LEAD FOIL ON WINE BOTTLES

1473

(MIC)

of 0-06

mg/L

After

a

total of 13

days’ topical mupirocin

therapy, further isolates of MRSA were obtained and the MIC to mupirocin had increased to 4 mg/l. By this time her lesions had healed except for a sacral erosion and the leg ulcer. Despite a further 8-day course of topical mupirocin we were unable to eradicate

carriage of MRSA (mupirocin MIC 16 mg/1). We felt it would be difficult to eradicate carriage of any Staph aureus until her skin had healed. 4 weeks after mupirocin was discontinued the patient was still colonised with mupirocin-resistant MRSA (MIC 16 mg/1). Rahman et al describe high-level mupirocin resistance (MIC 700 mg/1), probably plasmid-mediated and readily lost on sub-culture. The two key patients had received long-term therapy with mupirocin (1-9 months) for chronic skin disorders. Baird and Coia describe low-level mupirocin resistance (MIC 32-64 mg/1) in dermatology patients. The resistance appeared to be stable and led to treatment failure in two patients. This is in accord with in-vitro training of low-level mupirocin resistance (MIC 40 mg/1) in previously susceptible strains of Staph aureus.1 Low-level resistance to mupirocin after long-term treatment is perhaps not surprising, but our case suggests that in-vivo resistance can occur earlier than expected. Long-term therapy with mupirocin should probably be avoided, especially in patients with skin disorders which are not expected to resolve quickly. Department of Microbilogy, University College Hospital,

M. D. SMITH M. SANGHRAJKA

London WC1E 6AU

Department of Geriatrics, Middlesex Hospital,

S. LOCK

London 1. Casewell MW, Hill RLR. In-vitro activity of

mupirocin ("pseudomonic acid") against clinical isolates of Staphylococcus aureus. J Antimicrob Chemother 1985; 15: 523-31.

RESISTANCE TO

BETA-LACTAM/CLAVULANATE

SIR,-Dr Masterton and colleagues (Oct 24, p 975) report resistance to ’Timentin’ (ticarcillin plus potassium clavulanate) during treatment of Pseudomonas aeruginosa septicaemia. Resistance to this &bgr;-lactan/&bgr;-lactamase inhibitor combination seems to have been due to selection of a bacterial variant with unusual &bgr;-lactamase production. The &bgr;-lactamase seems to have been of the chromosomal type but resistance to &bgr;-lactam/ calvulanate combination is more likely to arise from plasmid &bgr;-lactamases. During the past six months an increasing number of amoxycillin/clavulanate or ticarcillin/clavulanate resistant Escherichia coli strains (minimum inhibitory concentration [MIC] 16-8 mg/l of amoxycillin + clavulanate) have appeared in at least two hospitals in Madrid. The frequency may be more than one-third of that for arrioxycillin-resistant E coli. We have studied five of these strains. All produced exclusively plasmid-mediated TEM-1 type &bgr;-lactamase, which proved to be normally inhbitied by potassium clavulanate in spectrophotometric assays. Resistance to amoxycillin/clavulanate was-transferable by conjugation or by transformation to the susceptible recipient strain E coli HB101. All resistant transconjugants or transformants produced from four to fifty times more TEM-1 &bgr;-lactamase than the same E coli HB101 strain harbouring the plasmid pMM4::Tn3, which contains a single TEM-1 gene. In two transconjugants the amount of TEM-1 &bgr;-lactamase was similar to the corresponding to the E coliHB101 strain harbouring the small plasmid pUC8 (more than 50 copies of the THM-1gene). This strain was highly resistant ’

MIC AND

&bgr;-LACTAMASE PRODUCTION OF E COLI HB101

TRANSFORMANTS CONTAINING PLASMIDS OF AMOXYCILLIN CLAVULANATE RESISTANT E COLI STRAINS

amoxycillin clavulanate, indicating the importance of the number of TEM-1 genes (or total amount of &bgr;-lactamase) in the pattern of resistance observed. In general, there was a good correlation between the amoxicyllin clavulanate MIC and the &bgr;-lactamase level of strains (table). Although other mechanisms of resistance to &bgr;-lactam clavulanate combinations are possible in E coli (eg, chromosomal or plasmid &bgr;-lactamases with decreased susceptibility to clavulanate) bacterial resistance seems to be based on the overproduction of clavulanatesusceptible &bgr;-lactamases. These &bgr;-lactamases are good clavulanate inhibitors and their overproduction ensures extra inhibition of amoxycillin or ticarcillin. The clinical and epidemiological consequences of this new type of bacterial resistance remain to be evaluated. J. L. MARTINEZ E. CERCENADO M. RODRIGUEZ-CREIXEMS Microbiology Services, M. F. VINCENTE-PEREZ Hospital Ramon y Cajal A. DELGADO-IRIBARREN and Hospital Gregorio Marañon, Madnd 28034, Spain F. BAQUERO to

DYSGONIC FERMENTER ORGANISMS AND POST-SPLENECTOMY RISKS

SIR,—Your Oct 3 editorial (p 777) again stresses the serious consequences of overwhelming post-splenectomy sepsis (OPSI). Much emphasis is still placed on the pneumococcus as the cause of such infections. Dysgonic fermenter 2 (DF-2) is a less well recognised cause. However, 18 cases of septicaemia, sometimes complicated by disseminated intravascular coagulation’2 and the Waterhouse-Friedrichsen syndromehave been reported in splenectomised patients, and meningitis after DF-2 septicaemia in an asplenic individual has also been recorded.’ Two-thirds of such infections occur within 5 years of splenectomy, although sepsis may occur as early as 8 months’ and as late as 30 years2 after the

operation. A striking feature in OPSI due to DF-2 is onset after a dog bite or scratch, noted in 13 reports. 3 other patients had had close contact with dogs but had no history of a bite or scratch; 1 case followed a cat bite;4 and Butler et all cite a case of DF-2 sepsis in a splenectomised animal trainer who worked with coyotes, bears, and tigers. Given the frequency with which DF-2 is found in the oral microflora of dogs and catsb asplenic individuals should be advised not to keep dogs or cats. Department of Microbiology, Manchester Royal Infirmary, Manchester M1 3 9WL

K. G. KERR

1 Findling JW, Pohlmann GP, Rose HD. Fulminant gram-negative bacillaemia (DF-2) following a dog bite in an asplenic woman. AmJ Med 1980; 68: 154-56. 2. Kalb R, Kaplan MH, Tenenbaum MJ, Joachim GR, Samuels S. Cutaneous infection at dog bite wounds associated with fulminant DF-2 septicaemia. Am J Med 1985; 78: 687-91. 3 Chaudhun

AK, Hartley RB, Maddocks AC. Waterhouse-Friedrichsen syndrome by a DF-2 bacterium. J Clin Pathol 1981; 34: 172-73. 4. Carpenter PD, Heppner BT, Gnann JW DF-2 bacteraemia following cat bites. Am J Med 1987; 82: 621-23 5. Butler T, Weaver RE, Venkata Ramani TK, et al. Unidentified gram negative rod infection. Ann Intern Med 1977; 86: 1-5. 6. Westwell AJ, Spencer MT, Kerr KG. DF-2 bacteraemia following cat bites. Am J Med (in press). caused

LEAD FOIL ON WINE BOTTLES

SIR,—The warning issued to wine drinkers by the Ministry of Agriculture, Fisheries, and Food (Nov 14, p 1164) that lead foil on wine bottles can be a health hazard reminds us of an experiment we did about ten years ago. The lead seal was removed from a bottle of red wine and a corkscrew was carefully introduced to about half the depth of the cork. The cork was drawn until about two-thirds was visible; the corkscrew was removed and the cork sliced across to expose a virgin surface. The needle of a syringe was inserted through the remaining cork and used to withdraw 5 ml wine from the bottle (A). The lower portion of cork was then removed and a glass of wine poured out over the rim of the bottle (B). Two further samples were similarly obtained after the top had been wiped with a cloth (C) and after vigorous cleaning with a damp towel (D). The concentrations of lead in each of the four samples of mature

1474 wine extracted were in gg/1, A 57, B 320, C 250, and D 100, confirming that lead can be extracted from the rim of a bottle capped with lead foil. Individuals persistently drinking wine of the quality associated with these seals could, therefore, have a greatly increased dietary intake of lead. Whether the lead or the associated alcohol contributes the greater health hazard was not, however, considered in this experiment. Department of Biochemistry, University of Surrey, Guildford, Surrey GU2 5XH

VINCENT MARKS ANDREW TAYLOR

Medicine and the Law Death of an Epileptic Patient in

a

Prison Medical

Wing ON Oct 30,

1984, a man with a long history of epilepsy and with

schizophrenia with paranoid delusions

was arrested after a serious assault on his father. He was remanded to Brixton prison where he had recurrent seizures. The family were concerned and asked that a consultant neuropsychiatrist examine him to determine whether he was fit to plead. His condition became serious and he was admitted to the Maudsley Hospital as an emergency. At Brixton medical unit, the provisional diagnosis was an intracranial lesion, but the hospital’s diagnosis was repeated epileptic convulsions. His condition improved under treatment and on Jan 20, 1985, he was returned to the hospital unit at Brixton where treatment with phenytoin was continued. On March 1, having been found fit to plead, he was convicted of the assault and a hospital order was made under the Mental Health Act. The family were disturbed because for some days the prisoner had been unwell. His mother was not able to see him when she visited Brixton on March 6, because he had had two attacks of petit-mal and he was to be seen by the doctor. On March 7 and 8 she was again told he was not well, and her daughter was told the same thing on March 9, 10, and 11. Apparently, during the evening of March 11 he had a grand-mal seizure and was put to bed. He was due to be transferred to a mental hospital on March 12, but, on that day, at 1.30 am, during a routine check, he was found dead in his room. His age when he died was 38. After necropsy the cause of death was given as status epilepticus. The blood level of phenytoin was 3 mg/1, equivalent to 5 mg/1 in plasma. At the inquest, the question was raised, but not resolved, as to whether this figure indicated that he had not been receiving the proper dose of phenytoin. Evidence was given by the prison nursing staff that he had had a number of grand-mal and petit-mal fits in the week before his death and on the night he died he had had another grand-mal seizure. The prison medical officer said he had not seen him before his death, although other doctors, whom he did not name, had treated him. The coroner refused a request by counsel for the deceased’s family that the doctors involved in treatment be called as witnesses. The coroner also refused to leave to the jury a verdict of lack of care, because he believed that such a verdict would offend against rule 42 of the Coroners Rules 1984 in that it appeared to determine a question of civil liability as against the prison governor or the Home Office. The jury, who had sat continuously from 10.49 am until’ about 4 pm with a short break just before the coroner’s summing up, returned a verdict of death by misadventure. The deceased’s parents applied for judicial review and for a declaration that the jury were entitled to return a verdict of lack of care and for an order quashing the inquisition on the grounds that the coroner had wrongly refused to call as witnesses the doctors involved in treatment in the days preceding death; and that he refused a request to direct disclosure of the prison’s medical notes relating to treatment from Jan 7, 1985, to March 12, 1985.

Inquest Verdict Quashed The Divisional Court quashed the verdict and ordered a new inquest. Lord Justice Croom-Johnson said that deaths of prisoners in custody were a special category which required particularly

once serious questions had been raised about the deceased’s treatment, it was incumbent on the coroner to adjourn the inquest to allow the calling of evidence of the treatment given, even though it meant adjourning the proceedings, which was inconvenient. "Whether the worries or suspicions of the family were justified or wholly unjustified, it was in the public interest that they should be examined sympathetically so long as they went to a verdict which it was legitimate for the jury to return. The coroner should at least have approached the problem in that spirit." A verdict of lack of care was permissible and appropriate where the death was caused by neglect of the deceased’s condition and where some other person had a real opportunity of doing something effective in rendering care which would have prevented the death. "The opportunity should have been a real one of doing something effective. This verdict should not be used as a means of levelling disguised criticism at people who do not act in an emergency or take a wrong or inadequate decision in such cases." It should not attribute blame or fault to a particular individual. In this case, such a verdict might have been possible if there had been evidence that insufficient medical treatment’had been given to the deceased. Mr Justice Peter Pain agreed. The Divisional Court said by way of "final criticism" that the inquest was conducted for too long without a break before a jury which must have been tired. The same jury began an earlier inquest at 10.49 am. After bringing in their verdict, they began their hearing of the deceased’s inquest at 12.17 pm and it ended at 4.41 pm. At about 4 pm before the summing up, there was a 15-minute break. By then the jury had sat continuously for over five hours without refreshment. The coroner had asked the jury whether they were tired or in discomfort at about 1 pm and 2 pm and, receiving no assent, he had decided to carry on. This was wrong. Jurors were not used to sitting for long hours, as were professional men; by the end some of them were likely to have lost concentration and much of the evidence was technical and medical. It was not enough to leave it to the jurors to speak up and ask for a break; it was for the tribunal-in this case, the coroner-to decide on what breaks were needed or to indicate clearly to the jury what might be involved by sitting on and to give some indication of how long proceedings were likely to take. As Mr Justice Peter Pain put it, "The picture that I have of this jury trying to grapple with a complex medical problem with empty stomachs and full bladders troubles me." A second inquest, held in June, lasted three days and produced a verdict that death was due to natural causes aggravated by lack of care. The evidence indicated that no one doctor at Brixton had overall charge of the prisoner’s care. Two doctors had treated him and both thought the other was chiefly responsible. The prisoner died on a Tuesday; the previous Friday, one of the two doctors had seen him and said to the nursing officer, "this man needs treatment--contact the other doctor urgently". The message was never relayed. No doctor actually saw the deceased between Friday and Tuesday. He was said to have been doubly incontinent and psychotic, lying on the floor of his cell for that time. Each doctor apparently placed responsibility for treatment on the other, and the nurses transferred their responsibility to the doctors. It emerged from the evidence at the second inquest that the deceased had seemingly not had 12 out of 18 doses of phenytoin he was due to be given in the week before he died. The coroner said that "this appeared to have been a lack of continuity and in his case the system had slipped up". The deceased’s mother has been granted legal aid and is pursuing a civil action for damages.

thorough investigations. Accordingly,

R v Southwark Coroner, Ex Parte Hicks. Divisional Court, CroomJohnson LJ and Peter Pain J. Jan 26, 1987. [1987] 1 WLR 1624.

DIANA BRAHAMS, Barrister-at-law.

Informed Consent:

a

Canadian Case in

a

British

Perspective A FULL report! now published of the Saskatchewan Court of Appeal decision in Haughian v Paine makes it clear that the Appeal Court did not find the defendant surgeon negligent, as I said it did (Oct 31, p 1038), in failing to recommend conservative treatment for herniation of a cervical disc. His diagnosis was correct and surgery