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MEDICAL JOURNALVol 119 No 1243 ISSN 1175 8716 Why the tuberculosis incidence rate is not falling in
New Zealand
Dilip Das, Michael Baker, Kamalesh Venugopal, Susan McAllister Abstract
Aims To assess the role of migration from high-incidence countries, HIV/AIDS
infection, and prevalence of multi-drug resistant organisms as contributors to
tuberculosis (TB) incidence in New Zealand (NZ) relative to ongoing local
transmission and reactivation of disease.
Methods TB notification data and laboratory data for the period 1995 to 2004 and
population data from the 1996 and 2001 Census were used to calculate incidence rates
of TB by age and ethnicity, country of birth (distinguishing high and low -incidence
countries), and interval between migration and onset of disease. Published reports of
multi-drug-resistant TB for the period 1995 to 2004 were reviewed. Anonymous HIV
surveillance data held by AIDS Epidemiology Group were matched with coded and
anonymised TB surveillance data to measure the extent of HIV/AIDS coinfection in
notified TB cases.
Results Migration of people from high-TB incidence countries is the main source of
TB in NZ. Of those who develop TB, a quarter does so within a year of migration, and
a quarter of this group (mainly refugees) probably enter the country with pre-existing
disease. Rates of local TB transmission and reactivation of old disease are declining
steadily for NZ-born populations, except for NZ-born Māori and Pacific people under
40. HIV/AIDS and multi-drug-resistant organisms are not significant contributors to
TB incidence in NZ and there is no indication that their role is increasing.
Conclusion TB incidence is not decreasing in NZ mainly due to migration of TB
infected people from high-incidence countries and subsequent development of active
disease in some of them in NZ. This finding emphasises the importance of regional
and global TB control initiatives. Refugees and migrants are not acting as an
important source of TB for most NZ-born populations. Those caring for them should
have a high level of clinical suspicion for TB.
It is well documented that tuberculosis (TB) incidence rates in the developed worldrapidly declined after the Second World War. However, in the mid to late 1980s, thedecline was halted and many countries experienced an increase in TB incidencerates.1 Occurrence of human immunodeficiency virus (HIV) infection and acquired immunedeficiency syndrome (AIDS),1,2 emergence of multi-drug-resistant (MDR)organisms,1 and increased migration from high-incidence countries,1 have beenimplicated as causes for the TB increase.
New Zealand (NZ) also followed this declining trend in TB incidence up to the mid-1980s. Since then, the incidence rate has plateaued.3 TB in people who haveemigrated from high-incidence countries has been thought to be one factor preventing URL: http://www.nzma.org.nz/journal/119-1243/2248/ a further decline in TB incidence in NZ. Specifically, inadequate screening ofmigrants who are subsequently shown to have active disease soon after arriving hasbeen suspected to be one factor contributing to this pattern.4,5 However, it is importantto assess the relative importance of other potential factors, notably the role ofHIV/AIDS infection, increasing drug resistance (particularly MDR), and the potentialdecline in the effectiveness of local TB-control programmes. This paper uses datafrom several surveillance sources to analyse the relative importance of these factors inpreventing the further fall in the TB incidence rate in NZ.
This paper is largely based on analysis of TB surveillance data for the years 1995–2004 and 1996 and2001 Census data (see the preceding article for a description of these data sources).6 Migration—The TB surveillance system records country of birth and, for migrants, their date of
arrival in NZ. These data allow cases born in low TB incidence countries to be distinguished from
those born in high-TB incidence countries (defined as all countries except Australia, Austria, Belgium,
Canada, Czech Republic, Denmark, Finland, France, Germany, Greece, Holland, Iceland, Ireland,
Israel, Italy, Luxembourg, Malta, Monaco, NZ, Norway, Slovakia, Sweden, Switzerland, the UK, and
USA).7
We calculated the crude incidence rate by migrant region and country (for countries contributing onaverage more than one TB case a year) using census data on country of birth to provide thedenominator. We also examined the TB notifications of people born in low- and high-incidencecountries according to the interval between time of arrival in NZ and the date of notification.
Transmission and reactivation in NZ—TB cases were divided into categories based on probable
transmission setting and timing of infection.
This classification used a combination of: The age group classification split the population into those <40 years where infection is likely to be dueto relatively recent transmission and those ≥40 where TB is more likely to be due to reactivation ofinfection acquired many years previously. In the older group, however, some recent transmissioncannot be ruled out as evidenced by studies using genetic fingerprinting.8 HIV/AIDS coinfection—Medical practitioners diagnosing a case of AIDS are required to notify this in
a coded form to the local Medical Officer of Health (MOH). Nationally, AIDS notifications are
compiled by the AIDS Epidemiology Group at the University of Otago, Dunedin. HIV infection is
under laboratory-based surveillance. Two laboratories—one in Auckland Hospital and the other at the
Institute of Environmental Science and Research Limited (ESR)—do the confirmatory ‘Western Blot’
test for HIV and report positive results in a coded form to the AIDS Epidemiology Group.
TB is an AIDS defining condition in HIV-positive persons. So, by definition, an HIV-positive personwith TB also has AIDS. The AIDS Epidemiology Group matched the coded list of people with AIDSand HIV infections with the similarly coded list of TB notifications to detect people coinfected withHIV and TB.
AIDS is notified anonymously with a code using the first two letters of surname, first initial of givenname, sex, day, month, and year of birth.9 We calculated the proportion of TB patients coinfected withHIV each year and examined the trend.
Multi-drug resistance—Three mycobacteriology laboratories (in Auckland, Wellington, and Waikato
hospitals) test antimicrobial susceptibility of all Mycobacterium tuberculosis and Mycobacterium bovis
isolated from human specimens in NZ. ESR matches these with TB case notifications and analyses the
data to describe the distribution of TB-drug resistance in NZ. We reviewed reports for the period 1995
to 2001,10 and annual reports of anti-TB-drug resistance for subsequent years (2002-2004),11 to assess
the role of multi drug resistance in local transmission of the disease.
URL: http://www.nzma.org.nz/journal/119-1243/2248/ Migration—For the 10-year period 1995–2004, country of birth status (NZ or
overseas) was reported for 89.3% (3367/3772) of notified cases. Of those for whom
country of birth status was known, 35.4% (1193) were born in NZ and 64.6% (2174)
were born overseas.
Table 1 presents numbers and crude incidence rates of TB by region and selectedcountries (those with an average of more than one case per year). Most of theoverseas-born cases were from three regions of the world—Asia, Africa, and PacificIslands.
Countries (in descending order) contributing an average of more than 5 cases a yearwere India, China, Somalia, Samoa, Philippines, Tonga, Korea, Cook Islands,Vietnam, and Cambodia. Tuvalu contributed more than 5 cases per year for the period2000–2004. Very high rates were observed in people born in Ethiopia (3209.9 per100,000) and Somalia (1924.4 per 100,000) in the 1995–1999 period.
Among people born in high-incidence countries, the numbers of TB notifications washighest within the first year of arrival, and then decreased substantially in subsequentyears (Figure 1). About a quarter (28.3% or 144 / 508) of people who were notifiedwith TB within 1 year of migration from a high-incidence country were identified ashaving active TB within 2 months of arrival in NZ.
In contrast, very few people from lower-incidence countries were notified with TBwithin 1 year of arrival in NZ (Figure 2). Most of those who developed the disease didso 20 years or more after arrival (Figure 2).
Table 2 shows TB numbers and rates in NZ- and overseas-born populations accordingto broad age and ethnic groups. Compared to NZ-born people of Pacific and Otherethnicity, TB rates were much higher in their overseas-born counterparts. Thisdifference indicates that exposure to TB overseas rather than local transmission is thepredominant mode of acquiring TB in people of these ethnic groups.
Rates of TB in overseas born populations generally declined over the 10-year period,with the exception of Pacific people <40 years, where there was a slight increase.
URL: http://www.nzma.org.nz/journal/119-1243/2248/ Table 1. Incidence of tuberculosis by country of birth, New Zealand, 1995–2004
Country of birth
1995–1999
2000–2004
Population1
Population 2
High TB incidence countries
Total Africa
Total Asia
Total Pacific Islands
Total for high incidence
countries
Low TB incidence countries
Total for low incidence
countries
Overall Total
1 Census 1996, 2 Census 2001, 3 Annual incidence rate per 100,000.
URL: http://www.nzma.org.nz/journal/119-1243/2248/ Figure 1. Interval between migration and notification of tuberculosis in cases
born in high-incidence countries, New Zealand, 1995-2004
Figure 2. Interval between migration and notification of tuberculosis in cases
born in low-incidence countries, New Zealand, 1995-2004
URL: http://www.nzma.org.nz/journal/119-1243/2248/ Table 2. Incidence of tuberculosis in New Zealand-born and overseas-born populations by ethnicity and age group, New Zealand, 1995-
2004
Country of birth &
1995–1999
2000–2004
Ethnicity
Rate Ratio
Rate Ratio 95% CI of
Cases Population1 Rate3
95% CI of RR Cases Population2
New Zealand-born
Overseas born
1 Census 1996, 2 Census 2001, 3 Annual incidence rate per 100,000, CI= Confidence interval. There were 270 and 182 TB cases, respectively, for the 1995–99 and 2000–04 periods that had missing values for eithercountry of birth, ethnicity, or age. These cases were excluded. 4 This rate is used as the reference value for all rate ratios presented in this table.
URL: http://www.nzma.org.nz/journal/119-1243/2248/ Transmission and reactivation in NZ—In the NZ-born population (Table 2), TB
incidence varied markedly by age group and ethnicity. In 2000–2004, rates ranged
from <0.5 per 100 000 (in Europeans <40 years) up to 23.8 per 100,000 (in Pacific
people <40 years). TB rates in NZ-born populations were generally higher in older
age groups (≥40 years) except for Pacific people (where these rates were based on
very small numbers of cases).
TB rates declined in most NZ-born populations except for Māori and Pacific people<40 years, in whom there were statistically non-significant increases between 1995–1999 and 2000–2004. Of particular note was the statistically significant decline in theTB rate for NZ born Europeans <40 years, which is the largest single sub-populationidentified in Table 2.
Multi-drug-resistant TB (MDR-TB)—MDR-TB is defined as TB resistant to at
least isoniazid and rifampicin. Published reports on anti-TB drug resistance showed
that MDR-TB is rare in NZ, with a total of 19 cases recorded in 10 years since
national surveillance of anti-TB drug resistance began in 1995.10,11 Eighteen of the 19
MDR-TB cases identified were people born overseas and presumed to have acquired
the MDR-TB overseas. The remaining MDR-TB case was also born overseas, but
multi drug resistance appeared to have developed during treatment in NZ. There is no
documented evidence that MDR-TB has been transmitted within NZ up to 2004.
HIV/AIDS coinfection—In the 10-year period (1995-2004), out of 3,772 notified TB
cases, 45 (1.2%) were diagnosed with HIV infection. The annual proportion of TB
cases with HIV showed a non-significant declining trend over this 10-year period
(Figure 3).
Figure 3. Percentage and trend of tuberculosis cases coinfected with HIV, New
Zealand, 1995–2004
1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 URL: http://www.nzma.org.nz/journal/119-1243/2248/ Discussion
This analysis has shown that migration of TB-infected people from higher incidencecountries is the dominant factor driving the incidence of this disease in NZ. Bycomparison, rates in most NZ-born populations are static or declining, indicating thatlocal transmission is being effectively controlled for most population groups. Thisanalysis has also shown that HIV/AIDS and TB drug resistance are not making asignificant contribution to the burden of TB in NZ.
Amongst people migrating from countries classified as ‘high-TB incident’, rates ofdisease vary enormously. Large contributors (more than 5 cases per year) withparticularly high rates include India, China, Somalia, Philippines, Vietnam, Cambodiaand Korea (Table 1).12 A similar pattern has also been seen in Australia.13 However,this observation has some limitations. Denominators used to calculate the rates inTable 1 are from 1996 and 2001 Census data. They do not represent the actual numberof people with specific country of birth in other years (other than 1996 and 2001). Asthe numbers of people born in some of the countries are small, a change in theirnumber could have a large effect on the rates.
A quarter (508 out of 2036) of TB cases born in high-incidence countries werenotified within 1 year of migration. This population of 508 included 144 cases(28.3%), who developed TB within 2 months of arrival. Most of these people arelikely to be refugees who had active TB on their arrival in NZ. This assumption issupported by the findings of TB screening for quota refugees at Mangere RefugeeResettlement Centre.14 Screening, within 6 weeks of arrival, of 1405 refugees fromJuly 1995 to July 1998 found that 2% of them had active disease.
If 2% is taken as the prevalence rate of TB in newly arrived refugees, then NZ canexpect to see 15 TB cases per year in the quota refugee population (750 refugees peryear). Other groups that are not screened for TB before entry include short-termvisitors, who may in a few instances have active TB on arrival in NZ.
Results of this analysis provide considerable reassurance that migrant populations arenot acting as an important source of TB transmission to most NZ-born populations.
The largest NZ-born population considered in this analysis, those of Europeanethnicity aged <40 years, experienced a significant decline in TB incidence over thesetwo time periods. This is despite the rise in absolute numbers of TB cases in migrantpopulations from high incidence countries that occurred over this time period. Thisobservation is consistent with the experience of other countries such as Australia, thathas also found that TB transmission tends to occur within defined populationgroups.13 The NZ-born populations that experienced modest, though non-significant, increasesin TB rates were Māori and Pacific people <40 years. NZ-born Pacific people <40have a significant burden of disease. There are several possible explanations for theseobservations, including: a potential decline in the effectiveness of local TB controlmeasures; increased exposure to Pacific migrants with TB; increasing ease oftransmission (from such factors as higher levels of household crowding); for Pacificpeople increased visiting to ancestral home countries; or a chance finding. These URL: http://www.nzma.org.nz/journal/119-1243/2248/ possible contributing factors need further investigation to identify opportunities forimproved prevention and control.
This study found that HIV is making only a small contribution to TB incidence in NZ.
Woodhouse, by analysing the data from Auckland Hospital Infectious Disease Unit,reported an increasing incidence of HIV/TB coinfected cases from the 1985–95period to 1996-2001 period.15 However, our study based on national data for a 10 yearperiod, did not find any increasing trend either in the number or in the proportion ofcoinfected cases. The findings of this study (and also of the previous reports)16,17indicate that HIV is an insignificant contributor to TB in NZ, unlike some othercountries,1,2 and there is no indication that its contribution is increasing.
Drug resistance also does not appear to be making a significant contribution to TBtransmission in NZ. Multi-drug resistance among TB isolates in NZ (0.6%) is lowcompared to the global median (1.7%), Australia (2.0%), United States (1.4%), andEngland and Wales (1.5%).18 Indeed, there is no indication that MDR-TB isincreasing in NZ or is being transmitted.
One other potential source of TB infection in NZ is the large reservoir ofMycobacterium bovis-infected animals. A separate combined epidemiological andmicrobiological investigation has shown that these animal reservoirs are making onlya small contribution to TB infection in humans (2.7% over the 1995 to 2002 period)and incidence from this source is not increasing.19 One limitation of this study is the possible numerator-denominator bias in calculatingincidence rate by ethnicity. Though prioritised ethnicity was used both for thenumerator and denominator, it is possible that these were not collected in the sameway.6 While ethnicity in the census (denominator) is self-reported, surveillance(numerator) data are more likely to contain health professional reported ethnicity. It isknown that in comparison to census data, hospital records are more frequently codedwith sole rather than multiple ethnicities.20 The implication for this is underestimationof the Māori rates.6 In conclusion, the findings of this study clearly indicate that migration from high TB-incidence countries is the predominant source of TB in NZ, and this contribution isincreasing over time. This source of TB is supplemented in a smaller way bytransmission to young Pacific people,17 local outbreaks,6 and reactivation of latentinfection in the NZ born population.
It is envisaged that (for economic, social, and humanitarian reasons) NZ will continueto accept immigrants (including refugees) from high-TB incidence countries in future.
We therefore need to constantly identify approaches to improve the swift detectionand treatment of TB in these populations.12 One area where improvements could bemade is the systematic screening of family reunification refugees. For quota refugees,there is an organised system of screening soon after their arrival. The system forfamily reunification is not as well organised.
In 2005 the NZ Immigration Service introduced stricter migrant health screening.
These measures included full medical certificate (including chest X-ray) for peoplewishing to stay in NZ for more than 12 months, temporary entry chest X-raycertificate for people wishing to stay for more than 6 months (but less than 12 URL: http://www.nzma.org.nz/journal/119-1243/2248/ months), and chest X-ray for international students and working holiday makers.21The effects of these changes have yet to be seen.
At the time of entering NZ far greater numbers of immigrants have latent TB infection(LTBI) rather than active disease and LTBI is not detected by chest X-ray. Soclinicians who are caring for immigrants and refugees (particularly from Asia, Africaand Pacific Islands) need to be very vigilant for features of TB. Early detection andtreatment of cases improves clinical outcomes and minimises the further spread ofdisease.
Ultimately, TB needs to be seen as a regional and global health problem. Increasingaid and development assistance can contribute to preventing and controlling thishealth threat. Other countries, notably the United States, have also seen value insupporting TB control in neighbouring counties.22 NZ is well placed to supportregional TB control efforts, and at the same time help to protect NZ from this disease.
Disclaimer: Parts of this work are based on data and information provided by the Institute of
Environmental Science & Research Limited (on behalf of the Ministry of Health) and Statistics NZ.
However, the analyses, conclusions, opinions, and statements expressed herein are those of the authors,
and are not necessarily those of the Institute of Environmental Science & Research Limited, the
Ministry of Health, or Statistics NZ.
Author information: Dilip K Das, Public Health Medicine Trainee, Department of
Public Health, Wellington School of Medicine and Health Sciences, University of
Otago, Wellington; Michael Baker, Senior Lecturer, Department of Public Health,
Wellington School of Medicine and Health Sciences, University of Otago,
Wellington; Kamalesh Venugopal, Biostatistician, Department of Public Health,
Wellington School of Medicine and Health Sciences, University of Otago,
Wellington; Sue McAllister, AIDS Epidemiology Group, Department of Preventive
and Social Medicine, University of Otago Medical School, University of Otago,
Dunedin
Acknowledgements: This work was carried out in the He Kainga Oranga/Housing
and Health Research Programme, Department of Public Health, Wellington School of
Medicine and Health Sciences, and was funded by the Health Research Council of
NZ.
Correspondence: Michael Baker, He Kainga Oranga/Housing and Health Research
Programme, Department of Public Health, Wellington School of Medicine and Health
Sciences, PO Box 7343, Wellington South. Fax: (04) 389 5319; email
michael.baker@otago.ac.nz
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URL: http://www.nzma.org.nz/journal/119-1243/2248/

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