1020

end and indeed may be one of the weakest methods. Still, it might be well for such a ban to be introduced so that anti-smoking organisations can then begin to focus their influence on winning the most effective measures. Or, to be more positive: pass the ban and then in the climate created by that ban move on to even more

effective steps. Smoke-free European (Newsletter of the European Union of Nonsmokers),

Melgund Centre, Edinburgh EH7 4BU, 1.

UK

PHILLIP WHIDDEN

Chapman S, Borland R, Hill D, Owen N, Woodward S. Why the tobacco industry fears the passive smoking issue. Int J Health Serv 1990; 3: 417-27.

SIR,-I strongly support Mr Dean’s article on European tobacco advertising. In the UK, at least 1000 young people start the tobacco habit every day, and of the children alive today in Europe, 5 million will die in middle age of tobacco-related disease. Faced with a few vicious dogs, the UK Government does not negotiate, it legislates. Why does it not apply the same ethical principle and legislate against tobacco advertising? Does it always have to come down to money? Wythenshawe Hospital, Manchester M23 9LT, UK

ASHLEY WOODCOCK

State of British psychiatry SiR,—In your Sept 28 editorial you state that British psychiatry is

happy with itself. In 1991 a happy medical specialty would be hard to find-and might prove to be have hypomania precipitated by bereavement. But your reasons for this unhappiness seem banal: too rapid change; no control over our destiny; arguments about theory and practice. Do you recommend the quiet certainties of the cemetery? Psychiatry is showing healthy signs of life, growth, and not

differentiation. With respect to research, it is only too true that the opportunities provided by new technology cannot be taken up as we would like. We are horrified by the dwindling funds for all scientific research in the UK, and we are very troubled by the shortage of research posts and poor academic prospects. But these feelings are shared by a

large and unhappy company. You should supply references for your accusations of poor treatment, demoralised staff, and absent psychiatrists. But perhaps you refer to the College’s own audits-electroconvulsive therapy for instance-or to the regular external audits (far more extensive than for any other specialty) by the Health Advisory Service and the Mental Health Act Commission. The findings may be uncomfortable, but at least we are turning over our stones. Why throw them all around the glasshouse? Are we unique in our deficiencies? I await the reports of the new Clinical Standards Group with interest. 133 Sydenham Hill, London SE26 6LW, UK

J. L. T. BIRLEY

Increased community-acquired septicaemic infection with group B streptococci SIR,-Dr Eykyn and colleagues (Aug 17, p 446) note an increase in

community-acquired septicaemic infections with group B streptococci (Streptococcus agalactiae) in adults. Our experience in Scotland from September, 1989, to August, 1991, based on weekly

from laboratories to the Communicable Diseases Scotland at the Glasgow Royal Infirmary, shows similarities and and Unit, some differences. Over these 2 years there were 94 cases of group B streptococcal bacteraemia in adults. Of these 75 were serious invasive infections in non-puerperal adults. This represents 1% (75 of 7304) of the total number of adults with bacteraemia. Patients were aged 16-98 years (mean 57). The female to male ratio was 1-2/1. There were 3 deaths-2 due to infective endocarditis and 1 unknown cause. 4 patients had group B streptococcal endocarditis and accounted for 3% (4 of 132) of all cases of infective endocarditis. 2 patients were returns

reported to have septic arthritis, 1 of whom had a mixed infection with S pyogenes (group A streptococcus). No cases of endophthalmitis were reported. The group B streptococcus is

an uncommon cause

of infective

endocarditis, accounting for only 62 reported cases world wide from 1962 to 1985.1 Most patients had underlying cardiac disease or other risk factors.1,2 We have seen 7 patients with group B streptococcal endocarditis since 1985, 6 of whom have been reported.3,4 Only 1 patient had previous valvular disease. The infections were all characterised by acute presentation, aggressive course with major arterial emboli, and high mortality. Despite early diagnosis and appropriate intravenous antibiotics (penicillin and an aminoglycoside) 5 patients died-2 after valve replacement and 3 before surgery could be undertaken. All 7 isolates of group B streptococci were typed by the streptococcus reference laboratory at the Central Public Health Laboratory, Colindale, London: 3 were type III, 2 type I b/c, 1 type II, and 1 type I a. The observed increase in group B streptococcal endocarditis in adults may well result from increased recognition of the organism, or because the epidemiology of endocarditis is constantly changing.5 Perhaps it does indeed represent a true increase in incidence of group B streptococcal endocarditis. University Department of Bacteriology, Royal Infirmary, Glasgow G4 0SF, UK

A. CHRISTINE MCCARTNEY BISHAN THAKKER

Communicable Diseases Scotland Unit, Ruchill Hospital, Glasgow

WILLIAM J. REILLY

University Department of Medical Cardiology, Royal Infirmary, Glasgow

STUART M. COBBE

Watanakunakorn C. Group B streptococcal endocarditis: report of and review of the literature 1962-1985. Rev Infect Dis 1986; 8: 175-88. 2. Lerner PI, Gopalakrishna KV, Wolinsky E, McHenry MC, Tan JS, Rosenthal M. Group B streptococcus (S agalactiae) bacteremia in adults: analysis of 32 cases and review of the literature. Medicine 1977; 56: 457-73. 3. Pringle SD, McCartney AC, Marshall DAS, Cobbe SM. Infective endocarditis caused by Streptococcus agalactiae. Int J Cardiol 1989; 24: 179-83. 4. Marshall DAS, McCartney AC, Pringle SD, Cobbe SM. Infective endocarditis. Int J Cardiol 1990; 26: 387-88. 5. Watanakunakorn C. Changing epidemiology and newer aspects of infective endocarditis. Adv Intern Med 1977; 22: 21-47. 1.

Gallagher PG, seven cases

Fatal outcome of pyruvate loading test in child with restrictive cardiomyopathy SiR,—Cardiologists and neurologists should be warned of the potential danger of a pyruvate loading test,1-5 which is recommended in the diagnosis of mitochondrial enzyme deficiency. We report a fatal outcome in a 9-year-old boy. The child was admitted because of decreased exercise capacity, wheezing, orthopnoea, and mild cyanosis for six months. He had striking hepatomegaly, congestion of jugular veins, and a loud, split second sound. Electrocardiography revealed pronounced atrial enlargement and right ventricular hypertrophy. On echocardiography dilatation of both atria with normal dimensions and contractility of the ventricles were noted. Heart catheterisation showed pulmonary hypertension and typical square-root sign on the left ventricular pressure curve. Pericardial biopsy was done to rule out constrictive pericarditis. We diagnosed restrictive cardiomyopathy. Because the aetiology of this disorder is still obscure, screening for mitochondrial enzyme defect was planned. Basal blood lactate was slightly increased (2-4 mmol/1). Pyruvate loading test was done by Gabreels’ method.1-5 After overnight fasting an intravenous infusion of sodium pyruvate 0-5 g/kg bodyweight was given over 10 min. Venous blood samples were obtained from his other arm. The patient was anxious before and during the first minutes of the test. Between 6 and 12 min after infusion he started to complain of precordial pain and a suffocating feeling. Shortly after the 12 min blood sample was taken the child had sudden loss of vision, he became unconscious, had a tonic convulsion, and stopped breathing. Attempts at resuscitation were unsuccessful. Since cardiac monitoring was not done, it is unclear whether the cause of death was asystole, ventricular fibrillation, or an abrupt fall in blood

State of British psychiatry.

1020 end and indeed may be one of the weakest methods. Still, it might be well for such a ban to be introduced so that anti-smoking organisations can...
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