752
Correspondence
CID 1992; 15 (October)
Table 1. Summary of clinical findings for patients with infections due to Pseudomonas aeruginosa. Risk factor for Age (y)
CDC stage
CD4 cell count
P. aeruginosa infection
Type of infection
Infection
Positive culture(s)
I 2 3 4 5 6 7 8
22 26 23 19 20 31 27 36 21 30 28 28 22 41 29
II II II III II II III IV-CI II IV-CI IV-CI IV-CI III II IV-CI
NO NO NO 290 635 432 264 II 381 5 10 55 306 157
IVDU IVDU IVDU IVDU IVDU IVDU,DNB IVDU None IVDU None Neutropenia None IVDU None Surgery/DNB
C C C C C N C C C C N C C C N
Bacteremia Bacteremia Pneumonia Right-sided endocarditis Bacteremia/pneumonia Bacteremia/ophthalmitis Bacteremia Bacteremia Right-sided endocarditis Bacteremia/pneumonia Pneumonia/sepsis Invasive otitis externa Osteomyelitis Pneumonia/empyema Peritonitis
Blood Blood Lung aspirate Blood Blood/sputum Blood/eye aspirate Blood Blood Blood Blood/sputum Blood/skin Discharge from ear Bone aspirate Pleural fluid Blood/ascitic fluid
9 10 II 12 13 14 15
22
NOTE. CDC == Centers for Disease Control; NO barriers; and N = nosocomially acquired.
Cure Cure Cure Cure Cure Blindness Cure Cure Cure Relapse Relapse/death Cure Cure Cure Relapse/death
= not done; IVDU = intravenous drug use; C = community acquired; DNB = disruptions of natural
cording to the classification of the Centers for Disease Control (CDC), was IV-CI, had no known risk factor. The second noteworthy observation from our series, which is consistent with the report by Kielhofner et aI., is the unfavorable outcome of P. aeruginosa infections despite adequate treatment (in all the cases with ceftazidime or piperacillin in combination with aminoglycosides) of the patients with IV-Cl-classified HIV infection. This contrasts with the good response of patients in earlier stages of HIV disease, lending support to the importance of the immune response in the defense against and control of P.
aeruginosa. In our series, like that of others [2], most P. aeruginosa infections in HIV-infected adult patients occurred in the context of known risk factors (in ours, mostly intravenous drug addiction). However, we concur with Kielhofner et al. in noting the importance of these factors, given the unfavorable outcome and mini-
Bacteremia Due to Vancomycin-Resistant Enterococcus faecium of Van B Phenotype During Prophylaxis with Vancomycin SIR-The glycopeptide antibiotics vancomycin and teicoplanin are used in the treatment ofserious infections due to enterococci in cases of resistance or allergy to {Hactam agents. Enterococci resistant to these antibiotics have been described recently [I]. The resistant strains are readily divided into three classes, Van A, Van B, and Van C, on the basis of the level of resistance to
Correspondence: Dr. Pascal Pouedras, Laboratoire de BacteriologieVirologie, CHU Pontchaillou, 35033 Rennes Cedex, France.
Clinical Infectious Diseases 1992;15:752-3 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0047$02.00
Outcome of this episode
mum response of these patients to conventional therapy when these infections occur in conjunction with advanced HIV disease.
Fernando Lozano, Juan E. Corzo, Carmen Nogales, and Fernando Garcia-Bragado Infectious Diseases Unit (Department 0/ Internal Medicine) and the Department o/Microbiology, University Hospital o/Valme. Seville. Spain References I. Kielhofner M, Atmar RL, Hamill RJ, Musher OM. Life-threatening Pseudomonas aeruginosa infections in patients with human immunodeficiency virus infection. Clin Infect Dis 1992; 14:403-11. 2. Rolston KVI, Radentz S. Rodriguez S. Bacterial and fungal infections in patients with the acquired immunodeficiency syndrome. Cancer Detect Prev 1990; 14:377-81.
vancomycin and teicoplanin and whether the resistance is inducible [2]. Van B strains show inducible, moderate levels of resistance to vancomycin but remain susceptible to teicoplanin [3]. Recently, we isolated Enterococcus faecium of class B from the blood and stool ofone patient while she was receiving vancomycin prophylaxis. A 52-year-old woman with acute myelogenous leukemia was admitted to the hematology department for cytotoxic chemotherapy. At that time, vancomycin prophylaxis (1 g iv every 12 hours) was administered for 24 days. Peak serum levels of vancomycin of between 19 and 40 #Lg/mL were reported on several occasions. The regimen for selective antimicrobial decontamination of the digestive tract consisted of administration of oral colimycin and fluconazole. On day 9, the patient had a high fever (40°C), and ceftazidime and amikacin were empirically added to the therapeutic regimen. All blood cultures remained negative. Fever resolved on day 15, but the appearance of hypo-
Downloaded from http://cid.oxfordjournals.org/ at Florida Atlantic University on July 24, 2015
Case no.
CID 1992; 15 (October)
Correspondence
753
thermia necessitated more blood cultures. E. faecium was recovered from four blood cultures. The isolates were highly resistant to streptomycin but not to gentamicin, moderately resistant to penicillin (MIC, 16 ~g/mL) and sensitive to ampicillin (MIC, 2 ~g/mL). Broth microdilution and macrodilution MIC and MBC testing revealed that the MIC of vancomycin was 64 ~g/mL (MBC, >128 ~g/mL) and the MIC ofteicoplanin was 0.25 ~gl mL (MBC, 32 ~g/mL). Several stool cultures during her 1month hospitalization yielded E. faecium with the same Van B phenotype. Therapy with vancomycin was discontinued on day 19, and that with ampicillin and gentamicin was begun. All further blood cultures were negative, and her temperature rapidly returned to normal. Stool cultures done 1 and 2 months after discharge from the hospital yielded the same isolate, although the patient had no clinical infection due to E. faecium. Glycopeptide resistance was considered extremely rare until 1988, when Uttley et al. [4] described an outbreak of infection due to vancomycin-resistant enterococci in a London hospital. Since that time, additional reports on the emergence of vancomycin-resistant enterococci have appeared in the literature. Low incidences of serious infections caused by enterococci of Van B phenotype have been reported [5-7], but the failure of the diskagar diffusion test to detect this low-level resistance could explain this rare occurrence. We describe a case of colonization and subsequent bacteremia with a Van B strain occurring in a patient suffering from debilitating underlying disease. Digestive colonization by this strain obviously persisted over a longer period of time in the absence of selective antimicrobial pressure. This observation suggests that this strain can be a part of the normal flora of the digestive tract of this patient. The biochemical mechanism of vancomycin resistance is not yet understood. Leclercq et al. [8] showed that the vancomycin resistance of their Van A strains could be induced by subinhibitory concentrations of the drug. In the present report, the patient had received vancomycin for 17 days prior to detection of
the first positive blood culture. Vancomycin prophylaxis with subinhibitory concentrations appears to have provided the selective pressure for producing an organism resistant to the drug and to have led to colonization and infection with this organism. Emergence of vancomycin resistance during the course of vancomycin prophylaxis is troublesome, and the clinical and therapeutic consequences have still to be established.
Fatal Intrauterine Infection Associated with Mycoplasma hominis
strong evidence that M. hominis is linked to maternal fever postabortion and postpartum [4, 5] and is associated with chorioamnionitis, spontaneous abortion, and stillbirth [4-9]. However, it has been clearly established that healthy pregnant women delivering healthy infants are frequently asymptomatically colonized with M. hominis [1]. Accordingly, we present a case of stillbirth following intrauterine infection in which M. hominis was detected in the internal organs of the fetus by culture and by the recently developed polymerase chain reaction (PCR) [10]. A 37-year-old gravida 2 para 1 woman was admitted at 24 weeks gestation because of imminent premature labor. The pregnancy was uneventful and the patient had no history of illness. Findings of physical examination on admission were remarkable for the absence of fever or other signs of systemic infection. No uterine tenderness was detected. Amniotic membranes were intact although they were bulging through the cervical os, which was dilated to 4 cm. The peripheral white blood cell count (WBC) was 17.1 X 109IL. Ultrasonography of the fetus and uterus revealed no abnormalities. For preventing immature partus, a cerclage of the cervix was put in place. Vaginal cultures at this time yielded Gardnerella vaginalis. Two days
Correspondence: Dr. Jacques F. Meis. Department of Medical Microbiology. University Hospital Nijmegen. 6500 HB Nijmegen. The Netherlands.
Clinical Infectious Diseases 1992;15:753-4 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0048$02.00
Laboratoire de Bacteri%gie- Vir%gie. Hopita/ Pontchai//ou, Rennes. and Laboratoire de Bacteriologie- Virologie, Hopital Henri Mondor, Paris, France
References I. Johnson AP. Uttley AHC, Woodford N, George RC. Resistance to van-
2. 3.
4. 5.
6.
7.
8.
comycin and teicoplanin: an emerging clinical problem. Clin Microbioi Rev 1990;3:280-91. Shlaes OM. AI-Obeid S, Gutmann L. Vancomycin-resistant enterococci. APUA Newsletter 1989;7:1-8. Williamson R. AI-Obeid S. ShlaesJH. Goldstein FW. Shlaes OM. Inducible resistance to vancomycin in Enterococcus faecium 0366. J Infect Dis 1989; 159: 1095-104. UttIey AHC, Collins CH, Naidoo J, George RC. Vancomycin resistant enterococci [letter]. Lancet 1988;1:57-8. Kaplan AH. Gilligan PH, Facklam RR. Recovery of resistant enterococci during vancomycin prophylaxis. J Clin Microbiol 1987; 26: 1216-8. Sahm OF. Kissinger J. Gilmore MS, et al. In vitro susceptibility studies of vancomycin-resistant Enterococcus faeca/is. Antimicrob Agents Chemother 1989;33: 1588-91. Handwerger S. Perlman DC, Altarac 0, McAuliffe V. Concomitant highlevel vancomycin and penicillin resistance in clinical isolates of enterococci. C1in Infect Dis 1992; 14:655-61. Leclercq R, Derlot E, Weber M. Duval J, Courvalin P. Transferable vancomycin and teicoplanin resistance in Enterococcus faecium. Antimicrob Agents Chemother 1989;33: 10-5.
Downloaded from http://cid.oxfordjournals.org/ at Florida Atlantic University on July 24, 2015
SIR-Mycoplasma hominis and Ureaplasma urealyticum are generally considered commensals of the urogenital tract. The potential pathogenic role of these genital mycoplasmas in nongonococcal urethritis, pelvic inflammatory disease, and infertility has been reviewed previously [1]. Extragenital infections include septic arthritis, wound infection, prosthetic valve endocarditis, peritonitis, brain abscess, septicemia, ventriculoperitoneal shunt infection, neonatal encephalitis, and meningitis [2, 3]. The latter three infections are most likely the result of intrauterine infection or colonization during passage through the birth canal, with subsequent development of infection [4]. There is
Pascal Pouedras, Roland Leclercq, Pierre-Yves Donnio, Jean-Marie Sire, Renaud Mesnard, and Jean-Loup Avril
Correspondence
CID 1992; 15 (October)
Table 1. Summary of clinical findings for patients with infections due to Pseudomonas aeruginosa. Risk factor for Age (y)
CDC stage
CD4 cell count
P. aeruginosa infection
Type of infection
Infection
Positive culture(s)
I 2 3 4 5 6 7 8
22 26 23 19 20 31 27 36 21 30 28 28 22 41 29
II II II III II II III IV-CI II IV-CI IV-CI IV-CI III II IV-CI
NO NO NO 290 635 432 264 II 381 5 10 55 306 157
IVDU IVDU IVDU IVDU IVDU IVDU,DNB IVDU None IVDU None Neutropenia None IVDU None Surgery/DNB
C C C C C N C C C C N C C C N
Bacteremia Bacteremia Pneumonia Right-sided endocarditis Bacteremia/pneumonia Bacteremia/ophthalmitis Bacteremia Bacteremia Right-sided endocarditis Bacteremia/pneumonia Pneumonia/sepsis Invasive otitis externa Osteomyelitis Pneumonia/empyema Peritonitis
Blood Blood Lung aspirate Blood Blood/sputum Blood/eye aspirate Blood Blood Blood Blood/sputum Blood/skin Discharge from ear Bone aspirate Pleural fluid Blood/ascitic fluid
9 10 II 12 13 14 15
22
NOTE. CDC == Centers for Disease Control; NO barriers; and N = nosocomially acquired.
Cure Cure Cure Cure Cure Blindness Cure Cure Cure Relapse Relapse/death Cure Cure Cure Relapse/death
= not done; IVDU = intravenous drug use; C = community acquired; DNB = disruptions of natural
cording to the classification of the Centers for Disease Control (CDC), was IV-CI, had no known risk factor. The second noteworthy observation from our series, which is consistent with the report by Kielhofner et aI., is the unfavorable outcome of P. aeruginosa infections despite adequate treatment (in all the cases with ceftazidime or piperacillin in combination with aminoglycosides) of the patients with IV-Cl-classified HIV infection. This contrasts with the good response of patients in earlier stages of HIV disease, lending support to the importance of the immune response in the defense against and control of P.
aeruginosa. In our series, like that of others [2], most P. aeruginosa infections in HIV-infected adult patients occurred in the context of known risk factors (in ours, mostly intravenous drug addiction). However, we concur with Kielhofner et al. in noting the importance of these factors, given the unfavorable outcome and mini-
Bacteremia Due to Vancomycin-Resistant Enterococcus faecium of Van B Phenotype During Prophylaxis with Vancomycin SIR-The glycopeptide antibiotics vancomycin and teicoplanin are used in the treatment ofserious infections due to enterococci in cases of resistance or allergy to {Hactam agents. Enterococci resistant to these antibiotics have been described recently [I]. The resistant strains are readily divided into three classes, Van A, Van B, and Van C, on the basis of the level of resistance to
Correspondence: Dr. Pascal Pouedras, Laboratoire de BacteriologieVirologie, CHU Pontchaillou, 35033 Rennes Cedex, France.
Clinical Infectious Diseases 1992;15:752-3 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0047$02.00
Outcome of this episode
mum response of these patients to conventional therapy when these infections occur in conjunction with advanced HIV disease.
Fernando Lozano, Juan E. Corzo, Carmen Nogales, and Fernando Garcia-Bragado Infectious Diseases Unit (Department 0/ Internal Medicine) and the Department o/Microbiology, University Hospital o/Valme. Seville. Spain References I. Kielhofner M, Atmar RL, Hamill RJ, Musher OM. Life-threatening Pseudomonas aeruginosa infections in patients with human immunodeficiency virus infection. Clin Infect Dis 1992; 14:403-11. 2. Rolston KVI, Radentz S. Rodriguez S. Bacterial and fungal infections in patients with the acquired immunodeficiency syndrome. Cancer Detect Prev 1990; 14:377-81.
vancomycin and teicoplanin and whether the resistance is inducible [2]. Van B strains show inducible, moderate levels of resistance to vancomycin but remain susceptible to teicoplanin [3]. Recently, we isolated Enterococcus faecium of class B from the blood and stool ofone patient while she was receiving vancomycin prophylaxis. A 52-year-old woman with acute myelogenous leukemia was admitted to the hematology department for cytotoxic chemotherapy. At that time, vancomycin prophylaxis (1 g iv every 12 hours) was administered for 24 days. Peak serum levels of vancomycin of between 19 and 40 #Lg/mL were reported on several occasions. The regimen for selective antimicrobial decontamination of the digestive tract consisted of administration of oral colimycin and fluconazole. On day 9, the patient had a high fever (40°C), and ceftazidime and amikacin were empirically added to the therapeutic regimen. All blood cultures remained negative. Fever resolved on day 15, but the appearance of hypo-
Downloaded from http://cid.oxfordjournals.org/ at Florida Atlantic University on July 24, 2015
Case no.
CID 1992; 15 (October)
Correspondence
753
thermia necessitated more blood cultures. E. faecium was recovered from four blood cultures. The isolates were highly resistant to streptomycin but not to gentamicin, moderately resistant to penicillin (MIC, 16 ~g/mL) and sensitive to ampicillin (MIC, 2 ~g/mL). Broth microdilution and macrodilution MIC and MBC testing revealed that the MIC of vancomycin was 64 ~g/mL (MBC, >128 ~g/mL) and the MIC ofteicoplanin was 0.25 ~gl mL (MBC, 32 ~g/mL). Several stool cultures during her 1month hospitalization yielded E. faecium with the same Van B phenotype. Therapy with vancomycin was discontinued on day 19, and that with ampicillin and gentamicin was begun. All further blood cultures were negative, and her temperature rapidly returned to normal. Stool cultures done 1 and 2 months after discharge from the hospital yielded the same isolate, although the patient had no clinical infection due to E. faecium. Glycopeptide resistance was considered extremely rare until 1988, when Uttley et al. [4] described an outbreak of infection due to vancomycin-resistant enterococci in a London hospital. Since that time, additional reports on the emergence of vancomycin-resistant enterococci have appeared in the literature. Low incidences of serious infections caused by enterococci of Van B phenotype have been reported [5-7], but the failure of the diskagar diffusion test to detect this low-level resistance could explain this rare occurrence. We describe a case of colonization and subsequent bacteremia with a Van B strain occurring in a patient suffering from debilitating underlying disease. Digestive colonization by this strain obviously persisted over a longer period of time in the absence of selective antimicrobial pressure. This observation suggests that this strain can be a part of the normal flora of the digestive tract of this patient. The biochemical mechanism of vancomycin resistance is not yet understood. Leclercq et al. [8] showed that the vancomycin resistance of their Van A strains could be induced by subinhibitory concentrations of the drug. In the present report, the patient had received vancomycin for 17 days prior to detection of
the first positive blood culture. Vancomycin prophylaxis with subinhibitory concentrations appears to have provided the selective pressure for producing an organism resistant to the drug and to have led to colonization and infection with this organism. Emergence of vancomycin resistance during the course of vancomycin prophylaxis is troublesome, and the clinical and therapeutic consequences have still to be established.
Fatal Intrauterine Infection Associated with Mycoplasma hominis
strong evidence that M. hominis is linked to maternal fever postabortion and postpartum [4, 5] and is associated with chorioamnionitis, spontaneous abortion, and stillbirth [4-9]. However, it has been clearly established that healthy pregnant women delivering healthy infants are frequently asymptomatically colonized with M. hominis [1]. Accordingly, we present a case of stillbirth following intrauterine infection in which M. hominis was detected in the internal organs of the fetus by culture and by the recently developed polymerase chain reaction (PCR) [10]. A 37-year-old gravida 2 para 1 woman was admitted at 24 weeks gestation because of imminent premature labor. The pregnancy was uneventful and the patient had no history of illness. Findings of physical examination on admission were remarkable for the absence of fever or other signs of systemic infection. No uterine tenderness was detected. Amniotic membranes were intact although they were bulging through the cervical os, which was dilated to 4 cm. The peripheral white blood cell count (WBC) was 17.1 X 109IL. Ultrasonography of the fetus and uterus revealed no abnormalities. For preventing immature partus, a cerclage of the cervix was put in place. Vaginal cultures at this time yielded Gardnerella vaginalis. Two days
Correspondence: Dr. Jacques F. Meis. Department of Medical Microbiology. University Hospital Nijmegen. 6500 HB Nijmegen. The Netherlands.
Clinical Infectious Diseases 1992;15:753-4 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1504-0048$02.00
Laboratoire de Bacteri%gie- Vir%gie. Hopita/ Pontchai//ou, Rennes. and Laboratoire de Bacteriologie- Virologie, Hopital Henri Mondor, Paris, France
References I. Johnson AP. Uttley AHC, Woodford N, George RC. Resistance to van-
2. 3.
4. 5.
6.
7.
8.
comycin and teicoplanin: an emerging clinical problem. Clin Microbioi Rev 1990;3:280-91. Shlaes OM. AI-Obeid S, Gutmann L. Vancomycin-resistant enterococci. APUA Newsletter 1989;7:1-8. Williamson R. AI-Obeid S. ShlaesJH. Goldstein FW. Shlaes OM. Inducible resistance to vancomycin in Enterococcus faecium 0366. J Infect Dis 1989; 159: 1095-104. UttIey AHC, Collins CH, Naidoo J, George RC. Vancomycin resistant enterococci [letter]. Lancet 1988;1:57-8. Kaplan AH. Gilligan PH, Facklam RR. Recovery of resistant enterococci during vancomycin prophylaxis. J Clin Microbiol 1987; 26: 1216-8. Sahm OF. Kissinger J. Gilmore MS, et al. In vitro susceptibility studies of vancomycin-resistant Enterococcus faeca/is. Antimicrob Agents Chemother 1989;33: 1588-91. Handwerger S. Perlman DC, Altarac 0, McAuliffe V. Concomitant highlevel vancomycin and penicillin resistance in clinical isolates of enterococci. C1in Infect Dis 1992; 14:655-61. Leclercq R, Derlot E, Weber M. Duval J, Courvalin P. Transferable vancomycin and teicoplanin resistance in Enterococcus faecium. Antimicrob Agents Chemother 1989;33: 10-5.
Downloaded from http://cid.oxfordjournals.org/ at Florida Atlantic University on July 24, 2015
SIR-Mycoplasma hominis and Ureaplasma urealyticum are generally considered commensals of the urogenital tract. The potential pathogenic role of these genital mycoplasmas in nongonococcal urethritis, pelvic inflammatory disease, and infertility has been reviewed previously [1]. Extragenital infections include septic arthritis, wound infection, prosthetic valve endocarditis, peritonitis, brain abscess, septicemia, ventriculoperitoneal shunt infection, neonatal encephalitis, and meningitis [2, 3]. The latter three infections are most likely the result of intrauterine infection or colonization during passage through the birth canal, with subsequent development of infection [4]. There is
Pascal Pouedras, Roland Leclercq, Pierre-Yves Donnio, Jean-Marie Sire, Renaud Mesnard, and Jean-Loup Avril
