Vancomycin-resistant Enterococcus durans
1
1105 Vancomycin-resistant Enterococcus durans SIR,-Enterococci are emerging as significant pathogens, responsible for at least 4% of hospital-acquired infection in the UK and about 10% of such infections in the US. Treatment is seriously compromised by the emergence of strains resistant to the few antibiotics normally useful against this genus. Of concern is the recent appearance of vancomycin resistance, especially in Enterococcus faecium but also in other species, which have been detected at various centres in the UK.1 We report vancomycin- resistant E durans, with evidence of transfer of this organism within the renal transplant unit at the Royal London Hospital. The first patient was in the renal unit between May 16 and 19, 1992, and again between June 4 and 17. Enterococcus sp was isolated from the urine once during each admission and was resistant to vancomycin by disc diffusion (5 µg disc). Only the second isolate was available for further characterisation. The second patient was in the unit from May 25 to June 17, 1992. Culture of a central-line tip on May 28 yielded, after 5 days’ fluid enrichment, a vancomycin- resistant enterococcus. The isolates from the two patients were identified by API-20S as E durans (with poor discrimination from Lactococcus lactis) and confirmed to have the group D streptococcal antigen with a Streptex grouping kit. API-50S also gave the most likely identity as E durans, with both isolates having the same profile. The minimum inhibitory concentration of vancomycin was over 256 mg/1, and that of teicoplanin was 16 mg/1 for both isolates. The high resistance to vancomycin and teicoplanin suggests that the isolates bear the VanA resistance determinant. The isolates were also resistant to erythromycin, benzylpenicillin, rifampicin, and ampicillin, but susceptible to chloramphenicol. Total DNA restriction patterns of the two isolates were compared.2 Four different restriction enzymes were used, Sstl, SaIl, PvuII, and BscI, cutting the DNA at different frequencies. In all cases the two isolates produced identical patterns, which were different from a reference strain (NCTC 8174) and another clinical isolate of E durans. Isolates from the two renal transplant patients were therefore indistinguishable, leading us to conclude that the organism had spread within the unit. Fortunately no further isolates of this strain have been identified, nor were vancomycin-resistant enterococci isolated during a previous survey in this hospital (M. Guiney and G. Urwin). This incident emphasises that vancomycin resistance can occur in enterococcal species other than E faecium, that the organisms can spread between patients, and that effective antimicrobial treatment of enterococcal infections is being severely threatened by acquired resistance determinants. We thank B. Duke, M. Guiney, and the staff of the Royal London Hospital Medical Microbiology Department. Department of Medical Microbiology, London Hospital Medical College, London E1 2AD, UK L. M. C. HALL H. Y. CHEN R. J. WILLIAMS 1. Anon. Vancomycin-resistant enterococci. Commun Dis Rep 1992; 2: 121. 2. Hall LMC, Duke B, Guiney M, Williams R. Typing of Enterococcus species by DNA restriction fragment analysis. J Clin Microbiol 1992; 30: 915-19. Thrombolysis with recombinant tissue-type plasminogen activator in renal venous thrombosis in infancy SIR,-Bilateral renal venous thrombosis in infancy frequently leads to chronic renal failure,’ and thrombectomy or fibrinolytic therapy with streptokinase and urokinase has been successful in both adults and infants.2,3 We present our results in eight babies with renal venous thrombosis (bilateral, n = 4; uni-lateral and vena cava, n = 3; renal veins, vena cava, and aorta, n = 1) treated with recombinant tissue-type plasminogen activator (rt-PA). In these patients, all treated with neonatal resuscitation, thrombosis followed the placement of vascular catheters, sepsis, haemolytic- uraemic syndrome, exsiccosis, fetopathia diabetica, or heterozygous antithrombin III and protein C deficiency. 48 h after the initial clinical symptoms (oliguria, haematuria, hypertension) diagnostic procedures including duplex ultrasound were done and rt-PA started at 0-1-0-2 mg/kg over 10 min with additional continuous rt-PA infusion and low-dose heparin. Individual rt-PA doses, the duration and complications of therapy, and the final outcome (mean observation period, 9 [7-48] months) are shown in the table. To avoid reocclusion when rt-PA infusion was ended, heparin infusion was enhanced and substitution with antithrombin III concentrate began.4 PATIENTS’ DETAILS *Patient 6 had normal bleeding and perforative duodenitis on day 1 and afterwards, respectively During rt-PA therapy we saw no decrease in fibrinogen or plasminogen concentrations as a sign of systemic fibrinolytic activation induced by rt-PA. Five infants had renal recovery (normal creatinine clearance, normal radiological and radionuclide imaging). Complications of the basic disease led to death in one preterm infant 2 weeks after successful thrombolysis. In one patient heparinisation after complete reperfusion was ineffective; partial reocclusion with an atrophic kidney occurred during follow up. Because of the severity of the basic disease in patient 6, rt-PA 9 mg/kg per day was necessary5 to achieve reperfusion of the aorta and renal veins while peritoneal dialysis was done. Later rt-PA therapy was stopped because of intra-abdominal bleeding due to perforative duodenitis. This patient is undergoing further peritoneal dialysis at home 8 months after thrombolysis. No other severe side-effects (eg, cerebral intraventricular bleedings) occurred. We believe thrombolytic therapy with rt-PA in infants with renal venous thrombosis is a logical therapeutic regimen because prompt lysis of renal venous thrombosis may prevent or minimise loss of renal function, especially when there is bilateral occlusion, and because of the short half-life, less systemic fibrinolytic activation and local enhancement of plasminogen concentration, which is important in infants with physiologically reduced plasminogen concentrations." Department of Haematology and Oncology, Centre for Paediatrics, Klinikum der J W Goethe-Universitat, 6000 Frankfurt/Main, Germany U. NOWAK-GÖTTL D. SCHWABE W. SCHNEIDER R. SCHLÖSSER W. KREUZ 1. Stapleton FB, Jones DP, Green RS. Acute renal failure in neonates: incidence, etiology and outcome. Pediatr Nephrol 1987; 1: 314-20. 2. Bromberg WD, Firlit CF. Fibrinolytic therapy for renal vein thrombosis in the child. J Urol 1990; 143: 86-88. 3. Pritchard SL, Culham JAG, Rodgers PCJ. Low-dose fibrinolytic therapy in infants. J Pediatr 1985; 106: 594-98. 4. Egbring R, Seitz R, Behling T, Bethke C. Die Prophylaxe von Reocclusion von Infarktegafäßen nach intrakoronarer Thrombolyse: Einfluß von Antithrombin III? Hamostaseologie 1988; 9: 3-7. 5. Levy M, Benson LN, Burrows PE, et al. Tissue plasminogen activator for the treatment of thromboembolism in infants and children. J Pediatr 1991; 118: 476-72. 6. Nieuwenhuizen W, Verheijen TH, Vermond A, Chang GTG. Plasminogen activation by tissue activator is accelerated in the presence of fibrinogen cyanogen bromide fragment FCB-2. Biochim Biophys Acta 1983; 755: 531-33. 7. Seifried E, Transwell P, Rijken DC, Barett-Bergshoeff MM, Capf SU, Kluft C. Pharmacokinetics of antigen and activity of recombinant tissue-type plasminogen activator after infusion in healthy volunteers. Drug Res 1988; 38: 418-22. 8. Andrew M. Development of the hemostatic system in the neonate and young infant. Am J Pediatr Hematol Oncol 1990; 12: 95-104.
Transcript of Vancomycin-resistant Enterococcus durans
1105
Vancomycin-resistant Enterococcus durans
SIR,-Enterococci are emerging as significant pathogens,responsible for at least 4% of hospital-acquired infection in the UKand about 10% of such infections in the US. Treatment is seriouslycompromised by the emergence of strains resistant to the fewantibiotics normally useful against this genus. Of concern is therecent appearance of vancomycin resistance, especially in
Enterococcus faecium but also in other species, which have beendetected at various centres in the UK.1 We report vancomycin-resistant E durans, with evidence of transfer of this organism withinthe renal transplant unit at the Royal London Hospital.The first patient was in the renal unit between May 16 and 19,
1992, and again between June 4 and 17. Enterococcus sp was isolatedfrom the urine once during each admission and was resistant tovancomycin by disc diffusion (5 µg disc). Only the second isolatewas available for further characterisation. The second patient was inthe unit from May 25 to June 17, 1992. Culture of a central-line tipon May 28 yielded, after 5 days’ fluid enrichment, a vancomycin-resistant enterococcus.The isolates from the two patients were identified by API-20S as
E durans (with poor discrimination from Lactococcus lactis) andconfirmed to have the group D streptococcal antigen with aStreptex grouping kit. API-50S also gave the most likely identity asE durans, with both isolates having the same profile. The minimuminhibitory concentration of vancomycin was over 256 mg/1, and thatof teicoplanin was 16 mg/1 for both isolates. The high resistance tovancomycin and teicoplanin suggests that the isolates bear the VanAresistance determinant. The isolates were also resistant to
erythromycin, benzylpenicillin, rifampicin, and ampicillin, butsusceptible to chloramphenicol. Total DNA restriction patterns ofthe two isolates were compared.2 Four different restriction enzymeswere used, Sstl, SaIl, PvuII, and BscI, cutting the DNA atdifferent frequencies. In all cases the two isolates produced identicalpatterns, which were different from a reference strain (NCTC 8174)and another clinical isolate of E durans.
Isolates from the two renal transplant patients were thereforeindistinguishable, leading us to conclude that the organism hadspread within the unit. Fortunately no further isolates of this strainhave been identified, nor were vancomycin-resistant enterococciisolated during a previous survey in this hospital (M. Guiney and G.Urwin).This incident emphasises that vancomycin resistance can occur in
enterococcal species other than E faecium, that the organisms canspread between patients, and that effective antimicrobial treatmentof enterococcal infections is being severely threatened by acquiredresistance determinants.
We thank B. Duke, M. Guiney, and the staff of the Royal London HospitalMedical Microbiology Department.
Department of Medical Microbiology,London Hospital Medical College,London E1 2AD, UK
L. M. C. HALLH. Y. CHENR. J. WILLIAMS
1. Anon. Vancomycin-resistant enterococci. Commun Dis Rep 1992; 2: 121.2. Hall LMC, Duke B, Guiney M, Williams R. Typing of Enterococcus species by DNA
restriction fragment analysis. J Clin Microbiol 1992; 30: 915-19.
Thrombolysis with recombinant tissue-typeplasminogen activator in renal venous
thrombosis in infancySIR,-Bilateral renal venous thrombosis in infancy frequently
leads to chronic renal failure,’ and thrombectomy or fibrinolytictherapy with streptokinase and urokinase has been successful inboth adults and infants.2,3 We present our results in eight babieswith renal venous thrombosis (bilateral, n = 4; uni-lateral and venacava, n = 3; renal veins, vena cava, and aorta, n = 1) treated withrecombinant tissue-type plasminogen activator (rt-PA). In thesepatients, all treated with neonatal resuscitation, thrombosisfollowed the placement of vascular catheters, sepsis, haemolytic-uraemic syndrome, exsiccosis, fetopathia diabetica, or heterozygousantithrombin III and protein C deficiency.
48 h after the initial clinical symptoms (oliguria, haematuria,hypertension) diagnostic procedures including duplex ultrasoundwere done and rt-PA started at 0-1-0-2 mg/kg over 10 min withadditional continuous rt-PA infusion and low-dose heparin.Individual rt-PA doses, the duration and complications of therapy,and the final outcome (mean observation period, 9 [7-48] months)are shown in the table. To avoid reocclusion when rt-PA infusionwas ended, heparin infusion was enhanced and substitution withantithrombin III concentrate began.4
PATIENTS’ DETAILS
*Patient 6 had normal bleeding and perforative duodenitis on day 1 and afterwards,respectively
During rt-PA therapy we saw no decrease in fibrinogen orplasminogen concentrations as a sign of systemic fibrinolyticactivation induced by rt-PA. Five infants had renal recovery(normal creatinine clearance, normal radiological and radionuclideimaging). Complications of the basic disease led to death in onepreterm infant 2 weeks after successful thrombolysis. In one patientheparinisation after complete reperfusion was ineffective; partialreocclusion with an atrophic kidney occurred during follow up.Because of the severity of the basic disease in patient 6, rt-PA 9
mg/kg per day was necessary5 to achieve reperfusion of the aorta andrenal veins while peritoneal dialysis was done. Later rt-PA therapywas stopped because of intra-abdominal bleeding due to perforativeduodenitis. This patient is undergoing further peritoneal dialysis athome 8 months after thrombolysis. No other severe side-effects (eg,cerebral intraventricular bleedings) occurred.We believe thrombolytic therapy with rt-PA in infants with renal
venous thrombosis is a logical therapeutic regimen because promptlysis of renal venous thrombosis may prevent or minimise loss ofrenal function, especially when there is bilateral occlusion, andbecause of the short half-life, less systemic fibrinolytic activationand local enhancement of plasminogen concentration, which isimportant in infants with physiologically reduced plasminogenconcentrations."
Department of Haematology and Oncology,Centre for Paediatrics,Klinikum der J W Goethe-Universitat,6000 Frankfurt/Main, Germany
U. NOWAK-GÖTTLD. SCHWABEW. SCHNEIDERR. SCHLÖSSERW. KREUZ
1. Stapleton FB, Jones DP, Green RS. Acute renal failure in neonates: incidence, etiologyand outcome. Pediatr Nephrol 1987; 1: 314-20.
2. Bromberg WD, Firlit CF. Fibrinolytic therapy for renal vein thrombosis in the child.J Urol 1990; 143: 86-88.
3. Pritchard SL, Culham JAG, Rodgers PCJ. Low-dose fibrinolytic therapy in infants.J Pediatr 1985; 106: 594-98.
4. Egbring R, Seitz R, Behling T, Bethke C. Die Prophylaxe von Reocclusion vonInfarktegafäßen nach intrakoronarer Thrombolyse: Einfluß von AntithrombinIII? Hamostaseologie 1988; 9: 3-7.
5. Levy M, Benson LN, Burrows PE, et al. Tissue plasminogen activator for thetreatment of thromboembolism in infants and children. J Pediatr 1991; 118:476-72.
6. Nieuwenhuizen W, Verheijen TH, Vermond A, Chang GTG. Plasminogen activationby tissue activator is accelerated in the presence of fibrinogen cyanogen bromidefragment FCB-2. Biochim Biophys Acta 1983; 755: 531-33.
7. Seifried E, Transwell P, Rijken DC, Barett-Bergshoeff MM, Capf SU, Kluft C.Pharmacokinetics of antigen and activity of recombinant tissue-type plasminogenactivator after infusion in healthy volunteers. Drug Res 1988; 38: 418-22.
8. Andrew M. Development of the hemostatic system in the neonate and young infant.Am J Pediatr Hematol Oncol 1990; 12: 95-104.
