1
446 4 of the E faecium isolates were from patients on the same paediatric oncology ward and 4 (3 children, 1 adult) were from liver transplant recipients on different wards. Enterococci were the most common blood culture isolates from liver transplant recipients in our hospital from 1975 to 1990; Efaecium accounted for half of such isolates. Although cross-infection with HLGR Efaecalis has been described previously,2 lack of an effective and available typing method for E faecium limited our investigation of the relation between isolates. However, as judged by plasmid analysis, the 4 isolates from patients on the paediatric oncology ward were indistinguishable but were not the same as those from liver transplant patients. Also, on the basis of plasmid content there were at least two types among the 4 isolates from liver transplant patients. All the isolates from paediatric oncology patients had streptomycin MICs of 32-64 mg/1, whereas the isolates from the liver transplant patients were highly resistant (MIC > 2000 mg/1) to streptomycin. Streptomycin susceptibility (which Woodford et al did not report) may be a useful epidemiological marker and, if isolates are not highly resistant to streptomycin, the agent might be useful therapeutically.3 Wade et al described HLGR Efaecium in liver transplant patients at King’s College Hospital (KCH), London. We first detected HLGR E faecium on Dec 27, 1989, in a patient who had been transferred from KCH to Addenbrooke’s Hospital on Dec 21,1989, as part of the paediatric liver transplant programme, which at that time was conducted jointly by the two hospitals. The patient was subsequently transferred back to KCH at the end of January, 1990. Although we cannot be sure where the strain originated, national and international interhospital transfer to tertiary referral units are likely to lead to the introduction of HLGR Efaecium. Similarly, methicillin-resistant Staphylococcus aureus was introduced to the two hospitals during the same transplant programme. HLGR in Efaecium may not be as uncommon as the lack of European reports would suggest, which may reflect the fact that not all laboratories speciate clinically significant enterococci or test for HLGR. Clinical Microbiology and Public Health Laboratory, Addenbrooke’s Hospital, Cambridge CD2 2QW, UK RICHARD BENDALL ROD WARREN DEREK BROWN 1. Spiegel CA. Laboratory detection of high-level aminoglycoside-aminocyclitol resistance m Enterococcus spp. J Clin Microbiol 1988; 26: 2270-74. 2 Zervos MJ, Dembinski S, Mibesell T, Schaberg DR High-level resistance to gentamicin in Streptococcus faecalis: risk factors and evidence for exogenous acquisition of infection. J Infect Dis 1986, 153: 1075-83. 3. Nachamkin I, Axelrod P, Talbot GH, et al. Multipy high-level-aminoglycoside- resistant enterococci from patients in a university hospital. J Clin Microbiol 1988; 26: 1287-91. Increased community-acquired septicaemic infection with group B streptococci in adults SiR,--Group B streptococci are recognised pathogens in non- pregnant adults, but septicaemic infections such as endocarditis are unusual, and only one case of metastatic endophthalmitis with this organism seems to have been reported.1 In many, but not all, reported cases of group B streptococcal septicaemia, underlying conditions, especially diabetes, malignant disease, and liver failure and/or alcohol abuse, have been present.2 We have noted a striking increase in septicaemic group B streptococcal infection in adults, and to monitor this and investigate the implicated strains, two of us (S. J. E. and S. E. J. Y.) have been following cases in England and Wales since July, 1990. Preliminary findings confirm an increase in these infections. After 9 months, we have received reports of 16 patients with endocarditis (3 with metastatic endophthalmitis), who accounted for 4% of all cases of endocarditis reported to the Public Health Laboratory Service Communicable Disease Surveillance Centre (CDSC) during this period, together with 1 case of metastatic endophthalmitis plus septic arthritis and 1 case of vertebral osteomyelitis. In an investigation during 1981 and 1982 of endocarditis by the Medical Services Study Group of the Royal College of Physicians there were only 3 patients with group B streptococcal infections, accounting for 0-5% of the 544 episodes. At St Thomas’ Hospital we have seen 10 patients with group B streptococcal endocarditis since 1970, and 5 of them have presented in the past 18 months. Data from CDSC (S. E. J. Y.) show that the number of adults (over 15 years) with group B streptococcal bacteraemia reported per year has steadily increased since 1975, but the proportion of all reported adults with bacteraemia caused by this organism has only increased from 0-6% (29/4871) in 1975 to 1.0% (322/32 270) in 1990, with no detectable recent increase. However, these data include all adults with group B bacteraemia (including puerperal women) and not merely those with serious invasive infection. Typing of the group B streptococci from these septicaemic infections (BDC) has not shown a predominant type, but type III strains, so common in neonatal infections, are seldom seem. Detailed investigation of the isolates is proceeding. Why has the frequency of these infections increased? And are they confmed to the UK? We would ask colleagues (both in the UK and elsewhere) who encounter such patients to report them to us at CDSC and to submit the strains (and patients’ serum if possible) to the Division of Hospital Infection, for typing and further investigation. Microbiology Department, St Thomas’ Hospital, London SE1 7EH, UK SUSANNAH J. EYKYN Communicable Disease Surveillance Centre, Colindale, London NW9 SUSAN E. J. YOUNG Division of Hospital Infection, Central Public Health Laboratory, Colindale, London NW9 BARRY D. COOKSON 1. Farber BP, Weinbaum DL, Dummer JS. Metastatic bacterial endophthalmitis. Arch Intern Med 1985; 145: 62-64. 2. Edwards MS, Baker CJ. Streptococcus agalactiae (group B streptococcus). In: Mandell GL, Douglas RG, Bennett JE, eds. Principles and practice of infectious diseases. New York: Churchill Livingstone, 1990: 1554-63. 3. Bayliss R, Clarke C, Oakley CM, et al. The microbiology and pathogenesis of infective endocarditis. Br Heart J 1983; 50: 513-19. Complete nerve deafness after abuse of co-proxamol SiR,—A 44-year-old woman was admitted to hospital with a 4-month history of increasing deafness and weight loss (she weighed 30 kg on admission). Over the previous 4 years she had noticed intermittent episodes of deafness; tinnitus developed a week before admission. Pyoderma gangrenosum had developed 8 years earlier but no underlying cause for it had been found. Audiological tests confirmed severe bilateral sensorineural deafness. A family member disclosed that the patient had been prescribed ’Distalgesic’ (co-proxamol: dextropropoxyphene plus paracetamol) as analgesia for abdominal adhesions after salpingo-oophorectomy 20 years earlier and had continued to take it since then. She obtained the drug by persistently asking for a prescription from her general practitioner, by using a friend’s prescription, and by taking tablets from the drug supply in the unit in which she worked. Normally she took about four co-proxamol tablets daily but in the months during which the deafness had become more severe she had increased her usage to thirty tablets, partly because of pain from her pyoderma ulcers and partly through an inability to control tablet intake. Just before the admission she had obtained 2000 tablets. Paracetamol was found in her blood while she was in hospital. The nurses observed self-induced vomiting and laxative purgation by the patient, and she had excoriations over the knuckles of her right hand from this practice. She admitted to the vomiting and purgation. 20 years earlier she had perceived herself as overweight and had dieted. Her body mass index was 12.7 7 kg/m (healthy range 20-25), confirming anorexia nervosa. As she increased her co-proxamol intake the deafness worsened and her eating disorder de-stabilised. She could not stop losing weight because she was so upset by her deafness. The patient has gained 10 kg while on a specialist eating disorder unit. Psychotherapy has proved difficult because of her total deafness. She has stopped abusing co-proxamol, methadone being the withdrawal agent. Her skin ulcers improved greatly with her weight gain.

Increased community-acquired septicaemic infection with group B streptococci in adults

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4 of the E faecium isolates were from patients on the samepaediatric oncology ward and 4 (3 children, 1 adult) were from livertransplant recipients on different wards. Enterococci were the mostcommon blood culture isolates from liver transplant recipients inour hospital from 1975 to 1990; Efaecium accounted for half of suchisolates. Although cross-infection with HLGR Efaecalis has beendescribed previously,2 lack of an effective and available typingmethod for E faecium limited our investigation of the relationbetween isolates. However, as judged by plasmid analysis, the 4isolates from patients on the paediatric oncology ward wereindistinguishable but were not the same as those from liver

transplant patients. Also, on the basis of plasmid content there wereat least two types among the 4 isolates from liver transplant patients.All the isolates from paediatric oncology patients had streptomycinMICs of 32-64 mg/1, whereas the isolates from the liver transplantpatients were highly resistant (MIC > 2000 mg/1) to streptomycin.Streptomycin susceptibility (which Woodford et al did not report)may be a useful epidemiological marker and, if isolates are nothighly resistant to streptomycin, the agent might be useful

therapeutically.3Wade et al described HLGR Efaecium in liver transplant patients

at King’s College Hospital (KCH), London. We first detectedHLGR E faecium on Dec 27, 1989, in a patient who had beentransferred from KCH to Addenbrooke’s Hospital on Dec 21,1989,as part of the paediatric liver transplant programme, which at thattime was conducted jointly by the two hospitals. The patient wassubsequently transferred back to KCH at the end of January, 1990.Although we cannot be sure where the strain originated, nationaland international interhospital transfer to tertiary referral units arelikely to lead to the introduction of HLGR Efaecium. Similarly,methicillin-resistant Staphylococcus aureus was introduced to thetwo hospitals during the same transplant programme.HLGR in Efaecium may not be as uncommon as the lack of

European reports would suggest, which may reflect the fact that notall laboratories speciate clinically significant enterococci or test forHLGR.

Clinical Microbiologyand Public Health Laboratory,

Addenbrooke’s Hospital,Cambridge CD2 2QW, UK

RICHARD BENDALLROD WARRENDEREK BROWN

1. Spiegel CA. Laboratory detection of high-level aminoglycoside-aminocyclitolresistance m Enterococcus spp. J Clin Microbiol 1988; 26: 2270-74.

2 Zervos MJ, Dembinski S, Mibesell T, Schaberg DR High-level resistance to

gentamicin in Streptococcus faecalis: risk factors and evidence for exogenousacquisition of infection. J Infect Dis 1986, 153: 1075-83.

3. Nachamkin I, Axelrod P, Talbot GH, et al. Multipy high-level-aminoglycoside-resistant enterococci from patients in a university hospital. J Clin Microbiol 1988;26: 1287-91.

Increased community-acquired septicaemicinfection with group B streptococci in

adults

SiR,--Group B streptococci are recognised pathogens in non-pregnant adults, but septicaemic infections such as endocarditis areunusual, and only one case of metastatic endophthalmitis with thisorganism seems to have been reported.1 In many, but not all,reported cases of group B streptococcal septicaemia, underlyingconditions, especially diabetes, malignant disease, and liver failureand/or alcohol abuse, have been present.2We have noted a striking increase in septicaemic group B

streptococcal infection in adults, and to monitor this and investigatethe implicated strains, two of us (S. J. E. and S. E. J. Y.) have beenfollowing cases in England and Wales since July, 1990. Preliminaryfindings confirm an increase in these infections. After 9 months, wehave received reports of 16 patients with endocarditis (3 withmetastatic endophthalmitis), who accounted for 4% of all cases ofendocarditis reported to the Public Health Laboratory ServiceCommunicable Disease Surveillance Centre (CDSC) during thisperiod, together with 1 case of metastatic endophthalmitis plusseptic arthritis and 1 case of vertebral osteomyelitis. In an

investigation during 1981 and 1982 of endocarditis by the MedicalServices Study Group of the Royal College of Physicians there wereonly 3 patients with group B streptococcal infections, accounting for

0-5% of the 544 episodes. At St Thomas’ Hospital we have seen 10patients with group B streptococcal endocarditis since 1970, and 5of them have presented in the past 18 months.

Data from CDSC (S. E. J. Y.) show that the number of adults(over 15 years) with group B streptococcal bacteraemia reported peryear has steadily increased since 1975, but the proportion of allreported adults with bacteraemia caused by this organism has onlyincreased from 0-6% (29/4871) in 1975 to 1.0% (322/32 270) in1990, with no detectable recent increase. However, these datainclude all adults with group B bacteraemia (including puerperalwomen) and not merely those with serious invasive infection.Typing of the group B streptococci from these septicaemic

infections (BDC) has not shown a predominant type, but type IIIstrains, so common in neonatal infections, are seldom seem.Detailed investigation of the isolates is proceeding.Why has the frequency of these infections increased? And are

they confmed to the UK? We would ask colleagues (both in the UKand elsewhere) who encounter such patients to report them to us atCDSC and to submit the strains (and patients’ serum if possible) tothe Division of Hospital Infection, for typing and further

investigation.Microbiology Department,St Thomas’ Hospital,London SE1 7EH, UK SUSANNAH J. EYKYNCommunicable Disease Surveillance Centre,Colindale, London NW9 SUSAN E. J. YOUNGDivision of Hospital Infection,Central Public Health Laboratory,Colindale, London NW9 BARRY D. COOKSON

1. Farber BP, Weinbaum DL, Dummer JS. Metastatic bacterial endophthalmitis. ArchIntern Med 1985; 145: 62-64.

2. Edwards MS, Baker CJ. Streptococcus agalactiae (group B streptococcus). In: MandellGL, Douglas RG, Bennett JE, eds. Principles and practice of infectious diseases.New York: Churchill Livingstone, 1990: 1554-63.

3. Bayliss R, Clarke C, Oakley CM, et al. The microbiology and pathogenesis of infectiveendocarditis. Br Heart J 1983; 50: 513-19.

Complete nerve deafness after abuse ofco-proxamol

SiR,—A 44-year-old woman was admitted to hospital with a4-month history of increasing deafness and weight loss (she weighed30 kg on admission). Over the previous 4 years she had noticedintermittent episodes of deafness; tinnitus developed a week beforeadmission. Pyoderma gangrenosum had developed 8 years earlierbut no underlying cause for it had been found. Audiological testsconfirmed severe bilateral sensorineural deafness.A family member disclosed that the patient had been prescribed

’Distalgesic’ (co-proxamol: dextropropoxyphene plus paracetamol)as analgesia for abdominal adhesions after salpingo-oophorectomy20 years earlier and had continued to take it since then. She obtainedthe drug by persistently asking for a prescription from her generalpractitioner, by using a friend’s prescription, and by taking tabletsfrom the drug supply in the unit in which she worked. Normally shetook about four co-proxamol tablets daily but in the months duringwhich the deafness had become more severe she had increased her

usage to thirty tablets, partly because of pain from her pyodermaulcers and partly through an inability to control tablet intake. Justbefore the admission she had obtained 2000 tablets. Paracetamolwas found in her blood while she was in hospital.The nurses observed self-induced vomiting and laxative

purgation by the patient, and she had excoriations over the knucklesof her right hand from this practice. She admitted to the vomitingand purgation. 20 years earlier she had perceived herself as

overweight and had dieted. Her body mass index was 12.7 7 kg/m(healthy range 20-25), confirming anorexia nervosa.As she increased her co-proxamol intake the deafness worsened

and her eating disorder de-stabilised. She could not stop losingweight because she was so upset by her deafness.The patient has gained 10 kg while on a specialist eating disorder

unit. Psychotherapy has proved difficult because of her totaldeafness. She has stopped abusing co-proxamol, methadone beingthe withdrawal agent. Her skin ulcers improved greatly with herweight gain.