Apparent epidemic of HCV infection in a haemodialysis unit

D. Marchesi1, E. Minola2 and O. Vicari3

1 Department of Nephrology and Dialysis 2 Department of Infectious Diseases 3 Department of Immunohematology, Ospedali Riuniti di Bergamo, Bergamo, Italy

Sir,

Haemodialysis units have been recognized as a high-risk environment for the transmission of blood-borne infections. In our unit we had an outbreak of non-A, non-B hepatitis involving over 40 patients between 1980 and 1985 [1]. After that we started a preventive programme based on universal precautions to minimize the risk of exposure to hepatitis C virus (HCV), with good results [2]. Actually, from 1990 to March 1997 we had no cases of seroconversion to HCV antibodies among new patients starting haemodialysis treatment. Surprisingly, from March 1997 to January 1998 we had five new cases, as reported in Table 1Go. We were seriously considering the possibility of a new cluster of HCV infection which might have been favoured by our lowering attention for universal precautions of blood-borne infections.


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Table 1.
 
In all our patients who had positive HCV antibodies (Abbott HCV EIA 3.0, Abbott Labs, USA) we analysed HCV genotype with inverse hybridization (Amplicor extraction, Roche, immunoblotted Innolipa, Nuclear Laser) and classified them as suggested by Simmonds et al. [3]. In January 1997 we had 36/143 haemodialysis patients with HCV antibodies. We found genotype 1B in 16/36 (44.4%), genotypes 2 in 15/36 (41.6%), and undetermined genotype in 5/36 haemodialysis patients (13.9%). In our geographical area the presence of HCV antibodies is 3–6%, depending on age. We therefore controlled the distribution of different genotypes in a non-selected, successively enrolled group of 453 patients with community acquired HCV infection. We found genotype 1A in 41/453 haemodialysis patients (9.1%), genotype 1B in 204/453 (34.9%), genotypes 2 in 158/453 (24.9%), genotype 3A in 33/453 (7.3%), genotype 4 in 5/453 (1.1%) and undetermined genotype in 12/453 (2.6%).

We then controlled the day and turn of dialysis of all five patients from June 1996 to January 1998. We found that only patients No. 4 and 5 were regularly dialysed in the same room and turn. Moreover, the genotyping of our five new cases revealed different HCV subtypes.

We conclude that this apparent cluster of HCV infection was not an epidemic but corresponded to independent infections, possibly related to surgical procedures (patients Nos 1,3 and 4) or community acquired infection (patient No. 2). Only one out of the five cases was potentially acquired in the dialysis unit. After January 1998 we followed the usual procedure to avoid exposure to HCV and until January 1999 no other cases have occurred. This observation led to a debate with dialysis staff as to the importance of respecting universal precaution measures in the unit. We think that it is useful to maintain permanent alertness on blood-borne infections.

References

  1. Marchesi D, Arici C, Poletti E, Mingardi G, Minola E, Mecca G. Outbreak of Non-A, Non-B hepatitis in centre haemodialysis patients: a retrospective analysis. Nephrol Dial Transplant 1988; 3: 795–799[Abstract]
  2. Arici C, Gregis GP, Marchesi D, Mingardi G, Mecca G, Bellavita P. Effectiveness of a preventive programme for Non-A, Non-B hepatitis in a large dialysis unit. Nephrol Dial Transplant 1990; 5: 902–903[ISI][Medline]
  3. Simmonds P, Holmes EC, Cha TA et al. Classification of hepatitis C virus into six major genotypes and a series of subtypes by phylogenetic analysis of the NS5 region. J Gen Virol 1993; 74: 2391–2399[Abstract]