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In Other Words
Dark Winters Ahead
Emerging Infectious Diseases, Vol. 7, No. 3, May-June 2001, Atlanta During the 1990s, the eruption of military conflicts posed one of the strongest stimuli for the reemergence of infectious diseases in poor nations. The civil wars in Angola, Rwanda, and Sudan produced devastating outbreaks of African sleeping sickness, cholera, and polio, even though experts had ...
Emerging Infectious Diseases,
Vol. 7, No. 3, May-June 2001, Atlanta
During the 1990s, the eruption of military conflicts posed one of the strongest stimuli for the reemergence of infectious diseases in poor nations. The civil wars in Angola, Rwanda, and Sudan produced devastating outbreaks of African sleeping sickness, cholera, and polio, even though experts had believed that these infections had been eliminated a decade or so earlier.
New links between political turmoil and public health crises are forcing the traditional foreign-policy community to consider the latest trends in global disease. Enter Emerging Infectious Diseases, a seven-year-old bimonthly journal published by the Centers for Disease Control and Prevention (CDC) in Atlanta. The journal provides a valuable service by studying infectious agents like the West Nile or Ebola viruses, which have the potential to emerge because of new human or animal migrations or environmental changes. A recent article by Scott Dowell, the acting associate director for global health at the CDC’s National Center for Infectious Diseases, examines the seasonal aspects of infectious disease, offering insights that could prove useful to global public health initiatives as well as antibioterrorism efforts around the world.
In an article titled "Seasonal Variation in Host Susceptibility and Cycles of Certain Infectious Diseases," Dowell explains how human viral epidemics seem to depend on the calendar, suddenly appearing and disappearing with the seasons. A good example is the regular January arrival of influenza in the United States. Similarly, rotavirus gastroenteritis appears in the southwestern United States and then slowly migrates to northeastern cities like Boston and Washington, D.C., striking young children during the winter months. Some 200 years ago, these same cities faced predictable and devastating summer epidemics of yellow fever introduced by cargo ships carrying infected mosquitoes from the West Indies.
Dowell argues that this seasonal variation of infection might not depend solely on the weather, as is commonly thought. He notes that the same viral infection — such as influenza — can appear on both sides of the equator during January, despite it being winter in the North and summer in the South. Because some aspects of human physiology (including sensitivity to light and certain immunities) also vary with the calendar, Dowell maintains, the regular arrival of certain epidemic infections might be explained by seasonal changes in human susceptibility to microbial invasion.
On this particular point, Dowell’s hypothesis is less convincing since it diminishes the crucial role of the infectious agent itself in producing a clinical infection. Indeed, infectious pathogens have coevolved with humans in an intricate and remarkable dance that has taken millions of years. Recognizing the tentative nature of his hypothesis, Dowell calls for fellow researchers to review past clinical trials for further evidence. Nevertheless, Dowell’s larger emphasis on the seasonal nature of infection has important implications for the implementation of public health efforts. For instance, when national immunization days are held in polio- and measles-endemic regions of the developing world, they are best conducted well before the seasonal onset of these infections, thus allowing sufficient time for a child’s immune system to respond to the vaccine. The same time urgency applies to so-called days of tranquility when vaccinations help to implement effective cease-fires in war-torn areas of Central Asia and sub-Saharan Africa.
Dowell’s insights can also help those who seek to mitigate the potential impact of bioterrorism attacks. U.S. civil defense officials are concerned by the similarity between the early symptoms produced by biological warfare agents — such as bacterial agents of tularemia and Q fever — with the symptoms produced by influenza. In the initial stages of infection, all three will produce fever, chills, headaches, muscle pains, and appetite loss. The similarity may delay the detection of biological attacks during the winter, when public health officials might erroneously attribute an increase in complaints of such symptoms to a common flu outbreak.
Responding to such concerns, the CDC has initiated a national system of Centers for Public Health Preparedness to ensure that local health workers can respond to a bioterrorism attack. Similarly, the U.S. Defense Department’s Advanced Research Projects Agency is developing new technologies aimed at differentiating infectious agents used as biological weapons from common seasonal viruses. However, such efforts are far from sufficient. A January 2001 CDC report concluded that the nation’s public health infrastructure is not prepared to detect a bioterrorist event. In June 2001, the Center for Strategic and International Studies and the Johns Hopkins University Center for Civilian Biodefense Studies simulated a bioterrorist attack in a war game exercise known as "Dark Winter." Their conclusion: A smallpox attack on the United States would produce massive civilian casualties and rapid breakdown of the country’s essential institutions. Unfortunately, the United States remains years away from replenishing key vaccine stockpiles and even further from having improved detection technologies in place.