Weber was brought the first host in 1938 and had to keep the disease alive with new hosts from the Gestapo—which they were always willing to supply, though in small lots so he never had more than a few laboratory subjects at a time. He was never told where that first host came from but he surmised South America. Later, in 1940 when the laboratory was at Buchenwald, the Gestapo supplied him with a slow but steady trickle of Gypsies.
What he had discovered when I joined the project in 1941 was that infection was only successful by fluid transport from the infected host, infection was in two phases, and there were at least two components to the disease.
In one experiment, Weber took fluid from a toter Mann and filtered three samples, one through a 100 micron filter, one through a 50 micron filter, and one through a Chamberland filter. The 100 micron wash caused full infection. The 50 micron also caused a partial infection involving quick and sudden pain, followed by an inevitably fatal stroke. He called this partial infection type I-A. The Chamberland wash caused a particularly quick and virulent form of rabies—Weber referred to that as type I-B. Hence, Weber’s hypothesis of two components for a full infection, one large and the other the rabies virus. He had isolated a worm as the possible large component in that, when collected and washed of any contaminants, it seemed to cause an I-A infection similar to the infection caused by the 50 micron wash. When the Chamberland wash was recombined with the worm, full infection ensued.
Weber had even characterized the partial infections and the stages of the full infection. I found it interesting that the partial infections were both dismal, painful affairs, while the full infection showed up first as euphoria, followed by sleepiness and coma. The subject awoke in a few days as a toter Mann.
Even so, I was surprised that there hadn’t been more discovered in four years. After all, Weber had the tote M?nner themselves and their inherent ability to infect others. The Gestapo was willing to provide a constant, if limited, supply of hosts. But Weber’s horror of contagion was so strong that every step had to be examined minutely until he had determined to his satisfaction that he could properly protect himself and his staff. Dissection was a long and tedious process; vivisection was almost impossible. I suppose I could not blame him. Even a partial infection would be fatal and full infection always resulted in another toter Mann. No one wanted to risk that.
Thus, my first task was the design and construction of a dissection and histology laboratory where Weber could disassemble the subjects in safety. It was not a difficult task. I came to Buchenwald in July. By the end of the month I had the design and began construction. Weber dissected his first wriggling subject by the first of September.
My fuel work had been much more interesting. It was exacting, exciting work with great applications. Here, I was barely more than a foreman. The war in Russia seemed to be going well and I wondered if I should have protested more to Willem.
But Elsa and our son Helmut loved Weimar. The city was pretty in a storybook way. It didn’t hurt that the bombers left Weimar largely undisturbed, instead striking in Germany proper. It lent the city a relative calm. Several young couples had taken over the empty housing. This was early in the war and food and petrol, though rationed, were still plentiful.
I didn’t work weekends and the three of us spent many summer days in the Park on the Ilm. It occurred to me, during those pleasant hours watching Helmut playing in front of Goethe’s House, that this was, perhaps, a better use of my time than the factory or the lab.