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understanding that individual results would not be available, and that some couples may have misunderstood the test and assumed that a negative result was truly negative for both partners.

worn

Furthermore, the value of information about carrier

drain of the shower:

status for had been of carriers not mentioned to patients-they were siblings carrier in an information about testing explanatory leaflet given rather than having non-directive counselling by trained staff. Although the frequency of non-patemity is much less than the 10% widely quoted, it may still be a substantial difficulty for genetic screening programmes.3 2% or so non-paternity has been reported amongst the parents of CF children4 but non-paternity rates may be higher in a population where the risk of CF is not perceived as high and might not be seen by the mother to justify the complications of

by a doctor who had handled her sputum container. Ps cepacia cultured from gloves or cup before use. S21/PO:B (the profile of Ps cepacia colonising patient Y) was cultured from the was not

assigning paternity explicitly. Wald wishes to spare carriers whose partners test negative anxiety because they "cannot be reassured" by a residual risk higher than the pre-test risk (risk of affected fetus is 1/500 in contrast with 1/2500 pre-test). It is quite possible that women may perceive this risk as low, be glad to be able to inform their family, and, if they do have an affected child, be less upset than if they had been given an inappropriately low risk result by couple screening. It is only ethical to withhold information about carrier status if the benefits of doing so are rigorously proven. Genetic testing requires non-directive counselling by trained staff to allow individuals to make a truly informed choice. Medical Genetics, Medical School, University of Aberdeen, Aberdeen AB9 2ZD, UK

ZOFIA MIEDZYBRODZKA JOHN DEAN NEVA HAITES

1 Cox TK, Chakravarti A. Detection of cystic fibrosis gene carners: comparison of two

screening strategies by simulations Am J Hum Genet 1991; 49 (suppl 4): 327. 2. Pelias MZ. Duty to disclose in medical genetics: a legal perspective. Am J Med Genet

1991, 39: 347-54. 3.

Macintyre S, Sooman A. Non-paternity and prenatal genetic screening. Lancet 1991;

4.

Shrimpton AE,

338: 869-71. McIntosh I, Brock DG. The incidence of different cystic fibrosis the Scottish population: effects on prenatal diagnosis and genetic counselling. J Med Genet 1991; 28: 317-21.

mutations

in

Pseudomonas cepacia in inpatients with cystic fibrosis SIR, Pseudomonas cepacia is

recognised as an important pathogen in patients with cystic fibrosis (CF).1-3 Patients colonised with this organism seem to be at increased risk of pulmonary exacerbations and death.’ Ps cepacia tends to be resistant to antibiotics and disinfectants, and pulmonary infection is very now

difficult to treat and to prevent, because modes of transmission and factors involved in pulmonary colonisation are not established. A 1984 study’ in CF patients suggested nosocomial transmission but a link with epidemic pulmonary colonisation was not confirmed. A longitudinal study" suggested a nosocomial source for colonisation but Ps cepacia was not cultured from solutions or environmental surfaces. Ribotyping of isolates has suggested person-to-person transmission of Ps cepacia in CF, and the failure of other investigators to recover Ps cepacia from the hospital environment was cited in support of that view.5 We have used ribotyping and bacteriocin typing*’ to characterise Ps cepacia isolated from environmental surfaces in a hospital room

occupied by 2 CF patients. The 2 women (X and Y, aged 26 and 27) had been admitted with exacerbations of bronchiectasis and they had shared a two-bed room for two weeks and used the same shower. Both were known to be colonised by Ps cepacia, but with different strains. Selective medium7 was used for culture studies. Swabs were first moistened in minimal broth containing polymyxin (300 U/ml). After primary inoculation swabs were incubated at 30°C for 48 h and turbid broths were subcultured. Culture plates were incubated at 30°C and checked for growth at 24 h intervals up to 72 h. Ps cepacia was identified biochemically (API 20 NE system; API-bioMerieux). Ps cepacia bacteriocin type S3/PO:ribotype A was cultured from the sputum of patient X and isolates with similar profiles were also cultured from a drinking cup used by patient X and from gloves

Isolates from water in a vase of flowers and from soil in a plantpot differed in typing profile from the organisms colonising the

patients. This study

demonstrates both the value of selective media for isolation of Ps cepacia from environmental sites and surfaces and the potential for indirect transmission of Ps cepacia between patients. LiPuma et all favoured person-to-person transmission and concluded that unnecessary contact between colonised and noncolonised CF patients should be avoided. Others doubt if ordinary social contact between colonised and non-colonised patients is harmful.2 We found that CF patients can contaminate environmental surfaces with Ps cepacia, confirming that indirect transmission is possible. We did not isolate Ps cepacia from a CF patient in the room next to patients X and Y who had frequent social contact with them. Our findings suggest the need for reasonable precautions in the management of colonised patients. What is meant by "reasonable" in this context has yet to be defmed, and until the precise mode of transmission of this opportunist pathogen is known a policy of segregating colonised from non-colonised CF patients must remain controversial. We thank

Dr Ty Pitt for arranging the ribotyping.

Department of Medical Microbiology, University of Edinburgh Medical School, Edinburgh EH8 9AG, UK, Respiratory Unit, Western General Hospital, Edinburgh. and Central Public Health Laboratory, London NW9

J. W. NELSON C. J. DOHERTY P. H. BROWN A. P. GREENING M. E. KAUFMANN J. R. W. GOVAN

I, Corey M, et al. Pseudomonas cepacia infection in cystic fibrosis: an emerging problem J Pediatr 1984; 104: 206-10. Simmonds EJ, Conway SP, Ghoneim ATM, Ross H, Littlewood JM. Ps cepacia: a new pathogen in patients with cystic fibrosis referred to a large centre in the United Kingdom. Arch Dis Child 1990; 65: 847-77. Gilligan PH. Microbiology of airway disease in patients with cystic fibrosis. Clin

1. Isles A, Maclusky 2.

3.

Microbiol Rev 1991; 4: 35-51. 4. Tablan OC, Martone WJ, Doershuk CF, et al. Colonisation of the respiratory tract with Ps cepacia in cystic fibrosis: risk factors and outcomes. Chest 1987; 91: 527-32. 5. LiPuma JJ, Dasen SE, Nielson DW, Stem RC, Stull TL Person-to-person transmission of Ps cepacia between patients with cystic fibrosis. Lancet 1990; 336: 1094-96. 6 Rabkin CS, Jarvis WR, Anderson RL, et al. Ps cepacia typing systems: collaborative study to assess their potential in epidemiologic investigations. Rev Infect Dis 1989; 11: 600-07. 7. Gilligan PH, Gage PA, Bradshaw LM, Schidlow DV, Decicco BT. Isolation medium for the recovery of Ps cepacia from the respiratory secretions of patients with cystic fibrosis. J Clin Microbiol 1985; 22: 5-8.

Antithrombin III and arterial disease SIR,-Dr Meade and colleagues (Oct 5, p 850), in their prospective investigation of the relation between antithrombin IIIII and subsequent death from arterial disease, find that there are more deaths from arterial disease in the lower and upper thirds of the antithrombin III distribution than in the middle third. We examined the distribution of fatal and non-fatal well documented atherothrombotic events in 953 patients with pre-existing coronary, cerebral, or peripheral ischaemic disease followed for 24 months in

Pseudomonas cepacia in inpatients with cystic fibrosis.

1525 understanding that individual results would not be available, and that some couples may have misunderstood the test and assumed that a negative...
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