Claudia Newbold
The Threat of Emerging Infection MLA 59
Robert Siegel
May 31, 1998
Web page at http://www2.netcom.com/~schopnew/newbold.html
Tuberculosis in San Francisco
Introduction
Emerging infectious diseases have been defined as "diseases of infectious origin whose incidence in humans has increased within the past two decades or threatens to increase in the near future". (IOM) Using this definition, Tuberculosis (TB) qualifies as an emerging infectious disease in the San Francisco Bay Area. The battle against TB in the 1990's, however, lacks the optimism of the TB battles after World War II, when drug discoveries led public health officials to believe that TB eradication was not only possible but merely a matter of time. Surrounding the re-emergence of TB in San Francisco is a host of complex factors that diminish significantly the prospects for outcomes similar to that achieved after the war and through the 1970's.
Brief history of tuberculosis (NJMS)
The bacterial agent for TB is the mycobacterium tuberculosis and is believed to have existed since at least 4000 BCE, coincident with the beginnings of stationery and concentrated populations, combined with the domestication and confinement of cattle. It has been postulated that these changes facilitated the spread of tuberculosis from person to person as well as from animal to human. Paleopathological evidence and archaeological discoveries have been used in an attempt to determine the earliest evidence of TB. Fragments of spinal columns from Egyptian mummies as old as 3700 BCE suggest the possibility of mycobacterium tuberculosis; however, more persuasive evidence is found in mummies dating from 1000 BCE.
Around 460 BCE, Hippocrates identified TB, then referred to as phthisis pulmonaris (consumption), as a widespread disease causing high mortality. In the seventeenth century, pathological and anatomical descriptions of the disease appeared, including references to specific changes in the lungs and cavities. Around the same time, it was suggested that the disease was infectious.
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In 1720, English physician Benjamin Marten’s writings evidenced the first understandings of the epidemiological nature of the disease when he conjectured that "exceedingly minute animals" could be responsible for the lesions and other symptoms of TB (Marten). He also conjectured that repeated exposure to a consumptive patient was necessary in order for the disease to be passed from one person to another.
145 years later, in 1865, Jean-Antoine Villemin, a French military doctor postulated a specific microorganism as the cause of TB. He was also successful in demonstrating that TB could be passed from humans to cattle and from cattle to rabbits (Villemin). In 1882, Robert Koch discovered the staining technique allowing him to view mycobacterium tuberculosis. The name tuberculosis was adopted because of the tubercles found in the bodies of fatal cases.
Following the discovery of the bacteria, the development of more advanced therapies followed relatively rapidly. The discovery of radiation in 1895 by Konrad Roentgen provided the means by which the disease could be monitored. Finally, beginning in 1943 and following through 1963, a series of anti-TB drugs were developed.
Symptoms and complications
The mycobacterium tuberculosis is most frequently spread to another person when a person with TB disease of the lungs or throat coughs or sneezes and the tubercle bacilli is transformed into airborne particles. People who are nearby can inhale these bacilli. Approximately 10% of those infected will develop the disease in their lifetime and only those persons who have developed the disease can spread it to others. While TB is highly contagious, research has shown that continuous contact with a person who has TB is necessary to become infected.
Once the bacilli is inhaled, it settles in the lungs. The bacilli grows and multiplies and is spread, by passing through the blood, to other parts of the body, such as kidney, spine, and brain. Despite the fact that TB can take hold in different parts of the body, most TB disease can be traced directly to infection in the lungs or throat. Common symptoms include a bad cough that
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lasts longer than 2 weeks, pain in the chest, and coughing up blood or sputum. Other symptoms include weakness or fatigue, weight loss, loss of appetite, chills, fever, and night sweats.
The physical manifestation of the disease, which led to its name, is the formation of small modules called tubercles. These tubercles are collections of cells that can take on a variety of characteristics. As the disease progresses, "TB presents as an acute necrotizing pneumonic process in either or both upper-lung fields…There may be liquefaction and bronchial involvement, with rapid intrabronchial spread to adjacent lobes of lung resulting in 'galloping consumption'" (Rom 469). In end stage pulmonary TB, death occurs from complications, most commonly pneumothorax or hemoptysis.
Epidemiology
The timing for developing the disease varies – some people develop the disease within three to six weeks of exposure, others may not develop the disease until years later. Not surprisingly, this later group is the least likely to receive therapy as they exhibit no symptoms and don’t feel sick. It is now believed that this later group develops the disease at a point when their immune system becomes vulnerable. The following people are among those who are commonly immune suppressed:
1. Babies and young children
2. Those with HIV, AIDS, diabetes mellitus, silicosis, cancer of the head or neck,
Leukemia or Hodgkin’s disease, severe kidney disease, low body weight.
3. Those undergoing certain medical treatment, such as corticosteroid treatment or
Organ transplants.
4. Those with substance abuse problems.
Nearly 2/3 of all TB cases occurs among blacks, Hispanics, Asians, and Native Americans. Other groups with high rates of disease include immigrants, refugees, and migrant workers from countries where the disease is prevalent. Research now shows that people with HIV have a much higher incidence of TB. 7-10% of those with HIV and 33-50% of those with
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AIDS will develop TB every year, versus the general population whose risk is 10% in their lifetimes.
Worldwide, the World Health Organization estimates that approximately 1/3 of the world's population is infected with mycobacterium tuberculosis. Of those who ultimately develop the disease, WHO estimates that 3 million people will die every year, representing approximately 36% of those diagnosed with the disease. The fatality rate increases to 50% for untreated patients and to 80% when multidrug-resistant TB (MDR-TB) occurs in immunocompromised individuals. The highest incidence of TB now occurs in those countries of Africa, Asia, and Latin America roughly corresponding with the lowest gross national product. The Wall Street Journal, on May 26, 1998, quoted the WHO as stating that "tuberculosis is the No. 1 killer of women of childbearing years around the world…more than 1.2 million women died of the disease in 1997, accounting for 9% of death. War, the No. 2 killer, caused 4% of deaths" (WSJ A1). In the United States, TB was the leading cause of death until the first decade of this century. By 1969, the U.S. death rate fell to 4 out of 100,000 from 188 out of 100,000 with the disease in 1904.
Treatment protocols
Sanatorium care was the first therapeutic approach to dealing with TB, beginning in the mid-1800s and continuing until chemotherapy was fully accepted as the treatment of choice. It was believed that by providing a patient with fresh air, healthy diet, rest, and exercise, a person could recover from TB, although there is no proof that any patient recoveries were attributable to the "cure", as it was known. In the early 1900s, the first surgical procedure was introduced, which consisted of collapsing the lung in order to promote the healing of cavitary lesions through a reduction in respiratory movement.
In 1944, streptomycin was first used in TB patients, with dramatic results. However, resistant bacteria developed within months. After trial and experimentation, it was shown that a combination of two to four drugs was effective in eliminating the disease. The "cocktail" usually prescribed includes 4 drugs: isoniazid (1952), rifampin (1963), pyrazinamide (1954) and ethambutol (1962) or streptomycin. If the patient fails to follow the protocol and TB becomes
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active again, there is a high probability that the disease will now be drug resistant. In this case, more toxic medications must be added to the "cocktail". Second-line medications include ethionamide, protionamide, pyrazinamide, cycloserine, capreomycin, viomycin, and kanamycin. To ensure full recovery from the disease, this expensive protocol must be followed meticulously for between 6 to 22 months. The cost of treating a patient averages $15,000; for an MDR-TB patient the cost soars to $250,000.
Re-emergence of Tuberculosis in San Francisco
In San Francisco, Tuberculosis began a gradual re-emergence beginning in the early 1980's after steady declines since the early part of the century. The table "Cases of Tuberculosis in San Francisco 1920-1977" shows 1,4ll new cases reported in 1920, thereafter declining to 242 new cases in 1997. The drop is even more dramatic when viewed as a percentage of total population. For example, in 1920, the 1,411 cases represented 278.5 cases per 100,000 population. In 1997, the 242 cases represented 32 cases per 100,000 population.
Mortality has also plummeted according to information for the period 1920 through 1965. The table "Tuberculosis Mortality in San Francisco 1920-1965" shows total deaths in 1920 from all forms of TB of 670, dropping in 1965 to 61 deaths. The TB Clinic at San Francisco General Hospital did not have mortality information after 1965; however, they indicated that deaths are relatively rare in San Francisco now.
In 1965, the San Francisco Department of Public Health published a statistical report (SF-1965) showing the distribution of the 485 new cases for 1965 by each of five health districts. The eastern half of the city, comprising 4 of the 5 health districts, contributed 83.1% of the new cases, with the western half of the city contributing only 13.6% of the cases. The remaining 3.3% of cases could not be attributed to a specific district. The distribution of cases correlated with higher density of population, greater concentration of ethnic-cultural groups, and a lower socio-economic status. The table "Tuberculosis Cases in San Francisco by Ethnic Group" shows that
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whites comprised the majority of cases in 1965 (52.3%), with other groups comprising from 1.4% to 22.5%.
Beginning in the early 1980's, TB began a gradual re-emergence in San Francisco, as represented by the increase in new cases in the table "Case of Tuberculosis in San Francisco 1920-1997". The Institute of Medicine (IOM), in 1994, identified factors responsible for disease re-emergence, some of which have been cited as factors in San Francisco's battle with TB. Two factors implicated in the increased number of new cases in San Francisco include the following:
Immigration. Increased immigration has contributed to the spread of TB, as immigrants are more likely to live in poor and crowded conditions where the disease is more easily transmitted. Other factors promoting the spread of TB include their reluctance to seek medical help, and the difficulties involved in developing culturally sensitive outreach programs. Moreover, immigrants who are here illegally usually try to avoid any contact with government officials or their representatives. The table "Tuberculosis Cases in San Francisco by Place of Birth 1981-1997", shows that over 50% of new TB cases in San Francisco occurred in foreign born individuals during this time period.
Gisela F. Schecter, former Director of the TB Clinic at San Francisco General Hospital describes the impact of immigration on the incidence of TB in San Francisco:
Over the past 20 years, the SFGH TB control program has faced 2 major challenges. Just as Federal funding for TB dried up in the 1970's, the human consequences of the collapse of the South Vietnamese government and the rise to power of the Khmer Rouge in Cambodia were manifested in the United States as a huge tide of refugees. The first surge was predominantly Vietnamese beginning in 1975 and the second surge in 1979 through 1981 and later included Cambodians, Laotians and Vietnamese. All three countries had always had high rates of tuberculosis, but now made even higher because of the deprivations of war. Rates of TB among refugees were similar to U.S. rates of 100 years ago and management was complicated by language and cultural barriers. Even
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before this refugee influx, foreign-born immigrants had made up a substantial proportion of San Francisco TB cases. Now, during 1979-1981, 80% of all TB cases were among foreign-born. The SFGH TB program responded very quickly by hiring and training translators and health workers from among the refugees themselves. In 1981, Dr. Gary Slutkin took over the TB program and successfully sought CDC (Centers for Disease Control) cooperative agreement funds to augment outreach to the refugee communities and to begin a directly observed therapy program, in which patients with active disease are managed by having a nurse in clinic, or a health worker in the field observe each dose of medication prescribed on a daily or twice weekly basis. This program began in 1982 (Schecter, undated).
AIDS. Not surprisingly, the high incidence of AIDS in San Francisco is also a factor in the re-emergence of tuberculosis. Again, Gisela Schecter provides the historical perspective:
The second major challenge faced by the SFGH TB program was AIDS. After taking over the SFGH TB clinic in late 1984, the author noted than an unusual number of white, middle-class gay men were developing active tuberculosis. The AIDS epidemic was in full force in San Francisco, one of the epicenters of AIDS in the United States. As might be predicted in a disease manifested by severe compromise of cellular immunity, persons with AIDS were highly susceptible to reactivation of latent tuberculosis, and to the rapid development of severe TB after exposure to an infectious case. SFGH was among the first programs in the country to publish reports on the epidemiology and treatment of AIDS-related tuberculosis (Schecter, undated).
Three additional factors are implicated in the persistently high rates of TB in San Francisco:
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Homelessness, substance abuse, and poverty. These social factors have been persistent contributors to TB for as long as records have been maintained for San Francisco. Gisela Schecter has noted, for example, that in the 1950's and 1960's, "there was a continuous parade of men in hospital gowns and robes crossing the street to the liquor store on the corner of 23rd St. and Utah" from the TB ward in the old San Francisco General Hospital (Schecter, undated).
Homeless persons have historically been at greater risk for TB due to their poor living conditions, high rates of HIV and other diseases, high rates of substance abuse, and late detection of TB. See table "Tuberculosis Cases in San Francisco and Social Factors". The Department of Public Health reported that:
TB cases among the homeless and injecting drug users (IDUs) increased between 1993 and 1995…TB case rates in areas that have the highest density of homeless and transiently housed individuals are 200-300 cases per 100,000 population which are rates comparable to those in Central Africa and 30 times the national case rate. Homeless cases peaked in 1995 accounting for 18.6% of all TB cases. Among the homeless, 67% to 82% are U.S. born, and have an exceptionally high rate of substance abuse…Between 1993 and 1996, of those whose substance histories were known, 73% to 94% abused alcohol, injected substances, or used other illicit drugs (94% in 1996). For the past three years one in four TB cases (25%) in San Francisco were substance abusers (SFEPI-1996, 8).
Elements of San Francisco Tuberculosis Control Program
Except for MDR-TB, it has been widely accepted that the "knowledge, medications, and techniques for the effective prevention and control of tuberculosis have been available for decades. Failure to apply what has been shown to work well results primarily from lack of funds, but in the final analysis, this omission derives from lack of political commitment and financial
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appropriations" (Rom 69). In contrast to other regions, the control program developed by San Francisco is considered a model in the United States. Since the early years of the 20th Century, San Francisco has prided itself on being in the forefront of TB control. By control is meant the effectiveness of surveillance in the early stages of the disease and compliance with chemotherapy treatment. It is extremely important in this regard to understand that the use of mandatory treatment programs was eliminated many years ago in the U.S. As a result, the effectiveness of any control program is directly dependent upon gaining the trust, confidence, and most of all, the cooperation of TB patients.
The TB Clinic manages San Francisco's tuberculosis control program at The San Francisco General Hospital, located at 1001 Potrero Avenue. Masae Kawamura is the current Director of the TB Clinic. The Clinic's directly-observed therapy (DOT) program contains 5 key elements (Schecter 165-168):
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5. Incentives to complete chemotherapy treatment. Other incentives provided to patients include food, drink, and television during their Clinic visits, grocery coupons, clothing store coupons, restaurant coupons, bus tokens, and assistance with housing and social services.
The San Francisco TB Clinic boasts a success rate for DOT of 98%.
Current challenges
The Centers for Disease Control published a report in 1989 titled "A Strategic Plan for the Elimination of Tuberculosis in the United States" (Footnote i). Since the CDC designated San Francisco as one of three locations to house a Model Tuberculosis Center, key organizations have formed cooperative and collaborative relationships to address many needs (Footnote ii). Critical to the success of these organizational efforts are advances in research (Footnote iii), more effective surveillance (Footnote iv), education (Footnote v), treatment, measurement, and assessment.
In its 1997 report, San Francisco summarized the challenges the City faces in controlling TB:
Targeted screening of higher risk groups through outreach efforts, community awareness and the use of preventive therapy with increased focus on the homeless and HIV infected is believed to be making its impact. Despite these promising statistics, TB case rates in San Francisco remains 4 times the national rate and double the California rate. HIV, substance abuse, poverty, homelessness and immigration continue to fuel the high rates of TB. Prevention of TB cases among foreign-born San Francisco residents will be the major challenge in the coming years as the percentage of TB cases in this group increases (SF-1997, 1).
Decreases in TB cases for non-Hispanic whites and African Americans have come at the expense of cases among other minorities. See table "Tuberculosis Cases in San Francisco by Place of Birth" which shows that the percentage of foreign-born in San Francisco contributing to
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new TB cases is again on the rise after declines in through 1992. According to San Francisco's
1997 report, this increase underscores "the need to continue targeted education, screening and contact investigation among underserved minority populations (SF-1997, 1).
With recent improvements in the health status of AIDS patients, the percentage of tuberculosis cases in AIDS patients has declined. From the high point in 1991, compared to 1997, the percentage of tuberculosis cases involving AIDS patients declined from 25% to 11%.
Complicating factors of the 1990's include modern concerns about patient rights and the right to privacy. Gisela Schecter describes the privacy issues raised by the new populations exposed to tuberculosis:
The appearance of TB in persons with AIDS raised new issues about confidentiality and involuntary isolation that had not been raised in the past. An important dialogue about individual civil rights versus the demands of protecting the public health swirled around the airborne disease, TB. Open lines of communication between AIDS activists and the Department of Public Health allowed the effective management of TB to continue (Schecter, undated).
Future challenges
In addition to the challenges described above, MDR-TB is of growing concern to public health officials, whether occurring as a result of noncompliance with drug protocols or from new strains of MDR bacilli. New York City is considered the hot spot for MDR-TB currently, but San Francisco is also an area for watch out for. Studies have already demonstrated rates approach 20% of drug resistance in San Francisco to any of the TB medications. See table titled "Drug Resistance in Tuberculosis Cases in San Francisco 1993-1997" for levels of drug resistance during this time period. As a consequence of San Francisco's high success rate for DOT (see page 10), public health officials here are focusing on MDR-TB occurring in individuals prior to moving to San Francisco and MDR-TB due to new strains of MDR bacilli. At the present time, there is no clear answer as to how MDR-TB will be dealt with in San Francisco.
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Other MDR diseases are sure to have a spillover effect on TB cases in San Francisco. MDR-HIV, for example, will undoubtedly cause more TB cases in San Francisco, given the relatively high incidence of HIV in San Francisco and the strong correlation between HIV and TB. A recent genetic analysis by Stanford University researchers shows that at least 1/2 of viral samples from 200 Bay Area AIDS patients are partially MDR to the new drug therapies, and 20% are completely MDR (SFMN 1A). It is not yet known whether MDR-HIV is a co-factor for MDR-TB. Another complicating factor between MDR-TB and MDR-HIV is the fact that the respective medications are antagonistic to one another, leaving patients and their doctors with agonizing choices over which illness to treat. In addition, with the spread of AIDS to more minority population groups, the social and cultural issues associated with treating TB will become a greater issue in the future.
Citations
Institute of Medicine (IOM), "Emerging Infections: Microbial Threats to Health in the United States". Washington, D.C.: National Academy Press, 1992.
Marten, Benjamin. "A New Theory of Consumption, More Especially of Phythisis or Cunsumption of the Lungs", London, 1720.
New Jersey Medical School National Tuberculosis Center (NJMS), "Brief History of Tuberculosis", online at
Rom, William N., Stuart M. Garay. Tuberculosis. Little, Brown and Company: New York, 1996.
San Francisco Department of Public Health (SF-1965), "Statistical Report 1965", pages 31-37.
San Francisco Department of Public Health, Bureau of Epidemiology and Disease Control (SFEPI-1996), San Francisco Epidemiologic Bulletin, "Tuberculosis in San Francisco, 1996", Vol. 13, Nos. 3/4, Mar./Apr. 1997.
San Francisco Department of Public Health (SF-1997), TB Control Section, "Tuberculosis in San Francisco, 1997".
San Francisco Department of Public Health, Bureau of Epidemiology and Disease Control (SFEPI-1996), San Francisco Epidemiologic Bulletin, "Tuberculosis in San Francisco, 1996", Vol. 9, Nos. 7/8, July/August 1993.
San Jose Mercury News, "HIV defying newest drugs", May 30, 1998. Also refers to
http://hivdb.stanford.edu for information on recent research by Stanford University.
Schecter, Gisela F., M.D., MPH (Schecter). "Supervised Therapy in San Francisco", Clinics in Chest Medicine, Volume 18, Number 1, March 1997.
Schecter, Gisela F., M.D., MPH (Schecter, undated). "Tuberculosis at San Francisco General Hospital", undated memorandum.
Stanford Center for Tuberculosis Research (Stanford), online at
The Francis J. Curry National Tuberculosis Center (NTC), online at
www.nationaltbcenter.edu/
The Wall Street Journal, "World-Wide" column, May 26, 1998.