156 was isolated. On routine testing this found to be resistant to chloramphenicol and tetracycline, and the zone of inhibition round the penicillin disc (1-55 units) was reduced from the expected 10 mm to 7 mm, measured radially from the edge of the disc. By the agar dilution method, using a minimal-growth endpoint, the minimum inhibitory concentration (M.LC.) of penicillin was 0-25 {j.g/ml compared with an mt.i.c. of 0-03 g4nl for a sensitive strain. The M.i.c.s of tetracycline and chloramphenicol were both 20 g/ml. The inoculum used in these tests was about 106 organisms. Although this pneumococcus almost certainly was not indigenous to the U.K. its isolation makes it necessary for those treating serious pneumococcal disease to be aware that multiply resistant strains of the organism are close to, if not already on, our shores. A patient with a pneumococcal meningitis due to a strain with the M.i.c.s reported would be unlikely to respond adequately to treatment with penicillin’ or chloramphenicol.3 In respect of the treatment of such an infection we would add that its ampicillin M.i.c. was 0.15 ug/mi compared with 0.07 for a penicillin-sensitive strain; however, experience elsewhere3 has shown that much higher M.i.cs may be found. It has been said that testing pneumococci with high-concentration discs prevents the detection of significant penicillin resistance.4,5Although we use low-concentration discs, the zone of inhibition round an 8 unit tablet (’Neo-sensitabs’, A/S Rosco, Denmark) with the strain reported was reduced from a radius measured from the edge of the disc of 14 mm for a sensitive strain, to 10 mm.
23, Danish nomenclature)
was
We thank Dr M. T. Parker for
typing
the strain.
Public Health Laboratory Plymouth General Hospital, Plymouth PL4 8NN
TRIMETHOPRIM-RESISTANT KLEBSIELLA AEROGENES
SIR,-Reports trimethoprim-resistant coliforms1,2z a comparison of trimethoprim resistance among prompted Klebsiella aerogenes strains isolated from patients in hospital and from patients seen in general practice. Between Nov. 1, 1977, and April 30, 1978, 200 strains of K. aerogenes were isolated in our laboratory from first urine specimens-142 from hospital inpatients or patients recently discharged from hospital and 58 from patients in general practice or hospital outpatients. Sensitivity to trimethoprim was determined by agar dilution, plates of DST agar containing 2 fLg/ml being inoculated with 1:100 dilutions of an overnight broth culture by a Denley multipoint inoculator; a control plate with no antibiotic was also inoculated. The plates were incubated at 370C for 18-24 h. Resistance to trimethoprim was detected in 46 (32%) of the hospital strains but in only 4 (6%) of the general practice or outpatient strains. The higher resistance-rate in hospital patients may be due to the greater use of co-trimoxazole in hospitals in Ayrshire than in the community. of
Microbiology Department, Ayrshire Central Hospital, Irvine KA12 8SS
ROSEMARY E. T. MCGILL
THROMBOSIS AND FACTOR-IX CONCENTRATES
SIR,-The development of clinical evidence of deep-vein a 63-year-old man with therapeutic fibrinolytic
thrombosis in 4. 5. 1. 2.
Hansman, D., Devitt, L., Riley, I. Br. med J. 1973, iii, 405. Dixon, J. M. S. Lancet, 1974, ii, 474. Marks, P. J., Bruten, D. M., Speller, D. C. E. Lancet, 1977, ii, 774. Brumfitt, W., Hamilton-Miller, J. M. T., Grey, D. ibid. p 926.
blockade 5 days after a prostatectomy would not surprise the average surgeon. Whilst Dr Machin and Dr Miller’ were right to report the thrombotic complication in their patient with haemophilia B, they were wrong to assume a causal relationship between it and the administration of Oxford factor-ix concentrate. The use of this concentrate had converted their patient to a non-haemophilic state, and there is no reason to believe that in that state he would be any less prone to postoperative thrombosis than anyone else. Northern Regional Hæmophilia Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP
Service,
PETER
JONES
ENVIRONMENTAL DEPRIVATION AND ENRICHMENT IN COMA
SIR,-In considering what role synaptic reinnervation in recovery of function after brain damage Galbraith et al .2 correlated the rate of synaptic reinnervation in rats with the rate of recovery from coma due to head injury in man. The two recovery patterns, graphically illustrated by Galbraith et al., resemble patterns of other recuperative processes-most notably, in the context of brain function, that of the "catch-up phenomenon". They also resemble condensed forms of familiar, normal patterns of developmental processes from birth to maturity. Both recovery and developmental processes are highly susceptible to environmental factors. The effects of enriched or impoverished environments on maturation and development of the intact young brain have been reviewed elsewhere.4 In the intact adult sensory deprivation soon causes widespread impairment of intellectual and perceptual processes accompanied by changes in cerebral electrical activity.5 When the brain has been physically injured we can draw on experience with adult rats experimentally brain damaged at birth, from which Schwartz6 concluded "... that the deleterious effects of neonatal brain damage can be significantly offset by an enriched environment". In the comatose patient, although the problem is primarily cerebral and only secondarily related to the surroundings, there is, in effect, a state of environmental deprivation. Even the stimuli provided by the early hours and days of the emergency and by intensive treatment and repeated neurological examinations are not sufficiently strong, frequent, or persistent to compensate for severe sensory impairments. Nevertheless, the rate and degree of recovery from coma, and, probably, of synaptic reinnervation, can often be importantly enhanced. At the Institutes for the Achievement of Human Potential (I.A.H.P.) experiments started before 1955 with intensively enriched environments in comatose children progressed so that by 1965 coma treatment procedures were sufficiently developed and results impressive enough to warrant organisation of a special coma team. The team designs and applies orderly and systematic I.A.H.P. programmes of environmental inputs through all five sensory pathways, at a frequency, intensity, and duration far above those in the usual hospital, institutional, or home environment. We present here a preliminary report of the first pilot study of these I.A.H.P. procedures in sixteen consecutive patients in severe coma, admitted to hospitals in Nassau County, N. W., unaffiliated to I.A.H.P. The study was done independently by one of us (M.D.D.) who is also unattached to I.A.H.P. All functional evaluations of patients were made on the Glasgow
might play
1. Machin, S J , Miller, B. R. Lancet, 1978, i, 1367. 2. Galbraith, S., Jennett, B., Raisman, G. Lancet, 1978, i, 710. 3. Tanner, J. M. Child Devel. 1973, 34, 817. 4. LeWinn, E. B. Human Neurological Organisation, Springfield, 1969. 5. Zubek, J. P., Wilgosh, L. Science, 1973, 140, 306. 6. Schwartz, S. J. comp. Physiol. Psychol. 1964, 57, 72.
Illinois,
23, Danish nomenclature)
was
We thank Dr M. T. Parker for
typing
the strain.
Public Health Laboratory Plymouth General Hospital, Plymouth PL4 8NN
TRIMETHOPRIM-RESISTANT KLEBSIELLA AEROGENES
SIR,-Reports trimethoprim-resistant coliforms1,2z a comparison of trimethoprim resistance among prompted Klebsiella aerogenes strains isolated from patients in hospital and from patients seen in general practice. Between Nov. 1, 1977, and April 30, 1978, 200 strains of K. aerogenes were isolated in our laboratory from first urine specimens-142 from hospital inpatients or patients recently discharged from hospital and 58 from patients in general practice or hospital outpatients. Sensitivity to trimethoprim was determined by agar dilution, plates of DST agar containing 2 fLg/ml being inoculated with 1:100 dilutions of an overnight broth culture by a Denley multipoint inoculator; a control plate with no antibiotic was also inoculated. The plates were incubated at 370C for 18-24 h. Resistance to trimethoprim was detected in 46 (32%) of the hospital strains but in only 4 (6%) of the general practice or outpatient strains. The higher resistance-rate in hospital patients may be due to the greater use of co-trimoxazole in hospitals in Ayrshire than in the community. of
Microbiology Department, Ayrshire Central Hospital, Irvine KA12 8SS
ROSEMARY E. T. MCGILL
THROMBOSIS AND FACTOR-IX CONCENTRATES
SIR,-The development of clinical evidence of deep-vein a 63-year-old man with therapeutic fibrinolytic
thrombosis in 4. 5. 1. 2.
Hansman, D., Devitt, L., Riley, I. Br. med J. 1973, iii, 405. Dixon, J. M. S. Lancet, 1974, ii, 474. Marks, P. J., Bruten, D. M., Speller, D. C. E. Lancet, 1977, ii, 774. Brumfitt, W., Hamilton-Miller, J. M. T., Grey, D. ibid. p 926.
blockade 5 days after a prostatectomy would not surprise the average surgeon. Whilst Dr Machin and Dr Miller’ were right to report the thrombotic complication in their patient with haemophilia B, they were wrong to assume a causal relationship between it and the administration of Oxford factor-ix concentrate. The use of this concentrate had converted their patient to a non-haemophilic state, and there is no reason to believe that in that state he would be any less prone to postoperative thrombosis than anyone else. Northern Regional Hæmophilia Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP
Service,
PETER
JONES
ENVIRONMENTAL DEPRIVATION AND ENRICHMENT IN COMA
SIR,-In considering what role synaptic reinnervation in recovery of function after brain damage Galbraith et al .2 correlated the rate of synaptic reinnervation in rats with the rate of recovery from coma due to head injury in man. The two recovery patterns, graphically illustrated by Galbraith et al., resemble patterns of other recuperative processes-most notably, in the context of brain function, that of the "catch-up phenomenon". They also resemble condensed forms of familiar, normal patterns of developmental processes from birth to maturity. Both recovery and developmental processes are highly susceptible to environmental factors. The effects of enriched or impoverished environments on maturation and development of the intact young brain have been reviewed elsewhere.4 In the intact adult sensory deprivation soon causes widespread impairment of intellectual and perceptual processes accompanied by changes in cerebral electrical activity.5 When the brain has been physically injured we can draw on experience with adult rats experimentally brain damaged at birth, from which Schwartz6 concluded "... that the deleterious effects of neonatal brain damage can be significantly offset by an enriched environment". In the comatose patient, although the problem is primarily cerebral and only secondarily related to the surroundings, there is, in effect, a state of environmental deprivation. Even the stimuli provided by the early hours and days of the emergency and by intensive treatment and repeated neurological examinations are not sufficiently strong, frequent, or persistent to compensate for severe sensory impairments. Nevertheless, the rate and degree of recovery from coma, and, probably, of synaptic reinnervation, can often be importantly enhanced. At the Institutes for the Achievement of Human Potential (I.A.H.P.) experiments started before 1955 with intensively enriched environments in comatose children progressed so that by 1965 coma treatment procedures were sufficiently developed and results impressive enough to warrant organisation of a special coma team. The team designs and applies orderly and systematic I.A.H.P. programmes of environmental inputs through all five sensory pathways, at a frequency, intensity, and duration far above those in the usual hospital, institutional, or home environment. We present here a preliminary report of the first pilot study of these I.A.H.P. procedures in sixteen consecutive patients in severe coma, admitted to hospitals in Nassau County, N. W., unaffiliated to I.A.H.P. The study was done independently by one of us (M.D.D.) who is also unattached to I.A.H.P. All functional evaluations of patients were made on the Glasgow
might play
1. Machin, S J , Miller, B. R. Lancet, 1978, i, 1367. 2. Galbraith, S., Jennett, B., Raisman, G. Lancet, 1978, i, 710. 3. Tanner, J. M. Child Devel. 1973, 34, 817. 4. LeWinn, E. B. Human Neurological Organisation, Springfield, 1969. 5. Zubek, J. P., Wilgosh, L. Science, 1973, 140, 306. 6. Schwartz, S. J. comp. Physiol. Psychol. 1964, 57, 72.
Illinois,
