CID 1992; 15 (October)
Aortic Valve Endocarditis Due to Escherichia coli SIR-Endocarditis caused by Escherichia coli is rare despite the frequency of bacteremia due to this organism. Only 19 cases were reported during 1945-1990 [I]. We report a further case, in which resistance ofthe E. coli isolate to the bactericidal action of serum may have contributed to pathogenesis. A 52-year-old woman presented in March 1992 with right loin pain, rigors, and fever. Similar episodes had occurred each month for the previous 4 months. Cultures of blood and a mid-
Correspondence: Dr. Selwyn D. R. Lang, Department of Microbiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand.
the groups as the "A. calcoaceticus-A. baumannii" complex [10]. Most acinetobacter isolates ofthese groups are glucose acidifying; therefore, these new groupings would largely correspond to the previous "A. calcoaceticus subspecies anUratus." This unification of groups may be appreciated for its simplification, although another nomenclatural change might add to the confusion of the taxonomy of Acinetobacter.
Lenie Dijkshoorn and Jos van der Toorn Department of Clinical Microbiology. Rotterdam University Hospital, Rotterdam; and Kluyver Laboratory of Biotechnology, University of Technology, Delft, the Netherlands References I. Gradon JD, Chapnick EK, Lutwick, LI. Infective endocarditis of a native valve due to Acinetobacter: case report and review. C1in Infect Dis 1992; 14: 1145-8. 2. J uni E. Genus III Acinetobacter Brisou and Prevot 1954, 727a' . In: Krieg NR, ed. Bergey's manual of systematic bacteriology. Vol. I. Baltimore: Williams and Wilkins, 1984:303-7. 3. Skerman VBD, McGowan V, Sneath PHA. Approved lists of bacterial names. Int J Syst Bacteriol 1980;30:241. 4. Bouvet PJM, Grimont PAD. Taxonomy of the genus Acinetobacter with the recognition of Acinetobacter baumannii sp. nov., Acinetobacter haemo(vticus sp. nov., Acinetobacter johnsonii sp. nov., and Acinetobacter junii sp. nov., and emended descriptions of Acinetobacter calcoaceticus and Acinetobacter Iwoffii. Int J Syst Bacteriol 1986;
36:228-40. 5. Nishimura Y, Ino T, Iizuka H. Acinetobacter radioresistens sp. nov. isolated from cotton and soil. Int J Syst Bacteriol 1988;38:209-11. 6. Tjernberg I, Ursing J. Clinical strains of Acinetobacter classified by DNA-DNA hybridization. APMIS 1989;97:595-605. 7. Moore WEe, Moore LYH. Index of the bacterial and yeast nomenclatural changes. Washington, DC: American Society for Microbiology,
1989:2-3. 8. Bouvet PJM, Jeanjean S. Delineation of new proteolytic genomic species in the genus Acinetobacter. Res Microbiol 1989; 140:291-9. 9. Dijkshoorn L, Tjernberg I, Pot B, Michel MF, Ursing J, Kersters K. Numerical analysis of cell envelope protein profiles of Acinetobacter classified by DNA-DNA hybridization. Syst Appl Microbiol 1990;
13:338-44. 10. Gerner-Smidt P, Tjernberg I, Ursing J. Reliability of phenotypic tests for identification of Acinetobacter species. J Clin Microbiol 1991;
29:277-82.
stream urine specimen processed at a private laboratory shortly before her admission yielded E. coli susceptible to amoxycillinf clavulanate, trimethoprim, cefaclor, gentamicin, and ceftriaxone but resistant to amoxycillin. Urine contained 100 X 106 white blood cells (WBCs) per liter but no red cells. Her general practitioner prescribed cefaclor for 4 days and then amoxycillinf clavulanate. On admission she was hypotensive and febrile. There was no heart murmur or stigmata of bacterial endocarditis. At that time, there was no growth from urine; however, further blood cultures yielded E. coli. The peripheral WBC count was 20 X 109fL, the serum glucose level was 11.9 mmolfL, and the serum creatinine level was 0.1 mmolfL. An ultrasonogram showed a 5-mm right renal calculus but no dilatation of the collecting system and no perirenal or intrarenal collections. Fever persisted despite therapy with gentamicin followed by that with ceftriaxone (I g daily), and the peripheral WBC count
Downloaded from http://cid.oxfordjournals.org/ at Florida Atlantic University on July 14, 2015
DNA group 2 (A. baumannii) has been found to be highly prevalent in clinical isolates in France [4], while DNA group 3 was predominant among clinical isolates in Sweden [6]. Strains from hospital outbreaks were found to belong to DNA group 2 (A. baumannii) [9]. Overall, the knowledge of the ecology and clinical relevance of the different groups is still poor. For identification of Acinetobacter isolates belonging to DNA groups I through 12, a scheme of phenotypic tests has been described [4]. However, a recent study has shown that phenotypic identification can be problematic [9], and this was especially the case for DNA group I (A. calcoaceticus), group 2 (A. baumannii), group 3, and group 13 [6], which are genetically and phenotypically closely related [4, 6]. Thus, today, at least 17 different groups (seven of which have species names) can be distinguished within the genus by DNADNA hybridization. Presumptive identification of a number of groups may be performed by phenotypic tests or by inspection of protein electrophoretic profiles [9]. However, unambiguous identification requires DNA hybridization, which is laborious and not a current method in routine microbiology. It may be questioned whether it is necessary to identify Acinetobacter isolates according to the recent classification. It is our opinion that the clinical laboratory's identification of the organisms to the genus level may suffice as long as Acinetobacter isolations are incidental. Furthermore, a few additional tests such as those for the aerobic acidification of glucose and growth at 44°C may be used for presumptive identification of DNA group 2 (A. baumannii) [4]. This approach is not satisfactory for tracing epidemic strains during outbreaks; in these situations, isolates have to be typed by combinations of typing methods, e.g., biotyping and comparative protein electrophoretic typing [10]. For a better knowledge of the ecology and pathology of the different DNA groups, however, the precise DNA group of isolates must be determined, and this would require rapid methods for unambiguous identification. We hope that these methodsperhaps new molecular techniques-will soon be available for this purpose. Finally, given the close relationship of DNA groups I, 2, 3, and 13 [6] at different levels of DNA expression [4, 6, 9], researchers have considered lumping these groups together into one species, "A. calcoaceticus" (in sensu lata), thus giving the DNA groups the rank of subspecies [6], or referring to
Clinical Infectious Diseases 1992;15:749-50 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0043$02.00
749
Correspondence
750
Correspondence
Metronidazole and Pancreatitis SIR-In their article, Corey et al. [I] report the case ofa 63-yearold woman with Crohn's disease who develops acute pancreatitis coincident with the administration of metronidazole that disappears upon discontinuance of the drug's administration. The authors base their diagnosis on the clinical picture and the rise in enzyme concentrations (results of pancreatic ultrasonography and computed tomography were normal). The absence of other risk factors suggests a pathogenic relationship between metronidazole and the pancreatitis. For implicating a pharmaceutical agent as the cause of a disease, demonstration of the following is necessary: the disease occurs during the administration of the drug; the disease disappears once use of the drug is discontinued; the disease can be induced by renewed administration ofthe medication; and there are no other possible causes.
Correspondence: Dr. M. Yebra, Servicio de Medicina Interna I, Cl1nica Puerta de Hierro, San Martin de Porres 4, 28035 Madrid, Spain.
Clinical Infectious Diseases 1992;15:750-1 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0044$02.00
The rarity of E. coli endocarditis may be due in part to the bactericidal activity of the complement system against most isolates that cause bacteremia. In an experimental model of endocarditis in rabbits, Durack and Beeson showed that serum-sensitive E. coli caused endocarditis in II % of rabbits, while serum-resistant E. coli caused endocarditis in 91 %of rabbits [2]. Of general clinical isolates of E. coli, approximately one-third are human serum-resistant, one-third are partially sensitive, and one-third are extremely sensitive [3]. Similarly, two of the four E. coli isolates we tested from patients with bacteremic pyelonephritis were serum-resistant, in addition to the isolate that caused endocarditis. Thus, serum resistance is unlikely to be the only factor accounting for the rarity of endocarditis due to this organism. Recurrent bacteremia, the presence of which was suggested by the history of recurrent rigors over 4 months, may have been a factor in our case. Bacterial adherence properties of pathogenic strains to valvular tissue may also be important [4].
Nigel J. Raymond, Max D. Robertson, and Selwyn D. R. Lang Departments of Medicine and Microbiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand
References I. Watanakunakorn C, Kim J. Mitral valve endocarditis caused by a serumresistant strain of Escherichia coli. Clin Infect Dis 1992; 14:501-5. 2. Durack DT, Beeson PB. Protective role of complement in experimental Escherichia coli endocarditis. Infect Immun 1977; 16:213-7. 3. Vosti KL, Randall E. Sensitivity ofserologically classified strains ofEscherichia coli of human origin to the serum bactericidal system. Am J Med Sci 1970;259: 114-9. 4. Gould K, Ramirez-Ronda CH, Holmes RK, Sanford JP. Adherence of bacteria to heart valves in vitro. J Clin Invest 1975;56: 1364-70.
In the case to which we refer, it appears that all these postulates are reasonably fulfilled (although metronidazole administration was not reinitiated so as not to expose the patient to further risk) except the last condition, with regard to which we wish to point out two considerations. First, several authors [2-5] have reported cases of pancreatitis associated with Crohn's disease, a fact that was briefly referred to in the article by Corey et al. In their review of the medical literature, Matsumoto et al. [5] gathered some 40 cases, in 13 of which there was no other cause than Crohn's disease itself to explain the pancreatitis. Of these, five patients had duodenal involvement and the pancreatic picture was considered to be secondary to this involvement. In the remaining eight patients, there was no duodenal involvement and no convincing pathogenic mechanism was found to explain the pancreatic inflammation. It is interesting that in some of the patients of the latter group, no correlation was found between the activity ofCrohn's disease and the course of pancreatitis [5]. On the other hand, in a study by Katz et al. [6], 8% of 97 patients with Crohn's disease had hyperamylasemia that was not associated with clinical pancreatitis. These authors found no relation between hyperamylasemia and the drugs employed or the duration, location, and activity of the basal disease. Follow-up data for the amylase levels were not included in the study.
Downloaded from http://cid.oxfordjournals.org/ at Florida Atlantic University on July 14, 2015
rose to 68 X 109IL. Further blood cultures were negative. Six days after presentation she developed complete heart block, hypotension, and acute renal failure. A soft systolic murmur was noted. Echocardiography showed a possible septal myocardial abscess, but no valvular abnormality was seen. The cardiothoracic surgical service recommended control ofsepsis before contemplation of surgery. Progressive cardiac failure ensued despite ventilation, cardiac pacing, and inotropic support, and the patient died on the 8th hospital day. At autopsy the heart was of normal size. There was a 15-mm vegetation on the ventricular aspect of the aortic valve, with perforation of a cusp. Within the upper interventricular septum a 15-mm abscess and an extensive area ofinduration containing acute inflammatory cells were noted. There was a 20-mm calculus in the right kidney with pyelonephritis, and hepatic and splenic infarcts were noted. The serum sensitivity of the E. coli isolated from the patient was tested by incubation with fresh pooled human serum according to the method described by Watanakunakorn and Kim [I]. Colony counts were carried out hourly for 3 hours. Normal saline and heat-inactivated serum were used as controls. The E. coli isolated from the patient showed no reduction in colony counts, thus indicating serum resistance. Four E. coli isolates from women with bacteremic pyelonephritis were similarly tested; two of the four isolates were serum-sensitive and two were resistant. Watanakunakorn and Kim [I] recently reported a case of E. coli endocarditis in which the isolate was also serum-resistant, and they reviewed the clinical features ofanother 18 cases from the literature. Our patient was typical in terms of age, the urinary source of infection, the presence of hyperglycemia, and the fatal outcome but was unusual in having aortic valve involvement, a myocardial septal abscess, and complete heart block.
CID 1992; 15 (October)
Aortic Valve Endocarditis Due to Escherichia coli SIR-Endocarditis caused by Escherichia coli is rare despite the frequency of bacteremia due to this organism. Only 19 cases were reported during 1945-1990 [I]. We report a further case, in which resistance ofthe E. coli isolate to the bactericidal action of serum may have contributed to pathogenesis. A 52-year-old woman presented in March 1992 with right loin pain, rigors, and fever. Similar episodes had occurred each month for the previous 4 months. Cultures of blood and a mid-
Correspondence: Dr. Selwyn D. R. Lang, Department of Microbiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand.
the groups as the "A. calcoaceticus-A. baumannii" complex [10]. Most acinetobacter isolates ofthese groups are glucose acidifying; therefore, these new groupings would largely correspond to the previous "A. calcoaceticus subspecies anUratus." This unification of groups may be appreciated for its simplification, although another nomenclatural change might add to the confusion of the taxonomy of Acinetobacter.
Lenie Dijkshoorn and Jos van der Toorn Department of Clinical Microbiology. Rotterdam University Hospital, Rotterdam; and Kluyver Laboratory of Biotechnology, University of Technology, Delft, the Netherlands References I. Gradon JD, Chapnick EK, Lutwick, LI. Infective endocarditis of a native valve due to Acinetobacter: case report and review. C1in Infect Dis 1992; 14: 1145-8. 2. J uni E. Genus III Acinetobacter Brisou and Prevot 1954, 727a' . In: Krieg NR, ed. Bergey's manual of systematic bacteriology. Vol. I. Baltimore: Williams and Wilkins, 1984:303-7. 3. Skerman VBD, McGowan V, Sneath PHA. Approved lists of bacterial names. Int J Syst Bacteriol 1980;30:241. 4. Bouvet PJM, Grimont PAD. Taxonomy of the genus Acinetobacter with the recognition of Acinetobacter baumannii sp. nov., Acinetobacter haemo(vticus sp. nov., Acinetobacter johnsonii sp. nov., and Acinetobacter junii sp. nov., and emended descriptions of Acinetobacter calcoaceticus and Acinetobacter Iwoffii. Int J Syst Bacteriol 1986;
36:228-40. 5. Nishimura Y, Ino T, Iizuka H. Acinetobacter radioresistens sp. nov. isolated from cotton and soil. Int J Syst Bacteriol 1988;38:209-11. 6. Tjernberg I, Ursing J. Clinical strains of Acinetobacter classified by DNA-DNA hybridization. APMIS 1989;97:595-605. 7. Moore WEe, Moore LYH. Index of the bacterial and yeast nomenclatural changes. Washington, DC: American Society for Microbiology,
1989:2-3. 8. Bouvet PJM, Jeanjean S. Delineation of new proteolytic genomic species in the genus Acinetobacter. Res Microbiol 1989; 140:291-9. 9. Dijkshoorn L, Tjernberg I, Pot B, Michel MF, Ursing J, Kersters K. Numerical analysis of cell envelope protein profiles of Acinetobacter classified by DNA-DNA hybridization. Syst Appl Microbiol 1990;
13:338-44. 10. Gerner-Smidt P, Tjernberg I, Ursing J. Reliability of phenotypic tests for identification of Acinetobacter species. J Clin Microbiol 1991;
29:277-82.
stream urine specimen processed at a private laboratory shortly before her admission yielded E. coli susceptible to amoxycillinf clavulanate, trimethoprim, cefaclor, gentamicin, and ceftriaxone but resistant to amoxycillin. Urine contained 100 X 106 white blood cells (WBCs) per liter but no red cells. Her general practitioner prescribed cefaclor for 4 days and then amoxycillinf clavulanate. On admission she was hypotensive and febrile. There was no heart murmur or stigmata of bacterial endocarditis. At that time, there was no growth from urine; however, further blood cultures yielded E. coli. The peripheral WBC count was 20 X 109fL, the serum glucose level was 11.9 mmolfL, and the serum creatinine level was 0.1 mmolfL. An ultrasonogram showed a 5-mm right renal calculus but no dilatation of the collecting system and no perirenal or intrarenal collections. Fever persisted despite therapy with gentamicin followed by that with ceftriaxone (I g daily), and the peripheral WBC count
Downloaded from http://cid.oxfordjournals.org/ at Florida Atlantic University on July 14, 2015
DNA group 2 (A. baumannii) has been found to be highly prevalent in clinical isolates in France [4], while DNA group 3 was predominant among clinical isolates in Sweden [6]. Strains from hospital outbreaks were found to belong to DNA group 2 (A. baumannii) [9]. Overall, the knowledge of the ecology and clinical relevance of the different groups is still poor. For identification of Acinetobacter isolates belonging to DNA groups I through 12, a scheme of phenotypic tests has been described [4]. However, a recent study has shown that phenotypic identification can be problematic [9], and this was especially the case for DNA group I (A. calcoaceticus), group 2 (A. baumannii), group 3, and group 13 [6], which are genetically and phenotypically closely related [4, 6]. Thus, today, at least 17 different groups (seven of which have species names) can be distinguished within the genus by DNADNA hybridization. Presumptive identification of a number of groups may be performed by phenotypic tests or by inspection of protein electrophoretic profiles [9]. However, unambiguous identification requires DNA hybridization, which is laborious and not a current method in routine microbiology. It may be questioned whether it is necessary to identify Acinetobacter isolates according to the recent classification. It is our opinion that the clinical laboratory's identification of the organisms to the genus level may suffice as long as Acinetobacter isolations are incidental. Furthermore, a few additional tests such as those for the aerobic acidification of glucose and growth at 44°C may be used for presumptive identification of DNA group 2 (A. baumannii) [4]. This approach is not satisfactory for tracing epidemic strains during outbreaks; in these situations, isolates have to be typed by combinations of typing methods, e.g., biotyping and comparative protein electrophoretic typing [10]. For a better knowledge of the ecology and pathology of the different DNA groups, however, the precise DNA group of isolates must be determined, and this would require rapid methods for unambiguous identification. We hope that these methodsperhaps new molecular techniques-will soon be available for this purpose. Finally, given the close relationship of DNA groups I, 2, 3, and 13 [6] at different levels of DNA expression [4, 6, 9], researchers have considered lumping these groups together into one species, "A. calcoaceticus" (in sensu lata), thus giving the DNA groups the rank of subspecies [6], or referring to
Clinical Infectious Diseases 1992;15:749-50 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0043$02.00
749
Correspondence
750
Correspondence
Metronidazole and Pancreatitis SIR-In their article, Corey et al. [I] report the case ofa 63-yearold woman with Crohn's disease who develops acute pancreatitis coincident with the administration of metronidazole that disappears upon discontinuance of the drug's administration. The authors base their diagnosis on the clinical picture and the rise in enzyme concentrations (results of pancreatic ultrasonography and computed tomography were normal). The absence of other risk factors suggests a pathogenic relationship between metronidazole and the pancreatitis. For implicating a pharmaceutical agent as the cause of a disease, demonstration of the following is necessary: the disease occurs during the administration of the drug; the disease disappears once use of the drug is discontinued; the disease can be induced by renewed administration ofthe medication; and there are no other possible causes.
Correspondence: Dr. M. Yebra, Servicio de Medicina Interna I, Cl1nica Puerta de Hierro, San Martin de Porres 4, 28035 Madrid, Spain.
Clinical Infectious Diseases 1992;15:750-1 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0044$02.00
The rarity of E. coli endocarditis may be due in part to the bactericidal activity of the complement system against most isolates that cause bacteremia. In an experimental model of endocarditis in rabbits, Durack and Beeson showed that serum-sensitive E. coli caused endocarditis in II % of rabbits, while serum-resistant E. coli caused endocarditis in 91 %of rabbits [2]. Of general clinical isolates of E. coli, approximately one-third are human serum-resistant, one-third are partially sensitive, and one-third are extremely sensitive [3]. Similarly, two of the four E. coli isolates we tested from patients with bacteremic pyelonephritis were serum-resistant, in addition to the isolate that caused endocarditis. Thus, serum resistance is unlikely to be the only factor accounting for the rarity of endocarditis due to this organism. Recurrent bacteremia, the presence of which was suggested by the history of recurrent rigors over 4 months, may have been a factor in our case. Bacterial adherence properties of pathogenic strains to valvular tissue may also be important [4].
Nigel J. Raymond, Max D. Robertson, and Selwyn D. R. Lang Departments of Medicine and Microbiology, Middlemore Hospital, Otahuhu, Auckland, New Zealand
References I. Watanakunakorn C, Kim J. Mitral valve endocarditis caused by a serumresistant strain of Escherichia coli. Clin Infect Dis 1992; 14:501-5. 2. Durack DT, Beeson PB. Protective role of complement in experimental Escherichia coli endocarditis. Infect Immun 1977; 16:213-7. 3. Vosti KL, Randall E. Sensitivity ofserologically classified strains ofEscherichia coli of human origin to the serum bactericidal system. Am J Med Sci 1970;259: 114-9. 4. Gould K, Ramirez-Ronda CH, Holmes RK, Sanford JP. Adherence of bacteria to heart valves in vitro. J Clin Invest 1975;56: 1364-70.
In the case to which we refer, it appears that all these postulates are reasonably fulfilled (although metronidazole administration was not reinitiated so as not to expose the patient to further risk) except the last condition, with regard to which we wish to point out two considerations. First, several authors [2-5] have reported cases of pancreatitis associated with Crohn's disease, a fact that was briefly referred to in the article by Corey et al. In their review of the medical literature, Matsumoto et al. [5] gathered some 40 cases, in 13 of which there was no other cause than Crohn's disease itself to explain the pancreatitis. Of these, five patients had duodenal involvement and the pancreatic picture was considered to be secondary to this involvement. In the remaining eight patients, there was no duodenal involvement and no convincing pathogenic mechanism was found to explain the pancreatic inflammation. It is interesting that in some of the patients of the latter group, no correlation was found between the activity ofCrohn's disease and the course of pancreatitis [5]. On the other hand, in a study by Katz et al. [6], 8% of 97 patients with Crohn's disease had hyperamylasemia that was not associated with clinical pancreatitis. These authors found no relation between hyperamylasemia and the drugs employed or the duration, location, and activity of the basal disease. Follow-up data for the amylase levels were not included in the study.
Downloaded from http://cid.oxfordjournals.org/ at Florida Atlantic University on July 14, 2015
rose to 68 X 109IL. Further blood cultures were negative. Six days after presentation she developed complete heart block, hypotension, and acute renal failure. A soft systolic murmur was noted. Echocardiography showed a possible septal myocardial abscess, but no valvular abnormality was seen. The cardiothoracic surgical service recommended control ofsepsis before contemplation of surgery. Progressive cardiac failure ensued despite ventilation, cardiac pacing, and inotropic support, and the patient died on the 8th hospital day. At autopsy the heart was of normal size. There was a 15-mm vegetation on the ventricular aspect of the aortic valve, with perforation of a cusp. Within the upper interventricular septum a 15-mm abscess and an extensive area ofinduration containing acute inflammatory cells were noted. There was a 20-mm calculus in the right kidney with pyelonephritis, and hepatic and splenic infarcts were noted. The serum sensitivity of the E. coli isolated from the patient was tested by incubation with fresh pooled human serum according to the method described by Watanakunakorn and Kim [I]. Colony counts were carried out hourly for 3 hours. Normal saline and heat-inactivated serum were used as controls. The E. coli isolated from the patient showed no reduction in colony counts, thus indicating serum resistance. Four E. coli isolates from women with bacteremic pyelonephritis were similarly tested; two of the four isolates were serum-sensitive and two were resistant. Watanakunakorn and Kim [I] recently reported a case of E. coli endocarditis in which the isolate was also serum-resistant, and they reviewed the clinical features ofanother 18 cases from the literature. Our patient was typical in terms of age, the urinary source of infection, the presence of hyperglycemia, and the fatal outcome but was unusual in having aortic valve involvement, a myocardial septal abscess, and complete heart block.
CID 1992; 15 (October)
