The Island of the Colorblind

These were some of the clues and contradictions, John continued, which faced Kurland and Mulder when they came here in the 1950s – and which are so difficult to reconcile by any single theory. Kurland was at first inclined to think in terms of a genetic origin. He looked at the early history of the island, and how a near genocide reduced the population from 100,000 to a few hundred – the sort of situation which disposes to the spread of an abnormal trait or gene (as with the achromatopsia on Pin-gelap) – yet there was no simple Mendelian pattern linking those with the disease. He wondered, in the absence of such a pattern, whether this was a gene with ‘incomplete penetrance.’ (He wondered too if a genetic predisposition to lytico-bodig might also have a paradoxical, selective advantage – perhaps increasing fertility or conferring immunity to other diseases.) But he had to wonder whether there might not be some environmental factor, in addition to a genetic susceptibility, a ‘necessary adjunct,’ as he put it, to developing the disease.

In the late 1950s he extended his studies to the very large population of Chamorros who had migrated to California. They had, he observed, the same incidence of lytico-bodig as the Chamorros in Guam, but the disease might only develop ten or twenty years after they had left Guam. There were, on the other hand, a few non-Chamorro immigrants who seemed to have developed the disease a decade or two after moving to Guam and adopting a Chamorro lifestyle.

Could the environmental factor, if there was one, be an infectious agent, a virus, perhaps? The disease did not appear to be contagious or transmissible in any of the usual ways, and no infectious agent could be found in the tissues of those affected. And if there was such an agent, it would have to be one of a very unusual sort, one which might act as a ‘slow fuse’ – John repeated the phrase for emphasis – a slow fuse in the body, setting off a cascade of events which only later might manifest as clinical disease. As John said this, I thought of various post-viral neurodegenerative syndromes, and especially again of my postencephalitic patients, who in some cases only started to show symptoms decades after the initial encephalitis lethargica – sometimes as much as forty-five years later.

At this point in the story, John started pointing emphatically through the window. ‘Look!’ he said. ‘Look! Look! Cycads!’ Indeed I saw cycads all round, some growing wild but many, I now saw, cultivated in gardens, as we drove to Talofofo to visit another patient of John’s, a former mayor of the village, whom everyone called the Commissioner.

Cycads only grow in tropical or semitropical regions and were new, alien, to the early European explorers when they first saw them. At first glance, cycads bring to mind palms – indeed the cycad is sometimes called a sago palm – but the resemblance is superficial. Cycads are a much more ancient form of life, which arose a hundred million years or more before there were palms or any other flowering plants.

There was a huge native cycad, at least a century old, growing in the Commissioner’s yard, and I stopped to gaze at this splendid tree, fondled a stiff, glossy frond, then caught up with John at the front door. He knocked on the door, and it was opened by the Commissioner’s wife, who ushered us into the main room where her husband sat. Sitting in a massive chair – rigid, immobile, and parkinsonian, but with a sort of monumental quality, the Commissioner looked younger than his seventy-eight years and still exuded a sense of authority and power. Besides his wife, there were his two daughters and a grandchild – he was still, for all his parkinsonism, very much the patriarch of the house.