A primer for pandemics [Archives:2006/940/Health]

April 24 2006

By: H. T. Goranson
A few times each year, the world is reminded that a pandemic threat is immanent. In 2003, it was SARS. Today, it is a potential avian virus similar to the one that killed 30 million people after 1914.

“Bird flu” has already shown that it can jump from fowl to humans, and now even to cats, which indicates that it might be the next global killer. But there are many other potential pandemics, and many are not even viruses. Bacteria, prions, parasites, and even environmental factors could suddenly change in a way that slays us. It is widely predicted that when this happens, the economic and human losses will exceed that of any previous war.

Indeed, it is humbling to remember that some of history's most deadly invasions were carried out by single-cell organisms, such as cholera, bubonic plague, and tuberculosis. Countries with the resources to do so are making resistance plans against pandemics – limited strategies that would protect their own citizens. Most governments are hoping that early detection will make containment possible.

Containment depends heavily on vaccines, but vaccines are only part of the answer. While they are a good defense against many viruses, each vaccine is highly specific to the threat. Viruses are parasites to cells, and each virus attacks a particular type of cell. The virus is shaped so that it can drill into a particular feature of that cell and inject parts of itself inside, confusing the cell into making more viruses and destroying itself in the process. With their very specific forms, the most effective anti-viral vaccines must be designed for a narrow range of factors.

Sometimes the tailored nature of viruses works in our favor. For example, they usually find it difficult to jump between species, because they would have to change their structure. But if large numbers of a host – say, birds – encounter a great number of people, eventually the virus will find a way to prosper in a new type of cell.

Birds are the greatest concern today only because the spread is easy to see. But AIDS jumped from monkeys and several types of flu jumped from swine. Deadly mutations of any kind need to be identified urgently, so that an effective vaccine can be designed before the strain becomes comfortable in the human body. Unfortunately our present methods of detection are not sensitive enough.

This is even more worrying when you realize that scientists should also be monitoring bacteria, prions, and parasites. There are more bacteria than any other life form. Many live harmlessly in our bodies and perform useful functions. They evolve and adapt easily, which means that they learn to sidestep our drugs over time. Bacteria should be checked for two types of mutation: adaptation by a hostile form that enables it to become super-immune to drugs, or a deadly mutant strain that appears in one of the multitude of “safe” bacteria.

Prions are a relatively new discovery. They are made from proteins similar to those that the body uses during healthy operations, which means that they are able to fool the body's tools into making more prions. They have only recently been recognized as the cause of several infectious diseases, including mad cow disease and Creutzfeldt-Jakob Disease, which kill by crowding out healthy brain cells. Many nerve, respiratory and muscle diseases might also be caused by prions.

Finally, parasites, simple animals that infect us, are already classified as pandemics. Malaria afflicts 300 million people and is the world's biggest killer of children. Many parasites are worms: hookworm (800 million people infected), roundworm (1.5 billion), schistosomes (200 million), and the worm that causes Elephantiasis (150 million).

There are also antagonists that are currently ignored. Environmental chemicals and particulates might warrant their own categories. Or consider combinations of problems, such as these chemical infectors mixing with airborne pollens, and apparently pushing up incidences of asthma. New fungal infections are even scarier and might be harder to treat.

The bottom line is that we can't predict where the threat will emerge, so we need a distributed, intelligent detection system. In practical terms, how should it be built?

“Detectors” would have to be expert enough to know when an ordinary-looking symptom is actually an emergency. They would be located everywhere, with an emphasis on vulnerable regions. Initial warning signs of a pandemic are most likely to appear in the developing world, but detection nodes should be positioned in every country, with the least possible expense. This is not as difficult as it sounds. The key is to harness existing infrastructure.

Medical infrastructure exists everywhere, in some form. It also tends to be the least corrupt of institutions in regions where that is a problem. Medical centers and clinics would be expected to investigate the cause of ailments in a large number of their patients, even in cases where the symptoms seem common. A small amount of additional scientific expertise and lab equipment would need to be added to a public health system that serves ordinary needs.

Enhancing existing resources would be effective for two reasons. First, illness is more likely to be reported in a city hospital than at a specialist institute. Second, the investment would boost latent public health in that region.

For poor regions, investment in equipment and training would have to come from wealthier counterparts. Rich countries could justify the expense in terms of the savings that would result from early detection of a major threat. Tropical climates and urban slums are humanity's front line against pandemics, and they should be equipped properly.

Public health is an important asset for any nation. With so much at stake, it makes sense to place sentinels near every swamp, city, public market, and farmyard on earth.

H. T. Goranson is the Lead Scientist of Sirius-Beta Corp and was a Senior Scientist with the US Defense Advanced Research Projects Agency.

Copyright: Project Syndicate, 2006.