Part 18 (1/2)

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 ma.s.sively 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 ma.s.sive dose lived nearly three minutes, but he also succ.u.mbed 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.

SGOT : 40 : 75.

SED RATE : 9 : 29.

AMYLASE : 70-200 : 450.

Some of the results were easy to understand, others were not. The hematocrit, for example, was rising because Jackson was receiving transfusions of whole blood and packed red cells. The BUN, or blood urea nitrogen, was a test of kidney function and was mildly elevated, probably because of decreased blood flow.

Other a.n.a.lyses were consistent with blood loss. The reticulocyte count was up from 1 to 6 per cent.Jackson had been anemic for some time. He showed immature red-cell forms, which meant that his body was struggling to replace lost blood, and so had to put young, immature red cells into circulation.

The prothrombin time indicated that while Jackson was bleeding from somewhere in his gastrointestinal tract, he had no primary bleeding problem: his blood clotted normally.

The sedimentation rate and SGOT were indices of tissue destruction. Somewhere in Jackson's body, tissues were dying off.

But the pH of the blood was a bit of a puzzle. At 7.31, it was too acid, though not strikingly so. Hall was at a loss to explain this. So was the computer.

SUBJECT CODED JACKSON, PETER.