Infectious diseases

Endemic STDs in remote communities: the challenge for STD control High rates of STDs in Australian Aboriginal communities point to limitations in current surveillance and control methods MJA 1997; 166: 456 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". - ©MJA1997 A recent MJA editorial recognised Australia's achievements in controlling sexually transmitted disease (STD), but emphasised that the necessary aim must be "striving to eliminate endemic disease".1 Two articles in this issue of the Journal2,3 highlight the problems in the path of this objective -- and some of the potential solutions. Our information on the extent of STD in the population is largely derived from a passive notification system. Sentinel sites that routinely screen their client population for STDs and community surveys supplement the data from notification systems. Sentinel surveillance for HIV is conducted at urban sexual health clinics and data are collated nationally by the National Centre for HIV Epidemiology and Clinical Research, but there is no national collection of sentinel data for STD outside sexual health clinics. Our understanding of the epidemiology of STD outside the cities and towns is incomplete. What you test for is what you see, and our passive notification systems may be blind to much STD in the community Nationally, notifications of gonorrhoea and syphilis have declined in recent years,4 but celebration may be premature. The community-based survey reported in this issue by Skov et al. demonstrates that our notification systems may not provide an accurate picture of STD distribution in Australia.2 Their study found a far higher rate of gonorrhoea and chlamydia than would have been expected from previous notification data. Notifications made as a result of their community screening were responsible for a significant part of the 59% increase in notifications of gonorrhoea in South Australia in 1995.5 What you test for is what you see, and our passive notification systems may be blind to much STD in the community. At present, notifications are more often received from communities that recognise STD as an important health issue. Thus, communities that act on their responsibility for sexual health and STD control run the risk of being denigrated because of their apparently high rates of STD, while other communities not active in sexual health may have similar or bigger problems that remain largely hidden. The problem of detecting cases of STD is also an issue in evaluating the extent of their complications, which often form the greatest burden of disease. As shown in the report by Mein and Bowden (page 464 of this issue of the Journal),3 this burden falls heavily upon women in Aboriginal communities. What is perhaps most alarming in their case review is that only 45% of patients admitted to a gynaecological ward with suspected pelvic inflammatory disease were tested appropriately for STD (by endocervical swab). The rates of infection calculated by Mein and Bowden are therefore only the minimum estimate of gonococcal and chlamydial infection in pelvic inflammatory disease. The effort to control STD in Aboriginal communities can be facilitated by using new technology. In particular, tests based on the polymerase chain reaction (PCR) can diagnose chlamydia and gonorrhoea from urine samples. Such samples can be collected and processed more easily than swabs, and the procedure is more acceptable to Aboriginal people. This application of PCR technology is still in its infancy, and there may be some interpretation problems. The PCR test detects DNA or RNA, but does not tell us if the material comes from an infectious organism or from non-infectious remnants of a resolving infection. Another problem is that PCR testing does not allow the determination of antibiotic sensitivity patterns. Sentinel surveillance activities (involving culture for gonorrhoea to determine trends in antimicrobial resistance) must continue so that control efforts are not frustrated by drug resistance. PCR technology can be used in two ways in STD control. Firstly, in community surveys, such as that described by Skov et al.2 This survey, a collaborative effort between Aboriginal and government health services, required considerable infrastructure and community consultation, which were facilitated by the TriState STD/HIV Project (funded by the Western Australian, South Australian, Northern Territory and Commonwealth health departments). The collaborative approach of the TriState STD/HIV Project offers a model for undertaking surveys of this nature. A second application is through increased opportunistic testing by health care workers at consultations unrelated to sexual health. This approach is not necessarily easier than community surveys and represents a challenge to Aboriginal communities with limited access to health resources and a different cultural perspective on sexual matters. Opportunistic testing cannot be undertaken without prior consultation with the community and the development of guidelines on who should be tested and when. The risk of acquiring an STD is not evenly distributed within Aboriginal communities and a better understanding of social and sexual networks is needed. Mechanisms will need to be in place to inform people of test results and to ensure their treatment, and that of their contacts. The provision of adequate and acceptable community-based health services that recognise the importance of STD and have the capacity and will to detect, follow up and treat cases should be a priority. This will involve the active participation of the communities concerned and is perhaps the biggest challenge facing funders and providers of health services. HIV is already present in Aboriginal communities but its extent is limited at present.6 Experience in Africa (where the main focus of successful prevention programs is the provision of quality STD health services, encouragement of early presentation and availability of effective treatment) suggests that our ability to control bacterial STD will be a major determinant in controlling the spread of HIV.7 The two reports published in this issue of the Journal2,3 suggest that we have a long way to go in controlling STD in remote communities. We have the technology to enable non-invasive testing for gonorrhoea and chlamydia. We now have to use it effectively to detect, treat and reduce the level of endemic disease. The challenge is there for public health professionals and involved communities. Russell G Waddell Clinic Manager, STD Control Branch South Australian Health Commission Fairley CK. Sexual health -- reaching out [editorial]. MJA 1997; 166: 341-342. Skov SJ, Miller P, Hateley W, et al. Urinary diagnosis of gonorrhoea and chlamydia in men in remote Aboriginal communities. MJA 1997; 166: 468-471. Mein J, Bowden FJ. A profile of inpatient STD-related pelvic inflammatory disease in the Top End of the Northern Territory of Australia. MJA 1997; 166: 464-467. Hart G. STD epidemiology in Australasia: syphilis and gonorrhoea. Venerology 1992; 5: 115-120. South Australian Health Commission 1996. Sexually transmitted diseases in South Australia. Epidemiologic report no. 9 -- 1995. Adelaide: SAHC, 1995. Feachem RGA. Valuing the past, investing in the future: evaluation of the National HIV/AIDS strategy 1993-1994 to 1995-1996. Canberra: Department of Health, Housing and Community Services, 1995. Grosskurth H, Mosha F, Todd J, et al. Impact of improved treatment of sexually transmitted diseases on HIV infection in rural Tanzania: randomised controlled trial. Lancet 1995: 346; 530-536. - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Russell G Waddell

Urinary diagnosis of gonorrhoea and chlamydia in men in remote Aboriginal communities Steven J Skov, Penny Miller, Wayne Hateley, Ivan B Bastian, Jenny Davis and Peter W Tait MJA 1997; 166: 468 For editorial comment see Waddell Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - ©MJA1997 Abstract Aims: (1) To evaluate the acceptability and validity of an intervention based on urine tests for diagnosis and treatment of gonorrhoea and chlamydia in men in remote Aboriginal communities. (2) To provide a prevalence estimate of these infections in the male population in the surveyed communities. Methods: First-void urine samples from 460 men in remote communities and 33 men in the Alice Springs Gaol were tested for gonorrhoea and chlamydia with at least one of polymerase chain reaction (PCR), enzyme immunoassay (EIA) and culture (gonorrhoea only). Results: One hundred and three men (20.9%) were infected with gonorrhoea or chlamydia. The prevalence of infection for gonorrhoea only was 11.7%, for chlamydia only 4.1% and for dual infection 5.1%. Eighty-eight infected men and 45 of their sexual partners were recorded as having been treated within two months of testing. PCR tests detected the largest number of infections and were the easiest to use. Conclusions: The prevalence of these infections was higher than anticipated. Urine PCR tests were acceptable to men and are well suited to the remote-community setting. As an effective alternative to urethral swabs, they permit a range of community-based strategies to address high rates of infection with gonorrhoea and chlamydia. MJA 1997; 166: 468-471 Introduction The rates of sexually transmitted diseases (STDs) in central Australia, particularly gonorrhoea and chlamydia, are among the highest in Australia and indeed the world,1,2 despite a modest decline in gonorrhoea over the past 15 years (according to notifiable diseases data from the health departments of South Australia, Western Australia and the Northern Territory). Although these infections are more common in this region than in the rest of Australia among both Aboriginal and non-Aboriginal people, most of the excess morbidity occurs among Aboriginal people (health departments' data). Many factors contribute to this situation. Dispossession, unemployment and their sequelae are the fundamental determinants of the poor health of Aboriginal people and also underlie the observed high levels of STDs. The serious under-resourcing of central Australian health services, the difficulty in maintaining confidentiality in small communities, the stigma attached to STDs, the unpleasant nature of urethral and endocervical swabs and, in particular, the frequent lack of male health care workers -- all militate against effective STD programs.3-5 Urine tests for the detection of gonorrhoea and chlamydia are now commercially available. Enzyme immunoassay (EIA) tests have sensitivities above 80% and specificities above 93%,6-9 while polymerase chain reaction (PCR) tests have reported sensitivities of 90%-100% and specificities of 98%-100%.10-14 These technologies offered exciting possibilities to address some of the difficulties in delivering STD services, so, after receiving approval from the Alice Springs Institutional Ethics Committee, the Tri-State STD/HIV Project (TSP), in collaboration with Nganampa Health Council (NHC) and the Central Australian Aboriginal Congress (CAAC), both organisations controlled by Aboriginal communities, undertook the programs described in this article. Methods The study was undertaken in four parts. Phase I: NHC provides health services to several remote Aboriginal communities and conducts annual syphilis serology screening programs in these communities. NHC maintains a population register, and all persons between the ages of 12 and 40 years who are in the communities during the screening programs are sought out and asked to participate. In April 1995, 189 men participating in this program in three communities serviced by NHC were asked to give a first-void urine sample in addition to the blood sample for the syphilis test. Phase II: In June 1995, another 218 men in the remaining three NHC communities had urine tests only; all males over the age of 12 who were present in the communities at the time were asked to participate. Phase III: In October 1995, a further 53 men were tested who had not been previously tested. Phase IV: CAAC, as part of its many functions, provides the health service to the Alice Springs Gaol. In June 1995, 33 new inmates were asked to give a first-void urine sample as part of their comprehensive health check on admission. Diagnostic tests used for gonorrhoea were culture, EIA (Abbott Gonozyme, Chicago, IL) and PCR (Roche Amplicor CT/NG, Branchburg, NJ) and for chlamydia were EIA (SYVA MicroTrak II, Palo Alto, CA) and PCR (Roche Amplicor, Branchburg, NJ) (Box 1, below). If there was insufficient urine for all tests, the order of priority was to do PCR first, then culture, chlamydia EIA and finally gonococcal EIA. To check for cross-contamination between PCR specimens, all Phase III specimens that provided sufficient urine were divided before any PCR procedures were performed. When a positive result was obtained the other half of the original sample was retested. Chocolate and/or Thayer-Martin agar plates incubated in candle jars or CO2 gaspacks were used for gonococcal culture. BioCult GC tubes (Orion Diagnostica, Espoo, Finland), which contain a modified Thayer-Martin dipslide and a CO2-generating tablet, were also trialled. Culture media were inoculated with sediment from 10 mL of centrifuged urine and incubated for up to 72 hours at 35oC on-site and/or at Western Pathology in Alice Springs. Neisseria gonorrhoeae was identified by standard methods: typical morphology of colonies, oxidase paper test, microscopy with Gram stain, and latex agglutination (Phadebact GC, Boule Diagnostics AB, Huddinge, Sweden). Urine samples for EIA and PCR were prepared on-site according to the test manufacturer's specifications and then sent to Western Pathology in Alice Springs for processing. Male Aboriginal health workers and registered nurses in each clinic were responsible for liaison with the community and collection of specimens. Each man was asked to give 25-40 mL of first-void urine in a sterile collection jar. No urethral swabs were sought. Initial preparation of urine specimens for transport to the laboratory was completed within three hours of collection. A diagnosis of infection was made and treatment was initiated if any test was positive. Resident clinic staff were responsible for offering treatment, further investigation and safe-sex education to infected men and their sexual partners. Results Study population We tested urine samples from 493 men, of whom 460 lived in six remote communities and 33 were gaol inmates. Acceptability to clients was high, with fewer than 10 men (exact count not possible) declining testing. The 460 men from remote communities represented about 60% of the male population over the age of 12 in the area serviced by the participating clinics (Box 2, below). The proportion of men tested in different communities varied from 28% to 85%. The rate of infection Based on all methods of diagnosis combined, 103 of the men tested (20.9%) were found to be infected with either gonorrhoea or chlamydia. The rate of infection in different communities varied between 14.5% and 26%. Among the gaol inmates, who originated from all parts of the southern NT, seven (21.2%) were infected. Most infections (90.3%) occurred in men aged 15-39 years and the five-year age-specific prevalence of infection in this group varied from 22% to 27% (Box 2, above). Treatment and follow-up Eighty-eight men were treated within two months of testing. The average delay between testing and treatment was 18 days. Forty-five sexual partners of infected men were also recorded as having been treated. Performance of the tests used Different combinations of tests were used in different phases. The volume of urine received from each man varied, so it was not always possible to do all the intended tests. A summary of the numbers of specimens subjected to the various tests and their relative performance is shown in Box 3 (below). During Phase II, culture for gonorrhoea using both BioCult GC tubes and standard Thayer-Martin plates was performed on 193 urine specimens. Thirteen diagnoses were made with the BioCult GC tubes and only seven were made with standard Thayer- Martin plates: all cases positive on Thayer-Martin plates were also positive on the BioCult GC tubes. During Phase III, 19 of the 20 initially positive PCR results were retested (in one case there was insufficient urine). In 18 of these cases there was complete agreement between the first and second test. One chlamydia-positive specimen was negative on the second testing. However, because of delays in transport, the tests on this specimen were done at six and eight days after collection, well in excess of the four days maximum recommended by the test manufacturers. Discussion These results highlight the need for improvements in current STD control, including surveillance programs. Based on routine clinic activity and notifications, NHC reported only 38 men with either gonorrhoea or chlamydia during the whole of 1994 (health departments' notifiable diseases data), compared with the 96 cases detected in this study. Other regions of Australia that have comparable notification rates of these infections1 may have similar problems in underdetection. The variation in participation rates in different communities and age-groups was largely attributable to the numbers of people who happened to be present at the time of the study (people in these remote communities being highly mobile), the working relationship between community members and the health staff, and the assiduousness of the health staff in conducting the program. In central Australia it is often considered, without specific evidence, that people who do not participate in such programs may be at higher risk of infection. Recent work by NHC showed no difference in rates of syphilis infection between those tested during the main body of a screening program and those tested later as part of an effort to test non-participants (Dr Penny Miller, unpublished data). The screening programs in our study were intended to identify the most effective and practical tests for everyday use in remote clinics. Collection of urethral swabs was avoided because it would not have been acceptable to the community. Hence, the study lacked a diagnostic "gold standard" and could not formally evaluate sensitivities and specificities. The published specificities of all the tests were high -- above 98% for urine PCR tests.10-14 The procedures used in Phase III demonstrated no problems with cross-contamination in PCR testing. Several studies have suggested that urine PCR tests for chlamydia are more sensitive than urethral-swab culture and highly specific.10-13 Less work has been done on urine PCR for diagnosing gonococcal infection, but two studies indicate sensitivities above 90% and specificities of 100%.13,14 In ideal conditions, the sensitivities of urethral-swab microscopy and culture are 90%-98%,15,16 but are likely to be much less in remote communities because of high staff turnover, the use of non-nutritive transport media, and frequently prolonged transport times. In such circumstances, urine PCR may be as good as or better than urethral-swab microscopy and culture for diagnosis of gonorrhoea. In any event, according to local management protocols,17 all men presenting to clinics with urethritis are offered immediate treatment for both gonorrhoea and chlamydia. In terms of practical application, PCR was superior to culture for gonorrhoea and EIA for both infections. PCR tests detected more infections with either organism than did the other tests (Box 3). Assuming that the high published specificities for the PCR tests held under field conditions, this increased rate of detection would be attributable to a superior sensitivity. The PCR test was also the easiest to use: urine is simply stored and transported at 4¡-8¡C in the same jar used to collect it. The urine must then be processed in the laboratory within four days (test manufacturer's instructions), which is usually feasible in most remote situations. In contrast, both EIA tests used require centrifuging before transport, and the SYVA MicroTrak II EIA required addition of a transport buffer. However, PCR tests do not provide information about antibiotic susceptibility. If PCR technology is to be used as the principal diagnostic tool for gonorrhoea, there would need to be accompanying sentinel systems for gonococcal culture and antibiotic susceptibility. We found that culture of first-void urine was positive in 72% of diagnoses of gonorrhoea. Sensitivities of 70%-100% for urine culture of gonorrhoea have been reported.18,19 On this basis, urine culture in addition to urine PCR for diagnosis of gonorrhoea could be performed routinely at sentinel sites and during similar programs to those reported here in order to maintain antibiotic-sensitivity surveillance. In the field situation, the BioCult GC tubes detected more gonorrhoea than standard Thayer-Martin plates and were easier and more convenient to use. The accuracy, ease of use and acceptability to men of urine PCR tests suggest several strategies to make clinical services more accessible to people, reduce the amount of disease in the community and identify individuals who are in need of safe-sex education. The use of urine tests for routine diagnosis may encourage more men to present with an STD, even if there is no male practitioner present. Health services could adopt active case-finding strategies such as opportunistic testing when people present for other reasons, including annual comprehensive health checks or community surveys. Such strategies are under consideration by health services in central Australia. For example, CAAC is seeking funding to establish an outreach program via a mobile clinic to make comprehensive well-men's check-ups, including STD checks, accessible to Aboriginal men in Alice Springs. We also examined screening as an STD control strategy. With fewer than 10 men refusing to participate, these programs resulted in 88 men who had either gonorrhoea or chlamydia and at least 45 of their sexual partners being treated. We did not have the resources to determine whether the men were symptomatic at the time of the test. However, none of them had presented to the clinic for treatment. When these findings are considered in the light of routine notifications and our own local experience, it is likely that most of these people would not have been diagnosed and treated outside these programs. Health services catering to remote Aboriginal communities in other parts of Australia may wish to consider this new technology and its usefulness in comprehensive STD education and control programs. Acknowledgements The Tri-State STD/HIV Project (TSP) is jointly funded and managed by the Commonwealth Department of Health and Family Services, Territory Health Services, the South Australian Health Commission and the Western Australian Health Department. The work would not have been possible without the support of the clinical staff of Nganampa Health Council (NHC) and the Central Australian Aboriginal Congress (CAAC). Technical advice and material resources were contributed by the TSP, NHC, CAAC, Western Pathology, Alice Springs Hospital laboratory, the Australian Army, the Northern Territory AIDS/STD Unit, Roche Diagnostics, and the Institute of Medical and Veterinary Science. John Kaldor, Russell Waddell, Frank Bowden and John Boffa all commented on earlier drafts of this paper. References National Notifiable Diseases Surveillance System. Annual report of the National Notifiable Diseases Surveillance System. Commun Dis Intell 1994; 18: 518-548 . De Schryver A, Meheus A. Epidemiology of sexually transmitted diseases: the global picture. Bull World Health Organ 1990; 68 (5): 639-654. Scrimgeour D, Rowse T. Evaluation of STD control activities in central Australia. Menzies School of Health research report. Alice Springs: Menzies School of Health, 1992. Warchivker I. Variations in health care expenditure in the Alice Springs Rural District in 1993-94. Aust N Z J Public Health 1996; 20: 11-13. McDermott R, Beaver C. Models of horizontal equity in resource allocation in Aboriginal health. Aust N Z J Public Health 1996; 20: 13-15. Roongpisuthipong A, Lewis JS, Kraus SJ, Morse SA. Gonococcal urethritis diagnosed from enzyme immunoassay of urine sediment. Sex Trans Dis 1988; 15: 192-195. Schachter J, Pang F, Parks RM, et al. Use of gonozyme on urine sediment for diagnosis of gonorrhoea in males. J Clin Microbiol 1986; 23: 124-125. Moncada J, Schachter J, Shafer MA, et al. Detection of Chlamydia trachomatis in first catch urine samples from symptomatic and asymptomatic males. Sex Trans Dis 1994; 21: 8-12. Sanders JW, Hook EW, Welsh LE, et al. Evaluation of an enzyme immunoassay for detection of Chlamydia trachomatis in urine of asymptomatic men. J Clin Microbiol 1994; 32: 24-27. Jaschek G, Gaydos CA, Welsh LE, Quinn TC. Direct detection of Chlamydia trachomatis in urine specimens from symptomatic and asymptomatic men by using a rapid polymerase chain reaction assay. J Clin Microbiol 1993; 31: 1209-1212. Bianchi A, Scieux C, Brunat N, et al. An evaluation of the polymerase chain reaction Amplicor Chlamydia trachomatis in male urine and female urogenital specimens. Sex Trans Dis 1994; 21: 196-200. Bauwens JE, Clark AM, Loeffelholz MJ, et al. Diagnosis of Chlamydia trachomatis urethritis in men by polymerase chain reaction assay of first-catch urine. J Clin Microbiol 1993; 31: 3013-3016. Mahony JB, Luinstra KE, Tyndall M, et al. Multiplex PCR for detection of Chlamydia trachomatis and Neisseria gonorrhoeae in genitourinary specimens. J Clin Microbiol 1995; 33: 3049-3053. Komeda H, Deguchi T, Yamamoto H, et al. Detection of Neisseria gonorrhoeae in first-voided urine sediments from male urethritis patients by polymerase chain reaction. Kansenshogaku Zasshi 1992; 66: 1209-1212. Judson FN. Gonorrhoea. Med Clin North Am 1990; 74: 1353-1366. Lind I. The laboratory diagnosis of gonorrhoea. In: Facklam R, Laurell G, Lind I, editors. Recent developments in laboratory identification techniques. Amsterdam: Excerpta Medica, 1979. Central Australian Rural Practitioners' Association. The CARPA Standard Treatment Manual. 2nd ed. Alice Springs: Institute for Aboriginal Development, 1994. Woods ER, Galvez LM, Talis AL, Jean Emans S. First catch urine sediment for Chlamydia trachomatis and Neisseria gonorrhoeae in adolescent males with pyuria. J Adolesc Health 1991; 12: 329-334. Feng WC, Medeiros AA, Murray ES. Diagnosis of gonorrhoea in male patients by culture of uncentrifuged first-voided urine. JAMA 1977; 289: 896-898. (Received 24 June, accepted 17 Oct, 1996) Authors' details Tri-State STD/HIV Project, Alice Springs, NT. Steven J Skov, MPH, FAFPHM, Medical Officer, Tri-State STD/HIV Project. Nganampa Health Council, Alice Springs, NT. Penny Miller, MB BS, STD/HIV Program Coordinator. Wayne Hateley, STD/HIV Aboriginal Health Worker. Royal Darwin Hospital, NT. Ivan B Bastian, MB BS, MSc, Microbiology Registrar. Australian Army, Darwin, NT. Jenny Davis, Medical Technician. Central Australian Aboriginal Congress, Alice Springs, NT. Peter W Tait, MB BS, DipRACOG, FRACGP, Acting Senior Doctor. Reprints will not be available. Correspondence: Dr Penny Miller, Nganampa Health Council, PO Box 2232, Alice Springs, NT 0871. - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Steven J Skov · Penny Miller · Wayne Hateley · Ivan B Bastian · Jenny Davis · Peter W Tait

Is screening of Australian blood donors for HTLV-I necessary? Gordon S Whyte MJA 1997; 166: 478 For editorial comment see Kaldor Subsequently cited in Wong et al. Should we be screening blood donors for hepatitis G virus? The case against screening. MJA 1998; 169: 375-377 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - The decision to screen blood for HTLV-I - Blood donor data collection - Extrapolation of State data to national data - New and repeat Australian donors - Screening of donors - Prevalence and incidence of HTLV-I - Risk of HTLV-I transmission - Discussion - Acknowledgement - References - Authors' details - ©MJA1997 Abstract Objective: To re-examine the 1992 decision by Australian Red Cross for its blood banks to screen blood donors for antibody to human T-cell lymphotropic virus type I (HTLV-I) by determining the risk of its transmission by blood transfusion. Methods: Data on patterns of return behaviour by repeat blood donors in Victoria were modelled to deduce the number of donors giving repeat donations in Australia from March 1993 to December 1995. Data on annual donor and issued cellular blood products from 1992 to 1995 were obtained from national Red Cross statistics. From the numbers of donations given by repeat donors, together with the number of new donors, the number tested for HTLV-I was deduced. The number and characteristics of donors screened positive for HTLV-I antibody were collated. The crude prevalence of HTLV-I was calculated by dividing the number of donors with HTLV-I by the total number of donors (repeat donors and new donors). The incidence of HTLV-I was calculated by dividing the number of seroconversions in repeat donors by the cumulative period of donor exposure. Results: Sixteen homologous and five autologous donors were found to be positive for HTLV-I; none seroconverted and no clear risk factors for HTLV-I were identified. The prevalence of HTLV-I in Australian donors is 1 in 100 000 and the incidence less than 1 in 1 million person-years. In the absence of HTLV-I screening, the calculated risk of a transfused patient developing HTLV-I infection is 1 in 370 000, with a risk of developing HTLV-I disease of 1 in 9 to 15 million. Conclusion: Three possible future courses of action for screening for HTLV-I are to screen every donation, to screen only new donors or to discontinue screening altogether. Using the information in this study, public discussion should be encouraged to assist stakeholders to agree on an acceptable level of risk and an appropriate level of screening for HTLV-I in Australia. MJA 1997; 166: 478-481 Introduction Human T-cell lymphotropic virus type I (HTLV-I) is endemic in all continents including Australia,1,2 where in some Aboriginal communities it is present in up to 14% of individuals.3-6 HTLV-I was first described in cases of aggressive T-cell leukaemia in southern Japan7 and in a T-cell lymphoma in a Jamaican patient.8 In areas endemic for the virus, 2% to 4% of those infected rapidly develop fatal leukaemia, with a peak incidence in the sixth decade of life.9 Progressive spastic myelopathy (or tropical spastic paraparesis), first reported in association with HTLV-I infection in Caribbean patients,9 occurs infrequently (0.25%).9 Transmission of HTLV-I is primarily by sexual contact and by infected cellular blood products (packed red cells, platelet-rich plasma and whole blood); breast milk is a major route of HTLV-I transmission in communities where the virus is endemic.10 In predominantly white communities, occasional cases of HTLV-I infection, in the absence of any risk factors, may represent transmission across several generations in a family.11 In a survey of 11 121 Northern Territory blood donors in 1991-1992, only one donor (with no evident risk factors) was confirmed as HTLV-I seropositive.6 Since March 1993, all Australian blood donors have been screened for antibody to HTLV-I. The decision to implement screening was made by the National Executive of the Australian Red Cross in February 1992, despite a lack of agreement among some government advisory bodies. The decision to screen for a rare transfusion-transmitted disease can be re-examined in the light of the results of HTLV-I screening of Australian blood donors from 1993 to 1995. The decision to screen blood for HTLV-I in Australia In October 1986, the American Red Cross proposed that, when a test became available, blood donors should be screened for HTLV-I as this retrovirus could be spread by blood transfusion and had been detected in blood donors.12 In November 1988, the United States Food and Drug Administration recommended testing of whole blood and cellular blood products for antibodies to HTLV-I,13 which was followed by a public review of the issues involved.14 Universal screening was also introduced in Canada, France, the Netherlands and Sweden. In Australia, after recommendations by the Red Cross National Blood Transfusion Committee (in September 1989 and later in March 1991) for HTLV-I screening to be funded, the then Federal Minister for Health sought advice from the National Health and Medical Research Council (NHMRC) in January 1992. In July 1991, the Communicable Diseases Standing Committee of the NHMRC had decided that the costs of screening Australian blood supplies (for HTLV-I) outweighed any public health benefits. This position was endorsed in 1992 by the Public Health Committee of the NHMRC15 and published by the Executive of the NHMRC in December 1992.16 However, the NHMRC also stated ". . . decisions on screening may have to be made on other than public health grounds".16 In February 1992, in the absence of a decision from NHMRC and acting on legal advice, the National Blood Transfusion Committee of the Australian Red Cross recommended that cellular blood products be screened from May 1992.17 By March 1993, although some State governments refused to fund HTLV-I screening, all Red Cross Blood Banks had commenced routine testing for HTLV-I under instruction from the Red Cross National Executive. A report by the Australian Health Ethics Committee, which was endorsed by the NHMRC in November 1993, stated that the cost of screening for HTLV-I was considerable and the risk to the community was low, and that "the spectre of large damages (litigation) . . . probably had a significant influence on the reasoning leading to implementation".17 It considered that the risk of transfusing HTLV-I-infected blood, although real, was rare. The report concluded that a decision not to screen all blood in Australia for HTLV-I would not be unethical.17 Blood donor data collection Data on the number of individuals who donated whole blood in Victoria between March 1994 and December 1995 and the interval from the date of the previous donation were extracted from Victorian Red Cross Blood Bank records. Patients attending for autologous, directed or therapeutic donations were excluded, as were donors returning for repeat testing or counselling only. Plasma donors were excluded because HTLV-I is not transmitted by plasma. The 1994-1995 attendance pattern was comparable with attendance patterns of repeat donors attending in June and July between 1993 and 1996 and was therefore applicable. Data on the number of whole blood collections in Australia and the number of new donors each year were obtained from the annual statistics of the Australian Red Cross Society. Data on the number of blood donations and the number of issues of cellular blood products in Australia for the financial years 1992-95 were obtained from national Red Cross statistics. Extrapolation of State (Victorian) data to national data Donor attendance patterns Repeat donors give many donations, so it is necessary to deduce the number of donors tested for HTLV-I from the total number of donations. The total number of repeat donations is used to calculate the number of repeat donors giving the donations by using a hypothetical model, together with the number of donations given by new donors. Using this information, the prevalence of HTLV-I in donors can then be estimated. Iterative model: The pattern of return after previous donations by Victorian repeat donors was applied to a hypothetical model in which 1000 donations were given each month over 34 months. Using an iterative spreadsheet model, the number of donors giving 1000 repeat donations each month from March 1993 to December 1995 was calculated (Figure, below). It was assumed that all repeat donors in Australia had a similar pattern of repeat donation. By analogy, the proportion of repeat donors contributing the 34 000 donations from repeat donors in the model was applied to the total number of donations from repeat donors in Australia over the 34-month period. To apply the model, it was assumed that the same number of repeat donations was given each month and that the discounting effect of donor rejection was constant over time. The number of Victorian donors and the intervals between donations were extrapolated to all repeat donations in Australia between March 1993 and December 1995 to derive a figure for donor exposure in person-years. "Donor exposure" is the sum of the time between one donation and the next for all donation intervals during the period. The sex and age distribution of Victorian donors was extrapolated to all Australian donors. Prevalence, incidence and risks of HTLV-I The number and characteristics of donors confirmed positive for HTLV-I were provided by Red Cross blood banks in each State and Territory. Donors were confirmed positive if their plasma reacted in triplicate with one of seven HTLV-1 enzyme-linked immunosorbent assay screening tests (Genetic Systems; Abbott; Cambridge recombinant/Ortho; Serodia particle-agglutination; Murex; Sanofi Platelia new; Organon Teknica), as approved by the National Reference Laboratory, and showed a diagnostic pattern on a western blot. The crude prevalence of HTLV-I was calculated by dividing the number of donors with HTLV-I by the total number of donors tested (repeat donors and new donors). The incidence of HTLV-I was calculated by dividing the number of seroconversions in repeat donors by the cumulative period of donor exposure. The risk of disease transmission was calculated from the infectivity rate for HTLV-I and the long-term risk of HTLV-I disease in patients. New and repeat Australian donors The return patterns for repeat donors over the period remained much the same. No donors returned within 12 weeks of donating blood. Of the donors who returned after making a previous donation, 0.29, 0.74, 0.84, 0.89, 0.92 and 0.94 had returned after successive quarters and 0.06 had returned after 18 months. Across Australia, first-time donors gave 335 183 whole blood donations and repeat donors gave 2 038 927 whole blood donations between March 1993 and December 1995. The proportion of first-time donations over the four fiscal years from July 1992 was 0.14, 0.14, 0.14, and 0.13, respectively. Screening of donors for HTLV-I By applying the pattern of return for repeat donors in Victoria to a hypothetical figure of 1000 donations a month over 34 months from repeat donors, it was concluded that the 34 000 donations would have been given by 19 197 donors in Victoria who had returned within 18 months. Furthermore, 6% (2040) would have been given by repeat donors whose previous donation was more than 18 months previously. By applying the Victorian model to the national statistics, it was concluded that over the 34 months 2 038 927 donations were given by 1 273 550 repeat donors. In addition, there were 335 183 new donors and donations. Therefore, a total of 1 608 733 individuals had been screened for HTLV-I. Some States had begun testing for HTLV-I before March 1993, but the high proportion of repeat donors in Australia, the small number of infected donors and the absence of serconversion permit the assumption that they would have been identified if screening had been delayed to March 1993. Prevalence and incidence of HTLV-I in blood donors To December 1995, 21 donors had been confirmed positive for HTLV-I in Australia, each on the first occasion the donor was tested. Five of the blood collections were for autologous transfusion. There were no seroconversions (a change in serological status from negative to positive) during the study period. Two donors were identified before June 1992, with 5, 8 and 6 in each subsequent 12 months. More men and more first-time donors were positive than expected, but the age distribution matched that of the general donor population (Box, below). There were no clear patterns of disease acquisition, although four of the five donors born in endemic areas were aged less than 40. Therefore, the crude prevalence of HTLV-I in Australian blood donors was 16 in 1 608 733, or 1 in 100 546. In Victoria, repeat whole blood donors gave 358 332 donations between March 1994 and December 1995, with intervals from the previous donation of up to 23.5 years. The repeat donors represent 11 851 014 person-weeks of exposure, or 227 904 person-years. By extrapolation, 2 038 927 repeat donations in Australia represent 1 296 785 person-years of exposure. There were no seroconversions. Therefore, the crude incidence of HTLV-I in Australian blood donors was less than 1 in 1 000 000 person-years. Risk of HTLV-I transmission via blood transfusion The risk of transmitting HTLV-I in Australia by blood transfusion over the study period was calculated from the number of donations given by 16 donors in 2 374 110 donations. The spreadsheet calculations showed that 1.6 million donors gave 2.4 million donations, so 16 donors would have given 24.6 donations. Therefore, the risk of receiving blood infected with HTLV-I before testing was about 1 in 100 000. The infectivity rate has been recently reported as 0.27,18 so only 1 in 370 000 transfusion recipients would become infected. Relatively few (2.5%-4%) people with HTLV-I infection not acquired by blood transfusion risk developing disease after 10 to 30 years.19 Therefore, the risk of developing HTLV-I disease from blood transfusion in Australia without testing would have been 1 in 9 to 15 million. Transfusion recipients, particularly those who are immunocompromised, may have a shorter incubation period,20 and infants of infected mothers have a 25% chance of becoming infected.21 If universal screening were discontinued, then the risk of transfusing infected blood would progressively return to the pretesting situation because of the recruitment of new donors from a population with the same characteristics as at present, as well as the retirement of repeat donors who have already been screened. In the absence of seroconversion, if only previously untested donors are screened for HTLV-I then there will be a zero risk of transmitting HTLV-I by blood transfusion. However, seroconversion has been reported in Dutch, French and American studies.22-24 If only the 14% of donations by new donors are screened, then the costs to Red Cross and the community would be significantly reduced. Discussion Our results have shown that the prevalence of HTLV-I in Australian donors is 1 in 100 000. By comparison, the prevalence of hepatitis C virus in new Victorian donors is 1 in 560; of hepatitis B virus, 1 in 650; and of HIV, 1 in 27 000. However, the introduction of universal blood screening for these diseases has reduced the risk to the transfused population for hepatitis C virus to 1 in 150 000, for hepatitis B virus to 1 in 150 000 and for HIV to 1 in 1.3 million.25 The risk of transfusing HTLV-I-infected blood would have been 1 in 100 000 without screening. In the United Kingdom, HTLV-I has been found in 1 in 20 000 donors; in the United States, in 1 in 6000; and in Sweden and the Netherlands, in 1 in 50 000.19 The decision by the Australian Red Cross to commence testing of all blood donations for HTLV-1 was contentious. Red Cross had shown that HTLV-I was present in the Australian blood supply,9 and believed that testing should be undertaken to ensure the safety of the blood supply as well as its own credibility.26 Our findings have shown that in the three years since screening began 16 Australian blood donors were found with HTLV-I. Without screening, the risk of viral transmission by blood transfusion would have been 1 in 100 000. On the other hand, the NHMRC and some State governments believed that universal screening was not justified on public health grounds. The findings in this study show that the risk of a blood transfusion recipient developing HTLV-I-related disease as a result of transfusion is about 1 in 10 million; these data were not available when Red Cross made their decision for universal screening. From the perspective of Red Cross and transfusion recipients, screening affords the certain benefit27 of the removal of the threat of HTLV-I infection from transfusion whatever the future risk of developing leukaemia. From a public health perspective, the certain benefit is the prevention of the very low risk of leukaemia or spastic paraparesis. Stakeholders (Australian Red Cross Blood Service, State and Federal governments and the community) would be assisted by public discussion of an acceptable level of risk and appropriate level of screening for rare transfusion-transmitted diseases; HTLV-I provides a suitable test case. It may be appropriate to screen only new donors for HTLV-I (at a lower cost) now that the donor base has been repeatedly screened. However, it is likely that Red Cross would need a form of statutory defence, such as that provided in Victoria for HIV and hepatitis C virus,28 if it were to apply less-than-universal screening for HTLV-I and other conditions of low risk to public health. Acknowledgement I thank the Directors of each State Blood Transfusion Service for providing the figures for HTLV-I and for constructive and critical comment. References Doherty RR. HTLV-I in Australia and Oceania: long term resident or recent immigrant? Med J Aust 1996; 164: 84-86. Gallo RC. A surprising advance in the treatment of viral leukemia. N Engl J Med 1995; 332: 1783-1784. Ascher D, Goudsmit J, Poeroy K, et al. Antibodies to HTLV-I in populations of the south western Pacific. J Med Virol 1988; 26: 339-351. Bastian I, Hinuma Y, Doherty RR. HTLV-I among Northern Territory Aborigines. Med J Aust 1993; 159: 12-16. Bastian I, Gardner J, Webb D, Gardner I. Isolation of a human T-lymphotropic virus type I strain from Australian Aboriginals. J Virol 1993; 67: 843-851. Bastian I, Dent J, McFarlane R, et al. HTLV-I among Northern Territory blood donors. Med J Aust 1993; 159: 7-12. Hinuma Y. Natural history of the retrovirus associated with a human leukemia. Bio essays 1985; 3: 205-209. Poeisz B, Ruscetti F, Gazdar A, et al. Detection and isolation of type C retrovirus particle from fresh and cultured lymphocytes of a patient with cutaneous T-cell lymphoma. Proc Natl Acad Sci U S A 1980; 77: 7415-7419. Hollsberg P, Hafler DA. Pathogenesis of diseases induced by human lymphtropic virus type 1 infection. N Engl J Med 1993; 328: 1173-1182. Nakano S, Ando Y, Saito K, et al. Primary infection of Japanese infants with adult T-cell leukemia associated retrovirus (ATLV): evidence for viral transmission from mothers to children. J Infect 1986; 12: 205-212. May JT, Stent G, Schnagl RD. Antibody to human T-cell lymphotropic virus type I in Australian Aborigines [letter]. Med J Aust 1988; 149: 104. Barnes D. HTLV-I: to test or not to test. Science 1988; 242: 372-373. Parkman PD. HTLV-I antibody testing; instruction of all registered blood establishments. Bethesda: Food and Drug Administration, 1988. Public Health Service Working Group. Licensure of screening tests for antibody to human lympotropic virus type I. MMWR Morb Mortal Wkly Rep 1988; 37: 736-747. Anon. Blood tests would drain funds: medics. Courier Mail 1992 June 5: 15. National Health and Medical Research Council, Communicable Diseases Standing Committee. HTLV-I screening: outcome of consideration by the Executive. Canberra: NHMRC, 4 December 1992. National Health and Medical Research Council. Case study of screening blood donations for human T-cell lymphotropic virus type I: Report of the Australian Health Ethics Committee. Canberra: NHMRC, November 1993. Donegan E, Lee H, Operskalski GM, et al. Transfusion transmission of retroviruses: human T-lymphotropic virus type I and II compared with human immunodeficiency virus type I. Transfusion 1994; 34: 478-483. Pagliuca A, Pawson R, Mufti GJ. HTLV-I screening in Britain. BMJ 1995; 311: 1313-1314. Kaplan JE, Litchfield B, Roualt C, et al. HTLV-I associated myelopathy associated with blood transfusion in the United States. Neurology 1991; 41: 192-197. Sugiyama H, Doi H, Yamaguchi K, et al. Significance of post-natal mother-to-child transmission of human T-lymphotropic virus type-1 on the development of adult T-cell leukemia/lymphoma. J Med Virol 1986; 20: 253-260. Vrielink H, van der Poel CL, Reesink HW. Efficacy of selected versus random blood donor screening for anti HTLV-I antibodies [letter]. Vox Sang 1995; 68: 251-252. Courouce AM, Pillonel J. Transfusion-transmitted viral infections. N Engl J Med 1996; 335: 1609-1610. Schreiber GB, Busch MP, Kleiman SH, Korelitz JJ. The risk of transfusion-transmitted viral infections. N Engl J Med 1996; 334: 1685-1690. Whyte G S, Savoia H F. The effectiveness of donor selection for reducing the risk of HCV, HBV and HIV in new blood donors in Victoria. Med J Aust . In press. Wylie B. HTLV-I: is donor screening really necessary? [editorial] Med J Aust 1993; 159: 4-5. McGuire A, Henderson J, Mooney G. The economics of health care. London: Routledge, 1994: 112. Health Act 1958 (Vic.), s. 139. Melbourne: The Law Printer, 1995.(Received 5 Aug 1996, accepted 18 Feb 1997) Authors' details Australian Red Cross, Blood Bank of Victoria, Southbank, VIC. Gordon S Whyte, FRACP, FRCPA, Director. Reprints will not be available. Correspondence: Dr G S Whyte, PO Box 354, Southbank, VIC 3205. E-mail: rcbb AT peg.apc.org ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Gordon S Whyte

Hepatitis C: waiting for the Grim Reaper Encouraging drug users to adopt non-injecting routes of administration may be the most effective way of controlling the hepatitis C epidemic MJA 1997; 166: 284 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". - - ©MJA1997 Until the controversial Grim Reaper campaign alerted Australians to the seriousness of its newly recognised AIDS epidemic, citizens of the Lucky Country were complacent about infections. Fortunately, the HIV epidemic has been stabilised among injecting drug users (IDUs) in Australia by a harm reduction/public health approach to intravenous drug use. Now we have evidence of another important viral epidemic -- hepatitis C. Despite it being arguably the commonest life-threatening infection in Australia, alarm bells have not yet been rung for hepatitis C. We are beginning to recognise hepatitis C as a public health problem comparable in magnitude with HIV The incidence and prevalence of hepatitis C in Australia are far higher than those of HIV infection. An estimated 130 000 Australians have been infected with hepatitis C virus (HCV) over the last 20 years, with about 6000 new chronic infections a year through injecting drug use alone.1 In contrast, an estimated 15 450 people have been infected with HIV by all routes of transmission, with about 500 new infections a year between 1994 and 1996.2 Although a smaller proportion of individuals infected with HCV experience serious morbidity and mortality, and only after a longer delay (10%-20% are estimated -- conservatively -- to develop cirrhosis within 20 years and 5% of these develop hepato cellular carcinoma within five years),3 the far larger pool of infected people and longer duration of illness suggest that the total health and economic burden of hepatitis C in Australia is considerable and may well surpass HIV before too long. The task of bringing hepatitis C under control is daunting. While the pieces of the hepatitis C jigsaw puzzle are still being assembled, injecting drug use is undeniably the major mode of transmission in Australia and other developed countries. In this issue of the Journal, Sladden and colleagues found that 85% of hepatitis C notifications involved IDUs. Their epidemiological study analysed notifications of hepatitis C from a community sample and assigned risk factors for a high proportion of respondents. However, the high non-response rate of 53% and the statistically significant differences between respondents and non-respondents qualify their findings. In contrast to Sladden and colleagues' results, a United States study estimated a much lower proportion of IDUs among hepatitis C notifications, but could not assign risk factors for as high a proportion of respondents.4 As official policy in the US advocates "zero tolerance" for any illicit drug use, it is hardly surprising that many American IDUs were apparently intimidated from revealing their risk behaviour. Australian national surveillance data (of uncertain quality) accord with Sladden and colleagues' results -- about 85% of hepatitis C virus infections involve IDUs.1 Current hepatitis C incidence in IDUs is now estimated to be about 15 per 100 person-years.1 IDUs entering prison on more than one occasion are at even greater risk.5 These alarming figures are consistent with those for other countries.6 Hepatitis C seroprevalence in a large cohort of IDUs in the United States was 65% for those who had injected for one year or less and 85% when the cohort was followed up for 49-72 months.7 Indeed, a recent review1 of published studies of the epidemiology of hepatitis C among Australian IDUs traces the epidemic back to at least 1971, soon after injecting drug use became established in this nation. Clearly, the epidemic will be halted only if it is controlled among IDUs. Could a harm reduction/public health approach control hepatitis C among IDUs? Such an approach, which includes needle exchange and methadone treatment programs, has already been successful in stabilising the HIV epidemic among IDUs in Australia. In contrast, the US "War on Drugs", which has resulted from the official policy of "zero tolerance" for any illicit drug use, has had catastrophic public health consequences. In 1994, IDUs accounted for only 2.5% of AIDs cases in Australia,8 compared with 28% in the US in 1993.9 While the prevalence of AIDS (per million population) in the United States was 4.3 times that in Australia in 1988, by 1992 this ratio had increased to 6.4,10 fuelled by an uncontrolled epidemic among IDUs and a secondary epidemic among heterosexual contacts of HIV-positive IDUs in the US. Despite the success of the harm reduction/public health approach in controlling the HIV epidemic and slowing the spread of hepatitis B among IDUs in Australia, it appears not to have reduced the incidence of hepatitis C.1 There is a very real possibility that hepatitis C transmission among IDUs requires only minimal breaches of infection control guidelines.1 Hepatitis C virus is an order of magnitude more infective than HIV,11 and hepatitis C has a far higher baseline prevalence than HIV infection. Consequently, while expanding needle exchange and methadone treatment programs may reduce hepatitis C incidence, this is unlikely to control the epidemic. The approach of eliminating importation or global production of injectable drugs continues to enjoy some support, especially during long election campaigns, but it is increasingly apparent that this is an expensive fantasy. Even a major architect of Nixon's "War on Drugs", the former White House adviser John Erlichman, testified to a US Senate Subcommittee: "the people in the federal government . . . know darn well that the massive war they have mounted on narcotics is only going to be effective at the margins. If they don't know it, they ought to know it."12 Reducing drug supply or demand is seemingly a more realistic objective, but the evidence of past decades provides little grounds for optimism. While attempts to eliminate harm from illicit drugs almost universally fail, efforts to reduce harm generally succeed. Therefore, encouraging drug users to adopt non-injecting routes of administration (sniffing, smoking, snorting or swallowing) appears to offer our best hope for achieving hepatitis C control among IDUs. Smoking of heroin has overtaken injecting in popularity in many parts of the United States, the United Kingdom and the Netherlands.13 Reasons differ between these countries but are thought to include, in the US, the scarcity of sterile injecting equipment, coupled with drug users' fear of contracting HIV infection through needle sharing, and (most importantly) the recent drop in price and increase in purity of available heroin. In other countries, the increased availability of heroin base, which has a lower melting point than heroin hydrochloride and is thus more suitable for smoking, has played a part. A strategy of promoting non-injecting routes of administration also offers the hope of reducing the growing epidemic of drug overdoses, which claim about 500 young Australian lives each year. We are beginning to recognise hepatitis C as a public health problem comparable in magnitude with HIV. The recent inclusion of hepatitis C in the Third National HIV/AIDS Strategy means that it will at least be included in a national policymaking apparatus, which delivered splendid, internationally recognised results for HIV/AIDS. Only when there is a national commitment to raise levels of awareness about the seriousness of this epidemic will Australia stand a chance of controlling hepatitis C. Until Australia embarks on a major national awareness-raising exercise, such as a "Grim Reaper"-style public education campaign, the band will continue to play on for hepatitis C as it once did for HIV. Alex Wodak Director, Alcohol and Drug Service, St Vincent's Hospital, Sydney, NSW. Crofts N, Jolley D, Kaldor J, et al. The epidemiology of hepatitis C virus infection among injecting drug users in Australia. J Epi Comm Health. In press. National Centre in HIV Epidemiology And Clinical Research. An epidemiological assessment of the HIV epidemic in Australia. Technical Appendix 1. Evaluation of the HIV/AIDS Strategy 1993-4 to 1995-6. Canberra: AGPS, 1996: 9-16. Albertis A, Realdi G. Parenterally acquired non-A, non-B (type C) hepatitis. In: McIntyre N, Benhamou J-P, Bircher J, et al., editors. Oxford textbook of clinical hepatology. Oxford: Oxford University Press, 1991: 605-617. Alter MJ, Hadler SC, Judson FN et al. Risk factors for acute non-A, non-B hepatitis in the United States and association with hepatitis C virus infection. JAMA 1990; 264: 2231-2235. Crofts N, Stewart T, Hearne P, et al. Spread of blood borne viruses among Australian prison entrants. BMJ 1995; 310: 285-288. MacDonald M, Crofts N, Kaldor J. Transmission of hepatitis C virus: rates, routes and cofactors. Epidemiol Rev. In press. Garfein RS, Vlahov D, Galai N, et al. Viral infections in short-term injection drug users: the prevalence of the hepatitis C, B human immunodeficiency and human T-lymphotropic viruses. Am J Pub Health 1996; 86: 655-661. National Research Council and Institute of Medicine. Preventing HIV transmission. The role of sterile needles and bleach. Washington DC: National Academy Press. 1995. National Centre For Epidemiology And Clinical Research. Australian HIV surveillance report. 11: 14. April. 1995. Feachem RGA. Valuing the past -- investing in the future. Evaluation of the national HIV/AIDS strategy 1993-94 to 1995-96. Canberra: Commonwealth Department of Human Services and Health, AGPS, 1995. Gerberding JL. Management of occupational exposure to blood-borne viruses. N Engl J Med 1995; 332: 444-451. Baum D. Smoke and mirrors. The war on drugs and the politics of failure. Boston: Little Brown and Company, 1996. Wodak A, Crofts N. Once more unto the breach: controlling hepatitis C in injecting drug users. Addiction 1996; 91: 181-184. - - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Alex Wodak

Hepatitis C transmission on the north coast of New South Wales: explaining the unexplained Tim J Sladden, Alan R Hickey, Therese M Dunn and John R Beard MJA 1997; 166: 290 For comment see Wodak Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Exposures - Transmission to sexual partners and offspring - Discussion - Acknowledgements - References - Authors' details - - ©MJA1997 Abstract Objective: To determine the routes of hepatitis C virus (HCV) transmission in an Australian community. Design: Questionnaire-based, cross-sectional survey of notified HCV cases. Subjects and setting: All cases notified to the New South Wales North Coast Public Health Unit between 1 January 1993 and 30 September 1994. Outcome measures: Frequency of potential transmission exposures (parenteral and sexual); most likely primary exposure; HCV infection rates in sexual partners and offspring. Results: 467 subjects responded (47% of resident cases). Of these, all but one reported actual or potential blood exposures (injecting drug user [IDU], 85%; IDU with sharing of injection equipment, 76%; pre-1990 blood transfusions, 6%; other blood exposures, 8%). Most subjects reported multiple exposures and none reported sexual contact as the only potential exposure. Of 233 sexual partners tested for HCV, 83 were positive; 54 of these were questioned and all had other parenteral exposures. Only three children out of 91 children tested were positive for HCV (two expressing maternal antibodies). Conclusions: In contrast with previous studies, possible HCV transmission modes were identified for almost all respondents. Most respondents in this community were IDUs. Non-parenteral transmission appeared minimal. Novel approaches to preventing HCV transmission in IDUs are needed. MJA 1997: 166; 290-293 Introduction Few studies have investigated transmission of hepatitis C virus (HCV) in representative, population-based samples.1-3 Most previous studies have examined patient series,4-6 those at risk (e.g., transfusion recipients and injecting drug users [IDUs])7-9 or other particular groups (e.g., blood donors, pregnant women and prisoners).10-12 Previous studies have also failed to identify exposures in significant numbers of cases (up to 45% of respondents).1-5,8 HCV transmission is predominantly parenteral13 (via shared drug injection equipment, infected blood products [almost entirely before screening was introduced in February 1990], unsterile skin penetration practices [e.g., tattooing, ear/skin piercing, acupuncture], needlestick and "sharps" injuries and shared personal items, such as toothbrushes and razors14 ). However, patient-to-patient transmission (via contaminated anaesthetic circuitry)15 and surgeon-to-patient transmission (via percutaneous injury)16 have both been demonstrated. Sexual transmission without blood contact appears rare,5,6,8,13 but the risk of blood exposure may be increased by sexual contact during menstruation and anal intercourse. Vertical transmission also appears rare.8,13,17 Both sexual and vertical transmission appear viraemia-dependent,8,9,13,17 and may be facilitated by genital lesions.6,17 Nipple trauma may enable postnatal transmission.18 Household transmission is probably restricted to infected personal items.19 Arthropod vectors have not been identified. Despite evidence that there is no risk of transmission via casual contact, community concern about hepatitis C transmission remains evident in the discrimination reported anecdotally by people with HCV. Clarification of how HCV is transmitted is needed both to allay this concern and to allow the development of new prevention strategies.20 One focus of the current Australian hepatitis C epidemic is the north coast of New South Wales (NSW), where the notification rate (201/100 000 residents) is double the NSW rate (103/100 000 residents),21 and nearly three times the Australian average (74/100 000 residents).22 We investigated the mode of transmission in notified cases in residents on the NSW north coast over a 21-month period. Methods All people diagnosed with HCV infection (through duplicate second generation anti-HCV antibody tests) who were notified to the North Coast Public Health Unit between 1 January 1993 and 30 September 1994 were invited to participate. Subject name, diagnosis and contact address were verified with attending doctors. Questionnaires were mailed to subjects with covering letters, consent statements, and reply-paid return envelopes. Non-respondents were recontacted by mail six weeks later. Data, with identifying codes removed, were entered into a restricted-access database. We developed a questionnaire that included demographic questions, a checklist of possible ways the subject may have contracted hepatitis C (see Box 1) and questions about the HCV status of the subject's current sexual partner and, for women, of their children. The questionnaire was pilot-tested on clients of a local sexual health service. The study and questionnaire were approved by the North Coast Region Health Service Ethics Committee. For subjects with multiple potential exposures, exposures were ranked according to expected risk, and the exposure with the highest risk was considered the most likely primary exposure. Parenteral exposures were assumed to be higher risk than sexual exposure and ranked as: High risk -- (in descending order of risk) injecting drug use (IDU) (with and without reported sharing of injection equipment), receipt of pre-1990 blood products, dialysis and transplants; Medium risk -- needlestick injuries, tattooing, or blood splashes into a cut, eye or mouth (i.e., during an accident or fight); and Potential or low risk -- origin from countries where medical services have used inadequate infection control procedures in the past (such as reuse of needles) or where unsterile tattooing or scarification is common (including the Mediterranean area, Eastern Europe, Asia, South America, Africa and the Middle East),23 post-1989 blood transfusion, ear or skin piercing and other clinical procedures. Transmission between study subjects and their current sexual partners was investigated; a modified questionnaire which included only the checklist of potential transmission routes was mailed to all HCV-positive partners. Household and social contact were examined when no other exposure was reported. Subjects with only low-risk or no parenteral exposures were offered testing for HCV RNA by polymerase chain reaction (PCR) to confirm their hepatitis C status. Demographic characteristics of respondents and non-respondents were compared with chi-squared tests and t tests, and sharing of injection equipment by current and former IDUs was compared with chi-squared tests. Results Of 1487 notified cases, 487 were excluded (395, temporary residents or non-residents; 67, with address unknown; seven, aged under 18 years; 18, other reasons), leaving a study population of 1000. Questionnaires were returned by 467 (46.7%). Respondents differed significantly from non-respondents in sex and age distributions: respondents included a significantly higher proportion of women than non-respondents (respondents: 219/467 [47%]; non-respondents: 212/533 [40%]; chi-squared = 4.42, P = 0.035) and were significantly older (respondents: mean age, 37.4 years; 95% confidence interval [CI], 36.6-38.3; range, 18-86; non-respondents: mean age, 34.9 years; 95% CI, 34.4-35.5; range, 18-62); t [unequal variances] = 4.70; df = 852, P < 0.001). Exposures Potential HCV exposures are shown in Box 1. Almost all 467 respondents reported at least one potential transmission exposure and most reported multiple exposures. The potential exposure with the highest expected risk was classified as the most likely primary exposure. Most respondents (398 [85%]) were IDUs (222 men, 176 women), including 287 (72%) former IDUs (although 45 [11%] of these reported stopping during the survey period). None of the 19 subjects aged over 60 years were IDUs. Of the IDUs, 354 (89%) reported having shared injection equipment. Frequency of sharing injection equipment by IDU status is shown in Box 2 (below). Current IDUs reported sharing significantly less than former IDUs ( chi-squared = 5.82; df = 1; P= 0.016). Hepatitis B infection was reported by 184 subjects (39%); 175 of these (95%) were IDUs. All but 11 sharers of injection equipment and all non-sharer IDUs reported other parenteral exposures (Box 1). Among subjects who were not IDUs, the most likely primary exposure (Box 1) was pre-1990 blood transfusion for 30 (6%), dialysis for two (0.4%), needle-stick injuries for six (1%) (including three health care workers, one with a known exposure to hepatitis C virus, a garbage collector and the partner of an IDU), tattooing for four (0.9%), blood splashes for four (0.9%), origin in a "high-risk" country for three (0.6%), post-1989 blood transfusion for two (0.4%), skin piercing for 13 (3%) and medical procedures for four (0.8%). About a third of subjects (151 [ 32%]) reported past or current HCV-positive sexual partners. However, 147 (97%) also had potential blood exposures (141, IDU; three, blood transfusion; and one each, tattoos, needlestick injury and blood splash). The remaining four had low-risk potential blood exposures (pierced ears or skin for three and a clinical procedure for one). Thus, sexual contact did not occur without concurrent or potential blood exposure(s). Sharing of personal items (e.g., toothbrushes) also could not be excluded for subjects reporting sexual contact. For 15 subjects, no sexual exposure and only low-risk potential parenteral exposures were reported. Another subject reported no risk factors. Polymerase chain reaction (PCR) was offered to these 16 to confirm their anti-HCV antibody test results. Ten were lost to follow-up (including the subject with no risk factors), three were confirmed HCV-positive (all had had clinical procedures, two had pierced ears and the third had social contact with an HCV-positive person) and three were HCV-negative, indicating either resolved infections or false positive initial antibody results. Transmission to sexual partners and offspring Three-hundred-and-twenty subjects (69%) had current sexual partners. Of 233 partners who had been tested for HCV, 83 (36%) were positive, 138 negative and 12 had unknown results. Of the positive partners, 80 (96%) were partners of IDUs, with independent parenteral exposures determined for 54 (68%) and unknown for the rest. Of the negative partners, 70 (51%) practised "unsafe" sex (defined as unprotected oral, anal or vaginal sex) with study subjects. Among the 219 women subjects, 173 had had children; 56 had had one child tested for HCV and 35, a second child. Only three children were anti-HCV positive -- two infants expressing maternal anti-HCV antibodies, and a three-year old. Discussion Many studies have investigated HCV transmission in limited patient series or specific groups,4-12 and full identification of exposures has been difficult.1-5,8 Our study was a population-based survey, and we were able to identify potential blood exposures for 99% of respondents. However, the response rate was low (47%), reflecting the difficulties of community-based surveys and, possibly, community sensitivities about bloodborne viruses. In addition, there were small but statistically significant age and sex differences between respondents and non-respondents, with a higher proportion of women among respondents and most older subjects responding. However, none of the 19 subjects aged over 60 years were IDUs. We suggest that non-IDUs would be more likely to respond than IDUs, and that a higher response rate in non-IDUs accounted for the age difference between respondents and non-respondents. Questionnaire comprehension was not thought to be a problem as the north coast population is predominantly English-speaking (96%).24 The high proportion of subjects declaring use of illicit drugs in the 60 years and under age group (89%) implies they were reporting truthfully. Therefore, we postulate that the respondents were representative of those infected with HCV in this community. If more respondents had denied injecting drugs, selection bias due to non-response of IDU subjects might have been a legitimate concern. Our results suggest that, on the NSW north coast, injecting drug use with sharing of injection equipment accounted for transmission in 76% of all people with hepatitis C. Transmission during injecting drug use remained possible in a further 9% who denied sharing injection equipment, as unrecognised contamination of such equipment (e.g., spoons, filters, water or swabs), poor recall or denial of sharing may have occurred. Apart from IDU, other high- or medium-risk blood exposures appeared to be responsible for a further 10% of respondents, and all but one of the remaining 5% had low-risk or potential blood exposures, with 1% of these also having sexual contact. While rates of IDU (past or current) may be relatively high on the NSW north coast, we suggest that almost all HCV transmission is via blood exposure, with varying proportions of different types of blood exposure in different populations. Thus, there appeared to be minimal HCV transmission via sexual, perinatal, household, occupational or social contact, provided blood exposures were avoided. Supplemental testing identified some false positives among the few subjects without obvious blood exposures. While a third of subjects had had sexual contact with HCV-positive partners, all of these had additional blood exposures (high risk for 95%, medium risk for 2% and low risk for 3%). Our results should help allay community concern about HCV transmission via casual contact. Sexual transmission appears to be minimal, but the risk may increase with menstruation, anal sex, concurrent STDs that involve scratching, sores or blisters, and increasing viraemia (often observed in early, acute stages of HCV infection). Uninfected partners should also avoid oro-facial abrasions of infected sexual partners (e.g., from toothbrushing or razor cuts). People with hepatitis C who are contemplating having children would be advised to seek medical advice regarding their HCV-RNA PCR status, hepatic enzyme function, and clinical symptoms as markers of viral activity. The low frequency of unexplained transmission in this study (< 1%) was almost entirely attributable to the high rate of reporting of injecting drug use. Other studies have found much lower rates of injecting drug use in HCV-positive subjects, but have been unable to explain transmission in a much higher proportion (27%-45%),1,3-5 possibly because of reluctance to admit illicit drug use. In our study, the privacy afforded by the self-administered questionnaire may have encouraged more truthful reporting than may occur in an interview or clinic situation. Many IDUs were former users, suggesting not only reluctance of current IDUs to participate, but also that much HCV infection is due to past drug use. Current IDUs shared injection equipment significantly less often than former IDUs, indicating increased awareness of the dangers and the effectiveness of needle and syringe exchange programs. However, sharing of injection equipment remains the commonest route of transmission of HCV, responsible for an estimated 10 000 new infections each year in Australia.25 The proportion of cases due to IDU will increase with blood product screening. This emphasises the need for transmission prevention and harm-minimisation programs, especially targeting adolescents before any experimental drug-taking. Community development and peer education of IDUs to promote safer injecting practices should be strengthened.26 The impacts of improved access to needle and syringe exchange and methadone programs, campaigns to encourage non-injecting routes of drug administration, development of non-reusable syringes,25 supply of heroin to registered users27 and provision of "safe-house" injecting venues on HCV transmission all need to be investigated. Acknowledgements Kieran Mutimer and staff at the Lismore Sexual Health and AIDS Service assisted with piloting and circulating questionnaires. References Alter MJ, Hadler SC, Judson FN, et al. Risk factors for acute non-A, non-B hepatitis in the United States and association with hepatitis C virus infection. JAMA 1990; 264: 2231-2235. Mistry SA. Hepatitis C notifications in the Australian Capital Territory, January to June 1993. Comm Dis Intell 1995; 19: 183-188. Curran M. Acute hepatitis C notifications and associated risk factors in Australia, 1995 first quarter report. Comm Dis Intell 1995; 19: 615-617. Strasser SI, Watson KJR, Lee CS, et al. Risk factors and predictors of outcome in an Australian cohort with hepatitis C virus infection. Med J Aust 1995; 162: 355-358. Weinstock HS, Bolan B, Reingold AL, Polish LB. Hepatitis C virus infection among patients attending a clinic for sexually transmitted diseases. JAMA 1993; 269: 392-394. Tor J, Llibre JM, Carbonell M, et al. Sexual transmission of hepatitis C virus and its relation with hepatitis B and HIV. BMJ 1990; 301: 1130-1133. Crofts N, Hopper JL, Bowden DS, et al. Hepatitis C virus infection among a cohort of Victorian injecting drug users. Med J Aust 1993; 159: 237-241. Meisel H, Reip A, Faltus B, et al. Transmission of hepatitis C virus to children and husbands by women infected with contaminated anti-D immunoglobulin. Lancet 1995; 345: 1209-1211. Bresters D, Mauser-Brunschoten EP, Reesink HW, et al. Sexual transmission of hepatitis C virus. Lancet 1993; 342: 210-211. Kaldor JM, Archer GT, Buring ML, et al. Risk factors for hepatitis C virus infection in blood donors: a case-control study. Med J Aust 1992; 157: 227-230. Fairley CK, Leslie DE, Nicholson S, Gust ID. Epidemiology and hepatitis C in Victoria. Med J Aust 1990; 153: 271-273. Anand CM, Fonseca K, Walle RP, et al. Antibody to hepatitis C virus in selected groups of a Canadian urban population. Int J Epidemiol 1992; 21: 142-145. van der Poel CL, Cuypers HT, Reesink HW. Hepatitis C virus six years on. Lancet 1994; 344: 1475-1479. Davis AR. Contaminated razor blades as a possible source of hepatitis C virus infection [letter]. Med J Aust 1995; 163: 275. Chant K, Kociuba K, Munro R, et al. Investigation of possible patient-to-patient transmission of hepatitis C in a hospital. NSW Public Health Bull 1994; 5: 47-51. Esteban JI, Gomez J, Martell M, et al. Transmission of hepatitis C virus by a cardiac surgeon. N Engl J Med 1996; 334: 555-560. Zanetti AR, Tanzi E, Paccagnini S, et al. Mother-to-infant transmission of hepatitis C virus. Lancet 1995; 345: 289-291. Grayson ML, Braniff KM, Bowden DS, Turnidge JD. Breastfeeding and the risk of vertical transmission of hepatitis C virus [letter]. Med J Aust 1995; 163: 107. Davis AR, Kowalik AM. Hepatitis C virus transmission to heterosexual partner: bedroom or bathroom hazard? [letter] Med J Aust 1996; 164: 126. Strasser SI. Hepatitis C: questions still to be answered [editorial]. Med J Aust 1996; 164: 132-133. Sladden TJ, Hickey AR, Beard JR. Hepatitis C on the North Coast of NSW [letter]. Med J Aust 1995; 162: 166. Longbottom H, Evans D, Myint H, Hargreaves J. Annual Report of the National Notifiable Diseases Surveillance System. Comm Dis Intell 1994; 18: 521, 533. National Health and Medical Research Council Hepatitis C Working Party. Draft report on a strategy for the detection and management of hepatitis C virus in Australia. Canberra: NHMRC, 1996. Census Applications. Socio-economic profile of the north coast of New South Wales. Lismore: North Coast Regional Co-ordination Pilot Program, NSW Premier's Department, 1996. Wodak A, Crofts N. HIV revisited: preventing the spread of blood-borne viruses among injecting drug users. Aust J Public Health 1994; 18: 239-240. Feachem RGA. Valuing the past. . .investing in the future. Evaluation of the National HIV/AIDS Strategy 1993-94 to 1995-96. Canberra: Commonwealth Department of Human Services and Health, 1995 (ISBN 0644356944). Bammer G, editor. Feasibility research into the controlled availability of opioids. Canberra: NCEPH/AIC, 1991 (ISBN 0731512359). (Received 8 Feb, accepted 20 Nov, 1996) Authors' details North Coast Public Health Unit, NSW Health Department, Lismore, NSW. Tim J Sladden, MSc, MPH, Epidemiologist; Alan R Hickey, RN, Research Assistant; Therese M Dunn, BAppSc(Comp), Research Assistant; John R Beard, MB BS, FAFPHM, Director. Reprints: Mr T J Sladden, North Coast Public Health Unit, NSW Health Department, PO Box 498, Lismore, NSW 2480. E-mail: tslad AT doh.health.nsw.gov.au - - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Tim J Sladden · Alan R Hickey · Therese M Dunn · John R Beard

A cruel and unusual punishment Sentencing prisoners to hepatitis infection as well as to loss of liberty is a violation of human rights MJA 1997; 166: 116 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". - ©MJA1997 Prison authorities and governments must realise that the responsibility for the infection of a prisoner with a bloodborne virus, because means for prevention were not available within the prison, rests with them. We justify depriving people of their liberty for transgressing social norms on the grounds of protecting society or rehabilitating the person. However, in the case of illicit drug use, there is little evidence that either of these objectives is achieved by current approaches. Imprisonment exposes injecting drug users to greater risks of infection with bloodborne viruses (such as hepatitis B and C) than in the community. About half of all injecting drug users have histories of imprisonment; about half of all prisoners have histories of injecting drug use; and about half of all imprisoned injecting drug users inject drugs in prison.1 Infection with hepatitis C virus (HCV) is common among Australian injecting drug users and prisoners. Butler and colleagues' study of prisoners entering the New South Wales correctional system (in this issue of the Journal) showed that almost a third were seropositive for HCV, rising to two-thirds of those with a history of injecting drug use. HCV infection was significantly associated with a history of previous imprisonment, which accords with the results of other studies.2 Similarly, surveys of Australian injecting drug users find that histories of incarceration are among the strongest associations with HCV seropositivity. 3 A major survey of prison entrants in Victoria found high incidences of infection with both HCV and hepatitis B virus (HBV) among returning prison entrants -- 41 per 100 person-years among young male injecting drug users.4 While these data do not prove that infections are acquired in prison, the prison environment makes spread of blood-borne viruses more likely. The boredom, frustration and hopelessness felt by many prisoners potentially contribute to drug use. Many prisoners have no investment in the future, which will probably contain little except unemployment, further drug use and further imprisonment -- 64% of prison entrants in Victoria have been imprisoned previously. 5 They may believe they have nothing to lose (and some escape to gain) from drug use. In addition, prison policies may aggravate the problem of disease transmission. For example, sharing of injecting equipment is much more common in prison (where equipment is very scarce) than outside (where it is relatively freely available). 1 Efforts to detect drug use, such as urine screening, may drive prisoners from smoking marijuana (which has metabolites that can be detected in the urine for many days) to injecting heroin and amphetamines (which are rapidly cleared from the body). Prison practices may also prevent prisoners taking precautions against spread of bloodborne viruses. For example, despite official policy, urine screening is alleged by prisoners to be anything but random; in some prisons, prisoners claim that a request for bleach (for disinfecting injecting equipment) is followed the next day by a urine test. 6 Sanctions against drug use, such as loss of contact visits as punishment for a "dirty" urine, simply reinforce the original reasons for drug use. 6 Prisons take people from diverse settings who would not otherwise meet, create the opportunity to spread bloodborne viruses among them and then send them back to their original social networks as potential sources of infection. The situation varies for different bloodborne viruses. Despite the opportunities for transmission by injecting drug use, there has been very little transmission of HIV in Australian prisons. 7 However, this is not because conditions are not right for such transmission. It is because there is very little HIV among prison entrants as a result of harm reduction programs in the general community -- fewer than 5% of Australian injecting drug users were seropositive for HIV. 4 The recognition that reducing the spread of HIV is a more urgent priority than eradicating drug use (were the latter possible) has allowed our national AIDS and drug strategies to adopt such harm-reduction approaches (e.g., needle and syringe exchange and methadone maintenance programs). On the other hand, HCV is causing an epidemic among Australian injecting drug users that will be difficult to control. 2 Prisons are a key to this control; without rational approaches to the twin problems of injecting drug use and of HCV transmission in prisons, the epidemic will continue. The first step should be the recognition that incarceration offers nothing but ill to most injecting drug users. Alternative approaches to their problems will benefit both them and society. A serious reconsideration of the opportunities for spread of bloodborne viruses in prisons is the next step. Measures should include everything from lowering the cost to prisoners of razors and toothbrushes (so they will not share them), to provision of sterile injecting and tattooing equipment, peer education programs, transition programs to assist movement back to society (including referral to needle exchanges), proper drug substitution and drug treatment programs and hepatitis B vaccination. 8 It cannot be said often enough that the punishment is deprivation of liberty, and that is all. Prisoners should have available to them all the means for protecting themselves against infection with bloodborne viruses that are available outside prison, without qualification. Prison authorities and governments must realise that the responsibility for the infection of a prisoner with a bloodborne virus, because means for prevention were not available within the prison, rests with them. Nick Crofts Head, Epidemiology and Social Research, The Macfarlane Burnet Centre for Medical Research, Melbourne, VIC. Crofts N, Webb-Pullman J, Dolan K. An analysis of trends over time in social and behavioural factors related to the transmission of HIV among injecting drug users and prison inmates. Evaluation of the National HIV/AIDS Strategy 1993-94 to 1995-96, Technical Appendix 4. Canberra: AGPS, 1996. Crofts N, Stewart T, Hearne P, et al. Spread of blood-borne viruses among Australian prison entrants. BMJ 1995; 310: 285-288. Crofts N, Jolley D, Kaldor J, et al. The epidemiology of hepatitis C virus infection among Australian injecting drug users. J Epidemiol Community Health. In press. Kaldor JM, Elford J, Wodak A, et al. HIV prevalence among IDUs in Australia: a methodological review. Drug Alcohol Rev 1993; 12: 175-184. Victorian Correctional Services Annual Prison Census, 1995. Melbourne: Department of Justice, 1996. Crofts N, Thompson S, Wale E, Hernberger F. Risk behaviours for blood-borne viruses in a Victorian prison. Aust N Z J Criminol 1996; 29: 20-28. Dolan K, Hall W, Wodak A, Gaughwin M. Evidence of HIV transmission in an Australian prison [letter]. Med J Aust 1994; 160: 734. Dolan K, Wodak A, Penny R. AIDS behind bars. AIDS 1995; 9: 825-832. - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Nick Crofts

Hepatitis B and C in New South Wales prisons: prevalence and risk factors Tony G Butler, Kate A Dolan, Mark J Ferson, Linda M McGuinness, Phillip R Brown and Peter W Robertson MJA 1997; 166: 127 For comment see Crofts Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Laboratory methods - Statistical methods - Results - Participants - Serology and risk factors - Discussion - Acknowledgements - References - Authors' details - ©MJA1997 Abstract Objectives: To determine the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection among inmates entering the New South Wales correctional system and to examine risk factors for infection. Design: Cross-sectional survey. Setting: Reception Centre at Long Bay Correctional Centre, Sydney, New South Wales, June to December 1994. Participants: 408 adult male inmates received at the reception centre (28% of the 1450 new inmates eligible for compulsory HIV testing). Outcome measures: Presence of HBV core and surface antibody and surface antigen; HCV antibody; risk factors; inmates' knowledge about risk factors. Results: 37% of inmates tested positive for HCV antibody, 31% for HBV core antibody and 3.2% for HBV surface antigen (indicating recent infection or carrier status). Among those who reported a history of injecting illegal drugs, rates rose to 66% for HCV antibody and 43% for HBV core antibody. Prevalence of HBV and HCV antibodies was similar in Aboriginal and non-Aboriginal inmates, but HBV antigen carrier rate was significantly higher among Aboriginals (12% versus 2.2%). Knowledge about hepatitis risk factors was poor (only 20% named injecting drug use), although recidivists were significantly better informed than those new to the correctional system. Multivariate analysis identified injecting drug use, past exposure to hepatitis B virus and previous imprisonments as significant predictors for HCV infection, and age over 25 years and HCV antibodies for HBV infection. Conclusions: Results suggest that about a third of adult male prisoners entering the NSW correctional system may have been infected with HBV or HCV. Measures such as education about hepatitis risk factors and HBV vaccination are needed to reduce hepatitis transmission in this population. MJA 1997; 166: 127-130 Introduction The reported high prevalence of hepatitis B and C in prison populations is attributed to the disproportionate number of people in prisons who engage in risk behaviours, particularly injecting illegal drugs.1-8 It is estimated that up to 60% of inmates are committed for drug-related offences.9 Further, an Australian study estimated that during their incarceration 25%-44% of inmates occasionally injected illegal drugs, 14%-34% engaged in occasional anal intercourse and 5%-18% did both.10 Among inmates entering the Victorian prison system in 1991 and 1992, 39% were positive for hepatitis C antibody (including 64% of those reporting a history of injecting illegal drugs), 33% were positive for hepatitis B antibody and 2.5% for hepatitis B surface antigen.11 There are no recent studies of the prevalence of infection with hepatitis B and C viruses (HBV and HCV) in New South Wales prisons. Our study aimed to determine the prevalence of HBV and HCV infection among inmates entering the NSW correctional system and to examine the risk factors associated with these infections. Methods The study was performed at the Reception Centre at Long Bay Correctional Centre, Sydney, NSW, from June to December 1994. The Reception Centre receives about 51% of adult males entering the NSW correctional system, most of whom are then transferred to other prisons. At the time of our survey, all inmates entering NSW prisons were routinely screened for the human immunodeficiency virus (HIV) by public health nurses of the Corrections Health Service. Inmates were also invited to participate in the hepatitis survey. Recruitment depended on the nurses' availability to enrol inmates during HIV screening, and in busy periods it was not always possible to enrol all new inmates. No information was sought from those who did not agree to participate. Inmates who agreed to participate were briefed on the project and informed that a consent form had to be signed, a blood specimen was needed, and a risk factor questionnaire would be administered by the nurse. Nurses also asked inmates to describe ways in which hepatitis can be transmitted. All inmates who tested positive for HBV and HCV antibodies were counselled by public health nurses. HCV-positive inmates routinely receive follow-up liver function tests. Inmates who reported having had HBV vaccination were given booster vaccination if antibody tests indicated they were not immune. All other inmates who tested negative for HBV core antibody were offered hepatitis B vaccination. Ethics approval for the study was granted by the Eastern Sydney Area Health Service Ethics Committee and the NSW Department of Corrective Services. Laboratory methods HBV core antibody (indicating past exposure) was tested with an anti-HBc enzyme immunoassay kit (General Biologicals, Taiwan). Samples positive for HBV core antibody were tested for HBV surface antigen (indicating carrier status) with the HBsAg-enzyme immunoassay (Murex, Dartford); positive results were confirmed by HBs reverse passive haemagglutination assay (Serodia, Tokyo). Inmates who reported having been vaccinated against hepatitis B were tested for HBV surface antibody with the HBsAb-enzyme immunoassay (General Biologicals, Taiwan). A level of 30 IU/mL was considered the minimum necessary for immunity. HCV antibody was detected with the Innotest HCVAbIII assay (Innogenetics, Belgium). Reactive samples were retested in duplicate and, if again reactive, were tested with anti-HCV (Murex, Dartford). Samples that were reactive in each of the two types of assay were classified as positive, and those with discrepant results as equivocal. Statistical methods Relative risks were calculated with the statistical software Epi Info-6,12 and logistic regression was performed with the software SPSS-6. 13 The c 2 test was used to test for association between Aboriginality and serostatus. Results Participants About 1450 inmates were tested for HIV at the Long Bay Reception Centre between June and December 1994. Of these, 410 adult males (28%) consented to be screened for HBV and HCV antibodies. It is not known how many of the remainder were not invited to participate and how many refused. Two inmates were counted twice as they were released and reincarcerated during the study period. Results of their second tests were excluded from the analysis. The 408 subjects were aged 17-73 years (mean, 30.6 years; standard deviation, 10.1), and 296 (73%) had been imprisoned previously. Country of origin was: Australia, 80%; Europe, 8.6%; New Zealand and the Pacific Islands, 3.5%; Asia, 2.7%; the Middle East, 2.7%; and elsewhere or unknown, 2.5%. Forty-one inmates (10%) identified themselves as Aboriginal. Serology and risk factors Prevalence of HBV and HCV antibodies and HBV antigens is shown in Box 1 (below). About a third of inmates were positive for HBV core antibody (31%) or for HCV antibody (37%), with 21% positive for both. Among those who reported having received HBV vaccination, only 34% had HBV surface antibody levels (indicating immunity). No significant differences were found between Aboriginal and non-Aboriginal inmates in prevalence of HBV core and HCV antibodies. However, the HBV carrier rate was significantly higher among Aboriginals (12% versus 2.2%; c2 =11.8; P < 0.001). Among those reporting hepatitis B vaccination, more Aboriginals (50%) than non-Aboriginals (32%) had developed immunity, but the difference was not significant. The association between risk behaviours and HBV and HCV infection is shown in Box 2. The risk of each infection was significantly increased by a history of injecting drug use, previous imprisonment, sharing of injecting equipment, age over 25 years, injecting drug use during previous imprisonment, and tattooing (P< 0.05 or less). Risk also increased significantly with increasing numbers of previous imprisonments (P< 0.01 or less). Risk of HCV infection was also significantly increased by tattooing, sex with an injecting drug user and presence of HBV antibodies (P< 0.001). Among the 67 inmates who reported injecting drug use during a previous imprisonment, 77% were positive for HCV antibody and 56% for HBV antibody. In addition, among the 150 inmates positive for HCV antibody, only 14 (9%) did not report a history of injecting drug use. The following independent variables were entered into a logistic regression model, with HBV and HCV infection as separate outcome variables: injecting drug use, sex with an injecting drug user, tattoos, Aboriginality, age group (over 25 years versus 25 years and under), previous imprisonment, and HBV or HCV infection. For HCV infection, significant predictors were injecting drug use (odds ratio [OR], 19.9; P< 0.001), presence of HBV antibody (OR, 5.6; P< 0.001), and previous imprisonment (OR, 3.9; P< 0.001). For HBV infection, significant predictors were presence of HCV antibody (OR, 6.2; P< 0.001), and age over 25 years (OR, 3.4; P< 0.001). Among the 85 inmates positive for both HBV and HCV antibodies, 83 (98%) reported previous imprisonment, 78 (92%) reported injecting drug use, 40 (47%) reported sharing injecting equipment, 64 (75%) had tattoos, and 31 (36%) reported being tattooed in prison. Inmates' knowledge of risk factors for hepatitis B and C transmission is shown in Box 3 (below). Few inmates were knowledgeable about risk factors, with injecting drug use nominated by only 20% and tattooing by only 2%. However, those who had been imprisoned previously were significantly more likely to identify injecting drug use as a risk factor than those new to the correctional system, and significantly less likely to answer "no idea" about risk factors. Discussion Our results agree with those of a 1991-1992 study of Victorian prison inmates.11 We found that 37% of inmates were positive for HCV antibodies (39% in Victoria), 31% for HBV antibodies (33% in Victoria), and 3.2% for HBV surface antigen B (2.5% in Victoria). Our results also agree with those of two Victorian studies, which found rates of 62% and 68%, respectively, for HCV infection among injecting drug users.8,14 Extrapolating our results to the current NSW male prison population of over 6000 implies that almost 2000 inmates are likely to have been exposed to HBV, about 200 are HBV carriers, and over 2000 are HCV-antibody-positive. In contrast, there were 25 HIV-positive inmates in NSW correctional centres at the time of the study (0.4%; 23 male and 2 female) (unpublished data). NSW prison inmates are offered hepatitis B vaccination if their sentences exceed six months and they are considered "at risk". However, inmates with shorter sentences may also be at risk. We believe that all inmates have the right to be protected from possible infection and that all should start a course of hepatitis B vaccination on entry to the correctional system. It may be appropriate to use recently described accelerated vaccination schedules, which provide protective levels of anti-hepatitis B surface antibody relatively quickly.15 In addition, if hepatitis B vaccination courses are not completed in prison, inmates should be educated about the need to complete them after release. We found that among the 108 inmates (26%) who reported having had hepatitis B vaccination only a third were immune, possibly because of failure to complete the recommended vaccination schedule. Vaccination history could not be verified. We found that previous imprisonment was a significant risk factor for HCV infection, suggesting that measures to minimise the spread of hepatitis within prisons are essential. In addition, as many injecting drug users spend time in prison, it is an appropriate point for intervention to break the cycle of infection by educating them about risks for hepatitis transmission and providing vaccination. Prison education programs seem to have improved awareness about transmission of hepatitis, as inmates with a prison history were more likely to know the role of injecting drug use and less likely to have "no idea" about hepatitis transmission. However, knowledge was still poor, and only 2% of inmates identified tattooing as a risk factor for hepatitis transmission, which is of concern given the popularity of tattooing in this population. The link between tattooing and HCV infection has been identified elsewhere,16,17 and should receive more emphasis in hepatitis education programs. The recent decision by the NSW Department of Corrective Services to make condoms available in prisons may reduce hepatitis transmission. Other measures, such as removing obstacles for accessing bleach, and needle exchange, should also be considered in the fight to curb the spread of hepatitis. Our findings suggest that chronic hepatitis may become one of the prison system's major health concerns over the next two decades. Acknowledgements The study was funded in part by a grant from the NSW Health Department AIDS/Infectious Diseases Branch. We wish to thank the nursing staff at the NSW Corrections Health Service for assistance in data collection (Amanda Christensen, Sheryl Frewin, Marion Grey, Cherylyn Jesson, Linda Kemp, Jodie Lee, and Sandra Parsons). References Acedo A, Campos A, Bauza J, et al. HIV Infection, hepatitis, and syphilis in Spanish prison [letter]. Lancet 1989; 2: 226. Hull HF, Lyons LH, Mann JM, et al. Incidence of hepatitis B in the penitentiary of New Mexico. Am J Public Health 1985; 75: 1213-1214. Koplan JP, Walker JA, Bryan JA. Prevalence of hepatitis B surface antigen and antibody at a state prison in Kansas. J Infect Dis 1978; 137: 505-506. Melico-Silvestre A, Pombo V, Pereira A, et al. Seroepidemiological survey of transmissible infections in Portuguese prisoners [letter]. AIDS 1991; 5: 780-781. Decker M, Vaughn W, Brodie J, et al. Seroepidemiology of hepatitis B in Tennessee prisoners. J Infect Dis 1984; 150: 450-458. Chiaramonte M, Trivello R, Renzulli G, et al. Hepatitis B virus infection in prisons. J Hyg Camb 1982; 89: 53-58. Vlahov D, Nelson K, Quinn T, Kendig N. Prevalence and incidence of hepatitis C virus infection among male prison inmates in Maryland. Eur J Epidemiol 1993; 9: 566-569. Fairley CK, Leslie DE, Nicholson S, et al. Epidemiology and hepatitis C virus in Victoria. Med J Aust 1990; 153: 271-273. Corrections Health Service. Strategic Plan 1993-1998. Sydney: NSW Health Department, 1994. Douglas RM, Gaughwin MD, Ali RL, et al. Risk of transmission of the human immunodeficiency virus in the prison setting [letter]. Med J Aust 1989; 150: 722. Crofts N, Stewart T, Hearne P, et al. Spread of blood borne viruses among Australian prison entrants. BMJ 1995; 310: 285-288. Epi Info [computer program], version 6.0. Atlanta, Ga: Centers for Disease Control, 1994. SPSS-6: Statistical package for the social sciences [computer program], version 6. Chicago, Ill: SPSS Inc, 1994. Crofts N, Hopper J, Bowden S, et al. Hepatitis C virus infection among a cohort of Victorian injecting drug users. Med J Aust 1993; 159: 237-241. Bayas J, Bruguera M, Martin V, et al. Hepatitis B vaccination in prisons: the Catalonian experience. Vaccine 1993; 11: 1441-1444. Kaldor J, Archer, G, Buring M, et al. Risk factors for hepatitis C virus infection in blood donors: a case-control study. Med J Aust 1992; 157: 227-230. Holsen DS. Prevalence of antibodies to hepatitis C virus and association with intravenous drug abuse and tattooing in a national prison in Norway. Eur J Clin Microbiol Infect Dis 1993; 12: 673-676. (Received 10 Jan, accepted 21 Oct, 1996) Authors' details New South Wales Health Department, AIDS/Infectious Diseases Branch, Sydney, NSW. Tony G Butler, MSc, Public Health Officer. National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW. Kate A Dolan, BSc, Research Officer. South Eastern Sydney Area Health Service, Sydney, NSW. Mark J Ferson, FRACP, FAFPHM, Director of Public Health. NSW Corrections Health Service, Long Bay Correctional Centre, Sydney, NSW. Linda M McGuinness, Grad Dip HSc, RN, Assistant Director of Nursing; Phillip R Brown, MBA, FAFPHM, Chief Executive Officer. Microbiology Department, Prince of Wales Hospital, Sydney, NSW. Peter W Robertson, PhD, Serologist. No reprints will be available. Correspondence: Mr T G Butler, NSW Health Department, AIDS/Infectious Diseases Branch, Locked Bag 961, North Sydney, NSW 2059. - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Tony G Butler · Kate A Dolan · Mark J Ferson · Linda M McGuinness · Phillip R Brown · Peter W Robertson

In February 1996, vivax malaria was diagnosed in a man from a remote community in far north Queensland who had not visited a malarious area for the past 19 years. Microscopy and DNA studies of blood from other residents of the community did not identify a source of infection. It was suspected the infection was transmitted by mosquitoes from a neighbour who had been infected in Papua New Guinea, but whose blood was not available for DNA tests. Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia". Introduction - Clinical record - Investigations - Discussion - Acknowledgements - References - Authors' details Introduction We report a case of Plasmodium vivax malaria that we conclude was acquired in far north Queensland in early 1996. There has been only one other report of malaria acquired in mainland Australia 1 since the country was declared malaria-free by the World Health Organization in 1981. Clinical record A 31-year-old white male presented to a Cairns general practitioner in early February 1996 with a two-day history of fever, headaches, generalised aches and pains, lethargy and loss of appetite. Two days later he was hospitalised with vomiting and dehydration; he was given intravenous fluids and discharged within 24 hours. He remained unwell and consulted his general practitioner again the following day. A full blood count showed: lymphocytopenia (lymphocytes, 0.71 x 10 9 /L; normal, 1.5-4.0 x 10 9 /L); neutropenia (neutrophils, 1.95 x 10 9 /L; normal, 2.0-7.5 x 10 9 /L); and thrombocytopenia (platelets, 33 x 10 9 /L; normal, 150-450 x 10 9 /L). Haemoglobin concentration was in the normal range. On review of the routine blood film, schizonts of P. vivax were noticed, and malaria was diagnosed six days after onset of symptoms. The patient was treated with standard doses of chloroquine and primaquine, 2 and has remained well since. The patient had never received a blood transfusion nor used intravenous drugs. He had travelled to Papua New Guinea (PNG) 19 years before presentation, and for most of 1995 had worked as a tradesperson in a remote Aboriginal community in far north Queensland. Over the 1995 Christmas-New Year period he spent seven days in Cairns, followed by 12 days south of Cairns, at Mission Beach. For the next 24 days before onset of symptoms, he worked at the community in far north Queensland. Investigations Because the average incubation period for P. vivax malaria is 15 days (range, 12-17 days), 3 we investigated the possibility that the patient acquired malaria via a mosquito bite while at the community. It lies about 15¡ south of the Equator, 40 km from the coast of the Gulf of Carpenteria and about 450 km northwest from the closest international airport, at Cairns. The climate early in the year is monsoonal -- hot and humid with intermittent, heavy rainfall. Most of the population of about 1200 is Aboriginal. Investigations of source: After diagnosis of the index case, blood films were collected from 20 residents of the community who were considered possible sources of infection. These comprised: A person who had been diagnosed with P. vivax malaria in June 1995 (this had been acquired in PNG, and the person had remained well after appropriate treatment); All 13 people who presented to the community health centre with an undiagnosed fever within three weeks of the diagnosis of the index case; and Six people who had recently travelled from PNG. Further blood samples for DNA amplification by polymerase chain reaction were collected from five of these six people (blood was not available from one woman who had visited PNG in December 1995). Malaria parasites were seen in the blood films of only one of these 20 people. This person was Melanesian, had arrived in Australia from PNG in November 1995 and had taken no malaria-prophylactic drugs. No parasites were found in thin peripheral blood films, but three early ring trophozoites were seen in thick films. Although definitive species identification could not be made on morphological grounds, DNA amplification detected only P. falciparum (A Baddeley, Centre for Public Health Sciences, Brisbane, and A Saul, Queensland Institute of Medical Research, Brisbane, personal communication). The person was treated accordingly. 2 No evidence of malaria was found by DNA amplification in the other four people tested. The woman whose blood was not available for DNA amplification was also Melanesian, from PNG; she had lived in Australia for about four years and was related to the person with P. falciparum parasitaemia (who was staying with her). Although her house was about 2 km away from the home of the index patient, the latter often spent the evening socialising nearby. Both homes are about 50 m from a creek that runs along the periphery of the community. Investigations of vector: Two days after diagnosis of the index case, surface waters at the community (such as puddles, wheel ruts, ditches, swamps and drains) were surveyed for mosquito larvae with a standard 350-mL dipper. Adult mosquitoes were collected in Centers for Disease Control (CDC) light traps, baited with carbon dioxide and 1-octen-3-ol. Traps were placed beside the creek, in the central built-up part of the community and near the homes of the index patient and of the person with P. falciparum parasitaemia and his relative. Larvae were stored in 70% ethanol and adult mosquitoes at -70oC before identification. 4 Results are shown in the Box. Most Anopheles larvae were collected from small puddles and wheel ruts near the creek. Most adult Anopheles mosquitoes were also collected near the creek, with fewer at the two houses, and very few from the central part of the community. A larvicide, ( S )-methoprene, was used to treat surface waters where Anopheles larvae were breeding, and a residual insecticide, deltamethrin, was used for the thickly vegetated zone along the creek (along the periphery of the community). Further CDC light traps were set a week after initial mosquito collections, in the same locations along the creek as previously. Many Anopheles mosquitoes (12%, An. farauti s.l.) were still present (see Box). Discussion We believe that this case represents local mosquitoborne transmission of P. vivax malaria at the community in far north Queensland, because: The index patient had not been to a malarious area for 19 years. Although very long incubation periods and late hypnozoite relapses of P. vivax malaria (caused by reactivation of the dormant hepatic stage of the parasite) have been reported from temperate zones, 4,5 P. vivax malaria acquired in tropical regions, such as the Western Pacific region (including PNG), typically has a short incubation period (12-17 days), and relapses quickly (average, six weeks later). The usual duration of untreated P. vivax malaria is 1.5-5 years.3 Therefore, we conclude that this episode is not a late hypnozoite relapse of P. vivax malaria acquired in PNG. The index patient was at the community during the usual incubation period for P. vivax malaria. A competent malaria vector was present. There is strong evidence that An. farauti s.l. is the most important potential malaria vector in Australia, 6 and we showed that breeding An. farauti s.l. were present at the community. Further, although the index patient's home was screened, he often slept outside on the verandah because of the oppressive climate, and therefore was accessible to An. farauti s.l. mosquitoes during their peak biting hours (sunset to midnight). 7 There was a possible source of infection at the community. Although we did not identify another individual with P. vivax malaria, we believe that the woman whose blood was not available for DNA studies was infected. She had recently travelled to PNG, where P. vivax malaria is endemic, and our concerns are strengthened by the finding of low-level P. falciparum parasitaemia in her asymptomatic relative, who had recently come from the same region. Although she reported taking chloroquine and doxycycline prophylaxis during her visit, chloroquine-resistant malaria is well described in PNG. In addition, this prophylaxis will not prevent hypnozoite relapses. 3 Malaria symptoms may be less obvious in those who have chronic malaria, and may be further reduced by self-medication, which is common among PNG nationals (unpublished observations). Therefore, although we have not been able to prove that there was a source of infection (i.e., an untreated imported case) at the community, we believe that she was a possible source. There was no evidence of modes of transmission other than via mosquitoes (e.g., via contaminated blood). When an isolated case of malaria cannot be epidemiologically linked with another case of malaria, it is defined as "cryptic". 8 However, for the above reasons, we believe that this was a case of "introduced" malaria (malaria transmitted by mosquitoes from an imported case in an area where malaria does not usually occur). 8 Two episodes of locally acquired malaria in mainland Australia in 15 years attest to the rarity of local transmission, 6 despite frequent importations, particularly into the malaria-receptive north of Australia. 9 Nevertheless, sensitive and timely surveillance must be maintained to ensure that locally acquired cases are promptly recognised and investigated. Intensive mosquito-control measures may be needed, and other cases should be sought and treated promptly. Treatment should include primaquine as a gametocidal agent for P. falciparum . 10 Acknowledgements We commend Heather Moseley for detecting malaria parasites in the index patient's blood film when malaria was not expected. We wish to thank Dr Bill Glavin and the health staff at the community for assistance with the investigation. References Walker J. The role of a diagnostic reference laboratory in malaria surveillance. Comm Dis Intell 1996; 20: 302-304. Antibiotic Guidelines Subcommittee, Victorian Drug Usage Advisory Committee. Antibiotic guidelines. 8th ed. Melbourne: Victorian Medical Postgraduate Foundation, 1994: 103-107. Gilles HM. The malaria parasites. In: Gilles HM, Warrell DA. Bruce-Chwatt's essential malariology. 3rd ed. London: Edward Arnold, 1993: 12-34. Lee DJ, Woodhill AR. The Anopheline mosquitoes of the Australasian region. Sydney: Australian Medical Publishing Company, 1944. Department of Zoology, University of Sydney, monograph no. 2. Bradley D, Newbold CI, Warrell DA. Malaria. In: Weatherall DJ, Ledingham JGG, Warrell DA. Oxford textbook of medicine. 3rd ed. Oxford: Oxford University Press, 1995: 835-862. Bryan JH, Foley DH, Sutherst RW. Malaria transmission and climate change in Australia. Med J Aust 1996; 164: 345-347. Service MW. The Anopheles vector. In: Gilles HM, Warrell DA. Bruce-Chwatt's essential malariology. 3rd ed. London: Edward Arnold, 1993: 96-123. Zucker JR. Changing patterns of autochthonous malaria transmission in the United States: a review of recent outbreaks. Emerg Infect Dis 1996; 2: 37-43. Longbottom H. Epidemiology of malaria in Australia 1991-1995. Comm Dis Intell 1996; 20: 84-87. Warrell DA. Treatment and prevention of malaria. In: Gilles HM, Warrell DA. Bruce-Chwatt's essential malariology. 3rd ed. London: Edward Arnold, 1993: 164-195. Received 5 Aug, accepted 26 Nov 1996 Authors' details Tropical Public Health Unit, Cairns, QLD. Dianne L Brookes, RN, Public Health Nurse; Scott A Ritchie, PhD, Medical Entomologist; Andrew F van den Hurk, BAppSc, Vector Control Officer. Cairns Base Hospital, Cairns, QLD. Julie R Fielding, BAppSc, Supervising Scientist (Haematology); Mark R Loewenthal, DTM&H, FRACP, Infectious Diseases Physician. No reprints will be available. Correspondence: D L Brookes, RN, Tropical Public Health Unit, PO Box 1103, Cairns, QLD 4870. E-mail: troppub AT citec.qld.gov.au

Dianne L Brookes · Scott A Ritchie · Julie R Fielding · Mark R Loewenthal

Outbreak of cryptosporidiosis linked to an indoor swimming pool Jennifer M Lemmon, Jeremy M McAnulty and Jason Bawden-Smith MJA 1996; 165: 613 Subsequently cited in Sinclair I, Fairley CK, Hellard ME. Protozoa in drinking water: is legislation the best answer? MJA 1998; 169: 296-297. Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - Authors' details - ©MJA1996 Abstract Objective: To determine the extent and source of a community outbreak of cryptosporidiosis. Design: Questionnaire-based survey and matched case-control study. Setting: Sutherland area in southern Sydney, September 1994 to January 1995. Participants: 70 patients reported by pathology laboratories to have stool specimens positive for cryptosporidia, of whom 43 were surveyed; 35 were compared with age- and neighbourhood-matched controls. Main outcome measures: Demographic characteristics and potential risk factors in the two weeks before onset of illness. Results: Laboratories reported 70 cases of cryptosporidiosis between September 1994 and January 1995. We found no association between illness and foods consumed or contact with people with diarrhoea or sick animals in the two weeks before onset. Seventeen of the case group (49%) reported swimming in a particular indoor swimming pool, compared with only seven controls (20%) (odds ratio, 3.7; P = 0.015). Cryptosporidial oocysts were detected in water from the swimming pool in January 1995. Conclusions: The outbreak of cryptosporidiosis was probably associated with ingestion of water from the indoor swimming pool, presumably contaminated by infected bathers. Recommendations: As it is difficult to eradicate cryptosporidia from swimming pools by either disinfection or filtration, we recommend that:People with recent diarrhoea should avoid public swimming pools; and Non-toilet-trained and faecally incontinent swimmers should be provided with alternative swimming facilities with separate water and filtration systems. To enable appropriate public health responses:Doctors and pathology laboratories should consider cryptosporidiosis in patients with diarrhoea lasting longer than three days; and Laboratory reporting of cryptosporidia to local health departments should be mandatory in all States and Territories. MJA 1996; 165: 613-616 Introduction The protozoan Cryptosporidium parvum was first recognised as a cause of illness in humans in 1976. 1 In the 1980s, cryptosporidia were reported to cause life-threatening, cholera-like illness in the immunosuppressed. 2 Subsequently, cryptosporidia were reported to produce a spontaneously resolving illness in the immunocompetent, characterised by diarrhoea with profuse watery stools lasting days to months, abdominal pain, nausea, vomiting, malaise and low-grade fever. 3 There is no known effective treatment. 4 Cryptosporidia (Figure 1) are common in the environment and are excreted in the faeces of those infected. They can be transmitted through contact with infected cattle, sheep and other animals, 5-7 person-to-person contact, 8 contaminated water supplies 4,9 and swimming. 10-12 Cryptosporidial infection was not a notifiable disease in New South Wales at the time of the study, and many laboratories do not routinely screen stool specimens for crypto sporidia. 3 Thus, we do not know the incidence of this disease in the community, nor the relative importance of different modes of transmission. In January 1995, a general practitioner in the Sydney suburb of Sutherland reported to the Southern Sydney Public Health Unit increases in numbers of patients presenting with watery diarrhoea and of stool specimens positive for cryptosporidia at a local laboratory. We therefore investigated the extent and source of this outbreak of crypto sporidiosis. Figure 1: Cryptosporidium oocysts from a faecal specimen. Modified Ziehl-Neelson stain; original magnification x 1000 (slide courtesy of Dr Stephen A Neville). Methods Methods were similar to those used by McAnulty et al. 10 and included a case survey and investigation of likely sources of the cryptosporidia, by comparison of cases and matched controls and an environmental study. Case survey In January 1995, the five major pathology laboratories serving the Sutherland area (defined as the area bounded by the Pacific Ocean to the east, Georges River to the north and the Royal National Park to the south) were asked to report all stool specimens in which crypto sporidia had been detected since September 1994. Two of the pathology laboratories examined stool specimens microscopically for cryptosporidial oocysts with a modified Ziehl-Neelsen acid-fast stain (modified by decolorising with hydrochloric acid and ethanol and counterstaining with malachite green) if structures suggestive of protozoa were seen on wet-mount examination. 13 The other three laboratories did not screen for cryptosporidia unless requested by the referring medical practitioner. Case patients were defined as people with a stool specimen positive for cryptosporidia between 1 September 1994 and 20 January 1995. Because of the high rate of person-to-person spread, cases were classified as primary (first to report diarrhoea in a household) and secondary (subsequent household cases). All people diagnosed as case patients after 1 December 1994 (and reported before 20 January 1995) and aged over 18 years were interviewed by telephone in January 1995 with a 34-item structured questionnaire. Interview was with parents if the patient was less than 18 years old. The questionnaire asked about the illness and about potential risk factors in the two weeks before onset of illness, including travel outside Sydney; childcare attendance; contact with other people with diarrhoea, or with pets and domestic animals; swimming; and sources of drinking water. The period of two weeks was chosen to include the incubation period for cryptosporidiosis of 1-12 days (average, about seven days). 14,15 People diagnosed before 1 December 1994 were not interviewed in detail because of the potential for poor recall given the time since infection. Case-control study To identify likely sources of infection, we compared potential risk factors of case patients with those of matched control subjects who had had no gastrointestinal symptoms in the previous two weeks, selected from a computerised telephone directory. Each matched control subject lived in the same street as (or within two streets of) the case patient and was matched for age within three years (for case patients younger than eight years), five years (for case patients aged 8-25 years), or 10 years (for case patients older than 25 years). Control subjects were administered a 23-item questionnaire on potential risk factors, referring to the two weeks before Christmas 1994. We chose this period as it was relatively easily identified by subjects and the season was similar or identical to that during the outbreak, so that conditions for swimming (a potential risk factor) were comparable. Differences in characteristics and risk factors between primary and secondary cases were tested for significance with either the c 2 test or, if expected cell size was less than five, with a two-tailed Fisher exact test. Differences between matched pairs of cases and controls were tested for significance with the probability of the maximum likelihood estimate of the odds ratio. 16 Swimming pool investigation We investigated a community swimming pool visited by some case patients (pool A), examining filtration systems and maintenance and chlorination records for the period November 1994 to January 1995. In addition, samples of poolwater and filter backwash water (water passed backwards through the filter to clean it) from this pool were tested for Crypto sporidium oocysts and Giardia cysts. For testing, water was filtered through a polycarbonate membrane (pore size, 2 m m for Cryptosporidium oocysts, or 5 m m for Giardia cysts), which was washed clean; washings were mixed with fluorescent antibody specific for either cryptosporidia or giardia. Particles were sorted by size and fluorescence with a flow cytometer and their identity confirmed by microscopy. 17 Filtration systems used at local government-owned swimming pools in the inner, eastern and southern areas of Sydney were surveyed. Operators were asked over the telephone about the type of filtration system used and whether general-use pools shared their water and filtration systems with pools for infants. Results Case survey We identified 70 cases of cryptospori diosis diagnosed between 1 September 1994 and 20 January 1995. Fortnightly incidence is shown in Figure 2. Characteristics and potential risk factors of the 43 case patients reported between 1 December 1994 and 20 January 1995 are shown in Box 1. (Another five case patients were diagnosed in the week to 20 January but not reported until later and so were not surveyed.) Symptoms included diarrhoea (42 of the 43 patients, 98%), cramping abdominal pain (23, 53%), vomiting (21, 49%), nausea (16, 37%) and fever (16, 37%). None of the people affected reported being immunocompromised; more than half were children aged under 4.5 years. Twenty-eight cases were primary and 15 secondary. The only significant differences between the primary and secondary cases were that secondary-case patients were more likely to be male (80% of secondary cases versus 36% of the primary cases; P < 0.01) and, as expected, were more likely to have had contact with people with diarrhoea (100% of secondary cases versus 25% of primary cases; P < 0.001). Figure 2: Cases of cryptosporidiosis diagnosed by laboratories in the Sutherland area of Sydney, 1 September 1194 - 20 January 1995 (specimen date was unknown for two cases). Case-control study Of the 43 cases reported between 1 December 1994 and 20 January 1995, five were excluded from the case-control study as they lived outside the Sutherland area, and three were excluded as matched controls could not be identified. As primary- and secondary-case patients reported similar potential risk factors, both sets of patients were included in the case-control study. Potential risk factors in the case and control groups are compared in Box 2. There was no association between illness and attendance at childcare, contact with people with diarrhoea, and drinking bottled water or city water. Although more of the case group than the control group reported swimming in the two weeks surveyed, the difference was not significant. However, significantly more in the case group than in the control group reported swimming in pool A. There was no significant association between cryptosporidiosis and swimming in any other pool. Swimming pool investigation Pool A is an indoor heated swimming pool located in a popular community swimming complex that caters for all ages from infants to adults. Average daily attendance between 1 September and 1 December 1994 was 1269 people (range, 1092-1443). The complex includes three outdoor pools (none associated on epidemiological grounds with cryptosporidiosis), as well as the indoor pool. The indoor pool comprises a 25-metre swim area, a teaching and aquarobics area (used by infant and toddler learn-to-swim classes), and a "bubble" area (with air jets, and popular with children). It contains about 1.6 million L of water and has a rapid sand filtration system, separate from the filtration systems for the outdoor pools. Chlorine levels in pool A, documented every three hours between 6 am and 9 pm daily, ranged from 0.55 to 5.0 mg/L. The New South Wales Health Department recommends that chlorine levels for indoor pools be maintained at 1.5 mg/L for those heated to less than 26¡C, and at a minimum of 2.0 mg/L for warmer pools. 18 Pool A was heated to more than 26¡C, and chlorine levels were in the recommended range 28% of the time. Eleven Cryptosporidium oocysts and 57 Giardia cysts were detected in a 55-L sample of the pool water taken in January 1995, but none in a 500-mL sample of filter backwash water. Among the 20 local government-owned pools surveyed, filtration used sand at 19, and fine-grade diatomaceous earth (a porous form of silica, composed of the fossilised shells of a type of alga) was used in the other. At all these pool complexes, general purpose pools and infants' pools shared water and filtration systems. As a result of the investigation, management at pool A erected signs warning patrons of the possibility of pool-water contamination and instructing that people who were not toilet-trained, who were faecally incontinent or who had had diarrhoea in the previous week should not enter the pool. The public was warned through a press release of the possible connection between the pool and cryptosporidiosis. On 20 January 1995, to allay public concern, pool A operators decided to replace the water in the pool and the outbreak subsequently abated. Discussion This is the first report of an outbreak of cryptosporidiosis associated with swimming in Australia. The outbreak, which lasted several months, was also the largest reported point-source outbreak of crypto sporidiosis in Australia. As many laboratories do not routinely screen for cryptosporidia, and as doctors may not order examination of stool specimens and people with diarrhoea may not consult a doctor, 3,9 there were undoubtedly many more cases of cryptosporidiosis than those reported. This outbreak probably began when the water in indoor swimming pool A was contaminated with cryptosporidia from an infected bather. The likelihood of contamination was increased by the pool's use by infants and children too young to be faecally toilet trained (crypto sporidia are present in the faeces of those infected). The infective dose of C. parvum causing illness in humans remains unclear, but recent evidence suggests it is very low (e.g., a dose of 30 oocysts has been reported to cause infection in a healthy volunteer). 19 While chlorine levels in pool A were not optimal, higher levels would have been unlikely to have prevented the outbreak, as cryptosporidial oocysts are extremely resistant to chlorine and can survive many days in chlorinated water. 20 We do not know if protection from ultraviolet light in the indoor pool may have enhanced cryptosporidial survival. While swimming at pool A was strongly associated with crypto sporidiosis, it explained only 49% of cases. No other single pool was significantly associated with illness and, as the epidemic subsided with draining of pool A, others were not tested. However, it is possible that others in the case group were infected at pools other than pool A (although not identified in our survey), or by direct contact with people with the disease, given the small infective dose. The localised nature of the outbreak and the age distribution of those affected (i.e., children or parents) indicated that drinking Sydney water was not a likely source of the outbreak. Detection of cryptosporidial oocysts in water from pool A confirmed the epidemiological findings that C. parvum contaminated the pool. However, the viability of the organisms detected is unknown. Although Giardia cysts were also detected, they are relatively sensitive to chlorine and unlikely to be viable. 20 Furthermore, local laboratories reported no increase in detection of Giardia cysts in stool specimens. Sand filtration systems have been implicated in previous swimming pool-related outbreaks of cryptosporidiosis, 10 and almost all of the local government-operated pools surveyed relied on this type of filtration. An uneven sand surface in this type of filter -ay reduce its efficiency. 11 Alternative filtration systems, such as those with diatomaceous earth, may be more effective in removing oocysts. However, swimming pools with malfunctioning diatomaceous earth filters have also been implicated in outbreaks of crypto sporidiosis. 12 There is not enough information on the comparative effectiveness of different filtration systems to warrant recommending one form of filtration over another at present. Because of the difficulty of eradicating cryptosporidia from swimming pools by either disinfection or filtration, preventing similar outbreaks depends on reducing contamination through the cooperation of swimmers and pool operators. 11 Patrons who have had diarrhoea in the previous week, who are faecally incontinent or not toilet trained should be discouraged from using the pool by signs at the pool entrance and in the change rooms. Similar recommendations have been made for controlling swimming pool-associated crypto sporidiosis in the United States. 10 In addition, new swimming pool complexes should provide separate facilities with their own filtration systems for patrons who are not toilet trained or who are faecally incontinent. People using these facilities should avoid swallowing pool water. Screening swimming pools for crypto sporidia would be of little use at present, as current detection methods do not determine oocyst viability and consequent ability to cause disease. In 1995, a Centers for Disease Control and Prevention workshop concluded that current knowledge about cryptosporidia, and about waterborne cryptosporidiosis in particular, is minimal and does not provide a scientifically sound basis for many essential decisions about the public health risks associated with infection. 21 In Australia, we do not know the incidence of cryptosporidiosis in the community or the extent to which swimming pools contribute to transmission. A first step in obtaining this information is to make cryptosporidiosis a notifiable disease and to encourage doctors and laboratories to consider cryptosporidiosis as a diagnosis in patients with diarrhoea lasting longer than three days. In 1995, South Australia was the only Australian State to require routine reporting of cryptosporidial detection by laboratories and doctors to public health authorities. Since then, Victoria and Queensland have introduced the requirement and New South Wales followed suit on 1 December 1996. Introducing this requirement in all States and Territories would assist in early detection and control of future outbreaks of cryptosporidiosis. Acknowledgements We thank Dr Philip Lye (Sutherland Division of General Practice), Sugermans Pathology (Hurstville), Dr Gary Grohmann (Australian Water Technologies) and the staff of the former Southern Sydney Public Health Unit for their assistance. References Nime FA, Burek JD, Page DL, et al. Acute enterocolitis in a human being infected with the protozoan Crypto sporidium . Gastroenterology 1976; 70: 592-598. Current WL. Cryptosporidiosis parvum : household transmission [editorial]. Ann Intern Med 1994; 120: 518-519. Berkelman RL. Emerging infectious diseases in the United States, 1993. J Infect Dis 1994; 170: 272-277. Gallaher MM, Herndon JL, Nims LJ, et al. Crypto sporidiosis and surface water. Am J Public Health 1989; 79: 39-42. Miron D, Kenes J, Dagan R. Calves as a source of an outbreak of cryptosporidiosis among young children in an agricultural closed community. Pediatr Infect Dis J 1991; 10: 438-441. Casemore DP. Sheep as a source of human cryptosporidiosis. J Infect 1989; 19: 101-104. Reif JS, Wimmer L, Smith JA, Dargatz DA, Cheney JM. Human cryptosporidiosis associated with an epizootic in calves. Am J Public Health 1989; 79: 1528-1530. Newman RD, Zu SX, Wuhib T, et al. Household epidemiology of Cryptosporidium parvum infection in an urban community in northeast Brazil. Ann Intern Med 1994; 120: 500-505. MacKenzie WR, Hoxie NJ, Proctor ME, et al. A massive outbreak in Milwaukee of Cryptosporidium infection transmitted through the public water supply. N Engl J Med 1994; 331: 161-167. McAnulty JM, Fleming DW, Gonzalez AH. A community-wide outbreak of cryptosporidiosis associated with swimming at a wave pool. JAMA 1994; 272: 1597-1600. Joce RE, Bruce J, Kiely D, et al. An outbreak of cryptosporidiosis associated with a swimming pool. Epidemiol Infect 1991; 107: 497-508. Sorvillo FJ, Fujioka K, Nahlen B, et al. Swimming- associated cryptosporidiosis. Am J Public Health 1992; 82: 742-744. Rusnak J, Hadfield TL, Rhodes MM, Gaines JK. Detection of Cryptosporidium oocysts in human fecal specimens by an indirect immunofluorescence assay with monoclonal antibodies. J Clin Microbiol 1989; 27: 1135-1136. Jokiph LJ, Jokiph DMM. Timing of symptoms and oocyst excretion in human cryptosporidiosis. N Engl J Med 1986; 315: 1643-1647. Benenson AS. Control of communicable diseases manual. 16th ed. Washington: American Public Health Association, 1995. Dean AG, Dean JA, Coulombier D. Epi Info Version 6. Atlanta (GA): Centers for Disease Control and Prevention, 1994. Vesey G, Narai J, Ashbolt N, et al. Detection of specific microorganisms in environmental samples using flow cytometry. Methods Cell Biol 1994; 42: Pt B: 489-522. Marsh C. Guidelines for disinfecting public swimming pools and spa pools. Sydney: New South Wales Health Department, 1991. DuPont HL, Chappell CL, Sterling CR, et al. The infectivity of Cryptosporidium parvum in healthy volunteers. N Engl J Med 1995; 332: 13: 885-859. Korich DG, Mead JR, Madore MS, et al. Effects of ozone, chlorine dioxide, chloride and monochloramine on Cryptosporidium parvum oocyst viability. Appl Environ Microbiol 1990; 56: 1423-1428. Centers for Disease Control and Prevention. Assessing the public health threat associated with waterborne cryptosporidiosis: report of a workshop. MMWR Morb Mortal Wkly Rep 1995; 44 (no. RR-6): 15. (Received 17 Apr, accepted 12 Aug 1996) Authors' details Southern (now South Eastern) Sydney Public Health Unit, Sydney, NSW. Jennifer M Lemmon, BNurs, ICC, RGN, Infectious Diseases Consultant; Jeremy M McAnulty, MB BS, MPH, Director; currently, Specialist Medical Adviser, New South Wales Department of Health; Jason Bawden-Smith, MEnvStudies, Environmental Health Officer. No reprints will be available. Correspondence: Ms J M Lemmon, South Eastern Sydney Public Health Unit, PO Box 482, Kogarah, NSW 2217. To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Jennifer M Lemmon · Jeremy M McAnulty · Jason Bawden-Smith

An outbreak of Japanese encephalitis in the Torres Strait, Australia, 1995 Jeffrey N Hanna, Scott A Ritchie, Debra A Phillips, Jack Shield, M Clare Bailey, John S Mackenzie, Michael Poidinger, Bradley J McCall and Phillip J Mills MJA 1996; 165: 256-260 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - Register to be notified of new articles by email - - ©MJA1996 Abstract Objectives: To determine the distribution of virus infection during an outbreak of Japanese encephalitis (JE) in the Torres Strait, and to describe the environmental factors facilitating the outbreak. Design: Human and porcine serological surveys for JE virus activity throughout the Torres Strait, and mosquito and household surveys on the island of Badu. Setting: The island of Badu (where the clinical cases occurred) and the other islands of the Torres Strait, Australia, during April-May 1995. Results: The serological surveys identified recent JE virus infection among residents or domestic pigs on at least nine outer Torres Strait islands. A JE virus, confirmed by nucleotide sequencing, was isolated from two asymptomatic Badu residents. Virus isolations and mosquito surveys implicated Culex annulirostris as the major vector involved in the outbreak. There was prolific Cx. annulirostris breeding in a variety of water bodies close to and within the Badu community. Over half (53%) of the households kept pigs in pens, and many (63%) of the pigpens were situated near standing water; in 56% of these "wet" pigpens Cx. annulirostris was breeding. Conclusions: There was evidence of widespread JE virus activity throughout the outer islands of the Torres Strait. We suggest that migratory birds and/or wind-blown mosquitoes could have imported the virus into the Torres Strait from a focus of viral activity, possibly in Papua New Guinea, thereby initiating the outbreak. A combination of environmental factors, with large numbers of domestic pigs in close proximity to human dwellings and mosquito breeding sites, undoubtedly facilitated the outbreak on Badu. MJA 1996; 165: 256-260 Introduction Over a two-week period in March-April 1995, three cases of Japanese encephalitis (JE) occurred among residents of the island of Badu in the Torres Strait, Australia 1 ( Box 1). Although JE is widespread throughout Asia, 3 the Torres Strait outbreak is the first time that it has been recognised in Australia. J E is caused by a mosquito-borne flavivirus, and results in an acute illness characterised by headache, fever, convulsions, depressed level of consciousness and coma. It has a high case-fatality rate and there is a high prevalence of neurological sequelae in those who survive the acute illness. However, infection with the JE virus does not invariably cause disease; there is a high ratio of asymptomatic to symptomatic infections. 3 The JE virus is maintained in a natural cycle involving water birds such as egrets and herons. Pigs are very efficient amplifying hosts for the virus and therefore almost always contribute to outbreaks of JE in human populations. However, humans and other large verte brates, such as horses, are not efficient amplifying hosts, and are therefore "dead-end" hosts for the JE virus. 3 The outbreak was assumed to have been caused by a mosquito-borne virus, and Murray Valley encephalitis (MVE) virus (the major cause of arboviral encephalitis in Australia) was first suspected. Although the current status of flavivirus infections in the Torres Strait is uncertain, MVE and other Australian flaviviruses (Alfuy, dengue, Kokobera, Kunjin, Stratford and Sepik viruses) have been reported from either Cape York or Papua New Guinea (PNG). 4 Once laboratory findings confirmed the outbreak as JE, further investigations were undertaken. Methods Serological survey In April 1995, a serological survey was undertaken among residents of Badu. A non-random convenience sample was used. Human sera were screened for the presence of (i) flavivirus IgG and IgM by enzyme-linked immunosorbent assay (ELISA) 5 and haemagglutination inhibition assay, 6 and (ii) antibodies to JE, MVE and Kunjin viruses by plaque reduction neutralisation assay. 7 Sera testing positive for flavivirus IgM by ELISA were fractionated by ultracentrifugation over a sucrose gradient. IgM fractions were then tested for haemagglutination-inhibiting antibodies against JE, MVE and Kunjin viruses. 8 A diagnosis of a recent JE virus infection was made if there was a fourfold or greater rise in haemagglutination-inhibiting antibody titres in paired sera tested in parallel, or if JE virus IgM antibody and JE neutralising antibody were detected in serum at significantly higher titres than antibody to MVE and Kunjin viruses. Blood samples for serological studies were also collected from domestic animals, in particular pigs, on Badu. The animal sera were screened for the presence of total (i.e., IgM and IgG) antibody to JE, MVE and Kunjin viruses by haemagglutination inhibition assay. A portion of the sera positive for total JE antibody by haemagglutination inhibition assay was then tested by plaque reduction neutralisation assay. The presence of neutralising antibody at significantly higher titres to JE virus than to MVE and Kunjin viruses was considered evidence of exposure of an animal to JE virus. Isolation of virus Virus isolations were attempted from human sera obtained from residents of Badu: 100 m L of serum was inoculated onto confluent monolayers of C6/36 ( Aedes albopictus ) cells. 9 Viral growth was monitored by testing the culture super natant for haemagglutinating ability. Box 2 details the method used for identification of virus isolates. Mosquito survey Because the outbreak was initially suspected to be MVE, mosquito surveillance focused on the primary vector of MVE in Australia, Culex annulirostris . 4 Commencing on 7 April, larval and adult mosquito surveys were conducted within a 1-km radius of the centre of the Badu community. Mosquito larvae were sampled with a 350 mL dipper and adult mosquitoes were trapped with Centers for Disease Control light traps -- eight, each baited with 1 kg of dry ice (carbon dioxide) and 1-octen-3-ol (octenol; release rate 10 mg/h), 16 were run overnight at locations throughout the community on four occasions throughout April 1995. Household survey In May 1995, environmental health staff undertook a house-to-house survey to interview one adult resident of each household on Badu about household characteristics that may have contributed to the outbreak of JE. These included the presence of backyard pigs and horses and the state of repair of waste disposal (drainage and sewerage) systems. Survey of other communities To determine the extent of recent JE infection, blood was taken from convenience samples of people residing on 12 other outer islands, three inner islands and seven Cape York communities. Blood was also taken from pigs from eight other outer islands, three inner islands and two Cape York communities. Results Serological survey Two hundred and fifteen Badu residents were tested for JE infection: 35 people had serological evidence of recent JE infection (Box 3), and 21 of these had a fourfold or greater rise in JE-specific antibody titres in paired sera. All 11 pigs from Badu (tested by plaque reduction neutralisation assay) showed serological evidence of JE infection (Box 3). Most of the horses (7/10) and dogs (10/16) tested also showed serological evidence of JE infection, but not one of six chickens was positive. Isolation of virus JE virus was isolated from the sera of two Badu residents, both of whom remained asymptomatic. Nucleotide sequences obtained by reverse transcriptase-polymerase chain reaction (RT-PCR) amplification showed that the two viruses (designated FU and NO) were definitely strains of JE, with a 90% nucleotide homology with other strains of JE virus but with less than 70% homology with other flaviviruses. Both Badu isolates were very closely related, with 99% homology with each other. Detailed sequence comparison of the prM region of the viruses with that of other JE virus isolates showed that the Badu viruses were most closely related (92% homology) to other viruses of genotype III, 12,13 especially WTP-70/22 (from Malaysia) and B1065 (from southern Thailand) (Figure 1). The nucleotide sequences of JE-FU and JE-NO have been deposited in GenBank (the international computerised depository of genomic-sequence information), with accession numbers L43565 ( prM ) and L48968 ( NS5 ) for JE-FU, and L43566 ( prM ) and L48967 ( NS5 ) for JE-NO. Mosquito survey Numerous water bodies contained large numbers of Cx. annulirostris larvae. There were extensive swampy areas close to the community, and those contaminated by horse faeces had high larval densities ( >= 10 larvae/dip). A waterhole on the inland side of the community contained a large amount of grass clippings, rubbish and horse faeces; high larval densities were found along the margins. Many of the concrete-lined drains running through the community were overgrown with vegetation and contained mosquito-infested accumulations of water. High densities were also found in some of the defective household waste disposal systems (see below), and in pools in horse hoofprints. A total of 22 190 adult mosquitoes were trapped in the Badu community in April. Aedes kochi , Aedes culiciformis and Cx. annulirostris comprised 99% of the collection, with means of 364, 243 and 127 adult mosquitoes per trap, respectively. While the largest collections of Cx. annulirostris (up to 607 per trap) were taken from swampy areas near the community, collections of more than 100 per trap were taken within the community and close to houses. Eight JE viruses were isolated from 2871 Cx. annulirostris mosquitoes collected at Badu, but not from any other species (S A Ritchie, D A Phillips and A K Broom, unpublished data). Six of the isolates were from mosquitoes collected from within the community. Household survey An adult resident from 97 of the 102 houses in the community was interviewed for the household survey. Fifty-one (53%) of the households kept pigs; 35 (69%) of the pigpens were within 50 metres of the house. There were 179 domestic pigs in the community, an average of 3.5 (range, 1-11) per pig-rearing household. On inspection, 32 (63%) of the pigpens were situated either over or surrounded by standing water, and in 18 (56%) of these "wet" pigpens Cx. annulirostris was breeding. The householders of 15 (15%) of the houses owned a total of 18 horses; they were all kept in paddocks within 500 metres of the houses. The interviewees reported that 62 (64%) of the 97 houses had defective waste disposal systems: 49 of these houses had either waste water or raw sewage overflowing from septic tanks either into the house or into the yard, with 10% of the defective septic tanks containing Culex larvae. Survey of other communities A total of 1242 human serum samples were collected from the other communities. Twenty people from three other outer islands had serological evidence of recent JE virus infection. There was no evidence of JE infection in those tested from the inner islands or from the Cape York communities (Box 3). There was no evidence of any prior infection (i.e., only IgG JE antibodies) in any individual. Of the 182 pig sera collected from the other communities, 121 (66%) were tested by plaque reduction neutralisation assay. There was serological evidence of JE infection in pigs from all eight other outer islands, but no evidence of infection in pigs from the inner islands and Cape York Peninsula (Box 3). Discussion The human serological survey indicated that people from four outer islands had been recently infected with the JE virus. The porcine serological survey found evidence of JE activity in pigs from another five outer islands. Therefore, the two surveys indicated widespread, and presumably recent, JE virus activity in at least nine of the outer Torres Strait islands. There was no evidence of either human or porcine infection in the communities surveyed on the inner islands or on Cape York. The lack of evidence of prior infection in those tested suggests that the 1995 outbreak was the first incursion of the JE virus into the Torres Strait. Nucleotide sequencing studies clearly defined the virus strains isolated from the two people from Badu (and presumably the virus that infected people and pigs throughout the outer Torres Strait islands) as JE virus, and that the isolates were distinct from, but related to, virus strains that were circulating in southern Thailand, Malaysia and Indonesia between 1968 and 1983. 12 The virus differed, however, from a newly recognised genotype known to be circulating in Indonesia in 1980-1981. A strain (JKT-6468, Figure 1) of this latter genotype has been isolated from culicine mosquitoes collected from Flores, east of Bali, and is therefore the closest known isolate to Australia. 13 JE virus has not been isolated or reported as causing human disease in either PNG or Irian Jaya. Although no evidence of JE virus has been demonstrated conclusively in a number of serological surveys, there was possible JE seropositivity in a few single-serum specimens collected in 1956-1957 in the Western Province of PNG. 17 More recently, antibody to JE virus was detected by competitive ELISA in at least 23% of human sera collected in the Western Province in 1989 (R A Hall and J S Mackenzie, unpublished data), and 49% of porcine sera collected in the Western Province in 1995 were positive for neutralising antibody to JE virus (J Shield and R A Lunt, unpublished data). Thus, it seems possible that JE virus has become enzootic in parts of southwestern PNG. The northwestern islands (Boigu, Dauan and Saibai), because of their closeness to PNG, receive Papuan visitors virtually every day, raising the question of whether a viraemic visitor could have brought the JE virus across from PNG to the Torres Strait. However, humans, as "dead-end" hosts of the JE virus, have a low level of JE viraemia of short duration. 3 On the other hand, a viraemic pig imported from PNG, being a very efficient amplifying host, might have initiated the Torres Strait outbreak. However, the Australian Quarantine Act 1908 (Cwlth) prohibits the movement of live animals from PNG to the Torres Strait. The ban is actively enforced and respected; since the appointment of the first indigenous Quarantine Officers in 1982 they have not had occasion to seize even one illegally imported pig (P Stephen, Australian Quarantine and Inspection Service, personal communication). Therefore, we believe it most unlikely that an imported pig initiated the outbreak. Over 100 species of bird migrate annually between Australia and New Guinea, usually in a predictable seasonal pattern. 18 A further 63 species cross the Torres Strait at irregular intervals; these include numerous aquatic species, including wading birds. 18 The rufous night heron ( Nycticorax caledonicus ), for example, is a common nomad found throughout the Torres Strait; 18 it is closely related to the black-crowned night heron ( N. nycticorax ), a principal bird species implicated in the natural JE virus bird-mosquito cycle in Asia. 19 Experimental JE virus infection of the rufous night heron produces levels of viraemia that are quite adequate to infect the most efficient JE vector in Asia ( Culex tritaeniorhynchus ). 20 From December to April the prevailing wind in the region is from the northwest, raising the possibility that the dispersal of "wind-blown" mosquitoes could have carried the JE virus from New Guinea to the Torres Strait. Indeed, it has been reported that female Cx. annulirostris mosquitoes "can disperse at least 12 km and probably further"; 21 the northernmost outer islands are all less than 10 km from the PNG coastline (Box 1). We therefore suggest that two natural phenomena -- viraemic migratory birds and/or infectious wind-blown mosquitoes -- are plausible mechanisms for the importation of the JE virus from New Guinea to the Torres Strait, thereby initiating the outbreak. Cx. annulirostris was undoubtedly the major vector at Badu, and presumably at the other outer islands. Multiple JE virus isolations were made from Cx. annulirostris but not from any other mosquito species. The very small (fewer than one adult mosquito per trap) collections of Culex quinquefasciatus and Culex bitaeniorhynchus (both recognised as being either "marginal" or "occasional" vectors of the JE virus in Asia) 3 indicate that these species were of no importance in this outbreak. Cx. annulirostris was breeding in abundance in a variety of sites close to the community. However, the natural surface waters were extensive, and produced the most mosquitoes. The waterhole with run-off watercourses passing through the community meant that there was extensive mosquito breeding close to the $omestic pigs and to the people. The close proximity of the blocked drains to many of the houses also made them a significant risk. Defective waste disposal systems may also have contributed to the outbreak. The most striking combination of environmental factors contributing to the outbreak was the large number of domestic pigs adjacent to human dwellings and prolific mosquito breeding sites (Figure 2). The density of pigs, the abundance of the vector species and the human population density are all critical factors in determining the risk of human infection. 3,22 Horses, although "dead-end" hosts for the JE virus, 3 nevertheless contributed to the outbreak by providing numerous hoofprint breeding sites, nutrient (i.e., faeces) to the larvae and bloodmeals for female mosquitoes. 23 We need to determine the likelihood of future incursions of the JE virus into the Torres Strait. At the same time there is a clear need not only to reduce the mosquito breeding potential but also to improve the environmental conditions on the islands. Meanwhile, an inactivated JE vaccine has been offered to the inhabitants of the outer islands to confer protection while these risk assessment studies and risk reduction interventions are being implemented. 24 Acknowledgements Many people assisted with the investigation of the outbreak. We thank the staff of the Community Health Centers throughout the Torres Strait, Torres Strait Public Health Program, Tropical Public Health Unit, Australian Quarantine and Inspection Service, Queensland Department of Primary Industries, Laboratory of Microbiology and Pathology and the Australian Animal Health Laboratory. We are particularly grateful to Dr Ted Tsai (Division of Vector-Borne Viral Diseases, Centres for Disease Control and Prevention, USA) for his expert advice and support. References Hanna J, Ritchie S, Loewenthal M, et al. Probable Japanese encephalitis acquired in the Torres Strait. Commun Dis Intell 1995; 19: 206-208. The Torres Strait Health Workshop Working Party. Torres Strait Health Strategy. Thursday Island: Torres Strait Health Council, 1993. Vaughn DW, Hoke CH Jr. The epidemiology of Japanese encephalitis: prospects for prevention. Epidemiol Rev 1992; 14: 197-221. Mackenzie JS, Lindsay MD, Coelen RJ, et al. Arboviruses causing human disease in the Australasian zoogeographic region. Arch Virol 1994; 136: 447-467. Burke D, Nisalak A, Ussery M. Antibody capture immunoassay detection of Japanese encephalitis virus immunoglobulin M and G antibodies in cerebrospinal fluid. J Clin Microbiol 1982; 16: 1034-1042. Clarke DH, Cassals J. Techniques for haemagglutination and haemagglutination inhibition with arthropod borne viruses. Am J Trop Med Hyg 1958; 7: 561-573. Gorman BM, Leer JR, Filippich C, et al. Plaquing and neutralization of arboviruses in the PS-EK line of cells. Aust J Med Technol 1975; 6: 65-71. Field PR, Murphy AM. The role of specific IgM globulin estimations in the diagnosis of acquired rubella. Med J Aust 1972; 2: 1244-1248. Igarashi A. Isolation of a Singh's Aedes albopictus cell clone sensitive to dengue and chikungunya viruses. J Gen Virol 1978; 40: 531-544. Pierre V, Drout M-T, Deubel V. Identification of mosquito-borne flavivirus sequences using universal primers and reverse-transcriptase-polymerase chain reaction. Res Virol 1994; 145: 93-104. Sellner LN, Coelen RJ, Mackenzie JS. A one-tube, one manipulation RT-PCR reaction for detection of Ross River virus. J Virol Methods 1992; 40: 255-264. Chen W-R, Tesh RB, Rico-Hesse R. Genetic variation of Japanese encephalitis virus in nature. J Gen Virol 1990; 71: 2915-2922. Chen W-R, Rico-Hesse R, Tesh RB. A new genotype of Japanese encephalitis virus from Indonesia. Am J Trop Med Hyg 1992; 47: 61-69. Ni H, Barrett ADT. Nucleotide and deduced amino acid sequence of the structural protein genes of Japanese encephalitis viruses from different geographical locations. J Gen Virol 1995; 76: 401-407. Sumiyoshi H, Mori C, Fuke I, et al. Complete nucleotide sequence of the Japanese encephalitis virus genome RNA. Virology 1987; 161: 497-510. Ritchie SA, Kline DL. Comparison of CDC and EVS light traps baited with carbon dioxide and octenol for trapping mosquitoes in Brisbane, Queensland (Diptera: Culicidae). J Aust Entomol Soc 1995; 34: 215-218. Anderson SG, Price AVG, Nanadai-Koia, Slater K. Murray Valley encephalitis in Papua and New Guinea: II. Serological survey, 1956-1957. Med J Aust 1960; 2: 410-413. Draffan RDW, Garnett ST, Malone GJ. Birds of the Torres Strait: an annotated list and biogeographical analysis. The Emu 1983; 83: 207-234. Buescher EL, Scherer WF, McClure HE, et al. Ecologic studies of Japanese encephalitis virus in Japan. IV. Avian infection. Am J Trop Med Hyg 1959; 8: 678-688. Boyle DB, Dickerman RW, Marshall ID. Primary viraemia responses of herons to experimental infection with Murray Valley encephalitis, Kunjin and Japanese encephalitis viruses. Aust J Exp Biol Med Sci 1983; 61: 655-664. Bryan JH, O'Donnell MS, Berry G, Carvan T. Dispersal of adult female Culex annulirostris in Griffith, New South Wales, Australia: a further study. J Am Mosq Control Assoc 1992; 8: 398-403. Gingrich JB, Nisalak A, Latendresse JR, et al. Japanese encephalitis virus in Bangkok: factors influencing vector infections in three suburban communities. J Med Entomol 1992; 29: 436-444. Kay BH, Boreham PFL, Fanning ID. Host-feeding patterns of Culex annulirostris and other mosquitoes (Diptera: Culicidae) at Charleville, southwestern Queensland, Australia. J Med Entomol 1985; 22: 529-535. Hanna J, Barnett D, Ewald D. Vaccination against Japanese encephalitis in the Torres Strait. Commun Dis Intell 1996; 20: 188-190. (Received 9 Feb, accepted 27 May 1996) o Authors' details Tropical Public Health Unit, Queensland Health, Cairns, QLD. Jeffrey N Hanna, MPH, FAFPHM, Public Health Physician. Scott A Ritchie, PhD, Medical Entomologist. World Health Organization Collaborating Centre for Arbovirus Reference and Research, Laboratory of Microbiology and Pathology, Queensland Health, Brisbane, QLD. Debra A Phillips, BSc, MASM, Supervising Scientist. Queensland Department of Primary Industries, Cairns, QLD. Jack Shield, BVSc, Veterinary Officer. Torres Strait Public Health Program, Queensland Health, Thursday Island, QLD. M Clare Bailey, MAIEH, Environmental Health Officer. Department of Microbiology, The University of Queensland, Brisbane, QLD. John S Mackenzie, PhD, FASM, Professor of Microbiology. Michael Poidinger, PhD, Research Officer (NHMRC). Southern Zone Public Health Unit, Queensland Health, Upper Mount Gravatt, QLD. Bradley J McCall, MPH, FAFPHM, Public Health Physician. Queensland Health, Thursday Island, QLD. Phillip J Mills, Executive Officer, Torres Sector. Reprints: Dr J Hanna, Tropical Public Health Unit, Queensland Health, PO Box 1103, Cairns, QLD 4870. Email: troppubATcitec.qld.gov.au - Register to be notified of new articles by email - - To top of article - ©MJA1996 < URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Jeffery H Hanna · Scott A Ritchie · Debra A Phillip · Jack Shield · John S Mackenzie · Michael Poidinger · Bradley J McCall · Phillip J Mills

Age-specific HIV incidence among homosexually active men in Australia Matthew G Law, Philip S Rosenberg, Ann McDonald and John M Kaldor MJA 1996; 164: 715-718. This article has been published in the Medical Journal of Australia. Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Author's Details - Table - Figure 1 - Figure 2 Register to be notified of new articles by email - To Current Issues list - ©MJA1996 Abstract Objective: To estimate age at HIV infection among homosexually active men in Australia. Design: Age-specific back-projection estimates of HIV incidence. Methods: Monthly counts of AIDS among homosexually active men diagnosed by 30 June 1994 and reported by 31 March 1995 were obtained from the National AIDS Registry and were adjusted for reporting delays. The progression rate to AIDS was estimated from a large cohort study of HIV-infected homosexual men, with adjustment for the effect of age at HIV infection and the effect of antiretroviral and prophylactic treatments. Results: The median age at HIV infection was estimated to have decreased from 31 years of age between 1982 and 1984 to between 23 and 27 years in the periods 1987 to 1989 and 1990 to 1994. Despite the trend to a younger median age at HIV infection during the current epidemic, HIV incidence was estimated to have declined in all age groups from a peak in the mid-1980s. This decline was more pronounced in the older age groups, with more modest reductions in age groups under 30 years. Conclusion: Most HIV infections among homosexually active men since 1987 appear to have occurred in men aged under 30 years. This has implications for education programs aimed at preventing HIV infection among homosexually active men. MJA 1996; 164: 715-718 Introduction A rapid increase in HIV incidence in Australia in the early 1980s (with a peak of around 3300 cases per year in the mid-1980s, followed by a rapid decline) was reported by both the National Working Group on HIV Projections in 19921 and the Evaluation of the National HIV/AIDS Strategy in 1996.2Cumulative HIV incidence to the end of 1993 was estimated to be between 13 000 to 19 000 cases, with a preferred estimate of 15 200 cases. The estimated annual incidences of HIV infection from 1981 to 1993 for homosexually active men, for heterosexual women, and for women and heterosexual men who were intravenous drug users, are shown in the Box.3 About 85% of both AIDS cases and diagnosed HIV infections in Australia have been in men who have had homosexual contact.4 Over the period of the current AIDS epidemic, it could be expected that a new generation of homosexual men has become sexually active and at risk of HIV infection. An important question, therefore, is whether and how HIV incidence among younger homosexually active men has changed over time. The method of back-projection has become the preferred method for estimating past HIV incidence, and for projecting future AIDS incidence, in most developed countries.5-7 Here, using an extension of the back-projection method,8 we estimate the age at HIV infection among homosexually active men in Australia. Methods Our analyses were based on AIDS cases diagnosed by 30 June 1994 and reported to the National AIDS Registry (NAR) at the National Centre in HIV Epidemiology and Clinical Research by 31 March 1995 in men with a history of homosexual contact, including those who were intravenous drug users. These AIDS incidence data were adjusted for the reporting delay between the time of diagnosis to the time of entry of the case on the NAR.9 All estimates of HIV incidence were adjusted for underreporting of AIDS cases to the NAR, which is currently estimated to be about 10%.3 Age-specific HIV incidence was estimated using the back-projection method suggested by Rosenberg,8 in which the rate of progression to AIDS is assumed to be associated with age.10 To reflect the uncertainty in the rate of progression to AIDS, particularly beyond 10 years following HIV infection, we used two different progression-rate distributions derived from a large-cohort study of HIV-infected homosexual men.11 A faster progression-rate distribution was based on a median "time-to-AIDS" of nine years for people aged 30 at diagnosis of HIV infection, and the rate of progression to AIDS was taken to increase by 1.042 for each year the age at HIV infection was above 30, and to decrease by 1/1.042 for each year the age was below 30. A slower progression rate was based on a median "time-to-AIDS" of 9.8 years and an age-effect of 1.037. As the effect of age on modifying the progression rate to AIDS is uncertain and the assumption of an age-effect would lower the back-projection estimate of median age at HIV infection, we also analysed the progression rates with the age-effects at both zero and half of the above values. The extended definition of AIDS adopted in Australia in January 1988 was assumed to result in a 10% increase in the rate of progression to AIDS.12 The effect of antiretroviral and prophylactic treatments on the progression rate was incorporated into the analysis by assuming that 20% of HIV-infected people were first diagnosed as HIV positive at diagnosis of AIDS and so would not have received treatment before the diagnosis of AIDS,13 and that zidovudine became available in Australia from mid-1987 and was accepted and tolerated by up to 90% of people with diagnosed HIV infection. The effect of treatment was assumed to be a modest 20% reduction in the rate of progression to AIDS and to gradually diminish during ex- tended use, consistent with randomised clinical trials of zidovudine.14-16 We also did further analyses assuming a stronger treatment effect which corresponded to a 50% reduction in the progression rate. Back-projections were conducted for five time periods (early 1977 to mid-1981, mid-1981 to mid-1984, mid-1984 to mid-1986, mid-1986 to mid-1989 and mid-1989 to mid-1994) and for five age groups (17 to 20, 21 to 24, 25 to 29, 30 to 39 and 40 to 59 years). To allow direct comparison of estimates of HIV incidence in different age groups and time periods, estimates of HIV incidence in a given age group and time period were standardised by dividing the estimated total number of new HIV infections by the product of the number of age-years and calendar-years. Results There were 4661 cases of AIDS diagnosed by 30 June 1994 and reported to the NAR by 31 March 1995 among homosexually active men. After adjusting for reporting delays, analyses were based on 4769 cases of AIDS. We did not analyse other exposure categories as there were too few AIDS cases in these categories. The patterns of HIV incidence were similar for both the faster and the slower progression-rate distributions, with a rapid increase in the annual number of HIV infections in the early 1980s to a peak of between 2600 and 3100 per year in the mid-1980s, followed by a steep decline. The faster progression rate gave a smaller estimate of the cumulative HIV incidence to 30 June 1994 than the slower progression rate: 11 800 HIV infections, compared with 14 700, respectively. Both the pattern of HIV incidence and the cumulative HIV incidence estimated by the age-specific analysis are consistent with the non-age-specific back-projections for homosexually active men shown in the Box. The median age at HIV infection was similar for both the faster and slower progression-rate distributions (Figures 1a and 1b). As the epidemic developed, there was a decline in the median age at HIV infection, from 31 years in 1982 to 1984, to 23 and 25 years for both the faster and slower progression-rate distributions, respectively, in 1987 to 1989, and to 25 and 27 years in 1990 to 1994. The age-effect of zero on the progression rate to AIDS gave similar results, showing a decline in median age at HIV infection from 34 and 33 years for both the faster and slower progression-rate distributions, respectively, in 1982 to 1984, to 24 and 26 years, respectively, in 1987 to 1989, and to 27 and 28 years, respectively, in 1990 to 1994. Analyses which assumed half the age-effect also gave similar results. Figure 1: Estimated median age at HIV infection by calendar year (a) faster progression-rate distribution, (b) slower progression-rate ditribution (see text) Although the median age at HIV infection has declined during the epidemic, HIV incidence has declined in all age groups from a peak in the mid-1980s (Figures 2a and 2b). However, this decline has been more pronounced in the older age groups; most HIV infections in recent years appear to have been in men under 30 years. HIV incidence was similar in the age groups 21 to 24, 25 to 29 and 30 to 35 years in 1982 to 1984, but by 1990 to 1994 HIV incidence was substantially higher in the 21 to 24 years age group. Figure 2: Estimated HIV incidence by age group at HIV infection and by calendar year (a) faster progression-rate distribution, (b) slower progression-rate ditribution (see text) Sensitivity analyses which assumed a stronger treatment effect (a 50% reduction in the progression rate to AIDS) gave similar results and are not shown. Discussion The decrease in the estimated median age at HIV infection among homosexually active men, as shown by our age-specific back-projection analysis, has previously been reported using similar methods in the United States,17 and has also been observed in open cohorts of homosexual men attending genitourinary medicine clinics in London between 1988 and 1994.18 Since 1991, another Australian source of information about new HIV infections has been reported cases to the NAR of newly acquired HIV infection. Diagnosed HIV infections are considered to be newly acquired if the person had a negative HIV test within a year of their positive HIV test or if a HIV seroconversion illness was diagnosed. About 200 newly acquired HIV infections are reported each year,4 and the median age of these people has been around 30 to 31 years since 1991 (more than the median age of between 25 and 27 years estimated by the age-specific back-projection analyses in our study). However, HIV incidence since 1991 has been estimated to be around 500 cases per year,3 so only about 40% of these cases are diagnosed each year as newly acquired. It is possible that this 40% is a biased sample of all new HIV infections and, in particular, slightly older than new HIV infections which are not diagnosed as newly acquired. Back-projection analyses are based on assumptions that are subject to uncertainty, in particular the assumed progression-rate distributions. The available Australian data were part of a large- cohort study of HIV-infected homosexual men,11 and indicate that the overall progression rate in homosexually active men in Australia is broadly consistent with both the faster and slower progression-rate distributions that were assumed in the age-specific back-projections. Other major sources of uncertainty are in the modifying effect of age at HIV infection and the effect of antiretroviral and prophylactic treatments on the progression rate to AIDS. The general trend of decreasing age at HIV infection was, however, a robust feature of sensitivity analyses which investigated these uncertainties, suggesting that this trend is at least qualitatively correct. Examining the history of the HIV epidemic among homosexually active men in Australia lends further support for a decreasing age at HIV infection. When the HIV epidemic began in Australia around 1980, homosexually active men of all ages were at risk of infection. As the epidemic progressed, new homosexual men were at risk of HIV infection as they became sexually active, generally at a younger age. Thus, the age distribution of homosexually active men at risk of HIV infection (and hence of those already infected) would be expected to have decreased as the epidemic progressed. The estimates of HIV incidence were standardised for the number of calendar-years and age-years in each time period and age group. This allows direct comparison of HIV incidence if the number of homosexually active men can be assumed to be constant across different age groups over the time period of the epidemic. Based on the 1991 census,19 the resident male population in Australia was fairly uniformly distributed across the age range 15 to 44 years (at about 140 000 men per age-year) but there were fewer men in older age groups. In the age range 17 to 39 years, however, direct comparison of the standardised estimates of HIV incidence appears valid, provided that the proportion of homosexual men is constant over the age range. One feature of our analyses which requires cautious interpretation is the apparent small increase in HIV infection in some age groups between 1987 to 1989 and 1990 to 1994. As few people infected with HIV in the most recent period would be expected to have progressed to AIDS, these figures are uncertain. The most appropriate interpretation is that the number of new HIV infections has been reasonably stable in all age groups between 1987 and 1994. In conclusion, age-specific back-projections suggest that the median age at HIV infection among homosexually active men has decreased over the period 1982 to 1994, and that most HIV infections in more recent years have occurred in men aged under 30. These results suggest that education programs aimed at preventing HIV infections in homosexually active men should be targeted towards younger age groups, in particular homosexually active men in their early twenties. Register to be notified of new articles by email - To Current Issues list - ©MJA1996 Acknowledgements The National Centre in HIV Epidemiology and Clinical Research is funded by the Australian National Council on AIDS through the Commonwealth AIDS Research Grants Committee. The authors thank the National HIV Surveillance Committee and the doctors who reported AIDS cases under national surveillance procedures. References National Working Group on HIV Projections. Estimates and projections of the HIV epidemic in Australia, 1981-1994. Internal technical report 1. Sydney: National Centre in HIV Epidemiology and Clinical Research, April 1992. Valuing the past . . . investing in the future. Evaluation of the National HIV/AIDS Strategy 1993-94 to 1995-96. Canberra: Commonwealth Department of Human Services and Health, 1995. National Centre in HIV Epidemiology and Clinical Research. Estimates and projections of the HIV epidemic in Australia, 1981-1997. In: Technical appendix no. 1: An epidemiological assessment of the HIV epidemic in Australia. Evaluation of the National HIV/AIDS Strategy 1993-94 to 1995-96. Canberra: Commonwealth Department of Human Services and Health, 1996. National Centre in HIV Epidemiology and Clinical Research. Australian HIV Surveillance Report, Vol. 12, No. 1. Sydney: National Centre in HIV Epidemiology and Clinical Research, 1996. Brookmeyer R, Gail MH. A method for obtaining short-term projections and lower bounds on the size of the AIDS epidemic. J Am Stat Soc 1988; 3: 301-308. Taylor JM. Models for the HIV infections and AIDS epidemic in the United States. Stat Med 1989; 8: 45-58. Becker NG, Watson LF, Carlin JB. A method of non-parametric back-projection and its application to AIDS data. Stat Med 1991; 10: 1527-1542. Rosenberg PS. Backcalculation models of age-specific HIV incidence rates. Stat Med 1994; 13: 1975-1990. Brookmeyer R, Liao J. The analysis of delays in disease reporting: methods and results for the acquired immunodeficiency syndrome. Am J Epidemiol 1990; 132: 355-365. Rosenberg PS, Goedert JJ, Biggar RJ, for the multicenter Hemophilia Cohort Study and the International Registry of Seroconverters. Effect of age-at-seroconversion on the natural AIDS incubation distribution. AIDS 1994; 8: 803-810. Biggar RJ and the International Registry of Seroconverters. AIDS incubation in 1891 HIV seroconverters from different exposure groups. AIDS 1990; 4: 1059-1066. Selik RM, Buelher JW, Karon JM, et al. Impact of the 1987 revision of the case definition of Acquired Immune Deficiency Syndrome in the United States. J AIDS 1990; 3: 73-82. Kaldor JM, French MAK. When do patients present with HIV infection? Med J Aust 1993; 158: 37-38. Volberding PA, Lagakos SW, Koch MA, et al. Zidovudine in asymptomatic human immunodeficiency virus infection: A controlled trial in persons with fewer than 500 CD4-positive cells per cubic millimeter. N Engl J Med 1990; 322: 941-949. Cooper DA, Gatell JM, Kroon S, et al. Zidovudine in persons with asymptomatic HIV infection and CD4+ cell counts greater than 400 per cubic millimeter. N Engl J Med 1993; 329: 297-303. Concorde Coordinating Commitee. Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Lancet 1994; 343: 871-881. Rosenberg PS, Biggar RJ, Goedert JJ. Declining age at HIV infection in the United States [letter]. N Engl J Med 1994; 330: 789-790. Miller E, Waight PA, Tedder RS, et al. Incidence of HIV infection in homosexual men in London, 1988-94. BMJ 1995; 311: 545. Australian Bureau of Statistics. Australia in profile. Canberra: ABS, 1993. (Catalogue No. 2821.0.) (Received 13 Nov 1995, accepted 2 April 1996) Authors' details National Centre in HIV Epidemiology and Clinical Research, The University of New South Wales, Sydney, NSW. Matthew G Law, MSc, Statistician. Ann McDonald, MPH, Senior Research Assistant. John M Kaldor, PhD, Professor of Epidemiology. National Cancer Institute, Rockville, USA. Philip S Rosenberg, PhD, Biostatistician. No reprints will be available. Correspondence: Mr M G Law, National Centre in HIV Epidemiology and Clinical Research, The University of New South Wales, 376 Victoria Street, NSW 2010. E-mail: mlaw@nchecr.unsw.edu.au Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Matthew G Law · Philip S Rosenberg · Ann McDonald · John M Kaldor

Teaching hospital medical staff to handwashJames Tibballs Electronically published Tuesday April 30 1996 This article was published in the Medical Journal of Australia on 1 April 1996. Readers may print a single copy for personal use. No further reproduction or distribution of the article in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Abstract - Introduction - Methods - Results - Group performance - Cohort performance - Discussion - Author's Details - Figure - Table 1 - Table 2 - - ©MJA1996 AbstractObjective: To increase the frequency of handwashing by medical staff. Design: A prospective study of handwashing before and after patient contact. Setting: A paediatric intensive care unit in a tertiary hospital. Participants: 61 intensive care unit medical staff and visiting medical staff. Interventions: A five-phase behaviour modification program: (i) unobtrusive observation for four weeks to obtain a baseline handwashing rate; (ii) overt observation for five weeks (preceded by written advice); (iii) overt observation continued for four weeks with performance feedback; (iv) all observation and feedback discontinued for seven weeks; and (v) unobtrusive observation for five weeks to obtain a residual rate. Results: 939 patient contacts were observed. The baseline handwashing rates before and after patient contact were 12.4% and 10.6%, respectively. During overt observation, the respective rates increased and plateaued at 32.7% and 33.3%, but increased further (to 68.3% and 64.8%) during the period of performance feedback. The residual handwashing rates, observed unobtrusively seven weeks after the cessation of performance feedback, were 54.6% before and 54.9% after patient contact. Conclusions: Performance feedback is moderately effective in training hospital medical staff to handwash. MJA 1996; 164: 395-398 IntroductionHandwashing is one of the most important measures for preventing and controlling nosocomial infection.1-4 Despite this, handwashing practices before and after patient contact by all hospital staff, and especially by physicians, are poor.5-9 Educational programs to improve handwashing by increasing awareness of nosocomial infection have had limited success,10-12 suggesting that an innovative approach is needed.13 A training program for nurses with observation and performance feedback as a behaviour modification technique was successful in the short term, but the relative effects of observation and performance feedback were inseparable.14 My study assessed the frequency of handwashing by medical officers in association with patient contact and determined the effects of observation and performance feedback. MethodsThe study was conducted over a five-month period in the Intensive Care Unit (ICU), Royal Children's Hospital, Melbourne, and was approved by the hospital ethics committee. The ICU is an 18-bed multidisciplinary unit treating critically ill infants and children. During the study, 807 patients were admitted: 37% had undergone cardiac surgery, 27% had respiratory illnesses, 9% had general medical illnesses, 8% had newborn medical and surgical illnesses, 8% had trauma, and 8% had undergone neurosurgery and 3% general surgery. Mechanical ventilation was provided for 84% of patients. Most had invasive monitoring or therapeutic devices inserted into peripheral arteries, peripheral or central veins, the thoracic cavity, the urinary bladder or the extradural space. The mortality rate was 5.9%. The subjects of the study were any medical officers who made hand contact with any patient in the ICU. The ICU is newly constructed and comprises four rooms adjacent to each other along a corridor. Windows enable vision between rooms and into each room from the corridor. Handwashing basins are located in each room within two to three metres of each bed and in the corridor. A choice of handwashing solutions are provided at each basin. During the study these were: (i) a mixture of 1% chlorhexidine gluconate, 70% ethyl alcohol and emollients; (ii) 2% aqueous chlorhexidine gluconate; (iii) 7.5% aqueous povidone-iodine; and (iv) domestic bar soap. Paper-towel dispensers are located at each basin. I observed patient contact and handwashing practices of medical officers during ward rounds; at other times this observation was by instructed members of the nursing staff. Observations were made between the hours of 7 am and 6 pm on weekdays. Handwashing was regarded as any action to cleanse the hands with water and one of the available handwashing agents, or with a handwashing agent alone. No judgement was made about the duration or efficacy of the handwashing technique. Observations were recorded with the names of subjects and the patients involved. However, anonymity was preserved for data analysis and feedback purposes. Patient contact was defined as any contact by the hands of a medical officer with a patient's skin or an indwelling invasive device during a procedure in which the hands could be contaminated with the patient's blood, secretions or excretions. Contact with bed linen, bed frames, medical records or monitoring equipment was not regarded as patient contact. Typical patient contact involved procedures such as examining wounds, inserting intravenous or arterial catheters, aspirating endotracheal tubes, performing echocardiographic examinations, auscultating the chest, palpating the chest or abdomen, manipulating chest drains or urinary catheters, inserting tracheal or gastric tubes, and withdrawing blood from intravascular catheters. Handwashing was assessed before and after contact with a patient. Handwashing was not recorded if the subject was not observed immediately before patient contact, or could not be observed after contact until handwashing had been performed, or contact with another patient had occurred. Departure from the ICU area without handwashing was regarded as failure to handwash. Contact by the subject with his or her own skin, secretions or a mucous membrane (e.g., nasal mucosa) after handwashing but before patient contact was registered as failure to handwash. Medical officers were not requested to handwash, and the ICU did not have any information about handwashing displayed (other than the performance feedback when this part of the study was reached). The behaviour modification program was divided into five phases1. Weeks 1-4: unobtrusive observation (only hospital personnel involved in the study knew this was happening). At the end of this phase, 19 medical officers who worked in the ICU or visited frequently were requested verbally to estimate their own handwashing rates before patient contact. 2. Weeks 5-9: overt observation; this was preceded by written advice to all medical staff of the intention to study handwashing in ICU. Subjects were not informed which aspect of handwashing was to be studied, although, if requested, information was not to be withheld (no medical staff requested clarification). 3. Weeks 10-13: overt observation with performance feedback; at the beginning of this phase all results collected thus far were displayed as brightly coloured histograms on 40 x 60 cm sheets of paper showing the group percentage handwashing rate before and after patient contact. These were placed in strategic locations used by the medical staff in ICU, but were out of sight of patients and visitors. Data were updated weekly for the four weeks. After two weeks of performance feedback, results of group data collected up to that time were mailed to the medical officers. 4. Weeks 14-20: observations and feedback were discontinued. 5. Weeks 21-25: unobtrusive observation, after which these data were added to the histograms displayed in the ICU. Handwashing by members of the cohort who were requested to estimate their own handwashing rate and who participated in all phases of the program was analysed separately and is also reported here. ResultsGroup performanceSixty-one medical officers were observed making 939 patient contacts. Twelve were full-time senior or junior ICU staff, and the remainder full-time or part-time senior staff from other disciplines or junior full-time staff. Half the observations (470/939) were made by the investigator, and half by nursing staff. The aggregate handwashing rates before and after patient contact during phases of the program are presented in The aggregate handwashing rates before and after patient contact during phases of the program are presented in Table 1. The week-to-week variation within each phase and between each phase is shown in the Figure. During overt observation the handwashing rate rose from the baseline level (determined by unobtrusive observation), with the peak rate occurring in Week 3 of this five-week period. It rose again during performance feedback, peaking in the last week of this phase. During the second period of unobtrusive observation, seven weeks after performance feedback, the handwashing rate was lower but still showed a more than fourfold increase over baseline levels. There was a gradual decline from week to week during this last phase of unobtrusive observation. Cohort performanceNineteen medical officers estimated their own handwashing rate before patient contact after the first phase of covert observation. Their mean estimate was 66% (range, 30%-95%). Several commented that other medical officers washed their hands infrequently. Fourteen of these 19 subjects subsequently participated in the remain- ing phases of the program. Among this cohort, the mean self-estimated handwashing rate was 73% (range, 50%-95%), compared with the covertly observed rate for this cohort of 8.6% before and 10.8% after patient contact, with an individual mean rate of 10% (range, 0-33%). The performance of the cohort during the other phases of the program is shown in Table 2. Significant improvement in handwashing before and after patient contact was observed during overt observation and performance feedback. The improved performance of these 14 subjects was maintained after the period without observation. DiscussionPatients in intensive care units are at greater risk of nosocomial infection than those elsewhere in hospitals: they are already critically ill; are subject to multiple hand contacts from a wide variety of staff; have indwelling invasive therapeutic and monitoring devices; and often receive non-specific antimicrobial therapy. Reports of nosocomial infection in intensive care units show infection rates varying from 13% to 26%,15-19 whereas hospital-wide nosocomial infection rates are about 5%-10%.20-23 Physicians freely acknowledge that handwashing is important in the control of nosocomial infection, and suggest pressure of work, a lack of patient contact, detrimental effects of handwashing agents on skin and the more important needs of the patient as reasons for not handwashing.4 Infection control is rarely taught in medical school,24 and poor handwashing practices may be learnt from peers at the bedside.25 In the first phase of this study, I found the handwashing rate among medical staff to be lower than rates reported previously (13%-28%,5 21%6 and 15%7). Physicians were observed unobtrusively as it is known that observation alone may alter behaviour, a phenomenon otherwise known as the "Hawthorne effect" (after the Hawthorne works of the Western Electric Company, where job performance was improved by the presence of observers).26 This effect was confirmed firstly by the abrupt increase in handwashing which accompanied notification of my intention to observe handwashing and again during the performance feedback phase. Despite the relative lack of handwashing in relation to patient contact by hospital staff and its possible detrimental consequences, few reports of attempts to improve handwashing have been published. "Educational programs" which aim to increase medical staffs' awareness of nosocomial infection and the importance of handwashing have not been successful. In an intensive care unit the handwashing rate among physicians increased to only 17% after an educational program (in-service teaching rounds, poster displays, specific requests to handwash and unspecified performance feedback to all staff).10 Another study, in a paediatric ambulatory setting, found that physicians did not respond to written and verbal requests to handwash before patient contact.27 Moreover, my study showed that medical staff have an inflated impression of their own handwashing performance, which may possibly prejudice learning. Educational programs to teach nurses to handwash have also been unsuccessful. The failure of one consisting of poster displays and the distribution of booklets on isolation policy was attributed to a lack of motivation.11 Another strategy to improve handwashing is the installation of handwashing machines. This was associated with improvement over a short period in a small group of nurses and physicians, but it was abandoned when there was an outbreak of methicillin-resistant Staphylococcus aureus.28 Several "training programs" to increase handwashing have been more successful than educational awareness programs. A program for nurses consisted of observation and daily feedback of handwashing performance from the previous day; the handwashing rate after patient contact rose from 59% to 92% during a three-week period.14 However, the relative effects of observation and performance feedback could not be separated. Among food handlers in a university cafeteria, performance feedback alone was successful in training to handwash.29 Performance feedback is an intervention frequently used in organisational behaviour management to improve performance.30 In my study, it resulted in an increase in handwashing among medical officers which was sustained at a rate six times the baseline in about two-thirds of contacts with patients. Regular programs are required to maintain an acceptable standard of performance among permanent staff10 and to compensate for departure and entry of staff members. In my study the difference in handwashing performance between the whole group of medical officers and a cohort within the group may be attributed to staff turnover outside the cohort or, alternatively, to greater exposure to the program, or may be a consequence of being asked to estimate their own handwashing rate. The cohort achieved and maintained a higher handwashing rate than the group as a whole. For reasons of economy and efficacy, behaviour intervention rather than educational awareness programs appears preferable in educating medical staff to handwash. Acknowledgements I thank Dr Gerald Elsworth, formerly of the Centre for the Study of Higher Education, University of Melbourne, for helpful suggestions concerning the design of the study. I thank the ICU nurses, particularly Sharon Kinney. (©MJA 1996; 164: 14-17) To beginning of this article ReferencesDaschner F. Useful and useless hygienic techniques in intensive care units. Intensive Care Med 1985; 11: 280-283. Davies PA. Please wash your hands. Arch Dis Child 1982; 57: 647-648. Steere AC, Mallison GF. Handwashing practices for the prevention of nosocomial infections. Ann Intern Med 1975; 83: 683-690. Larson E, Killien M. Factors influencing handwashing behaviour of patient care personnel. Am J Infect Control 1982; 10: 93-99. Albert RK, Condie F. Hand-washing patterns in medical intensive care units. N Engl J Med 1981; 304: 1465-1466. Donowitz LG. Handwashing technique in a pediatric intensive care unit. Am J Dis Child 1987; 141: 683-685. De Carvalho M, Lopes JMA, Pellitteri M. Frequency and duration of handwashing in a neonatal intensive care unit. Pediatr Infect Dis J 1989; 8: 179-180. Larson E. Compliance with isolation technique. Am J Infect Control 1983; 11: 221-225. Meengs MR, Giles BK, Chisholm CD, et al. Hand washing frequency in an emergency department. Ann Emerg Med 1994; 23: 1307-1312. Conly JM, Hill S, Ross J, et al. Handwashing practices in an intensive care unit: the effects of an educational program and its relationship to infection rates. Am J Infect Control 1989; 17: 330-339. Williams E, Buckles A. A lack of motivation. Nursing Times 1988; 84: 60-64. Doebbeling BN, Stanley GL, Sheetz CT, et al. Comparative efficacy of alternative hand-washing agents in reducing nosocomial infections in intensive care units. N Engl J Med 1992; 327: 88-93. Goldmann D, Larson E. Hand-washing and nosocomial infections. N Engl J Med 1992; 327: 120-122. Mayer JA, Dubbert PM, Miller M, et al. Increasing handwashing in an intensive care unit. Infect Control 1986; 7: 259-262. Daschner FD, Frey P, Wolff G, et al. Nosocomial infections in intensive care wards: a multicenter prospective study. Intensive Care Med 1982; 8: 5-9. Donowitz LG, Wenzel RP, Hoyt JW. High risk of hospital-acquired infection in the ICU patient. Crit Care Med 1982; 10: 355-357. Potgieter PD, Linton DM, Oliver SO, Forder AA. Nosocomial infections in a respiratory intensive care unit. Crit Care Med 1987; 15: 495-498. Donowitz LG. High risk of nosocomial infection in the pediatric critical care patient. Crit Care Med 1986; 14: 26-28. Craig CB, Connelly S. Effect of intensive care unit nosocomial pneumonia on duration of stay and mortality. Am J Infect Control 1984; 12: 233-238. McLaws M-L, Gold J, King K, et al. The prevalence of nosocomial and community-acquired infections in Australian hospitals. Med J Aust 1988; 149: 582-590. Meers PD, Ayliffe GAJ, Emmerson AM, et al. Report on the national survey of infection in hospitals, 1980. J Hosp Infect 1981; 2(Suppl): 13-17. Haley RW, Culver DH, White JW, et al. The nationwide nosocomial infection rate. A new need for vital statistics. Am J Epidemiol 1985; 121: 159-167. Mayon-White RT, Ducel G, Kereselidze T, Tikomirov E. An international survey of the prevalence of hospital-acquired infection. J Hosp Infect 1988; 11(Suppl A): 43-48. Moss F, Cochrane JPS, Yudkin JS. Introducing medicine to tomorrow's doctors. Lancet 1987; 1: 203-205. Larson E, McGinley KJ, Grove GL, et al. Physiologic, microbiologic and seasonal effects on the skin of health care personnel. Am J Infect Control 1986; 14: 51-59. Roethlisberger FJ, Dickson WJ. Management and the worker. Cambridge, Mass: Harvard University Press, 1942. Lohr JA, Ingram DL, Dudley SM, et al. Handwashing in paediatric ambulatory settings. Am J Dis Child 1991; 145: 1198-1199. Wurtz R, Moye G, Jovanovic B. Handwashing machines, handwashing compliance and potential for cross-contamination. Am J Infect Control 1994; 22: 228-230. Geller ES, Eason SL, Phillips JA, Pierson MD. Interventions to improve sanitation during food preparation. J Organizational Behav Manage 1980; 2: 229-240. Prue DM, Fairbank JA. Performance feedback in organizational behavior management: a review. J Organizational Behav Manage 1981; 3: 1-16. (Received 26 Jun, accepted 5 Dec 1995) Author's detailsIntensive Care Unit, Royal Children's Hospital, Melbourne, VIC. James Tibballs, MEd, FFICANZCA, Deputy Director. Reprints: Dr J Tibballs, Intensive Care Unit, Royal Children's Hospital, Flemington Road, Parkville, VIC 3052. E-mail: tibballjATcryptic.rch.unimelb.edu.au (©MJA 1996; 164: 14-17) < URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

James Tibballs

Vaccine-preventable childhood diseases in Australia Too much disease, not enough vaccination: what more can we do? MJA 1996; 164: 61 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". - ©MJA1997 In 1994, there were 17 442 notifications of vaccine- preventable diseases in Australia.1 This disgraceful situation exists despite the ready availability of free, safe and effective vaccines. Particularly damning were the 8661 cases of pertussis, measles, mumps, rubella and Haemophilus influenzae type b notified in children up to school leaving age (19 years old) -- all diseases for which a national immunisation program has been in place for many years! Why do we still have so much disease despite good vaccines and good delivery systems? While there is a lack of uniform reliable data on vaccination coverage, it would seem our national childhood vaccination rates are inadequate. The Australian Bureau of Statistics' 1989-90 National Health Survey reported that, according to parental recall, 53% of children up to six years of age had been vaccinated in accord with the National Health and Medical Research Council (NHMRC) vaccination schedules.2 Unpublished data from State health departments include the report of a 1991 cluster survey in Victoria of 630 children aged 18 months to 3 years which found that 88% were fully vaccinated against diphtheria, pertussis, tetanus, polio and measles (John Carnie, Manager, Infectious Diseases Unit, Victorian Department of Health and Community Services, Melbourne, personal communication); a 1994 ACT report found that only 67% of 236 children at school entry (aged about five years) were fully vaccinated (Ms Ann Kempe, Immunisation Coordinator, ACT Department of Health and Community Care, Canberra, personal communication). Whatever the true vaccination coverage, continuing notifications (in the thousands) of cases of measles, with its well-known risks of encephalitis, bronchopneumonia and subacute sclerosing panencephalitis (SSPE), highlight how much still needs to be done. In the United Kingdom a recent national measles-rubella immunisation program has successfully terminated measles virus circulation in schools; in March and April 1995, there were four confirmed cases of measles in England and Wales; three cases had recently arrived in the country, and the other occurred in an unvaccinated 15-month-old child.3 In Australia there were 229 measles notifications for the same period (National Notifiable Diseases Surveillance System, personal communication). there is still a lack of awareness on the part of parents and even some health practitioners of the benefit-risk equation for vaccination On the other hand, notifications of invasive Haemophilus influenzae type b have decreased from at least 3.5 cases per 100 000 population in 19911 to 1 case per 100 000 in 1994.1 Within three years we may see less than a quarter the number of cases of childhood bacterial meningitis recorded in 1990 -- evidence of the benefit of effective vaccination. The National Childhood Immunisation Committee has implemented a number of initiatives over the past two years to increase vaccination coverage rates in line with the goals of the 1993 NHMRC National Childhood Immunisation Strategy.4 More than 30 000 copies of a kit, which included the fifth edition of the Australian immunisation procedures handbook,5 were distributed to general practitioners and other vaccination service providers. A parents' guide to immunisation, Understanding childhood immunisation,6 was also produced and widely distributed; a recent mass media awareness campaign offers this booklet free to enquirers through a toll-free telephone number (1800 671 811). Such initiatives have received broad professional and community support from organisations such as the Australian Medical Assocation, the Royal Australian College of General Practitioners, the Australian College of Paediatrics, the Australian Institute of Environmental Health, the Sudden Infant Death Association and the NHMRC. Technical considerations also play a role in ensuring the optimal efficacy of vaccines: guidelines and systems for cold-chain maintenance have been implemented (some local studies have suggested that some vaccine providers have difficulty maintaining vaccines at between 2-81/4C7,8 ); knowledge of the thermolability of reconstituted measles-mumps- rubella vaccines and of oral polio vaccine at room temp erature is another important consideration. The safety and efficacy of vaccines are apparent to all but a few. A scheme to record, follow-up and regularly publish significant adverse events following vaccination has been under way since March 1995 (general practitioners and other providers notifying respective State or Territory health authorities by telephone). The data are collated, reviewed and published monthly in Communicable Diseases Intelligence. Adverse event rates of less than 1% have been recorded, although the data are as yet incomplete. Nevertheless, there is still a lack of awareness on the part of parents and even some health practitioners of the benefit-risk equation for vaccination, at least for some vaccines. A few individuals who propagate tired myths of exaggerated vaccination harm, however sincerely, make it more difficult to provide concerned parents with balanced benefit-risk information. To address this problem Commonwealth funding of $24 million has been allocated towards childhood vaccination during 1995-96 and 1996-97. Most of this outlay is provided to the States and Territories to purchase NHMRC standard childhood immunisation schedule vaccines in return for their undertaking to provide a coordinated program. Some of this funding will be used to obtain better information about vaccination coverage via the Australian Childhood Immunisation Register, which commenced on 1 January 1996. Information from the Register will enable resources to be targeted effectively to assist areas with the lowest coverage rates. Combination 4-in-1 (tetravalent) and 5-in-1 (pentavalent) vaccines (e.g., against diphtheria, tetanus, polio, Haemophilus influenzae type b and hepatitis B), less reactogenic acellular pertussis vaccines, as well as a varicella vaccine, are soon to appear on local markets. On the eve of the third millennium, once again we as a nation will need to debate the cost-benefit of disease prevention. In this debate we must acknowledge how far we have come in the two hundred years since Jenner's successful inoculations against smallpox, and how far we have yet to go. Gavin W Frost Senior Medical Adviser, AIDS/Communicable Diseases Branch Commonwealth Department of Human Services and Health, Canberra, ACT Monica Johns Senior Project Officer, National Childhood Immunisation Program Commonwealth Department of Human Services and Health, Canberra, ACT Hargreaves J, Longbottom H, Myint H, et al. Annual Report of the National Notifiable Diseases Surveillance System 1994. Commun Dis Intell 1995; 19: 542-574. Australian Bureau of Statistics. 1989-90 National Health Survey Children's Immunisation Survey, Australia. Canberra: ABS, 1992. (Catalogue No. 4379.0.) Interruption of measles transmission in school schildren, 1995. Wkly Epidemiol Rec 1995; 70: 215-216. National Health and Medical Research Council. National Immunisation Strategy. Canberra: NHMRC/AGPS, 1993. National Health and Medical Research Council. The Australian immunisation procedures handbook. 5th ed. Canberra: AGPS, 1995. Herceg A, Shelley S. Understanding childhood immunisation. Canberra: Commonwealth Department of Human Services and Health, 1995. Liddle JL, Harris MF. How general practitioners store vaccines. A survey in south-western Sydney. Med J Aust 1995; 162: 366-368. Herceg A, Longbottom H. A national immunisation provider survey. Canberra: Commonwealth Department of Human Services and Health, 1995. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Gavin W Frost · Monica Johns

Drug-resistant Streptococcus pneumoniae: the beginning of the end for many antibiotics? Peter J Collignon and Jan M Bell, on behalf of the Australian Group on Antimicrobial Resistance (AGAR)* Abstract - Introduction - Methods - Antibiotic sensitivity testing - Statistical analysis - Results - Discussion - Acknowledgements - References - Authors' details - ©MJA1997 Abstract Objective: To determine the levels of antibiotic resistance in Streptococcus pneumoniae in Australia. Design: Prospective, Australia-wide, laboratory-based survey. Setting: 27 hospital and private laboratories around Australia, from January 1994 to August 1995. Subjects: First 100 patients with clinically significant isolates of S. pneumoniae at each laboratory. Outcome measures: Resistance to penicillin (determined from penicillin minimum inhibitory concentration [MIC] measured by the Etest), erythromycin, trimethoprim-sulfamethoxazole, tetracycline, chloramphenicol, cefotaxime and ceftriaxone. Results: A total of 2396 isolates were tested (including 537 invasive isolates and 740 from children). Penicillin resistance was seen in 161 isolates (6.7%), including 17 with high level resistance. Penicillin resistance rates were significantly lower in invasive than in non-invasive strains (3.7% versus 7.6%; odds ratio [OR], 0.47; 95% confidence interval [CI], 0.28-0.77; P = 0.001). There was no significant difference in penicillin resistance rates between children ( < 15 years) and adults (7.3% versus 6.5%; OR, 1.14; 95% CI, 0.80-1.63; P = 0.47). Resistance rates were higher for most other antibiotics than for penicillin (chloramphenicol, 6%; erythromycin, 11%; tetracycline, 15%; and trimethoprim-sulfamethoxazole, 42%). No high level resistance was seen to third generation cephalosporins, but 17 of 109 penicillin-resistant isolates tested (16%) displayed intermediate resistance to cefotaxime. Rates of antibiotic resistance varied between States, with the lowest rates in Tasmania. Conclusions: Antibiotic resistance levels in S. pneumoniae are increasing in Australia and high level penicillin resistance is being encountered for the first time (including in invasive strains). This will lead to an increasing number of therapeutic dilemmas and possible therapeutic failures, especially important in meningitis. MJA 1996; 164: 64 Introduction The pneumococcus (Streptococcus pneumoniae) continues to be a common cause of serious and life-threatening infections, including pneumonia, bacteraemia and meningitis. It is also a frequent cause of respiratory tract infections, such as otitis media and sinusitis.1-4 A major advance was made in the treatment of these infections with the introduction of penicillin 50 years ago. Until relatively recently, pneumococci were considered so uniformly sensitive to penicillin (with minimum inhibitory concentrations [MICs] < 0.02 mg/L) that sensitivity tests were usually not performed. It was from Australia in 1967 that the first clinically significant isolate of a penicillin-resistant pneumococcus was reported.5 However, penicillin resistance was not a major clinical problem in this country, although it caused major problems elsewhere, particularly in Papua New Guinea and South Africa.1-3 In the late 1970s and the 1980s, rates of resistance (including multiple resistance) increased in Western countries, particularly in Spain (with resistance levels of 50%).1,2,3 A recent United States study found 25% of invasive S. pneumoniae isolates were penicillin-resistant.6 Resistance rates are usually higher in children, and the distribution of resistance varies within countries and population groups.1,2,3,6 In an Australia-wide study of over 1800 isolates of S. pneumoniae in 1989, we found that only 1% were penicillin-resistant,7 a lower rate than in most other Western countries. However, some communities (especially Australian Aboriginals) have relatively high rates of resistance.8 Because of the worldwide increase in resistance to many antibiotics and the implications of penicillin resistance in S. pneumoniae for treatment of life-threatening conditions (particularly meningitis), we undertook a further study of resistance to penicillin and other commonly used antibiotics in clinically significant S. pneumoniae isolates from both the community and hospitals. Methods Twenty-seven hospital and private laboratories from around Australia parti cipated. From January 1994, each laboratory tested the first 100 consecutive clinically significant isolates. The rate of collection varied from 5 to 20 months, with all laboratories filling their quota in August 1995. Patients' sex, age, specimen site and inpatient or outpatient status were recorded prospectively. Clinically significant isolates were defined as those isolated either from normally sterile sites (e.g., cerebrospinal fluid and blood [invasive isolates]) or from specimens that made contact with mucosal surfaces (e.g., sputum) if they were associated with an increased white cell count on gram staining and would normally have been reported as clinically significant. Throat or surveillance swabs were excluded, as were duplicates of clinically significant isolates. S. pneumoniae was identified by colonial morphology, a -haemolysis on blood agar plates, susceptibility to optochin and/or bile solubility. Antibiotic sensitivity testing Isolates were tested for susceptibility to penicillin, erythromycin, trimethoprim-sulfamethoxazole, tetracycline and chloramphenicol by the standardised routine method of each laboratory. Methods included disc diffusion with either National Committee for Clinical Laboratory Standards (NCCLS)9 (14 laboratories) or Calibrated Dichotomous Sensitivity (CDS)10,11 (7 laboratories); agar dilution12 with either Isosensitest agar (Oxoid) (2 labora tories) or Mueller-Hinton agar (3 lab oratories); and the ATB system (BioMerieux sa , Marcy-l'Etoile, France) (1 laboratory). The MIC of penicillin was also determined for each isolate by the Etest on Mueller-Hinton agar supplemented with 5% blood;13,14 plates were incubated at 35¡C in 5% CO 2 for 20-24 hours. 14 The interpretive criteria of the NCCLS15 were used for susceptibility categorisation of Etest values (susceptible, MIC < 0.06 mg/L; intermediate resistance, MIC = 0.125-1 mg/L; and high level resistance, MIC > > 2 mg/L). For the study, antibiotic resistance was defined as decreased susceptibility (both intermediate and high level resistance),6,12 and multidrug resistance as decreased susceptibility to two or more of the antibiotic agents tested. Isolates from normally sterile sites and those that appeared resistant to penicillin or chloramphenicol by routine susceptibility testing or had penicillin MICs > > 0.047 mg/L were forwarded to Monash Medical Centre for further susceptibility testing: Etest strips were used to determine cefotaxime and ceftriaxone MICs. Statistical analysis Fisher's two-tailed exact test was used to calculate P values. Calculations were performed with True Epistat software.16 Results A total of 2396 isolates from different patients were tested. The average age of the patients was 41.6 years (range, < 1 day to 98 years); 32% were children ( < 15 years) and 60% were male. The percentage of penicillin-resistant isolates from each specimen site is shown in Box 1; the overall rate of penicillin resistance was 6.7%, with rates in individual laboratories ranging from 0 to 13%. High level resistance was seen in 17 isolates, including two from normally sterile sites. The rate of penicillin resistance was significantly lower among invasive isolates than among non-invasive isolates (3.7% versus 7.6%; odds ratio [OR], 0.47; 95% confidence interval [CI], 0.28-0.77; P = 0.001) (Box 2). The rate of penicillin resistance was slightly higher among children ( < 15 years) than among adults, but the difference was not statistically significant (7.3% versus 6.5%; OR, 1.14; 95% CI, 0.8-1.63; P = 0.47). Resistance to antibiotics other than penicillin was common (Boxes 2 and 3). Rates varied around Australia, with the lowest rates for nearly all antibiotics in Tasmania and the highest in the eastern States, particularly Queensland and New South Wales. The rate of penicillin resistance was highest in South Australia. Very high levels of resistance were seen for trimethoprim-sulfamethoxazole (29%-52%). All five antibiotics were tested on 1895 isolates; 267 (14%) were multi resistant, with 159 (8%) resistant to three or more antibiotics and 31 (1.6%) to all five (Box 3). Of 124 penicillin-resistant isolates tested, 72 (58%) were resistant to three or more non--lactam agents; 40% were resistant to chloramphenicol; 52% to erythromycin; 64% to tetracycline; and 78% to trimethoprim-sulfamethoxazole. Of the 1771 pencillin-susceptible isolates, 101 (6%) were resistant to three or more non--lactam agents; 3% to chloramphenicol; 8% to erythromycin; 12% to tetracycline; and 39% to trimethoprim- sulfamethoxazole . Of 109 penicillin-resistant isolates tested with cefotaxime, 17 (16%) had intermediate resistance (MIC, 1 mg/L). These comprised 12 of 13 isolates with high-level penicillin resistance and 5 of 96 with intermediate penicillin resistance. Only three of the 109 isolates had intermediate resistance to ceftriaxone (all with high-level penicillin resistance). Discussion We found that the level of penicillin resistance among S. pneumoniae isolates was six times higher than that found in 1989 in the only other large multicentre Australian study,7 but fortunately it was still lower than in most other countries. Penicillin resistance rates are very high in Third World countries, and in some areas of Western Europe and the USA.1-3 However, the rate of rise in resistance in Australia appears very similar to that seen in the early 1980s in countries such as Spain1-3 and in the early 1990s in the United States;6 there, only 0.02% of isolates nationally were penicillin-resistant in the early 1980s and still only 1.3% in 1992,6 but a recent study found a rate of 25%, with much higher rates in some subgroups (e.g., 40% in white children). Of equal concern was that 3% of isolates had high level resistance to both penicillin and third generation cephalosporins.6 Over the next few years, we are likely to see similar rates of resistance developing in Australia. The finding of high level penicillin resistance among S. pneumoniae isolates in Australia is of particular concern; in meningitis caused by organisms with any level of penicillin resistance, penicillin treatment is likely to fail.1-3,17,18 Penicillin resistance has consequences for other related drugs, as in S. pneumoniae it is not due to -lactamase production (as in Staphylococcus aureus ), but to changes in the target for penicillin (the penicillin-binding proteins).1,2,19 This change increases the MICs for all -lactams, including the third generation cephalosporins.1,2,19 However, the levels of third generation cephalosporins achieved in cerebrospinal fluid are still high enough to eradicate organisms with intermediate penicillin resistance.1-3,18 Alternative regimens include combination therapy with vancomycin, third generation cephalosporins and rifampicin, as well as newer agents such as meropenem, teicoplanin and quinolones (under investigation),1 but none has been adequately evaluated. Of even greater concern are the implications of the rapid rise in resistance to third generation cephalosporins noted in the United States. Primary resistance to these drugs is less frequent than to penicillin, but requires less genetic change.1,19 In some areas up to 27% of penicillin-resistant pneumococci have high level resistance to cefotaxime.1 This leads to therapeutic failure of these agents, yet they are the main treatment for the increasingly common intermediate penicillin-resistant strains. No high level cefotaxime-resistant strains were seen in our study or have been reported in Australia, to our knowledge. However, given the worldwide spread of resistant pneumococci in the recent past, they will inevitably be seen soon in Australia and leave us with major therapeutic dilemmas in the treatment of meningitis. In life-threatening situations other than meningitis (e.g., bacteraemia), high dose intravenous penicillin appears sufficient to eradicate organisms with intermediate resistance, as drug levels achievable in serum are still much higher than the MIC.1,2,3 There is, however, controversy, and many recommend use of either cefotaxime or ceftriaxone.1,3 For organisms with high level resistance, the most appropriate agent is unclear. However, we would favour vancomycin. In non-life-threatening infections with penicillin-resistant pneumococci, the most appropriate antibiotics are less clear. In otitis media, amoxycillin still appears the best choice,20,21 as drug levels achieved in the middle ear can still exceed the MICs of strains with intermediate resistance (although higher doses may be needed). Other oral agents available in Australia for use in children (cefaclor, trimethoprim, erythromycin and cefpodoxime) do not reach adequate levels to eradicate resistant isolates.20,21 Third generation cephalosporins, such as ceftriaxone, are active, but their parenteral route is likely to preclude their use. Combining clavulanic acid with amoxycillin is no advantage, as the resistance is not due to -lactamase. For high level penicillin-resistant isolates there does not appear to be a satisfactory oral agent. The reasons for the increasing resistance in S. pneumoniae worldwide are not completely understood, although antibiotic pressure appears to be a major factor.1 A few resistant clones were shown to have spread from one continent to others (e.g., from Spain to the United States and Iceland) and then through the local population, undergoing minor genetic changes in the process.1,3,19 The pneumococcus can acquire DNA molecules from other bacteria that probably include viridans group streptococci (e.g., Streptococcus mitis), which form part of the normal flora of the nasopharynx.1,19 While it would probably be impossible to eradicate carriage of these resistant organisms from the population, it may be possible to reduce the rate of increase in resistance by minimising the prescription of unnecessary antibiotics. Other strategies, such as vaccination, may be necessary. Unfortunately, the currently available vaccine is a polysaccharide and therefore a poor immunogen, especially in young children. Studies are under way to assess a conjugated pneumococcal vaccine (i.e., a carbohydrate with protein carrier), but vaccine development is difficult as there are over 80 serotypes of pneumococci (compared with only one commonly invasive serotype of Haemophilus influenzae -- type b). However, at present most of the resistant organisms belong to relatively few serotypes.1,2,3 A vaccine containing most of these might not only decrease life-threatening disease, but might also decrease carriage of the organisms, as was found for the H. influenzae type b (Hib) vaccine.1 However, as the pneumococcus can acquire DNA from other organisms,1,19 the number of resistant serotypes is likely to increase. Our study was one of the largest in the world where all organisms were clinically significant and all were assessed for MIC for penicillin. It is valuable not only for showing the rate of resistance (both intermediate and high level), but also for providing a baseline to assess future changes in resistance and to differentiate subtle shifts in resistance in the whole population of pneumococci from the introduction of resistant clones. In the past, determining MICs was time-consuming, laborious and not routine. The recent development of the Etest (which consists of a strip of paper impregnated with increasing concentrations of antibiotic from one end to the other) has simplified the procedure. This technological advance, along with the willingness of so many laboratories around Australia to participate in the project, has allowed us to obtain information essential for guiding us in making appropriate antibiotic choices and designing empiric therapy for these emerging threats. Acknowledgements We wish to thank the many doctors, scientists and technicians at the participating laboratories who donated their time and resources to carry out this project. The penicillin Etest strips were supplied by Australian Laboratory Services Pty Ltd at cost price. Eli Lilly provided funding for many of the participants to meet at the twice-yearly AGAR meeting. Cefotaxime and ceftriaxone Etest strips were donated by AB Biodisk (Sweden). References Lister PD. Multiply-resistant pneumococcus: therapeutic problems in the management of serious infection. Eur J Clin Microbiol Infect Dis 1995; 14 Supp 1: 18-25. Klugman K. Pneumococcal resistance to antibiotics. Clin Microbiol Rev 1990; 3: 171-196. Schreiber J, Jacobs M. Antibiotic-resistant pneumococci. Pediatr Clin North Am 1995; 42: 519-537. Collignon P. Penicillin-resistant pneumococci: will the recent Olympics bring back to Australia more than gold? Med J Aust 1992; 157: 655-657. Hansman D, Bullen M. A resistant pneumococcus. Lancet 1967; 2: 264-265. Hofmann J, Cetron M, Farley M, et al. The prevalence of drug resistant Streptococcus pneumoniae in Atlanta. N Engl J Med 1995; 333: 481-486. Collignon P, Bell J, on behalf of AGAR. Streptococcus pneumoniae : how common is penicillin resistance in Australia? Aust N Z J Med 1992; 22: 473-476. Hansman D, Morris S, Gregory M, McDonald B. Pneumococcal carriage amongst Australian aborigines in Alice Springs, Northern Territory. J Hyg (Camb) 1985; 95: 677-684. National Committee for Clinical Laboratory Standards. Performance standards for antimicrobial disk susceptibility tests. 5th ed. Approved standard. Document M2-A5. Villanova, Pa: NCCLS, 1993. Bell SM, Gatus BJ, Pham JN, et al. CDS users group newsletter No. 6. Sydney: The Prince of Wales Hospital, 1993. Bell SM. Additions and modifications to the range of antibiotics tested by the CDS method of antibiotic sensitivity testing. Pathology 1988; 20: 303-304. National Committee for Clinical Laboratory Standards. Methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically. 3rd ed. Approved standard. Document M7-A3. Villanova, Pa: NCCLS, 1993. Jorgensen JH, Ferraro MJ, McElmeel ML, et al. Detection of penicillin and extended spectrum cephalosporin resistance among Streptococcus pneumoniae clinical isolates by use of the Etest. J Clin Microbiol 1994; 32: 159-163. AB Biodisk . Etest Technical Guide 5B. Solna, Sweden: AB Biodisk , 1995. National Committee for Clinical Laboratory Standards. Performance standards for antimicrobial susceptibility testing. 5th informational supplement. Document M100-S5. Villanova, Pa: NCCLS, 1994. True Epistat [computer program]. Version 5.0. Richardson, TX: Epistat Services, 1994. Collignon P, Bell J, Hufton I, Mitchell D. Meningitis caused by a penicillin- and chloramphenicol-resistant Streptococcus pneumoniae . Med J Aust 1988; 149: 497-498. Friedland I, McCracken G. Management of infections caused by antibiotic-resistant Streptococcus pneumoniae . N Engl J Med 1994; 331: 377-382. Tomasz A. The pneumococcus at the gates. N Engl J Med 1995; 333: 514-515. Barnett E, Klein J. The problem of resistant bacteria for the management of acute otitis media. Pediatr Clin North Am 1995; 42: 509-517. Nelson C, Mason E, Kaplan S. Activity of oral antibiotics in middle ear and sinus infections caused by penicillin-resistant Streptococcus pneumoniae : implications for treatment. Pediatr Infect Dis J 1994; 13: 585-589. (Accepted 30 Nov 1995) Authors' details Infectious Diseases Unit, Woden Valley Hospital, Canberra, ACT. Peter J Collignon, FRACP, FRCPA, Head of Unit, Microbiologist and Infectious Diseases Physician. Department of Microbiology and Infectious Diseases, Monash Medical Centre, Melbourne, VIC. Jan M Bell, BSc(Hons), BA, Scientist. * Australian Group on Antimicrobial Resistance (AGAR). For this study AGAR consisted of the microbiology laboratories at: ACT: Woden Valley Hospital (Peter Collignon, Linda Halliday). NSW: Concord Hospital (Joan Yap, Tom Gottlieb, Glenn Funnell); Illawarra Regional Hospital (Keith Wise, Rodney Jones); Liverpool Hospital (Denise Daley, Rosemary Munro); Prince of Wales Hospital (Jeanette Pham, Barrie Gatus, Sydney Bell); Royal North Shore Hospital (Clarence Fernandes); Royal Prince Alfred Hospital (Richard Benn, Barbara Yan, Alison Vickery). QLD: Mater Misericordiae Hospital, Brisbane (Martyn Tilse, Janet Montgomery); Princess Alexandra Hospital (Graeme Nimmo, Jacqueline Schooneveldt); Royal Brisbane Hospital (Narelle George, Joan Faoagali); Sullivan, Nicolaides and Partners (Jenny Robson, Sylvia van der Valk); Toowoomba Base Hospital (David Farrell). SA: Flinders Medical Centre (Hendrik Pruul); Institute of Medical and Veterinary Science (Irene Lim, Richard Lumb); Queen Elizabeth Hospital (Peter Lawson, David Grove). TAS: Diagnostic Pathology (which includes Hobart Pathology and Launceston Pathology) (Barbara Henderson, Danny McColl, Gary Fenton); Launceston General Hospital (Erika Cox, Veronica Lyons); Royal Hobart Hospital (Keith Ott, Rob Peterson). VIC: Alfred Hospital (John Spicer, J Clare Franklin); Dorevitch Pathology (Liz Snashall); Heidelberg Repatriation Hospital (Barrie Mayall, Angie Chan, Vicki Moritz); Melbourne Pathology (Christine Hargreaves); Monash Medical Centre (Dianne Olden, Jan Bell, John Turnidge); Royal Children's Hospital and Microbiological Diagnostic Unit (Geoff Hogg, Marion Easton, Janet Strachan). WA: Fremantle Hospital (David McGechie, Neil Stingemore, Graham Francis); Royal Perth Hospital (Keryn Christiansen, Claire Khinsoe, Geoff Coombs). Reprints: Dr P J Collignon, Infectious Diseases Unit, Woden Valley Hospital, PO Box 11, Woden, ACT 2606. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Peter J Collignon · Jan M Bell · the AGAR

Editorial Hydatid disease: medical problems, veterinary solutions, political obstacles Prevention of human hydatidosis requires new strategies, political support and collaboration between government departments It is to be hoped that in the near future Australia will cease to have the unenviable reputation of being the home of perhaps the most important parasitic disease common to man and domesticated animals, which carries with it the added stigma that it is preventable.1 Seventy years later, the hopes of Sir Ian Clunies Ross, the first chairman of the Commonwealth Scientific and Industrial Research Organisation (CSIRO), have not been fulfilled; the problem is still with us. Australians have been very good at treating human hydatidosis but very poor at preventing it. Notorious under-reporting of cases of hydatid disease has made it easier for authorities to remain inactive to the need for control. In this issue of the Journal, Jenkins and Power (page 18) have effectively documented the failure of the New South Wales (NSW) and Australian Capital Territory (ACT) health care systems to take the problem seriously. Their survey of medical records from hospitals and health care services identified 195 new cases of hydatidosis (172 in NSW, and 23 in the ACT) during the six-year period 1987-1992. This compares with official notifications of 37 and three cases, respectively, during the (partially overlapping) five-year period 1990-1994.2 New cases presented predominantly in the north-eastern and south-eastern Tablelands and in metropolitan areas. Whereas the latter could have included some patients from rural areas, 60% of the urban cases were migrants who had most probably contracted hydatidosis outside Australia. Their presentation to city practitioners may present diagnostic difficulties if medical awareness of hydatidosis is less acute than in endemic rural areas. Would complete notification of all cases (assuming that it could be achieved) alleviate the problem? Apart from causing transient embarrassment, I believe it would have little impact. Certainly, accurate incidence figures are essential for assessing any pattern of change in a disease, but there are other major obstacles interfering with successful hydatid control in mainland Australia. In Tasmania, a concerted campaign involving collaboration between government and community organisations over several decades eliminated transmission of hydatid disease to humans,3 but in the larger mainland areas problems stem from the disease failing to conform to a pattern to which health care systems are designed to respond. Firstly, hydatidosis occurs in a limited number of regions, and centrally directed health programs operate on a state-wide basis (with a strong urban bias). Secondly, hydatidosis, although a human disease, requires veterinary, agricultural and educational expertise for effective prevention. Thirdly, the treatment of hydatidosis is exclusively surgical (and undertaken at a high standard in Australia) but its prevention is not ( in a way, surgery is as relevant to hydatid control as panel beating is to the prevention of road accidents. Fourthly, because successful prevention requires diverse skills, hydatidosis is not accepted as the responsibility of any one bureaucracy. Health, agriculture, education and conservation all have a role, but collaboration across such a range of portfolios to solve a regional problem is apparently unthinkable. And finally, the coup de grace ( there are no votes in hydatids. The largest and longest operating control campaign on the mainland (under the auspices of which the research of Jenkins and Power was undertaken) succumbed after a decade in which it received no State funding whatsoever: the Government eliminated the campaign and left the parasite! To what extent would complete prevention of human hydatidosis be attainable if political support and collaboration between government departments were coupled with the enthusiasm of many in rural communities who have attempted the task in the past? Ongoing investigations of hydatidosis epidemiology in Australia indicate that the textbook description of the life cycle of Echinococcus granulosus is no longer comprehensive.4 Surveys of parasite prevalence in regions with a high incidence of human hydatidosis consistently reveal a high prevalence of infection in wild dogs (including dingoes) as definitive hosts, and in macropods (kangaroos and wallabies) and feral pigs as intermediate hosts.5 In the light of these findings, the practice of baiting pigs in national parks, and thus providing an appetising source of echinococcal infection for wild dogs, may require re-examination. Contrary to earlier beliefs, foxes have been found to carry the parasite,6 and they frequent urban locations such as barbecue areas where their habit of demarcating territories by depositing faeces may introduce a significant human hazard.7 Dogs living in Perth suburbs but used for recreational pig hunting have been found to carry the parasite.8 It is not clear whether these new patterns of hydatidosis represent changes in the parasite, in its ecosystem, or in both. The extent to which human activity has contributed to the changes is also unclear. Increasingly, there are indications that the concept of separate wildlife and domestic animal strains of the parasite is breaking down and that a single strain, albeit manifesting host-determined phenotype variation, may have the capacity to infect both types of host in each of the traditional wildlife and domestic cycles. The domestic and wildlife strains of E. granulosus do not appear to be genetically distinguishable.9 Consequently, the wildlife cycle is likely to be of considerable human health importance. A case of hydatidosis in a child from the Southern Tablelands was the first documented instance of human disease produced by the wildlife strain.10 When a serious decision to combat hydatidosis is taken, it is clear that new strategies will be required. Peter J McCullagh Senior Fellow, Division of Clinical Sciences John Curtin School of Medical Research Australian National University, Canberra, ACT 1. Clunies Ross I. A survey of the incidence of Echinococcus granulosus (Batsch) or hydatid disease in New South Wales. Aust Vet J 1926; 2: 56-67. 2. Longbottom H, Hargreaves J. Human hydatid surveillance in Australia. Commun Dis Intell 1995; 19: 448-451. 3. Goldsmid JM, Pickmere J. Hydatid eradication in Tasmania. Point of no return. Aust Fam Physician 1987; 16: 1672-1674. 4. Constantine GC, Thompson RCA, Jenkins DJ, et al. Morphological characterization of adult Echinococcus granulosus as a means of determining transmission patterns. J Parasitol 1993; 79: 55-61. 5. Schartz PM, Chai J, Craig PS, et al. Epidemiology and control of hydatid disease. In: Thompson RCA, Lymbery AJ, editors. The biology of Echinococcus and hydatid disease. Wallingford, UK: CAB International, 1995: 233-302. 6. Obebdorf DL, Matheson MJ, Thompson RCA. Echinococcus granulosus infection of foxes in south-eastern New South Wales. Aust Vet J 1989; 66: 123-124. 7. Jenkins DJ, Craig NA. The role of foxes, Vulpes vulpes, in the epidemiology of Echinococcus granulosus in urban environments. Med J Aust 1992; 157: 754-756. 8. Thompson RCA, Lymbery AJ, Hobbs RP, Elliot AD. Hydatid disease in urban areas of Western Australia: an unusual cycle involving western grey kangaroos (Macropus fuliginosus), feral pigs and domestic dogs. Aust Vet J 1988; 65: 188-190. 9. Lymbery AJ, Thompson RCA, Hobbs RP. Genetic diversity and genetic differentiation in Echinococcus granulosus (Batsch, 1786) from domestic and sylvatic hosts on the mainland of Australia. Parasitology 1990; 101: 283-289. 10. Thompson RCA, Nott DB, Squire J, Rennell D. Evidence that the Australian sylvatic strain of Echinococcus granulosus is infective to humans [letter]. Med J Aust 1987; 146: 396-397.

Peter J McCullagh

Human hydatidosis in New South Wales and the Australian Capital Territory, 1987-1992 David J Jenkins and Karen Power Abstract - Authors' details - Introduction - Methods - Results - Discussion - Acknowledgement - References - Box 1 - Box 2 - Figure 1 - Figure 2 - Figure 3 - ©MJA1996 - For editorial comment, see McCullagh Objective: To determine the prevalence of human hydatidosis in New South Wales and the Australian Capital Territory. Methods: Data on human hydatid infection occurring between 1987 and 1992 were collected retrospectively from 25 hospitals and 13 health services in New South Wales and four hospitals in the Australian Capital Territory. Mean annual prevalences of human hydatidosis were determined for shires in eastern New South Wales and data on infection in immigrants and Australian-born patients were compared. Results: 321 patients were diagnosed with hydatid disease, 1987-1992; 195 were new cases and 117 readmissions (nine cases were not identified as new or recurrent). Most patients lived in the eastern half of New South Wales (which includes the Australian Capital Territory), half in rural areas and half in the major coastal cities. Most Australian-born rural patients lived in 39 shires in the north-eastern and south-eastern Tablelands. Sixty per cent of the patients in major cities were born overseas. Conclusions: Hydatid infection occurs more commonly in south-eastern Australia than the official figures suggest. In rural areas of the north-eastern and south-eastern Tablelands hydatid infection is of public health importance. The national notification system must be improved and control campaigns alerting the public to the dangers of hydatid infection promoted. (MJA 1996; 164: 18-21) Introduction The tapeworm genus Echinococcus is an important zoonosis which is endemic in many parts of the world. The only species occurring in Australia is Echinococcus granulosus. It was probably introduced with infected domestic livestock during European settlement and is now widespread in domestic livestock and wildlife, with wildlife acting as an important reservoir.1 Dogs (domestic and wild) and foxes are the definitive hosts (Figure 1). Humans become infected by the ingestion of eggs passed in faeces of dogs. Oncospheres released from the eggs penetrate the intestinal mucosa and, via the portal system, lodge in the liver, lungs, muscle or other organs, where the hydatid cysts form. Because of inadequate reporting, the prevalence of human hydatid infection in Australia is unknown. From the earliest published studies human hydatidosis in New South Wales has occurred mainly in people living in rural areas in the eastern half of the State associated with the Great Dividing Range.2-4 Dew, in 1928, reported a relatively even distribution of patients with hydatidosis in eastern New South Wales, but subsequent reports showed an increasing trend for patients to be concentrated in the north-eastern and south-eastern Tablelands.3-5 To assess the health risk associated with E. granulosus, a retrospective survey of hydatid infection was conducted between 1987 and 1992 by examining records of patients with hydatidosis from hospitals and health services in New South Wales (NSW) and the Australian Capital Territory (ACT). Methods All the public and private hospitals and area and district health services in NSW and the ACT were asked to supply data of patients with confirmed hydatidosis who were admitted between January 1987 and December 1992. After approval of our written request, all institutions ( four hospitals in the ACT and 25 hospitals and 13 health services in NSW ( supplied data comprising: - Sex; - Date of admission; - Date and country of birth; - Place of residence at admission; - Cyst location; and - Whether the infection was new or recurrent. We maintained patient confidentiality by using initials only for individual identification. Multiple admissions for the same patient were identified from admission dates, initials, age, sex and general location of residence at the time of admission. We calculated mean annual prevalences of infection using 1991 Census data.6 Results Three hundred and twenty-one patients with confirmed hydatidosis were treated between 1987 and 1992. These comprised 195 new cases (107 males and 88 females), 117 recurrent cases (27 cases had their first treatment before this survey began) and nine cases not identified as new or recurrent. Two hundred and eighty-two patients (172 new cases and 110 recurrent cases [including those not classified as new or recurrent]) were treated in NSW and 39 patients (23 new cases and 16 recurrent and unclassified cases) were treated in the ACT (16 and 14, respectively, of those treated in the ACT lived in NSW). Rural patients Except in three cases, hydatid infection in rural patients, most of whom were Australia-born, occurred in the eastern half of NSW at higher altitudes, mainly associated with the Great Dividing Range (Figure 2). There were concentrations of patients in the north-eastern and south-eastern Tablelands, and these two areas were connected by a corridor parallel to the coast where further cases occurred. The mean annual prevalence of human hydatidosis in rural NSW was 2.6 cases per 100 000 rural population. Cases occurred in 15 shires [counties] in the north-east and 24 shires in the south-east. On a shire-to-shire basis, the mean annual prevalence of infection ranged from 0.3 to 17.7 and 0.5 to 23.5 (cases per 100 000 population), respectively, in these two areas (Box 1). Four of the cases (three new and one recurrent) were in Aboriginal people. These four cases represented a mean annual prevalence of hydatid infection of 1.1 cases per 100 000 in the Aboriginal population of NSW. Urban patients There were 152 cases diagnosed from the three major metropolitan centres of NSW (Sydney, Newcastle and Wollongong), which included 98 new cases, mostly in patients born overseas (60%); in rural areas the reverse was evident (85% of rural patients were born in Australia). Of the patients born overseas, all were living in NSW, except one ACT resident. The mean annual prevalence of infection was calculated for 25 ethnic groups (each with a population of over 1000) resident in NSW (Box 2). The highest mean annual prevalence occurred in the Iranian population (6.6 cases/100 000) and the lowest in the German population (0.5 cases/100 000). Most cases came from the Greek and Lebanese communities and communities of people from the former Yugoslavia (13, 10 and 8, respectively), but because of their relatively large populations in NSW, these cases represented only a mean annual prevalence of 4.8, 3.2 and 2.2, respectively. Age distribution Age-group distribution profiles of the patients born in Australia and those born overseas are compared in Figure 3. All age groups are represented among Australian-born patients with hydatidosis, especially the older age groups, whereas the immigrant population, being generally younger, has fewer cases in the older age groups. Cyst location Infection in the liver occurred most commonly (157 of the 195 new cases); 13 cases involved infection in the lungs and four had infection in both liver and lungs. Infection in other less common sites were two each in the spleen, pancreas and leg muscle and one each in the diaphragm, pelvic area, arm muscle, brain, adrenal gland and gallbladder. Discussion Retrospective survey data on human hydatidosis cannot give an accurate picture of the prevalence of infection. A number of cases are not seen in hospitals because the infection is asymptomatic, or does not require surgical intervention, and mistakes in coding may occur. However, these data remain a useful indication of infection prevalence. Our study confirmed the concentration of hydatidosis in the north-eastern and south-eastern Tablelands reported previously.3-5 The narrow corridor parallel to the coast in the central part of the State is an area where there have been few cases reported previously, but where considerable urban development has occurred over the last decade, and previously undiagnosed patients may have moved to this region. Population movement from country areas to cities may also account for many of the Australian-born patients diagnosed in urban areas. However, it is also possible for urban residents to be exposed to eggs of E. granulosus. Recent studies have identified infection with E. granulosus in dogs of a recreational pig hunter living in suburban Perth,7 and in dogs of Perth residents living in uncleared areas on the outskirts of the city.8 Foxes infected with E. granulosus have been found in the suburbs of Canberra.9 The older age of the Australian-born compared with the immigrant patients largely reflects the different age-group structures of the two groups. In 1990, 88.3% of immigrants were aged less than 45 years when they arrived in Australia and 27.4% were less than 14 years of age.10 Migrants may be already infected when they arrive as children, but the long latent period of hydatid disease means it is first detected in adulthood. It is difficult to explain why most Australian-born patients were detected in the age group 31 to 40 years whereas most immigrants were not detected until 41 to 50 years. Infections in immigrants may be caused by a different strain type of E. granulosus with a slower cystic growth rate. Alternatively, there may be a reluctance among newer immigrants to consult local doctors. The migrants infected with hydatid disease origin(Box 2)ated in countries where E. granulosus is endemic. The order of ranking of countries according to the mean annual prevalence of hydatid infection in their migrant populations in NSW closely reflected the relative importance of human hydatidosis in their countries of origin. The range of prevalences in the migrant populations were no higher than those recorded in shire populations in north-eastern and south-eastern NSW. In at least three of these shires the prevalence of human hydatidosis was two to three times higher than the highest level recorded in a migrant population. Three of the urban patients and one of the rural patients born in Australia were Aboriginals. The three urban Aboriginal patients are likely to be from a rural background, but as their place of birth was unknown it was not possible to calculate a prevalence of hydatid infection for rural Aboriginal people. The mean annual prevalence of 1.1 cases per 100 000 for the total Aboriginal population of NSW is about a third of the prevalence in the rural non-Aboriginal population. Few cases of hydatid disease in Aboriginal people have been reported. All the reports are from studies in Western Australia during the 1970s, where Aboriginals were always highly represented: 15/57 cases11 and 13/31 cases.12 Our data represent the first report of hydatid infection in Aboriginal people in NSW; a previous study reported E. granulosus infection in a dog from a NSW Aboriginal community.13 The reason for human hydatidosis not being perceived as a problem in Australia can be attributed largely to under-reporting of this notifiable disease;5 this has been a problem for many years,,5,12,14,15 with no signs of improvement. Only 17 of the 321 new and recurrent cases identified in this study had been notified, and in a retrospective study in Victoria for the 12 months up to July 199116 only two of the 50 new or recurrent cases had been notified. Disease recurrence after operative treatment is an important aspect of human hydatid infection. A carefully conducted follow-up study of 39 patients treated surgically in Australia first drew attention to this problem;17 22% had had recurrent infection by 30 months, mainly caused by cyst rupture before surgery. In our study, 37.5% of patients (for whom information on new or recurrent infection status was supplied) were treated for recurrent infection. Effective chemotherapy of patients with hydatid infection would substantially reduce the cost of treatment. This topic has been reviewed,18 and the most promising drug studied was albendazole. Data from studies on 253 patients indicated that albendazole was an effective cure in 28%, 51% showed improvement, 18% were unchanged and in 2% the cysts continued to grow.19 The most appropriate use of albendazole may be as an adjunct to surgery. Rupture of cysts and spilling of protoscoleces (which can form new cysts) into the body cavity during surgery is a constant risk, but an immediate postoperative course of albendazole will greatly reduce the chance of new cysts developing.20 Hydatid disease is preventable, and education is one of the most effective tools to achieve this. It is important that State and Federal governments take a responsible attitude towards increasing community awareness, and implement control strategies through education, either by themselves or by funding organisations such as the Australian Hydatid Control and Epidemiology Program. Control of this parasite in Australia requires a long term commitment; the alternative is that hydatid disease will continue to incapacitate individuals and be an additional financial drain on an already overstretched health service. Acknowledgements The authors gratefully acknowledge the assistance of the staff of the medical records departments of the following hospitals: Albury, Armidale and New England, Bathurst, Broken Hill, Calvary (ACT), Camperdown, Casino and District, Cooma, Dubbo, Goulburn, Grafton, Grenfell, Griffith, Inverell, John James Memorial (ACT), Lismore, Orange, Parkes District, Prince Henry, Prince of Wales Children's, Queanbeyan, Royal Canberra (ACT, now closed), Royal North Shore, Royal Prince Alfred, St Vincent's, St Vincent's Private, Tamworth, Wagga Wagga, Westmead and Woden Valley (ACT); also the following area and district health services: Brunswick-Byron, Central Coast, Cooma, Hunter, Illawarra, Macleay Valley, Manning Valley, Queanbeyan, South Western Sydney, Southern Sydney and Tumut, Wentworth. We also thank Ms Celia Moss (Australian Bureau of Statistics) and Ms Irene Pasaris (ACT Health Department) for their help and advice and Dr M W Lightowlers, Dr E Bennet, Dr P McCullagh and Professor R C A Thompson for their suggestions in the preparation of the manuscript. This study was funded partly through contributions from the Shire Councils of Bega Valley, Boorowa, Cooma-Monaro, Crookwell, Gunning, Harden, Snowy River, Tumbarumba, Yarrowlumla, Yass and Young, Queanbeyan City Council and the ACT Health Authority. Dr Jenkins' salary was funded by the National Health and Medical Research Council of Australia. (©MJA 1996; 164: 14-17) References Schantz PM, Chai J, Craig PS, et al. Epidemiology and control of hydatid disease. In: Thompson RCA and Lymbery AJ, editors. The biology of Echinococcus and hydatid disease. Wallingford, UK: C A B International, 1995: 233-302. Dew HR. Hydatid disease. Its pathology, diagnosis and treatment. Sydney: The Australasian Medical Publishing Company Ltd, 1928. Christopher PJ, Lopez WA. Hydatid disease notifications in New South Wales. Med J Aust 1970; 1: 54-56. Little JM. Hydatid disease at Royal Prince Alfred Hospital, 1964 to 1974. Med J Aust 1976; 1: 903-908. Schreuder S. Survey of hospital admissions for hydatidosis in New South Wales and the Australian Capital Territory, 1982-1987. Aust Vet J 1990; 67: 149-151. Australian Bureau of Statistics. 1991 Census of population and housing. State comparisons. Canberra: ABS, 1993. (Catalogue No. 2731.0.) Thompson RCA, Lymbery AJ, Hobbs RP, Elliot AD. Hydatid disease in urban areas of Western Australia: an unusual cycle involving western grey kangaroos (Macropus fuliginosus), feral pigs and domestic dogs. Aust Vet J 1988; 65: 188-190. Thompson RCA, Robertson ID, Gasser RB, Constantine CC. Hydatid disease in Western Australia: a novel approach to education and surveillance. Parasitol Today 1993; 9: 431-433. Jenkins DJ, Craig NA. The role of foxes Vulpes vulpes in the epidemiology of Echinococcus granulosus in urban environments. Med J Aust 1992; 157: 754-756. Australian Bureau of Statistics. Migration, Australia. Canberra: ABS, 1994. (Catalogue No. 3412.0.) Joske RA. The changing pattern of hydatid disease, with special reference to hydatid of the liver. Med J Aust 1974; 1: 129-132. Stein GR, McCully DJ. Hydatid disease in Western Australia (1957-1967). Med J Aust 1970; 1: 848-850. Jenkins DJ, Andrew PL. Intestinal parasites in dogs from an Aboriginal community in New South Wales. Aust Vet J 1993; 70: 115-116. Davies P, Nicholas WL, Beard TC. Hospital records of hydatid disease in Victoria for 1970 to 1974. Med J Aust 1977; 2: 493-495. Beard TC. Hydatids in Australia ( the present position in man. Aust Vet J 1979; 55: 131-135. Taylor K. Hydatids in 1992: public health lessons. Update. A quarterly bulletin of infectious diseases. Victoria: Department of Health and Community Services, 1993; 2: 63-64. Little JM, Hollands MJ, Ekberg H. Recurrence of hydatid disease. World J Surg 1988; 12: 700-704. Morris DL, Richards KS. Hydatid disease current medical and surgical management. Oxford: Butterworth-Heinemann Ltd, 1992: 94-118. Horton RJ. Chemotherapy of Echinococcus infection in man with albendazole. Trans R Soc Trop Med Hyg 1989; 83: 97-102. Morris DL, Taylor DH. Optimal timing of postoperative albendazole prophylaxis in E. granulosus. Ann Trop Med Parasitol 1988; 82: 65-66. (Received 11 Apr, accepted 27 Sep 1995) Authors' details Australian Hydatid Control and Epidemiology Program, Canberra, ACT. David J Jenkins, MSc, PhD, Research Officer. Karen Power, BApplSci, Field Officer.

David J Jenkins · Karen Power