Avoparcin and animal feedstuff

Avoparcin and animal feedstuff

We also agree with Yudkin and Coppack that, despite compelling epidemiological data and at least one positive clinical trial, these observations are i...

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We also agree with Yudkin and Coppack that, despite compelling epidemiological data and at least one positive clinical trial, these observations are insufficient to establish a causal relation between glucose and cardiovascular disease, and, as we originally stated, dysglycaemia should be regarded as a potentially modifiable risk factor. Until the results of further research are available, rises in plasma glucose can identify people at increased cardiovascular risk, and strategies currently proven to reduce this risk may be especially effective in this group. If this research proves that glucose elevation is itself a modifiable causal risk factor for cardiovascular disease, therapies to lower glucose into the non-diabetic range in high-risk patients may further decrease cardiovascular risk. *Hertzel C

Gerstein, Salim Yusuf

Department of Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5 1

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Scheidt-Nave C, Barrett-Connor E, Wingard DL, Cohn BA, Edelstein SL. Sex differences in fasting glycemia as a risk factor for ischemic heart disease death. Am J Epidemiol 1991; 133: 565-76. Donahue RP, Abbott RD, Reed DM, Yano K. Postchallenge glucose concentration and coronary heart disease in men of Japanese ancestry. Honolulu Heart Program. Diabetes 1987; 36: 689-92. Singer DE, Nathan DM, Anderson KM, Wilson PWF, Evans JC. Association of HbA1c with prevalent cardiovascular disease in the original cohort of the Framingham heart study. Diabetes 1992; 41: 202-08. Andersson DKG, Svardsudd K. Long-term glycemic control relates to mortality in type II diabetes. Diabetes Care 1995; 18: 1534-43. Genuth S. Exogenous insulin administration and cardiovascular risk in NIDDM and IDDM. Ann Intern Med 1996; 124: 104-09.

Avoparcin and animal feedstuff SiR-The apparent confidence of Mudd (May 18, p 1412)’ and the Roche organisation that avoparcin use in animals will not influence glycopeptide resistance in human enterococcal pathogens must be questioned. Experience in both the UK2 and Germany3 strongly suggests that the resistance determinant, the van A gene, can be selected by avoparcin when the product is used as a feed additive, that it can enter the human food chain, and be incorporated into the bowel flora of patients. No new families of antimicrobials have been developed recently yet bacterial resistance to those available continues apace. There is now much public concern about additives fed to animals that are destined for human consumption. There needs to be full debate on how and when we use antimicrobials (be they glycopeptides or fluoroquinolones) in animals and man. Commercial considerations of food production have to be balanced against potential adverse effects on man. Do I hear an echo of the bovine spongiform encephalopathy (BSE) debate? Richard Wise City Hospital NHS Trust, Birmingham B18 7QH, UK

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Mudd A.

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1412. Bates J,

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Vancomycin

resistance and

avoparcin.

Lancet 1996; 347:

Jordens Z, Selkan JB. Evidence for an animal origin of vancomycin resistant enterococci. Lancet 1993; 342: 490-91. Klare I, Heier H, Clans H, Reissbrodt R, Witte W. Van A mediated from animal

high level glycopeptide resistance in Enterococcus faecium husbandry. FEMS Microbiol Lett 1995; 125: 165-72. SIR We agree with Gerstein and Yusufthat there is a continuous relation between the risk of cardiovascular disease (CVD) and raised blood glucose concentration. We also feel that hyperinsulinaemia could be another risk factor for CVD. There is now ample evidence, both experimental and epidemiological,2 that insulin is a risk factor for coronary artery disease. Stout3 has proposed that mild hyperglycaemia inhibits endothelial cell activity, resulting in or potentiating an injury to the endothelial barrier. Insulin would then cause proliferation and migration of smooth muscle cells and would enhance the lipoprotein receptor activity through the injured endothelium. Individuals would have a higher insulin response before the onset of dysglycaemia, which could be a defence mechanism to prevent dysglycaemia. Initially individuals are hyperinsulinaemic, and when the increased insulin response reaches a threshold value (insulin resistance) dysglycaemia sets in. A continuous relation between risk of CVD and classic risk factors such as cholesterol, blood pressure, and glucose implies that there should not be any cutoff values for these variables, over which they are regarded as risk factors; levels may differ from individual to individual because of the presence or absence of other risk factors. Individuals should be assessed overall for the risk of CVD. Attention should be focused on lifestyle modification to achieve weight reduction, dietary change, and exercise to reduce morbidity and mortality from CVD in the general population.

Pankaj Malhotra, *Rajesh Kumar, Savita Kumari, M Meghachandra Singh Department

of Community and Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh 160 012, India

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Gerstein HC, Yusuf S. Dysglycaemia and risk of cardiovascular disease. Lancet 1996; 347: 949-50. Morris AD, Petrie JR, Connell MC. Insulin and hypertension. J Hypertens 1994; 12: 633-42. Stout RW. The impact of insulin upon atherosclerosis. Horm Metab

Res 1994; 26: 125-28.

Newly recognised hantavirus in Siberian lemmings SIR-The list of known hantaviruses has increased since the of PCR to amplify viral genomic sequences from rodenttissue samples. Hantaviruses such as Sin Nombre from the USA’ and Tula from Europe2 were first seen as new genotypes and only later identified as unique serotypes. We report a newly detected hantavirus carried by lemmings, the most abundant mammal species in the arctic tundra.3 Siberian lemmings (Lemmus sibiricus) were collected during a Swedish-Russian Tundra Ecology Expedition in the summer of 1994 and kindly provided by Vadim Fedorov and Karl Fredga (University of Uppsala, Sweden). We screened liver samples of 61 animals from two localities on Taimyr Peninsula, Siberia. Six lemmings were found to contain hantavirus antigen by immunoblotting with rabbit antisera raised against recombinant nucleocapsid protein of Puumala virus. These results were consistent with earlier findings of hantavirus antigen in lemmings from arctic Siberia.4 Each positive sample was injected into Norwegian lemmings, Lemmus lemmus, a closely related species. Our laboratory colony originated from Finse, Norway, and has been maintained since 1994. The virus was successfully passaged in 4/6 laboratory lemmings as judged by the presence of antigen in lungs (4/6) and/or the development of antibodies (3/6). Lung tissues of antigen-positive lemmings were used for RNA isolation, reverse transcription, and nested PCR. Amplicons (354 base pairs in length) from the S(mall) genomic segment were prepared from two specimens and sequenced. Phylogenetic analyses of the virus-specific sequences, identical in both lemmings, indicated that they use

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