We determined the prevalence of hepatitis C virus (Hepatitis C Virus) antibodies among health-care workers at risk of occupational contact with blood and body fluids and among source patients in reported blood-exposure incidents. Anonymised stored blood samples from health-care workers immunised against hepatitis B virus since 1991 (n = 1053) and blood samples from source patients in needlestick injuries (retrospective and prospective) since 1989 (n = 373) were analysed. 3 (0.28%) of the serum samples from health-care workers were found to be anti-Hepatitis C Virus-positive. 17 (8-5%) of 200 source patients tested retrospectively between January 1989 and January 1992, and 24 (13.9%) of 173 source patients tested prospectively between January 1992 and June 1993 were anti-Hepatitis C Virus-positive. During the second period, 15 (10.6%) of 142 source patients tested for human immunodeficiency virus (HIV) were positive and 7 (3.8%) of 184 source patients tested for hepatitis B surface antigen were positive. 6 of 24 (25%) Hepatitis C Virus-infected patients were diagnosed only after the incident; for hepatitis B, 2 (33%) of patients were diagnosed after the incident, and for HIV all patients were previously diagnosed.

The seroprevalence of Hepatitis C Virus among these health-care workers is no higher than that reported in blood donors. This suggests that there has not been significant occupational transmission of Hepatitis C Virus to these health-care workers despite the high prevalence of Hepatitis C Virus (often covert) among source patients in reported blood exposure in the same hospital.

Lancet 1994; 343:1618-20

Health-care workers are at risk of infection by blood-borne viruses through needlestick injuries and other blood-exposures. Transmission of hepatitis virus (Hepatitis C Virus) after accidental blood inoculation has been recorded and several studies on the occupational risk of Hepatitis C Virus infection have been reported. Occupational infection with Hepatitis C Virus may have serious long-term implications: establishment of a carrier state, chronic liver disease, and possible transmission to patients. Understandably, health-care workers are anxious about the possibility of Hepatitis C Virus infection when a needlestick injury occurs. We studied the prevalence of Hepatitis C Virus antibodies among health-care workers with direct and indirect clinical contact. In the same hospital, we assessed the potential for occupational transmission of Hepatitis C Virus infection by measuring its seroprevalence among patients involved in reported blood-exposure incidents.

The Occupational Health Unit at The Royal Free NHS Trust Hospital, London, UK, has well-established protocols for hepatitis B (HBV) immunisation of staff and for managing needlestick injuries? Staff who are at risk of blood exposures at work (doctors, nurses, and laboratory and ancillary staff) are offered HBV immunisation with subsequent testing of antibody response. Several thousand staff have been immunised and many of these have had frozen serum samples stored. This allowed us to investigate the prevalence of Hepatitis C Virus by a second-generation enzyme immunoassay antibody test (Ortho Diagnostics, High Wycombe, UK) and supplementary tests with Ortho immunoblot assay (RIBA II) on any repeatedly reactive samples.

Individuals to be tested were those on a computer database of staff immunised against HBV and tested for response since January 1991, stratified by age (< 24 years, 25 to 39 years, and > 40 years); and two occupational groups, those with direct clinical exposure (medical and nursing staff) and those with indirect clinical exposure (laboratory and ancillary staff). There were 1053 stored serum samples available; aliquots were decanted into unlabelled containers, coded for age group and occupational group, and randomly numbered. These anonymous samples were then tested for Hepatitis C Virus antibodies.

Aliquots of all available 200 source patients in reported blood-exposure incidents January 1986 to December 1991 with stored serum samples were decanted into unlabelled containers and tested anonymously for hepatitis C antibodies.

From January 1992, identified source patients in blood exposure incidents have been routinely asked for consent to be tested for Hepatitis C Virus antibodies in addition to our previous practice of requesting testing for HIV antibodies and HBV surface antigen (HBsAg). 245 source patients were identified up to June 1993, of whom 184 were tested for HBsAg, 142 for HIV antibodies, and 173 for antibodies to Hepatitis C Virus. If any sample was found to be positive for Hepatitis C Virus antibodies, supplementary tests were undertaken and the staff member involved in the incident was offered follow-up tests for serum liver enzymes and hepatitis C antibodies for one year.

The overall seroprevalence of Hepatitis C Virus antibodies amongst 1053 health care workers was 0.28% (table 1). There appeared to be a trend for hepatitis C antibodies to be found more frequently in older age groups, but the number of positive samples (3) was very small. 17 (8.5%) of the 200 source patients involved in blood exposures from January 1989 to January 1992 were Hepatitis C Virus-antibody positive. From January 1992 to June 1993, 24 (13.9%) of 173 source patients tested were Hepatitis C Virus-antibody positive (table 2). In addition, 15 (10.6%) of 143 source patients were HIV-antibody positive and 6 (3.8%) of 184 source patients were HBsAg-positive (table 2).

Table 2 also shows that all 15 source patients who were HIV-positive had been diagnosed before the needlestick injury. In contrast, 2 of 6 (33%) patients infected with HBV and 6 of 24 (25%) infected with Hepatitis C Virus were diagnosed only after the incident.

None of the health-care workers followed up after the 24 Hepatitis C Virus antibody-positive blood exposures since January 1992 has seroconverted for Hepatitis C Virus, nor have there been any HBV or HIV seroconversions in our hospital following infected blood exposures to date.

An increased prevalence of markers of HBV infection was recognised among health-care workers before widespread immunisation. Epidemiological and experimental studies have indicated that Hepatitis C Virus can be transmitted by the parenteral route, and it is known that infected blood transfusions are an important route of transmission.

There have been several reports of Hepatitis C Virus transmission following needlestick injuries and one report of transmission by a human bite. A study of New York dentists[2] found that 2% bad antibodies to Hepatitis C Virus compared with 0'1% among controls. A study of German hospital staff reported a seroprevalence of 0.58% compared with 0.24% among blood-donor controls. In contrast, a UK study of dental surgeons reported that none had antibodies to Hepatitis C Virus compared with a 0.3% seroprevalence among local blood donor controls.

A recent prospective study of hospital employees estimated the risk of Hepatitis C Virus transmission to be 4% after needlestick exposure to anti-Hepatitis C Virus-positive blood. A Japanese study found the risk of transmission from a single needlestick accident with Hepatitis C Virus RNA-positive blood to be 10%. The apparent difference was most likely due to the use of different markers for Hepatitis C Virus infection in the two studies. The present study shows that the seroprevalence of Hepatitis C Virus infection among health care workers in potential contact with blood in our hospital is no higher than the 0.3% previously reported in UK blood donors. There is presently a seroprevalence rate for Hepatitis C Virus of 0.07% in new blood donors in north London and our figure of 0.28% is somewhat higher. Nonetheless, seroprevalence amongst staff is low. This is encouraging and suggests that there has not been significant occupational transmission of hepatitis C to these workers in the past.

The high seroprevalence of Hepatitis C Virus in source patients probably reflects the type of patients in the hospital, which has a large liver unit, and renal dialysis and haemophilia units. Incidents involving patients known to be infected with a blood-borne virus may also be more likely to be reported. Recent guidance concerning occupational exposure to Hepatitis C Virus states that routine Hepatitis C Virus-antibody testing from identifiable source patients of unknown Hepatitis C Virus status is presently not justified. However, in this study, 25%of source patients infected with Hepatitis C Virus were identified as such only after the blood exposure incident (table 2). Therefore, if the resources are available, we suggest it is appropriate to test--with consent--all source patients of unknown Hepatitis C Virus status. In this way, the health-care worker involved in the blood exposure incident can be counselled as early as possible about the risk of transmission and either reassured or given informed advice about follow-up procedures.

The results of this study indicate that there is a continuing risk of exposure to blood-borne viruses from blood exposure incidents in this hospital. The fact that Hepatitis C Virus and HBV infection in a number of patients in blood exposure incidents was not known at the time of the incident (see table 2) argues in favour of universal precautions for blood and body fluids,ts which is the policy in our hospital. The Hepatitis C Virus seroprevalence among staff should not lead to complacency. Efforts to reduce blood exposures are important as the best way to reduce the risk of occupational transmission of HIV, HBV, and Hepatitis C Virus.

We thank Toyin Shobande and Chris Gooch for their help with this study, and the Medical Research Council for financial support.

Table 1: Prevalence of hepatitis C antibodies in health-care workers with clinical contact

Age (years)    Clinical exposure group         Total

               Direct           Indirect

</=24          0/246 (0%)       0/84 (0%)      0/330 (0%)

25-39          1/186 (054%)     0/174 (0%)     1/360 (028%)

>/=40          0/184 (0%)       2/179 (1-12%)  2/363 (0.55%)

Total          1/616 (016%)     2/437 (0.46%)  3/1053 (0.28%)

Table 2: Results of testing for blood-borne viruses in identified source patients In reported blood exposure incidents (January 1992-June 1993)

Marker   Serological status of patient

         Tested before Incident  Tested after  Total tested

                                 incident

           No      No        No       No       No       No

         tested  positive  tested  positive  tested  positive

HBsAg      77       4        107      2        184      6

HIVAbS     53      15         90      0        143     15

HCVAbs     54      18        119      6        173     24

There are 245 identified source patients in 285 blood exposure incidents reported January 1992 to June 1993. Reasons for not testing source patients after the incident, despite a policy of requesting testing in each patient (unless previously tested), have been described elsewhere. HBSAg= hepatitis 8 surface antipen, HIVAbs = human immunodeficiency virus antibodies, HCVAbS = hepatitis C virus antibodies.

References

Cariani E, Zonaro A, Primi D, etal. Detection of hepatitis C virus RNA and antibodies after needlestick. Lancet 1991; 337: 850.

Klein R, Freeman K, Taylor PE, Stevens CE. Occupational risk factors for hepatitis C virus infection among New York City dentists. Lancet 1991; 338: 1539-42.

Kiyosawa K, Sodeyama T, Tanaka E. Hepatitis C in hospital employees with needlestick injuries. Ann Interm Med 1991; 115: 367-69.

Mitsui T, Iwano K, Masuko K, etal. Hepatitis C virus infection in medical personnel after needlestick accident. Hepatology 1992; 16: 1109-14.

Cockcroft A, Soper P, Insall C, et al. Antibody response after hepatitis B immunisation in a group of health care workers. BrJ Indust Med 1990; 47: 199-202.

Oakley K, Gooch C, Cockcroft A. Review of management of incidents involving exposure to blood in a London teaching hospital. BMJ 1992; 304:949-51.

West DJ. Risk of hepatitis B infection in health care workers in USA. Am J Med Sci 1984; 287: 26-33.

Garson J, Tedder RS, Briggs M, et al. Detection of hepatitis C vital sequence in blood donations by nested PCR and prediction of infectivity. Lancet 1991; 335::1419.

Schlipkopter U, Roggendorf M, Cholmakow K, Weise A, Deinhardt F. Transmission of hepatitis C virus from a haemodialysis patient to a medical staff member. Scand J Infect Dis 1990; 22:757.

Vaglia A, Nicolin R, Puro V, et al. Needlestick hepatitis C virus seroconversion in a surgeon. Lancet 1990; 336: 1315-16.

Seeff LB. Hepatitis C from a needlestick injury. Ann Interbn Med 1991; 115:411.

Dusheiko GM, Smith M, Scheuer PJ. Hepatitis C virus transmitted by human bite. Lancet 1990; 336: 503--04.

Jochen AB. Occupationally acquired hepatitis C virus infection. Lancet 1992; 339: 304.

Herbert A-M, Walker DM, Davies KJ, Bagg J. Occupationally acquired hepatitis C virus infection. Lancet 1992; 339: 304-05.

Maciennan S, Barbara JA, Hewitt P, Moore C, Contreras M. Screening blood donations for Hepatitis C Virus. Lancet 1992; 339: 131-32.

Ryan KE, MacLennan S, Barbara JAJ, Hewitt PE. Follow-up of anti-Hepatitis C Virus positive blood donors. Br Med J 1994; 308: 696.

Centres for Disease Control. Update: universal precautions for prevention of transmission of human immunodeficiency virus, hepatitis B virus and other blood borne pathogens in health care settings. MMWR 1988; 37: 377-88.

 PHLS Hepatitis Subcommittee. Hepatitis C virus: guidance on the risks and current management of occupational exposure. Comm Dis Rep 1993; 3: R135-139.

~~~~~~~~

By Jane Zuckerman, Gillian Clewlay, Paul Griffiths and Anne Cockcroft

Occupational Health Unit (J Zuckerman MD, A Cockcroft FRCP), and Department of Virology, Division of Communicable DIsease, Royal Free NHS Trust and Royal Free Hospital School of Medicine, London, UK (G Clewely esc, Prof P Griffiths MRCPath

Correspondence to: Jane Zuckerman, Occupational Health Unit, Royal Free Hospital of Medicine, 5 Rosslyn Hill, London NW3 5UL, UK