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Ebola, Global Health, In the News, Infectious Disease

Ebola: This outbreak is different

Ebola: This outbreak is different

15038945315_7613c40e54_zMisinformation about Ebola blankets the web. To clarify priories, and spur action, Stanford global health specialist Michele Barry, MD, penned a strongly worded essay published today in Boston Review:

In the United States, the few cases imported have incited irrational fear which is not only unwarranted but actually undermines an appropriate response to the outbreak. By focusing on quarantine, we are ignoring the need for centralized public health systems and training to deal with inevitable cases of Ebola.

Ebola is not spread through air, water or food, but end-stage sick patients can have over a billion viral particles in a cubic centimeter — or about a fifth of a teaspoon — of blood making contact with bodily fluids highly contagious.

This Ebola outbreak is different, she says. Previously, the virus stayed close to its forest reservoir in Central Africa. Now, it’s in large cities, spreading through heavily populated areas that have been decimated by poverty and conflict.

As the virus spread, the World Health Organization was slow to respond, Barry writes. “The WHO was alerted to the cluster of cases in Guinea by March, but did not sound the alarm until August. Why did this happen?”

And what, now, can be done?

In actuality, the solution to this Ebola crisis is not drugs, mass quarantine, vaccines or even airdrops of personal protective gear. The real reasons this outbreak has turned into an epidemic are weak health systems and lack of workforce; any real solution needs to address these structural issues.

We have the tools to spot emerging outbreaks and to stop them. We know how to prevent transmission of Ebola. Orchestrating an international response, however, one that considers the welfare of patients and healthcare workers, the resilience of healthcare systems and the triumph of reason — that needs some work.

Previously: Stanford physician shares his story of treating Ebola patients in Liberia, How to keep safe while operating on Ebola patients and Ebola: A look at what happened and what can be done
Photo from the European Commission DG ECHO

Global Health, Infectious Disease, Stanford News

Stanford physician shares his story of treating Ebola patients in Liberia

Stanford physician shares his story of treating Ebola patients in Liberia

P1030655For a month, emergency physician Colin Bucks, MD, found himself in the remote, dense jungle of northeast Liberia in the heat of the battle against Ebola. A clinical assistant professor of surgery at Stanford, Bucks was a volunteer with the International Medical Corps at a new tent-like unit hastily built to accept the continuing stream of Ebola patients in the hard-hit West African country.

The facility, a series of low, tin-roofed, concrete buildings, were primitive in design but had very effective methods for controlling infection, including spigots everywhere that dispensed virus-killing doses of chlorine and protective gear for covering the body head to toe. Aside from providing basic care, such as fluid and electrolyte replacement, Bucks said much of his time was spent comforting patients, who were physically isolated from family members because of the threat of infection.

P1030673“In this setting (in West Africa), there is an additional barrier because you have one physical degree of separation, as your head, your hands, your face are completely covered. But that doesn’t preclude the same level of connection to the patient and the same sense of responsibility and care,” said Bucks, who left Liberia Oct. 22 and is now isolated at his home in Redwood City, Calif. “There may be a higher percentage of sad cases because Ebola has a high-case fatality rate, so there is an added burden there. But there is a similarity to working a tough case in rural Liberia to working a tough case in a U.S. critical care unit.”

He said the unit received patients from a nearby hospital, as well as those brought in by makeshift ambulances that might travel as much as eight hours to retrieve ailing victims. “We would get these reports everyday from the ambulance – we have four cases and three flat tires. The roads would be blocked with trees. They would have to drive through dense jungles. The ambulance stories were by far the most riveting.”

Colin Trish PPEBucks said the caregivers at the unit, which included 125 Liberians, were able to save just under half the patients who came in, with each survivor serving as an important ambassador to the community.

“The public health message was blanketing the country, but there was still a lot of fear and misunderstanding,” he said. “People are scared to come to the hospital. People are scared to undergo treatment. It helped every time we had patients discharged as cured.”

Bucks, who is now following recommendations and Stanford requirements to remain in isolation for 21 days, says there is a desperate need for other U.S. volunteers like himself to help contain the spread of the virus. “There needs to be a rational policy that facilitates health-care workers going to and from the U.S. Policy should help this – not impede this. But you need an organized response on West Africa. Otherwise we will be fighting a much bigger battle in the U.S. and around the globe.”

Previously: How to keep safe while operating on Ebola patients, Experience from the trenches in the first Ebola outbreak, Ebola: A look at what happened and what can be done and Dr. Paul Farmer: We should be saving Ebola patients
Photos courtesy of Colin Bucks

Imaging, Immunology, Infectious Disease, Neuroscience, Research, Stanford News

Some headway on chronic fatigue syndrome: Brain abnormalities pinpointed

Some headway on chronic fatigue syndrome: Brain abnormalities pinpointed

patchbrainHow can you treat a disease when you don’t know what causes it? Such a mystery disease is chronic fatigue syndrome, which not so long ago was written off by many physicians as a psychiatric phenomenon because they just couldn’t figure out what else might be behind it. No one was even able to identify an anatomical or physiological “signature” of the disorder that could distinguish it from any number of medical lookalikes.

“If you don’t understand the disease, you’re throwing darts blindfolded,” Stanford neuroradiologist Mike Zeineh, MD, PhD, told me about a week ago. Zeineh is working to rip that blindfold from CFS researchers’ eyes.

From a release I wrote about some breaking CFS research by Zeineh and his colleagues:

CFS affects between 1 million and 4 million individuals in the United States and millions more worldwide. Coming up with a more precise number of cases is tough because it’s difficult to actually diagnose the disease. While all CFS patients share a common symptom — crushing, unremitting fatigue that persists for six months or longer — the additional symptoms can vary from one patient to the next, and they often overlap with those of other conditions.

A study just published in Radiology may help to resolve those ambiguities. Comparing brain images of 15 CFS patients with those from 14 age- and sex-matched healthy volunteers with no history of fatigue or other conditions causing similar symptoms, Zeineh and his colleagues found distinct differences between the brains of patients with CFS and those of healthy people.

The 15 patients were chosen from a group of 200 people with CFS whom Stanford infectious-disease expert Jose Montoya, MD, has been following for several years in an effort to identify the syndrome’s underlying mechanisms and speed the search for treatments. (Montoya is a co-author of the new study.)

In particular, the CFS patients’ brains had less overall white matter (cable-like brain infrastructure devoted to carrying signals rather than processing information), aberrant structure in a portion of a white-matter tract called the right arcuate fasciculus, and thickened gray matter (that’s the data-crunching apparatus of the brain) in the two places where the right arcuate fasciculus originates and terminates.

Exactly what all this means is not clear yet, but it’s unlikely to be spurious. Montoya is excited about the discovery. “In addition to potentially providing the CFS-specific diagnostic biomarker we’ve been desperately seeking for decades, these findings hold the promise of identifying the area or areas of the brain where the disease has hijacked the central nervous system,” he told me.

No, not a cure yet. But a well-aimed ray of light that can guide long-befuddled CFS dart-throwers in their quest to score a bullseye.

Previously: Unbroken: A chronic-fatigue patient’s long road to recovery, Deciphering the puzzle of chronic-fatigue syndrome and Unraveling the mystery of chronic-fatigue syndrome
Photo by Kai Schreiber

Global Health, In the News, Infectious Disease, Microbiology, Public Health

Exploiting insect microbiomes to curb malaria and dengue

Original Title: Aa_FC2_23a.jpgEvery year, more than 200 million people are affected by malaria and 50 to 100 million new dengue infections occur. Now, a group of scientists from Johns Hopkins University may have found a novel way of curbing both diseases: by “vaccinating” mosquitos against the parasite that causes malaria and the virus that causes dengue. The researchers are using the bacteria Chromobacterium, which prevents the pathogens from effectively invading and colonizing mosquito guts.

As Science magazine reported last week:

Like humans and most other animals, mosquitoes are stuffed with microbes that live on and inside of them—their microbiome. When studying the microbes that make mosquitoes their home, researchers came across one called Chromobacterium sp. (Csp_P). They already knew that Csp_P’s close relatives were capable of producing powerful antibiotics, and they wondered if Csp_P might share the same talent.

In another experiment, done with mosquitoes that weren’t pretreated with antibiotics, Csp_P-fed mosquitoes were given blood containing the dengue virus and Plasmodium falciparum, a single-celled parasite that causes the most deadly type of malaria. Although a large number of the mosquitoes died within a few days of being infected by the Chromobacteriumthe malaria and dengue pathogens were far less successful at infecting the mosquitoes that did survive, the team reports today in PLOS Pathogens. That’s good news: If the mosquito isn’t infected by the disease-causing germs, it is less likely to be able to transmit the pathogens to humans.

The bacteria also inhibited growth of Plasmodium and dengue in lab cultures, indicating that Csp_P is producing compounds that are toxic to both pests. One possible application of these toxins is to develop treatment drugs for people already infected with malaria or dengue. Real-world applications of this research are many years in the future, but it hints at a whole new way of dealing with otherwise intractable diseases.

Previously: Close encounters: How we’re rubbing up against pathogen-packing pestsClosing the net on malaria and Fighting fire with fire? Using bacteria to inhibit the spread of dengue
Photo by Sanofi Pasteur

Immunology, Infectious Disease, Microbiology, Public Health, Research, Stanford News

Paradox: Antibiotics may increase contagion among Salmonella-infected animals

Paradox: Antibiotics may increase contagion among Salmonella-infected animals

cattleMake no mistake: Antibiotics have worked wonders, increasing human life expectancy as have few other public-health measures (let’s hear it for vaccines, folks). But about 80 percent of all antibiotics used in the United States are given to livestock – chiefly chickens, pigs, and cattle – at low doses, which boosts the animals’ growth rates. A long-raging debate in the public square concerns the possibility that this widespread practice fosters the emergence of antibiotic-resistant bugs.

But a new study led by Stanford bacteriologist Denise Monack, PhD, and just published in Proceedings of the National Academy of Sciences, adds a brand new wrinkle to concerns about the broad administration of antibiotics: the possibility that doing so may, at least  sometimes, actually encourage the spread of disease.

Take salmonella, for example. One strain of this bacterial pathogen, S. typhimurium, is responsible for an estimated 1 million cases of food poisoning, 19,000 hospitalizations and nearly 400 deaths annually in the United States. Upon invading the gut, S. typhimurium produces a potent inflammation-inducing endotoxin known as LPS.

Like its sister strain S. typhi (which  causes close to 200,00o typhoid-fever deaths worldwide per year), S. typhimurium doesn’t mete out its menace equally. While most get very sick, it is the symptom-free few who, by virtue of shedding much higher levels of disease-causing bacteria in their feces, account for the great majority of transmission. (One asymptomatic carrier was the infamous Typhoid Mary, a domestic cook who, early in the 20th century, cheerfully if unknowingly spread her typhoid infection to about 50 others before being forcibly, and tragically, quarantined for much of the rest of her life.)

You might think giving antibiotics to livestock, whence many of our S. typhi-induced food-poisoning outbreaks derive, would kill off the bad bug and stop its spread from farm animals to those of us (including me) who eat them. But maybe not.

From our release on the study:

When the scientists gave oral antibiotics to mice infected with Salmonella typhimurium, a bacterial cause of food poisoning, a small minority — so called “superspreaders” that had been shedding high numbers of salmonella in their feces for weeks — remained healthy; they were unaffected by either the disease or the antibiotic. The rest of the mice got sicker instead of better and, oddly, started shedding like superspreaders. The findings … pose ominous questions about the widespread, routine use of sub-therapeutic doses of antibiotics in livestock.

So, the superspreaders kept on spreading without missing a step, and the others became walking-dead pseudosuperspreaders. A lose-lose scenario all the way around.

“If this holds true for livestock as well – and I think it will – it would have obvious public health implications,” Monack told me. “We need to think about the possibility that we’re not only selecting for antibiotic-resistant microbes, but also impairing the health of our livestock and increasing the spread of contagious pathogens among them and us.”

Previously: Did microbes mess with Typhoid Mary’s macrophages?, Joyride: Brief post-antibiotic sugar spike gives pathogens a lift and What if gut-bacteria communities “remember” past antibiotic exposures?
Photo by Jean-Pierre

Chronic Disease, Health Costs, Infectious Disease, Research

Despite steep price tag, use of hepatitis C drug among prisoners could save money overall

Despite steep price tag, use of hepatitis C drug among prisoners could save money overall

pills-384846_640There’s nothing free about the revolution that’s shaking up hepatitis C treatment. A slew of newer drugs, including sofosbuvir, are nearly eliminating the virus with fewer side effects than the old standbys, pegylated interferon and ribavirin, which had limited effectiveness and caused fatigue, nausea and headaches. But at a cost of $7,000 a week, it seems obvious they are more expensive.

Not necessarily, however, says Jeremy Goldhaber-Fiebert, PhD. Working with colleagues including former Stanford graduate student Shan Liu, PhD, Goldhaber-Fiebert developed a model that examines the overall costs and benefits of treating hepatitis C with sofosbuvir rather than the traditional drugs in prisons. Prisoners are more likely than those in the general population to be infected with hepatitis C, a virus that attacks the liver, because it can be transmitted through intravenous drug use and unclean tattoos.

The researchers found that the high upfront cost saves money in later years by reducing the number of liver transplants and other more invasive treatments needed. In accordance with standard practices, this  study examined the overall societal cost without accounting for the source of the money. For example, the prison system’s are more likely to spend more money upfront, although savings might be recouped by Medicaid or other private insurers several decades later. From our release:

“Overall, sofosbuvir is cost-effective in this population, though its budgetary impact and affordability present appreciable challenges,” said Goldhaber-Fiebert,who is also a faculty member at Stanford’s Center for Health Policy/Center for Primary Care and Outcomes Research, which is part of the university’s Freeman Spogli Institute for International Studies.

Goldhaber-Fiebert called hepatitis C a “public health opportunity.”

“Though often not the focus of health-policy research, HCV-infected inmates are a population that may benefit particularly from a highly effective, short-duration treatment,” he said.

The research appears in this week’s Annals of Internal Medicine.

Previously: Fortune teller: Mice with ‘humanized’ livers predict HCV drug candidate’s behavior in humans, A primer on hepatitis C and For patients with advanced hepatitis C, benefits of new drugs outweigh costs
Photo by stevepb

Ebola, Global Health, Infectious Disease, Patient Care, Stanford News, Surgery

How to keep safe while operating on Ebola patients

How to keep safe while operating on Ebola patients

surgical instrumentsAmid the Ebola crisis, two U.S. surgeons with a combined 30 years of working in developing countries have stepped forward to help disseminate well-defined protocols for operating on any patient with the virus or at-risk of having contracting the virus.

In an op-ed piece published today in the San Jose Mercury News, the two surgeons first ask, then answer, their own question: “Why should anyone care about surgery and Ebola? Ebola is a virus.” Their answer is that patients still have accidents. They still need things like appendectomies and C-sections and treatment for gunshot wounds.

The piece points to shocking news reports like those of 16-year-old Shacki Kamara, a patient in Sierra Leone who died of gunshot wounds to his leg during the Ebola quarantine of West Point, Liberia because people were afraid to operate on him. The growing fear of operating on anyone suspected of having contracted the Ebola virus, which is transmitted by bodily fluids, is a flashback to the early days of the AIDS crisis when operating room personnel and physicians often declined to treat patients, said Stanford surgeon Sherry Wren, MD, who co-authored the op-ed with Johns Hopkins surgeon Adam L. Kushner, MD, founder and director of Surgeons OverSeas. The two wrote:

With supportive medical care, patients may survive an Ebola infection. Without surgery for severe trauma, obstructed labor, a strangulated hernia, or a perforated ulcer, some patients may die. The moral dilemma is overwhelming. How does one operate on a patient infected with Ebola, yet at the same time protect the surgical staff?

Last week, the two came together to write an Ebola surgery protocol and send it to a number of surgical organizations, and the largest one – the American College of Surgeons – immediately accepted and posted it on their website. The response to the new guidelines was immediate and overwhelming, Wren said. In Africa, 10 countries have since adopted the protocol. Press articles on the guidelines have also appeared around the world, including in the New York Times and Washington Post and on Al Jazeera. Wren told me in a phone interview that she was both a bit surprised and overwhelmed by the reaction:

I’ll tell you, it was amazing. I’ve seen very few things in surgery go that fast. There was a need to start the discussion. It was never my intent to be the definitive Ebola expert. I’ve never seen a case of Ebola in my life. We expanded existing  CDC guidelines for prevention of transmission of other infections such as HIV and hepatitis and then added common sense from years of  experience operating.

Both Wren and Kushner acknowledged the “unsung heroes” who bravely choose to treat Ebola patients and stress the importance of working to keep them as safe as possible by increasing the availability of supplies of protective gear especially in West Africa and working toward increased training for health care workers. As they state in their op-ed:

 The management of Ebola is new to many clinicians in the United States and elsewhere. We hope to see more training, protocols and personal protective supplies to lower risks to surgical staff and patients. Just as surgery is a necessary part of a functioning health system, surgery must be part of the discussion during this time of Ebola; otherwise, the death toll will not only include those unfortunate to have died from the virus but also those unlucky to have developed a treatable surgical condition in this time of Ebola.

Previously: Experience from the trenches in the first Ebola outbreak, Ebola: A look at what happened and what can be done, Paul Farmer: We should be saving Ebola patients, Ebola panel says 1.3 million cases possible, building trust key to containment and Should we worry? Stanford’s global health chief weighs in on Ebola
Photo by Badly Drawn Dad

Ebola, Events, Global Health, Infectious Disease

Experience from the trenches in the first Ebola outbreak

Experience from the trenches in the first Ebola outbreak

512px-Ebola_virus_emNoted infectious disease expert Donald Francis, MD, PhD, was “a quiet doctoral student” at Harvard when he was called in to fly into the remote bush of southern Sudan in 1976 to help with one of the world’s first documented outbreaks of Ebola. The federal Centers for Disease Control and Prevention dispatched him for a two-week assignment that stretched into two months, as he saw villages demolished by the virus and helped bury some 274 bodies, he told a group of 70 science writers earlier this week in San Francisco.

Like today’s epidemic in West Africa, most people who contracted the disease were caregivers, either at home or at the make-shift tent hospital, or people assisting at funerals, where bodies were literally dripping with blood, he said. A single drop contains many thousands of viral particles, so all it took was a simple scratch of the nose with a contaminated finger to become infected.

Remarkably, none of his team members became infected, though they took risks, including storing viral samples in unsafe vials, and flying in and out of the treatment area when they were supposed to be in quarantine, he said.

Unlike today’s epidemic, the outbreak burned itself out because it took place in the remotest of areas.

“This was a very good place to control an outbreak – very rural, very isolated,” said Francis, co-founder and executive director of Global Solutions for Infectious Diseases.

Francis is the former director of the CDC’s AIDS Laboratory Activities and was among the first to suggest that AIDS was caused by an infectious agent. He has worked in epidemics around the world and helped eradicate smallpox from Sudan, India and Bangladesh before he became involved in the AIDS epidemic.

But his early work was in Ebola. During that first outbreak in Sudan, his five-member team worked with local nurses, some of whom were sickened by the virus but recovered. “I had patients who were so sick that the whole skin of their feet would slough off,” he said. And though the survivors were in a weakened state, losing as much as 20 percent of their body weight, they were determined to continue caring for their fellow villagers, he said.

He said today’s epidemic in West Africa presents a number of “worrisome challenges,” as it is occurring in a part of the world beset by political and social chaos.

“You have social chaos, socio-economic lack of resources, and hospitals that are just set up for transmission of the virus,” he said.

He said Ebola “can be controlled, but once it becomes so broad (as is currently the case), you lose that capability.” He expressed little hope that the current epidemic could be contained anytime soon: “I expect it will play out very badly for at least a year.”

Previously: Ebola: A look at what happened and what can be done,  Dr. Paul Farmer: We should be saving Ebola patients, Ebola panel says 1.4 million cases possible, building trust key to containmentShould we worry? Stanford’s global health chief weighs in on Ebola and Biosecurity experts discuss Ebola and related public health concerns and policy implications
Photo by CDC/ Dr. Frederick A. Murphy

Ebola, Global Health, In the News, Infectious Disease

Ebola: A look at what happened and what can be done

Ebola: A look at what happened and what can be done

As of September 28, the World Health Organization (WHO) estimates that, so far, more than 7,100 people have been infected with and more than 3,300 have died from the Ebola virus. These estimates of what has happened are almost certainly far too low; the estimates of what will happen are terrifyingly high. The current Ebola epidemic may well become the worst human disaster in this century. And we are not doing enough about it.

Ebola is unlikely to become a major problem in the developed world. But… it seems increasingly likely that hundreds of thousands, and quite possibly millions, of men, women, and children will be struck down by this ghastly plague

What happened?

Researchers will be trying to answer that question for years. This is the 24th known outbreak of Ebola virus disease since it was first recognized in 1976. All of the other outbreaks burned themselves out quickly, after between one and 425 people had been infected. Over nearly 40 years, fewer than 2,500 people are known to have become infected and fewer than 1,500 to have died. The outbreaks were all in Central Africa; they killed people in scattered villages, with few Western connections and fewer Western media on site.

However, the current outbreak started in West Africa, not Central Africa. I suspect this change in location will prove to be the key change, not so much in how it has affected human responses but how it has affected human susceptibility. Yes, the health infrastructures in Guinea, Liberia, and Sierra Leone were very poor (and are now far worse), but they were no worse than those in the Democratic Republic of Congo, South Sudan, or Uganda, the sites of most of the earlier outbreaks. But the lands where this outbreak start are more densely populated and better connected. Instead of burning out in one or two villages, hidden away in dense jungle, the virus spread from village to village, from village to town, and eventually from town to city. When it hit Monrovia, the slum-ridden, million-person capital of Liberia, an explosion was probably inevitable. (It has recently begun to expand in Freetown, the capital of Sierra Leone, as well as Conakry, the capital of Guinea.)

The growth of the epidemic has brought with it the growth of terror and the destruction of already tenuous trust, both in governments and in modern health care. It has also brought death from other, treatable conditions that cannot now be treated in health care systems that Ebola has collapsed. It has brought restricted transportation and supplies and, as a result, in some places, sharply higher food prices. It may eventually bring, in spots, starvation.

Recriminations have already started. Why didn’t the West provide powerful help in March 2014, when the epidemic (already about a year old) began to be noticed? Or why hasn’t Western science, expensively pursuing the latest “me too” drug for common Western conditions, produced a treatment, cure, or vaccine for Ebola? These critiques seem too harsh. No previous epidemic has ever ballooned like this one, even in Central Africa. And the chance of an epidemic outside those traditional regions, let alone in the West, appeared remote.

And while some have pointed fingers at the West, others have focused on the behavior of the affected West African populations. Much has been made of their reluctance to abandon traditional methods of burying their dead, their lack of trust in modern medicine, and even their physical attacks on health care workers. But before blaming the victims for their poor infection control measures, put yourself in their shoes. A five year old – perhaps your five year old – is feverish and vomiting. She is crying and holding her arms out to you for comfort, for help. In West Africa you would not have the chance to telephone for an ambulance, with well-protected professionals to treat the child. Touching her could kill you. But what would it do to you – what would it make of you – to ignore her? As Benjamin Hale wrote in Slate, Ebola is a fantastically cruel disease, turning against us our own compassion, care, and love.

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Cancer, Infectious Disease, Pediatrics, Research, Stanford News

Summer’s child: Stanford researchers use season of birth to estimate cancer risk

Summer’s child: Stanford researchers use season of birth to estimate cancer risk

Four_seasons

One of the hardest parts of unraveling childhood cancers is understanding what causes them. In recent years, evidence has been mounting that cancer and many other chronic diseases begin early in life – and perhaps even in utero. To untangle some of these early causes of cancer in children and young adults, Stanford epidemiologist and family physician Casey Crump, MD, PhD, is partnering with researchers at Lund University in Sweden, a working relationship was set up by Marilyn Winkleby, PhD, MPH, professor emeritus of medicine here. The team is using Sweden’s national registries for birth certificates and medical records to track how factors during gestation and soon after birth – called perinatal factors – affect cancer risks.

Because Sweden has a national health care system, it’s relatively easy to track the course of illness in individuals. By comparison, the U.S.’s health care system is fragmented across dozens of health care providers and insurers, so getting medical records for a single person that might span decades is a much more difficult prospect.

Crump’s team is focusing on cancers that are common in childhood and early adulthood: brain tumors, leukemia and lymphoma among them. Two papers published earlier this year examine how the time of year a child is born affects cancer risk. The most recent, published ahead of print in April in the International Journal of Cancer, examined whether the season of birth was linked to the risk of developing either Hodgkin’s lymphoma or non-Hodgkin’s lymphoma later in life. Crump explained:

Lymphomas are among the most common cancers in childhood but the causes are still largely unknown. It’s been hypothesized that infectious exposures, such as Epstein Barr virus and others may play an important role, but it’s still unclear what the critical age window of susceptibility might be. We had an opportunity to use season of birth from birth records as a proxy for infectious exposures in the first few months of life, and see the relationship between that and subsequent risk of Hodgkin’s and non-Hodgkin’s lymphoma – following these people from birth through childhood and on into young adulthood.

The researchers found that children born in spring or summer had a higher risk of developing non-Hodgkin’s lymphoma later in life compared to kids born in winter. The team didn’t find any similar seasonal pattern for risk of Hodgkin’s lymphoma. The results lend additional support to the “delayed exposure hypothesis.” Children born in spring or summer may not be exposed to critical pathogens during a critical early period of immune system development, leaving them vulnerable later in life. Children born in the fall or winter, by comparison, do get that important exposure at just the right time. Crump was quick to note that season of birth provides only a rough estimate of these exposures, since the team didn’t have accurate measures of exposures to Epstein Barr or other viruses, but he also added that these results “shed additional light on possible pathways of risk that may contribute to the development of non-Hodgkin’s lymphoma.”

A similar study published in January in the International Journal of Epidemiology found that children born in spring and summer had a higher chance of developing melanoma later in childhood or early adulthood. The team hypothesized that spring and summer babies are exposed to more UV radiation in warm summer months in the first few months of life – an exposure that fall and winter babies are less likely to have.

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