Journal of the New Zealand Medical Association, 13-October-2006, Vol 119 No 1243
Tuberculosis in New Zealand: poverty casts a long shadow
Mark Thomas, Rod Ellis-Pegler
In an era concerned with the real or imagined threats from epidemics of “new” infectious diseases such as AIDS, SARS, and pandemic influenza, it is easy to forget the continued burden of disease caused by that “old” infectious disease, tuberculosis.
The white plague, as it was known in the past, killed famous names from this part of the world too. Robert Louis Stevenson (1894), Hone Heke (1909), and Katherine Mansfield (1923) are just some of the more notable examples.
In this issue of the New Zealand Medical Journal, Michael Baker and his colleagues remind us, in two articles,1,2 that tuberculosis has not gone away but instead continues to cause disease and death—disproportionately affecting the poor and recent immigrants.
These epidemiologic associations are not new. At the end of the nineteenth century, New Zealand was a favoured destination for British men with consumption, hopeful that a change in climate would improve their chances of survival. At that time, tuberculosis was the leading cause of death in the colony and each year killed approximately 100 of the 100,000 residents of Auckland.3
The migration to New Zealand of Europeans with tuberculosis during the nineteenth and early twentieth centuries has been followed by subsequent waves of migrants with high rates of tuberculous infection; from the Pacific Islands in the 1960s and 1970s, South East Asia in the 1980s, and Africa in recent years. The inevitable result of the introduction of tuberculosis to New Zealand by the early European settlers was transmission of the disease to Māori, followed by high rates of disease and death in Māori in particular.
Tuberculosis has always been a disease of poverty. Death rates due to tuberculosis in Māori men were 10 times those of non-Māori men as recently as the 1970s and 1980s,4 and the incidence of tuberculosis in Māori during the last decades remains approximately 10 times that in Europeans.1
The recent resurgence of tuberculosis in New Zealand, fuelled by immigrants from third world countries with high rates of infection,2 has also occurred in most other wealthy countries. In some countries, most notably the USA where the public health system and laboratory susceptibility testing were allowed to atrophy in the latter part of the 20th century, intersecting epidemics of tuberculosis and HIV infection led to explosive outbreaks of multi-drug resistant tuberculosis (MDR TB) (defined as resistance to at least rifampicin and isoniazid) in the most deprived members of society, such as prison inmates and homeless people.5
Fortunately this has not occurred in New Zealand. Overlapping systems based on clinician and laboratory reporting of tuberculosis have ensured relatively high notification rates. Reference laboratories in Auckland, Hamilton, and Wellington test the susceptibility of all Mycobacterium tuberculosis isolates in New Zealand.
Initial diagnosis and antimicrobial selection is predominantly in the hands of chest and infectious disease physicians, and a strong public health service has provided an effective supervision of outpatient treatments with anti tuberculous medicines. As a result, there has been only one case of locally generated MDR TB, and overall MDR TB constitute only 0.6% of all isolates.2 Nevertheless, MDR TB were causative (in 2005) in 2.0% of overseas-born cases.6
Even more serious are the recent reports7 of extensive (the official term has been decreed “extensive” rather than “extremely”) drug-resistant M. tuberculosis isolates (XDR TB); bacteria which are not only MDR TB but also have resistance to at least three of the second line agents, viz. aminoglycosides, polypeptides, fluoroquinolones, thioamides, cycloserine, and para-aminosalicylic acid.
XDR TB have been found throughout most of the world, and in a recent evaluation7 constituted 4%, 19%, and 15% of MDR TB in the USA, Latvia, and South Korea respectively. Patients infected with such variants of tuberculosis do badly.
The recent report from Kwazulu-Natal in South Africa8 of an outbreak of 53 patients with XDR TB and (at least in the 44 tested) HIV infection—52 of whom died within an average of 25 days—has brought a brutal immediacy to these issues. Once again, intercepting epidemics of tuberculosis and HIV infection with appalling outcomes.
It is gently reassuring that there is no evidence of an important contribution to tuberculosis in New Zealand from those coinfected with HIV,2 but our clinical impression from Auckland, where we treat a large cohort of those with HIV infection, is that that may not continue to be true of 2005 and 2006 once evidence is available for those years.
While outbreaks of tuberculosis in New Zealand usually involve an average of 10 persons and almost exclusively occur in Pacific or Māori communities, the recent still-evolving epidemic in Palmerston North is atypical. There, about 1800 boys from Palmerston North Boys High School have been evaluated after the diagnosis of infectious tuberculosis in an immigrant boy.
Initial reports9 indicate 194 Mantoux-positive boys (i.e. ca. 11% infected), with 12 of them diagnosed as probable tuberculous disease and being treated. The remaining 182 Mantoux-positive boys will receive chemoprophylaxis. These are both very high infection and disease rates so there can be no rest from endless vigilance.
Improved control of tuberculosis in New Zealand will result from enhanced detection of infection in immigrants and a nationwide reduction in poverty.10 The new immigration protocols introduced late last year,11 which require stricter migrant and visitor health screening as Das et al outline,2 should produce a modest immediate reduction in the burden of disease.
Given the increasing risk of reactivation of latent tuberculous infection with increasing age, it will be decades before the full benefits will accrue, however. Indeed, we can expect continued tuberculous disease in recently arrived immigrants as they age over the next 30 to 40 years.
Finally, the doctor caring for a recent immigrant, Pacific, or Māori patient with fever, respiratory symptoms, and/or weight loss should remember the high rate of tuberculosis in such patients. Failing to enquire about past exposure to tuberculosis, ascribing illness to other causes of lung disease (most commonly pneumonia and asthma), and failing to request a chest X-ray, were the most significant causes of delay in diagnosing patients with pulmonary tuberculosis in Auckland during the late 1990s.12
Beware the recent Asian immigrant with fever and chronic illness or even the recent Asian immigrant who is afebrile and has just a single persistently enlarged cervical lymph node!
Author information: Mark Thomas, Infectious Disease Physician, Rod Ellis-Pegler, Infectious Disease Physician; Infectious Diseases Unit, Auckland City Hospital, Grafton, Auckland
Correspondence: Dr Rod Ellis-Pegler, Department of Infectious Disease, Auckland Hospital, Private Bag 92024, Auckland. Fax: (09) 307 4940; email: RodEP@adhb.govt.nz
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