Blacks’ High TB Rate May Be Linked to Genetics : Medicine: A study discovers the importance of the earliest stage of the body’s response to the disease. The finding may outweigh differences in racial susceptibility.
The disproportionately high rate of tuberculosis among blacks, long blamed on social factors such as crowding and poverty, may result in part from a greater innate susceptibility to tuberculosis infection, a surprising new study has found.
The study of 25,398 nursing home residents found that blacks are twice as likely as whites to become infected with the organism that causes tuberculosis--even when the two groups live under identical social conditions with equal opportunity for exposure to the disease.
“It seems that black people are at greater risk of this,” said Dr. Joseph Bates of the University of Arkansas College of Medicine. “This would imply some fundamental differences in their immune mechanisms at the very initial point where infection becomes established.”
The study, published today in the New England Journal of Medicine, found that blacks in 165 racially integrated nursing homes in Arkansas had double the “infectibility” of their white counterparts when exposed to Mycobacterium tuberculosis.
The lead author of the paper, Dr. William W. Stead, suggested that the reason for the difference appears to be genetic: Certain cells appear to present a more penetrable first-line defense against tuberculosis infection in blacks than in whites, he said.
“What we’re talking about is a pre-immune defense,” said Stead, director of the tuberculosis program at the Arkansas Department of Health. He said that perhaps more significant than the racial difference is the discovery of the importance of the earliest stage of the body’s response to tuberculosis infection.
Tuberculosis is an infectious disease that affects the lungs primarily, but may also involve other organs. Once one of the most common causes of death in the world, it now strikes about 22,500 Americans annually and results in about 2,000 deaths.
It has long been recognized that blacks are disproportionately affected. But health officials have tended to blame social factors--poverty, crowding, poor nutrition and limited access to medical care.
Stead began his study inadvertently after an outbreak of TB in an Arkansas nursing home in 1978. In an attempt to control the outbreak, Stead began requiring nursing homes to test all new residents for tuberculosis infection upon admission.
Later, those who had initially tested negative were retested. Stead based the findings in his paper on those men and women discovered by the second round of testing to have become infected while living in the integrated homes.
According to the paper, 13.8% of the blacks became infected while living in the nursing homes, compared to 7.2% of the whites. The nearly 2-1 ratio was relatively constant regardless of the size of the nursing home.
Blacks were also more likely to become infected regardless of the race of the resident found to have spread the infection. Even in homes where the sole infectious resident was white, blacks were more likely than whites to become infected.
Stead speculated that the racial difference may be traceable to the behavior of certain cells that defend the lungs against infection. Those cells, called macrophages, may be less able to fend off tuberculosis infection in blacks than in whites, Stead said.
Stead said his theory finds support in the laboratory research of a microbiologist at the University of Colorado School of Medicine. Alfred Crowle has found that macrophages in the tissues of blacks are more susceptible to tuberculosis infection than macrophages from whites.
“I look at this paper as an important contribution to the idea that there are racial differences in susceptibility to infectious disease,” Crowle said in a telephone interview. “And people need to be aware of that in order to take advantage of advances in medicine.”
Stead emphasized that the racial difference occurred at the earliest stage of exposure to infection. He found no racial difference in the proportion of infected people who then came down with the disease in the absence of preventive therapy.
“So the immune system seemed to handle it equally for the two races--after the infection had taken place,” Stead said in an interview. He said the initial response of the macrophages, which scavenge microorganisms, occurs before the immune system even kicks in.
The idea of racial differences in defense against infectious diseases is not new. Blacks are less susceptible than whites to malarial parasites as a result of a hereditary difference in hemoglobin, a critical protein involved in transporting oxygen from the lungs to tissues.
In a separate paper, published this month in Archives of Ophthalmology, researchers at Johns Hopkins University in Baltimore reported that a large epidemiological survey had found that blindness and visual impairment is twice as common in blacks as in whites.
The researchers studied 5,300 blacks and whites from East Baltimore in an attempt to estimate the prevalence of eye problems in urban populations. Only in old age do whites exceed the rate of blindness and visual impairment among blacks, they found.
The researchers did not speculate on the reasons for the racial difference, which has been suggested in previous studies.
“This association highlights the importance of race as an indicator of high-risk populations that need additional programmatic resources directed towards blindness prevention,” they wrote.
