![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
![]() |
How long are TB patients infectious? CMAJ 2000;163(2):157 In response to: D. Ahmad, W.K.C. Morgan We agree that the infectiousness of TB patients diminishes rapidly once effective treatment is initiated. However, there is considerable evidence against dogmatic claims that patients are no longer infectious after 2 weeks of treatment. Among the sentinel contributions of Wells and Riley was the finding that a single viable TB bacillus, once inhaled, is sufficient to produce infection.1 Viable mycobacteria can persist in sputum for weeks after the onset of therapy,2and isoniazid-susceptible TB bacilli in droplet nuclei containing isoniazid were demonstrated to remain viable after 12 hours airborne.3 Of course, mycobacteria need not survive this long to produce secondary infection if circumstances favour rapid dissemination (e.g., close proximity, no mask use, poor ventilation). These are precisely the circumstances once respiratory isolation is discontinued. Smear-negative patients can and do transmit TB. Such patients accounted for 17% of secondary transmission in San Francisco.4 There is also evidence that some mycobacteria are much more infectious than others. This was first suggested by Riley's finding of highly variable infection risks related to patients with similar clinical characteristics.5 Valway reported a community outbreak where extremely high tuberculin conversion rates followed trivial contacts and demonstrated accelerated growth of the relevant isolate in a mouse model.6 At present it is impossible to prospectively identify or differentially isolate patients harbouring such organisms. Community studies suggested that within stable households, transmission to identified contacts (with long-standing antecedent exposure) greatly diminished or ceased once effective treatment was initiated. However, most of these studies had serious design flaws. The only randomized controlled trial of confinement versus outpatient treatment took place in India, where nearly all contacts evaluated were already infected.7 It is inappropriate to extrapolate these data to the hospital setting. Hospitals now house sizeable numbers of patients infected with HIV, and other heavily immunosuppressed people. All of these individuals are at increased risk for infection and disease and most have never previously been exposed to TB. The comments of D. Ahmad and W.K.C. Morgan also rest on the dangerous assumption that all infecting organisms are drug susceptible. Multidrug resistance is uncommon in Canada (12% of cases), but resistance to isoniazid was seen in 8.7% of Montreal cases [Evidence].8 In these patients, the response to standard therapy may be slower (or nonexistent, in multidrug resistance cases). The laboratory diagnosis of drug resistance cannot be established within 2 weeks. The release of smear-positive, drug-resistant patients onto general medical wards after 2 weeks of "standard therapy" has been documented to fuel nosocomial TB outbreaks in the United States, and the attendant risks cannot be overstated.9 Before hospitalized smear-positive patients move to general ward rooms, they must clearly respond to treatment. This entails a significant reduction in bacillary load, most reliably documented by conversion of the smear and supported by clinical parameters such as weight gain and resolution of fever. In some cases this may take 2 weeks or less; in others, much longer. Patients returning to stable households in which contacts have already been evaluated and treated (where appropriate) can indeed be discharged before smear conversion, provided there is clinical evidence of improvement and a suitable follow-up plan. As with other clinical decisions, we believe that a more reasoned approach is preferable to the indiscriminate application of a standard "recipe" regardless of the (cook)books in which it has previously appeared.
Kevin Schwartzman
References
© 2000 Canadian Medical Association or its licensors |