Free Zika by Donald G. McNeil Page A

Guillain-Barré syndrome a year earlier, in early 2015, as soon as Zika had turned intense. It had been noticed by the health authorities, there had been worrying headlines in Brazil, and some scientists had noted French Polynesia’s experience, but it had not alarmed the whole world. He found Patricia Brito, a 20-year-old bakery cashier who was in intensive care for 40 days and said it was “more terrifying than any horror movie,” and Geraldo da Silva, a 43-year-old construction worker who said he had felt he was “drowning in a sea of mud.”
    Another rare Zika complication that was a footnote in the academic articles about Polynesia eventually made headlines because it caused the first American death. It was an unstoppable case of immune thrombocytopenic purpura, a tongue-twister of a name that means “purple skin caused by leaking capillaries caused by low platelets (thrombocytes) caused by an immune system problem.”
    The first American to die of Zika was not a baby but a Puerto Rican man in his 70s. He succumbed in February 2016, but the connection to Zika wasn’t confirmed for two months. First, the health department and its CDC advisers had to find the antibodies in his blood—antibody testing takes much longer in tropical areas because dengue and yellow fever cross-react on the preliminary antibody tests, creating false positives. To distinguish them from each other, scientists must do “neutralization assays,” a version of the same work that Zika’s discoverers did in mice, but carried out in flat flasks of live cultured cells instead. It is faster than using whole mice, but still takes days or weeks. Then they had to dig up his medical records and interview his family and his doctors to be sure he hadn’t had anything else.
    The man was reasonably healthy for his age before developing Zika symptoms in January, quite early in the island’s outbreak. He recovered, and everything looked fine. But a few days later, he demonstrated “bleeding manifestations,” which the initial CDC report did not detail but, given the later diagnosis, presumably included blood leaking from his gums and nostrils as well as petechiae, tiny dot-like bruises all over his skin caused by leaky capillaries. If the bleeding doesn’t stop, the dots grow until they merge, becoming purpura.
    That would have alarmed him and his family. He went to a doctor, who hospitalized him. In less than 24 hours, he was dead.
    Immune thrombocytopenic purpura (ITP) is related to Guillain-Barré, except that the antibodies triggered by the late immune reaction don’t attack the nerve cells. They attack the platelets, which the blood needs in order to clot. Without them, one simply bleeds to death internally. If ITP had occured in Brazil, it had not appeared in headlines or in medical literature. By the time the death in Puerto Rico was confirmed, it had been declared the cause of death in three cases in Colombia.
    But that was a very rare condition. Another frightening possibility surfaced when I was in conversation with Dr. W. Ian Lipkin, the famous virus hunter who runs the Columbia University Center for Infection and Immunity.
    I asked him about the theory that microcephaly might be a consequence of an initial dengue infection that was followed by Zika.
    He argued that microcephaly didn’t need a viral one-two punch. Several years earlier, he said, his lab had given monkeys Bornavirus (a rare virus that attracted little attention until it killed three German squirrel breeders) and their babies had been microcephalic.
    What people didn’t realize, he said, was that microcephaly was just the tip of the iceberg. Regarding Brazilian kids whose mothers had Zika but who appeared healthy at birth, he said, “I wouldn’t be surprised if we saw big upswings in ADHD, in autism, in epilepsy, and in schizophrenia.”
    That was a horrible thought, I replied. I’d assumed most