Public Health and Communicable Diseases - SA Health - SA.Gov.au

Edition 4 /2006 South AustraliaPublic Health and Communicable DiseasesEditorial - Agent-Host-EnvironmentDr Scott CameronSenior LecturerMaster of Applied Epidemiology and Population Health (NCEPH)Australian National University Associate ProfessorDiscipline of Public HealthThe University of AdelaidePublic Health surveillance forCommunicable Diseases in SouthAustraliaEmerging communicablediseases: Pandemic and AvianInfluenzaVector-borne diseases in Australia269The limited resourcing of some public health units and the enticing ease ofdata management and analysis using computers sees some public healthinvestigations conducted exclusively by telephone, using someone else’squestionnaire followed by staring at a screen expecting an answer to appear.Communicable disease-related investigations constitute a high proportion ofthe acute epidemiology conducted in public health units. In general they areretrospective investigations into events that have put a host into effectivecontact with an agent of disease. That is they had a shared environment.They represent natural experiments where cases are linked by virtue of theirbeing infected with apparently similar, or the same agents. The cases have theanswers to the puzzle of their infection and it is the task of the investigators totry and find the correct questions to ask of them.Half of the papers in this edition of the Bulletin address issues where suchmethods will fail to yield information that would underpin effective publichealth actions. These issues involve the need to understand in depth, thesocial and cultural make-up of particular groups, their understanding of illness,their health-seeking behaviour, their concepts of disease and the impact ofstigma. Furthermore, exploration of their attitudes to intervention, preventionand therapy are vital to the development of rational policy.The recognition that such broad-based investigations are necessary is notnew. Aspects of the environment in its broadest sense have been included inconsiderations of the incidence and distribution of disease for millennia.Hippocrates for instance ascribed racial and local climate factors asdeterminants of disease. Some places were seen to be inherently badfor health and others had been made so by humans themselves. He alsopointed to the inequities inherent in social status determined by law andpolitical regimes. These grew naturally from the adoption of agriculture andsocial gradients which were generally regarded as unchangeable. There werepeasants on which all others depended, then artisans perhaps, and the upperclasses associated with religion and ruling.Infections, kidney andcardiovascular disease inAboriginal communitiesHepatitis C virus infection inprisonsReflections on John Snow’sPump Handle: Is there a need foran infection control program inSouth Australian prisons?Immunisation – a new era forvaccinesVaccine safety and CommunityAttitudes in SAChlamydia - closing the stabledoorSexually transmitted infectionsin Central Australia – time forconcerted actionThe Impact of Health CareAssociated InfectionCOMMUNICABLE DISEASECONTROL BRANCHInfection Control ServiceCommunicable Disease ControlBranch ReportNotifiable Diseases in SouthAustralia1216212325303234374044

In the early 1800s Chadwick identified the appallingliving conditions of industrial England as causes of illhealth in workers, resulting in their inability to perform inthe workplace as well as they otherwise might. At thistime the miasma theory of disease was predominantand environment was ascribed the status of agent.With Koch’s discoveries from the mid-1870s, cameconcerted attention upon the diad of biological agentand host with less emphasis on the environment. Thusbegan an era where the emphasis of public health was(rightly) communicable disease. These are illnessesdue to specific infectious agents or their toxic productstransmitted from another infected host or from ananimate or inanimate reservoir.The recognition that an understanding of diseasedynamics could be usefully described by the triadhost-agent-environment arose in the 1920s withthe development of social and holistic medicine. Italso came to be the basis of training by AlexanderLangmuir and the Epidemic Intelligence Service and theconcept of ‘shoe leather epidemiology’ was promoted.Importantly, this required investigators to go into thefield to interview cases, their families, industry andother informants such as local health workers andgovernment officials.However, it was always necessary to view theenvironment as a multi-level construct ranging fromcellular interactions, to person to person interactions andto the influences at community and country level. Therehas been an evolving process of developing theory thateffectively integrates these multiple levels of factors thatcan all be viewed as causes of disease 1 .Classical epidemiology is being integrated with socialor cultural investigations as this theory evolves. This isimportant for several reasons. Firstly it reinforces theneed to fully understand the nature of a problem beforedesigning a solution and we see an increasing emphasison introducing ethnographic techniques into traditionalcommunicable disease investigations 2 . Secondly thisinvolves a mix of research methods – quantitative andqualitative to reach that understanding with betteranalytic methods to handle the data from mixed methodresearch becoming available. Finally, just as illness anddisease can be better understood with this paradigm, sotoo can appropriate means of intervention be devised.Clearly, the overwhelming message is that appropriateresources must be invested for adequate fieldinvestigations to secure reliable research findings whichcan be translated into feasible policy.References1. Kreiger N. Theories for social epidemiology in the 21 stcentury: an ecosocial perspective. Int. J Epidemiol.2001;30:668-677.2. Weiss MG. Cultural epidemiology: an introduction andoverview. Anthropology and Medicine 2001;8(1):5-29.Public Healthsurveillance forCommunicable Diseasesin South AustraliaIntroductionCameron MoffattEpidemiology Registrar,Communicable Disease Control BranchDepartment of HealthMaster of Applied Epidemiology ProgrammeAustralian National UniversityCommunicable disease control remains a high priorityfor population health. In Australia, many of the controlsfor communicable diseases already exist outside of thehealth system. These include things such as education,clean water, secure food sources, systems for disposalof refuse and sewage and adherence to regulationssuch as building codes. Disease surveillance helps toidentify cases when breakdowns in these systems mayhave occurred, however the pathogens responsible forthese diseases are frequently evolving, readily exploitingopportunities for change and transmission. In particularviruses transmitted in the air or by respiratory secretionshighlight the need for systems capable of detecting andmonitoring the presence of such pathogens.This paper examines public health surveillance with aparticular focus on notifiable conditions, using wherepossible relevant South Australian examples. Includedis an examination of effective public health surveillanceand its core aims; the main types of surveillancesystems used for monitoring communicable diseases;discussion of the importance of notifiable conditions;specific reporting systems and surveillance; the analysisand dissemination of surveillance data; and concludingremarks.What is public health surveillance?Public health surveillance is the systematic and on-goingassessment of the health of a community, including thetimely collection, analysis, interpretation, disseminationand subsequent use of that data. 1An effective public health surveillance system collectsrelevant data on a problem of public health importance,allowing users of the system to classify and interpretthat data to enable appropriate interventions to beapplied. All surveillance systems need to include thiscapacity for data collection and analysis as well astimely distribution of that data to those responsible forimplementing prevention and control measures.

Emphasis on particular goals of public healthsurveillance may vary between different levels of publichealth responsibility. Some goals are achieved mosteffectively by a regional public health unit while othermore strategic aims are best managed by state-baseddisease surveillance units or the CommonwealthDepartment of Health and Ageing. In South Australia,data generated through communicable diseasesurveillance is most typically used as a prompt foroutbreak investigation, monitoring of disease trends andfor initiating disease control initiatives. This does notpreclude the use of such data for other means includingepidemiological research and programme development.Table 1 lists the goals seen in effective public healthsurveillance.Table 1: Goals of effective public health surveillanceGoals of Surveillance• To detect cases or clusters of cases thereby enablinginterventions to be implemented that preventtransmission or reduce morbidity and mortality.• To assess the public health impact of a health eventor determinant and measure trends.• To demonstrate the need for public healthintervention programmes and resources.• To monitor the effectiveness of disease preventionand control measures and intervention strategies.• To identify high-risk populations or geographic areasto target interventions and guide analytical studies.• To develop hypotheses leading to analyticstudies about disease causation, transmission ordevelopment.Types of surveillance systemsPublic health surveillance systems have traditionallybeen classified as being passive, active or sentinel,and all three types are utilised in the surveillance ofcommunicable diseases in SA. 2Passive surveillancePassive disease surveillance usually refers tomonitoring of data supplied to health authorities bydoctors and laboratories as a requirement under law.Communicable disease surveillance is heavily reliant onpassive surveillance, using both clinical and laboratorynotifications, however these systems are likely tounderestimate the true burden of illness as many peoplewith notifiable conditions may only have mild illnessand do not seek care, while others may be incorrectlydiagnosed or may not receive laboratory testing toconfirm a diagnosis. For example Campylobactergastroenteritis, with over 15,000 notifications nationally,is the most common notifiable cause of foodbornedisease in Australia, with SA having the highest statenotification rate (173 per 100,000). 2 Yet estimates ofits true prevalence in Australia are thought to exceed200,000 cases per year. 3 Nevertheless the patternsseen over time are informative and provide the basis forpublic health action.Active surveillanceTo preclude issues with under reporting, particularlyfor more serious conditions, more vigorous means ofdetection may be used. In SA additional laboratorytesting of all bloody stools for the presence of Shigatoxigenic Escherichia coli is undertaken, 4 as cases wouldnot be detected via routine microbiological examinationor a specific clinical diagnosis. This supplementarysurveillance was implemented in response to a largeoutbreak of Haemolytic Uraemic Syndrome (HUS)caused by fermented sausage contaminated with E.Coli. 5 This type of surveillance is particularly useful inestablishing prevalence rates for conditions where theremay be a lack of data or where cases occur sporadically.Another illustration of active surveillance is theprocess of case ascertainment during an outbreakinvestigation. If a hospital intensive care doctornotified two cases of HUS a likely response would beto contact other intensive care unit and renal units toactively find more cases. Active systems can validatethe representativeness of passive systems, enablemore complete reporting of conditions or be used inconjunction with or part of specific epidemiological oroutbreak investigations.Sentinel surveillance systemsSentinel surveillance systems are established for thepurpose of enabling simple, early detection of disease.Animals are often used to provide this early warning. InAustralia, the Sentinel Chicken Surveillance Programmewas established to detect increases in flavivirus activity. 6The programme involves regular testing of a numberof chicken flocks across Australia for seroconversion toMurray Valley encephalitis virus and Kunjin virus in orderto determine levels of risk to human populations fromthese viruses.Sentinel healthcare providers are another example, withclinicians collecting data on selected indicators to assistin estimating the size of a problem among the generalpopulation. The Australian Sentinel Practice Research andEvaluation Network is one such example, with GeneralPractitioners (GP) collecting data on presentations forinfluenza-like illness (ILI). Such presentations couldpossibly represent an early expression of increasedinfluenza activity. In SA this data is combined withlaboratory reporting of influenza and ILI presentationsto emergency departments, to provide evidence of theimpact of seasonal influenza activity (Figure 1 next page).

The collection of notifiable disease data is facilitatedby the use of a standard notification form. Theseforms seek common core data that includes patientidentification, age, sex, Indigenous status, residentiallocation, date of onset and details of the reportingdoctor. Clinical judgment on the cause of disease,identification of risk factors and the occurrence of othercases are important elements in surveillance, whilelaboratory notification often enables links between casesto be established that could not be achieved by medicalnotification alone. For certain invasive and vaccinepreventable conditions such as Haemophilus influenzaeinfection, meningococcal disease, pneumococcaldisease and Q Fever, more detailed data collection isroutinely performed on each case’s clinical presentation,such as their risk factors and vaccination status.Analysis and dissemination of surveillance dataAnalysis of surveillance data focuses on differencesbetween observed and expected rates of disease orcounts of cases. CuSUM (Cumulative Sum) analysis 8is the main statistical technique used to examineNDDMS surveillance data. These calculations take intoaccount current and previous observations to identifywhen the rate of a notifiable condition exceeds anestablished baseline. CuSUMs are also calculated at thelocal government area (LGA) level allowing geographicand spatial analysis of disease clustering (Figure 3).Where indicated data are orientated by person, placeor time using epidemic curves to plot rates of diseasenotifications over time, while line listings and geospatialmapping provide visual displays of disease clustering.The timely dissemination of data to those who need toknow is crucial to effective surveillance. In SA weeklyupdates of surveillance information are posted onlinevia the CDCB Public Health webpage http://www.dh.sa.gov.au/pehs/notifiable-diseases-summary/currentepi-features.htmIncluded are the current week’sepidemiological features, information on influenza andother respiratory illnesses, notification summaries, yearto date totals for notifiable conditions and a summary ofall outbreaks investigated in SA. Along with the otherstates and territories, SA then contributes a core set ofnotifiable disease data to the Commonwealth for thepurposes of national disease surveillance.ConclusionInformation derived from public health surveillanceguides public health practice. The passive reportingof notifiable conditions through the NDDMS willcontinue to provide the basis for communicable diseasemonitoring and intervention in SA. While this approachcan be considered as meeting current needs, thechanging epidemiology of communicable diseases isleading to a renaissance in surveillance techniques. Inorder to ensure sustainable, comprehensive and timelycollection of high quality public health data increasingrigour is being applied to surveillance practices throughimproved statistical analysis, more frequent evaluationand the use of web-based systems for data collectionand dissemination. The key challenge will be forgovernment to recognise that surveillance practicesneed to be every bit as dynamic as the pathogens theyseek to detect and prevent.Figure 3: Map of RRV cases by source of infection July 2005 - May 2006

References1. Teutsch SM. Considerations in Planning a SurveillanceSystem. In: Teutsch SM, editor. Principles andPractice of Public Health Surveillance. New York:Oxford University Press; 1994.2. Miller M, et al. Australia’s notifiable disease status,2003 Annual report of the National NotifiableDiseases Surveillance System. CommunicableDisease Intelligence. 2005;29(1):1-61.3. Hall G and Kirk M. Foodborne illness in Australia.National Centre for Epidemiology and PopulationHealth. Canberra: OzFoodNet Working Group; 2005.4. Combs BG, Raupach JCA, Kirk M. Surveillanceof Shiga toxigenic Escherichia coli in Australia.Communicable Disease Intelligence. 2005;29(4):366-369.5. Cameron AS, et al. Community Outbreak of HemolyticUremic Syndrome Attributable to Escherichia coliO111:NM - South Australia, 1995. Morbidity andMortality Weekly Report. 1995;44(29): 550-558.6. Department of Health and Ageing (DOHA).Surveillance systems reported in CDI, 2006.Communicable Disease Intelligence. 2006;30(1):156-160.7. Dicker RC. A brief review of the basic principles ofepidemiology. In: Gregg M, editor. Field Epidemiology.London: Oxford University Press; 2002.8. Hutwager LC, et al. Using Laboratory-BasedSurveillance Data for Prevention: An Algorithm forDetecting Salmonella Outbreaks. Emerging InfectiousDiseases. 1997;3(3):395-400.Emerging communicablediseases: Pandemic andAvian InfluenzaDr Ann KoehlerBSc, MBBS, FRCPA, MPHConsultant MicrobiologistCommunicable Disease Control BranchDepartment of HealthA pandemic (from Greek pan all + demos people) isan epidemic (an outbreak of an infectious disease) thatspreads across a large region or worldwide.There are three types of influenza virus, A, B, and C.Influenza A causes much of the seasonal influenzaoutbreaks that occur annually, as well as less frequentpandemics. Influenza B and C are ‘human’ viruses thatare not found in avian hosts, though C viruses havebeen isolated from pigs and dogs. Neither types B norC cause pandemics and both typically cause milderrespiratory illness than influenza A.Influenza A is a zoonotic infection in humans. Its naturalhosts are wild aquatic birds, principally ducks, gulls,and waders, in whom it causes asymptomatic infectionof the gastrointestinal tract 1 . All of the subtypes ofinfluenza A (16 different neuraminidase types [N] and9 different haemagglutinin types [H]) can be isolatedfrom these birds. (Neuraminidase and haemagglutininare molecules on the surface of the virus involvedin attachment and release from host cells, and areimportant inducers of antibody response 2 .) They caninfect a wide range of birds and mammals, includingaquatic mammals such as whales. When a subtypechanges and is able to infect humans readily it maybecome established as a human influenza strain.The origins of recently circulating strains of influenzaA in humans can be traced back to pandemics of the20 th century – H1N1 from the 1918-19 ‘Spanish’ flupandemic, H2N2 from the 1957-58 Asian flu, and H3N2from the 1968-69 Hong Kong flu pandemic. Of the threeinfluenza pandemics last century, the 1918 pandemicwas the worst human disease outbreak ever recorded,causing acute illness in 30% of the world’s population,and killing up to 40 million people, more than thosekilled by the “Black Death”. The first recorded pandemicoccurred in 1580, though no doubt they occurred beforethis, and 31 have been documented since, most recentlyin 1968-69 3 . It is inevitable that another one will occur,and by historical measures it is overdue.Influenza pandemics occur when the influenza virusmutates to produce a virulent strain for humans to whichthe existing population has not been exposed. Influenza

viruses are RNA viruses, and like all RNA viruses lack‘proofreading’ when they are replicating, making themgenetically unstable and variable. While each roundof RNA virus replication results in a mixed populationwith many variants, most of which are not viable, somehave potentially advantageous mutations that canbecome dominant under the right selective conditions.Reassortment of the viral genome occurs rapidly amonginfluenza viruses in nature, and is important in theappearance of pandemics in human populations.To date just over 100 people have died worldwidefrom the current H5N1 ‘bird flu’ infections which havegeographically encompassed countries housing morethan half the world’s population. Concern remainsin the medical and scientific community that H5N1may develop into the next pandemic influenza strain.Although most attention is focussed on the H5N1 virus,it is entirely possible that the next pandemic might becaused by a different influenza virus.Current human influenza viruses are believed to havearisen by genetic reassortment between previoushuman influenza viruses and nonhuman viruses, whenthere has been simultaneous infection of a host animalwith both avian and human influenza viruses. Thoughthere is no scientific proof to support it, the pig hasbeen the leading contender for the role of ‘mixingvessel’. The pig is the only mammalian species whichis domesticated, reared in abundance, and a commonhost for human influenza viruses, though mixing mayoccur in humans who are co-infected with two strains 4 .One remarkable exception to this mode of selectionof new strains was the 1918 pandemic strain, whichwas revealed by molecular sequencing in 2005 to beof purely avian origin 5 . The 1918 strain jumped species,from birds to humans, and there is concern that theH5N1 strain might do the same, or might recombinewith a human strain, either way producing a newpandemic strain. In recent years, purely avian influenzaviruses of subtypes H5, H7 and H9 have crossed thespecies barrier to directly cause disease, sometimesfatal, in humans in many Asian countries, as well asTurkey, Holland and Canada 6 .The majority of pandemic strains of human influenzafrom the 20 th century appear to have originated in China,with its large population of humans, pigs, and domesticand wild ducks. In temperate countries, influenza in pigsand humans tends to occur in winter, when free-flyingaquatic birds are absent. In tropical and subtropicalcountries such as Southern China, influenza occurs yearround in humans, pigs, and birds. There is interminglingof these species, and the opportunity for interspeciestransmission and genetic exchange among influenzaviruses 4 .Even though pandemic strains emerge only rarely,available information indicates that interspeciestransmission of influenza viruses may not be so rare,for up to 10% of persons with occupational exposureto pigs develop antibodies to swine influenza virus 7 .It remains unclear what viral and human geneticcharacteristics allow the transmission of avian influenzaviruses to humans. So far the H5N1 strain isolates fromhumans have not acquired gene segments from humaninfluenza virus strains.(Source: http://europa.eu.int/comm/health/ph_threats/com/Influenza/influenza_en.htm)

H5N1 is not yet readily transmissible from humanto human. The body temperature of birds is higherthan that of humans, at around 40 o C, and it has beensuggested that H5N1 has not yet adapted to the humanbody temperature, particularly in the upper airways.New research has also shown that H5N1 virus bindsto receptors which are present in the lungs rather thanin the upper airways 8 . Viral proliferation and sheddingthus occurs predominantly in the lower respiratorytract, reducing infectivity of droplets generated from theoropharynx during coughing and sneezing.Human disease associated with the H5N1 ‘bird flu’outbreak has been unusually severe, for reasons whichare not fully understood, though probably involveoverproduction of proinflammatory cytokines andevasion of their antiviral effects 9 . Reported mortalityrates have exceeded 50% which is much higher thanthat observed in seasonal influenza. Although human tohuman transmission has not been documented so far,it is interesting that many cases have occurred amongblood relatives. There have been no cases reportedamong persons involved in culling infected poultry,who could be expected to be at high risk of infection.This suggests that there may be a genetic element tosusceptibility, although this remains speculative.Will H5N1 cause the next pandemic? Never before hasthe emergence of an influenza pandemic been metwith such a high level of surveillance and preparedness.Close cooperation between the World Organisationfor Animal Health (OIE), and WHO, the human WorldHealth Organisation, has resulted in rapid responses tooutbreaks of avian influenza in both animals and humansworldwide. By “stamping out” infections in poultry, theopportunity for the virus to infect and mutate in humanshas been much reduced. Authorities believe it may bepossible to contain H5N1 through global cooperation.So far this has been helped by the low infectivity of thevirus to humans, and the fact that it has not adapted foreasy transmissibility between humans. If this changesor response teams become overwhelmed, then the nextpandemic may occur very soon.Should a pandemic occur, it will be met by anunprecedented public health response. The World HealthOrganisation, and governments in Australia and overseasare working on plans for containment and quarantine,administration of anti-virals and vaccines, maintenanceof essential services, and provision of acute medicalcare for up to one third of the population. Since the lastpandemic, we have developed technology allowing rapidtyping and surveillance of influenza viruses, vaccinesagainst influenza viruses, anti-viral drugs, better infectioncontrol knowledge and equipment, and sophisticatedcommunications to enable spread of information aroundthe world within minutes. However we also haverapid international transport, a much larger population,and communities whose structures have altereddramatically since the last pandemic, all of which willmake transmission of a pandemic virus easier. The rapidglobal spread of SARS illustrated the impact of a newviral respiratory illness that can be easily transmittedfrom human to human in the era of jet travel. The worldwatches with fear, awe, and hope that a killer pandemicwill not occur again.References1. Hinshaw VS, Webster RG. The natural history ofinfluenza A viruses. In: Beare AS, editor. 79-104. Basicand applied influenza research. Boca Raton, Fla., CRCPress, Inc.1982.2. Gerhard W, Mozdanowska K, Zharikova D. Prospectsfor universal influenza virus vaccine. Emerg Infect Dis.2006;12(4):569-74.3. Treanor JJ. Influenza virus. 2060-85. In: Mandell,Douglas, and Bennett’s principles and practice ofinfectious diseases. 6 th ed. Mandell GL, Bennett JE,Dolin R, editors. Philadelphia, Pen; Elsevier ChurchillLivingstone; 2005.4. Webster RG, Bean WJ, Gorman OT, et al. Evolutionand ecology of influenza A viruses. Microbiol Rev.1992;56(1):152-79.5. Tumpey TM, Basler CF, Aguilar PV, et al.Characterization of the reconstructed 1918 Spanishinfluenza pandemic virus. Science. 2005;310:77-80.6. Guan Y, Poon LLM. Cheung CY, et al. H5N1 influenza:a protean pandemic threat. PNAS. 2004;101(21):8156-61.7. Schnurrenberger, PR, Woods GT, Martin RJ. Serologicevidence of human infection with swine influenzavirus. Am Rev Respir Dis. 1970;102:356-361.8. Shinya K, Ebina M, Yamada S, et al. Avian flu:influenza virus receptors in the human airway. Nature.2006;440(7083):435-6.9. Seo SH, Hoffman E, Webster RG. Lethal H5N1influenza viruses escape host anti-viral cytokineresponses. Nat Med. 2002;8(9):950-4.

Vector-borne diseases inAustraliaVector-borne diseases in AustraliaDr Peng Bi*, MBBS PhDSenior Lecturer in EpidemiologyDepartment of Public HealthThe University of AdelaideDr Ying Zhang MBBS, MMedSciDepartment of Public HealthThe University of AdelaideVector-borne diseases notified to the National NotifiableDiseases Surveillance System (NNDSS) includemosquito-borne diseases caused by alphaviruses(Barmah Forest virus and Ross River virus) andflaviviruses (Dengue Fever/Dengue Shock Syndrome,Murray Valley encephalitis, Kunjin and Japaneseencephalitis), and malaria 1 . In the last decade, morethan 61,000 cases of vector-borne diseases have beennotified to the NNDSS, which accounts for 6.3% ofthe total notifications 2 . The commonest vector-bornediseases in Australia are Ross River virus infection andBarmah Forest virus infection, which represent more than80% of all notified vector-borne diseases. The proportionof notified vector-borne diseases has decreased in thepast ten years, from 16% of total notifications in 1996to 4% in 2005. However a significant factor in thistrend has been the introduction of a number of nonvector-borne notifiable diseases over the last ten years.Geographically, more than 85% of notified cases ofvector-borne diseases came from Queensland, NewSouth Wales and Western Australia. Ross River virusinfection is the most notified vector-borne disease inalmost all States and Territories except ACT. Rates ofnotified vector-borne diseases have fluctuated over thelast ten years; with considerable year to year variation.Ross River virus infection (RRV) and Barmah Forestvirus infection (BFV)RRV is the most common mosquito-borne disease inAustralia. There have been more than 41,000 casesnotified to NNDSS during the last decade with themost serious situation occurring in 1996 (Figure 1).The vertebrate reservoir hosts of RRV could includemarsupials, placental mammals and birds, for examplekangaroos, horses and rats. 3 There are over 40 speciesof mosquito vectors, with Aedes vigilax, Aedescamptorhynchus (saltmarsh along coastline) and Culexannulirostris (inland) being the most important. 3 In termsof seasonal distribution, peak incidence of the diseaseis through the summer and autumn months, when themosquito vectors are most abundant. Studies suggestthat climate variability is related to the transmission ofRRV. 4,5 BFV has been notified to NNDSS since 1995. Itis noticed that the number of BFV notifications in 2005increased 1.5 times compared with that in 1996 (Figure1). In NSW, the notified number of BFV cases increasedmore than 2 times compared with ten years ago, andan outbreak was observed in SA in 2005 and 2006.The increase in notified cases of BFV may also reflectincreased awareness among the general communityand GPs of the disease as well as changes in testingprocedures. Barmah Forest virus and Ross River virusdemonstrate many similarities. They have similar diseasesymptoms and seasonal distribution. Most affectedpeople by BFV and RRV are middle aged and thereseems to be no gender difference.Dengue and other notified Flavivirus infectionsDengue is the most common arboviral infection inthe world, with four distinct virus serotypes. 6 Aedesaegypti, the major vector, has adapted well to urbanenvironmental conditions such as poor housing,overcrowding and inadequate sanitation. 7 Globally, itis suggested that climate change could increase the

number of people living in areas of higher denguerisk, from 1.5 billion in 1990 to about 50-60% of globalpopulation in 2085 8 . In Australia, most notified cases ofdengue are from north Queensland, where the vectormosquito Aedes aegypti is endemic. The two mostserious epidemics noted in Queensland during the lastdecade were in 1998 and 2003 respectively (Figure 1),with more than 1,100 cases notified. To date, denguehas not caused outbreaks in southern parts of Australia.However, a recent study suggested that there might bea dengue threat for southern parts of Australia in thefuture. 9Other Flavivirus infections include Japanese encephalitis,Murray Valley encephalitis (MVE) and Kunjin (KUN) virusinfection with less than 100 notified cases annually inAustralia (Figure 1). For MVE and KUN viruses, the majorvector is Culex annulirostris, which breeds in freshwater.Most cases in this category are notified in northernAustralia. There has been only one case of MVE notifiedin South Australia during the last five years. Attentionshould be given to Japanese encephalitis in Australiain order to keep it under control. 10 This is particularlyimportant in north Queensland. Health professionalsneed to keep alert for the potential transmissionof Japanese encephalitis, including correct clinicaldiagnosis, health information sharing and exchange, andhealth education and promotion.MalariaAustralia has claimed to be malaria free since 1983.Since then all notified cases of malaria are believed to beimported and the notified cases have remained relativelystable during the last ten years, with around 700 casesper year (Figure 1). While there is currently no evidencefor local transmission of malaria within Australia, thereis potential for this to occur in view of the presence ofthe main mosquito vector Anopheles farauti. Studiesindicate that increases in the incidence of malaria arestrongly associated with higher temperatures andincreased rainfall. In Australia, the length and intensity ofwet seasons have a significant effect on the distributionof Anopheles farauti. 11 Climate modelling shows thatglobal warming will enlarge the potential range of thisvector, which could extend, by 2030, to a location 800km south of its present limit in Queensland. 12 Therefore,Australian health professionals should remain alert forthis potential risk.Situation in South AustraliaIn South Australia, RRV is the most important vectorbornedisease. There have been more than 1,600 RRVcases notified in the last ten years with the highestnumber occurring in the year 1997 (635 notified cases).There were four epidemics in the period 1992-2003,with the majority of cases acquired from regions alongthe River Murray. There was some evidence of spreadof the disease to regions in which activity of RRV hadnot been previously recognised, such as the Mid-Northand the South-East 13 . In terms of disease distributionamongst the population, it was found that the highestrates occurred in the 30–49 year age range. There wasno significant difference in disease rates between malesand females 13 . BFV is another important concern inSouth Australia, with a sharp increase in cases in 2005and 2006, and notifications ten times higher comparedto a decade ago. Factors contributing to this increaseinclude climatic variation and also increased awarenessamong the general community and GPs of the disease,as well as changes in testing procedures. Healthprofessionals including GPs should pay great attentionto RRV and BFV especially in the areas where the caseshave not identified before. Dengue and other notifiedFlavivirus infections, eg Murray Valley encephalitis, arenot a big threat in South Australia at the moment.Implications for public health practiceMosquito control may be the most effective way toprevent and control the spread of vector-borne diseases.Mosquito surveillance programs have been performed insome States and proved to be effective in identifying thedistribution of mosquito species, presence and activityof the arboviruses. 14,15 A national strategy to enhancethe routine mosquito monitoring and surveillance,which involves the collaboration with local council, Stategovernments and research organisations, could prove tobe most effective in controling and prevent in the spreadof the vector-borne diseases.In addition to maintaining high quality surveillance, anearly warning system should also be set up for bothmosquitos and arbovirus diseases. Time series analysisand spatial analysis 16,17 techniques could be performedto build a predictive model to highlight potential riskareas, using local vector data, meteorological data andother influencing factors eg population dynamics, landuse, vegetable types, reservoir information and socioeconomicindex. These predictive models could assistrisk assessment for policy makers and public healthpractitioners.In South Australia, fortunately, there are somerecent developments in mosquito management.The Environmental Health Service coordinated theimplementation of the SA Integrated MosquitoManagement Strategy (SAIMMS). “This process wasinitiated due to the need to promote and integratemosquito management practices throughout SA toensure that programs are as effective, economical andenvironmentally sensitive as possible”. 18 There are 15agencies in SA involved in this working group, includingthe Local Government Association, EPA, PIRSA and the10

AIEH. 18 Additionally, some work to set up predictivemodels for high-risk areas of mosquitos in SA isunderway.Personal protection measures, eg long sleeves andpants, mosquito repellents and mosquito coils arealso essential and effective to avoid mosquito bites.Education programs directed to communities at risk arean essential part of an effective public health strategy.These programs could include social marketing ofkey messages via the local media, eg radio, televisionprograms and newspapers, as well as creating healthpromoting environments in local communities, schools,and health services, to increase awareness andunderstanding about the effectiveness of personalprotection measures in the prevention of mosquitobornediseases.Another critically important issue is the potential risksfrom future environment change, eg increased tidesand temperature that could promote vector abundance,and then impact on the transmission of vector-bornediseases. It is very important for State governmentagencies, local councils and communities, researchorganisations and health professionals to have relevantadaptive measurements, including early warningsystem, routine vector management, pubic educationand awareness, research input, and collaboration acrossgovernment departments and organisations.References1. Australia’s notifiable diseases status: Annual report ofthe National Notifiable Diseases Surveillance System.[Accessed Feb 2006]. Available from: http://www.health.gov.au/internet/wcms/publishing.nsf/Content/cda-pubs-annlrpt-nndssar.htm.2. Calculation based on NNDSS data and the annualreports. [Accessed Feb 2006]. Available from: http://www.health.gov.au/internet/wcms/publishing.nsf/Content/Nationally+notifiable+diseases+%28NNDSS%29-1.3. Harley D, Sleigh A, Ritchie S. Ross River virustransmission, infection and disease: a crossdisciplinaryreview. Clinical Microbiology Review.2001;14(4): 909-932.4. Tong SL, Hu WB, McMichael AJ. Climate variabilityand Ross River virus transmission in Townsvilleregion, Australia, 1985-1996. Trop. Med. Int. Health.2004;9:298-304.6. World Health Organisation (WHO). Dengueprevention and control. [Accessed Feb 2006]. In.Available from: http://who.int/7. Kindhauser MK. Global defence against the infectiousdisease threat. Geneva: WHO; 2003.8. Hales S, de Wet N, Maindonald J, Woodward A.Potential effect of population and climate changeson global distribution of dengue fever: an empiricalmodel. Lancet. 2002;360:830-834.9. Russell RC, Williams CR, Sutherst RW, RitchieSA. Aedes (Stegomyia) albopictus--a denguethreat for southern Australia? Commun Dis Intell.2005;29(3):296-8.10. Solomon T, Ni H, Beasley DW, Ekkelenkamp M,Cardosa MJ, Barrett AD. Origin and evolution ofJapanese encephalitis in southeast Asia. J Virol.2003;77:3091–3098.11. Walker J. Malaria in a changing world an Australianperspective. International Journal for Parasitology.1998;28:947-53.12. Bryan J, Foley D, Sutherst R. Malaria transmissionand climate change in Australia. MJA. 1996;164:345-7.13. Horwood CM, Bi P. The incidence of Ross River virusdisease in South Australia, 1992 to 2003. CommunDis Intell. 2005;29(3):291-6.14. Environmental Health Services. Annual report ofHealth Department of Western Australia. [AccessedFeb 2006]. Available from: http://www.health.wa.gov.au/publications/annual_reports.cfm15. The New South Wales Arbovirus Surveillance &Mosquito Monitoring Program. [Accessed Feb 2006].Available from: http://medent.usyd.edu.au/projects/arbovirus%20surveillance.htm #achieve16. Gatton ML, Kelly-Hope LA, Kay BH, Ryan PA.Spatial-temporal analysis of Ross River virus diseasepatterns in Queensland, Australia. Am. J. Trop. Med.Hyg. 2004;71(5):629-635.17. Woodruff RE, Guest CS, Garner MG, Becker N, et al.Predicting Ross River virus epidemics from regionalweather data. Epidemiology. 2002 Jul;13(4):384-93.18. Personal communication with Renay Cooke,Environmental Health Service, Government of SouthAustralia.5. Woodruff, R, Guest, C, Garner, G, Becker, N, Lindsay,MF. Weather and climate as early warning systemindicators for epidemics of Ross River virus: a casesstudy in south-west western Australia. Epidemiology.2003;14: S94-S97.11

Infections, kidneyand cardiovasculardisease in AboriginalcommunitiesStephen McDonaldSenior Staff Specialist, Nephrology & TransplantationServicesExecutive Officer, Australia & New Zealand Dialysis andTransplant (ANZDATA) RegistryThe Queen Elizabeth HospitalThe parlous state of health among Aboriginal peoplein Australia has been extensively documented overthe past 20 years. Among the areas with the largestdifferentials in health status are those relating to kidneydisease, cardiovascular disease and infections. In thisarticle the published literature on rates of kidney diseaseand cardiovascular disease and infectious diseasesamong Aboriginal people will be briefly reviewed, andthen links between these conditions explored.Kidney diseaseHigher rates of all stages of kidney disease have beenshown among Australian Aboriginal people for sometime. Broadly speaking, rates of kidney disease areascertained in two ways. There are well-validatedmarkers of mild kidney disease. The earliest stages arereflected in abnormal levels of albumin (albuminuria)or protein in the urine (proteinturia), with more severestages reflected in abnormalities in serum creatinineor calculated glomerular filtration rate (GFR). Theprevalence of albuminuria has been studied in severalremote Aboriginal communities. Age-specific prevalencerates of over 50% have been described for some remoteNorthern Territory communities, with commensurateincreases in rates of reduced GFR. 1, 2 The pattern issimilar to other remote communities 3, 4 including onestudied in South Australia. 5 In these communities, as inother environments, these early markers strongly predictthe risk of later more serious disease. 6The most severe stage of kidney disease is end stagekidney disease (ESKD). This is the stage where formsof dialysis and kidney transplantation are required tomaintain life. In Australia, patients receiving thesetreatments are recorded in the Australia & New ZealandDialysis and Transplant (ANZDATA) Registry. Theincidence rate of Aboriginal people commencing dialysiseach year is substantially higher than non-Aboriginalpeople 7 . In addition there is an interaction with age,with the relative risk for ESKD for Aboriginal comparedto non-Aboriginal people substantially higher among the35-55 year age groups (Figure 1). As a methodologicalFigure 1. Age-specific incidence ratios for Aboriginal vsnon-Aboriginal ESKD in Australia, 1996-2001 (ANZDATARegistry).aside, this prevents calculation of a valid directly agestandardisedincidence ratio, as comparisons will varydepending on the structure of the reference population.Acute InfectionsAcute infectious illnesses are described at much higherrates among Aboriginal people. The actual relative riskvaries according to the type of infection studied andthe way the data is collected. The Australian Instituteof Health & Welfare report a two-fold increase in ratesof admission to hospital with infectious and parasiticdiseases. 8 These are nation-wide figures, and farhigher rates have been reported for remote and moredisadvantaged communities. For example, the pointprevalence of bacterial skin infections has been reportedto range from 10 to 70%. 9-12 Both upper and lower 8respiratory tract infections are also extremely common.Circulatory diseaseRates of circulatory (or cardiovascular) disease areextremely high among Aboriginal people, and this groupof diseases is a major contributor to the prematuremortality among Aboriginal people. 13 Age-specificrates of cardiovascular mortality are up to 10 times thenational average. 14 This situation is similar to that seenamong other indigenous groups. 15 The relative increasein hospital admission rates for circulatory disease amongAboriginal people is less marked that that of mortality,with rates 1.5-2 times that of non-indigenous peopleshown both in regional data 16 and national reports. 8 Thegreater relative risk for mortality than hospital admissionsuggests a number of possibilities, including greatercase-fatality rates, admission of sicker patients, ordifferences in practice patterns.12

Community-based reports of the prevalence ofcardiovascular disease (as opposed to risk factors)are more problematic. Earlier studies using restingECG-based criteria showed 10-20% of people in somecommunities had ECG changes of ischaemia. 17-19 Otherdata comes from a survey using exercise ECG testing, 20or surveys of case notes, 21 but these are difficult tointerpret in the absence of non-indigenous controls.When risk factors for circulatory disease (smoking,diabetes, obesity, hyperlipidaemia) are considered,there have been a large number of surveys with variabledegrees of increase in risk factors (for examples see 22-27).Are these problems related?This coexistence of high rates of infections, kidneydisease and circulatory disease raise questions abouthow they might be related. Links between thesediseases might occur through a number of possiblemechanisms.Strong links have been shown between kidneydisease and cardiovascular disease among nonindigenousgroups, and all stages of kidney diseasehave been shown to predict cardiovascular morbidityand mortality. 28-30 Although many community-basedstudies have examined risk factors for cardiovasculardisease among Australian Aboriginal people, few haveexamined the coexistence of cardiovascular and renaldisease. In one well-described cohort, the presence ofalbuminuria predicted cardiovascular mortality 31-32 ; inanother albuminuria and reduced GFR were associatedwith increased carotid intima-media thickness 2 . Othercross sectional studies of remote 4, 22, 23 and non-remote24,33Aboriginal communities have included assessmentsof risk factors, but not necessarily cardiovascular or renaldisease outcomes.There are some direct pathological links betweeninfections and kidney disease (and also infections andcardiac disease in rheumatic heart disease). The bestdescribed link between infection and kidney disease isthat of post-infectious glomerulonephritis (PIGN, alsoknown as post-streptococcal glomerulonephritis). Thisglomerulonephritis is triggered by an immunologicalreaction to infection, and one of the most important andmost common causes is Streptococcal skin infections.Epidemics of this disease have been described inNorthern Australia. 10-12 However, PIGN is responsibleonly for a very small number of the cases of ESKD inAustralia. 34 The situation underlying the increased ratesof kidney disease among Aboriginal people is likely tobe more complex than an increase in a single disease.Traditional dogma teaches that kidney function recoversfully after PIGN, however, there is evidence that PIGNamong Aboriginal people is not a benign process,and does predict later development of albuminuria /proteinuria. 35 A more likely theory is that a series ofinsults throughout life, beginning with smaller kidneyassociated with lower birthweight and progressingthrough higher rates of PIGN and thence diabetes andhypertension, explains the increased rate of kidneydisease among Aboriginal people. 36The list of risk factors for kidney disease andcardiovascular disease is very similar. Diabetes andhypertension are major risk factors for both diseases,and diabetes especially is prevalent at extremely highrates among some Aboriginal communities. Othershared risk factors extend beyond the traditional model.The presence of infection/inflammation is anotherobvious link. Very modest increases in C-reactive protein(a marker of inflammation) have been shown to be a riskfactor for cardiovascular disease in the non-Aboriginalpopulation 37 . Among Aboriginal people, greater increasesin CRP (consistent with those seen as a responseto bacterial infection) are well-described 38-40 and areassociated with the presence of albuminuria 38 andincreased carotid intima-media thickness. 41 It is likelythat these increases of CRP reflect shared associationswith bacterial infections rather than a direct causativerole of chronic bacterial role in atherosclerosis or kidneydisease. This is not to suggest repeated bacterial skin orlung infections cause cardiovascular or kidney diseasedirectly, but that they all share causal factors. Themost apparent of these are the living conditions, withovercrowding and other markers of poverty extremelycommon among Aboriginal people, particularly thoseliving in remote communities. Consistent with this isthe observation that rates of ESKD among AustralianAboriginal are particularly increased among those livingin remote areas. 42Increased rates of ESKD incidence in Australia havealso been associated inversely with markers of socioeconomicstatus among non-Aboriginal people. 43 Allthese observations are consistent with the paradigmexpounded by Marmot, where the influence of socioeconomicfactors is likely to be reflected in a numberof mediators, including increased household crowding,lower birth weight, higher rates of cigarette smoking andobesity. This relationship has been remarkably robustbetween different countries and cultures. 44ConclusionsLinks between renal and cardiovascular disease existat a number of levels among Australian Aboriginalpeople. In addition to the usual list of “traditional”cardiovascular risk factors, increased CRP over a rangeof CRP concentrations considerably greater than thatdescribed in non-indigenous settings is common, and isassociated with both renal and cardiovascular disease.These increased CRP concentrations are likely to reflectthe generalised burden of infection and thereby poor13

living conditions and health status among AboriginalAustralians. The approach to kidney and cardiovasculardisease prevention among Aboriginal people needs to bebroad-based, and extend beyond traditional risk-factorsto include consideration of infections both as a directpathologic cause, and more importantly of repeatedexposure to bacterial infection as a marker of a high-riskenvironment. A logical outcome of this is a broadeningof risk-factor modification approaches at both anindividual and community level.Finally, this area is an example of the value of diseaseregistries. Although ESKD is a relatively rare disease, thedocumentation and subsequent efforts to address thehigh rates of kidney disease among Aboriginal peoplebegan with the reporting of high rates of ESKD, and theepidemiology of ESKD has been an important basis forthe investigation in this area.Further readingThe themes in this brief review are further developed in36, 42, 45-47several manuscripts.References1. Hoy WE, Norman RJ, Hayhurst BG, et al. A healthprofile of adults in a Northern Territory Aboriginalcommunity, with an emphasis on preventablemorbidities. Aust N Z J Public Health. 1997;21:121-126.2. McDonald SP, Maguire GP, Hoy WE. Renal functionand cardiovascular risk markers in a remote AustralianAboriginal community. Nephrol Dial Transplant.2003;18:1555-1561.3. Eiser D. Microalbuminuria and cardiovascular riskfactors in Central Australian Aboriginal Communities.In: Department of Medicine, Melbourne, Universityof Melbourne;1995, 73.4. Rowley KG, Iser DM, Best JD, et al. Albuminuriain Australian Aboriginal people: prevalence andassociations with components of the metabolicsyndrome. Diabetologia. 2000;43:1397-1403.5. Shephard M, James J, Allen G, et al. A preventativemodel for Aboriginal kidney disease. In: Departmentof Renal Medicine (vol 1999), Flinders MedicalCentre, Adelaide; 1999.6. Hoy W, Wang Z, van Buynder P, et al. The naturalhistory of renal disease in Australian Aborigines.Part 2. Albuminuria predicts natural death and renalfailure. Kidney Int. 2001;60:249-256.7. McDonald SP, Russ GR. Current incidence, treatmentpatterns and outcome of end-stage renal diseaseamong indigenous groups in Australia and NewZealand. Nephrology. 2003;8:42-48.148. Trewin D, Madden R. The Health and Welfare ofAustralia’s Aboriginal and Torres Strait IslanderPeoples. ABS Catalogue number 4704.0. In:Australian Bureau of Statistics, Canberra; 2005.9. Carapetis JR, Connors C, Yarmirr D, et al. Success ofa scabies control program in an Australian aboriginalcommunity. Pediatr Infect Dis J. 1997;16:494-499.10. Nimmo GR, Tinniswood RD, Nuttall N, et al. Group Astreptococcal infection in an Aboriginal community.Med J Aust. 1992;157:521-522.11. Streeton CL, Hanna JN, Messer RD, et al.An epidemic of acute post-streptococcalglomerulonephritis among aboriginal children. JPaediatr Child Health. 1995;31:245-248.12. Van Buynder PG, Gaggin JA, Martin D, et al.Streptococcal infection and renal disease markersin Australian aboriginal children. Med J Aust.1992;156:537-540.13. Cunningham J, Condon JR. Premature mortality inAboriginal adults in the Northern Territory, 1979-1991.Med J Aust. 1996;165:309-312.14. Dempsey K, Condon J. Mortality in the NorthernTerritory 1979-1997. 1 ed. Darwin, Territory HealthServices; 1999.15. Durie MH. The health of indigenous peoples. BMJ.2003;326:510-511.16. Plant A, Condon J, Durling G. Northern Territoryhealth outcomes: morbidity and mortality 1979-1991.Darwin, NT Department of Health and CommunityServices; 1995.17. Bastian P. Coronary heart disease in tribal Aborigines :the West Kimberley survey. Aust N Z J Med.1979;9:284-292.18. Edwards FM, Wise PH, Thomas DW, et al. Bloodpressures and electrocardiographic findings inthe South Australian Aborigines. Aust N Z J Med.1976;6:197-205.19. Simons L, Whish P, Marr B, et al. Coronary riskfactors in a rural community which includesAborigines: Inverell Heart Disease PreventionProgramme. Aust N Z J Med. 1981;11:386-390.20. Markey P. The prevalence of ischaemic and rheumaticheart disease and risk factors in Aboriginal and non-Aboriginal footballers. In: Department of CommunityMedicine, Adelaide, University of Adelaide; 1996, 117.21. Sladden T. Cardiovascular disease risk factors inadults of an Aboriginal community. In: MenziesSchool of Health Research, Darwin, University ofSydney; 1990, 135.22. Smith RM, Spargo RM, Hunter EM, et al. Prevalenceof hypertension in Kimberley Aborigines and itsrelationship to ischaemic heart disease. An agestratifiedrandom survey. Med J Aust. 1992;156:557-562.

23. Gracey M, Spargo RM, Smith P, et al. Risk factorsfor ill-health in a remote desert-dwelling Aboriginalcommunity in Western Australia. Aust N Z J Med.1996;26:171-179.24. Guest CS, O’ Dea K, Larkins RG. Blood pressure,lipids and other risk factors for cardiovascular diseasein Aborigines and persons of European descentof southeastern Australia. Aust J Public Health.1994;18:79-86.25. Braun B, Zimmermann MB, Kretchmer N, et al.: Riskfactors for diabetes and cardiovascular disease inyoung Australian Aborigines. A 5-year follow-up study.Diabetes Care. 1996;19:472-479.26. Gault A, O’Dea K, Rowley KG, et al. Abnormalglucose tolerance and other coronary heart diseaserisk factors in an isolated Aboriginal community incentral Australia. Diabetes Care. 1996;19:1269-1273.27. Hoy WE, Mathews JD, McCredie DA, et al. Themultidimensional nature of renal disease: rates andassociations of albuminuria in an Australian Aboriginalcommunity. Kidney Int. 1998;54:1296-1304.28. Go AS, Chertow GM, Fan D, et al. Chronic KidneyDisease and the Risks of Death, CardiovascularEvents, and Hospitalization. N Engl J Med.2004;351:1296-1305.29. Hillege HL, Janssen WM, Bak AA, et al.Microalbuminuria is common, also in a nondiabetic,nonhypertensive population, and an independentindicator of cardiovascular risk factors andcardiovascular morbidity. J Intern Med. 2001;249:519-526.30. Janssen WM, Hillege H, Pinto-Sietsma SJ, et al. Lowlevels of urinary albumin excretion are associatedwith cardiovascular risk factors in the generalpopulation. Clin Chem Lab Med. 2000;38:1107-1110.31. Hoy W, Wang Z, van Buynder P, et al. The naturalhistory of renal disease: Part 1. Changes inalbuminuria and glomerular filtration rate over time ina community-based cohort of Australian Aborigineswith high rates of renal disease. Kidney Int.2001;60:243-248.32. Wang Z, Hoy WE. Albuminuria and incident coronaryheart disease in Australian Aboriginal people. KidneyInternational. 2005;68:1289-1293.33. Shaw JT, McWhinney B, Tate JR, et al. Plasmahomocysteine levels in indigenous Australians. Med JAust. 1999;170:19-22.34. McDonald SP, Excel L. ANZDATA Registry Report2005. Adelaide, Australia and New Zealand Dialysisand Transplant Registry; 2005.35. White AV, Hoy WE, McCredie D. Childhood poststreptococcalglomerulonephritis as a risk factorfor chronic renal disease in later life. Med J Aust.2001;174:492-496.1536. Hoy W, Vanbuynder P, Mathews JD, et al. Renaldisease and the environment: lessons fromAboriginal Australia. Nephrology. 2001;6:19-24.37. Ridker PM, Cushman M, Stampfer MJ, et al.Inflammation, aspirin, and the risk of cardiovasculardisease in apparently healthy men. N Engl J Med.1997;336:973-979.38. McDonald SP, Maguire GP, Duarte NL, et al. Creactive protein, cardiovascular risk, and renal diseasein a remote Australian Aboriginal community. Clin SciLondon. 2003;106:121-128.39. Rowley K, Walker KZ, Cohen J, et al. Inflammationand vascular endothelial activation in an Aboriginalpopulation: relationships to coronary diseaserisk factors and nutritional markers. Med J Aust.2003;178:495-500.40. Wang Z, Hoy WE. Population distribution of highsensitivity C-reactive protein values in AboriginalAustralians: A comparison with other populations.Clin Biochem. 2006;39:277-281.41. McDonald SP, Maguire GP, Duarte NL, et al. Carotidintima-media thickness, cardiovascular risk factorsand albuminuria in a remote Australian Aboriginalcommunity. Atherosclerosis. 2004;177:423-431.42. Cass A, Cunningham J, Snelling P, et al. End-stagerenal disease in indigenous Australians: a disease ofdisadvantage. Ethn Dis. 2002;12:373-378.43. Cass A, Cunningham J, Wang Z, et al. Socialdisadvantage and variation in the incidence of endstagerenal disease in Australian capital cities. Aust NZ J Public Health. 2001;25:322-326.44. Marmot M. Epidemiology of socioeconomic statusand health: are determinants within countries thesame as between countries? Ann N Y Acad Sci.1999;896:16-29.45. McDonald SP, Hoy W. Interfaces betweencardiovascular and renal disease among AboriginalAustralians. Adv Chronic Kid Dis. In Press; 2005.46. Hoy W, McDonald S, Cass A, et al. A broader view ofrenal disease: Findings in Aboriginal Australia. RecentAdv Microbiol. 2002; chapter 5: 75-96.47. Cass A, Cunningham J, Snelling P, et al. Exploring thepathways leading from disadvantage to end-stagerenal disease for indigenous Australians. Soc SciMed. 2004;58:767-785.

Hepatitis C virusinfection in prisonsCorresponding author:Ms Emma R Miller (MPH)Discipline of Public HealthSchool of Population Health and Clinical PracticeUniversity of AdelaideDr Peng Bi (MBBS, PhD)Discipline of Public HealthSchool of Population Health and Clinical PracticeUniversity of AdelaideAssociate Professor Philip Ryan (MBBS, FAFPHM)Discipline of Public HealthSchool of Population Health and Clinical PracticeUniversity of AdelaideHepatitis C virus (HCV) infection is one of the mostcommonly notified communicable diseases in Australia.Nationally, the HCV-prevalence (the proportion of thepopulation infected) is estimated at approximately1-1.5% and about 20,000 infections are newly notifiedeach year. 1, 2 Approximately 13,500 notifications havebeen made to the South Australian surveillance systemsince the introduction of mandatory notifications in thisjurisdiction in 1995 (Communicable Disease ControlBranch, Department of Health, surveillance data 2006).The number of infected persons around the world isestimated to be between 170 and 300 million people. 3-5Much of the escalating disease prevalence can beattributed to the high chronicity rate of the infectionup to 85% of those infected fail to clear the virus 6,8in combination with relatively low treatment uptake. 9Although only a small proportion of those infectedwill go on to develop the more severe sequelae ofthe disease, such as liver cirrhosis and hepatocellularcarcinoma, 8, 10-12 the sheer size of the infected populationhas clear and serious implications for health resourcesand community health.While injecting drug use is widely accepted as themost common primary risk factor for HCV infection,history of imprisonment has also been independentlyassociated with infection. 13-16 Approximately 10% ofall South Australian notifications for HCV in 2002 werereceived from the state’s prisons, as were 25% ofthose cases confirmed as new infections (or ‘incident’)cases. 17 Nonetheless, there have been relatively fewstudies on the prevalence of HCV-infection within prisonpopulations and only a few studies have investigatedHCV transmission in this particular setting. There hasbeen no previous work on HCV-infection in SouthAustralian prisons. The small amount of publishedwork in this area suggests that HCV prevalence amongprisoners is many times higher than that of the nonincarceratedpopulation. High background prevalencewill greatly increase the HCV risk for all individualsentering the prison system. High prison rates of HCV arepotentially an important contributor to escalating rates inthe general population.This paper reviews some of the literature on HCVin prisons, before briefly introducing a statewidestudy being undertaken by the University of Adelaide(Discipline of Public Health) in South Australian prisonsin conjunction with the South Australian Department ofHealth, the Department for Correctional Services andthe South Australian Prison Health Services. The studyis investigating the prevalence and transmission of HCVin the South Australian prison population. Some of theearly results from the study are also presented.HCV infection in prisons: what do we already know?There are a number of difficulties for researchers toovercome when investigating HCV infection in prisonpopulations. As discussed by Dolan, 18 two distinctpopulations exist within prisons, which are defined bytheir use of injection drugs. This has implications forsampling strategies when studying HCV prevalence inprison populations. Shorter periods of incarceration areassociated with nonviolent, drug-related offences, withthis offender sub-population likely to be at greater riskof HCV infection. Thus, the prevalence of HCV in prisonentrants might not necessarily be applicable to theoverall prison population. 19 Cohort (or follow-up) studies,usually incorporating serial HCV testing, will tend toexperience greater losses to follow-up in those servingshorter sentences, resulting in HCV transmissionestimates which are likely to be lower than the true rateof transmission in the prison.Despite these and other difficulties, all of the publishedstudies on HCV in prison have been able to demonstratevery strong evidence of the association betweeninjecting behaviour and, in particular, sharing injectingequipment and HCV infection in prisoners. Despite aclear overlap between injecting and tattooing practiceamong prisoners, 13, 18 most studies that investigatedtattooing in prison as a risk factor found there wasan excess risk for HCV infection associated with thispractice. 20-22 Sharing injecting equipment in prison isthe principal risk factor, however, with the scarcityof new equipment meaning that a single syringe isgenerally used multiple times by a very large numberof prisoners. 23-25 There is evidence that a small butsignificant number of prisoners are initiated into sharing13, 20,or injecting for the first time whilst incarcerated.26, 27The literature also suggests that, for some, riskbehaviours learnt in prison continue after release. 28-3016

HCV prevalence in prisonsWith some exceptions, and unlike the picture for othercommunicable diseases in this setting, HCV infectionappears to show a relatively consistent epidemiologicalpicture in prisons around the world, despite cleardifferences in political and socio-cultural contexts. Instudies of prison populations in the United Kingdom(UK) and the Republic of Ireland, the prevalence of HCVantibodyranged from 8% to 37%. Prevalences weremuch higher in those reporting a history of injecting druguse (IDU), ranging up to 81%. 27, 31-33 In the United States(US), between 23% and 41% of prisoners were HCVantibodypositive. 36-43 Those reporting IDU history hadthe highest prevalences (up to 96.6% in one study 38 ) andmost studies, in the US and elsewhere, also reportedthat females were more likely to be infected than maleprisoners.A study in Canada found 33% of prisoners wereHCV-antibody positive, representing an increase onthe prevalence noted in an earlier study in the sameinstitution (28%). 20 In Brazil 41% of the incarceratedpopulation were estimated to be HCV-infected – 87%in those reporting IDU. 45 HCV prevalence in prisonersreporting IDU in Spain and Greece were 92% and 81%respectively. 46, 47 Similar findings have been reported inDanish and Italian prisoners. 48In Australia, Butler et al 49 found that 37% of male prisonentrants to a New South Wales (NSW) prison were HCVantibodypositive, as were 66% of those reporting IDUand 48% of those with tattoos. In a later study of maleand female NSW prisoners, Butler et al 50 estimated 39%overall and 67% of female prisoners were HCV-antibodypositive. Crofts et al 51 found that 39% of Victorianprisoners were found to be HCV-antibody positive in asmaller sample of Victorian inmates who injected (n=51).Crofts et al later found an HCV-antibody prevalence of88%. 13 Very high HCV prevalences have subsequentlybeen identified in male and female Victorian prisoners(55% and 67% respectively), 22 and a recent surveyconducted among prisoners entering seven prisons inNSW, Western Australia, Tasmania and Queensland,reported an overall prevalence of 35%. 52HCV transmission in prisonsOnly very few studies of HCV transmission have beenpublished in Australia or worldwide. Typically, studiesemploying serial testing for HCV-antibody have foundsurprisingly low transmission rates in the prisonpopulations studied. For instance, two US studies reportrates between 0.4 and 1.1 new cases per 100 personyears*, having observed as low as only two new casesover 12 to 24 months of follow-up. 40, 41 In another USstudy in ‘recidivist’ female prisoners (defined as thoseentering prison more than once during the two yearstudy period), Macalino et al 42 estimated a relativelyhigh transmission rate of 18.2 per 100 person years.The authors point out, however, it was not possibleto attribute these cases to prison exposure since allof these women spent time outside prison during thestudy period.Crofts et al 51 calculated a transmission rate of 18.3 per100 person-years in Victorian prisoners. Unfortunately itwas not possible to determine whether these were alltransmitted in prison, as all ten cases had spent at leastsome time outside of prison during the period of followup.Butler et al 55 compared the results of two prisonentrant surveys conducted five years apart in NSWand noted 16 new HCV cases among 90 initially HCVnegative prisoners who had participated in both surveys.Six of these cases had been continuously incarceratedbetween surveys, giving a transmission rate of 4.5 per100 person years. In another study that did not reportthe overall person time at risk, four seroconversionswere also noted amongst 29 IDU-reporting prisoners inNSW who were followed up over 14 months. 56The only other published Australian studies examiningtransmission within the prison setting were casestudies. Haber et al 24 describe four cases of newlyacquired HCV-infection within a prison in NSW attributedto injecting drugs, lacerations sustained during a physicalassault and during a hair cut with barber shears. Post etal 21 describe another NSW case attributed to tattooing inprison.In summary, although direct evidence of HCVtransmission in prison exists, it has so far proven verydifficult to study in this setting and there is still noclear picture of the rate at which it might be occurring.Relatively small sample sizes and short observationperiods, losses to follow up in those serving shortersentences and multiple prisoner admissions andtransfers are examples of some of the inevitable (andpossibly insurmountable) problems which may impacton the ability of studies to investigate HCV transmissionin prison populations.The South Australian HCV in Prisons StudyWhile there have been some high quality Australianstudies on HCV in prisons, there has been no previouswork on the situation in South Australia (SA). The SAstudy has been underway for approximately 18 monthsand is being conducted by the Discipline of PublicHealth, University of Adelaide, in conjunction withvarious stakeholders. The study is being conductedthroughout the correctional system in SA and involves alleight publicly operated adult prison sites (representingapproximately 93% of the state’s incarcerated* Person years are calculated by summing all the years each population member spent at risk of infection (i.e. in prison). For example, if one new HCV casewas noted in two prisoners who had spent a combined period of 5 years in prison the transmission rate would be 1 in 5 years, or 20 per 100 person years.17

population). Data collection commenced in October2004 and was completed in January 2006.The SA HCV in Prisons Study is aimed at estimatingthe prevalence and transmission of HCV infection inthe incarcerated population. It will identify patterns ofrisk behaviour with respect to injecting drug use andtattooing at time of entry to prison and will evaluatethe impact of the prison environment on those riskbehaviours over time. The study has two main stages,the first of which is a cross-sectional study involvingcase note audits of all prisoners within the eightparticipating prisons. The other stage is a cohort study, inwhich prisoners were recruited as they entered prison,were offered HCV antibody tests and risk questionnairesand then were followed up over time.This study has formal approval from the following SouthAustralian ethics and research committees:• Aboriginal Health Research Ethics Committee• Department for Correctional Services ResearchManagement Committee• Department of Health Human Research EthicsCommittee• The Royal Adelaide Hospital Research EthicsCommittee• The University of Adelaide Human Research EthicsCommitteeEarly results of the SA HCV in Prisons studyOver 700 prison entrants were recruited to the cohortstudy over a period of ten months and the findings willbe available soon. Some of the findings from the crosssectionalstudy are already available online ahead of theirpublication later this year, 57 and are summarised here.The health records (or case notes) of 1347 prisonerswere available for auditing in January 2005. The auditcollected data on sex, age, Indigenous status and HCVantibody status at last test. The population included 1254males and 93 females, of whom approximately 30%overall had serological evidence of HCV infection. Ofthe 27% of prisoners who had no record of ever havingbeen tested, HCV prevalence increased to 41% overall40% of the males and 66% of the female prisoners(over 1.5 times the risk in females).Looking at age in groups based on thirds of the agedistribution of the population, those in the youngest agegroup (18 to 28 years) had the lowest risk for HCV (28%infected) and those in older age groups had significantlyhigher risk 52% of 29 to 36 years olds (1.8 times the riskin the lower age group) and 44% of those aged over 36years (over 1.5 times the risk) had tested HCV antibodypositive. Indigenous status was also associated withHCV antibody status, but with some prison specificvariation. Lower risk for Indigenous prisoners was seenin one prison in the north of the state (20%), whilesignificantly higher risk for Indigenous prisoners was inall other locations (57%). This difference is likely to bedue to the origins of the specific Indigenous populations,with many of the northern prison inmates originatingfrom more remote areas where IDU is less frequentthan in more urban Indigenous communities.Further findings from the cross sectional study willbe available soon, as will the first findings of thecohort study. In the meantime, these early findingsdemonstrate that the prevalence of HCV infection inthe SA prison system is very high overall, particularlyfor females, Indigenous prisoners in urban centresand those aged above 28 years. The findings clearlyunderscore the need to continue working with allstakeholders to ensure that acceptable solutions to thisserious public health problem are identified.Factors associated with HCV-antibody status in eight publicly operated prisons in South AustraliaJanuary 2005 (n=982**)* table adapted from Miller et al 57** excluding 362 individuals with no documented test history18

References1 Dore GJ, MacDonald M, Law MG, Kaldor JM.Epidemiology of hepatitis C virus infection inAustralia, Chapter 1 in Hepatitis C: an update. AustFam Physician. 2003;32 (Special feature) (10):2-5.2 Communicable Diseases Australia. National NotifiableDiseases Surveillance System [on line database].2006; Commonwealth Department of Health andAgeing (Accessed March 15 2006). Available from:http://www1.health.gov.au/cda/Source/CDA-index.cfm3 Sanchez JL, Sjogren MH, Callahan JD, Watts DM,et al. Hepatitis C in Peru: risk factors for infection,potential iatrogenic transmission, and genotypedistribution. Am J Trop Med Hyg. 2000;63:242-8.4 Lauer GM, Walker BD. Medical progress: hepatitis Cvirus infection. N Engl J Med. 2001;345 (1):41-52.5 Keeffe EB. Peginterferons in hepatitis C virus:virological, pharmacokinetic, and clinical implications[editorial]. Semin Liver Dis. 2003;23 (Supplement 1):1-2.6 Tillmann HL, Manns MP. Mode of hepatitis C virusinfection, epidemiology and chronicity rate in thegeneral population and risk groups. Dig Dis Sci.1996;41 (Supplement):27S-40S.7 Hoofnagle JH. Hepatitis C: the clinical spectrum ofdisease. Hepatology. 1997;26 (Supplement 1) (3):15S-20S.8 Farrell GC. Hepatitis C, other liver disorders, and liverhealth. NSW: MacLennan and Petty; 2002.9 Batey RG. Chronic Hepatitis C, Chapter 4 in HepatitisC an update. Aust Fam Physician. 2003;32 (Specialfeature) (10):15-20.10 Keefe EB, Hollinger B. The Consensus InterferonStudy Group. Therapy of hepatitis C: consensusinterferon trials. Hepatology. 1997;26 (Supplement1):101S-107S.11 Isaacson AH, Davis GL, Lau JY. Should we testhepatitis C virus genotype and viraemia level inpatients with chronic hepatitis C? J Viral Hepat.1997;4:285-92.12 Flamm SL. Chronic hepatitis C virus infection. JAMA.2003;289(18):2413-7.13 Crofts N, Thompson S, Wale E, Hernberger F. Riskbehaviours for blood-borne viruses in a Victorianprison. Aust N Z J Criminol. 1996;29:20-8.14 Stark K, Bienzle U, Vonk R, Guggenmoos-HolzmannI. History of syringe sharing in prison and risk ofhepatitis B virus, hepatitis C virus, and humanimmunodeficiency virus infection among injecting drugusers in Berlin. Int J Epidemiol. 1997;26(6):1359-66.15 Dolan K. The epidemiology of hepatitis C infection inprison populations. In: Commonwealth Departmentof Heath and Aged Care, editor. Hepatitis C:Informing Australia’s National Response. Canberra;2000, 61-93.1916 Dolan K. Surveillance and Prevention of Hepatitis CInfection in Australian Prisons. A discussion paper.Sydney. National Drug and Alcohol Research Centre,University of New South Wales; 2000; NDARCTechnical Report No. 95.17 STD Services of SA. Source of HCV Notifications. In.Adelaide; 2002.18 Dolan K. Why is there conflicting evidence of hepatitistransmission in prison? First Australasian Conferenceon Hepatitis C. Sydney;1997 March 16-18.19 Macalino GE, Hou JC, Kumar MS, Taylor LE, et al.Hepatitis C infection and incarcerated populations. IntJ Drug Policy. 2004;15:103-114.20 Ford PM, Pearson M, Sankar-Mistry P, Stevenson T, etal. HIV, hepatitis C and risk behaviour in a Canadianmedium-security federal penitentiary. Queen’sUniversity HIV Prison Study Group. Q J Med.2000;93(2):113-9.21 Post JJ, Dolan KA, Whybin LR, Carter IW, et al. Acutehepatitis C virus infection in an Australian prisoninmate: tattooing as a possible transmission route.Med J Aust. 2001;174(4):183-4.22 Hellard ME, Hocking JS, Crofts N. The prevalence andthe risk behaviours associated with the transmissionof hepatitis C virus in Australian correctional facilities.Epidemiol Infect. 2004;132:409-15.23 Seamark R, Gaughwin M. Jabs in the dark: injectingequipment found in prisons, and the risks of viraltransmission. Aust J Public Health. 1994;18(1):113-6.24 Haber PS, Parsons SJ, Harper SE, White PA, et al.Transmission of hepatitis C within Australian prisons.Med J Aust. 1999;171(1):31-3.25 Hughes RA. Drug injectors and the cleaning of needlesand syringes. Eur Addict Res. 2000;6(1):20-30.26 Gore SM, Bird AG, Burns SM, Goldberg DJ, et al.Drug injection and HIV prevalence in inmates ofGlenochil prison. Br Med J. 1995;310:293-6.27 Allwright S, Bradley F, Long J, Barry J, et al.Prevalence of antibodies to hepatitis B, hepatitis C,and HIV and risk factors in Irish prisoners: resultsof a national cross sectional survey. Br Med J.2000;321(7253):78-82.28 Danahar D. Louisiana update. Delta to explore newvenues in 1999. Faculty Notes - Delta Region AIDSEducation & Training Center. 1999;11(2):4.29 Dolan KA, Wodak AD, Hall WD. A bleach program forinmates in NSW: an HIV prevention strategy. Aust NZ J Public Health. 1998;22(7):838-40.30 MacDonald M, Zhou J, Buddle M. National needleand syringe program survey - Chapter 3. In: ANCD,editor. Dealing with risk: a multidisciplinary study ofinjecting drug use, hepatitis C and other blood-borneviruses in Australia. Canberra: Australian NationalCouncil on Drugs; 2003, 9-19.

31 Weild AR, Gill ON, Bennett D, Livingstone SJ, etal. Prevalence of HIV, hepatitis B, and hepatitisC antibodies in prisoners in England and Wales:a national survey. Commun Dis Public Health.2000;3(2):121-6.32 Gore SM, Bird AG, Cameron SO, Hutchinson SJ,et al. Prevalence of hepatitis C in prisons: WASH-Csurveillance linked to self-reported risk behaviours. QJ Med. 1999;92(1):25-32.33 Long J, Allwright S, Barry J, Reynolds SR, et al.Prevalence of antibodies to hepatitis B, hepatitisC, and HIV and risk factors in entrants to Irishprisons: a national cross sectional survey. Br Med J.2001;323(7323):1209-13.34 Richie BE, Freudenberg N, Page J. Reintegratingwomen leaving jail into urban communities: adescription of a model program. J Urban Health.2001;78(2):290-303.35 Gore SM, Bird AG, Burns S, Ross AJ, et al.Anonymous HIV surveillance with risk-factorelicitation: at Perth (for men) and Cornton Vale(for women) prisons in Scotland. Int J STD AIDS.1997;8(3):166-75.36 Baillargeon J, Wu H, Kelley MJ, Grady J, etal. Hepatitis C seroprevalence among newlyincarcerated inmates in the Texas correctionalsystem. Public Health. 2003;117(1):43-8.37 Ruiz JD, Molitor F, Plagenhoef JA. Trends in hepatitisC and HIV infection among inmates entering prisonsin California, 1994 versus 1999 [letter]. AIDS.2002;16(16):2236-2238.38 Ruiz JD, Molitor F, Sun RK, Mikanda J, et al.Prevalence and correlates of hepatitis C virus infectionamong inmates entering the California correctionalsystem. West J Med. 1999;170(3):156-60.39 Fox RK, Currie SL, Evans J, Wright TL, et al.Hepatitis C virus infection among prisoners in theCalifornia state correctional system. Clin Infect Dis.2005;41(2):177-186.40 Vlahov D, Nelson KE, Quinn TC, Kendig N. Prevalenceand incidence of hepatitis C virus infection amongmale prison inmates in Maryland. Eur J Epidemiol.1993;9(5):566-9.41 Macalino G, Vlahov D, Sanford-Colby S, Patel S,et al. Prevalence and incidence of HIV, hepatitisB virus, and hepatitis C virus infections amongmales in Rhode Island prisons. Am J Public Health.2004;94(7):1218-23.42 Macalino GE, Vlahov D, Dickinson BP, SchwartzpfelB, et al. Community incidence of hepatitis B and Camong reincarcerated women. Clin Infect Dis, 2005;41: 998-1002.43 Solomon L, Flynn C, Muck K, Vertefeuille J.Prevalence of HIV, syphilis, hepatitis B, and hepatitisC among entrants to Maryland correctional facilities.J Urban Health. 2004;81(1):25-37.2044 De P, Connor N, Bouchard F, Sutherland D. HIV andhepatitis C virus testing and seropositivity rates inCanadian federal penitentiaries: a critical opportunityfor care and prevention. Can J Infect Dis MedMicrobiol. 2004;15(4):221-5.45 Guimaraes T, Granato CF, Varella D, Ferraz ML, et al.High prevalence of hepatitis C infection in a Brazilianprison: identification of risk factors for infection. BrazJ Infect Dis. 2001;5(3):111-8.46 Pallas JR, Farinas-Alvarez C, Prieto D, Delgado-Rodriguez M. Coinfections by HIV, hepatitis B andhepatitis C in imprisoned injecting drug users. Eur JEpidemiol. 1999;15(8):699-704.47 Malliori M, Sypsa V, Psichogiou M, Touloumi G, et al.A survey of bloodborne viruses and associated riskbehaviours in Greek prisons. Addict. 1998;93(2):243-51.48 Babudieri S, Longo B, Sarmati L, Starnini G, et al.Correlates of HIV, HBV, and HCV infections in a prisoninmate population: results from a multicentre study inItaly. J Med Virol. 2005;76:311-317.49 Butler TG, Dolan KA, Ferson MJ, McGuinnessLM, et al. Hepatitis B and C in New South Walesprisons: prevalence and risk factors. Med J Aust.1997;166(3):127-30.50 Butler T, Spencer J, Cui J, Vickery K, et al.Seroprevalence of markers for hepatitis B, C and G inmale and female prisoners - NSW, 1996. Aust N Z JPublic Health. 1999;23(4):377-84.51 Crofts N, Stewart T, Hearne P, Ping XY, et al. Spread ofbloodborne viruses among Australian prison entrants.Br Med J. 1995;310(6975):285-8.52 Butler T, Boonwaat L, Hailstone S. National prisonentrants’ bloodborne virus survey 2004. Sydney:Centre for Health Research in Criminal Justice &National Centre in HIV Epidemiology and ClinicalResearch, University of New South Wales; 2005;ISBN: 0 7347 37440.53 Christensen PB, Krarup HB, Niesters HG, NorderH, et al. Prevalence and incidence of bloodborneviral infections among Danish prisoners. European JEpidemiol. 2000;16(11):1043-9.54 Champion JK, Taylor A, Hutchinson S, Cameron S,et al. Incidence of hepatitis C virus infection andassociated risk factors among prison inmates: acohort study. Am J Epidemiol. 2004;159(5):514-9.55 Butler T, Kariminia A, Levy M, Kaldor J. Prisoners areat risk for hepatitis C transmission. Eur JEpidemiol.2004;19(12):1119-1122.56 O’Sullivan BG, Levy MH, Dolan KA, Post JJ, et al.Hepatitis C transmission and HIV post-exposureprophylaxis after needle- and syringe-sharing inAustralian prisons. Med J of Aust. 2003;178(11):546-9.57 Miller ER, Bi P, Ryan P. The prevalence of HCVantibody in South Australian prisoners. J Infec. InPress, Corrected Proof available from: http://www.sciencedirect.com/science/article/B6WJT-4HNSG0G-5/2/c70e0d9f4b7f7656c46c1a3c2f287737.

Reflections on JohnSnow’s Pump Handle:Is there a need foran infection controlprogram in SouthAustralian prisons?Doreen RaeProject CoordinatorPrimary Health Care Services - Prisoner Health &Strategic ProjectsCentral Northern Adelaide Health ServicesOne hundred and fifty years ago John Snow (1813-1858),an icon in epidemiology, provided one of the earliestexamples of using epidemiologic methods to identifydisease risk and to recommend preventative actions.Snow was intent on cholera prevention and supportedthe unpopular view that cholera was transmitted bycontaminated water and not via bad air vapours. Hisstudies, and subsequent removal of a contaminatedwell’s pump handle, highlighted public health action,guided by epidemiological data, as a proven strategy tocontrol infectious diseases, stop epidemics and correctenvironmental causes of ill health. 1Reflections on past successes in controlling epidemicsin history may be useful in developing convincinganalogies for change in non-healthcare agencies. Indeed,this would highlight the value of systemic structuralinterventions as a catalyst. The pump handle analogy, forexample, could be instructive to prisons. Historical andcontemporary prison settings are recognised as sitesof disease transmission 4 and, globally there is an overrepresentationof blood-borne viruses among peopletemporarily accommodated in prisons. 2,3The high prevalence of blood-borne viruses amongprisoners is a risk to the health of correctional staff,uninfected prisoners and to the general community. 5,6Additionally, Australian and international studies revealthat:• The health status of people living in custody isgenerally lower than that of the rest of the population;• There are high rates of physical and mental disorderamong custodial populations; and• Social and economic disadvantage is identified as themajor causative or contributing factor to the ill healthof prisoners. 7Addressing infection control issues in prison settings ischallenging for both justice and public health, due to theincreasing complexities of managing growing numbersof transient, repeat offenders who present with trimorbiditiesassociated with unresolved drug issues and21significant chronic physical and mental problems. 8,7,9Traditionally, infection preventative strategies inprisons have emphasised changing individual prisonerbehaviours through infection control education andawareness campaigns. But although prisoner-targetededucational programs are essential, they are inadequateas a prevention strategy if the means of prevention arenot available to prisoners living with multiple medicaland psychosocial challenges in prison environments. 10Effective health-promoting strategies includeintersectoral partnerships, the development oforganisational health policies, and the acknowledgementthat all agents, not only health service providers, areresponsible for the health of the prison community. 11Due to community-supported sentencing practicesprison managers have exceeded the recommendedprison utilisation rates in the past decade. In mostdeveloped countries, similar sentencing trends havealso led to prison over-crowding. 12 In 2004, the SouthAustralian Department for Correctional Servicesdescribed the current high utilisation rate of prisons as‘problematic’. 13 As a result, more people, who wouldnot normally come together, mix and mingle in prison,as accommodation pressures necessitate frequentrelocations from prison-to-prison. Greater numbersof socially disadvantaged and unwell people move inand out of prison on a regular basis. 14 Overcrowdedconditions, accommodating transient populations inperpetual flux create ideal environmental conditions forthe transmission of infectious diseases. 15,16,17Providing leadership towards healthy environments forpeople in prisons is the responsibility of each state andterritory government and it is not a federal responsibilityas are some other national infection control initiatives.There are no national infection control guidelines forprisons as there are for other high-risk settings such ashealth care facilities and children’s day care centres.So who is responsible? Justice policy-makers in SouthAustralia are primarily directed to manage the separationof offenders from the general community, and areneither accountable nor suitably resourced to be activeparticipants in health promotion. Existing infectioncontrol programs are specific to other high-infectionrisksettings such as health care facilities and aged andchild-care centres, as these are essential for the nation’swelfare. To promote the health and safety of those livingand working in prisons, the need for an audited infectioncontrol program for both public and private prisonsin South Australia seems self-evident. Developing,implementing and monitoring an infection controlprogram for prison environments, with intersectoralcollaboration between the justice system and public,environmental and occupational health would be a steptowards a safer South Australian community.South Australia is a society with health policies that aimto improve the health of the most vulnerable groupsby implementing preventative measures and hospital-

avoidance strategies. To promote population healthby taking a ‘first-things-first’ preventative approach,beginning with a prison infection control program, 16would be analogous to removing the ‘pump handle’that is driving the present preventable blood-borne virusepidemic in the prison environment.Prison infection control preventative strategies couldinclude:• Up-to-date post-exposure control plans that minimisethe potential of employee and inmate exposures toblood-borne pathogens, both occupational and nonoccupational;• Systems to ensure staff and inmates are vaccinatedas recommended by national immunisation guidelinesand the outcomes audited; 18• Establishing and enforcing respiratory isolation policiesto a community standard;• Ensuring that personal protective equipment such aslatex gloves and eye shields are available to both staffand inmates;• Environmental hygiene inspections by qualifiedenvironmental health officers in prison food cateringareas, health care centres and hair dressing locations;and• Establishing infection control committees thatinclude prison management, health care providers,environment health officers, housekeeping,food services and occupational health industrialrepresentatives.A prison settings infection control program wouldremove the ‘pump handle’ from our correctionalsystem. It may be time to justify the introductionof a collaborative prison infection control program,underpinned by the hypothesis that our presentHepatitis C virus epidemic and its subsequent burdenof chronic disease will not be controlled unless newpartnerships are formed between the Justice and Healthsectors. Some international jurisdictions are creatingcollaborations, based on scientific evidence to controlprison-mediated infections, and are consequentlyprotecting the general community from contagion. Inthese pragmatic jurisdictions, both human suffering andhealth costs have been reduced. 19,20References1 Department of Health and Human Services, Centres forDisease Control and Prevention (CDC). 150th Anniversaryof John Snow and the pump handle. Morbidity andMortality Weekly Report (MMWR). 2004;53(34):783.Available from: http://www.cdc.gov/mmwr/PDF/wk/mm5334.pdf.2 Joint United Nations Programme on HIV/AIDS. WorldHealth Organization guidelines on HIV infection and AIDS inprisons. Geneva: World Heath Organization; 1993.3 Public Health Agency of Canada. Hepatitis C virustransmission in the prison/inmate population. Canada22Communicable Disease Report. 2004; 30(16):141-148.Available from: http://www.phac-aspc.gc.ca/publicat/ccdrrmtc/04vol30/dr3016ea.html4 Jurgens R. HIV/AIDS in prisons. Final report. Montreal.Canadian HIV/AIDS Legal Network; 1996. Available from:http://www.aidslaw.ca/maincontent/.htm5 Miller E. Hepatitis C infection in Australia: an ongoingepidemic. Public Health Bulletin South Australia. 2004;1:29-31.6 Hellard ME, Hocking JS and Crofts N. The prevalenceand the risk behaviours associated with the transmissionof hepatitis C virus in Australian correctional facilities.Epidemiol Infect. 2004;132:4009-415.7 Toma_evski T. Prison health: international standards andnational practices in Europe. Series 21. Helsinki Institute forCrime Prevention and Control (HEUNI) affiliated with theUnited Nations. Helsinki; 1992, 38.8 Australian Government Productivity Commission. Reviewof government services provision. Policy development, 7.9.Canberra: Corrective Services; 2004. Available from: http://www.pc.gov.au/gsp/rogs.html9 Butler T, Milner L. The 2001 New South Wales Inmate healthsurvey. Sydney: Corrections Health Service (NSW); 2003.10 Dolan K, Rouen DA. Evaluation of an educational comic onharm reduction for prison inmates in New South Wales. Int JForensic Psychol. 2003;1(1):138-141.11 World Health Organization. Ottawa charter for healthpromotion. Health Promot Int. 1986;1(4):i-v.12 Australian Government Productivity Commission. Review ofgovernment services provision. Canberra: Corrective Services.Available from: http://www.pc.gov.au/gsp/rogs.html13 Australian Government Productivity Commission. Reviewof government services provision. South Australiancomments, 7.33. Canberra. Corrective Services; 2004.Available from: http://www.pc.gov.au/gsp/rogs.html14 Kawachi I, Kennedy BP, Wilkinson RG. Crime: socialdisorganization and relative deprivation. Soc Sci Med.1999;48:719-731.15 Crofts N. A cruel and unusual punishment. Med J Aust.1997;166:116.16 Bick J. Infection control in the correctional setting.Infectious Diseases in Corrections Report. July/Aug2004. Available from: http://www.idcronline.org/archives/julyaug04/article.html17 Nelles J, Fuhrer A, Hirsbrunner HP, Harding TW. Provisionof syringes: the cutting edge of harm reduction in prisons?Education and Debate. Brit Med J. 1998;317:270-273.18 National Health and Medical Research Council (NHMRC).The Australian immunisation handbook. 8th Ed. Canberra.Commonwealth of Australia; 2003.19 Lines R, Jürgens R, Betteridge G, Stöver H, et al. Prisonneedle exchange: lessons from a comprehensive review ofinternational evidence and experience. Montreal. CanadianHIV/AIDS Legal Network; 2004. Available from: http://aidslaw.ca20 Centres for Disease Control and Prevention. Prevention andcontrol of infections with hepatitis viruses in correctionalsettings. Atlanta. Morbidity and Mortality Weekly Report(MMWR). 2003;52(RR-1). Available from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5210a9.htm

Immunisation– a new era for vaccinesHelen MarshallHead, Paediatric Trials Unit,Women’s and Children’s HospitalClinical Lecturer, Dept of Paediatrics,University of AdelaideClinical Lecturer, Dept of Public Health,University of AdelaideVaccines prevent up to three million deaths eachyear and 750,000 children are saved from disabilityglobally. 1 Recent advances in immunisation include themanufacture of several new vaccines including vaccinesto prevent Rotavirus (RV), the commonest causeof gastroenteritis in children and a vaccine with thepotential to substantially reduce the incidence of cervicalcancer in women.Rotavirus VaccinesRotavirus InfectionRotavirus infection causes approximately 440,000deaths worldwide every year in children under 5 yearsof age. 2 Most deaths from gastroenteritis occur indeveloping countries where children can experiencegreater than 12 episodes of diarrhea per year. Almost allchildren have been infected with RV by 2-3 years of age. 3There are an estimated 10,000 hospital admissionsand 115,000 GP visits annually attributable to RVinfection in children < 5 years in Australia. 4 Importantlygastroenteritis is a leading cause of morbidity andmortality in aboriginal children in Australia. Five outof 14 major serotypes are associated with almost allhuman rotavirus infections: G1, G2, G3, G4 and G9. 5Rotavirus VaccineThe first live oral RV reassortment vaccine, RotaShieldwas shown to provide 48% - 68% protection againstany RV disease when administered at 2, 4 and 6months of age. Following licensing in the USA in 1998and introduction into the routine schedule, the vaccinewas withdrawn form the market in 1999 followingseveral cases of intussusception after immunisation.The decision to remove RotaShield from the childhoodschedule in the USA remains controversial. 6 The riskof intussusception following administration of thisvaccine has recently been reassessed and estimatedto be as low as 1:32,000 (background risk of 18 to 56cases per 100,000 infant years). 6 More recently twonew RV vaccines have been manufactured, which arelikely to be available for use in Australia in the next12 months. A pentavalent human-bovine reassortant(G1, G2, G3, G4 and P[8]), 3 dose oral vaccine hasbeen developed by Merck Research Co (Rotateq) and amonovalent (P[8] G1), live attenuated 2 dose oral vaccinehas been developed by Avant Immunotherapeuticsfrom a live human RV strain and licensed to GSK23Biologicals (Rotarix). Pre-licensure studies with samplesizes including >60,000 infants have shown bothvaccines to be safe and efficacious against RV infectionwith no increased risk of intussusception followingadministration of these vaccines (Rotateq: RR 1.6; (95%CI 0.4, 6.4), Rotarix: RR 0.85 (95% CI 0.30, 2.42). 7,8Use of the vaccines is likely to lead to a reduction inthe burden of disease and health care costs associatedwith RV infection in Australian communities, howeverthe most significant potential benefits are reduction ofmorbidity and mortality in the developing world. TheWorld Health Organization has prioritised RV vaccineresearch and the RV Vaccine Programme based at PATHin Seattle, USA, aided by the Global Alliance for Vaccinesand Immunisation (GAVI) is assessing the informationrequired for early rotavirus introduction and accelerateduse in the global community. In addition to establishingRotavirus Vaccine Programs, surveillance for adverseevents associated with use of the new vaccines isimperative.Human Papilloma Virus VaccinesCervical cancer is preceded only by breast cancer as themost common cause of death from cancer in womenworldwide. In developing countries, where mass cancerscreening is not well established, cervical cancer isthe leading cause of death from cancer in womenparticularly affecting the 35-55 year age group. Mostdeveloping countries either have ineffective Pap smearscreening programs or have no such programs at all. 9In developed countries there has been a significantreduction in morbidity and mortality from cervicalcarcinoma due to the success of routine screeningusing the Pap smear. 10 However, despite the successof screening programs there is still significant morbidityand mortality from this disease in our community.Unfortunately not all women present for regularscreening and histologic and cytologic assessmentsof pap smears are subjective and may be prone tooperator error. 10 Pap smear screening alone is thereforenot entirely satisfactory as a preventative method forcervical cancer, even in the developed world and indeveloping countries is not practical.Cervical Carcinoma in Australian WomenThere are approximately 800-1000 new cases of cervicalcarcinoma diagnosed in Australian women each year. 11It is the 14th most common cause of cancer deathin Australian women. The lifetime risk of a womandeveloping cervical cancer is one in 130. In the 4 yearperiod from 2000 to 2003 there were 994 deaths fromcervical cancer in all states and territories comparedwith 1,081 from 1996 to 1999. 12Among aboriginal women there is evidence of a higherrate of cervical cancer compared with non-aboriginalwomen. In the period between 1995 and 1997 therewere 19 deaths (27.6 per 100 000 women) from cervical

cancer among aboriginal women. This represents morethan nine times the death rate of non-aboriginal women(3.0 per 100, 000 women). 11In some countries the incidence of cervical cancerappears to be increasing due to recent changes in risktaking behaviour in young women. 13 There was a 60%increase in incidence of cervical cancer in Finland inthe 1990s in young women. Over the same period oftime the number of lifetime sex partners significantlyincreased and the age at first intercourse decreased. 13Thus increasing exposure to HPV and other sexuallytransmitted infections is likely to explain the recentincrease in the incidence of cervical cancer observed inFinland in young women.Population studies in the 1980s and 1990s in variouscountries detected an association between humanpapilloma viruses (HPV) and cervical cancer. 14 Cervicalinfection with HPV is extremely common compared tothe incidence of cervical cancer. 15 However, particulartypes of HPV have a strong association with persistent14, 16-18infection and a high incidence of cervical cancer.Human Papilloma Virus as a cause of Cervical CancerThe association of cervical cancer and infectionwith a high-risk HPV type is supported by strongepidemiological evidence and by the detection ofHPV DNA in up to 99.7% of cervical cancers from allgeographic areas. 19 There are over 40 types of HPV,with 14 of these considered to be oncogenic. HPV16 isthe most prevalent high-risk HPV type and is presentin approximately 50% of cervical tumor specimensworldwide. HPV18 is the second most prevalent typeand is associated with approximately 16% of cervicalcancers, with the remaining tumors containing DNAfrom other high-risk types such as HPV45, 31 and 33. 20The persistence of HPV in the genital tract is a riskfactor for development of cervical cancer. 16-18Approximately 470,000 new cases of cervical cancerare diagnosed each year, and nearly 200,000 deathsare attributable to the disease. 21-23 Consequently, thesocial and economic costs of HPV-induced diseasesof the genital tract are enormous, and development ofprophylactic vaccines has been an important initiative.Human Papilloma Virus VaccineVaccines against the high-risk types HPV-16 and HPV-18 have been shown to be safe and immunogenicin previous trials, and have prevented incident andpersistent HPV-16/18 infection. The HPV vaccine isan inactivated virus vaccine which is not capableof replication or transfer of the virus to others. Twovaccines have been developed that are likely to beavailable in the next 12 months. Merck and Co. havedeveloped a quadrivalent vaccine, Gardasil whichcontains HPV 16, 18 (oncogenic types) and HPV 6and 11, benign types that are associated with genitalwarts. A bivalent vaccine, Cerverix has been developedby GSK which contains the leading oncogenic types,16 and 18. In Phase II and III studies, HPV vaccineshave been shown to be safe and 100% effective inpreventing persistent HPV infection. Recent publishedresults from a long term follow-up study of Cerverix,indicates long term (up to 4.5 years) protection againstpersistent infection and cervical intraepithelial neoplasia(CIN) changes with evidence of cross protection againstother oncogenic serotypes not included in the vaccine,including serotype 45. 24Pre-teen and young adolescent women will be animportant target population for vaccination, since itwill be important to protect prior to onset of sexualactivity and exposure to oncogenic HPVs. For HPVvaccine program to be effective, high coverage ratesespecially in high risk groups will need to be achieved.Linkages with other health care systems, improvedadult health services and education about the benefitsand availability of the HPV vaccine will be vital to theachievement of high levels of coverage. Implementationissues including provision of Government funding,decisions on whether both males and females willreceive the vaccine and the target age group are yet tobe determined.The future challenge for these new vaccines will beto develop innovative funding strategies to ensureadequate vaccine delivery to populations with thehighest burden of disease.References1. Global Alliance For Vaccines and Immunisation (GAVI).Fact sheet no. 169, March 2001.2. Parashar U, Hummelman E, Bresee J, Miller M et al.Global illness and deaths caused by rotavirus diseasein children. Emerg infect Dis. 2003;9:565-72.3. Bresee J, Glass R, Ivanoff B, Gentsch JR. Currentstatus and future priorities for rotavirus vaccinedevelopment, evaluation and implementation indeveloping countries. Vaccine. 1999;17(18):2207-22.4. Galati J, Harsley S, Richmond P, Carlin J. Healtheconomics and hospitalization data for RV infection.(Accepted to Aust N Z J Public Health subsequent tomanuscript amendment).5. Bonhoeffer J, Heath P. Update on new vaccinesand immunisation strategies. Current Paediatrics.2006;16:1-7.6. Simonsen L, Viboud C, Elixhauser A, Taylor R. More onRotaShield and intussusception: the role of age at thetime of vaccination. J Infect Dis. 2005;192(Suppl. 1):S36-43.7. Vesikari T, Matson D, Dennehy P, Van Damme P. Safetyand Efficacy of a Pentavalent Human – Bovine (WC3)Reassortant Rotavirus Vaccine. N Engl J Med.2006;354:23-33.8. Ruiz-Palacios G, Pérez-Schael I, Raúl Velázquez F,Abate H et al. Safety and Efficacy of an AttenuatedVaccine against Severe Rotavirus Gastroenteritis. NEngl J Med. 2006;354:11-22.9. Ponten J, Adami H,Bergstrom R,Dillner J, FribergL, Gustafsson l, Miller A, parkin D, Sparen P,Trichopoulos D. Strategies for global control ofcervical cancer. Int J Cancer. 1995;60:1-26.24

10. The Cancer Council of Australia. National CancerPrevention Policy 2001-2003; 2001. Available fromhttp://www.cancer.org.au/documents/National/CancerPreventionPolicy.pdf11. Australian Institute of Health and Welfare andAustralasian Association of Cancer Registries 2000.Cancer in Australia 1997: Incidence and MortalityData for 1997 and selected data for 1998 and 1999.Canberra: AIHW & AACR. Available from: http://www.aihw.gov.au/publications/can/ca97.12. The Australian Institute of Health and Welfare andAustralian Government Department of Health andAgeing for the National Cervical Screening Program2005. Cervical screening in Australia 2002-2003.Available from: http://www.aihw.gov.au/publications/can/csa02-03/csa02-03.pdf.13. Paavonen J, Halttunen M, Hansson B, NieminenP, Rostila T, Lehtinen M. Prerequisites for humanpapillomavirus vaccine trial: results of feasibilitystudies. Journal of Clinical Virology. 2000;19:25-30.14. Nobbenhuis M, Walboomers J, Helmerhorst T et al.Relation of human papillomavirus status to cervicallesions and consequences of cervical-screening: aprospective study. Lancet. 1999;354:20-5.15. Schiffman M, Brinton L, Devesa S, Fraumeni J.Cervical Cancer. In: Schottenfeld D, Fraumeni J.Cancer epidemiology and prevention. Second edition.New York.: Oxford University press; 1996.16. Bosch F. Epidemiology of human papillomavirusinfections: New options for cervical cancer prevention.Salud Pulica de Mexico. 2003;45(3):s326-339.17. Galloway D. Papillomavirus vaccines in clinical trials.The Lancet Infectious Diseases. 2003;3:469-475.18. Tyring S. Human papillomavirus infections:Epidemiology, pathogenesis and host immuneresponse. J Am Acad Dermatol. 2000;43:S18-26.19. Walboomers JM, Jacobs MV, Manos MM etal. Human papillomavirus is a necessary causeof invasive cervical cancer worldwide. J Pathol.1999;189:12-19.20. Clifford GM, Smith JS, Plummer M, Munoz N,Franceschi S. Human papillomavirus types in invasivecervical cancer worldwide: a meta-analysis. Br JCancer. 2003;88:63‐73.21. Parkin DM, Pisani P, Ferlay J. Estimates of theworldwide incidence from 25 major cancers in 1990.Int J Cancer. 1999;80:827-41.22. Parkin DM, Bray FI, Devesa SS. Cancer burdenin the year 2000. The global picture. Eur J Cancer.2001;37:S4-S66.23. Pisani P, Parkin DM, Bray F, Ferlay J. Estimates of theworldwide mortality from 25 major cancers in 1999.Int J Cancer. 1999; 83:18-29.24. Harper D, Franco E, Wheeler C, Moscicki A.Sustained efficacy up to 4.5 years of a bivalentL1 virus-like particle vaccine against humanpapillomavirus types 16 and 18: follow-up from arandomized control trial. The Lancet. 2006;10.1016/SO140 6736(06)68439-0.25VACCINE SAFETYand COMMUNITYATTITUDES IN SASarah DugdaleProject Officer, SA Vaccine Safety (SAVeS) Data LinkageProjectDepartment of HealthBackgroundSusan LewisNurse Consultant, South Australia ImmunisationCoordination Unit (SAICU)Department of HealthMike GoldSenior Lecturer, Department of PaediatricsUniversity of AdelaideHelen MarshallSenior Medical Officer, Paediatric Trials UnitUniversity of AdelaideDespite the immense public health benefit ofvaccination, 1,2,3 concern about the safety of vaccines isnow the most important issue to affect immunisationcoverage and the sustainability of immunisationprograms in developed countries. 4,5 Loss of confidencein vaccine safety can result in decreased vaccinecoverage and a resurgence of disease. 1,6,7 This hasbeen clearly demonstrated on a number of occasions,including the reappearance of whooping cough in Japanand Sweden in the 1970s, and measles in the UnitedKingdom in 1998. 6,7,8,9The three-in-one vaccine against diphtheria, tetanus andwhooping cough (DTP) was targeted by anti-vaccinecampaigners in a range of countries after a 1974 journalpublication stated it was linked to neurological reactions.In just two years DTP vaccine coverage in Japandropped from around 80% to 10%, and in Sweden from90% to 12% over 5 years. In some other countries thepersistent media reports even resulted in the vaccinebeing withdrawn from use. By the late 1970s whoopingcough epidemics affecting hundreds of thousands ofchildren were occurring in countries across the world,with 5000 cases in Australia by 1994. 6The UK measles outbreak in the late 1990s resultedfrom the controversial publication of an article byAndrew Wakefield in the Lancet, which purported anassociation between the Measles Mumps Rubella(MMR) vaccine and both autism and bowel disease.Although the article was later retracted, its effect onuptake of the vaccine was considerable; within 3 years

coverage had dropped by 21% and mumps cases were“spreading alarmingly”. 10Anxiety about vaccine safety had emerged long beforethese examples from the past three decades. SinceEdward Jenner developed the cowpox vaccine in 1796,community groups have been expressing their concernsabout the possible effects of vaccination. Figure 1is an etching by famous London social and politicalcommentator, James Gillray, circa 1800. It satirises thework of Jenner, showing him vaccinating an anxiouswoman with “vaccine pock hot from ye cow” whilstterrible cow-like growths erupt from the people he hasalready injected. 11Figure 1. “The cow pock – or - wonderful effects ofthe new inoculation,” James Gillray 1802.Vaccination remained controversial throughout the1800s, largely due to inadequate scientific explanationof the method, questionable evidence for its successand frequent side effects. Protest marches and vigorousresistance followed the introduction of legislation in1853 which declared cowpox vaccination compulsory.At the time, parental fears of the vaccine were mockedby Shieferdecker in his vignette “Dr. C. G. G. Nittinger’sEvils of Vaccination” 12 (Figure 2).Figure 2. “Dr. C. G. G. Nittinger’s Evils of Vaccination,”Christian Charles Schieferdecker 1856.One hundred and twenty years later however, thescientific proof and evidence of its success (coupledwith an improved vaccine and injection technique) weresufficient to finally eradicate smallpox disease from theworld. Unfortunately however, community concernsabout vaccine safety could not be eradicated. Theyhave remained to a greater or lesser extent, fluctuatingbackwards and forwards in each country and for eachvaccine depending on very specific local circumstances.The current challenge in developed countries is todescribe these circumstances in order to betterunderstand why, for example, Australia was affected bythe loss of confidence in DTP vaccine but was largelyunaffected by the Wakefield MMR crisis.Evaluation of vaccine safety in AustraliaLike all pharmaceuticals, no vaccine is 100% safe. Forthis reason all drugs in Australia, including vaccines,undergo strict evaluation before the Therapeutic GoodsAdministration approves licensure and supply. 13 Thisevaluation takes place during vaccine development,and comprises vaccine trials on a small number ofhealthy children with single vaccines and a short periodof follow-up safety assessment. Unfortunately, thisprocess has a limited capacity to identify adverse eventswhich are rare, delayed, occur with specific vaccinecombinations or in a sub-group of children with coexistingdisorders. 14,15Post-licensure surveillance, once vaccines are approvedand in use, is therefore critical for on-going safetyassessment. Its significance was recently demonstratedin the United States of America where, followingadministration of 12 million doses of oral rotavirusvaccine, a type of bowel disease was detected in somechildren within seven days of receiving the vaccine.Once recognised, the vaccine was promptly withdrawnfrom use globally. 16,17In Australia post-licensure vaccine safety is theresponsibility of the Adverse Drug Reactions AdvisoryCommittee (ADRAC) 18,13 which receives ad hoc reportsof suspected adverse drug reactions. 19 Like all passivesurveillance systems, ADRAC’s main limitation isunderreporting, which compromises the sensitivity ofdetecting significant events 20,21 and its ability to reliablymonitor vaccine safety. 2,22 In a study of adverse eventsfollowing BCG vaccination, researchers found theADRAC system only recorded 44% of cases identifiedthrough active surveillance. 23Some local health departments collect and reviewreports of Adverse Events Following Immunisation(AEFI), prior to notifying ADRAC. 13 Such is the casein South Australia (SA) where, in 1997, vaccine safetysurveillance and management was enhanced to includeactive promotion of reporting by parents; feedbackand advice concerning re-vaccination; and referral to aSpecial Immunisation Service for selected children.What do we know about parent attitudes to vaccinesand safety in SA?South Australia now has the highest level ofparental reporting of AEFI worldwide. Parents reportapproximately 63% of all childhood AEFI 24 comparedwith Australia as a whole (3.2%), the USA (7.2%) 26 and26

the Netherlands (8.5%), 27 whose surveillance systemsrely primarily on notifications from health professionalsand vaccine manufacturers.This commitment to parental reporting in SouthAustralia has fostered further research into attitudestoward vaccines and vaccine safety. From Case Study1, research conducted as part of the SA Vaccine SafetyData Linkage Project, we know that South Australianparents are highly supportive of vaccine safetymonitoring and generally believe vaccines are safe.This is supported by data from the Australian ChildhoodImmunisation Register, which places the proportionof “conscientious objectors” at around 2-3%. 28 Wealso know that parents are prepared to accept a newmethod of monitoring vaccine safety, called data linkage,provided their permission to participate is soughtbeforehand.The parents interviewed in Case Study 2, followingtheir child experiencing an AEFI, were not deterredfrom continuing their child’s vaccinations, howeverthey did require more information about adversereactions afterwards. This study also provided theSA Immunisation Coordination Unit with valuablesuggestions for improving the management of AEFI andreinforced the need for access to comprehensive riskbenefitinformation prior to immunisation. Finally, CaseStudy 3 has shown that the uptake of new vaccinessuch as chickenpox, is not so much influenced byconcern about side effects but rather lack of knowledgeabout the vaccine, as well as cost.ConclusionVaccine safety is a major component of a qualityimmunisation program. SA is leading the way in vaccinesafety monitoring and research regarding communityattitudes. The case studies presented here should givepolicy makers and immunisation providers reassurancethat public confidence in vaccines is currently high in SA.What is unclear however, is whether this confidencewill be adequate to protect us from another “Wakefieldesque”vaccine safety crisis. To avoid this risk in thefuture, immunisation providers and policy-makerswill need to work very closely with parents andkey stakeholders to maintain confidence, ensuretransparency and better understand what affects publicconfidence in vaccines.A symposium coordinated by the University of AdelaidePreventive Healthcare Research Cluster “Linking scienceto a shot in the arm” held in April 2006 provided aninvaluable opportunity to begin aligning these researchactivities with policy priorities. There is considerablescope for research in this area and those interested informing collaborations are encouraged to contact DrMike Gold on 08 8161 7266 for further information.The cornerstone of the South Australian vaccine safetysurveillance system is the active promotion of reportingby parents. If you suspect an AEFI or would like adviceon managing or reporting an AEFI, please contact SAICUon 08 8226 7177 9am-4.30pm Monday-Friday, or theChild and Youth Health Parent Helpline on 1300 364 10024hrs, 7 days a week.CASE STUDY 1Community and provider attitudes to vaccine safetyand data linkage: Acceptability findings from the SAVaccine Safety (SAVeS) Data Linkage ProjectData linkage (DL) is used to monitor vaccine safety inthe USA, UK, Scandinavia and Vietnam, and Australia’sfirst pilot project is presently being conducted inSA. Although DL can improve the quality of studiesevaluating vaccine safety, there is scant research onattitudes towards the method.To better understand community and immunisationprovider feelings regarding data linkage and vaccinesafety, surveys were conducted in 2004 and repeatedin 2005. Community attitudes were collected via the SAHealth Omnibus survey (n=3000), and immunisationprovider attitudes via postal survey (n=830).Preliminary results indicate that most respondentsbelieved adult and childhood vaccines are very safe(58-87%), however providers were more likely to thinkthis (P

CASE STUDY 2Parents’ experiences of an Adverse EventFollowing Immunisation in South Australia – aqualitative studyEffective systems are required to monitor vaccinesafety and to provide ongoing support for those whoexperience an Adverse Event Following Immunisation(AEFI). This study aimed to better understand theexperience and implications for parents when theirchild suffers an AEFI. Semi-structured interviewswere conducted in the homes of 10 parents whosechild had an AEFI reported during April 2005.Most parents were aware of the risk of commonside effects following immunisation however werenot aware of adverse reactions. Although they hadreceived varying amounts of information aboutcommon side effects they believed that knowledgeabout vaccine common side effects and adversereactions is necessary to enhance the immunisationprocess.Parents’ belief in immunisation remained unchangedand they all said they would continue to vaccinatetheir children, but with an increased knowledgeand heightened awareness of the risks of adversereactions. Their satisfaction with the managementof health services during and after the event wasaffected by the interest shown by health professionalsand the timeliness of the service.The parents in this study were not deterred fromcontinuing their child’s vaccination schedule followingan AEFI; however their needs changed, and they nowrequire more information about adverse reactions.Delivery of a timely service by an interested healthprofessional maintained parental satisfaction with themanagement of the health services.For further information contact Susan Lewis, SAImmunisation Coordination Unit:susan.lewis@health.sa.gov.auCASE STUDY 3Uptake of varicella vaccine in South Australia – across sectional survey of parental attitudes tovaricella vaccinationVaricella (chickenpox) vaccine was licensed for usein Australia in March 2000 and was included butnot funded in the Australian Standard VaccinationSchedule (ASVS) in 2003. This study aimed to assessthe uptake of varicella vaccine in South Australianchildren and to examine the main reasons thatdetermine a parent’s decision to have their childimmunised with varicella vaccine.A telephone survey was conducted in 2004 anddata were obtained from 613 households containingchildren less than 18 years of age. Six hundred andeighty children (55.7%) had a history of varicellainfection and 446 children (42.0%) had receiveda varicella vaccine. Almost 41% of susceptiblechildren aged 18 months to two years and 30.5%aged 2-4 years have no protection against varicella.Reasons why parents decided to have their childimmunised included concern about acquiring varicella(65.6%) and inclusion of the vaccine on the ASVS(10.8%). Excluding previous varicella infection, themost common reasons cited for not having childrenimmunised included lack of knowledge about thevaccine and cost. Concern about side effects (2.3%)was reported less commonly.Four years after the registration and licensing ofvaricella vaccine and one year following inclusionof the vaccine in the ASVS there is evidence ofincomplete coverage in children in South Australia.Federal Government funding for varicella vaccineshould result in high coverage rates, as the mainreasons why parents choose not to have their childimmunised would be addressed.For further information contact Helen Marshall,University of Adelaide: helen.marshall@adelaide.edu.au28

References1. Chen R and Hibbs B. Vaccine safety: Current andfuture challenges. Pediatr Ann. 1998;27(7):445-455.2. Chen R, Glasser J, Rhodes P, et al. Vaccine SafetyDatalink Project: A new tool for improving vaccinesafety monitoring in the United States. Pediatrics.1997;99(6):765-773.3. National Centre for Immunisation Research andSurveillance of Vaccine Preventable Diseases(NCIRS). Communicable Diseases Intelligence:Vaccine preventable diseases and vaccinationcoverage in Australia, 1999-2000. Canberra: AGPS;2002.4. Chen R. Vaccines risks: real, perceived andunknown. Vaccine.1999;17 (Suppl 3):S41-S46.5. National Institute of Public Health and Environmentin the Netherlands (RIVM). Adverse events followingimmunisation under the national vaccinationprogramme of the Netherlands: Number V11 -Reports in 2000. Bilthoven: RIVM; 2002.6. Gangarosa E, Galazka A, Wolfe C, et al. Impact ofanti-vaccine movements on pertussis control: theuntold story. Lancet. 1998;351:356-361.7. Ada G and Isaacs D. Vaccination: The facts, the fears,the future. St Leonards: Allen & Unwin,; 2000.8. Andrews N, Miller E, Taylor B, et al. Recall bias,MMR, and autism. Arch Dis Child. 2002;87:493-494.9. Ellenberg SS. Safety considerations for new vaccinedevelopment. Pharmacoepidemiol Drug Saf. 2001;10(5):411-415.10. ProMed Mail 6/8/200111. Gillray, J. The Cow Pock-or-the-Wonderful Effects ofthe New Inoculation! Publications of ye Anti-VaccineSociety. June 12, 1802. Available from:http://www-micro.msb.le.ac.uk/Tutorials/Pox/Pox13.html12. Schieferdecker CC. Dr. C. G. G. Nittinger’s Evils ofVaccination. Philadelphia: the editor, 1856. Availablefrom: http://www.sc.edu/library/spcoll/nathist/jenner2.html13. National Health and Medical Research Council(NHMRC). The Australian Immunisation Handbook.7th ed. Canberra: AGPSl 2000.14. Brewer T and Colditz G. Postmarketing surveillanceand adverse drug reactions: Current perspectives andfuture needs. JAMA. 1999;281(9):824-829.15. Jacobson R, Adegbenro A, Pankratz V, et al. Adverseevents and vaccination - the lack of power andpredictability of infrequent events in pre-licensurestudy. Vaccine. 2001;19:2428-2433.16. DeStefano F. The Vaccine Safety Datalink project.Pharmacoepidemiol Drug Saf. 2001;10:403-406Ggg.17. Murphy T, Gargiullo P, Massuodi M, et al.Intussusseption among infants given oral rotavirusvaccine. N Engl J Med. 2001;344:564-572.18. Gold M and Kempe A. Adverse Events FollowingImmunisation (AEFI) in Australia: Surveillanceand management. Adelaide: SA ImmunisationCoordination Unit; 2001.19. Department of Health and Ageing, TherapeuticGoods Administration. Adverse Drugs Reaction Unit.[Last updated 1/07/02, accessed 23/9/05]. Availablefrom: http://www.tga.gov.au/adr/20. Wattigney W, Mootrey G, Braun M, et al.Surveillance of poliomyelitis vaccine adverse events,1991 to 1998: Impact of a sequential vaccinationschedule of inactivated poliovirus vaccine followed byoral poliovirus vaccine. Pediatrics. 2001;107(5):e83.21. Chen R, Haber P, Mullen J. Surveillance of the safetyof simultaneous administration of vaccines. Ann N YAcad Sci. 1995;754:309-320.22. Andrews N. Statistical assessment of the associationbetween vaccination and rare adverse events postlicensure.Vaccine. 2002;20:S49-453.23. Turnbull F, McIntyre P, Achat H, et al. National studyof adverse reactions after vaccination with BacilleCalmette-Guérin. Clin Infect Dis. 2002;34:447-453.24. Dugdale, S. Adverse events in South AustralianChildren, 1997-2002. Master of Public Health Thesis.University of Adelaide; 2003.25. Lawrence G, Menzies R, Burgess M, etal. Surveillance of adverse events followingimmunisation: Australia 2000-2002. Commun DisIntell. 2003;27:307-323.26. Zhou W, Pool V, Iskander J, et al. Surveillancefor safety after immunization: Vaccine AdverseEvents Reporting System (VAERS) - United States,1991-2001. Morbidity and Mortality Weekly Report(MMWR). 2003;52:1-24.27. National Institute of Public Health and Environmentin the Netherlands (RIVM). Adverse events followingimmunisation under the national vaccinationprogramme of the Netherlands: Number V11 -Reports in 2000. Bilthoven: RIVM; 2002.28. Hull B, Lawrence G, MacIntyre CR, McIntyre P.Immunisation Coverage: Australia 2001. Canberra:Commonwealth Department of Health and Ageing;May 2002.29

Chlamydia -closing thestable doorDr Katrina AllenShineSAThe emergence of the deadly HIV in the early 1980ssaw a large increase in attention and funding for sexuallytransmitted infection clinics and, particularly in Australia,a major expansion in sexual health education andresearch, charted by the national survey of secondaryschool students’ sexual health. 1,2,3 Through the latterit has become clear that the message about HIV as asexually transmitted disease is being effectively taughtat later secondary school level. However what hasemerged over the time, as the studies have repeated, isthat knowledge about HIV is decreasing. Though thereis some improvement in knowledge about transmissionof Sexually Transmitted Infections (STIs), youngpeople’s knowledge of Chlamydia has not improved.Symptomatic of this lack of awareness is the knowledgethat condoms are primarily being used as contraceptionrather than infection protection. 3Genital Chlamydia is emerging as a significant publichealth problem for young people in particular, as mostWestern societies are experiencing a significant increasein infections particularly in people under 25. 4 Chlamydiais a fragile organism which infects mucus membranes.In genital infections, only 50 per cent of men and 30 percent of women experience symptoms, 5 but the infectioncan ascend in the genital tract to produce major diseasesuch as pelvic inflammatory disease in women, andchronic prostatitis and urethral strictures in men. 6 Inboth women and men the end result can be obstructiveinfertility as well as chronic pain and disease.As much of the burden of infection and disease occurs inthe young there has been considerable interest in raisingawareness of chlamydia infection in this population, aswell as in the health care providers for this population.For the latter this has largely taken the form of exploringthe possibilities of increasing screening for chlamydiain various sections of the population. Clearly screeningfor chlamydia is already part of the routine work of anSTI clinic, but the issue of screening of asymptomaticpopulations in the community has also been raised. Thishas been driven by the availability of less invasive meansof testing for chlamydia. Until recently chlamydia wastested for with an endocervical swab for women anda urethral swab for men, but the development of PCRamplification with chlamydia specific DNA has meantthat a first pass urine sample now provides an adequatesample for testing chlamydia. 6 This has meant screeningacross the community is easier, significantly increasingthe numbers of men being tested.The prevalence of chlamydia in South Australia is difficultto establish as the detection of infection mostly reflectsSTI screening and/or symptomatic screening. In 2000the ratio of women to men being tested was 4:1 buttesting is now more even between the sexes. Althoughchlamydia has been a notifiable disease in SouthAustralia since 1989, uneven testing left knowledge ofinfection rates in the male population unclear. What isnow emerging about chlamydia is that males tend tohave an infection for a shorter time than females. 7 Aswomen remain infective for longer periods it may bemost effective to screen and treat women to make adent in the rising infection rate.Routine screening, including treatment and follow-up ofpartners, has been shown to decrease the developmentof problematic complications. 8 For this reason andbecause the infection may be a marker for otherdisadvantage, 9 routine screening has been advocated bypublic health bodies both in Australia and overseas. Theidentification of chlamydia infection enables treatment,notification and treatment of infected partners.However there has been debate on which populationsshould be screened. Whole population screening isnot cost effective and most authorities favour eithertargeted or opportunistic screening. Possible populationstargeted for screening are all pregnant women in thefirst trimester, women seeking an abortion, womenattending family planning clinics or even all womenusing or requesting the injectable progesterone onlycontraception (Depo). Canadian guidelines include allsexually active women less than 25 years old and theUSA guidelines include all women aged under 20. 10The recognition of the link in identifying healthinequalities by chlamydia incidence has led to moreeffort to increase screening amongst vulnerable youngpeople, in an effort to identify and treat, and also totarget education and contraceptive access to decreasethe incidence of teenage pregnancy and abortion.Thus in Britain testing for chlamydia has moved intothe pharmacies in an effort to reach those groups ofteenagers and young people who have few health careattendances at clinics where opportunistic screeningmay occur. 5 This has inevitably led to questions ofaccess to treatment and contact tracing, but given theacceptability of testing for diabetes and high bloodpressure already available in many pharmacies, it maymake a significant contribution to reducing the stigmaassociated with chlamydia infection. Reduced stigmaand more acceptance of testing in the communitymay be an important step to encouraging effectivepreventative strategies.The simplicity and acceptability of the first pass urinetest has also led to an expansion of testing in menand education campaigns to encourage young men toget tested. 12 Most chlamydia infections are detectedby General Practitioners (GPs) and a major part ofincreasing testing for chlamydia in the community is30

increasing the awareness of GPs of the risk groupsand the opportunities for screening young people.While some categories are fairly obvious, such asanyone who is symptomatic, young women needingcontraception, emergency contraception or requestinga termination, young men rarely attend for checks whenasymptomatic. 12 Testing may need to be consideredwhen they attend with a sports injury or other minorcondition.There is good evidence showing effective detection ofwomen under 30 years of age who need emergencycontraception (EC). 13 The infection was identified bytesting at the time of accessing the EC in all but 2 ofthe 500+ women who were recruited. 13 The loss tofollow-up is high in post EC review in primary healthcare and so waiting until then to check for chlamydiais neither clinically nor economically effective. MakingGPs and other primary health care workers aware ofthe high incidence of chlamydia in people aged under25, particularly those with multiple sexual partnersand infrequent or inconsistent use of condoms, is animportant part of the strategy of identifying chlamydiainfection in the community, treating it and preventingits spread. This should include education for workersabout sexual health history taking, risk identification andeffective screening in their own practice.In addition it is clear from the surveys of young people’ssexual knowledge that more emphasis needs to begiven to educating young people about STIs, in particularchlamydia as the most common infection. Even with thisimprovement in knowledge the incidence of chlamydia isunlikely to change unless there is effort put in to supportyoung women in particular to apply their knowledgeabout safe sex. It is clear that the discourse of diseaserather than pleasure means that though many youngwomen know the theory of safe sex they do not feelable to apply protective measures when having sexbecause of complex emotional dynamics. 14 It is alsoclear from the New Zealand research and examplesthat unless very specifically targeted and marketed sexeducation is provided for boys and young men it is verydifficult to promote safe sex behaviors. 15In Australia there have been several efforts to considera national strategy on tackling the chlamydia infectionrates and various states have put forward their ownplans. The rising incidence of chlamydia and what itreflects about sexual risk taking, especially in the faceof a rising (though still very small) HIV infection rate,demands a prompt response from health care providers.It is clear that to be effective this response needs tomove beyond the traditional expansion of screening andinclude the education of health care providers in sexualhealth history taking, risk assessment and chlamydiainfection in the community. Any policy must focus onsexual health and relationships education for secondaryschool students, emphasizing relationship dynamics,safe sex behaviours and increased knowledge of thechlamydia as the most common STI. Finally, withoutinvolving young people who are most affected by thisdisease, any policy of national screening would likely beineffective.References1. Smith A, Agius P, Dyson S, Mitchell A, Pitts M.Secondary School Students and Sexual Health. LaTrobe University: Australian Research Centre in Sex,Health and Society; 1992.2. Smith A, Agius P, Dyson S, Mitchell A, Pitts M.Secondary School Students and Sexual Health. LaTrobe University: Australian Research Centre in Sex,Health and Society; 1997.3. Smith A, Agius P, Dyson S, Mitchell A, Pitts M.Secondary School Students and Sexual Health. LaTrobe University: Australian Research Centre in Sex,Health and Society; 2002.4. Hocking J, Fairley C, Counahan M, Crofts N.The pattern of notification and testing for genitalChlamydia trachomatis infection in Victoria, 1998-2000: An ecological analysis. Australian New ZealandJournal of Public Health. 2003; 27(4): 405-408.5. Anonymous. Chlamydia - a testing issue. Lancet.2005;365:630.6. Peipert JF. Genital Chlamydial infections. New Engl.J.Med. 2003;349:2424-30.7. Males have infection for a shorter time than females(Clinic 275 ref)**.8. Scholes D, Stergachis A, Heidrich FE, Andrilla H etal. Prevention of pelvic inflammatory disease byscreening for cervical chlamydial infection. N.Engl.J.Med. 1996;334(21):1362-6.9. Macleod J et al. Coverage and uptake of systematicpostal screening for genital Chalmydia trachomatisand prevalence of infection in the United Kingdomgeneral population: cross-sectional study. BMJ.2005;330:940.10. Department of Human Services. Chlamydia strategyfor Victoria (2001-2004). Melbourne, Victoria: PublicHealth Division, Department of Human Services;2001.11. Elliott KJ, Lambourn AJ. Sex, drugs and alcohol: twopeer-led approaches in Tamaki Makaurau/Auckland,Aotearoa/New Zealand. Journal of Adolescence.1999;22:503-13.12. ShineSA. Sexual Health Awareness Week Campaign2006. [Accessed May 2006]. Available from: http://www.shinesa.org.au/go/special-projects/sexualhealth-awareness-week/campaigns.13. Kettle H, Cay S, Brown A, Glasier A. Screening forChlamydia trachomatis infection is indicated forwomen under 30 using emergency contraception.Contraception. 2002;66:251-3.14. Goldman J, Bradley G. Sexuality education acrossthe life cycle in the new millennium. Sex Education.2001;197-217.15.Bradshaw SN. Sport, arts, resiliency and sex- amix for young men. Australasian Sexual HealthConference Handbook. Australasian Chapter ofSexual Health Medicine; 2005.31

Sexually transmittedinfections in CentralAustralia – time forconcerted actionFigure 2: Nationwide chlamydia notifications over 5years by year and State/TerritoryAhmed S. Latif, Kirsty S. SmithTristate STI/HIV Project, CDC, Sexual Health and BloodBorne Viruses UnitIntroductionSexually transmitted infections (STIs) are an importantpublic health problem not only because they can causeserious short term and long term complications butalso because they facilitate the transmission of humanimmunodeficiency virus (HIV) infection. Indigenouscommunities in Central Australia continue to experiencehigh rates of STIs including chlamydial infection,gonorrhoea, syphilis, trichomoniasis and genital herpes.Interventions for STI control in the region in the lastdecade have focussed on primary and secondaryprevention of infection through screening and casefinding and have had limited effect. An examinationof the national notification rates of chlamydial andgonococcal infection reveals extremely high annualisedinfection rates in the Northern Territory (NT). While ratesof infection of chlamydia and gonorrhoea in the rest ofAustralia are 200 per 100,000 or less, rates in the NTare more than three times greater 1 (Figures 1 and 2).Recognising the association between STIs and HIVtransmission, the World Health Organisation advises thatSTI management and control should form an integralpart of AIDS/HIV control programs globally 2 .Prevalence of STIs in the Central Australian CrossborderregionWithin the NT, STI rates are higher in the Alice Springsregion and most STI notifications in this region are fromindigenous communities in the area and from AliceSprings itself. 3, 4 The annual community based STI screenconducted over a 6-week period in 2005 revealed thatof 721 men aged between 14 and 35 years screened,119 (16.5%) had chlamydia and/or gonorrhoea and/orsyphilis, and of 808 women in the same age range, 177(21.9%) had an STI (Table 1).Table 1: Results of STI Screening in 2005 in remotecommunities in the Central Australian region of NTFigure 1: Nationwide gonorrhoea notifications over 5years by year and State/TerritoryThe trend of infection in NT communities is shown inFigure 3. It is noted that high rates of infection persistover the period of five years. The distribution of infectionthroughout the NT is not even. Higher rates of between25 and 33% occur in some remote communities and insome urban areas. STI control interventions includingSTI screening and treatment have been in place forsome years now in the Central Australian region.Rates of infection in the entire cross-border area arehigh, however control interventions have been moresuccessful in some areas than others. In WesternAustralia trends appear to be reducing gradually over theyears (Figure 4). Over the last 5 years In South Australiaa slight upward trend is noted, the rates of chlamydialand gonococcal infection previous to the period shownwere considerably higher (Figure 5).32

Figure 3:Trends in chlamydial and gonococcal infection inthe NT south of the Barkly tablelands – Summaryof crude prevalence rates obtained during annualcommunity-based STI screening of young personsover a 5-year periodFigure 2:Trends in chlamydial and gonococcal infection in theNgaanyatjaara Lands in WA over 5 years (Source:Tangey A. Report on STI Screen 2004. Sexual andreproductive health program. Ngaanyatjarra HealthService 6 .)Figure 5:Trends in chlamydial and gonococcal infection in theAnangu Pitjantjatjara Lands in northern SA – Resultsof annual STI Screening of young persons 2001-2005(Source: Nganampa Health Council. Annual Report2005 7 )*Prevalence rates (%) of infection prior to 2001 inthe Anangu Pitjantjatjara Lands in northern SA wereconsiderably higher:DiscussionThe tri-state cross-border region of Central Australiaexperiences high rates of chlamydial and gonococcalinfection. Infection rates persist at high levels despiteintensive coordinated control initiatives. There aremarked variations in prevalence rates geographicallyand in the NT it has been noted that extremely highrates of infection occur in some communities. Howeverit is encouraging to note that rates in the western andsouthern regions of Central Australia have decreasedover a period of time.A number of factors may be responsible for thedifference in rates between the NT and the WA and SAregions. Most notably, the health services in the WA andSA regions of central Australia are community controlled.The ownership of health care provision may have asignificant impact on the acceptability and effectivenessof services. It has been noted that during the annualSTI screen, the coverage rates of screening of thetarget groups over the years have been much betterin WA and SA when compared with those achieved inNT communities. The maintenance of population listsis prioritised enabling more accurate data analysis;testing for STIs opportunistically is an initiative that isencouraged and fully incorporated within the healthdelivery system in WA and SA and hence more personsconsidered to belong to high risk groups are offered STIscreening when they are seen at health facilities. Partnernotification and treatment are followed up rigorously,culturally appropriate education is promoted and finally,the community-controlled Nganampa and Ngaanyatjarrahealth services experience less staff turnover and enjoya more stable long term staffing situation. The mobilityof indigenous persons between remote communitiesand between communities and town is high 5 , and thisoften leads to poorer coverage rates particularly in theNT, during the annual targeted STI screen.Future directionWith the alarmingly high rates of STIs in indigenouscommunities the risk of becoming infected withoutengaging in “high-risk” behaviour is very high. In someareas one in every three young women and one in everyfour young men are infected, therefore any person whohas sex in such communities is at risk of becominginfected. With these prevalence rates it is absolutelyessential that early effective treatment be given toanyone at risk for infection and to consider presumptivetreatment of asymptomatic persons.The general lack of education of indigenous personsneeds to be addressed. The level of literacy andnumeracy is low and hence innovative educationalmethods need to be developed and used. These includethe participatory education methods developed for outof-schoolyouth.33

Early treatment of infections is essential in reducingtransmission of infection. This may be achieved throughhealth promotion and promotion of good health seekingbehaviour. Most individuals with infections are identifiedthrough screening and not as a result of havingsymptoms, hence screening of susceptible personsneeds to be continued and opportunistic screeningshould be encouraged.In order to make a difference a coordinated multisectoralapproach addressing many different factorsis necessary. There is an urgent need to coordinateeducational activities with the Department of Educationand to liaise with those working in the field of alcoholand other drugs to address the issue of substancemisuse and STI transmission.There is a great void in our knowledge concerningsexual behaviour and sexual networking in CentralAustralian indigenous communities. In order to developand disseminate appropriate safer sexual behaviourmessages there is a need to understand current normsin the area. Social and behavioural research needs to beconducted in this area.Finally, condoms should be accessible and freelyavailable in communities and there is a need to explorethe acceptability of female condoms to give women anopportunity to exercise greater control of their sexualhealth.References1. National Centre in HIV Epidemiology and ClinicalResearch. HIV/AIDS, viral hepatitis and sexuallytransmissible infections in Australia AnnualSurveillance Report 2005. National Centre in HIVEpidemiology and Clinical Research, The Universityof New South Wales, Sydney, NSW. Canberra, ACT:Australian Institute of Health and Welfare; 2005.2. World Health Organization Global Programme on AIDSmanagement of Sexually Transmitted Diseases.WHO/GPA/TEM/94.1. Geneva; 1994.3. Latif AS, Smith KS. STI screening conducted in NTDepartment of Health and Community Services andCommunity Controlled Health Services in CentralAustralia in 2004. NT Disease Control Bulletin. Centrefor Disease Control, NT Department of Health andCommunity Services. 2004;11:18-20.4. Miller PJ, Law M, Torzillo PJ, Kaldor J. Incident sexuallytransmitted infections and their risk factors in anAboriginal community in Australia: a population basedcohort study. Sex Transm Inf. 2001;77:21–25.5. Warchivker I, Japangati T, Wakerman J. The turmoilof Aboriginal enumeration: mobility and servicepopulation analysis in a central Australian community.Aust NZ J Public Health. 2000;4:444-449.6. Tangey A. Report on STI Screen. Sexual andreproductive health program. Ngaanyatjarra HealthService; 2004.7. Nganampa Health Council. Annual Report 2005.Alice Springs; 2005. Available from: http://www.nganampahealth.com.au34The Impact of HealthCare AssociatedInfectionIrene WilkinsonManager, Infection Control Service,Communicable Disease Control Branch.Healthcare associated infections (HAI) have long beenrecognised as a critical problem affecting the quality ofhealth care and are a principal source of adverse healthcare outcomes in Australian hospitals. 1 In overseasstudies, they have been shown to lead to increasedpatient morbidity and mortality, resulting in increasedlength of hospital stay, and additional diagnostictesting and treatment, with consequent increasedcosts to the health system. 2 In 1992 it was estimatedthat in the United States HAI affected over 2 millionpatients annually, at a cost in excess of $4.5 billion andhave been reported to account for 50% of all majorcomplications of hospitalisation. 3In 1999 the USA National Institutes of Health publisheda report entitled “To Err is Human” which addressed theincidence and impact of adverse events in healthcare, ofwhich HAI were a major contributor. 4 During the sameyear, the Department of Health in Britain published areport entitled “The Socio-Economic Burden of HospitalAcquired Infection”. 5 The aim of this study was to assessthe burden of HAI in terms of the costs to the publicsector, patients, informal carers and society as a whole.The researchers found that 7.8% of patients experienceda healthcare associated infection whilst still an in-patient,and a further 19.1% of surveyed patients experienceda possible HAI after discharge from hospital. Byextrapolation, HAI were estimated to cost the NHS £986million annually, of which £930 million was incurredduring the patients’ hospital stay and £56 million (or 6%of the total cost) was incurred post-discharge.There are little data on the cost of HAI in Australia,but recent estimates are provided in a report fromthe Expert Working Group of the Australian InfectionControl Association to the Commonwealth Departmentof Health and Ageing. 6 It is estimated that surgical siteinfections could be costing as much as $268 million peryear and that the total costs to the health care systemfor bloodstream infection may be as high as $686million. However, these figures should be viewed withcaution, since the lack of comprehensive surveillancedata in Australia make the estimation of the total burdenproblematic. There is little known about the relativecontribution of out-of-hospital expenses and societalcosts to the overall costs of nosocomial infection in

Australia, but there is no reason to suppose this wouldbe substantially different to the UK experience. Thusthe economic impact of HAI, a largely preventableconsequence of medical care, is not insubstantial.In an era when rising costs of healthcare are causingconcern, it is understandable that attention is beingfocussed on the potential resource savings that canbe made by the prevention of these adverse events.Healthcare associated infection impacts economicallyboth on the healthcare system and the community.From the perspective of a healthcare system operatingwithin a (more or less) fixed budget, the resources usedin treating healthcare associated infection are thereforeunavailable to provide valued health outcomes for otherpatients, the so-called “opportunity cost” of infection. 7From a societal perspective there are the indirect costssuch as lost productivity and litigation costs, as well asthe direct costs to patients and their carers in the formof out-of-pocket expenses for treatment and visits to theoutpatient department or general practitioner for followup,and possibly loss of income.The principal types of healthcare associated infectionare: bloodstream infection, surgical site infection,medical device-related infection such as intravenouscatheter insertion site infection or urinary catheterrelatedinfection, and ventilator-associated pneumonia.The most severe healthcare associated infectionin terms of patient morbidity and mortality isbloodstream infection (BSI), which is often acquired as aconsequence of medical device use, such as intravenousor urinary catheters, or mechanical ventilation or theymay occur secondary to surgical site or burn woundinfection. Of all the different types of healthcareassociated infection, BSIs are responsible for themost deaths and the greatest number of extra days inintensive care, and therefore incur the greatest costto the hospital and to society as a whole. 8 BSI alsocarries a substantial risk of further complications such asosteomyelitis or endocarditis, which can have long-termadverse consequences for the patient.Another significant problem for healthcare facilities ishow to control the emergence and spread of antibioticresistantbacteria. Several studies have linked theemergence of new antibiotic resistant strains to theoveruse, or inappropriate use of antibiotics. 9 Once thesestrains have emerged in a healthcare setting, strictadherence to infection control practices, especially handhygiene, becomes critical in preventing their spreadamongst other patients. Although most healthcareworkers are now well educated in the principles ofinfection control, lack of compliance with recommendedpractices remains a problem. The reasons mostcommonly cited for this situation include lack of time,and lack of properly designed and convenient facilities.It is often observed by infection control staff thathospitals these days appear to be designed for aesthetic35appeal over function, and when resources are scarce, itis often the hand washing and patient isolation facilitiesthat are cut.So how can these infections be prevented? The oftenquoted SENIC project in the United States demonstratedthat up to a third of all nosocomial infections could beprevented by the adoption of infection control programsthat had certain minimum requirements. 10 Theseincluded: routine surveillance, a full-time infectioncontrol practitioner per 250 beds, a trained hospitalepidemiologist, written infection control procedures, andfeedback of surgical wound infection rates to appropriatepersonnel. These elements have been incorporated intorecommended guidelines by the Society for HealthcareEpidemiology of America for the essential components ofan effective infection control program. 11For example, with appropriate infection controlmeasures the rate of BSI associated with medicaldevices can be significantly reduced. For intravenouscatheters, these measures include the use of: maximalsterile barrier on catheter insertion, a well-trained anddedicated intravenous catheter team, an alcoholic skindisinfectant preparation, and, most recently, the use ofantimicrobial catheters. 12 Adequate staffing may alsoimpact positively on the incidence of catheter-relatedBSI. The Centres for Disease Control and Preventionhave recently produced a set of guidelines for themanagement of intravenous catheters that include mostof the above interventions as recommendations for bestpractice. 13Routine targeted surveillance of HAI with regular andtimely feedback of results to clinicians has been shownto be an effective way of focussing attention on theseadverse events, and is useful for both illustrating themagnitude of the problem and for monitoring the effectof specific interventions. 14 This philosophy underpinsthe surveillance work of the Infection Control Service,which was established in 2001 with the aim of reducingthe incidence of HAI in South Australian healthcarefacilities. In this edition of the Public Health Bulletin, anarticle by Cope and Marwood summarises cumulativesurveillance data from the statewide healthcareassociated infection and antibiotic utilisation surveillancesystems. The HAI surveillance data illustrate theachievements obtained by South Australian infectioncontrol professionals, particularly in the area of infectionwith multi-resistant organisms, and bloodstreaminfection related to intravenous devices. Interpretationof antibiotic usage data is more complex, with usereflecting not only treatment of HAIs but also hospitaltreatment of community acquired infections, empiricuse for high risk patients and surgical prophylaxis.Using overseas published data on the cost of HAI, it iseasy to calculate that infection prevention programs canbe highly cost-effective. However, for administrators in

Australian hospitals, the optimum resource allocation forinfection prevention and control programs is uncertainand there has been very little information in the literaturespecific to Australian settings to guide such decisions.Historically, infection control programs have often beenviewed as expensive overheads with little appreciationof the potential of such programs to produce financialbenefits whilst simultaneously improving the outcomeof patient care. It is evident that more local researchneeds to be done in this area to guide the decisionmakers.References1. Wilson R, Runciman WB, Gibberd RW, HarrisonBT, Newby L, Hamilton JD. The quality in Australianhealth care study. The Medical Journal of Australia.1995;163:458-471.11. Scheckler W, Brimhall D, Buck A, et al. Requirementsfor infrastructure and essential activities of infectioncontrol and epidemiology in hospitals: a consensuspanel report. American Journal of Infection Control.1998;26:47-60.12. Saint S, Veenstra DL, Lipsky BA. The clinical andeconomic consequences of nosocomial centralvenous catheter-related infection: are antimicrobialcatheters useful? Infection Control and HospitalEpidemiology. 2000;21:375-380.13. Centers for Disease Control and Prevention.Guidelines for the Prevention of IntravascularCatheter-related infections. Morbidity and MortalityWeekly Report (MMWR). 2002;51:1-29.14. Haley RW. The scientific basis for using surveillanceand risk factor data to reduce nosocomial infectionrates. Journal of Hospital Infection. 1995;30:3-14.2. Smith SD, Doebbeling BN. Costs of nosocomialinfections. Current Opinion in Infectious Diseases.1996;9:286-290.3. Centres for Disease Control and Prevention. Publichealth focus: surveillance, prevention and controlof nosocomial infections. Morbidity and MortalityWeekly Report. 1992;41:783-787.4. Kohn L, Corrigan J, Donaldson M. To err is human:buiding a safer health system. Washington, DC:Institute of Medicine; 1999.5. Plowman R, Graves N, Griffin M, et al. The Socioeconomicburden of hospital acquired infection.London: DoH/PHLS; 1999.6. Australian Infection Control Association ExpertWorking Group. National Surveillance of HealthcareAssociated Infections in Australia. A Report to theCommonwealth Department of Health and AgedCare; 2001.7. Davey P, Hernanz C, Lynch W, Malek M, Byrne D.Human and non-financial costs of hospital-acquiredinfection. Journal of Hospital Infection. 1991;18:79-84.8. Wenzel RP. The economics of nosocomial infections.Journal of Hospital Infection. 1995;31:79-87.9. Weinstein RA. Controlling antimicrobial resistancein hospitals: infection control and use of antibiotics.Emerging Infectious Diseases. 2001;7:188-192.10. Haley RW, Culver DH, White JW, Morgan WM, EmoriTG. The efficacy of infection surveillance and controlprograms in preventing nosocomial infections inUS hospitals. American Journal of Epidemiology.1985;121:182-205.36

Communicable Disease Control BranchInfection Control ServiceChris CopeAnita MarwoodThe Infection Control Service monitors healthcareassociated infection and antibiotic utilisation, identifyingtrends and feeding back information to contributinghospitals. The information is used by contributors intheir continuous quality improvement activities. 1 Thesystem is voluntary and includes both public and privatehospitals. Currently the Service conducts statewidesurveillance for bloodstream infections, multi-resistantorganisms and antibiotic utilisation. The followinghighlight some of the important trends noted since thesurveillance began, and presents accumulated data upuntil the end of 2005.All rates are expressed per occupied bed days (OBDs).Staphylococcus aureus is the most common organismcausing BSI in hospital patients, and is associated witha high morbidity and mortality. The number of episodescaused by S.aureus has fallen steadily over the past fiveyears in South Australian hospitals (Figure 2).The proportion of S.aureus isolates that are methicillinresistant(MRSA), has also sustained a downward trendsince the peak in 2000 of almost 48% to approximately30% in the past two years. In addition to interventionsaimed at improving intravenous line care, other effortsto control the spread of MRSA have contributed to thispositive result.Figure 2: Trend in nosocomial inpatient S. aureusbloodstream infection for seven major metropolitanhospitals.BLOODSTREAM INFECTIONSBloodstream infection (BSI) data are contributedcurrently by 14 South Australian metropolitan hospitals(8 public and 6 private). Healthcare associated BSIdata have been provided by seven major metropolitanhospitals since July 1996 (5 public and 2 private).Enhanced surveillance using revised national BSIdefinitions commenced in January 2002. 2Although intravascular devices remain the primaryfocus of bloodstream infection, the total number ofintravenous line-related episodes has fallen significantlysince 2002 (Figure 1). This is attributed to severalinterventions in the major metropolitan hospitalstargeted at improving intravenous line managementincluding (but not limited to) the widespread introductionof alcohol-based hand gels and the introduction of adedicated “Line Nurse” in one major hospital.Figure 1: Trend in nosocomial bloodstream infectionsin SA metropolitan hospitals.MULTI-RESISTANT ORGANISMS (MRO)MRSA surveillance has been in progress sinceSeptember 2001 and data have been voluntarilysupplied by 16 hospitals (8 public and 8 private). MROsurveillance was expanded in 2002 to incorporate otherresistant epidemiologically significant organisms and upto the end of 2005 was contributed to by 15 hospitals (7public and 8 private).Methicillin-resistant Staphylococcus aureus (MRSA)There were 786 episodes of new healthcare associatedMRSA acquisitions reported during 2005. This includesboth infections and carriage without clinical symptoms.While identification of new MRSA isolations has onlydecreased marginally (Figure 3), the infection rate hasdecreased significantly from 2.9 per 10,000 OBDs in2002 to 1.6 per 10,000 OBDs in 2005 (p

Figure 3: Relationship between new acquisition andinfection rates to the overall burden of MRSA incontributing hospitals.Figure 5: New MRO acquisitions for all participatingcontributors, grouped by resistance category.This chart highlights the success of statewidesurveillance and quality improvement activities, sincethe overall infection rate continues to trend downwardsdespite a continuing high MRSA burden. It should benoted that both the burden and new acquisition rates aresensitive to the intensity of screening practices, whichhave increased in several hospitals over the period.*”Other” includes VRE vanA and vanB, carbapenemresistantEnterobacteriaceae or Acinetobacter species,and vancomycin intermediate Staphylococcus aureus.Figure 6: MRO acquisitions by specimen category.Figure 4: MRSA infection rates stratified by intensivecare units (ICU) and all clinical units combined.In 2005, for other MROs (excluding MRSA), urinecontinues to be the most common site of isolationfollowed by respiratory isolates (Figure 6).As Figure 4 illustrates, the rate of MRSA infectionis highest in those patients who are most at risk forinfection, i.e. intensive care unit patients.Other multi-resistant organismsDuring 2005 there were 120 new episodes of infectionor colonisation with multi-resistant organisms (MROs)other than MRSA reported. These were predominantlymulti-resistant Pseudomonas aeruginosa (MR-PAER) andextended spectrum beta-lactamase (ESBL) producingorganisms. Figures 5 and 6 present aggregate datafor the 15 contributing hospitals. The incident casesare presented rather than rates, because the overallnumbers are small.ANTIMICROBIAL UTILISATIONThe South Australian statewide antimicrobialutilisation program was established in November2001. The program collects in-hospital antimicrobialusage data from both metropolitan and countryhospitals. Currently 14 metropolitan hospitals, 7public and 7 private, are contributing to the program,the results of which are discussed below. Data fromNovember 2001 to November 2005 are reported. Theantimicrobial utilisation rates provided are calculatedusing the number of defined daily doses (DDDs) of theantimicrobial agent/class consumed per 1000 occupiedbed days (OBDs).Monthly analysis of aggregate data suggests an upwardtrend in total antimicrobial consumption (Figure 7).38

Figure 7: Total monthly aggregate antimicrobialusageFigure 10: Annual usage by class - ICUCorresponding aggregate usage rates for intensivecare units (ICU) suggest a downward trend (Figure8); however the considerable monthly fluctuations inantimicrobial usage in these units make assessment oftrends difficult. Analysis of usage within individual unitshas demonstrated a large variation in usage patterns.While statewide usage rates for some antimicrobialclasses appear to show no significant trend over thisperiod, increasing use of fluoroquinolones, in particularciprofloxacin, is evident for both total (Figure 11) and ICUusage (Figure 12).Figure 11: Total aggregate fluoroquinolone usageFigure 8: ICU monthly aggregate antimicrobial usage.Figure 12: ICU aggregate fluoroquinolone usageTotal aggregate annual usage rates by antimicrobial classare shown in Figure 9.Figure 9: Annual usage by class - total hospitalICU annual usage rates by antimicrobial class are shownin Figure 10.39In recent years, the emergence of a highly virulent formof Clostridium difficile, associated with high morbidityand mortality, has been reported in the USA and Canada,and has now also been documented in Europe. Diseaseassociated with this new strain has been shown tooccur with increased frequency and severity, and highrates of recurrence have also been noted. A clearassociation with the use of fluoroquinolones has beendemonstrated in outbreaks, with increased resistance tothese antimicrobials documented. 3

While ongoing monitoring and analysis over a longertime period is required to confirm changes in utilisationrates, some trends in usage of individual antimicrobialclasses and agents within classes are evident.Intervention programs to modify prescribing patternsfor classes linked to the emergence of multi-resistantspecies and other organisms, such as Clostridiumdifficile, should be considered a priority for all SouthAustralian hospitals.References1. Haley RW. The scientific basis for using surveillanceand risk factor data to reduce nosocomialinfection rates. Journal of Hospital Infection.1995;30(Supplement):3-14.2. An Expert Working Group of the Australian InfectionControl Association. Blood Stream Infection (BSI)Definition. National Surveillance of HealthcareAssociated Infection in Australia. Approved byHealthcare Associated Infections Advisory Committeeof Safety and Quality–Sept 04. Available from: http://www.safetyandquality.org/index.cfm?page=Action#suvlncdefine3. Bartlett J, Perl T. The New Clostridium difficile - WhatDoes It Mean? New England Journal of Medicine.2005;353(23):2503-5.For further information regarding either definitions usedor information discussed in this report please refer tothe “Definitions” section of the Infection Control Servicewebsite. http://www.healthsa.sa.gov.au/infectioncontrol/Communicable DiseaseControl Branch Report– 01 July to 31 December 2005VECTORBORNE DISEASESRoss River virusThere were 64 cases reported during this period. A totalof 57 cases were notified in 2004 (26 males, 38 females,age range: 8 to 85 years). The majority of cases eitherresided in or reported recent travel to the Riverland,South-East and Far North of South Australia.The last major outbreak of Ross River virus infections inSouth Australia occurred during the summer of 2000-2001. Figure 1 (see below) illustrates 3 to 4 yearly cyclicincreases in the number of cases of Ross River virusinfection.Barmah Forest virusIn the period under review, 15 cases of Barmah Forestvirus infection were reported. A total of four cases werereported for the same period in 2004. Of the 15 cases,ten (67%) either resided in or reported travel to ruralSouth Australia.An epidemic curve and source map illustrating RossRiver virus activity in South Australia can be viewedon our web site: http://www.health.sa.gov.au/pehs/.Information on preventing vector borne diseases andFight the Bite campaign can also be obtained by visitingthis website.Dengue feverThere were three reports of dengue fever in people whoreported recent travel to Asia (one male, two females,age range: 14 to 45 years).40

MalariaNineteen cases of malaria were reported (nine males,ten females, age range: 4 to 62 years). Of the 19 cases,13 were Plasmodium falciparum, five were Plasmodiumvivax and there was one mixed infection of Plasmodiumvivax and Plasmodium falciparum. Cases infected withPlasmodium falciparum reported exposure in Africawhile Plasmodium vivax cases reported recent travel toSouth-East Asia and the Pacific region.ZOONOSESQ feverThere were 6 reports of Q fever (five males, one female,age range: 22 to 53 years). Five cases reported variousrisk factors associated with animal contact and the othercase reported no known risk factors.VACCINE PREVENTABLE DISEASESPertussisA total of 757 cases were notified during this period.Cases were geographically dispersed throughoutmetropolitan and rural South Australia. For thecorresponding period in 2004 there were 800 pertussiscases reported. Figure 2 illustrates the increase innumber of cases reported by age grouping and year ofonset of illness.Invasive Haemophilus influenzaeEight cases of Haemophilus influenzae were notified(five males, three females, age range: 23 to 92 years).Of the eight cases, five were typed as non-groupable,the serogroup was unknown for two cases and one casewas identified as serogroup F.MumpsFive cases of mumps were notified during this period(one male, four females, age range: 25 to 65 years).Vaccination status was unknown for three cases and theother two cases had not been vaccinated.41

InfluenzaSouth Australian influenza surveillance combineslaboratory-confirmed cases reported by the Institute ofMedical and Veterinary Science and South Path, withclinical diagnoses of ‘influenza-like illness’ collected bythe Royal College of General Practitioners membersparticipating in the Australian Sentinel Practice Network,and emergency departments of several public hospitals.In the period under review, there were 167 influenza Aand 49 influenza B laboratory isolates reported.The strains from South Australia typed in 2005 by theWHO Collaborating Centre for Reference and Researchon Influenza (www.influenzacentre.org) were mainlyA/H3/California/7/2004-like and B/Shanghai/361/2002-like. There have also been positive cultures of A/H3/Wellington/1/2004-like, B/Hong Kong/330/2001-like andA/H1/New Caledonia/20/99-like.Invasive pneumococcal diseaseThere were 76 cases of pneumococcal disease reportedduring this period (37 males, 39 females, age range: 8months to 92 years). Four of the cases were indigenous.Eight (11%) cases were notified in children less than fiveyears of age. Four deaths were linked to this disease.GASTROINTESTINAL DISEASESCampylobacterCampylobacter infection remains the most commonlyreported notifiable disease in South Australia. In theperiod under review, 1238 notifications were receivedfor residents of metropolitan Adelaide and rural SouthAustralia. This compares with 1079 cases notified duringthe corresponding period in 2004.A cluster of 14 cases of Campylobacter infection wasassociated with a school in metropolitan Adelaide.An analytical study showed a significant associationbetween illness and eating a meal at the school. Thesource of the illness was not identified.CryptosporidiosisSixty three cases were reported (31 males, 32 females,age range: 1 month to 81 years). No clusters oroutbreaks were identified.Hepatitis AIn the period under review there were seven cases ofhepatitis A notified. Four of the seven cases were partof a cluster that was investigated by the CommunicableDisease Control Branch. Three of the four (two males,two females, age range: 7 to 52 years) cases resided in aremote South Australian town and the other resided in aneighbouring town. Two cases were indigenous. No directcontact between the four cases could be established.Health information and an expanded immunisationprogram were implemented in the local area.42The other three cases (three males, age range: 43 to 57years) reported recent overseas travel to endemic areasfor hepatitis A infection and interstate travel.ListeriosisFive cases of listeriosis were notified in the reportingperiod (three females, two males, age range: 53 to 73years). One of the cases was Listeria monocytogenesserogroup 4 and four cases were Listeriamonocytogenes serogroup 1.The four Listeria moncytogenes serogroup 1 cases wereinvestigated as a cluster. Prior to illness onset all caseshad admissions to one or several health care facilities.Three had underlying immuno-compromising illnessesand two died. Results of molecular typing established alink between contaminated food and illness in two casesassociated with one particular health care facility. Theremaining two cases had molecular typing different fromeach other and different from the common strain sharedby the contaminated food and the two cases associatedwith a particular health care facility.ShigellosisThere were 30 cases of shigellosis reported (11 males,19 females). Of these, Shigella flexneri type 4a mannitolnegative and Shigella sonnei biotype g were the mostfrequently reported species.Transmission of Shigella flexneri type 4a mannitolnegative was associated with living in remotecommunities in South Australia. In total, eight caseswere reported (three males, five females, age range: 4to 68 years); seven of these were indigenous.Eight cases of Shigella sonnei biotype g infection werenotified during this period (four males, four females,age range: 5 to 67 years). Six cases reported recentoverseas travel.Shiga toxin producing Escherichia coliThirteen cases were reported during the period underreview (five males, eight females, age range: 8 to90 years). The majority of cases were residents ofmetropolitan Adelaide. No common exposure or sourceof illness was identified among the cases.SalmonellosisIn the period under review, 294 cases of salmonellosiswere reported. The most commonly reported wereSalmonella Typhimurium phage type 64 (44 cases),Salmonella Typhimurium phage type 44 (29 cases),Salmonella Infantis (23 cases), Salmonella Typhimuriumphage type 9 (14 cases), Salmonella Typhimurium phagetype 108 (13 cases), Salmonella Typhimurium phage type135a (12 cases) and Salmonella Typhimurium phage type135 (11 cases).

Salmonella Typhimurium phage type 44The Communicable Disease Control Branch investigatedan outbreak of Salmonella Typhimurium phage type44 associated with a child care centre (16 cases)and community cases (13 cases) that occurredsimultaneously. Investigations were unable to identifythe source of the infections; however person to persontransmission is a likely explanation for the illness in thechild care centre.Salmonella ParatyphiThere were two cases of paratyphoid fever notifiedduring this period. One case was identified asSalmonella Paratyphi A in a 30 year old female and theother was identified as Salmonella Paratyphi B in a 19year old female. Both cases reported recent travel toAsia.Salmonella TyphiOne case was notified in a 26 year old female whoreported recent exposure in Africa.OUTBREAKS OF GASTROENTERITISDuring this period, a total of 16 outbreaks ofgastroenteritis were investigated by the CommunicableDisease Control Branch. Of the 16 outbreaks, 14 werereported in aged care facilities. Norovirus infectionwas identified as the infecting agent for eight of the14 outbreaks reported in aged care facilities. No agentwas identified for the other six outbreaks in aged carefacilities.Norovirus was also identified as the agent responsiblefor two sporadic outbreaks of gastrointestinal illness at arestaurant (22 patrons affected) and at a private function(ten persons affected).OTHER DISEASESLegionellosisThere were 30 sporadic cases of legionellosis reportedduring this period. Of the 30 cases 23 (14 males, ninefemales, age range: 25 to 88 years) were Legionellalongbeachae, four (three males, one female, age range:37 to 83 years) were Legionella pneumophila serogroup1 and three cases (two males, one female, age range:54 to 82 years) were Legionella pneumophila serogroup2. Legionella pneumophila serogroup 2 was detectedin a domestic hot water system. This is likely to be thesource of the infection for one of the cases of Legionellapneumophila serogroup 2.Invasive meningococcal diseaseThere were 18 laboratory confirmed cases ofmeningococcal disease reported (nine males, ninefemales, age range: 4 months to 77 years). Of the 18cases, 15 were identified as serogroup B, two wereidentified as serogroup C and one was identified asserogroup Y. There was one death in an 11 month oldchild from rural South Australia.The Public Health Bulletin South Australia is a publication of the S.A. Department of Health. The Bulletin aims to providecurrent data and information to practitioners and policy makers emphasising the value of orienting services towardsprevention, promotion and early intervention and to support effective public health interventions.The Editorial team welcomes correspondence and suggestions for public health/ primary prevention themes for futureeditions of the PHBSA. Please email phbsa@health.sa.gov.au or write toThe Managing Editor, Public Health Bulletin South Australia, Health Promotion Branch, Department of Health,PO Box 287, Rundle Mall, Adelaide 5000 or fax (08) 8226 6133. Comments and reports should be 500 – 600 words.Guidelines for authors are available from the managing editor.To add your name to the distribution list for the Public Health Bulletin South Australia please email: phbsa@health.sa.gov.auThe PHBSA can also be accessed in PDF format from http://www.dh.sa.gov.au/pehs/publications/public-health-bulletin.htmThe articles appearing in this publication represent the views of the authors and not necessarily those of the Minister forHealth or the Department of Health. No responsibility is accepted by the Minister for Health or the Department of Healthfor any errors or omissions contained within this publication. The information contained within the publication is forgeneral information only. Readers should always seek independent, professional advice where appropriate and no liabilitywill be accepted for any loss or damage arising from reliance upon any information in this publication.43

Notifiable Diseases in South Australia 1 July 2005 to 31 December 2005