1068
Correspondence
CID 1992; 15 (December)
5. Glynn AM, Slaughter RE, Brass e. D'Ambrosio R. Jusko WJ. Effects of ketoconazole on methylprednisolone pharmacokinetics and cortisol secretions. Clin Pharmacol Ther 1986;39:654-9. 6. Delpha IL, Zhu QM, Mo Z, Blaschke TF. Fluconazole is a potent inhibitor of antipyrine metabolism in vivo in mice. Drug Metab Dispos 1989; 17:49-53.
Seven Cases of BacteremiaDueto Ochrobactrum anthropi
tively. Patient I had a positive blood culture at the start of chemotherapy and 7 days later, during which time she had only trivial symptoms (occasional fever). Patient 2 was admitted with fever and pain at the site of a Hickman catheter that had been in place for 2 months. The five remaining infections occurred in patients in the intensive care unit with complex medical and surgical problems requiring numerous vascular access devices. We have found no epidemiological evidence of a common source or cross-infection. Although most patients received gentamicin empirically, this therapy was discontinued when the catheter was removed. One patient died as a result of factors unrelated to 0. anthropi infection. Blood cultures from patients 3 and 6 yielded Comamonas acidovorans in addition to 0. anthropi. All our cases of 0. anthropi sepsis have occurred in the last 3 years, and recent reidentification of oxidase-positive blood culture isolates (including Achromobacter species) of uncertain species failed to detect any previously unrecognized cases occurring since 1969. All our isolates were susceptible to gentamicin, tobramycin, amikacin, ciprofloxacin, imipenem, and trimethoprim-sulfamethoxazole and were resistant to amoxicillin,
SIR-Dr. Cieslak and colleagues [I] describe a single case of central venous catheter (CVC)-related sepsis caused by Ochrobactrum anthropi and make recommendations concerning antimicrobial therapy. We have encountered seven cases of clinically significant bacteremia with 0. anthropi that may help define the pattern of disease caused by this organism. Table I shows the clinical features of the patients. Five patients were in the intensive care unit; the remaining two were oncology patients. All had CVC-related sepsis. The two oncology patients (I and 2) were not profoundly immunosuppressed and had total white blood cell counts of9,OOO/mm 3 and 11,700/mm3, respec-
Correspondence: Dr. W. R. Gransden, Department of Microbiology, St. Thomas's Hospital, London SEI 7EH, United Kingdom. Clinical Infectious Diseases 1992;15:1068-9 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1506-0040$02.00
Table 1. Patient number
Clinical and microbiological features of patients with Ochrobactrum anthropi bacteremia. St Thomas's Hospital, London, 1969-1992.
Year
Age (y)/ sex
1989
13jF
2
1990
33/F
3 4
1990 1991
70/F 43/M
5
1991
28jF
6 7
1992 1992
71/F 65/M
Underlying disease/factor
Previous antimicrobial therapy
Rhabdomyosarcoma, chemotherapy Thymoma. chemotherapy
None
Fecal peritonitis Pancreatitis, acute renal and respiratory failure Acute renal failure after cesarean section Postcardiac surgery Postthoracic surgery
Cefuroxime + metronidazole Ceftazidime
NOTE. eve = central venous catheter. * Positive culture results obtained. t Death unrelated to infection.
None
Gentamicin, amoxicillin/ clavulanate Amoxicillin/clavulanate Ceftazidime, imipenem, and gentamicin
Focus of infection
Catheter removed
Outcome
None
Yes
Survived
Treatment
Hickman catheter* Hickman catheter* CVC CVC*
None
Yes
Survived
Gentamicin Gentamicin
Yes Yes
Survived Survived
eve-
Gentamicin
Yes
Survived
eve evc
Gentamicin Ciprofloxacin, imipenem
Yes No
Died t Died t
Downloaded from http://cid.oxfordjournals.org/ at University of Manitoba on September 8, 2015
tients with AIDS: therapeutic implications. In: Program and abstracts of the 7th International Congress on AIDS (Florence). 1991. 3. Foulds, G, Brennan DR, Wajszczuk C, et al. Fluconazole penetration into cerebrospinal fluid in humans. J Clin Pharmaco11988;28:363-6. 4. Blum RA, Wilton JH, Hilligoss DM, et al. Effect of fluconazole on the disposition of phenytoin. Clin Pharmacol Ther 1991;49:420-5.
CID 1992: 15 (December)
Correspondence
amoxicillin/clavulanate, azlocillin, ticarcillin, cefuroxime, cefotaxime, cefoxitin, ceftazidime, aztreonam, and trimethoprim, as determined by MICs. We contend that the epidemiological niche for O. anthropi is in CVC-related infections that may occur in any patient requiring such intervention and not exclusively in those who are immunocompromised. Isolation ofthe organism should raise suspicion of CVC-related infection. In our experience the infection can be successfully managed by removal of the infected catheter without resorting to antimicrobial therapy, a common practice with many CVC-associated infections.
SIR-We read with great interest the recent correspondence of Triesenberg et al. [I]. We describe an additional patient who developed group B streptococcal infection ofa prosthetic device (a pacemaker wire) following sigmoidoscopy. A 51-year-old nurse presented with chills, fever, and headache that developed abruptly the morning that she was admitted to the hospitaL She had undergone flexible sigmoidoscopic examination 2 days before the onset of chills and fever for rectal bleeding, which had been present for 5 days. No endoscopic biopsy had been performed and no prophylactic antibiotics had been administered. The patient had a history of allergy to penicillin and chronic liver disease caused by hepatitis C virus, and she had had a permanent pacemaker placed 20 days before admission. The patient was febrile on admission and had rigors. The pacemaker generator site on the chest wall appeared normal, and roentgenography of the chest revealed no abnormalities. She had a (previously described) grade 2/6 holosystolic murmur heard best at the cardiac apex. No diastolic murmurs were auscultated. No valvulopathies or vegetations were demonstrated on two-dimensional echocardiography. No peripheral skin lesions were found. Both sets of pretreatment blood cultures yielded group B streptococci. Despite receiving combined therapy with vancomycin and rifampin, the patient continued to manifest high fever, and the pacemaker was removed. The generator site showed no evidence of infection. Unfortunately, the pacemaker wire was not sent for microbiological examination. The patient's fever subsided rapidly following removal of the pacemaker generator and wire. After 14 days ofcombined antibiotic therapy, another pacemaker unit was implanted at a differ-
Correspondence: Dr. Larry M. Baddour, Department of Medicine. Suite 222 POB 1. University of Tennessee Medical Center at Knoxville. 1924 Alcoa Highway U-114. Knoxville. Tennessee 37920-6999. Clinical Infectious Diseases 1992;15:1069 © 1992by The University of Chicago. All rights reserved.
1058-4838/92/1506-0041$02.00
W. R. Gransden and Susannah J. Eykyn Division of Microbiology. United Medical and Dental Schools of Guy's and St Thomas's Hospitals. St Thomas's Campus. London. United Kingdom
References I. Cieslak TJ. Robb ML. Drabick CJ. Fischer GW.Catheter-related sepsis caused by Ochrobactrum anthropi: report of a case and review of related nonfermentative bacteria. Clin Infect Dis 1992; 14:902-7.
ent chest-wall site. She was discharged home and was followed as an outpatient. We believe that this patient's group B streptococcal infection was caused by the colonoscopic procedure, which resulted in transient bacteremia and secondary colonization of a recently inserted pacemaker wire. h is interesting that our patient was a nurse who worked in neonatal and pediatric intensive care units and occasionally cared for newborns with group B streptococcal disease. Thus it is possible that the source of our patient's group B streptococcal colonization was nosocomial [2]. Because of her underlying liver disease, she may have been less able to resolve the transient bacteremia caused by the endoscopic procedure and subsequently developed the pacemaker wire infection. Regardless, present recommendations of the American Heart Association do not support the routine use of prophylactic antibiotics for gastrointestinal endoscopic procedures, especially if the patient has a cardiac pacemaker [3]. A recent survey of cardiothoracic surgeons and cardiologists indicates that the majority (69%) follow these recommendations [4]. More intensive investigation of the use of antibiotic prophylaxis in patients undergoing lower gastrointestinal endoscopic examination will be required if additional case reports mirror our experience.
Larry M. Baddour and James W. Cox, Jr. Graduate School of Medicine. Department of Medicine. Divisions of Infectious Diseases and Cardiology. University of Tennessee Medical Center at Knoxville. Knoxville. Tennessee References I. Triesenberg SN. Clark NM. Kauffman CA. Group B streptococcal prosthetic joint infection following sigmoidoscopy. Clin Infect Dis 1992; 15:374-5. 2. Paredes A. Wong P. Mason EO Jr. et al. Nosocomial transmission of group B streptococci in a newborn nursery. Pediatrics 1976;59:67982. 3. Dajani AS. Bisno AI, Chung KJ. et al. Prevention of bacterial endocarditis. JAMA 1990;264:2919-22. 4. Vlay Sc. Prevention of bacterial endocarditis in patients with permanent pacemakers and automatic internal cardioverter defibrillators. Am HeartJ 1990;120:1490-2.
Downloaded from http://cid.oxfordjournals.org/ at University of Manitoba on September 8, 2015
Group B Streptococcal Infection of a Pacemaker Wire Following Sigmoidoscopy
1069
Correspondence
CID 1992; 15 (December)
5. Glynn AM, Slaughter RE, Brass e. D'Ambrosio R. Jusko WJ. Effects of ketoconazole on methylprednisolone pharmacokinetics and cortisol secretions. Clin Pharmacol Ther 1986;39:654-9. 6. Delpha IL, Zhu QM, Mo Z, Blaschke TF. Fluconazole is a potent inhibitor of antipyrine metabolism in vivo in mice. Drug Metab Dispos 1989; 17:49-53.
Seven Cases of BacteremiaDueto Ochrobactrum anthropi
tively. Patient I had a positive blood culture at the start of chemotherapy and 7 days later, during which time she had only trivial symptoms (occasional fever). Patient 2 was admitted with fever and pain at the site of a Hickman catheter that had been in place for 2 months. The five remaining infections occurred in patients in the intensive care unit with complex medical and surgical problems requiring numerous vascular access devices. We have found no epidemiological evidence of a common source or cross-infection. Although most patients received gentamicin empirically, this therapy was discontinued when the catheter was removed. One patient died as a result of factors unrelated to 0. anthropi infection. Blood cultures from patients 3 and 6 yielded Comamonas acidovorans in addition to 0. anthropi. All our cases of 0. anthropi sepsis have occurred in the last 3 years, and recent reidentification of oxidase-positive blood culture isolates (including Achromobacter species) of uncertain species failed to detect any previously unrecognized cases occurring since 1969. All our isolates were susceptible to gentamicin, tobramycin, amikacin, ciprofloxacin, imipenem, and trimethoprim-sulfamethoxazole and were resistant to amoxicillin,
SIR-Dr. Cieslak and colleagues [I] describe a single case of central venous catheter (CVC)-related sepsis caused by Ochrobactrum anthropi and make recommendations concerning antimicrobial therapy. We have encountered seven cases of clinically significant bacteremia with 0. anthropi that may help define the pattern of disease caused by this organism. Table I shows the clinical features of the patients. Five patients were in the intensive care unit; the remaining two were oncology patients. All had CVC-related sepsis. The two oncology patients (I and 2) were not profoundly immunosuppressed and had total white blood cell counts of9,OOO/mm 3 and 11,700/mm3, respec-
Correspondence: Dr. W. R. Gransden, Department of Microbiology, St. Thomas's Hospital, London SEI 7EH, United Kingdom. Clinical Infectious Diseases 1992;15:1068-9 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1506-0040$02.00
Table 1. Patient number
Clinical and microbiological features of patients with Ochrobactrum anthropi bacteremia. St Thomas's Hospital, London, 1969-1992.
Year
Age (y)/ sex
1989
13jF
2
1990
33/F
3 4
1990 1991
70/F 43/M
5
1991
28jF
6 7
1992 1992
71/F 65/M
Underlying disease/factor
Previous antimicrobial therapy
Rhabdomyosarcoma, chemotherapy Thymoma. chemotherapy
None
Fecal peritonitis Pancreatitis, acute renal and respiratory failure Acute renal failure after cesarean section Postcardiac surgery Postthoracic surgery
Cefuroxime + metronidazole Ceftazidime
NOTE. eve = central venous catheter. * Positive culture results obtained. t Death unrelated to infection.
None
Gentamicin, amoxicillin/ clavulanate Amoxicillin/clavulanate Ceftazidime, imipenem, and gentamicin
Focus of infection
Catheter removed
Outcome
None
Yes
Survived
Treatment
Hickman catheter* Hickman catheter* CVC CVC*
None
Yes
Survived
Gentamicin Gentamicin
Yes Yes
Survived Survived
eve-
Gentamicin
Yes
Survived
eve evc
Gentamicin Ciprofloxacin, imipenem
Yes No
Died t Died t
Downloaded from http://cid.oxfordjournals.org/ at University of Manitoba on September 8, 2015
tients with AIDS: therapeutic implications. In: Program and abstracts of the 7th International Congress on AIDS (Florence). 1991. 3. Foulds, G, Brennan DR, Wajszczuk C, et al. Fluconazole penetration into cerebrospinal fluid in humans. J Clin Pharmaco11988;28:363-6. 4. Blum RA, Wilton JH, Hilligoss DM, et al. Effect of fluconazole on the disposition of phenytoin. Clin Pharmacol Ther 1991;49:420-5.
CID 1992: 15 (December)
Correspondence
amoxicillin/clavulanate, azlocillin, ticarcillin, cefuroxime, cefotaxime, cefoxitin, ceftazidime, aztreonam, and trimethoprim, as determined by MICs. We contend that the epidemiological niche for O. anthropi is in CVC-related infections that may occur in any patient requiring such intervention and not exclusively in those who are immunocompromised. Isolation ofthe organism should raise suspicion of CVC-related infection. In our experience the infection can be successfully managed by removal of the infected catheter without resorting to antimicrobial therapy, a common practice with many CVC-associated infections.
SIR-We read with great interest the recent correspondence of Triesenberg et al. [I]. We describe an additional patient who developed group B streptococcal infection ofa prosthetic device (a pacemaker wire) following sigmoidoscopy. A 51-year-old nurse presented with chills, fever, and headache that developed abruptly the morning that she was admitted to the hospitaL She had undergone flexible sigmoidoscopic examination 2 days before the onset of chills and fever for rectal bleeding, which had been present for 5 days. No endoscopic biopsy had been performed and no prophylactic antibiotics had been administered. The patient had a history of allergy to penicillin and chronic liver disease caused by hepatitis C virus, and she had had a permanent pacemaker placed 20 days before admission. The patient was febrile on admission and had rigors. The pacemaker generator site on the chest wall appeared normal, and roentgenography of the chest revealed no abnormalities. She had a (previously described) grade 2/6 holosystolic murmur heard best at the cardiac apex. No diastolic murmurs were auscultated. No valvulopathies or vegetations were demonstrated on two-dimensional echocardiography. No peripheral skin lesions were found. Both sets of pretreatment blood cultures yielded group B streptococci. Despite receiving combined therapy with vancomycin and rifampin, the patient continued to manifest high fever, and the pacemaker was removed. The generator site showed no evidence of infection. Unfortunately, the pacemaker wire was not sent for microbiological examination. The patient's fever subsided rapidly following removal of the pacemaker generator and wire. After 14 days ofcombined antibiotic therapy, another pacemaker unit was implanted at a differ-
Correspondence: Dr. Larry M. Baddour, Department of Medicine. Suite 222 POB 1. University of Tennessee Medical Center at Knoxville. 1924 Alcoa Highway U-114. Knoxville. Tennessee 37920-6999. Clinical Infectious Diseases 1992;15:1069 © 1992by The University of Chicago. All rights reserved.
1058-4838/92/1506-0041$02.00
W. R. Gransden and Susannah J. Eykyn Division of Microbiology. United Medical and Dental Schools of Guy's and St Thomas's Hospitals. St Thomas's Campus. London. United Kingdom
References I. Cieslak TJ. Robb ML. Drabick CJ. Fischer GW.Catheter-related sepsis caused by Ochrobactrum anthropi: report of a case and review of related nonfermentative bacteria. Clin Infect Dis 1992; 14:902-7.
ent chest-wall site. She was discharged home and was followed as an outpatient. We believe that this patient's group B streptococcal infection was caused by the colonoscopic procedure, which resulted in transient bacteremia and secondary colonization of a recently inserted pacemaker wire. h is interesting that our patient was a nurse who worked in neonatal and pediatric intensive care units and occasionally cared for newborns with group B streptococcal disease. Thus it is possible that the source of our patient's group B streptococcal colonization was nosocomial [2]. Because of her underlying liver disease, she may have been less able to resolve the transient bacteremia caused by the endoscopic procedure and subsequently developed the pacemaker wire infection. Regardless, present recommendations of the American Heart Association do not support the routine use of prophylactic antibiotics for gastrointestinal endoscopic procedures, especially if the patient has a cardiac pacemaker [3]. A recent survey of cardiothoracic surgeons and cardiologists indicates that the majority (69%) follow these recommendations [4]. More intensive investigation of the use of antibiotic prophylaxis in patients undergoing lower gastrointestinal endoscopic examination will be required if additional case reports mirror our experience.
Larry M. Baddour and James W. Cox, Jr. Graduate School of Medicine. Department of Medicine. Divisions of Infectious Diseases and Cardiology. University of Tennessee Medical Center at Knoxville. Knoxville. Tennessee References I. Triesenberg SN. Clark NM. Kauffman CA. Group B streptococcal prosthetic joint infection following sigmoidoscopy. Clin Infect Dis 1992; 15:374-5. 2. Paredes A. Wong P. Mason EO Jr. et al. Nosocomial transmission of group B streptococci in a newborn nursery. Pediatrics 1976;59:67982. 3. Dajani AS. Bisno AI, Chung KJ. et al. Prevention of bacterial endocarditis. JAMA 1990;264:2919-22. 4. Vlay Sc. Prevention of bacterial endocarditis in patients with permanent pacemakers and automatic internal cardioverter defibrillators. Am HeartJ 1990;120:1490-2.
Downloaded from http://cid.oxfordjournals.org/ at University of Manitoba on September 8, 2015
Group B Streptococcal Infection of a Pacemaker Wire Following Sigmoidoscopy
1069
