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Not every person is so lucky. The World Health Organization estimates that there were more than two hundred million cases of malaria in the world in 2010, and that more than six hundred thousand people died from it. Most deaths occur in Africa, where, according to the WHO, a child dies of the disease every minute. People commonly assume that malaria is restricted to tropical climates such as sub-Saharan Africa, but we find instances of it all over the world — in Asia and in the Americas too, for example, with cases showing up annually in the United States and travellers returning to Canada with the disease in their blood. Some face the misfortune of periodic new bouts of malaria over the course of a lifetime. Malaria is not as much geographically specific as it is climate-related, and if global warming continues, the disease could present itself more often in northern climates.
It took scientists a long time to figure out that mosquitoes are the vectors of malaria. In the eighteenth century, for example, malaria raged in the sea islands off the coast of South Carolina. It was so bad that the spring and summer were known as the “sick season” on slave plantations, and some Southern whites left their plantations entirely to be run by African slaves until the season passed. It was thought at the time that noxious airs were responsible for the fatal illness.
It was not until medical breakthroughs in 1898, when the Scottish physician Sir Ronald Ross proved the complete life cycle of malaria in mosquitoes — for which he was awarded the Nobel Prize for medicine — that we came to understand that the disease is passed from one human being to another by means of the mosquito. Malaria is caused by any of four different plasmodium parasites, transmitted by the female anopheles mosquito, of which there are about twenty key species around the world.
You don’t have to touch the person who is infected. You don’t have to meet the person, or even be in the same room. Presumably, the infected person could die after having been bitten by the mosquito, and it wouldn’t matter to you. All that matters is that a female mosquito bearing sporozoites in its saliva glands chooses to bite you, and to spit into your bloodstream while it extracts a tiny hit of your blood. The disease usually shows up ten to fifteen days after the infective mosquito bite.
It is disturbing to stop and think about how malaria works, because the mosquito links the blood systems of people who don’t even know each other. It doesn’t stop with malaria. From human to human, mosquitoes can also transmit West Nile virus, dengue fever, yellow fever, and Japanese encephalitis. We are more connected than we think, and sometimes in dangerous ways. The more we learn about blood, the more we understand how all blood is hopelessly and forever intermingled, just like humanity itself, across culture, across gender, across age and race, and even across time.
SOMETIMES, THE VERY PERSON who is trying to keep you healthy can be the one who infects your blood and causes your demise. In the mid-nineteenth century, while working as an obstetrician in the Vienna General Hospital, the Hungarian physician Ignaz Semmelweis discovered that new mothers died from puerperal fever (a form of blood poisoning also known as childbed fever) at a far higher rate in a maternity ward in which doctors worked, than in a second maternity ward in which midwives worked. The problem was publicly known to such a degree that some pregnant women begged not to be admitted to the ward supervised by doctors and preferred to give birth in the streets. This was in the 1840s, about two decades before the British surgeon Joseph Lister built on the work of the French chemist Louis Pasteur and began to require — with great success — doctors to wash their hands and medical instruments between patients, to reduce the spread of germs.
Working a step ahead of his time, Semmelweis postulated that doctors and medical students were picking up “cadaverous particles” while dissecting cadavers, and carrying them into the maternity wards. When he prevailed upon physicians to wash their hands in a chlorinated lime solution between their autopsies and their maternity ward work, the maternal mortality rate from blood poisoning dropped dramatically. The resolution of this problem became an obsession for Semmelweis. He was convinced of the importance of his discovery but failed to convince his peers of the necessity of assiduous hand-washing to prevent rampant blood poisoning in maternity wards.
Contemporaries derided the work of Semmelweis, who lost his job at the Vienna hospital. Doctors would continue to spread disease from cadavers to patients, or from patients to patients, causing new mothers and others to die of blood poisoning for many more years, until the germ theory was accepted and hand-washing became the norm. Semmelweis suffered from various professional setbacks and personal problems. He was tricked into visiting an asylum, which he was not permitted to leave. Instead, he was straitjacketed and beaten.
Within two weeks of being detained, it appears, Semmelweis cut his finger during an altercation with asylum employees. The wound became gangrenous. Semmelweis developed blood poisoning — the very problem he had been trying to avert in maternity wards. Within two weeks of being “admitted” into the institution, Semmelweis died. The year was 1865. It was not until the following century that his passionate efforts to help women avoid blood poisoning in maternity wards led Semmelweis to be dubbed the “saviour of mothers.”
Likewise, Bruce Chown of Winnipeg could be considered the modern-day “saviour of babies.” Over the course of time, countless fetuses and newborns have died because — as we finally came to understand near the middle of the past century — their blood types were incompatible with that of their mothers. This is because an antigen, or molecule on the surface of the red blood cell, is present in most, but not all people. A person with this antigen is considered Rh-positive and will have a positive blood type. Someone without it is Rh-negative and will have a negative blood type. With regard to pregnancy and childbirth, this factor becomes critically important — and potentially fatal for the fetus or infant — when the mother is Rh-negative and the baby is Rh-positive. This can occur if the father is Rh-positive. If some of the baby’s red blood cells leak into the mother’s bloodstream — and this can happen during childbirth or in the case of miscarriage, abortion, or other in-uterine trauma — the mother will develop antibodies against the Rhesus factor in the baby’s blood cells. As a result, if the mother becomes pregnant again with an Rh-positive baby, the mother’s antibodies may attack the baby’s blood. This can result in jaundice, brain damage, and the death of the fetus or newborn child. Indeed, as recently as the early twentieth century, mortality from erythroblastosis fetalis — also known as hemolytic or Rh disease — was 50 percent. It accounted for 10 percent of fetal and neonatal deaths in Canada, and claimed the lives of some 10,000 babies annually in the United States.
There are now almost no such deaths in Canada, partly as a result of the pioneering work of Bruce Chown. In 1944, Chown — head of pediatrics at Winnipeg Children’s Hospital — founded a lab in the basement of the hospital to study the cause of Rh disease. Chown, who is described by the Canadian Medical Hall of Fame as one of the greatest Canadian physicians of all time, developed the first Rh exchange transfusion in Winnipeg in 1945, and went on to develop a facility with Connaught Laboratories to manufacture an Rh immune serum. By coating the fetus’s red blood cells and thus disguising their foreign nature, the serum tricks the mother’s bloodstream into thinking it’s compatible with that of the baby. Rh immunoglobulin was licensed for use in 1968, and soon helped prevent many more fetal neonatal fatalities in Canada and around the world. The Rh immune serum is developed from the donated plasma of an Rh-negative donor whose blood has developed Rh antibodies as a result of being exposed to Rh-positive blood cells.
The discovery of the Rh immune serum spurred again the drive to donate, and provided an outlet for the human need to save another’s life. Raymonde Marius, who was seventy-nine when I spoke with her in April 2013, gave plasma more than one thousand times over the course of forty years. After giving birth to five healthy children, she experienced three miscarriages. In the case of the final two losses, which took p
lace in the 1960s, Marius had to carry her fetuses to full term and deliver babies that she already knew had died. The deaths occurred because of the Rhesus disease: her blood type was incompatible with that of the fetuses growing in her womb.
After her own personal losses, Marius wanted to prevent other mothers from having miscarriages as she did. Because she had lost babies to Rh disease, her blood was rich with antibodies that could be used to create an immune system to give to other Rh-negative mothers who were likely to have Rh-positive babies.
When a doctor asked if she would consider donating plasma to be used to manufacture an immune serum, she entered a donation program that lasted four decades. She spent one evening a week, every week, donating plasma. “I started donating at the age of about thirty-seven and donated for forty-two years,” Marius told me. “It takes time to donate plasma. They take it. They spin it [in a centrifuge]. They remove the plasma. They take what they want and give us back the rest. And they do that twice. I was a fast blood donor. I had good veins. It took me sixty to seventy-five minutes to donate plasma.
“I got a plaque after the thousandth time (I donated blood). It was a nice plaque with my name on it. And I kept on donating after that.” Marius said that she was initially paid $5 per plasma donation, and that the amount later rose to about $60. She said they were paying for her time and for her travel expenses, not for her blood.
Cheryl Lawson is an employee at Cangene Corporation in Winnipeg, which pays donors to give plasma that is used to manufacture WinRho SDF, an immune serum globulin used to prevent fatalities due to Rh disease. Lawson estimates that Marius may have donated as many as 1,500 times before she finally stopped. The plasma donation program began in Winnipeg in the 1960s and had an active corps of twenty or thirty female donors at the time. Now the company has 102 regular donors — some male, but mostly female — who commit to a regular, long-term donation program, according to Lawson. The blood of the donor frequently has to be readied for donation. A donor may have to receive several blood transfusions to stimulate their own blood to produce the antibodies necessary to develop the serum. Clearly, all this work — undergoing blood transfusions to become a successful donor, and then donating regularly for years — stems from the desire to give. When I asked why she donated plasma weekly for forty years, Marius had a simple answer: “I was helping another mother. Without my plasma, she wouldn’t have been able to have a healthy baby.”
Blood keeps us alive, and — right down to our red and white blood cells — has the ability to save us. But as we have seen, it is dangerous too. It can turn against us, and it can turn against those we love most deeply too. The Bava Batra, the last of the three tractates of the Talmud, might indeed be prescient and wise beyond all reckoning when it warns, rather ominously: “I, blood, am the cause of all illness.”
AS THE AUTHOR OF Something Happened, a novel in which the main character worries, as only a hypochondriac will do, about how his body might do him in, the late Joseph Heller might have identified with this observation: there are so many ways that our blood betrays us! Some cancers involve a proliferation of white blood cells, and are generally treated by trying to destroy those same cells. Bleeding disorders are treated by blood transfusions, and by offering patients products to help their blood clot. Although not life-threatening by any means, and certainly not of the same order of magnitude as cancer or hemophilia, erectile dysfunction can certainly affect the quality of a man’s life, and can be treated by a number of means — pills, injection, implants — all of which aim to move blood into the penis. We can even inherit defects of the blood from our ancestors, or betray our own descendants by passing them along.
My son, Andrew, eighteen years old and winding up his first year at university as I write, is an active, slim man. He played hockey and soccer throughout his childhood. He goes to the gym. Gets on a bike. Likes to go running. When we were younger, he and my two eldest daughters, Geneviève and Caroline, would sometimes run with me. Some of my fondest memories involve running five-kilometre community races with them, on Father’s Day and on Thanksgiving. When they were young, I would run with whichever one was slowest in that particular race, so he or she wouldn’t feel alone. Now I wouldn’t be able to keep up with Andrew.
I had an ulterior motive for running with the children, Andrew especially. Sure, it’s good for the body, and relaxing for the soul. A great stress reliever, and something I have loved to do since my own childhood. But I took Andrew running for the same reason that I have tried to warn him, ever so gently, not to overdo the desserts. Perhaps not to stack an ice cream scoop on top of a piece of apple pie, all of that having followed a piece of cake. Teenagers eat like that, and many can get away with it. But I have worried about Andrew. He is in a long line of diabetics, and it shoots like an arrow through the male line of my family.
My grandfather, father, and older brother all developed diabetes at forty-three. When I passed that age, I counted my blessings. Maybe the disease had skipped over me. Perhaps all those years of running had saved me. But I was to have no such luck. I was diagnosed two years later. My grandfather and father died of complications related to diabetes.
Diabetes stands out as one of the most common defects of the pancreas, and thus the blood, to be passed from one generation to another. It has reached epidemic proportions in Canada and other countries. Diabetes associations in North America estimate that some twenty-six million Americans and three million Canadians suffer from the disease. It manifests itself in three basic ways. As the Canadian Diabetes Association notes, Type 1 diabetes usually shows up early in life and results from an inability of the pancreas to produce the hormone insulin, which regulates the amount of glucose (or sugar) in the blood. Type 2 diabetes presents itself more often in adulthood (although more children are being affected as the epidemic grows), and involves an inability of the pancreas to produce sufficient insulin or an inability of the body to use the insulin well. Finally, gestational diabetes occurs during pregnancy and is considered temporary.
The consequences of diabetes can be lethal. Excessively high levels of blood glucose eat away at our nerve endings, attacking the organs and the body’s extremities. This can lead to blindness and foot and leg amputations. It can also lead to kidney failure and death. Some people call the disease “the silent killer,” because diabetics do not generally experience significant pain or discomfort in the early phases of the disease. It’s a misnomer, however, because if it proceeds untreated or is poorly managed, the body will break down in the most excruciating ways, requiring operations, amputations, and dialysis.
I watched my father, Daniel G. Hill III, fall apart limb by limb. He had a wonderful, active, public life through most of his career as a sociologist, human rights activist, and writer about black history in Canada. His last years on the job were tough, but he made it through his final working stint as ombudsman for the province of Ontario. It was a five-year posting. I attended his swearing-in party, in 1984, and I remember driving him to the Ontario Legislature for it. He was still well enough to travel with my mother, go to work, and do battle on behalf of those who felt they had been treated badly by the Ontario government.
But he had good days and bad days, back then, and the day of his swearing-in was one of the bad ones. He was surely excited, and proud, and perhaps a tad anxious, going to the party. He called it glad-handing, when he went to social events and had to chat with a hundred well-wishers. He was the first black man to become the ombudsman of Ontario, and years earlier he had become the first director of the Ontario Human Rights Commission, and he was surely conscious of the social weight on his shoulders. He knew he had better not screw up on the job, do something stupid, or cause some scandal, because if he did the whole world would be looking to point fingers. To the best of my knowledge, he never screwed up on any job — certainly never enough to draw public opprobrium, or to jeopardize his own position.
I could see that he was worke
d up, in the passenger seat of the sedan that I drove to get him to the Legislature, but I was not prepared for what I saw. He became confused, irrational, demanding things that made no sense, and he appeared to be physically trembling. It upset me to see my father so out of it, on a day that he was expected to be in command of his faculties and to excite his well-wishers about the job that was ahead of him. He had invited many of our neighbours to the reception, and I recall that he was especially tickled and proud about that. With all the responsibilities that were about to fall on his shoulders as the person appointed to probe into accusations of wrongdoing by the very government that employed him, the thing my father obsessed about in the car was the neighbours: who was coming, if they had received their invitations, how they would react. This fussing on his part told me that something was wrong.
He got out of the car and started wandering off toward an employee of the Legislature who stood at the door, barking some sort of insane order. We got him inside and into a quiet room, and figured out that his blood sugars were probably low, and gave him a glass of apple juice. Fifteen minutes later, he was back to normal.
The irritability, irrationality, the trembling — all of this resulted from the amount of sugar in his blood. In the language of diabetics and their families, he was “having a low.” Glucometers — pocket-sized devices that measure blood sugar — were bigger, more cumbersome, and slower in the 1980s than they are now. You had to wait a while for the number to show up on a little screen, although it now takes all of five seconds to get the reading. I can’t remember for sure what his reading was that time, but it gave us all the information we needed to get the juice into him.