“A tapeworm is harmless and won’t necessarily cause its host to fall ill,” she said. “As a result, you can host even very long tapeworms for a long period of time without knowing that you’re infected. In the vast majority of cases, the tapeworm is discovered by chance, during an operation or an autopsy. They normally grow six to eight feet long, and when a tapeworm is discovered, the host is given medication that kills the tapeworm and it’s expelled from the host with feces. Unpleasant, certainly, but as I said, quite harmless.”
Søren was close to retching. At the same time his brain was troubled by a discrepancy.
“I’m not sure I quite understand,” he stuttered. “Professor Helland didn’t have a tapeworm, but carried…” Søren checked his notes, “cysticercus.” Dr. Bjerregaard waited patiently.
“That’s correct. However, I haven’t finished my explanation,” she said calmly. “The life cycle of parasites is a complex area, even for a great many biologists, and in order for you, as lay people, to understand what I’m telling you, I need to give you some basic information.” She suddenly looked at the two men as though she was enjoying herself tremendously.
“Yes, of course. Sorry,” Søren said. Henrik looked sick.
Søren expected Dr. Bjerregaard to launch into the second half of her disgusting lecture, but she merely said, “The logical conclusion is… ?” She looked sternly at the two men.
“That Helland ate shit,” Henrik blurted out. “Gross.”
Søren glared at Henrik.
“It means,” he said, addressing Dr. Bjerregaard, “that Helland somehow ingested a tapeworm egg.” On realizing the implications, he fell silent.
“Or, to be precise, 2,600 eggs,” Dr. Bjerregaard interjected. “If that’s the number of cysticerci Bøje found in the tissue of the diseased, then it would equal 2,600 eggs.”
Søren managed to suppress his revulsion to such an extent that he could follow her logic. “But he didn’t ingest a whole…” he checked his notes again, “proglottid?”
“That would be impossible to know.”
Søren detected a microscopic smile at the corner of her mouth.
“If the proglottid carried more than forty thousand eggs, you would have expected many more than 2,600 cysticerci. However, there might be several factors why only 2,600 managed to develop.” She shrugged. “The point is Lars Helland acted as the intermediate host, and that happens very rarely in these latitudes. During my thirty years here, I’ve only come across three cases of human intermediate host infection, and they were all discovered in people who had recently returned from countries with a high prevalence of Taenia solium, such as Latin America, non-Islamic Asia, and Africa. Do you know if Helland spent time in a high-risk country?”
“We’ll be checking that. The parasite theory is still very new to us,” he said, by way of apology, and continued, “How can you tell how long the cysticerci have been in Helland’s tissue?”
“The host body forms calcium capsules around the cysticercus, to protect itself from the foreign object, and in the capsule, the cysticercus awaits its next developmental stage. You can determine the exact age of the cysticercus by measuring the thickness of the calcium shell. This would normally take place in pigs, which will be eaten sooner or later, and this places an upper limit on how calcified the capsule becomes. However, humans are unlikely to be eaten, aren’t they? The growth of the cysticercus is generally very slow, and as Helland’s cysticerci were fairly large, I would estimate that they’d developed over a long period of time. The capsules were thick and the cysticerci would undoubtedly have demanded more and more room. To begin with, they would have caused Professor Helland only mild irritation, but in time they would have become a pathological condition, and I can’t imagine how he coped with it. Cysticerci have a preference for the central nervous system, and from records—from Mexico, for example, where the occurrence of humans infected with cysticerci is high—82 percent of cysticerci had attached themselves to nerve tissue. Otherwise they prefer muscular and subcutaneous tissue, in that order.”
“What about symptoms?” Søren asked. Bjerregaard pursed her lips.
“The symptoms of an infected patient depend on several factors. Generally, you’ll expect to find a positive correlation between the number of cysticerci and the extent of the symptoms. However, it depends on where the cysticerci are located. Forty thousand cysticerci located exclusively in muscle tissue can, in theory, cause less damage to their host than five unfortunately located cysticerci in nerve tissue. Muscular tissue tolerates the uninvited guests surprisingly well, and their presence may not cause muscular pain until the very late stages. However, if they are located in the central nervous system, it’s a completely different matter. As the cysticercus grows, it takes up more room and diverts blood supply from the surrounding tissue, and the tissue in the central nervous system is of far more critical importance for functionality than muscular tissue, for example. If the central nervous system is attacked, the patient will experience severe seizures of an epileptic nature, the same as have been observed in brain tumor patients. In addition, the patient will experience sudden blackouts, and very likely suffer from severe motor problems and spasms. Bøje Knudsen informed me the deceased had a fairly high concentration of cysticerci in his brain tissue, and he showed signs of multiple fractures and falls. That makes perfect sense.”
She allowed the conclusion to hang in the air before she continued. “If the cysticerci are discovered in time, the patient will be given medication and/or surgery, depending on the number of cysticerci, their location, and how advanced their development is. In the case of the deceased, the cysticerci weren’t discovered which, in itself, is incredible. To me, it’s a physiological mystery how the deceased managed to go to work on the day he died.”
A moment of silence followed, then Dr. Bjerregaard said, “Anything else I can do for you gentlemen today?”
Søren was taken aback. He wasn’t used to being shown the door before he had announced he had no further questions. Dr. Bjerregaard glanced at her watch and pursed her lips again.
“Can you explain how Helland was infected?” Søren said, refusing to be brushed off.
“No,” Dr. Bjerregaard replied. “I certainly can’t.”
She sounded almost hurt, and Søren realized what a stupid question it had been. It was the equivalent of asking the mechanic what caused a car crash.
“But, like I said,” she carried on, giving Søren a final look, “either he ingested feces, or something which had been in contact with infected feces—and all things considered, that’s highly unlikely. Or he worked with live tapeworms and was accidentally infected, which doesn’t really add up, either. There are parasites that infect their host through the skin, the blood-sucking Japanese mountain leech, for example, which causes bilharziasis, but Taenia solium has to be ingested via the digestive tract to complete its life cycle, so even if we assume the deceased had a work-related accident, I still can’t see how he could have been infected. You would expect a biologist who happens to drop a test tube to take precautions immediately, and you would most certainly not expect him to go to lunch without washing his hands after an accident involving Taenia solium. My guess is Professor Helland must have spent time in a high-risk area within the last six months, and that was where he was infected. It’s still hard to imagine how, but as I said, it does happen.”
Søren looked at Dr. Bjerregaard for a long time, before he said, “And if it’s none of the above?”
Bjerregaard stood up.