Clonal relationships in a shelter-associated outbreak of drug-resistant tuberculosis: 1983-1997.

SETTING: An outbreak of tuberculosis caused by Mycobacterium tuberculosis resistant to isoniazid and streptomycin (HS-resistant) was documented in Boston's homeless population in 1984. Isolate relatedness was confirmed at the time by phage typing. In the late 1990s, cases of HS-resistant tuberculosis in the homeless were also documented, confirmed by RFLP typing using IS6110. None of the phage typed isolates from the 1980s were viable for performing RFLP analysis. We attempted to determine, using mixed-linker PCR (M-L PCR) finger-printing, whether or not these cases were all due to the same strain of M. tuberculosis. DESIGN: Isolates from 10 HS-resistant patients-four non-viable isolates from the 1980s and six viable isolates from 1996-1997-were sent to the Centers for Disease Control and Prevention for M-L PCR fingerprinting. These results were combined with record reviews of older cases and an ongoing epidemiologic investigation. RESULTS: Eight of 10 of the isolates were clonal, and the other two were strongly suspected matches. Epidemiologic investigation determined that transmission continued to occur after the initial outbreak in 1984-1985, and that a streptomycin-monoresistant variant of the strain was also circulating. CONCLUSION: M-L PCR fingerprinting combined with epidemiology was able to document links between cases across 15 years.

Rifampin preventive therapy for tuberculosis in Boston's homeless.

An epidemic of isoniazid (INH)- and streptomycin (SM)-resistant tuberculosis began among Boston's homeless population in 1984. Individuals with skin test conversions who agreed to preventive therapy received either INH, rifampin, or a combination of INH and rifampin. A total of 204 individuals with documented tuberculin skin test conversions who did not have active tuberculosis at the time of the clinical evaluation for their positive skin test were eligible for preventive therapy. Data on type and length of preventive therapy were obtained from the Tuberculosis Clinic and the Boston Tuberculosis Registry records at Boston City Hospital. The individuals were followed for development of active tuberculosis. Six of 71 (8.6%) individuals who received no therapy, 3 of 38 (7.9%) in the INH group, and none in the rifampin or rifampin plus INH groups (49 and 37 persons, respectively) developed active tuberculosis. Patients in the rifampin group were significantly less likely to develop tuberculosis than patients in the no therapy group (p = 0.04; odds ratio [OR] = 0.00, 95% confidence interval [CI] = 0.00-0.91). Treatment with any rifampin-containing preventive therapy (rifampin or rifampin plus INH) was effective (p < 0.01 ) in preventing development of active disease. The three INH failures were with organisms that were resistant to INH.

Exogenous reinfection with tuberculosis in a shelter for the homeless.

We investigated an outbreak of tuberculosis in a large shelter for the homeless to assess the role of exogenous reinfection as opposed to reactivation of endogenous infection as the cause of secondary tuberculosis in this population. Exogenous reinfection is considered relatively unimportant in the United States and other developed countries. Of 49 shelter-related cases, 22 had cultures resistant to both isoniazid and streptomycin and of the same phage type, indicating recent transmission originating with a single index patient. The probable index patient had a 10-year history of isoniazid and streptomycin resistance--an uncommon pattern at the shelter during the three years preceding the outbreak. In 4 of the 22 cases, the patient had previously had documented tuberculosis infection or disease. These reinfected patients had extensive lung cavitation and numerous acid-fast bacilli on sputum smears--features associated with contagiousness. In contrast, patients with tuberculosis for the first time (primary tuberculosis) are usually less contagious. We conclude that exogenous reinfection may have been an important factor leading to highly contagious secondary cases and an acceleration of the usual pattern of tuberculosis transmission in this highly susceptible population.

Automatic control of blood pressures with multiple drug inputs.

Control of arterial blood pressure has been successfully achieved by infusing a single vasoactive drug. However, in clinical practice, blood pressures are frequently controlled using multiple drug infusions. This paper presents a computer based adaptive control algorithm for simultaneous infusions of both an inotropic agent and a vasoactive agent to maintain the blood pressures at desired levels. We present the dynamics of the system with a bilinear two-input, two-output model. A least-squares parameter estimation algorithm has been employed using an output error method. Results of computer simulations of an electrical analog model of the heart and circulatory system are presented.

Digital system for P-wave detection and synchronization of the artificial heart.

This paper describes the implementation of a microcomputer based P-wave synchronization system for the artificial heart. This system provides for synchronization of the cardiac prosthesis pump with P-wave signals from electrodes implanted in the remnant of the natural atrium. The device carries out the functions of P-wave detection and determines the duration of systole based upon a moving average of the time intervals between successive pulses. The system has been tested both on a mock circulatory system and in vivo on calves. The purpose of the paper is to provide details of the circuitry and algorithms used.