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Topics in Minority Health Tuberculosis Outbreak on Standing Rock Sioux Reservation -- North Dakota and South Dakota, 1987-1990
From 1987 through 1988, a cluster of cases of tuberculosis (TB) occurred among persons residing on the Standing Rock Sioux Reservation (Figure 1); recognition of this cluster prompted an epidemiologic investigation by the Indian Health Service (IHS), Standing Rock Sioux Tribal Health and Community Health Programs, South Dakota State Department of Health, North Dakota State Department of Health, and CDC. This report summarizes the findings of that investigation and follow-up public health interventions.
Standing Rock Sioux Reservation, which comprises approximately 3640 square miles, encompasses Sioux County, North Dakota, and Corson County and portions of Dewey and Ziebach counties in South Dakota (1981 resident American Indian population: 7958). The IHS provides clinical and preventive health services for the tribal population on the reservation through a hospital at Fort Yates, North Dakota; a clinic at McLaughlin, South Dakota; and field clinics in three outlying communities. Five TB cases were diagnosed in persons on the reservation in 1986 (rate: 62.8 per 100,000 persons), 10 cases in 1987 (rate: 125.7 per 100,000), six cases in 1988 (rate: 75.4 per 100,000), and two cases in the first 5 months of 1990. SIOUX COUNTY
From May 1987 through January 1988, seven cases of TB were reported in residents of the adjacent towns of Solen and Cannonball, Sioux County. The investigation linked transmission from an adult source patient to five of his contacts. In October 1987, the source patient (index patient A), a man with diabetes mellitus who resided in Solen, was hospitalized with sputum-smear-positive, cavitary TB. He had a documented positive tuberculin skin-test reaction in 1967 and was evaluated for TB in 1977 because of chest pain and hemoptysis.
At the time of diagnosis in 1987, he had a history of heavy alcohol consumption and lived in a house with approximately 20 persons. Of 33 identified contacts, six were diagnosed with TB, including two children who lived in the same house with the index patient, a child and a woman who lived in Cannonball, a man in Solen, and a man who lived outside the reservation (not included in Figure 1). The Mycobacterium tuberculosis phage type for index patient A was 1 (7,13), the same as that of one of the children living in his house and that of the woman living in Cannonball. Phage typing was not done for the other four contact cases. Of his 20 contacts with no previous record of tuberculin skin-test positivity, seven (35%) were positive; all seven completed a course of directly observed preventive therapy.
A seventh case occurred in a man (index patient B) living in Solen. Although he was a contact of index patient A, his isolate had a different phage type (phage type 1). In 1981, he was tuberculin skin-test positive but did not adhere to preventive therapy. In 1984, when his wife had onset of smear-positive pulmonary TB, index patient B did not receive preventive treatment. In April 1987, when he was evaluated because of shortness of breath, a chest radiograph indicated cavitation in the right upper lobe; however, TB was not diagnosed by his health-care providers. He was not evaluated further until November 1987, when he was hospitalized for massive hemoptysis; at that time, a chest radiograph indicated multilobe infiltration, and the sputum smear was positive for acid-fast bacilli. Of his nine contacts with no previous record of a positive skin test, four (44%) had positive tests; all four completed a course of directly observed preventive therapy. CORSON COUNTY
During 1987, four TB cases were reported among residents in the town of Little Eagle, Corson County (70 miles from Solen); three occurred among brothers, and one epidemiologically unrelated case occurred in a woman.
In October 1987, pulmonary TB was diagnosed in a disabled, bedridden man (index patient C). In December 1987, a chest radiograph obtained from one of his brothers indicated a small patchy lesion in the right upper lobe; this brother had a history of tuberculous pleural effusion in 1955 for which he was treated with isoniazid (INH), para-aminosalicylic acid, and streptomycin for an unknown duration. Because of negative sputum smears and cultures for mycobacteria and the small radiographic extent of the lesion, he was considered an unlikely source of disease for the index patient. The most likely source was a second brother who, in December 1987, was diagnosed with sputum-smear-positive, cavitary TB; his M. tuberculosis phage type was 1 (7,13). Phage typing was not done for the index patient. The father, who was deceased, was the only other member of the family with a reported history of TB. Although preventive therapy had been prescribed previously for several of the family members, including the probable source patient, adherence could not be assessed.
No patients with TB were identified among 36 other contacts of index patient C and the probable source patient. However, of 15 contacts with no previous record of a positive tuberculin skin test, six (40%) were positive; all six completed a course of directly observed preventive therapy with INH.
The unrelated case occurred in a woman who was diagnosed with genitourinary TB in March 1987; the phage type was 2 (7,13). Control and Prevention Response
Because of the high potential for TB transmission in the three communities, tuberculin skin-testing activities were expanded to schools and offered to the public. From October 1987 through February 1988, 724 persons were examined. Of these, 139 (19%) (including persons who were both tuberculin-positive and tuberculin-negative contacts, other persons with positive reactions, and persons who had previously had incomplete courses of preventive therapy) were placed on twice-weekly supervised preventive therapy; 137 persons completed at least 6 months of preventive therapy. One discontinued INH because of elevated liver enzymes; the other, who refused medication, subsequently had onset of TB and is currently receiving treatment. All persons with TB were treated with directly observed chemotherapy.
From February 1988 through May 1990, TB was diagnosed in seven other persons on the Standing Rock Sioux Reservation, four of whom were from Cannonball. Contact investigation did not indicate that any of these patients had been closely associated with any of the patients identified from October 1987 through January 1988, and no mycobacteriophage typing results of these cases were available. Reported by: Standing Rock Sioux Tribal Health and Community Health Representative Programs; L Volmer, Communicable Disease Control Program, KA Senger, State Epidemiologist, South Dakota State Dept of Health. F Heer, Div of Disease Control, S McDonough, MD, State Epidemiologist, North Dakota State Dept of Health. HL Rieder, MD, Federal Office of Public Health, Bern, Switzerland. TK Welty, MD, JS Takehara, MPH, Aberdeen Area Indian Health Svc, Rapid City, South Dakota. D Dailey, FNP, Indian Health Svc Unit, Ft. Yates, North Dakota. Mycobacteriology Laboratory, Respiratory Diseases Br, Div of Bacterial and Mycotic Diseases, Center for Infectious Diseases; Div of Tuberculosis Elimination, Center for Prevention Svcs, CDC.
Editorial Note: Since 1975, when national reporting of TB among American Indians and Alaskan Natives began, the incidence of TB in these groups has progressively declined (1,2). In 1987, 317 cases were reported to CDC, a rate of 20.0 per 100,000--4.7 times higher than the rate of 4.3 per 100,000 in the non-Hispanic white population (3). In comparison, the 10 reported cases in persons on the Standing Rock Sioux Reservation in 1987 resulted in a case rate of 125.7 per 100,000 population.
As TB becomes located in focal geographic areas (4), small outbreaks of TB are more likely to be recognized and should prompt rapid intervention and containment. The investigation in this report suggested that three independent sources of infection developed almost concurrently and resulted in persons with secondary cases that were potentially infectious and in persons with asymptomatic tuberculous infection. All three source patients had documented prior tuberculous infection, and preventive therapy had previously been prescribed for two. In two cases, patient delay in seeking treatment accounted for the extensive disease at the time of the diagnosis; in the third case, the failure to prevent progression from early TB to extensive infectious disease was attributable to lack of follow-up of a suspicious radiograph.
Although the incidence of TB has declined during the past 35 years, decreased clinical consideration by physicians can lead to unnecessary delays in diagnosis. Noncompliance with treatment remains one of the most serious constraints in effective TB control. Innovative ways to ensure adherence to prescribed treatment regimens, including fully supervised chemotherapy and preventive therapy (as was done in this outbreak), need to be implemented more widely, especially among high-risk populations (5,6).
The appropriate use of preventive therapy is crucial if TB is to be eliminated in the United States by the year 2010 (6). When taken as prescribed, INH preventive therapy is highly effective in preventing latent tuberculous infection from progressing to clinically apparent disease. The usual preventive therapy regimen is INH (10 mg/kg daily for children, 300 mg daily maximum for adults). The recommended duration of INH preventive treatment varies from 6 to 12 months of continuous therapy (7,8). To ensure that persons in high-risk groups comply with therapy, health-care personnel should, if necessary, directly observe the therapy. INH can be given twice weekly in a dose of 15 mg/kg (up to 900 mg) when therapy must be directly observed and resources are inadequate for daily therapy (7,8). Patients should be thoroughly educated about the disease and its treatment and should be monitored for toxicity to medication by appropriately trained personnel (8). The IHS has issued guidelines for TB control (9,10), modeled after recommendations by the American Thoracic Society and CDC (7) and adjusted to IHS-specific needs.
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3. Rieder HL, Bloch AB, Cauthen GM, Kelly GD, Snider DE Jr. Tuberculosis in the United States. JAMA 1989;262:385-9.
4. Bloch AB, Rieder HL, Kelly GD, Cauthen GM, Hayden CH, Snider DE Jr. The epidemiology of tuberculosis in the United States. Semin Respir Infect 1989;4:157-70.
5. Iseman MD, Sbarbaro JA, eds. National consensus conference on tuberculosis. Chest 1985;87:125S-32S.
6. CDC/Advisory Committee for Elimination of Tuberculosis (ACET). A strategic plan for the elimination of tuberculosis in the United States. MMWR 1989;38(no. S-3).
7. American Thoracic Society/CDC. Treatment of tuberculosis and tuberculosis infection in adults and children. Am Rev Respir Dis 1986;134:355-63.
8. CDC/Advisory Committee for Elimination of Tuberculosis (ACET). Screening for tuberculosis and tuberculous infection in high-risk populations and the use of preventive therapy for tuberculous infection in the United States: recommendations of the Advisory Committee for Elimination of Tuberculosis. MMWR 1990;39(no. RR-8).
9. Welty TK, Helgerson S, Tempest B, Johannes P. Control of tuberculosis among American Indians and Alaska Natives. The Indian Health Service Primary Care Provider 1989;14:53-4. 10. Welty TK, Follas R. IHS standards of care for tuberculosis. The Indian Health Service Primary Care Provider 1989;14:54-8.
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