The Boy on the Bridge

As soon as they’re underway, Greaves springs his seat strap and retreats from the crew quarters into the lab. He hopes he might get a little time to himself there, since working when they’re on the move isn’t a popular option. It’s too hard to compensate for the rocking of Rosie’s chassis. A few shattered test tubes and ruined samples were enough to wean most of the science team off the habit.

But not today. He is followed almost immediately by Rina. He’s afraid for a moment that she will offer to help him, but it seems she’s got a project of her own to pursue. She flashes him a smile as she moves past him towards the further workbench. It’s a weak smile. Greaves assigns it meaning c (you are my friend) on a list that goes all the way to n (I’m thinking of something that you wouldn’t understand).

“Getting harder and harder to work around me, isn’t it?” Rina asks, patting her protuberant belly. “Don’t let me get in your way, Stephen.”

He considers telling her that there is still more than a foot of clearance on either side of the central walkway if she stands in its centre. But he is almost certain (from her smile, which has now transitioned into a d) that she intends the comment as a joke. He offers a smile in return, usually the safest option, and goes back to his work.

From the crew quarters come the voices of Sealey and Akimwe. They are discussing Cordyceps, the great adversary—its cultural and historical significance, with special reference to Chinese folk legends about its life cycle. Greaves is well aware that the Chinese, almost three thousand years ago, saw the fungus sprouting from the exploded bodies of caterpillars and thought they had chanced upon a magical metamorphosis. A creature that was an animal in summer and a mushroom in winter! They prized Cordyceps as a treatment for heart disease and impotence, the distilled essence of life itself. Later generations found that the fungus could grow through damaged nerve tissue and partially repair it. There’s a prevailing theory that these medicinal uses of the fungus were the precursors to the hungry plague—the doorway through which Cordyceps infected human populations.

Tuning out the voices, Greaves prepares the tissue collected by the biopsy needle for examination. He uses the ATLUM, a machine perfected at Harvard’s Centre for Brain Science in the years immediately preceding the Breakdown. It’s a microtome, a lathe for slicing neural tissue into ultra-fine sections of a single cell’s thickness. The ATLUM mounts the sections onto a continuous ribbon of tape rather than onto conventional slides. It therefore allows the user—at least, the user with a scanning electron microscope ready to hand—to build up a three-dimensional view of brain structures and to follow them down through successive strata of tissue. Greaves finds the operation of the ATLUM utterly enthralling. It peels tissue samples the way you might peel an apple with your pocket knife, then rebuilds them into an apple again.

When he mounts and examines his sample, though, he is confused.

The children have already demonstrated that they are not at all like other hungries. Their behavioural repertoire is vast, perhaps as large as that of regular humans, so he expects to see little or no fungal penetration of the brain tissue. Instead he finds himself staring at a dense mat of fungal mycelia. The brain is one vast spider web of threads, woven about and through the regular neurons all the way from the outer cortex to the thalamus and transverse fissure. By volume, this brain is half human and half fungus.

But where is the damage? The human cerebral matter ought to have been hollowed out, devoured by the fungal invader. There ought to be a 55–80 per cent reduction in actual brain mass and a visible degeneration of whatever tissue still remains. A crust of microglial cells overlaying the damaged cortical areas. Myelin sheaths stripped away leaving bare neurons firing fitfully and futilely into synaptic gaps that have become mud wallows of necrotic juices. None of that is present. If this brain has been invaded, it is mounting a robust defence.

Or is this a moment rather than a state? Just a brief equilibrium before the cerebral tissue surrenders and the fungus carries the day? But in that case, how has the brain held out for so long, surrounded and besieged? There is some factor at work that he has never seen before, and the implications are immense. Almost dizzying.

Greaves raises his head from the eyepiece and looks around furtively. He feels for a moment as though the beating of his heart, the tremor in his breathing must have been noticed, but Rina isn’t looking at him at all. She is focused on her own work, her preoccupied calm contrasting with his own sudden burst of excitement and near-panic.

He goes back in. This time he abandons the microscope for a while, draws off another tissue sample and begins a series of tests for the presence of the major neurotransmitters—the chemicals that turn the brain from a lump of inert flesh into the world’s biggest communications hub. There are well over a hundred of these chemical couriers, but Greaves limits himself for the moment to a sample of about thirty: the ones that show up quickly in the presence of off-the-shelf reagents.

Half of the chemical transmitters are present in the same strengths and proportions as a normal human brain. The rest aren’t there at all.

Which is impossible.

He knows how Cordyceps is meant to work—how it works in every hungry studied so far. Seconds after primary infection, it floods the human host’s bloodstream where it proliferates with breathtaking speed. Carried through the blood-brain barrier, it lodges in the brain stem and launches a pre-emptive strike, deactivating normal neural functioning by destructive super-stimulation of the nerve cells. It burns the brain out.

Then it grows downwards again, into and through the spine, extending its mycelial system along the host body’s major afferent nerve trunks. With the brain out of the conversation, apart from a few powerful, instinctive behaviours controlled through the pons and medulla, the fungus is free to hijack the peripheral nervous system and use it to take direct control of the host’s motor functions.

So in a heavily infected brain, native neurotransmitter activity should be minimal to non-existent. There may still be a consciousness in there—the experts at Beacon have argued it back and forth without reaching a conclusion—but either way it doesn’t matter. The strings have been cut.

This brain is different. Structurally it’s intact and chemically it’s halfway functional: but what good is half a brain? You can’t drive a car if it has a carburettor but no spark plug, cylinders but no pistons. It’s not as though half a brain could run half the body’s systems. Your limbs can’t be made to move without dopamine or acetylcholine. You can’t have a proper sleep cycle without adenosine, or hunger and satiety reflexes without noradrenaline. So the fungus must still be running the show, surely, however healthy the brain tissue looks in cross-section.

M. R. Carey's books