The Andromeda Strain (22 page)

BURTON WAS WORKING in the autopsy room. He was nervous and tense, still bothered by his memories of Piedmont. Weeks later, in reviewing his work and his thoughts on Level V, he regretted his inability to concentrate.

Because in his initial series of experiments, Burton made several mistakes.

According to the protocol, he was required to carry out autopsies on dead animals, but he was also in charge of preliminary vector experiments. In all fairness, Burton was not the man to do this work; Leavitt would have been better suited to it. But it was felt that Leavitt was more useful working on preliminary isolation and identification.

So the vector experiments fell to Burton.

They were reasonably simple and straightforward, designed to answer the question of how the disease was transmitted. Burton began with a series of cages, lined up in a row. Each had a separate air supply; the air supplies could be interconnected in a variety of ways.

Burton placed the corpse of the dead Norway rat, which was contained in an airtight cage, alongside another cage containing a living rat. He punched buttons; air was allowed to pass freely from one cage to the other.

The living rat flopped over and died.

Interesting, he thought. Airborne transmission. He hooked up a second cage with a live rat, but inserted a millipore filter between the living and dead rat cages. This filter had perforations 100 angstroms in diameter—the size of a small virus.

He opened the passage between the two cages. The rat remained alive.

He watched for several moments, until he was satisfied. Whatever it was that transmitted the disease, it was larger than a virus. He changed the filter, replacing it with a larger one, and then another still larger. He continued in this way until the rat died.

The filter had allowed the agent to pass. He checked it: two microns in diameter, roughly the size of a small cell. He thought to himself that he had just learned something very valuable indeed: the size of the infectious agent.

This was important, for in a single simple experiment he had ruled out the possibility that a protein or a chemical molecule of some kind was doing the damage. At Piedmont, he and Stone had been concerned about a gas, perhaps a gas released as waste from the living organism.

Yet, clearly, no gas was responsible. The disease was transmitted by something the size of a cell that was very much bigger than a molecule, or gas droplet.

The next step was equally simple—to determine whether dead animals were potentially infectious.

He took one of the dead rats and pumped the air out of its cage. He waited until the air was fully evacuated. In the pressure fall, the rat ruptured, bursting open. Burton ignored this.

When he was sure all air was removed, he replaced the air with fresh, clean, filtered air. Then he connected the cage to the cage of a living animal.

Nothing happened.

Interesting, he thought. Using a remotely controlled scalpel, he sliced open the dead animal further, to make sure any organisms contained inside the carcass would be released into the atmosphere.

Nothing happened. The live rat scampered about its cage happily.

The results were quite clear: dead animals were not infectious. That was why, he thought, the buzzards could chew at the Piedmont victims and not die. Corpses could not transmit the disease; only the bugs themselves, carried in the air, could do so.

Bugs in the air were deadly.

Bugs in the corpse were harmless.

In a sense, this was predictable. It had to do with theories of accommodation and mutual adaptation between bacteria and man. Burton had long been interested in this problem, and had lectured on it at the Baylor medical school.

Most people, when they thought of bacteria, thought of diseases. Yet the fact was that only 3 per cent of bacteria produced human disease; the rest were either harmless or beneficial. In the human gut, for instance, there were a variety of bacteria that were helpful to the digestive process. Man needed them, and relied upon them.

In fact, man lived in a sea of bacteria. They were everywhere—on his skin, in his ears and mouth, down his lungs, in his stomach. Everything he owned, anything he touched, every breath he breathed, was drenched in bacteria. Bacteria were ubiquitous. Most of the time you weren’t aware of it.

And there was a reason. Both man and bacteria had gotten used to each other, had developed a kind of mutual immunity. Each adapted to the other.

And this, in turn, for a very good reason. It was a principle of biology that evolution was directed toward increased reproductive potential. A man easily killed by bacteria was poorly adapted; he didn’t live long enough to reproduce.

A bacteria that killed its host was also poorly adapted. Because any parasite that kills its host is a failure. It must die when the host dies. The successful parasites were those that could live off the host without killing him.

And the most successful hosts were those that could tolerate the parasite, or even turn it to advantage, to make it work for the host.

“The best adapted bacteria,” Burton used to say, “are the ones that cause minor diseases, or none at all. You may carry the same single cell of
Strep. viridians
on your body for sixty or seventy years. During that time, you are growing and reproducing happily; so is the
Strep
. You can carry
Staph. aureus
around, and pay only the price of some acne and pimples. You can carry tuberculosis for many decades; you can carry syphilis for a lifetime. These last are not minor diseases, but they are much less severe than they once were, because both man and organism have adapted.”

It was known, for instance, that syphilis had been a virulent disease four hundred years before, producing huge festering sores all over the body, often killing in weeks. But over the centuries, man and the spirochete had learned to tolerate each other.

Such considerations were not so abstract and academic as they seemed at first. In the early planning of Wildfire, Stone had observed that 40 per cent of all human disease was caused by microorganisms. Burton had countered by noting that only 3 per cent of all microorganisms caused disease. Obviously, while much human misery was attributable to bacteria, the chances of any particular bacteria being dangerous to man were very small. This was because the process of adaptation—of fitting man to bacteria—was complex.

“Most bacteria,” Burton observed, “simply can’t live within a man long enough to harm him. Conditions are, one way or another, unfavorable. The body is too hot or too cold, too acid or too alkaline, there is too much oxygen or not enough. Man’s body is as hostile as Antarctica to most bacteria.”

This meant that the chances of an organism from outer space being suited to harm man were very slim. Everyone recognized this, but felt that Wildfire had to be constructed in any event. Burton certainly agreed, but felt in an odd way that his prophecy had come true.

Clearly, the bug they had found could kill men. But it was not really adapted to men, because it killed and died within the organism. It could not be transmitted from corpse to corpse. It existed for a second or two in its host, and then died with it.

Satisfying intellectually, he thought.

But practically speaking they still had to isolate it, understand it, and find a cure.

Burton already knew something about transmission, and something about the mechanism of death: clotting of the blood. The question remained—How did the organisms get into the body?

Because transmission appeared to be airborne, contact with skin and lungs seemed likely. Possibly the organisms burrowed right through the skin surface. Or they might be inhaled. Or both.

How to determine it?

He considered putting protective suitings around an experimental animal to cover all but the mouth. That was possible, but it would take a long time. He sat and worried about the problem for an hour.

Then he hit upon a more likely approach.

He knew that the organism killed by clotting blood. Very likely it would initiate clotting at the point of entrance into the body. If skin, clotting would start near the surface. If lungs, it would begin in the chest, radiating outward.

This was something he could test. By using radioactively tagged blood proteins, and then following his animals with scintillometer scans, he could determine where in the body the blood first clotted.

He prepared a suitable animal, choosing a rhesus monkey because its anatomy was more human than a rat’s. He infused the radioactive tagging substance, a magnesium isotope, into the monkey and calibrated the scanner. After allowing equilibration, he tied the monkey down and positioned the scanner overhead.

He was now ready to begin.

The scanner would print out its results on a series of human block outlines. He set the computer printing program and then exposed the rhesus to air containing the lethal microorganism.

Immediately, the printout began to clatter out from the computer:

It was all over in three seconds. The graphic printout told him what he needed to know, that clotting began in the lungs and spread outward through the rest of the body.

But there was an additional piece of information gained. Burton later said, “I had been concerned that perhaps death and clotting did not coincide—or at least did not coincide exactly. It seemed impossible to me that death could occur in three seconds, but it seemed even more unlikely that the total blood volume of the body—five quarts—could solidify in so short a period. I was curious to know whether a single crucial clot might form, in the brain, perhaps, and the rest of the body clot at a slower pace.”

Burton was thinking of the brain even at this early stage of his investigation. In retrospect, it is frustrating that he did not follow this line of inquiry to its logical conclusion. He was prevented from doing this by the evidence of the scans, which told him that clotting began in the lungs and progressed up the carotid arteries to the brain one or two seconds later.

So Burton lost immediate interest in the brain. And his mistake was compounded by his next experiment.

It was a simple test, not part of the regular Wildfire Protocol. Burton knew that death coincided with blood clotting. If clotting could be prevented, could death be avoided?

He took several rats and injected them with heparin, an anticoagulating drug—preventing blood-clot formation. Heparin was a rapid-acting drug widely used in medicine; its actions were thoroughly understood. Burton injected the drug intravenously in varying amounts, ranging from a low-normal dose to a massively excessive dose.

Then he exposed the rats to air containing the lethal organism.

The first rat, with a low dose, died in five seconds. The others followed within a minute. A single rat with a massive dose lived nearly three minutes, but he also succumbed in the end.

Burton was depressed by the results. Although death was delayed, it was not prevented. The method of symptomatic treatment did not work.