Lessons from New York's tuberculosis epidemicBMJ 1998; 317 doi: https://doi.org/10.1136/bmj.317.7159.616 (Published 05 September 1998) Cite this as: BMJ 1998;317:616
Tuberculosis is a political as much as a medical problemand so are the solutions
In the late 1980s New York city witnessed a dramatic epidemic of tuberculosis. By 1990, with 3% of the US population, the city had 15% of the country's cases. From 1984 to 1991 incidence increased from 23 to 50/100 000, and in some poor areas rates were much higher. In central Harlem, for example, incidence rose from 90 to 220/100 000. Among black men aged 35-44 the incidence in 1991 was 469/100 000, almost 45 times the national average.1 Now, however, the number of cases and the incidence have both declined dramatically. How has this been achieved and what are the lessons for other places facing a tuberculosis epidemic?
Two aspects of the New York epidemic suggested that it was home grown rather than associated with immigration.2 Firstly, childhood tuberculosis rates (suggesting recent acquisition) were rising, particularly among black Americans. Between 1987 and 1990 cases in children under 15 rose by 97%, from 74 cases to 146; 92% of these cases occurred in children aged 4 or younger.3 Secondly, rates of acquired drug resistant tuberculosis were also rising. The percentage of cases resistant to at least one drug rose from 19% in 1987 to 28% in 1991, while resistance to at least both isoniazid and rifampicin (multidrug resistance) rose from 6% to 14%, most of it home grown.4
The causes were multifactorial but three are worth highlighting. Firstly, funding for tuberculosis control from the federal and state governments and the city had been slashed in the 1970s and had not recovered as rates had risen. Secondly, the city's Bureau of Tuberculosis Control suffered substantial internal problems, resulting in poor communication between inpatient facilities and community and outpatient services.5 Finally, through the 1980s the city had undergone major social upheavals. Neighbourhoods, particularly poor ones, were transformed by increases in overcrowding, inequality, homelessness, and the spread of HIV. The fracturing of communities both fanned the flames of the epidemic and made it much harder to encourage people with tuberculosis to adhere to treatment. 6 7
Ultimately failure of treatment compliance was at the heart of the epidemic of drug resistance. By 1989 completion of treatment rates across the city were only about 60% (and as low as 11% in some areas).8 This allowed patients with infectious tuberculosis to remain a threat to others; relapse was frequent; and, worst of all, drug resistant strains flourished.
The response to the epidemic by the city's public health officials has been remarkable. From a peak of over 3800 cases in 1992 the caseload has fallen to 1730 cases in 1997. Rates in children have fallen substantially, so that in 1997 there were only 56 cases of multidrug resistant tuberculosis (from a peak of 441 cases in 1992).9 This response was achieved broadly by improving infection control in institutional settings (to reduce nosocomial spread); improving coordination of the service; and, most importantly, improving treatment compliance largely through expanding directly observed therapy (DOT) programmes.
What lessons can be taken from the New York city experience? Firstly, tuberculosis is as much a social and political disease as a medical one. Even in affluent nations, when social disintegration is allied to a poor health infrastructure disastrous consequences result. The response to the city's tuberculosis epidemic has cost well over $1bn (£625m),10 and the human cost has been immeasurable. Secondly, without adequate surveillance methods delays in detecting problems — and therefore delays in response — will occur. For example, we need to know whether tuberculosis rates are increasing in early warning groups such as people with HIV infection11; in whom drug resistant strains are occurring; whether resistance is primary or acquired; whether the disease is home grown or not; and how much nosocomial spread is occurring before the unusual resistance patterns of multidrug resistant tuberculosis make it obvious. Thirdly, we must encourage our patients to adhere to treatment and know when they are not so we can help them.
We also need to know more about the most effective means of treatment. Now that the World Health Organisation is promoting the expansion of directly observed therapy, we need to know whether this is in fact the best, most cost effective approach. Many remain to be convinced and believe that the use of fixed dose combination treatments offer a different approach to control. This issue needs to be tested formally.
Finally, as we consider the global scale of the tuberculosis epidemic from the perspective of New York it is worth reflecting on a comment in the annual report of the New York City Board of Health in 1915, well before the advent of antituberculosis treatments: “The city can have as much reduction of preventable disease as it wishes to pay for. Public health is purchasable; within natural limitations a city can determine its own death rate.” The sentiments are as true today. Globally tuberculosis its preventable and treatable: it just depends on how much we are prepared to spend and how. Political will needs to be allied to a political and public health mandate.