causative organism in this case.
Introduction Gastro-enteritis
is the
most
common
manifestation
of infection
with
Campylobacterjejuni. x Campylobacter species are not often isolated from extraintestinal sites, the b l o o d stream being the most c o m m o n l y reported. ~ C. jejuni is a rare cause of peritonitis associated with continuous ambulatory peritoneal dialysis ( C A P D ) . 3 W e report a case in which pathogenicity was confirmed b y serological testing.
Case report T h e patient was a 63-year-old w o m a n with endstage renal failure due to chronic pyelonephritis and renal calculi. T r e a t m e n t with C A P D had b e g u n in July I987. In F e b r u a r y and April I988 she developed recurrent infections with Staphylococcus aureus at the exit-site of a T e n c k h o f f catheter. T h e s e were treated successfully with oral flucloxacillin. O n 7 July I988, the patient presented herself with a I2 h history of anorexia, nausea, vomiting and generalised abdominal pain associated with two cloudy peritoneal dialysis packs. T h e r e was no history of diarrhoea. O n examination, she appeared unwell, with a t e m p e r a t u r e of 38"3 °C, diffuse abdominal tenderness with peritonism, and crusting around the T e n c k h o f f catheter exit-site. Dialysate fluid was sent for microbiological investigations while she was given single intravenous doses of flucloxacillin and t o b r a m y c i n followed b y intraperitoneal flucloxacillin. S y m p t o m s and signs rapidly subsided. * Address correspondence to: Dr Keith A. Wise, Department of Microbiology, Wollongong Hospital; Wollongong, New South Wales 2500, Australia.
oi63-4453/9o/o4oo71 +05 $02.00/0
© I99O The British Society for the Study of Infection
72
D. J. G O O D M A N
A N D K. A. W I S E
T a b l e I Serological responses in a patient with C a m p y l o b a c t e r jejuni
peritonitis while being treated with C A P D Antibody titres Date
IgM
3o Jun 87 ~o May 88 I4 Jun 88 7 Jul 88 I8 Jul 88 8 Nov 88 30 May 89
4o 4° i6o 8o 8o 320 80 80 320 Episode of CAPD peritonitis 640 80 320 64o* I28O I28O 640* I28o I28o
R e f e r e n c e range
< 80
IgA
< 80
IgG
< 320
* IgM result not due to rheumatoid factor.
Staphylococcus aureus was again isolated from a swab of the catheter exitsite. After 3 days, campylobacter-like organisms were isolated from direct anaerobic cultures of the dialysate fluid. Aerobic and anaerobic blood culture bottles that had been inoculated with dialysate also grew the same organism. T h r e e days later the organism was formally identified as C, jejuni. At this stage the patient remained asymptomatic. Since the clinical significance of the organism isolated was uncertain, it was decided to complete a course of anti-staphylococcal therapy. Intraperitoneal cephalothin was given for 5 days followed b y oral cephalexin for 2 weeks. Faecal cultures were not p e r f o r m e d until i i days after the patient presented herself. Campylobacter species were not isolated. A b d o m i n a l ultrasound and C T scans, barium enema and colonoscopy were unremarkable. Laboratory results M i c r o s c o p y of the dialysate fluid revealed I72O × IO 6 p o l y m o r p h o n u c l e a r leucocytes/1 and IO x lO 6 red cells/l. A G r a m - s t a i n o f centrifuged sediment was negative. T h e dialysate was cultured on sheep blood and M c C o n k e y agars in an atmosphere of io % carbon dioxide in air at 37 °C, as well as on horse b l o o d agar anaerobically at 37 °C. Aerobic and anaerobic ' B a c t e c ' blood culture bottles were each inoculated with 5 ml dialysate. After 3 days of incubation, a very faint growth appeared only on the anaerobic plate. Gram-staining of the colonies revealed curved G r a m - n e g a t i v e rods consistent with the appearance of Campylobacter species. In b o t h blood culture bottles, inoculated with the dialysate, grew a similar organism. Biochemical tests and sodium dodecyl sulphate polyacrylamide gel electrophoresis confirmed the organism's identity as C. jejuni. Agar dilution antibiotic sensitivity testing showed the organism to be sensitive to erythromycin, tetracycline, gentamicin, norfloxacin, ciprofloxacin, chloramphenicol and ticarcillin.
Peritonitis caused by Campylobacter jejuni
73
Serial serum samples were tested for the presence of specific IgM, IgA and IgG antibodies to C. jejuni by means of a diffusion-in-gel enzyme-linked immunosorbent assay. A four-fold change in titre was considered significant. T h e results are shown in the accompanying Table I. Samples of serum stored from I year, 2 months, and I month earlier, all showed negative responses to all three classes of antibody. Serum collected IO days after the episode showed a significant rise in the titre of IgA, but not of IgG or IgM antibody. Four months after the episode, all three classes of antibody had risen in titre. A further sample of serum collected IO months after the episode showed that titres of all three remained elevated. Discussion
Campylobacter spp. are rarely implicated as a cause of CAPD peritonitis. 3 To our knowledge, only I I other cases have been described. Six were due to C. jejuni, 4-7 four to C. fetusf' s-x0 and one to C. coll. n A further five cases of spontaneous bacterial peritonitis due to Campylobacter spp. have also been reportedfl' 12-15 Only one of the reports involving CAPD included results of serological testing. 4 T h e mode of spread of C. jejuni to the dialysate fluid is uncertain. Our patient did not have a history of diarrhoea, and faecal cultures were not obtained until I I days after the onset of peritonitis. Initial treatment of CAPD peritonitis is usually directed at staphylococci and aerobic Gram-negative organisms unless the Gram-stain is positive. Initially, we treated our patient with I g flucloxacillin and Ioo mg tobramycin intravenously, followed by intraperitoneal instillation of 25o mg/1 flucloxacillin. Subsequently, 25omg/1 cephalothin was given intraperitoneally followed by oral cephalexin. Rapid symptomatic improvement and clearing of the dialysate fluid followed. Tobramycin has a half-life of up to 36 h in dialysis patients, Is hence the single dose of tobramycin would be active for a prolonged period. Similarly, the high concentrations of flucloxacillin and cephalothin achieved intraperitoneally may have inhibited the organism, even though C. jejuni is usually regarded as resistant in vitro, x' 17 Our isolate was sensitive to gentamicin in vitro, hence it may be assumed that it would also be sensitive to tobramycin. We believe that the prolonged activity of the initial dose of tobramycin, together with frequent changes of the CAPD pack, eradicated the organism from the peritoneal cavity of our patient. Pepersack and colleagues described the first case of C. jejuni CAPD peritonitis in I982. ~ Using a tube agglutination method, they demonstrated seroconversion to the strains of C. jejuni isolated from the patient's faeces and peritoneal fluid. Responses to individual classes of antibody were not reported. We found early seroconversion in respect of IgA followed by that in respect of IgM and IgG. These findings are consistent with an acute infection caused by C. jejuni although it is unusual for IgM to persist at such a high titre for Io months (B. Dwyer, personal communication). Also of interest, was the seroconversion in respect of IgA before that in respect of IgM, suggesting a source of the infection in the gut. Hence, we clearly demonstrated
74
D. J. GOODMAN AND K. A. WISE
s e r o c o n v e r s i o n r e l a t i n g to a c u t e a n d c o n v a l e s c e n t p h a s e s e r u m samples in respect of IgM, IgA and IgG. Gampylobacter jejuni is a r a r e cause o f C A P D p e r i t o n i t i s a l t h o u g h t h e dialysate fluid o f a few p a t i e n t s r e m a i n s c u l t u r e - n e g a t i v e in this s y n d r o m e . C u l t u r a l m e t h o d s t h a t e n h a n c e the g r o w t h o f fastidious o r g a n i s m s s h o u l d b e p e r f o r m e d so t h a t a c o r r e c t m i c r o b i o l o g i c a l diagnosis can allow t h e m o s t a p p r o p r i a t e antibiotics to b e p r e s c r i b e d . W e p e r f o r m d i r e c t c u l t u r e o n dialysate a n d also i n o c u l a t e it into ' B a c t e c ' b l o o d c u l t u r e m e d i u m in o r d e r to e n h a n c e t h e d e t e c t i o n o f fastidious o r g a n i s m s . I f g r o w t h is o b s e r v e d in t h e ' B a c t e c ' m e d i u m , a G r a m - s t a i n o f it will suggest t h e t y p e s o f m e d i a suitable f o r isolating t h e s e o r g a n i s m s . W e believe t h a t o u r p a t i e n t p r o b a b l y h a d an a c u t e a s y m p t o m a t i c g u t i n f e c t i o n w i t h C. jejuni f o l l o w e d b y C A P D p e r i t o n i t i s d u e to t h a t o r g a n i s m . D e m o n s t r a t i o n o f r e l a t e d s e r o c o n v e r s i o n c o n f i r m e d t h a t C. jejuni was t h e c a u s a t i v e o r g a n i s m in this case. (We thank M r Robert Warren, Serologist, Fairfield Hospital, Melbourne, for performing the serological studies; Wee Tee, Bacteriologist, Fairfield Hospital, Melbourne, for confirming the identity of the organism and for the sensitivity testing; and D r Peter Miach for granting permission to report this case.)
References
I. Tee W, Kaldor J, Dwyer B. Epidemiology of campylobacter diarrhoea. MedJ Aust 1986; 145: 499-5o3. 2. Schmidt U, Chmel H, Kaminski Z, Sen P. The clinical spectrum of Campylobacterfetus infections: report of five cases and review of the literature. Q J Med 198o; 196 431-442. 3. Vas SI. Infections of continuous ambulatory peritoneal dialysis catheters. In: Moellering RC, Ed. Infectious disease clinics of North America. Philadelphia: W. B. Saunders, 1989; Vol. 3 (2): 3Ol-328. 4. Pepersack, F, D'Haene M, Toussaint C, Schoutens E. Campylobacter jejuni peritonitis complicating continuous ambulatory peritoneal dialysis. J Clin Microbiol 1982; 16: 739-741. 5. Waters MJ, Andrew JH, Wright CA, Moran JE, Niall JF. Campylobacter jejuni peritonitis- treatment in a patient on CAPD. Dialysis 1985; 5 (2): 2-3. 6. Kristinsson KG, Spencer RC, Brown CB. Campylobacter peritonitis in continuous ambulatory peritoneal dialysis. J Infect 1986; 13: 199-2o4. 7. Fleming VA, McKinnon GT, Hooke DH, Wood CJ. Campylobacter peritonitis. Med J Aust 1989; 151: 239-24o. 8. Vernon SE, Dominguez C. Campylobacter and peritoneal dialysis. Ann Intern Med 1982; 96 : 534. 9. Wens R, Dratwa M, Potvliege C, Hansen W, Tielemans C, Collart F. Campylobacterfetus peritonitis followed by septicaemia in a patient on continuous ambulatory peritoneal dialysis. J Infect 1985 ; IO : 249-25 I. IO. Meigh JA, Wilkie ME, Ackrill P. Infection with Gampylobacter coli and Campylobacter fetus in a patient on continuous ambulatory peritoneal dialysis. J Infect 1988 ; 17: 189-191. II. Papasian CJ, Burdick C. Campylobacter peritonitis. Clin Microbiol Newsletter 1988; IO (13): lO2. 12. Targan SR, Chow AW, Guze LB. Spontaneous peritonitis of cirrhosis due to Campylobacter fetus. Gastroenterology 1976; 7I : 311- 313. 13. McNeil NI, Buttoo S, Ridgway GL. Spontaneous bacterial peritonitis due to Campylobacter jejuni. Postgrad Med J 1984; 6o: 487-488.
Peritonitis caused by Campylobacter jejuni
75
14. Domingo P, Mirelis B, Gimeno A, Cabezas R. Spontaneous peritonitis caused by Campylobacter jejuni in a cirrhotic patient. Med Clin (Barc) I985; 84: 416. 15. Ho H, Zuckerman MJ, Polly SM. Spontaneous bacterial peritonitis due to Campylobacter coli. Gastroenterology I987; 92 : 2024-2025. I6. Kucers A, Bennett N M c K . Tobramycin. In: The use of antibodies. A comprehensive review with clinical emphasis. 4th ed. London : William Heinemann Medical Books, r987 : 675-695. I7. Shanker S, Sorrell TC. Susceptibility of Campylobacterjejuni to twenty-three antimicrobial agents. Pathology I983 ; I5 : 61-63.
2 I , 71-75
CASE REPORT P e r i t o n i t i s c a u s e d b y Campylobacter jejuni a n d s e r o l o g i c a l l y c o n f i r m e d in a p a t i e n t b e i n g t r e a t e d w i t h c o n t i n u o u s ambulatory peritoneal dialysis David J. G o o d m a n and Keith A. Wise* Austin Hospital, Heidelberg, Victoria 3084, Australia Accepted for publication 26 January I99O
Summary A case of Campylobacter jejuni peritonitis in a patient being treated with continuous ambulatory peritoneal dialysis is described. The significance of the organism isolated from our patient was initially doubtful because of a rapid defervescence of symptoms with minimal specific antibiotic therapy, lack of a preceding diarrhoeal illness and the time taken to isolate and identify the organism. Serial serum IgM, IgA and IgG antibody estimations clearly showed an acute seroconversion confirming that the strain of C. jejuni isolated was the causative organism in this case.
Introduction Gastro-enteritis
is the
most
common
manifestation
of infection
with
Campylobacterjejuni. x Campylobacter species are not often isolated from extraintestinal sites, the b l o o d stream being the most c o m m o n l y reported. ~ C. jejuni is a rare cause of peritonitis associated with continuous ambulatory peritoneal dialysis ( C A P D ) . 3 W e report a case in which pathogenicity was confirmed b y serological testing.
Case report T h e patient was a 63-year-old w o m a n with endstage renal failure due to chronic pyelonephritis and renal calculi. T r e a t m e n t with C A P D had b e g u n in July I987. In F e b r u a r y and April I988 she developed recurrent infections with Staphylococcus aureus at the exit-site of a T e n c k h o f f catheter. T h e s e were treated successfully with oral flucloxacillin. O n 7 July I988, the patient presented herself with a I2 h history of anorexia, nausea, vomiting and generalised abdominal pain associated with two cloudy peritoneal dialysis packs. T h e r e was no history of diarrhoea. O n examination, she appeared unwell, with a t e m p e r a t u r e of 38"3 °C, diffuse abdominal tenderness with peritonism, and crusting around the T e n c k h o f f catheter exit-site. Dialysate fluid was sent for microbiological investigations while she was given single intravenous doses of flucloxacillin and t o b r a m y c i n followed b y intraperitoneal flucloxacillin. S y m p t o m s and signs rapidly subsided. * Address correspondence to: Dr Keith A. Wise, Department of Microbiology, Wollongong Hospital; Wollongong, New South Wales 2500, Australia.
oi63-4453/9o/o4oo71 +05 $02.00/0
© I99O The British Society for the Study of Infection
72
D. J. G O O D M A N
A N D K. A. W I S E
T a b l e I Serological responses in a patient with C a m p y l o b a c t e r jejuni
peritonitis while being treated with C A P D Antibody titres Date
IgM
3o Jun 87 ~o May 88 I4 Jun 88 7 Jul 88 I8 Jul 88 8 Nov 88 30 May 89
4o 4° i6o 8o 8o 320 80 80 320 Episode of CAPD peritonitis 640 80 320 64o* I28O I28O 640* I28o I28o
R e f e r e n c e range
< 80
IgA
< 80
IgG
< 320
* IgM result not due to rheumatoid factor.
Staphylococcus aureus was again isolated from a swab of the catheter exitsite. After 3 days, campylobacter-like organisms were isolated from direct anaerobic cultures of the dialysate fluid. Aerobic and anaerobic blood culture bottles that had been inoculated with dialysate also grew the same organism. T h r e e days later the organism was formally identified as C, jejuni. At this stage the patient remained asymptomatic. Since the clinical significance of the organism isolated was uncertain, it was decided to complete a course of anti-staphylococcal therapy. Intraperitoneal cephalothin was given for 5 days followed b y oral cephalexin for 2 weeks. Faecal cultures were not p e r f o r m e d until i i days after the patient presented herself. Campylobacter species were not isolated. A b d o m i n a l ultrasound and C T scans, barium enema and colonoscopy were unremarkable. Laboratory results M i c r o s c o p y of the dialysate fluid revealed I72O × IO 6 p o l y m o r p h o n u c l e a r leucocytes/1 and IO x lO 6 red cells/l. A G r a m - s t a i n o f centrifuged sediment was negative. T h e dialysate was cultured on sheep blood and M c C o n k e y agars in an atmosphere of io % carbon dioxide in air at 37 °C, as well as on horse b l o o d agar anaerobically at 37 °C. Aerobic and anaerobic ' B a c t e c ' blood culture bottles were each inoculated with 5 ml dialysate. After 3 days of incubation, a very faint growth appeared only on the anaerobic plate. Gram-staining of the colonies revealed curved G r a m - n e g a t i v e rods consistent with the appearance of Campylobacter species. In b o t h blood culture bottles, inoculated with the dialysate, grew a similar organism. Biochemical tests and sodium dodecyl sulphate polyacrylamide gel electrophoresis confirmed the organism's identity as C. jejuni. Agar dilution antibiotic sensitivity testing showed the organism to be sensitive to erythromycin, tetracycline, gentamicin, norfloxacin, ciprofloxacin, chloramphenicol and ticarcillin.
Peritonitis caused by Campylobacter jejuni
73
Serial serum samples were tested for the presence of specific IgM, IgA and IgG antibodies to C. jejuni by means of a diffusion-in-gel enzyme-linked immunosorbent assay. A four-fold change in titre was considered significant. T h e results are shown in the accompanying Table I. Samples of serum stored from I year, 2 months, and I month earlier, all showed negative responses to all three classes of antibody. Serum collected IO days after the episode showed a significant rise in the titre of IgA, but not of IgG or IgM antibody. Four months after the episode, all three classes of antibody had risen in titre. A further sample of serum collected IO months after the episode showed that titres of all three remained elevated. Discussion
Campylobacter spp. are rarely implicated as a cause of CAPD peritonitis. 3 To our knowledge, only I I other cases have been described. Six were due to C. jejuni, 4-7 four to C. fetusf' s-x0 and one to C. coll. n A further five cases of spontaneous bacterial peritonitis due to Campylobacter spp. have also been reportedfl' 12-15 Only one of the reports involving CAPD included results of serological testing. 4 T h e mode of spread of C. jejuni to the dialysate fluid is uncertain. Our patient did not have a history of diarrhoea, and faecal cultures were not obtained until I I days after the onset of peritonitis. Initial treatment of CAPD peritonitis is usually directed at staphylococci and aerobic Gram-negative organisms unless the Gram-stain is positive. Initially, we treated our patient with I g flucloxacillin and Ioo mg tobramycin intravenously, followed by intraperitoneal instillation of 25o mg/1 flucloxacillin. Subsequently, 25omg/1 cephalothin was given intraperitoneally followed by oral cephalexin. Rapid symptomatic improvement and clearing of the dialysate fluid followed. Tobramycin has a half-life of up to 36 h in dialysis patients, Is hence the single dose of tobramycin would be active for a prolonged period. Similarly, the high concentrations of flucloxacillin and cephalothin achieved intraperitoneally may have inhibited the organism, even though C. jejuni is usually regarded as resistant in vitro, x' 17 Our isolate was sensitive to gentamicin in vitro, hence it may be assumed that it would also be sensitive to tobramycin. We believe that the prolonged activity of the initial dose of tobramycin, together with frequent changes of the CAPD pack, eradicated the organism from the peritoneal cavity of our patient. Pepersack and colleagues described the first case of C. jejuni CAPD peritonitis in I982. ~ Using a tube agglutination method, they demonstrated seroconversion to the strains of C. jejuni isolated from the patient's faeces and peritoneal fluid. Responses to individual classes of antibody were not reported. We found early seroconversion in respect of IgA followed by that in respect of IgM and IgG. These findings are consistent with an acute infection caused by C. jejuni although it is unusual for IgM to persist at such a high titre for Io months (B. Dwyer, personal communication). Also of interest, was the seroconversion in respect of IgA before that in respect of IgM, suggesting a source of the infection in the gut. Hence, we clearly demonstrated
74
D. J. GOODMAN AND K. A. WISE
s e r o c o n v e r s i o n r e l a t i n g to a c u t e a n d c o n v a l e s c e n t p h a s e s e r u m samples in respect of IgM, IgA and IgG. Gampylobacter jejuni is a r a r e cause o f C A P D p e r i t o n i t i s a l t h o u g h t h e dialysate fluid o f a few p a t i e n t s r e m a i n s c u l t u r e - n e g a t i v e in this s y n d r o m e . C u l t u r a l m e t h o d s t h a t e n h a n c e the g r o w t h o f fastidious o r g a n i s m s s h o u l d b e p e r f o r m e d so t h a t a c o r r e c t m i c r o b i o l o g i c a l diagnosis can allow t h e m o s t a p p r o p r i a t e antibiotics to b e p r e s c r i b e d . W e p e r f o r m d i r e c t c u l t u r e o n dialysate a n d also i n o c u l a t e it into ' B a c t e c ' b l o o d c u l t u r e m e d i u m in o r d e r to e n h a n c e t h e d e t e c t i o n o f fastidious o r g a n i s m s . I f g r o w t h is o b s e r v e d in t h e ' B a c t e c ' m e d i u m , a G r a m - s t a i n o f it will suggest t h e t y p e s o f m e d i a suitable f o r isolating t h e s e o r g a n i s m s . W e believe t h a t o u r p a t i e n t p r o b a b l y h a d an a c u t e a s y m p t o m a t i c g u t i n f e c t i o n w i t h C. jejuni f o l l o w e d b y C A P D p e r i t o n i t i s d u e to t h a t o r g a n i s m . D e m o n s t r a t i o n o f r e l a t e d s e r o c o n v e r s i o n c o n f i r m e d t h a t C. jejuni was t h e c a u s a t i v e o r g a n i s m in this case. (We thank M r Robert Warren, Serologist, Fairfield Hospital, Melbourne, for performing the serological studies; Wee Tee, Bacteriologist, Fairfield Hospital, Melbourne, for confirming the identity of the organism and for the sensitivity testing; and D r Peter Miach for granting permission to report this case.)
References
I. Tee W, Kaldor J, Dwyer B. Epidemiology of campylobacter diarrhoea. MedJ Aust 1986; 145: 499-5o3. 2. Schmidt U, Chmel H, Kaminski Z, Sen P. The clinical spectrum of Campylobacterfetus infections: report of five cases and review of the literature. Q J Med 198o; 196 431-442. 3. Vas SI. Infections of continuous ambulatory peritoneal dialysis catheters. In: Moellering RC, Ed. Infectious disease clinics of North America. Philadelphia: W. B. Saunders, 1989; Vol. 3 (2): 3Ol-328. 4. Pepersack, F, D'Haene M, Toussaint C, Schoutens E. Campylobacter jejuni peritonitis complicating continuous ambulatory peritoneal dialysis. J Clin Microbiol 1982; 16: 739-741. 5. Waters MJ, Andrew JH, Wright CA, Moran JE, Niall JF. Campylobacter jejuni peritonitis- treatment in a patient on CAPD. Dialysis 1985; 5 (2): 2-3. 6. Kristinsson KG, Spencer RC, Brown CB. Campylobacter peritonitis in continuous ambulatory peritoneal dialysis. J Infect 1986; 13: 199-2o4. 7. Fleming VA, McKinnon GT, Hooke DH, Wood CJ. Campylobacter peritonitis. Med J Aust 1989; 151: 239-24o. 8. Vernon SE, Dominguez C. Campylobacter and peritoneal dialysis. Ann Intern Med 1982; 96 : 534. 9. Wens R, Dratwa M, Potvliege C, Hansen W, Tielemans C, Collart F. Campylobacterfetus peritonitis followed by septicaemia in a patient on continuous ambulatory peritoneal dialysis. J Infect 1985 ; IO : 249-25 I. IO. Meigh JA, Wilkie ME, Ackrill P. Infection with Gampylobacter coli and Campylobacter fetus in a patient on continuous ambulatory peritoneal dialysis. J Infect 1988 ; 17: 189-191. II. Papasian CJ, Burdick C. Campylobacter peritonitis. Clin Microbiol Newsletter 1988; IO (13): lO2. 12. Targan SR, Chow AW, Guze LB. Spontaneous peritonitis of cirrhosis due to Campylobacter fetus. Gastroenterology 1976; 7I : 311- 313. 13. McNeil NI, Buttoo S, Ridgway GL. Spontaneous bacterial peritonitis due to Campylobacter jejuni. Postgrad Med J 1984; 6o: 487-488.
Peritonitis caused by Campylobacter jejuni
75
14. Domingo P, Mirelis B, Gimeno A, Cabezas R. Spontaneous peritonitis caused by Campylobacter jejuni in a cirrhotic patient. Med Clin (Barc) I985; 84: 416. 15. Ho H, Zuckerman MJ, Polly SM. Spontaneous bacterial peritonitis due to Campylobacter coli. Gastroenterology I987; 92 : 2024-2025. I6. Kucers A, Bennett N M c K . Tobramycin. In: The use of antibodies. A comprehensive review with clinical emphasis. 4th ed. London : William Heinemann Medical Books, r987 : 675-695. I7. Shanker S, Sorrell TC. Susceptibility of Campylobacterjejuni to twenty-three antimicrobial agents. Pathology I983 ; I5 : 61-63.