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Screening patients for glycopeptide-resistant enterococci
226
Letters
Finally, we agree that training care is of the utmost importance.
to the Editor
and updating
S. V. Goddard R. P. D. Cooke
of staff involved
in PVC
Departments of Infection Control and Medical Microbiology, District General Hospital, Kings Drive, Eastbourne, East Sussex, BN21 ZLY, UK References
1. Nelson RRS, Tebbs SE, Richards N, Elliott TSJ. An audit of peripheral catheter care in a teaching hospital. r Hosp Infect 1996; 32: 65-69. 2. Elliott TSJ. Successful IV Therapy. Sweden: Viggo Spectramed 1991. 3. Wille JC, Blusst van Oud Alblas A, Thewessen APM. A comparison of two film-type dressings in central venous therapy. J Hasp Infect 1993; 23: 113-l 21.
Sir, Screening patients for glycopeptide-resistant
enterococci
In a recent article Dr Wade and colleagues described the emergence of multiply-resistant enterococci on a liver unit’ and presented some interesting data on screening for carriage of vancomycin-resistant enterococci (VRE) at different body sites. Because these organisms continue to emerge in our most severely ill hospitalized patients, and following the recent publication of guidelines in which patient screening is advocated,2 efficient screening protocols need to be determined. We wish to present data in relation to screening patients with renal and haematological diseases in Salford during an outbreak of colonization by Enterococcus faecium of the VanA phenotype. Screening of patients on the renal/haematology ward and the renal unit was performed twice at an interval of one week. All specimens were plated directly onto 100 mg/L neomycin blood agar and MacConkey agar and enriched for five days in nutrient broth containing 10 mg/L nalidixic acid. Broths were subcultured onto neomycin and MacConkey agars. Presumptive enterococci were characterized by standard laboratory methods and glycopeptide sensitivities were determined by the Stokes method. Results for individuals who had a ‘full screen’ taken (nose, throat, axilla, hands, faeces/perineum/rectum) are shown in Table I. Most patients had additional cultures of urine and lesions. In the first screen 19/77 patients had VRE detected at one or more sites. In the second screen 14/40 individuals were found to be colonized. In each screen five patients were positive by enrichment culture only. However, this does not necessarily imply that enrichment cultures are required in screening as 50 mg/L
Letters Table
I. Detection
of VRE
carriage
at different
227 sites in colonized
1st screen (N= 19) No. of patients positive at site (%)
Site(s) Perineum + urine + faeces/ rectal swab Perineum + faeces/rectal swab Faeces/rectal swab* Perineum* Urine” Vaginal swab* Hands Throat Nose Axilla * Denotes sole site of isolation ND, not done.
to the Editor
13/14 13/15 11/17 ‘i/17
(93) (87) (65) (41)
:::t “,g 2/18 (11) l/17 (5.9) l/19 (5.3) O/l9 (0)
patients
2nd screen (N= 14) No. of patients positive at site (%)
ll/ll 13/14 11/14 9/14 5/11
(100) (93) (79) (64) (45)
2,1:74) 2/14 (14) 2/14 (14) 2/14 (14)
in at least one patient.
neomycin agar has been shown to inhibit the growth of some isolates of VRE in the absence of enrichment3 and alternative media are available. No VRE were detected on MacConkey agar alone from any specimen. Most colonized patients could have been detected by culture of a perineal swab and faeces (or a rectal swab); this approach, plus examination of relevant clinical specimens for VRE infection, may provide an adequate screen.4 However, sensitivity could be usefully increased by additional screening of urine, probably by an enrichment method. No colonized patients would have been overlooked using our laboratory methods by omitting nose, throat, axilla, lesions (data not shown) or hand swabs. Routine screening of these sites would increase costs and is unlikely to be worthwhile for infection control purposes. P. R. Chadwick* J. Elliot P. Rowland M. G. L. Keaney L. A. Joseph
“Department of Microbiology, North Manchester General Hospital, Manchester, M8 6RB, UK Department of Microbiology, Hope Hospital, Salford M6 8HD, UK References
1. Wade JJ. The emergence of Enterococcus faecium resistant standard agents-a preliminary report. J Nosp Infect, 1995; 2. Hospital Infection Control Practices Advisory Committee. venting the spread of vancomycin resistance. Infect Control 105-113. 3. Chadwick PR, Oppenhein BA. Neomycin blood agar as a comycin-resistant Enterococcus faecium. J Clin Pathol, 1995;
to glycopeptides and other 30 (Suppl): 483-493 Recommendations for preHosp Epidemiol, 1995; 16: selective medium 48: 106X-1070.
for
van-
228
Letters
4. Yamaguchi E, Valena vancomycin-resistant
F, Smith Enterococcus
to the Editor
SM, Simmons A, Eng RHK. faecium. Am J Infect Control,
Colonisation pattern 1994; 22: 202-206.
of
Sir, Laboratory
acquired
verotoxin
producing infection
Escherichia
coli
(VTEC)
Verotoxin-producing Escherichia coli (VTEC) have emerged as a significant public health problem in the UK. Between 1990 and 1993 the annual incidences of infections with VTEC in England, Scotland and Wales have ranged from 0.5 to 4.0 cases per 100 000 population. Clinical manifestations of the infection range from mild diarrhoea to life threatening haemorrhagic colitis. Haemolytic uraemic syndrome (HUS) develops in 2-7% of the patients, and is particularly common in children.’ The commonest VTEC responsible for human infections is E. coli 0157: H7. Diagnosis of this infection is mainly by culture of E. coli 0157:H7 from faeces of infected patients. Such tests are performed routinely in most microbiology laboratories in the UK. Although the risk of acquiring infections is inherent in handling infected material in a microbiology laboratory, introduction of many safe practices has resulted in such accidents happening only rarely. In this letter we report a serious laboratory acquired infection with E. coli 0157:H7 in a laboratory worker. In the light of this and two other previously published reports, we propose that the hazard category of this organism is re-examined.2’3 A 40-year-old male microbiology laboratory worker presented in the casualty department at the Lewisham Hospital, London with symptoms of severe bloody diarrhoea of 12 h duration. On examination, he was pale, pyrexial (39.5’C) and dehydrated. The abdomen was diffusely tender without evidence of peritonism. Abdominal X-ray demonstrated a total colitis but no toxic dilatation. Sigmoidoscopy confirmed the presence of a uniform, haemorrhagic proctitis. There was no laboratory evidence of intravascular haemolysis or renal failure. The patient was rehydrated and empirical therapy was commenced with ciprofloxacin 500 mg twice daily. On the following day, cultures of faecal specimens yielded a heavy growth of E. coli 0157 which was sensitive to ciprofloxacin. The patient improved over the next few days, and was asymptomatic at the time of discharge. Detailed questioning revealed that he had been working until three days previously with E. coli 0157 isolates in a laboratory in Scotland which was involved in the investigation of an outbreak of VTEC infection. Because the onset of illness was within the incubation period (one to six days), the laboratory was contacted to explore the possibility of laboratory acquired infection.
Letters
Finally, we agree that training care is of the utmost importance.
to the Editor
and updating
S. V. Goddard R. P. D. Cooke
of staff involved
in PVC
Departments of Infection Control and Medical Microbiology, District General Hospital, Kings Drive, Eastbourne, East Sussex, BN21 ZLY, UK References
1. Nelson RRS, Tebbs SE, Richards N, Elliott TSJ. An audit of peripheral catheter care in a teaching hospital. r Hosp Infect 1996; 32: 65-69. 2. Elliott TSJ. Successful IV Therapy. Sweden: Viggo Spectramed 1991. 3. Wille JC, Blusst van Oud Alblas A, Thewessen APM. A comparison of two film-type dressings in central venous therapy. J Hasp Infect 1993; 23: 113-l 21.
Sir, Screening patients for glycopeptide-resistant
enterococci
In a recent article Dr Wade and colleagues described the emergence of multiply-resistant enterococci on a liver unit’ and presented some interesting data on screening for carriage of vancomycin-resistant enterococci (VRE) at different body sites. Because these organisms continue to emerge in our most severely ill hospitalized patients, and following the recent publication of guidelines in which patient screening is advocated,2 efficient screening protocols need to be determined. We wish to present data in relation to screening patients with renal and haematological diseases in Salford during an outbreak of colonization by Enterococcus faecium of the VanA phenotype. Screening of patients on the renal/haematology ward and the renal unit was performed twice at an interval of one week. All specimens were plated directly onto 100 mg/L neomycin blood agar and MacConkey agar and enriched for five days in nutrient broth containing 10 mg/L nalidixic acid. Broths were subcultured onto neomycin and MacConkey agars. Presumptive enterococci were characterized by standard laboratory methods and glycopeptide sensitivities were determined by the Stokes method. Results for individuals who had a ‘full screen’ taken (nose, throat, axilla, hands, faeces/perineum/rectum) are shown in Table I. Most patients had additional cultures of urine and lesions. In the first screen 19/77 patients had VRE detected at one or more sites. In the second screen 14/40 individuals were found to be colonized. In each screen five patients were positive by enrichment culture only. However, this does not necessarily imply that enrichment cultures are required in screening as 50 mg/L
Letters Table
I. Detection
of VRE
carriage
at different
227 sites in colonized
1st screen (N= 19) No. of patients positive at site (%)
Site(s) Perineum + urine + faeces/ rectal swab Perineum + faeces/rectal swab Faeces/rectal swab* Perineum* Urine” Vaginal swab* Hands Throat Nose Axilla * Denotes sole site of isolation ND, not done.
to the Editor
13/14 13/15 11/17 ‘i/17
(93) (87) (65) (41)
:::t “,g 2/18 (11) l/17 (5.9) l/19 (5.3) O/l9 (0)
patients
2nd screen (N= 14) No. of patients positive at site (%)
ll/ll 13/14 11/14 9/14 5/11
(100) (93) (79) (64) (45)
2,1:74) 2/14 (14) 2/14 (14) 2/14 (14)
in at least one patient.
neomycin agar has been shown to inhibit the growth of some isolates of VRE in the absence of enrichment3 and alternative media are available. No VRE were detected on MacConkey agar alone from any specimen. Most colonized patients could have been detected by culture of a perineal swab and faeces (or a rectal swab); this approach, plus examination of relevant clinical specimens for VRE infection, may provide an adequate screen.4 However, sensitivity could be usefully increased by additional screening of urine, probably by an enrichment method. No colonized patients would have been overlooked using our laboratory methods by omitting nose, throat, axilla, lesions (data not shown) or hand swabs. Routine screening of these sites would increase costs and is unlikely to be worthwhile for infection control purposes. P. R. Chadwick* J. Elliot P. Rowland M. G. L. Keaney L. A. Joseph
“Department of Microbiology, North Manchester General Hospital, Manchester, M8 6RB, UK Department of Microbiology, Hope Hospital, Salford M6 8HD, UK References
1. Wade JJ. The emergence of Enterococcus faecium resistant standard agents-a preliminary report. J Nosp Infect, 1995; 2. Hospital Infection Control Practices Advisory Committee. venting the spread of vancomycin resistance. Infect Control 105-113. 3. Chadwick PR, Oppenhein BA. Neomycin blood agar as a comycin-resistant Enterococcus faecium. J Clin Pathol, 1995;
to glycopeptides and other 30 (Suppl): 483-493 Recommendations for preHosp Epidemiol, 1995; 16: selective medium 48: 106X-1070.
for
van-
228
Letters
4. Yamaguchi E, Valena vancomycin-resistant
F, Smith Enterococcus
to the Editor
SM, Simmons A, Eng RHK. faecium. Am J Infect Control,
Colonisation pattern 1994; 22: 202-206.
of
Sir, Laboratory
acquired
verotoxin
producing infection
Escherichia
coli
(VTEC)
Verotoxin-producing Escherichia coli (VTEC) have emerged as a significant public health problem in the UK. Between 1990 and 1993 the annual incidences of infections with VTEC in England, Scotland and Wales have ranged from 0.5 to 4.0 cases per 100 000 population. Clinical manifestations of the infection range from mild diarrhoea to life threatening haemorrhagic colitis. Haemolytic uraemic syndrome (HUS) develops in 2-7% of the patients, and is particularly common in children.’ The commonest VTEC responsible for human infections is E. coli 0157: H7. Diagnosis of this infection is mainly by culture of E. coli 0157:H7 from faeces of infected patients. Such tests are performed routinely in most microbiology laboratories in the UK. Although the risk of acquiring infections is inherent in handling infected material in a microbiology laboratory, introduction of many safe practices has resulted in such accidents happening only rarely. In this letter we report a serious laboratory acquired infection with E. coli 0157:H7 in a laboratory worker. In the light of this and two other previously published reports, we propose that the hazard category of this organism is re-examined.2’3 A 40-year-old male microbiology laboratory worker presented in the casualty department at the Lewisham Hospital, London with symptoms of severe bloody diarrhoea of 12 h duration. On examination, he was pale, pyrexial (39.5’C) and dehydrated. The abdomen was diffusely tender without evidence of peritonism. Abdominal X-ray demonstrated a total colitis but no toxic dilatation. Sigmoidoscopy confirmed the presence of a uniform, haemorrhagic proctitis. There was no laboratory evidence of intravascular haemolysis or renal failure. The patient was rehydrated and empirical therapy was commenced with ciprofloxacin 500 mg twice daily. On the following day, cultures of faecal specimens yielded a heavy growth of E. coli 0157 which was sensitive to ciprofloxacin. The patient improved over the next few days, and was asymptomatic at the time of discharge. Detailed questioning revealed that he had been working until three days previously with E. coli 0157 isolates in a laboratory in Scotland which was involved in the investigation of an outbreak of VTEC infection. Because the onset of illness was within the incubation period (one to six days), the laboratory was contacted to explore the possibility of laboratory acquired infection.