ight through small bones and cartilage without
using a saw."

"How nice," Mary said. "I expect you enjoy yourself."

"I couldn't ask for better equipment," he replied noncommittally. With
deft motion of the handler he drew the scalpel down across the chest
and along the costal margins in the classic inverted "Y" incision.
"We'll take a look at the thorax first," he said, as he used the
handlers to pry open the rib cage and expose the thoracic viscera. "Ah!
Thought so! See that?" He pointed with a small handler that carried a
probe. "Look at those lungs." He swung a viewer into place so Mary could
see better. "Look at those abscesses and necrosis. It's Thurston's
Disease, all right, with secondary bacterial invasion."

The grayish solidified masses of tissue looked nothing like the normal
pink appearance of healthy lungs. Studded with yellowish spherical
abscesses they lay swollen and engorged within the gaping cavity of the
chest.

"You know the pathogenesis of Thurston's Disease?" Kramer asked.

Mary shook her head, her face yellowish-white in the glare of the
fluorescents.

"It begins with a bronchial cough," Kramer said. "The virus attacks the
bronchioles first, destroys them, and passes into the deeper tissues of
the lungs. As with most virus diseases there is a transitory
leukopenia--a drop in the total number of white blood cells--and a rise
in temperature of about two or three degrees. As the virus attacks the
alveolar structures, the temperature rises and the white blood cell
count becomes elevated. The lungs become inflamed and painful. There is
a considerable quantity of lymphoid exudate and pleural effusion.
Secondary invaders and pus-forming bacteria follow the viral destruction
of the lung tissue and form abscesses. Breathing becomes progressively
more difficult as more lung tissue is destroyed. Hepatization and
necrosis inactivate more lung tissue as the bacteria get in their dirty
work, and finally the patient suffocates."

"But what if the bacteria are controlled by antibiotics?"

"Then the virus does the job. It produces atelectasis followed by
progressive necrosis of lung tissue with gradual liquefaction of the
parenchyma. It's slower, but just as fatal. This fellow was lucky. He
apparently stayed out of here until he was almost dead. Probably he's
had the disease for about a week. If he'd have come in early, we could
have kept him alive for maybe a month. The end, however, would have been
th