Sometimes the sum of human wisdom is to be found, as writer Alexandre Dumas put it, within the words ‘wait and hope’.[1] And that was to be my treatment, to wait and to hope. My parents were given a multicoloured party horn to check the strength of my breathing (there was no home equipment small enough for a toddler). If the horn failed to unroll when I blew, it meant the paralysis had reached the muscles that pumped air into my lungs.
There is a photo of me sitting on my grandfather’s lap around this time. He is in a wheelchair. He’d caught polio in India aged twenty-five, and had been unable to walk since. I’d only ever known him like that, his strong arms wheeling uncooperative legs. In a way, it brought familiarity to this unfamiliar situation. Yet what linked us was also what separated us. We shared a symptom, but the mark of his polio was permanent; gbs, for all its misery, was usually a temporary condition.
So we waited and we hoped. The party horn never failed to unroll, and a lengthy recovery began. My parents told me gbs stood for ‘Getting Better Slowly’. It was twelve months before I could walk, and another twelve before I could manage anything resembling a run. My balance would suffer for years to come.
As my symptoms faded, so did my memories. Events became distant, left behind to another life. I can no longer remember my parents giving me chocolate buttons before the needles. Or how I subsequently refused to eat them – even on a normal day – fearing what would come next. The memories of games of tag at primary school have faded too, with me spending all of lunchtime as ‘it’, my legs still too weak to catch the others. For the twenty-five years that followed my illness, I never really spoke about gbs. I left school, went to university, completed a PhD. gbs seemed too rare, too meaningless to bring up. Guillain-what? Barré who? The story, which I never told anyway, was over for me.
Except it wasn’t quite. In 2015, I was in the Fijian capital Suva when I encountered gbs again, this time professionally. I’d been in the city to help investigate a recent dengue fever epidemic.[2] Transmitted by mosquitoes, the dengue virus causes sporadic outbreaks on islands like Fiji. Although symptoms are often mild, dengue can come with a severe fever, potentially leading to hospitalisation. During the first few months of 2014, over 25,000 people showed up at health centres in Fiji with a suspected dengue infection, putting a huge burden on the health system.
If you’re imagining an office perched on a sunny beach, you’re not picturing Suva. Unlike Fiji’s resort-laden Western division, the capital is a port city in the southeast of the main island, Viti Levu. The two main roads of the city loop down into a peninsula, forming the horseshoe shape of a magnet, with the area in the middle attracting plenty of rain. Locals who were familiar with British weather told me that I’d feel right at home.
Another, much older, reminder of home was to follow soon after. During an introductory meeting, a colleague at the World Health Organization (who) mentioned that clusters of gbs had been appearing on Pacific Islands. Unusual clusters. The annual par for the disease was 1 or 2 cases per 100,000 people, but in some places they’d seen double figures.[3]
Nobody ever worked out why I got gbs. Sometimes it follows an infection – gbs has been linked to flu and pneumonia, as well as other diseases[4] – but sometimes there’s no clear trigger. In my case, the syndrome was just noise, a random blip in the grand scheme of human health. But in the Pacific during 2014/15, gbs represented a signal, just like birth defects would soon do in Latin America.
Behind these new signals lay the Zika virus, named after the Zika Forest in southern Uganda. A close relative of the dengue virus, Zika was first identified in the forest’s mosquitoes in 1947. In the local language, Zika means ‘overgrown’[5] and grow it would, from Uganda to Tahiti to Rio de Janeiro and beyond. Those signals in the Pacific and Latin America in 2014 and 2015 would gradually become clearer. Researchers found increasing evidence of a link between Zika infection and neurological conditions: as well as gbs, Zika seemed to lead to pregnancy complications. The main concern was microcephaly, where babies develop a smaller brain than usual, resulting in a smaller skull.[6] This can cause a host of serious health issues, including seizures and intellectual disabilities.
In February 2016, triggered by the possibility that Zika was causing microcephaly,[7] who announced that the infection was a Public Health Emergency of International Concern, or pheic (pronounced ‘fake’). Early studies had suggested that for every 100 Zika infections during pregnancy, there could be between 1 and 20 babies with microcephaly.[8] Although microcephaly would become the primary concern about Zika, it was gbs that first brought the infection into health agencies’ focus, as well as into mine. Sitting in my temporary office in Suva in 2015, I realised that this syndrome, which had shaped so much of my childhood, was one I knew almost nothing about. My ignorance was mostly self-inflicted,
