Category Archives: Health


On June 10th, I traveled to the south of Gombe to visit the range of the little-known Kalande community of chimpanzees.

Map of Gombe National Park and chimpanzee ranges (from Rudicell et al., 2010)
Map of Gombe National Park and chimpanzee ranges (from Rudicell et al., 2010)

The Kalande community is one of three chimpanzee communities at Gombe.

The most famous, most intensively studied chimpanzees live in the Kasekela community in the center of the park. These are the chimpanzees that Jane Goodall has studied since 1960. They have the biggest range and the most members of the park’s three communities.

To the north of Kasekela live the Mitumba chimpanzees. This is a smaller community, which Deus Mjungu studied for his PhD research. The Mitumba community has fewer chimpanzees than Kasekela, but is still vigorous. They have a small range, but it includes excellent chimpanzee habitat with lots of food trees.

To the south is the Kalande community (also known as Bwavi). Most of the Kalande community’s range is grassland and woodland, with narrow strips of forest along the stream valleys. We know less about the Kalande chimpanzees than any of the others in Gombe. For the most part, these chimpanzees are still unhabituated, meaning they fear people. Researchers can follow the Kasekela and Mitumba chimpanzees around all day long, but they are lucky to get even fleeting glimpses of Kalande chimpanzees.

We aren’t even completely sure how many chimpanzees live in Kalande. Based on sightings and samples of genetically distinct individuals, there seem to be at least 9 chimpanzees in Kalande, but we don’t know for sure.

Skull from a male chimpanzee found dying in Kalande in 1994 or 1995.
Skull from a male chimpanzee found dying in Kalande in 1994 or 1995.

A small team of researchers monitor the Kalande chimpanzees. They collect fecal samples for genetic analysis, which enables us to keep track of individuals, even when we don’t know what they look like. Kalande has the highest rate of infection with the virus SIVcpz, which likely contributed to the decline of this community (Rudicell et al., 2010). Many females have left Kalande for other communities, both as part of the natural emigration process (females usually leave to join a new community when they are sexually mature), and because as Kalande declined, it eventually came to have too few males. Females seem to prefer living in communities with many males, both because many males are better able to defend the feeding territories that females need to survive and raise their offspring, and because females need unrelated males as mating partners. As the number of adult males in Kalande dropped down to one, or perhaps even zero, some Kalande females left for good, while others seem to have kept their Kalande home base, but visit Kasekela for mating.

Kat and Kazi, photographed when visiting Kasekela (20 April 2006)
Kat and Kazi, photographed when visiting Kasekela (20 April 2006)

Kati, for example, is a Kalande resident who has probably lived there since 1998.  Based on genetic data, we think she is the daughter of Patti who was known as Tita when she was younger. Since 2006, Kati has been making occasional visits to Kasekela. I saw her with her young son Kazi on one of these early visits. Of the Kalande chimps, Kati seems to fear people the least, which would make since if she grew up in Kasekela.

Deus and I took the boat to Kalande, where we met Ashaabu, one of the new Kalande research assistants. Ashaabu got his start working as a village Forest Monitor for his village’s forest reserve (part of the Greater Gombe Ecosystem project). Before going into the forest, we talked with Ashaabu for a while about which chimpanzees he has been seeing.

Kazi, who was just a little boy back in 2006, now seems to be the alpha male of Kalande, even though he is just a gawky adolescent. Based on how old Kazi looked back in 2006, I think he must be at least 12 years old now. Ashaabu says Kazi is around the size of the Kasekela male Fundi, who is about 14. The old male Renadi (or Leonard) hasn’t been seen for a number of years now, and I suppose must be dead. There might be another adolescent male, Pamera, but we don’t know for sure if he is still alive. Ashaabu has regularly seen Kati, Kazai, Katarina (Kati’s new baby), a big female without an infant, an adolescent female (who I think might be Pairott), and another young female around Kazi’s size. (Perhaps this is really Pamera? Might be hard to tell he’s a male if he’s still young and seen only briefly from a distance.) Ashaabu also mentioned Obedina, a female who had a big belly last year who might also have a new baby now.

After talking, we hiked into the forest, climbing a steep rocky path into Nyamagoma valley. Nyamagoma is the southernmost valley of the park, just north of Kazinga village. The path wound through an open woodland with a view of the lake below.

Ashaabu collecting Msongati fruits.
Ashaabu collecting Msongati fruits.

Along the way, we collected fruits and leaves for the isotope and nutrition projects. Given that Kalande has so much woodland, it will be interesting to see if the Kalande chimpanzees, or their foods, differ isotopically at all from those in Kasekela.

Ashaabu and Deus below a chimp nest.
Ashaabu and Deus below a chimp nest.

We followed the path down towards Nyamagoma Stream, where tall trees grew, shading the steep valley in green light. We didn’t see any chimpanzees, but we did see a number of nests. Chimpanzees build a new nest (or bed) in trees each night to sleep safely out of reach of any predators that might be lurking about. We found one cluster with five fresh nests, suggesting that up to seven chimpanzees might have slept there (if the group included Kati and Obedina and their new babies). It was encouraging to see so many fresh signs of chimpanzees using this valley. The Kalande community is still hanging in there, and perhaps they might recover, if the Kasekela males don’t catch Kazi and finish him off.

Ashaabu taking data on his tablet.
Ashaabu taking data on his tablet.

Ashaabu carried with him the tablet computer he had used as a Forest Monitor. He used the tablet to take pictures of the nests and enter the data, including GPS locations of the nests. It was quite stunning for me to think each of the villages around Gombe now has its own Forest Monitors, collecting data like this on their own village forest reserves, and loading it up regularly into the Cloud.









Director of Chimpanzee Research for Gombe Stream Research Centre.





Solving the origin of a major malaria parasite

A recent study by Beatrice Hahn and colleagues, published in Nature Communications, has solved a major puzzle about the origin of one of the parasites that causes malaria in people worldwide: Plasmodium vivax.

Malaria is one of the world’s deadliest diseases, killing perhaps a million people each year. Most of the people who die from malaria are in Africa, and most of them children. In areas where malaria is common, adults often have a degree of resistance to the disease, but still get sick enough now and then to miss many days of work, suffering from agonizing aches, fevers and chills. Even though most victims are children, many adults die as well, especially when their immune systems are weakened by other infections. Malaria thus has huge economic costs and has been cited as one of the main drags on economic growth for many tropical nations.

Malaria has had a huge impact on human history and evolution. Malaria is one of the major reasons that Africa resisted European colonialism for so long. Europeans visiting Africa died in droves until the discovery that a drug extracted from the bark of the South American cinchona tree, quinine, protects against malaria. Quinine is fairly awful stuff: when I took it to fight a particularly bad malaria infection, it caused vomiting and a painfully loud ringing of the ears. From the mid-20th Century on, more effective anti-malarial drugs have been produced, which have helped many millions of people survive this terrible disease. Visiting and working in the tropics for business, tourism or, say, field primatology, would be a lot more dangerous without these drugs.

Before the discovery of such drugs, and for the many millions of people in poor countries who still don’t have adequate access to them, malaria has served as a powerful source of selection pressure on human populations. Because malaria is so deadly, human populations with long exposure to the disease have evolved a number of different defenses.

Malaria was originally thought to be caused by the “bad air” (Italian: “mala aria) of swamps and marshlands. It is now known to be a group of similar disease caused by several different species of single-celled protozoans from the genus Plasmodium.  Plasmodium falciparum is the most deadly, and the most common in Africa. Plasmodium vivax is more common in Asia.  Because these parasites are different species, and only distantly related, tricks that work to defend against one species of parasite may not work agains the other. 

The most famous  anti-malarial adaptation is sickle-cell disease, which is caused by a single small change to a gene for hemoglobin, the protein that carries oxygen in red blood cells. This change changes the shape of the hemoglobin molecule.

Sickle cells in action. From:
Sickle cells in action. From:

Red blood cells are packed full of hemoglobin, and if cells have only the abnormal hemoglobin, they become abnormally curved (shaped like a sickle or a crescent moon). People with one copy of the gene for sickle-cell disease have higher resistance to Plasmodium falciparum.

People with two copies of the gene, though, have sickle-shaped that cells get stuck going through narrow capillaries, causing all sorts of problems, which shortened life expectancy before the development of modern medical treatments.

Falciparum malaria is such a dangerous  disease that having improved resistance more than offsets the risks of having children whose lives are shortened by inheriting two copies of the gene.

Nonetheless, sickle-cell trait seems a rather clumsy solution to the problem. Kind of like using hand grenades to protect yourself from tigers. The grenades can stop tigers fine, if you can throw them far enough. But if you don’t throw them far enough, they blow up too close and kill you instead. Perhaps sickle-cell is an emergency stop-gap measure that evolved too recently for all the kinks to be worked out yet.

A seemingly better solution to this sort of problem is the Duffy-negative trait, which provides resistance to a different species (Plasmodium vivax), with little apparent cost to people who have the trait.

To understand the tricks that have evolved to defend against different species of Plasmodia, it is useful to know something about the life cycles of these parasites. These life cycles are complex and involves different stages of sexual and asexual reproduction in various organs of different hosts, including the human liver, human red blood cells, mosquito guts, and mosquito salivary glands.

Malaria parasite life cycle. From:
Malaria parasite life cycle. From:

The malaria life cycle is a complicated solution to problems of replication, sex, and dispersal of Plasmodium genes. In most animals that we are familiar with, such as ourselves, individual organisms do the major work of replication, sex and dispersal. As individual organisms, we accomplish these goals by mating, raising kids, and sending them off to college, for example.

Malaria parasites have found ways to outsource most of this work to other organisms. To replicate, they turn human hosts into giant malaria factories, turning red blood cells into production centers that burst, releasing newly produced parasites into the blood stream, infecting new red blood cells, in an exponentially increasing production system that destroys millions of the host’s red blood cells. This is the part of malaria where the human host feels weak and miserable and suffers from alternating fevers and chills.

Most of this replication phase is asexual: making millions of copies of the same thing. This works fine within a single host, but if you want your babies to survive in the cruel and variable outside world, you need to boost their chances by introducing variation into their genes through sex. So towards the end of the cycle, the parasites start making male and female versions, the gametocytes. When mosquitoes suck the blood of an infected host, they suck up these gametocytes, which can then have sex with gametocytes picked up from other hosts. The offspring of the gametocytes then infest the mosquitoes gut, eventually sending sporocytes to the salivary glands, so they get injected into the next person the mosquito bites, starting the cycle over again. The mosquito thus serves as both a malaria parasite dating service and dispersal system. Kind of like college.

Anyway, a key part of the malaria parasites life cycle is getting into the host’s red blood cells. To do that, they use specific proteins on the surface of the blood cell, which serve to transport certain chemical signals across the cell membrane. Plasmodium vivax parasites use one specific kind of protein, the Duffy antigen receptor, to force their way into human red blood cells. In much of Africa, the indigenous people don’t have this receptor. There is thus no way for P. vivax to infect them. People who don’t have the Duffy antigen receptor may suffer some costs, such as increased susceptibility to asthma, but these costs don’t seem to be anywhere near as high as those imposed by sickle-cell trait. And of course they are much less than the costs of dying from malaria.

The African distribution of the Duffy-negative phenotype has been a puzzle, though, because P. vivax is very rare in Africa. The conventional wisdom has been that P. vivax evolved in Asia. How could a parasite that evolved in Asia, and is rare in Africa, select for parasite resistance in Africans? This would be as puzzling as if people in Africa were all born with some sort of inherent immunity to tiger attacks, even though there are no tigers in Africa.

Beatrice Hahn and her team have solved the problem by collecting poop from thousands of apes across Africa. I played a very small part in this study, by overseeing poop collection for a while at Gombe.

Humans are apes, and many diseases that infect humans can also infect other apes, or (like in the case of HIV) originally came from other apes. Malaria is no exception.  On a molecular scale, we are so similar to chimpanzees and gorillas that the  tricks pathogens use for getting into human cells often work for these cells in other apes as well.

Beatrice Hahn’s team has been collecting fecal samples from apes all across Africa as part of a study looking into the origins of HIV-1, the cause of the global AIDS pandemic. It turns out that the same samples, and same molecular methods, that are so useful for studying HIV, are equally useful for studying all sorts of other things that live inside humans and other apes, including other viruses and gut microbes.

Locations of ape study sites
Locations of ape study sites

It turns out that when apes are infected with malaria, they shed some of the malaria DNA out with their poop. Take some poop, put it in a jar of RNAlater, and you can recover all sorts of fascinating genes, including malaria genes.

(When Jimmy Fallon and Justin Timberlake visited Gombe some years ago, they seemed amused by all of our poop collection and made up a song about it: “Poop in a Jar.” Disappointingly, though, they don’t seem to have recorded this one yet.)

It turns out that gorillas and chimpanzees across Africa, but not bonobos, have malaria parasites that genetically are very close to Plasmodium vivax. Compared to the gorilla and chimpanzee parasites, the human vivax is much less genetically diverse. All the human P. vivax belongs to a single branch of the much bushier tree of African ape P. vivax.ncomms4346-f2

It thus looks very clear that P. vivax evolved in Africa, not in Asia, from a plasmodium population that infects other African apes. People must have carried P. vivax with them when dispersing from Africa some 60,000 years ago. More recently, human populations in Africa evolved the Duffy-negative phenotype that proved so effective that P. vivax became extinct in Africa.

This study underscores the importance of evolution in human lives. Evolution happens fast, and human populations continue to evolve in response to our environments. The parasites that infect us evolve even faster. Evolution leaves traces in the genomes of every living organism that can be used to solve innumerable fascinating puzzles. This study highlights the power of molecular methods to answer important questions, especially when combined with field studies.





Chimpanzees and humans have similar gut microbes

The human gut hosts numerous species of microbes (the microbiome) — so many that in our bodies, microbe cells outnumber human cells ten to one. Many of these microbes appear to be important for digesting our food and maintaining health, while others have been implicated in disease, such as Crohn’s disease and irritable bowel syndrome. Recent studies have found that human microbiomes can be broadly classified into three enterotypes based on the relative abundance of different microbe species. This finding raised the question: are these enterotypes the product of a long history of co-evolution between microbes and humans, or are they a recent product of changes in diet, such as those resulting from agriculture and processed foods?

Frodo feeding in an oil palm tree.

I played a small role in a recent study led by Howard Ochman that looked at this question. Ochman’s team examined chimpanzee fecal samples collected at Gombe as part of the ongoing study of SIVcpz led by Beatrice Hahn. By comparing the microbiomes of humans and chimpanzees, Ochman’s team found that the microbiomes of wild chimpanzees can be classified into similar enterotypes to those in humans. This suggests that these patterns of microbiome communities are evolutionarily ancient, predating the common ancestor of humans and chimpanzees (some 5 to 7 million years ago).


Causes of Death in Chimpanzees

As George Carlin says, “It’s inevitable when you buy the pet. You’re supposed to know it in the pet shop. It’s going to end badly. You’re purchasing a small tragedy.”

The same goes for studying animal behavior. Anyone who spends enough time in the field, getting to know the lives of animals, will also witness their deaths. In a new paper, “Pathologic lesions in chimpanzees (Pan troglodytes schweinfurthii) from Gombe National Park, Tanzania, 2004-2010,” we report on some of the things we’ve learned from chimpanzees who have died. This paper, led by Karen Terio at the University of Illinois, involved a large team of field researchers, veterinarians, and pathologists.

I started studying chimpanzees because I was interested in how they lived. But in studying their lives, I’ve seen many of their lives come to an end. In this way, studying chimpanzees is a bit like being an Elf in J. R. R. Tolkien’s Middle Earth. In Tolkien’s world, the Elves live for centuries, dying only if they encounter some mishap, such as being slain in battle. In a single life, an Elf such as Elrond watches sadly as generations of mortal men come and go. In a similar manner the generations of chimpanzees, though long by the standards of typical mammals, pass more quickly than those of our own species. Jane Goodall, who has been watching chimpanzees at Gombe since 1960, has seen entire generations come and go. Chimpanzees that Jane saw as newborn babies have grown old and died, and their children, grandchildren, and now great-grandchildren have been born. I’ve only been working at Gombe since 2001, but this is still long enough that many of the chimpanzees I’ve gotten to know there have since passed on: Fifi, Goblin, Vincent, Ebony, Andromeda, Patti, Ebony, Sherehe, Shangaa, Echo, Yolanda, Malaika, Kris, and others.

I knew each of the 11 chimpanzees we describe in this new paper, except for a stillborn baby. I was involved in various ways with documenting the ends of their lives, such as taking observations during their final days, helping with the recovery of their bodies after death, examining the bodies immediately after death, organizing and participating in the necropsies, burying the bodies and recovering their skeletons from their graves, after they had been buried for at least a year. My student Claire Kirchhoff examined these skeletons for evidence of trauma.

Determining the cause of death is important for many reasons, including understanding chimpanzee life histories and identifying threats to their conservation. Because my research focuses on aggression, it’s especially important for me to know the cause of death. Did they die from aggression, or some other cause? In each case, it’s important to document carefully the relevant evidence.

Graucho Marx said, “Outside of a dog, a book is man’s best friend. Inside of a dog, it’s too dark to read.”

I’ve never tried reading inside a dog, but I’ve ended up sending more time looking at the insides of chimpanzees than I ever expected. If I had known what the future held for me, I would have taken some proper anatomy courses. But fortunately at Gombe, we’ve benefited from a wide range of expertise, including the Health Monitoring Project led by Elizabeth Lonsdorf and Dominic Travis, and the virology study led by Beatrice Hahn. We’ve been able to store chimpanzee bodies in large freezers until we can assemble teams of experts to conduct necropsies. We send tissue samples to pathologists and molecular virologists to gain a finer grained understanding of the causes of death.

I study violence in chimpanzees, not because I like violence (I don’t), but because it plays such an important role in the lives of chimpanzees – and as one of the two species most closely related to humans, chimpanzee violence can help us understand violence in our own species. Chimpanzee violence caused 36% of deaths in this study – more than any other factor. Andromeda and Patti were killed during intergroup attacks. Vincent was killed by members of his own community. Ebony – found dead with a broken neck and puncture wounds – almost certainly killed by chimpanzees, and likely one or more of the males of his own community.

One of the humbling things about research is that often, even with all the expertise we can muster, there is much that we will never know for sure. One such case involves the adult female Echo, who became a long-term resident at Kasekela at about the same time that I did.  I caught my first glimpse of Echo during one of my first days in the field as Director of Field Research at Gombe, back in January 2004. While we were watching a large group of chimpanzees feeding in the trees above a steep valley, videographer Bill Wallauer pointed out a new immigrant female chimpanzee with a pretty face and an asymmetric, bumpy sexual swelling. Bill recognized her from pictures he had taken in 1999, and thought she might be a female seen during an intergroup encounter in 2003. We named her Echo because she seemed to keep bouncing back. Unusually, Echo had immigrated together with her juvenile daughter, who we named Eowyn, after the heroic shieldmaiden from Tolkien’s Lord of the Rings.

Eowyn inflicting fatal trauma on the Witch-King of Angmar

Usually, females only move from one community to another as adolescents, before they have children. Infants of immigrants face a high risk of being killed by the resident males, as nursing infants fathered by other males represent both genetic competition and an unwelcome form of contraception. But Echo chose a good time to immigrate: her daughter Eowyn was weaned, and Echo had a full sexual swelling. The Kasekela males left Eowyn alone, and Echo quickly conceived a daughter, Emela.

Genetic analysis of fecal samples confirmed that Echo used to live in the Kalande community. Her departure from Kalande showed just how bad the decline of that community had gotten. Usually, once females have settled into a community and have started having babies, they stay there for life. But females seem to prefer living in a community with multiple males, which may be important both to protect them from intergroup aggression and to provide them with some good options for mates. Echo left when the number of adult males in Kalande dropped to one.

We also learned that Echo was infected with SIVcpz, the virus that is the immediate precursor of HIV-1, which causes AIDS in humans. Four of the 11 chimpanzees in the new study were infected with this virus. Until recently, it was widely assumed that SIVcpz was harmless in chimpanzees. We learned from studying Gombe chimpanzees, though, that infection with this disease greatly increases mortality risk. Two of the chimpanzees in this study died from AIDS-like symptoms.

Echo and Emela

I particularly remember Echo from a day in March 2006. In the late afternoon, the chimpanzees climbed high into a hill above Kasekela valley, into an open woodland. They climbed into the short, stunted trees to feed, rest and groom. Echo climbed rested on a low limb and groomed with Tubi, Bahati and her son Baroza. All seemed peaceful and happy. Echo had immigrated successfully, settled into Kasekela, had a daughter, and made friends.

But this was not to last.

Paralyzed "Patina"

In November 2006, which happened to be my last month of being based full time at Gombe, field assistants monitoring the Kalande community reported that one of their females, Patina, was sick. Together with vet Iddi Lipende, I traveled down to Kalande to investigate. We found a female chimpanzee lying in a dry streambed, her legs apparently paralyzed. She looked at us fearfully. She was too weak even to shoo away the flies that gathered at the wounds she had inflicted on herself, dragging her broken body along the stones of the dry streambed. She died within a few days.

In the following months, analysis of genetic samples found something puzzling: new fecal samples continued to come in from a female who was an exact genetic match for Patina. Apparently it wasn’t Patina who lay dying in that streambed – it was someone else. Given that the Kalande chimpanzees aren’t habituated, a case of mistaken identity was not so surprising. But the puzzle remained: who was the female who died?

Around this time, Echo’s daughter Eowyn showed up in Kasekela without her mother – something unusual for such a young chimpanzee. And genetic analysis of the tissue from the dead female found that she was, in fact, Echo. She had gone back to her home community of Kalande and died there. In her weakened state, she looked so different that none of us had recognized her. Her infant Emela had disappeared and must have died as well.

The necropsy found that Echo had a broken spine, but we don’t know how she broke it. She didn’t have the other injuries typical of a chimp attack – no canine puncture wounds, missing fingers or toes – so it seems unlikely that chimpanzees had killed her. Did she fall from a tree? If so, why? Was she chased by other chimps? Or did she just have bad luck? We will never know.


Here are the publications where we report some of the findings discussed here:

Keele, B. F., J. H. Jones, K. A. Terio, J. D. Estes, R. S. Rudicell, M. L. Wilson, Y. Li, G. H. Learn, T. M. Beasley, J. Schumacher-Stankey, E. E. Wroblewski, A. Mosser, J. Raphael, S. Kamenya, E. V. Lonsdorf, D. A. Travis, T. Mlengeya, M. J. Kinsel, J. G. Else, G. Silvestri, J. Goodall, P. M. Sharp, G. M. Shaw, A. Pusey, E. and B. H. Hahn (2009). “Increased mortality and AIDS-like immunopathology in wild chimpanzees infected with SIVcpz.” Nature 460: 515-519.

Rudicell, R. S., J. H. Jones, E. E. Wroblewski, L. G. H., Y. Li, J. Robertson, E. Greengrass, F. Grossmann, S. Kamenya, L. Pintea, D. C. Mjungu, E. V. Lonsdorf, A. Mosser, C. Lehman, D. A. Collins, B. F. Keele, J. Goodall, B. H. Hahn, A. E. Pusey and M. L. Wilson (2010). “Impact of Simian Immunodeficiency Virus Infection on chimpanzee population dynamics.” PLoS Pathogens 6(9): e1001116.

Terio, K. A., M. J. Kinsel, J. Raphael, T. Mlengeya, I. Lipende, C. Kirchhoff, B. Gilagiza, M. L. Wilson, S. Kamenya, J. D. Estes, B. F. Keele, R. S. Rudicell, W. Liu, S. Patton, D. A. Collins, B. H. Hahn, D. A. Travis and E. V. Lonsdorf (2011). “Pathological lesions in chimpanzees (Pan troglodytes schweinfurthii) from Gombe National Park, Tanzania, 2004-2010.” Journal of Zoo and Wildlife Medicine 42(4): 597-607.


After starting this blog in August, I hardly blogged at all during the semester. Partly this was because with my teaching and other duties, I had little time to spare for blogging. And in what spare time I did have, I wasn’t thinking about blog topics. I was thinking about my Mom, who was fighting what turned out to be a losing battle with leukemia.

Years ago, as the stem cells in Mom’s bone marrow were going about their usual business of dividing to make cells that would in turn give rise to new blood cells, one of them made a mistake. A deletion occurred on Chromosome 9. That cell divided and gave rise to a whole lineage of cells with the same deletion. Over time, some other cells in that lineage arose with additional genetic errors that prevented them from making proper blood cells. Instead, they produced millions and millions of daughter cells that filled up Mom’s marrow with useless cells, crowding out the good cells.

Mom only became aware that there was a problem a couple of years ago, when she was diagnosed with Myelodysplastic Syndrome (MDS), which often develops into leukemia. And in Mom’s case it did. In March, on her birthday, she was diagnosed with Acute Myeloid Leukemia (AML) and soon started her first round of chemotherapy.

Mom faced all of this with remarkable courage. In the hospital, she joked, made light conversation, took photos of all her visitors, and kept her good humor through all of the indignities of hospital life – the flimsy gowns, the lack of privacy, the constant parade of people coming into the room to do this or that, the increasing need for other people to help with basic bodily functions. Mom accepted all of this gracefully. Though she did not like revealing her birth year to other people, in the hospital many times a day she cheerfully gave her name and birthdate to hospital staff, as required when receiving new medications or blood transfusions. She always liked to look her best. When the chemo caused her hair to fall out, she wore wigs and hats – but mainly to make her visitors comfortable. Over Skype, she asked us if we wanted to see the bald head, and showed us when we said yes, seeming entirely cheerful and matter-of-fact about the loss of the hair that she had been so careful to keep just so over the years.

As a family, we tried to learn as much as we could about Mom’s condition and treatments. Dad bought and diligently read a medical textbook on hematology. This information was interesting enough, and helped us understand what Mom was going through, but we never found what we were looking for: some hidden nugget that would help Mom live. And the scientific literature was far from comforting. Studies of AML (such as here and here) found that for most patients, even with the best treatments available, life expectancy was a matter of months rather than years, especially if they were older, had a background of MDS, and had multiple detectable genetic changes in their chromosomes.

I’m not sure what I imagined chemotherapy would be like, but the actuality was both more peaceful and more awful than I had expected. For the most part, it involved just waiting in the hospital room, attached to a rack full of IV bags dripping an array of different fluids, including saline solution, blood, plasma, and chemotherapy drugs, into a PICC line – a tube inserted into the arm that directed the incoming fluids right to the heart. At first, it hardly seemed like Mom was really sick. She was just like she always was, except confined to a hospital room and attached to an IV drip. But gradually the chemo did its job and took its toll, and Mom got sicker and sicker.

One of the chemotherapy agents that Mom received was Cytarabine. This is chemically nearly identical to cytosine, one of the four bases that make up DNA. It is similar enough that it gets incorporated into new DNA, but different enough that that new DNA doesn’t work properly, and the new cells die as a result. So all the rapidly dividing tissues – cancer cells, but also hair, skin, and the intestinal lining – suffer as a result, resulting in all the usual chemotherapy side effects.

Another chemo drug Mom had was Daunorubicin – a ruby colored compound isolated in the 1950s from soil-living fungus in Italy and named for a pre-Roman tribe, the Dauni. The bright ruby color of this drug made it look especially potent and menacing when it was injected. Daunorubicin molecules are just the right shape to slip in between successive base pairs in DNA strands, unwinding the DNA a bit and interfering with replication. Again, this wreaks havoc, not just on cancer cells, but also on all healthy tissues that rely on rapid cell division.

Mom endured two rounds of chemo, achieved remission, and came home, where before long, life almost seemed back to normal. She cooked dinners, played bridge, went to church, and even traveled across the country to see her newest grandchild. It started to seem that Mom was healthy and out of danger.

However, while the chemo had killed a lot of cells, it hadn’t completely wiped out the mutant stem cells. Instead, the few surviving mutant cells continued to replicate, acquiring new mutations on the way. By September, the leukemia was back, and just before Thanksgiving, it took Mom away from us.

The chemo took a terrible toll, but without it, what happened in November would have happened in March. Thanks to the chemo, Mom had a summer at home, visits from her children and grandkids, and time to say goodbye.

Mom wanted to live, but during what turned out to be her final hospital stay, she talked of how the quality of life, and the prospects for improving it, diminish. In one of our last conversations, she told me, “I had hoped to live long enough to see how things turned out for everyone. But then, even if we lived to be over 100, we would still want more.”

Mom was one of the very best people I have ever known, and it seems terribly unfair that she should be taken from us so soon. It’s hard to believe that such a vibrant person, so full of love and caring and thoughtfulness, the keeper of so many family memories and traditions, should be undone by the information copying errors of the tiny, mindless cellular machinery of her own body.

Around the time Mom got sick, my computer crashed. The Genius at the Apple Store said it was a problem with the logic board, and that there was really nothing to be done, since the repairs would cost about as much as a new computer, and that in a computer of such advanced age (nearly five years old!), more problems would soon be arising. Luckily I had my data backed up, and almost all the files on my old computer are now on my new computer. But Mom is gone. There’s no backing her up.

Religious minded people will be tempted to provide reassurance that Mom is in Heaven. That’s certainly what Mom believed, and if such a place exists, then surely she is there. But my own inclination is to think that we are material beings, and that our lives begin and end on earth. This materialist view provides its own comforts. “No Hell below us – above us, only sky.” There is no one to blame for the loss of loved ones: it just happens. But whatever one believes about the metaphysical, Mom left behind a great big hole here on earth.