Volume 168 Issue 3

Prevalence of tuberculosis infection in Melbourne secondary school students Paul D R Johnson, John B Carlin, Catherine M Bennett, Peter D Phelan Michael Starr, Jane Hulls and Terry M Nolan MJA 1998; 168: 106-110 Abstract - Introduction - Methods - Statistical analysis - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1998 Abstract Objective: To estimate the prevalence of asymptomatic Mycobacterium tuberculosis infection in Melbourne secondary school students. Design: Cross-sectional Mantoux testing of a partly random and partly targeted sample of secondary school students, designed to enable estimation of prevalence by region of birth. Setting: Fifty-one State and Catholic secondary schools in metropolitan Melbourne during 1995. Participants: Australian and overseas-born students in Years 9 and 10. Outcome measures: Proportions of students with positive Mantoux reactions (defined as induration at 48 hours of ≥5 mm with a history of recent exposure; ≥10 mm and no prior BCG vaccination; ≥15 mm and prior BCG vaccination). Results: Of 2586 students potentially eligible for testing, evaluable results were obtained from 1274 (49%). The overall prevalence of infection for Melbourne students in Years 9 and 10 was 2.5% (95% CI, 1.1-3.9%). Main predictors of a positive test were birth overseas and number of years residing overseas. Prevalence varied considerably by region of birth, and was very low in students born in Australia (0.7%), "other developed countries" (0.7%), and Southern Europe (0). The highest rates were observed in students born in Indochina (15.9%), other countries in South East Asia (10.2%), and Eastern Europe (10.2%). Conclusions: The risk of a young person becoming infected with M. tuberculosis while living in Melbourne is very low. Our results do not indicate a need for the reintroduction of mass screening in Victorian schools. If targeted screening were to be considered, the group most likely to benefit would be recently arrived migrants from Indochina. Introduction Human infection with Mycobacterium tuberculosis is usually clinically silent, and may then only be detectable by a positive Mantoux skin test. A minority of infected individuals develop active tuberculosis (TB), and those with pulmonary disease are the major source of new human infections. For M. tuberculosis to persist within a community over time, each person with pulmonary TB must infect an average of 20 others.1,2 In developed countries, the transmission rate is much lower than this, and the incidence of tuberculosis has declined steadily for many years.2 In the United States, a 32-year trend of declining TB notifications was reversed in the mid 1980s.3 This resurgence is thought to have resulted in at least 51 000 unexpected cases of the disease, and has been attributed to the impact of AIDS, urban decay, homelessness and high levels of migration from regions where TB is endemic.4 Recent increases in incidence have also been reported from other developed countries, including Denmark, Italy, the Netherlands, Spain, Switzerland, France and the United Kingdom.5 In Australia, the incidence of TB has remained constant during the 1990s (rates per 100 000 population of 5.95 in 1990 and 5.75 in 1995).6 In Victoria, the annual incidence of TB per 100 000 declined from 47 in 1954 to 6.2 in 1992;7 it was 6.35 in 1995.6 In 1970 40% of new cases of active tuberculosis in Victoria were in people born overseas, but by 1990 this figure had risen to 80%. Currently, most new TB patients are migrants from Indochina and South East Asia.7 Although intending adult migrants are screened by chest x-ray before their arrival in Australia, migrant children are generally not screened, partly because childhood tuberculosis is not normally transmissible. In a recent inner-Sydney study, 27% of foreign-born Year 8 students (159 of 580), compared with 2% of those born in Australia (20 of 1221), had positive Mantoux reactions.8 As adolescents appear to have an increased risk (compared with children over three years and adults) of developing active tuberculosis,9 this group may become a source of new, locally acquired infection. During 1995, we conducted a Mantoux survey of healthy metropolitan Melbourne secondary students in Years 9 and 10. Our aim was to estimate the prevalence of asymptomatic TB infection, and to identify specific groups of students by region of birth who may benefit from future targeted screening and intervention programs. Methods The study was a cross-sectional survey of secondary school students in the metropolitan region of Melbourne (population, 3.1 million, with people aged 12 to 17 years comprising approximately 8% [Australian Bureau of Statistics, 1996 Census]). To recruit enough overseas-born students for estimating prevalence by region of birth, we used a combination of targeted and random sampling, aiming to include schools where at least 4% of students were born overseas, plus a 5% random sample of all other schools. The Australian Bureau of Statistics (ABS) provided numbers and country of birth of Melbourne residents aged 12 to 17 years from the 1991 national census. The Directorate of School Education and the Catholic Education Office provided numbers of students at each school speaking a language other than English at home. These data were combined and used to select schools with high enrolments of overseas-born students. Independent schools were not included as they comprised only 18% of all Year 9 and Year 10 students (Directorate of School Education, personal communication), and we assumed that they would have a low proportion of recently arrived overseas-born students. Of 50 purposely selected and seven randomly selected schools approached, six and one, respectively, declined. The randomly selected school was replaced by a neighbouring school, so that 51 schools participated. Parents of all students in Years 9 and 10 at each participating school were provided with an explanatory letter and a short survey (in English and, if appropriate, one of 12 translations). The survey was part of a separate study on asthma, but included a question on country of birth and sought permission to approach students a second time for the TB study. The initial (asthma) survey was distributed to all 13 020 Year 9 and Year 10 students at the 51 schools; 9794 usable responses were obtained (75%). Respondents comprised 85% from purposely selected and 15% from randomly selected schools. From the returned surveys we created 12 notional region-of-birth groups, based partly on geography and partly on numbers of respondents to the first survey, and an additional group comprising Australian-born students with both parents born in Asia (Box 1). We aimed to enrol approximately 200 students from each group to allow us to estimate prevalence within each with a 95% confidence interval of ± 1.9% if the true prevalence were 2%, and ± 6.4% if the true prevalence were 30%. Selection for Mantoux testing was random, except when the number of respondents in a category was less than 200, in which case all respondents from that region were included. Parents of students selected for Mantoux testing were sent information letters, consent forms and a TB survey (in English and one of 14 translations). This survey sought parental consent for Mantoux testing and included questions on parents' country of birth, date of arrival in Australia and history of BCG vaccination. Mantoux testing (by two experienced nurses, with two assistants from the Victorian Tuberculosis Program) was performed at school. Responses on each TB survey were checked for completeness and each student's deltoids, forearms and scapulas inspected for the presence of BCG vaccination scars before testing, which involved intradermal injection of 0.1 mL of a 100 IU/mL solution of purified protein derivative (PPD; CSL Limited, Parkville, Vic.) to the volar aspect of the student's left forearm. A single batch of PPD was used throughout. At between 48 and 72 hours, the extent of transverse palpable induration was measured by ruler and recorded in millimetres. The study was approved by the Ethics in Human Research Committee of the Royal Children's Hospital. Statistical analysis We used the exact binomial method for confidence intervals and the chi-squared test for comparisons between groups. Logistic regression was used to estimate prevalences, adjusted for differences in duration of residence in Australia. As we had deliberately selected schools with high concentrations of foreign-born students, we estimated overall prevalence of infection by direct standardisation to the population distribution of region of birth in students aged 12 to 17 years in metropolitan Melbourne (1991 Census data, ABS). Results Of 2586 students (the results of our efforts to create the 13 groups) sent the TB survey, 620 (24.0%) did not return it, and 692 (27%) returned completed surveys but declined to be tested or were away on the day of testing. Test results were therefore available for 1274 students (49%). To explore the potential for response bias, survey response rates and acceptance of testing were compared between subgroups defined by age, sex and time since arrival in Australia (Box 2). Younger students and females were statistically more likely to return their surveys than older students and males (data not shown), but refusal to be tested did not vary between these subgroups. Proportions of students with Mantoux reactions that were positive by National Health and Medical Research Council criteria (≥5 mm with a history of recent exposure; ≥10 mm and no prior BCG vaccination; ≥15 mm and prior BCG vaccination8,10 ) were compared by region-of-birth group (Box 3). Birth overseas, number of years resident outside Australia (Box 4) and past BCG vaccination were predictors of a positive result. The crude prevalence was 5.3%. After standardisation by region of birth, we estimated that 2.5% of all students in Years 9 and 10 in metropolitan Melbourne had positive Mantoux results (95% CI, 1.1-3.9%). Students born in Australia, "other developed countries" and Southern Europe had the lowest rates (0.7%, 0.7% and 0, respectively). The highest rates were observed in students born in Indochina (15.9%), other countries in South East Asia (10.2%), and Eastern Europe (10.2%) (Box 3). Differences in mean number of years resident overseas between the groups prevented direct statistical comparison, so logistic regression was used to estimate the odds ratio for increase of risk for each year lived overseas (odds ratio per year, 1.15; 95% CI, 1.08-1.24), and to standardise rates by region so they could be compared directly. After this adjustment, statistically significant differences in prevalence by region persisted, but the ranking of some regions, most notably Eastern Europe, was altered (Box 3). Prevalence of TB in the group of Australian-born students with Asian-born parents was 3.6%. None of these students had received a prior BCG vaccination. This prevalence was fivefold higher than the background rate of 0.7% for other students born in Australia, but this difference did not reach statistical significance (P = 0.17, two-tailed Fisher's exact test). The 244 students with a result ≥10 mm and the two with a result ≥5 mm plus a history of exposure to someone known to have TB were referred to a special clinic at the Royal Children's Hospital for chest x-ray and clinical review. However, 10 students with indurations ≥10 mm declined to attend the clinic, five of whom had positive Mantoux reactions. Of the 236 students who attended the clinic, 174 had at least one BCG vaccination scar and/or documentary evidence of BCG vaccination and a Mantoux reaction < 15 mm; these were therefore considered to have negative results. Students with results positive by NHMRC criteria8,10 were offered isoniazid preventive therapy, provided there was no evidence of active disease and they had not been previously treated. Sixty-two students had positive Mantoux reactions. Of these, seven had previously been prescribed isoniazid preventive therapy, two had previously been treated for TB disease, and one (a recently arrived refugee from East Timor) had active pulmonary TB. Five students refused isoniazid therapy, and five were not offered therapy as they were considered to have a reduced risk (recent BCG). Forty-two students with positive Mantoux reactions were offered isoniazid preventive therapy; 38 (90%) completed six months of treatment. Multiple BCG scars (evidence of previous vaccinations) were common in students from Eastern Europe (mean number, 1.6; 33% of students with ≥2 scars) and the Middle East, whereas those from Indochina generally had only one (mean number, 0.9; 11% of students with ≥2 scars). Discussion The risk of a young person becoming infected with M. tuberculosis while living in Melbourne appears to be very low. The major determinant of the size of the Mantoux reaction in this study was birth overseas. However, most students with reactions to testing had also received at least one prior BCG vaccination, which complicates interpretation. Most Australian-born students had not been vaccinated, and the prevalence of infection in this group was very low (0.7%, giving a calculated annual risk of infection of 0.04% per year). The higher prevalence in Australian-born students with Asian-born parents may be the result of low-level transmission within migrant communities, although the apparent difference could have been due to chance. For those born overseas, the number of years spent outside Australia correlated positively with Mantoux results, indicating that the risk of infection increases with duration of residence in an endemic region. The prevalence of infection in Year 9 and Year 10 students in metropolitan Melbourne appeared to be approximately half that identified in a recent survey in Year 8 students in inner Sydney, both overall and within specific migrant subgroups.8 The authors of the Sydney study commented that the prevalence they identified was higher than previously reported in Australia and have since found a slightly lower prevalence in a further survey of younger students.11 Our lower rate may be the result of differing patterns of migration between Melbourne and Sydney, or the selection of our sample from the whole metropolitan region instead of just the inner city. Although only half of eligible students in our study were tested, we do not believe that our results are systematically biased in a way that would have led us to grossly underestimate prevalence. In particular, we found no association between recent arrival in Australia and the likelihood of refusing to be tested, and the group with the lowest participation rate (Eastern Europe) showed the second-highest prevalence. In retrospect, acceptance of testing may have been improved by selecting whole classes rather than individuals within a class for testing, and our two-stage study design allowed ample opportunity for students to withdraw. However, any future targeted screening program would need to select individuals from within a larger group, and part of our study rationale was to investigate the acceptability of such programs. Even if it were assumed that non-participants had twice the prevalence of those tested, the true prevalence would only be 50% greater than our estimates. There is controversy about the influence of BCG vaccination on the results of subsequent Mantoux testing. In countries with a high prevalence of TB infection, a single BCG vaccination is often given shortly after birth, but this is unlikely to influence the result of a Mantoux test 15 years later.12 By contrast, BCG given to older children or given several times during childhood probably does influence Mantoux reaction size.13 Although the current NHMRC guidelines make some allowance for past BCG vaccination, they could be further refined.13 For example, for recently arrived migrants who have received a single BCG vaccination early in life and who have lived for many years in a region of high prevalence it may be appropriate to use ≥10 mm to indicate a positive reaction, while for migrants from countries that routinely give three BCG vaccinations in childhood but have a lower prevalence of infection ≥20 mm may be more appropriate.13 Whether or not such refinements are introduced, the distinction between positive and negative reactions will remain somewhat arbitrary; a more reliable test is urgently required. Mass screening of secondary school students by Mantoux test was discontinued in Victoria over 10 years ago. Our results do not suggest that such programs need to be reintroduced, and recent overseas studies suggest that mass screening at school is unlikely to be cost effective.14-16 However, 24% of overseas-born students in our study had Mantoux reactions ≥10 mm, one of whom had active pulmonary disease and one-quarter of whom were considered eligible for isoniazid preventive therapy. If reactions of ≥10 mm for students born in a high-risk region with a history of having received a single BCG vaccination in infancy were considered positive, the number of students eligible for preventive therapy would increase further. If targeted screening were introduced, the group most likely to benefit would be recently arrived students from Indochina. We offered isoniazid therapy to students who tested positive because adolescents have an increased risk of developing active tuberculosis.9,17 However, we were mindful that isoniazid therapy is not entirely without risk even in young people,18-20 and that the risk of infection progressing to disease in an affluent society with a low prevalence of HIV infection may be much lower than the 10% often quoted.21 We cannot therefore be completely confident that wider use of isoniazid in this way would result in a net benefit to the Australian community. Acknowledgements This study was supported by a grant from the John Burge Estate administered by the Victorian Department of Human Services. We gratefully acknowledge the assistance of the principals, coordinators, teachers, students and parents at the participating schools. We also wish to thank the following individuals: Mary Randall, Mary McColl and staff of the Victorian Tuberculosis Program; Marita Dalton, Colin Powell, Department of Thoracic Medicine; and Susan Sawyer, Centre for Adolescent Health, Royal Children's Hospital. References Bates JH, Stead WW. The history of tuberculosis as a global epidemic. Med Clin North Am 1993; 77: 1205-1217. Styblo K. Recent advances in epidemiological research in tuberculosis. Tuberc Res 1980; 20: 1-63. Centers for Disease Control and Prevention. Tuberculosis morbidity -- United States, 1992. MMWR Morb Mortal Wkly Rep 1993; 42: 696-704. Snider DE Jr, Raviglione M, Kochi A. Global burden of tuberculosis. In: Bloom BR, editor. Tuberculosis: pathogenesis, protection and control. Washington DC: ASM Press, 1994: 3-12. Raviglione MC, Sudre P, Rieder HL, et al. Secular trends of tuberculosis in western Europe. Bull World Health Organ 1993; 71: 297-306. Oliver G, Harvey B. Tuberculosis notifications in Australia, 1995. Commun Dis Intell 1997; 21: 261-269. MacIntyre CR, Dwyer B, Streeton JA. The epidemiology of tuberculosis in Victoria. Med J Aust 1993; 159: 672-677. Alperstein G, Fett MJ, Reznik R, et al. The prevalence of tuberculosis infection among year 8 schoolchildren in inner Sydney in 1992. Med J Aust 1994; 160: 197-201. Comstock GW, Livesay VT, Woolpert SF. The prognosis of a positive tuberculin reaction in childhood and adolescence. Am J Epidemiol 1974; 99: 131-138. National Health and Medical Research Council. Tuberculosis in Australia and New Zealand into the 1990s. Canberra: AGPS, 1990. Alperstein G, Morgan KR, Fett MJ, et al. Prevalence of tuberculosis infection among primary school-entry children in Sydney. A N Z J Pub Health 1996; 20: 123-128. Menzies R, Vissandjee B. Effect of bacille Calmette-Guerin vaccination on tuberculin reactivity. Am Rev Resp Dis 1992; 145: 621-625. Ildirim I, Hacimustafaoglu M, Ediz B. Correlation of tuberculin induration with the number of Bacillus Calmette-GuŽrin vaccines. Ped Infect Dis J 1995; 14: 1060-1063. Driver CR, Valway SE, Cantwell MF, Onorato IM. Tuberculin skin test screening in schoolchildren in the United States. Pediatrics 1996; 98: 97-102. Mohle-Boetani JC, Miller B, Halper M, et al. School-based screening for tuberculous infection: a cost-benefit analysis. JAMA 1995; 274: 613-619. Starke JR. Universal screening for tuberculosis infection: school's out! JAMA 1995; 274: 652-653. Katz J, Kunofsky S. Logistics of chemoprophylaxis of tuberculosis. Chest 1971; 59: 600-605. Gal AA, Klatt EC. Fatal isoniazid hepatitis in a child. Ped Infect Dis J 1986; 5: 490-491. Israel HL, Gottlieb JE, Maddrey WC. Perspective: preventive isoniazid therapy and the liver. Chest 1992; 101: 1298-1301. Millard PS, Wilcosky TC, Reade-Christopher SJ, Weber DJ. Isoniazid-related fatal hepatitis. West J Med 1996; 164: 486-491. Haas DW, Des Prez RM. Mycobacterium tuberculosis . In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 4th ed. New York: Churchill Livingstone, 1995: 2213-2243. (Received 23 May, accepted 27 Sep, 1997) Authors' details Clinical Epidemiology and Biostatistics Unit, Royal Children's Hospital, Melbourne, VIC. Paul D R Johnson, FRACP, PhD, Research Officer, Royal Children's Hospital Research Institute (also, Infectious Diseases Physician, Department of Infectious Diseases and Clinical Epidemiology, Monash Medical Centre); John B Carlin, BSc(Hons), PhD, Deputy Head (also, Associate Professor, University of Melbourne, Department of Paediatrics); Catherine M Bennett, BSc(Hons), Research Officer; Jane Hulls, RN, Research Nurse; Terry M Nolan, PhD, FRACP, Head (also, Associate Professor, University of Melbourne, Department of Paediatrics). University of Melbourne, Department of Paediatrics, Royal Children's Hospital, Melbourne, VIC. Peter D Phelan, MD, FRACP, Stevenson Professor, and Head (currently, Emeritus Professor of Paediatrics). Department of Microbiology and Infectious Diseases, Royal Children's Hospital, Melbourne, VIC. Michael Starr, MB BS, FRACP, Paediatrician. Reprints: Dr P D R Johnson, Department of Infectious Diseases and Clinical Epidemiology, Monash Medical Centre, Clayton, VIC 3168. E-mail: Paul. Johnson AT med.monash.edu.au Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Paul D R Johnson FRACP, PhD · John B Carlin · Catherine M Bennett · Peter D Phelan · Michael Starr · Jane Hulls · Terry M Nolan

Tuberculosis in children in Australia: strategies for control David Isaacs and Craig M Mellis, on behalf of the Paediatric Special Interest Group of the Australasian Society for Infectious Diseases* and the Australasian Paediatric Respiratory Group** MJA 1998; 168: 121-124 Introduction - Epidemiology - Childhood tuberculosis - Child advocacy - Control of tuberculosis - Acknowledgements - References - Paediatric Special Interest Group of ASID - Australasian Paediatric Respiratory Group - Authors' details - - ©MJA1998 Introduction Globally, tuberculosis (TB) is responsible for more deaths per year than any other infection. The World Health Organization estimated that in 1990 there were 7.5 million new cases of TB; 1.3 million were in children under 15 years of age, of whom 450 000 died.1 TB is relatively rare in Australian children, but, because of the associated high morbidity and mortality and the risk of later reactivation of disease, it should not be neglected. This paper outlines strategies to control paediatric TB. Tuberculosis in childhood is different from that in adults, and requires different expertise. This position paper, a consensus by paediatric infectious disease and respiratory specialists, outlines strategies for managing childhood TB in Australia. A companion paper, in preparation, will address strategies applicable to New Zealand. A further paper will deal with specific details of management of paediatric tuberculosis, including diagnosis and treatment. Epidemiology While the incidence of TB in industrialised countries has fallen to very low levels with improving living conditions, in the United States the steady decline in incidence of TB has halted. From 1985 to 1992 there was a 20% increase in reported cases in both adults and children1-4 (although this situation has now improved5 ). Further, the US has experienced an increase in the prevalence of infection with multidrug-resistant strains of TB.2,4 This increase was the result of an association of HIV infection and TB, increasing poverty, immigration from countries with high TB prevalence, and decreased public health funding.4,5 The re-emergence of TB as a problem in the USA has caused other industrialised countries to re-examine policies for the prevention and management of this disease. Tuberculosis is not presently a major problem in Australia. Its incidence has remained stable since 1986 at 5.5-6.0 cases per 100 000 population per year.6-9 The number of notified cases in children aged 0-14 years has fallen from 70 in 1991, to 45 in 1992, 37 in 1993, and 33 in 1994.7-9 Two childhood deaths from TB were notified in 1992; none have been notified since. While most TB notifications are made from New South Wales and Victoria, the rate of notifications is highest in the Northern Territory. The notification rate is lowest in non-indigenous Australian-born people (1.5-2.0 per 100 000), while Aboriginality is associated with a higher incidence (10-13 per 100 000).8,9 However, being born overseas is associated with an even higher incidence, which has been consistently reported at around 15 per 100 000 for the past three years.7-9 Childhood tuberculosis Starke10 has emphasised the differences between paediatric and adult tuberculosis. Children generally have a much smaller bacterial population and there is less secondary resistance. Cavitary lesions are very rare, but children have a greater propensity for extrapulmonary disease. While children tolerate higher doses of medication relative to body weight, with lower rates of adverse reactions, paediatric formulations (syrups or soluble powders) are not always available. Paediatric tuberculosis is usually acquired from contact with an infected adult, and children with TB are generally at low risk of infecting others. Child advocacy In Australia, children with suspected or proven tuberculosis may be managed by paediatricians, at adult chest clinics, or by specialists in paediatric or adult infectious diseases.9 Given the low incidence of childhood cases, this variety of attending specialists is not surprising and does not necessarily mean that current management of paediatric TB is inappropriate. In large cities there may be enough children with TB or receiving preventive therapy to warrant specialised paediatric TB clinics that combine both paediatric and public health expertise. However, in many parts of Australia, children with TB or TB contact are managed in chest clinics by chest physicians who are expert in tuberculosis, but may lack paediatric knowledge and skills. On the other hand, the regional paediatrician, with experience in examining and managing children, may have little knowledge and experience of childhood tuberculosis. Although paediatric TB is rare, child contacts of adults with TB are much less rare, and preventive therapy of children requires expert knowledge and supervision.3,10 Guidelines on tuberculosis concentrate on adult aspects of TB, and tend to neglect paediatric aspects.11-13 As paediatricians are child advocates and experts in child health, they should be more involved in the care of children with TB,14 not necessarily as sole carers, but at least in consultation. Paediatricians can provide clinical expertise and advice in areas such as compliance with medication, particularly for very young children. Recommendation: Paediatricians should be consulted and involved in the management of TB in children whenever possible. [Consensus view, not addressed by the NHMRC TB Working Party.11] Control of tuberculosis The most critical aspect of control of tuberculosis is the existence of appropriate public health programs. The important strategies in TB control are: BCG vaccination; Screening of children at high risk; Contact tracing; and Appropriate duration of drug therapy. BCG vaccine Bacille Calmette-Guerin (BCG) vaccine was first used in humans in 1921, and few attempts have been made since then to develop improved vaccines against TB. BCG vaccine is moderately effective: a recent meta-analysis15 gave its protective efficacy as 50% against any TB disease, 64% against TB meningitis, and 71% against death from TB. Occasional cases of TB meningitis occur in children in Australia6-9 and might be prevented by BCG vaccination. The NHMRC TB Working Party currently recommends BCG vaccination for three groups of children:11 Aboriginal and Torres Strait Islander neonates in regions of high incidence; Neonates born to patients with leprosy (because of cross-protection by BCG against leprosy); and Children under the age of five years who will be travelling to live in countries of high TB prevalence for long periods. The NHMRC TB Working Party11 states that BCG vaccine should be considered for: Neonates who will be living in a household which includes immigrants or visitors recently arrived from countries of high TB prevalence (and neonates in families who have returned to visit the homes of relatives in countries of high prevalence); and Children and adolescents aged less than 16 years who continue to be exposed to a patient with active TB, and where the child or adolescent cannot be given preventive isoniazid therapy, or the person with active disease has organisms resistant to both rifampicin and isoniazid. We believe these latter two "considerations" should be changed to "recommendations" to prevent occasional, but devastating, cases of tuberculosis in these children. In particular, neonates whose parents are from South-East Asia or the Indian subcontinent should be given BCG at birth. There is currently no information on how many children receive BCG vaccine in Australia each year, either as an absolute number or as a proportion of those eligible. Clearly, such information would be a great advantage in analysing BCG vaccine efficacy, and thus in evaluating the current NHMRC recommendations. The Australian Childhood Immunisation Register, implemented in 1996, monitors compliance with some vaccines, but not with BCG as yet. Studies are needed on the proportion of eligible children who receive BCG vaccine, and on side effects of BCG vaccination. Recommendations: We support the indications for BCG vaccination as recommended by the NHMRC TB Working Party, but feel that BCG should be recommended in all five situations detailed above. [Consensus opinion based on the high rate of TB in children exposed to adults with TB. This recommendation has also been made in the Australian immunisation procedures handbook,16 but not by the NHMRC TB Working Party,11 in 1989.] We strongly urge the Federal Government to put in place mechanisms to audit the number of children vaccinated with BCG vaccine each year. [Consensus opinion.] Mantoux screening In Australia, Mantoux skin testing is usually performed with 10 tuberculin units of purified protein derivative (PPD), although one unit only may be used if there is a high risk of TB.16 In the United States,17 Mantoux skin testing is performed with five tuberculin units of PPD. US authorities' interpretation of a positive Mantoux skin test is shown in the Box; there is currently no recognised Australian interpretation of skin test positivity. At present, the Committee on Infectious Diseases of the American Academy of Pediatrics (the "Red Book" committee)17 recommends annual tuberculin testing of children at high risk, but not of children at low risk. Six months of isoniazid preventive therapy is recommended for children who are Mantoux positive without disease,12 as this is as effective as nine months' duration of therapy18 and has a better risk-benefit analysis.19 While Australian children are not routinely tested with tuberculin, two recent surveys of the Mantoux status of 13-year-old20 and six-year-old21 Sydney schoolchildren showed t hat being born overseas was the major risk factor for being Mantoux-positive. In addition, the later the child left the country of birth, the greater the risk of being Mantoux- positive. Australian-born children with one or both parents born overseas were not at increased risk of being Mantoux- positive compared with Australian-born children of Australian-born parents. As most Mantoux-positive children in Australia were born overseas, it is important to screen children who are migrating to Australia from countries with a high prevalence of TB. Short visits (e.g., holidays) overseas are associated with a low risk of becoming infected with TB. Although short term visitors to Australia occasionally transmit TB, screening them would be extremely difficult, and this is not done routinely. However, screening might be indicated in special circumstances (e.g., a visitor from a high endemic area with chronic respiratory symptoms). Routine annual Mantoux screening is not justified by the available data. Recommendations: Children born overseas who are migrating to Australia from a country with a high prevalence of tuberculosis should be screened by Mantoux testing with or without a chest x-ray on entry into Australia. [Based on evidence,20,21 but not currently recommended by the NHMRC TB Working Party.11] Children born in Australia should not be screened annually by Mantoux testing. [Based on evidence20,21 and consistent with NHMRC TB Working Party recommendations.11] Visitors to Australia from areas of high TB incidence should not be routinely screened, but neonates exposed to such visitors should be vaccinated with BCG. [Consensus opinion, consistent with Australian immunisation procedures handbook.16] Mantoux-positive children with no evidence of TB disease should be given preventive therapy with isoniazid for six months. [Based on evidence18,19 and consistent with NHMRC TB Working Party recommendations.11] Contact tracing Diligent tracing of the adult source of paediatric TB infection through public health networks continues to be an important step in preventing the spread of TB. Appropriate duration of drug therapy The emergence of highly resistant and multiply resistant strains of M. tuberculosis has re-emphasised the importance of good management of TB, and the development of innovative management and control strategies. The emergence of resistant strains is thought to be the result of failure of patients with TB to complete courses of chemotherapy. In New York, this was a consequence of failure to supervise patients' therapy as a result of cuts in health funding in the 1980s.4,5 In Australia, some States supervise all antituberculous therapy, while others use targeted supervision of patients considered to be at risk of being non-compliant. In general, there are insufficient public health staff to ensure supervision of preventive therapy with isoniazid. Continued supervision of therapy (either full or targeted supervision) is important to prevent the emergence of resistant strains in Australia, and requires funding. Recommendation: Specifically funded TB control programs need to be maintained in each State and Territory in Australia. [Consensus opinion.] This document has been discussed by the Writing Panel of the Paediatric Special Interest Group of the Australasian Society for Infectious Diseases (ASID), circulated to all members, and ratified by the ASID Council. It was discussed at the 1996 meeting of the Australasian Paediatric Respiratory Group, and circulated to all members for comment. It was sent to Dr Greg Stewart, Chair of the NHMRC Working Party on Towards elimination of tuberculosis II. Guidelines and protocols for controlling tuberculosis disease in Australia, and to the Public Health Association of Australia. Acknowledgements Helpful comments were received from Dr T Konstantinos, Dr Graeme Oliver, Dr Graham Simpson and Professor Louis Landau. References Raviglione MC, Snider DE, Kochi A. Global epidemiology of tuberculosis. Morbidity and mortality of a worldwide epidemic. JAMA 1995; 273: 220-226. Report from the Centers for Disease Control and Prevention: tuberculosis morbidity, United States, 1992. JAMA 1993; 270: 1525. Starke JR, Jacobs RF, Jereb J. Resurgence of tuberculosis in children. J Pediatr 1992; 120: 839-855. Drucker E, Alcabes P, Bosworth W, Schell B. Childhood tuberculosis in the Bronx, New York. Lancet 1994; 343: 1482-1485. Frieden TR, Fujiwara PI, Washro RM, Hamburg MA. Tuberculosis in New York City -- turning the tide. N Engl J Med 1995; 333: 229-233. Cheah D. Tuberculosis notification rates, Australia, 1991. Commun Dis Intell 1992; 16: 398-400. Hargreaves J. Tuberculosis notifications in Australia, 1992. Commun Dis Intell 1994; 18: 330-337. Hargreaves J. Tuberculosis notifications in Australia, 1993. Commun Dis Intell 1995; 19: 332-341. Oliver G. Tuberculosis notifications in Australia, 1994. Commun Dis Intell 1996; 20: 108-115. Starke JR. Multidrug therapy for tuberculosis in children. Pediatr Infect Dis J 1990; 9: 785-793. National Health and Medical Research Council. Tuberculosis in Australia and New Zealand into the 1990s. Canberra: AGPS, 1989. Grossman M, Hopewell PC, Jacobs RF, et al. Consensus: management of tuberculin-positive children without evidence of disease. Pediatr Infect Dis J 1988; 7: 243-246. NSW Health Department. Controlling tuberculosis in New South Wales. Sydney: NSW Health, 1993. Forfar JO. Child health in a changing society. Oxford: Oxford University Press, 1988. Colditz GA, Brewer TF, Berkey JCS, et al. Efficacy of BCG vaccine in the prevention of tuberculosis. JAMA 1994; 271: 698-702. 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Aust J Pub Health 1996; 20: 123-128. *Paediatric Special Interest Group of ASID R Benn, MA Burgess, D Burgner, D Caplan, J Carapetis, P Collignon, R Doherty, G Eagles, J Faoagali, M Ferson, K Forsyth, S Garland, GL Gilbert, D Gordon, K Grimwood, J Hanna, D Hansman, G Hogg, D Holdaway, M Holloway, D Isaacs, H Jeffery, C Jones, A Kakakios, A Kesson, D Lennon, D McCrossin, P McIntyre, A McGregor, D McIntosh, M Nissen, D Roberton, R Robins-Brown, J Robson, J Royle, L Voss, S Wesselingh, J Whitson, B Wild, A Yung. The writing panel of the Paediatric Special Interest Group of ASID comprised GL Gilbert, MA Burgess, M Ferson, S Garland, K Grimwood, G Hogg, D Isaacs, and P McIntyre. **Australasian Paediatric Respiratory Group H Allen, I Asher, P Van Asperen, G Bowes, B Clements, D Cooper, P Cooper, K Dawson, P Field, P Francis, N Freezer, J Gillies, M Haifer, M Harris, R Henry, A Isles, A Kemp, D Kennedy, L Landau, J Martin, CM Mellis, S Sawyer, B Masters, J Morton, T Olinsky, P Pattemore, P Phelan, C Robertson, P Robinson, P Sly, G Smith, P Le Souef, R Staugas, S Stick. Authors' details Australasian Society for Infectious Diseases, Sydney, NSW. David Isaacs, FRACP, Member of the Paediatric Special Interest Group; Craig M Mellis, FRACP, Member of the Australasian Paediatric Respiratory Group. Reprints will not be available from the authors. Correspondence: Associate Professor D Isaacs, Department of Immunology and Infectious Diseases, Royal Alexandra Hospital for Children, Westmead, NSW 2145. 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