Correspondence

Tuberculosis in a Child in North Dakota

N Engl J Med 2000; 342:1918-1919June 22, 2000

Article

To the Editor:

In an informative report, Curtis et al. describe extensive transmission of tuberculosis by an adopted nine-year-old child (Nov. 11 issue).1 However, I think the authors of the paper and the author of the accompanying editorial2 overlooked a factor that probably was involved in the development of tuberculosis in this child. It seems clear that the child was not infected in North Dakota, where the tuberculosis case rate is about 2 per 100,000 population, but rather in his native Marshall Islands, where the case rate is 104 per 100,000 population. A tuberculin skin test was performed shortly after his arrival in North Dakota in 1996, but unfortunately the result was not assessed. He apparently was well at that time, and his tuberculosis developed two years later.

Tuberculosis is common among persons from the Indian subcontinent who immigrate to the United Kingdom,3 in part because in the winter months dark-skinned people may be deficient in 1,25-dihydroxyvitamin D₃, an important immunoregulatory hormone.4-6 The Marshall Islands lie in the Pacific Ocean at a latitude of only 9 degrees north, where it is never cold enough to require staying indoors or dressing warmly. North Dakota is at about 46 degrees north, so there is a great difference in sunlight between the two locations for several months each year.

Finally, Douglas et al.7 have shown that the peak incidence of tuberculosis among persons with dark pigmentation who immigrate to the United Kingdom is in July (the month in which the tuberculosis of the source case was found), in contrast to the winter peak for other respiratory diseases. Perhaps the reason for the delayed development of tuberculosis after the winter nadir of vitamin D₃ is that it takes several months for a dormant tuberculosis infection to reactivate and produce sufficient symptoms for the illness to be diagnosed.

This experience should teach us that when dark-skinned people immigrate to northern states or Canada from areas where tuberculosis is common and sunshine abundant year round, we should be sure that they have adequate vitamin D to enable their immune system to function properly year round.

William W. Stead, M.D.
Arkansas Department of Health, Little Rock, AR 72205-3867

7 References

1. 1

   Curtis AB, Ridzon R, Vogel R, et al. Extensive transmission of Mycobacterium tuberculosis from a child. N Engl J Med 1999;341:1491-1495
   Full Text | Web of Science | Medline

2. 2

   Miller LC. Caring for internationally adopted children. N Engl J Med 1999;341:1539-1540
   Full Text | Web of Science | Medline

3. 3

   Davies PDO. A possible link between vitamin D deficiency and impaired host defence to Mycobacterium tuberculosis. Tubercle 1985;66:301-306
   CrossRef | Medline

4. 4

   Tsoukas CD, Provvedini DM, Manolagas SC. 1,25-Dihydroxyvitamin D₃: a novel immunoregulatory hormone. Science 1984;224:1438-1440
   CrossRef | Web of Science | Medline

5. 5

   Cadranel J, Hance AJ, Milleron B, Paillard F, Akoun GM, Garabedian M. Vitamin D metabolism in tuberculosis: production of 1,25(OH)₂ D₃ by cells recovered by bronchoalveolar lavage and the role of this metabolite in calcium homeostasis. Am Rev Respir Dis 1988;138:984-989
   CrossRef | Web of Science | Medline

6. 6

   Wilkinson RJ, Llewelyn M, Toossi Z, et al. Influence of vitamin D deficiency and vitamin D receptor polymorphisms on tuberculosis among Gujarati Asians in west London: a case-control study. Lancet 2000;355:618-621
   CrossRef | Web of Science | Medline

7. 7

   Douglas AS, Ali S, Bakhshi SS. Does vitamin D deficiency account for ethnic differences in tuberculosis seasonality in the UK? Ethn Health 1998;3:247-253
   CrossRef | Medline

Author/Editor Response

The authors reply:

To the Editor: Stead suggests a causal relation between 1,25-dihydroxyvitamin D₃ deficiency and the development of tuberculosis, on the basis of the temporal peak in the diagnosis of tuberculosis among dark-skinned immigrants from the Indian subcontinent and on the basis of other data suggesting impaired host defenses.1 However, this hypothesis of seasonal vitamin D deficiency is unlikely to account for the development of tuberculosis in the source case described in our report. Tuberculosis was diagnosed in this child in July, and the disease probably developed before the winter months. The boy was the source of the tuberculous osteomyelitis in his mother, whose symptoms started in December. This temporal sequence of events therefore suggests that his tuberculosis most likely developed in the fall and so was not influenced by a possible winter nadir in vitamin D₃, as suggested.

Secondary prevention is very important in the control of tuberculosis. Had the child we described been adequately screened for Mycobacterium tuberculosis infection on his arrival from a country with a high incidence of infection and treated appropriately, this outbreak could have been averted.

Renee Ridzon, M.D.
Amy Curtis, Ph.D., M.P.H.
Centers for Disease Control and Prevention, Atlanta, GA 30333

James Hargreaves, D.O.
Altru Health Care Systems, Grand Forks, ND 53206-6002

1 References

1. 1

   Davies PDO. A possible link between vitamin D deficiency and impaired host defence to Mycobacterium tuberculosis. Tubercle 1985;66:301-306
   CrossRef | Medline

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1. 1

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