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:
[graphic of disease spread in human body]
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.
He put the dead rats to one side, and then made his crucial mistake.
Burton did not autopsy the anticoagulated rats.
Instead, he turned his attention to the original autopsy specimens, the first black Norway rat and the first rhesus monkey to be exposed to the capsule. He performed a complete autopsy on these animals, but discarded the anticoagulated animals.
It would be forty-eight hours before he realized his error.
The autopsies he performed were careful and good; he did them slowly, reminding himself that he must overlook nothing. He removed the internal organs from the rat and monkey and examined each, removing samples for both the light and electron microscopes.
To gross inspection, the animals had died of total, intravascular coagulation. The arteries, the heart, lungs, kidneys, liver and spleen- all the blood-containing organs- were rock-hard, solid. This was what he had expected.
He carried his tissue slices across the room to prepare frozen sections for microscopic examination. As each section was completed by his technician, he slipped it under the microscope, examined it, and photographed it.
The tissues were normal. Except for the clotted blood, there was nothing unusual about them at all. He knew that these same pieces of tissue would now be sent to the microscopy lab, where another technician would prepare stained sections, using hematoxylin-eosin, periodic acid-Schiff, and Zenker-formalin stains. Sections of nerve would be stained with Nissl and Cajal gold preparations. This process would take an additional twelve to fifteen hours. He could hope, of course, that the stained sections would reveal something more, but he had no reason to believe they would.
Similarly, he was unenthusiastic about the prospects for electron microscopy. The electron microscope was a valuable tool, but occasionally it made things more difficult, not easier. The electron microscope could provide great magnification and clear detail-but only if you knew where to look. It was excellent for examining a single cell, or part of a cell. But first you had to know which cell to examine. And there were billions of cells in a human body.
At the end of ten hours of work, he sat back to consider what he had learned. He drew up a short list:
1. The lethal agent is approximately 1 micron in size. Therefore it is not a gas or molecule, or even a large protein or virus. It is the size of a cell, and may actually be a cell of some sort.
2. The lethal agent is transmitted by air. Dead organisms are not infectious.
3. The lethal agent is inspired by the victim, entering the lungs. There it presumably crosses over into the bloodstream and starts coagulation.
4. The lethal agent causes death through coagulation. This occurs within seconds, and coincides with total coagulation of the entire body vascular system.
5. Anticoagulant drugs do not prevent this process.
6. No other pathologic abnormalities are known to occur in the dying animal.
Burton looked at his list and shook his head. Anticoagulants might not work, but the fact was that something s the process. There was a way that it could be done. He knew that.
Because two people had survived.
17. Recovery
AT 1147 HOURS, MARK HALL WAS BENT OVER THE computer, staring at the console that showed the laboratory results from Peter Jackson and the infant. The computer was giving results as they were finished by the automated laboratory equipment; by now, nearly all results were in.
The infant, Hall observed, was normal. The computer did not mince words:
SUBJECT CODED- INFANT- SHOWS ALL LABORATORY VALUES WITHIN NORMAL LIMITS
However, Peter Jackson was another problem entirely. His results were abnormal in several respects.
SUBJECT CODED JACKSON, PETER
LABORATORY VALUES NOT WITHIN NORMAL LIMITS FOLLOW
TEST: NORMAL: VALUE
HEMATOC: 38-54: 21 INITIAL
25 REPEAT
29 REPEAT
33 REPEAT
37 REPEAT
BUN: 10-20: 50
COUNTS RETIC: 1: 6
BLOOD SMEAR SHOWS MANY IMMATURE ERYTHROCYTE FORMS
TEST: NORMAL: VALUE
PRO TIME: L2: 12
BLOOD PH: 7.40: 7.31