Published by
Stanford Medicine

Category

Infectious Disease

Behavioral Science, In the News, Infectious Disease, Research, Stanford News

Irrational fear of contagion fuels xenophobia, Stanford study shows

Irrational fear of contagion fuels xenophobia, Stanford study shows

face-mask-98640_1280I have a very distinct memory of my grandfather dying from leukemia in an Iowa hospital. I peered in through a glass window, too scared to don the white mask and gown to visit him myself, even though the protections were for him, not me. Granted, I was eight. But fear of disease, and fear of those who have disease, makes perfect sense to me, even now.

But, that realization is tempered by knowledge of the harmful effects of irrational fear, the topic of a recent study by a team of Stanford researchers. As described in a recent Graduate School of Business story:

Throughout history, minority or “out” groups have been blamed for the spread of infectious disease. In medieval Europe, for instance, Jews and gypsies were among those accused of spreading the deadly bubonic plague. In 1793, during the yellow fever epidemic in Philadelphia, local officials singled out actors, vaudevillians, and artists for transmitting the disease. But what is it about the fear of contagion that makes otherwise rational people buy into rumors about those they consider to be outsiders?

Organizational behavior researchers Hayagreeva Rao, PhD, and recent graduate Sunasir Dutta, PhD, developed an online pilot study where one group was told a new strain of flu had emerged, then asked about their views on immigration. The control group was simply asked about immigration.

Not surprisingly, the group told about the flu was less likely to support immigrant legalization. Dutta said he is convinced the results would be even more striking in the real world:

Practically speaking, the implications are clear: “Don’t do immigration reform during flu season,” says Rao.

The study also demonstrates the power of rumors to spur fear, even ethnic violence, Dutta said. And it illustrates the need for proactive, responsive communications, particularly in the beginning stage of epidemics when irrational fears can germinate.

Previously: Fear factor: Using virtual reality to overcome phobias, Fear of recurrence an issue for some cancer survivors and Looks of fear and disgust help us to see threats, study shows
Image by Openicons

Infectious Disease, Medical Education, Public Health, Research, Stanford News

A how-to guide on “galvanizing medical students” to administer flu vaccines

A how-to guide on "galvanizing medical students" to administer flu vaccines

image001Stanford’s Flu Crew, an initiative that gets medical students out into the campus and greater community administering flu vaccines, recently published a paper validating the importance of such initiatives for medical education and public health, and enumerating its best practices so other programs can follow in its footsteps.

Rachel Rizal and Rishi Mediratta were Flu Crew’s co-directors when we first wrote about their work in 2012. Rizal is now a fifth-year student and Mediratta a pediatrics resident at Stanford. They are lead authors on the article, “Galvanizing medical students in the administration of influenza vaccines: the Stanford Flu Crew,” which appears in the journal Advances in Medical Education and Practice.

I learned a lot about Flu Crew in an email exchange with Rizal, Mediratta, and a host of people they said were instrumental in this accomplishment. Catherine Zaw, a Stanford undergraduate who is a co-author on the recent paper, told me,”The Flu Crew concept has already spread to a couple of schools around the Bay Area, including UCSF, and I hope that with the publication of the paper, more medical schools will consider adopting it.”

The article is essentially a blueprint for replicating Flu Crew in other institutions. It describes Flu Crew’s innovative online-based curriculum, created by former Stanford medical student Kelsey Hills-Evans, MD (which she discussed in a post earlier this week). It lays out the planning needed to coordinate vaccination events, which in their case involves the medical school, undergraduate volunteers, the Vaden Student Health Center, Stanford’s Occupational Health Clinic, and community institutions like churches, libraries, and homeless shelters. And finally, it explains the impact on medical students’ attitudes to population health, as one of its main goals as a service-learning program is to provide students with experience in public health and patient interactions early on in their career.

Imee DuBose, MPH, who worked as operations manager at Occupational Health and was inspired by the “impressive professionalism” of Flu Crew’s student leadership to shift her career to student advising, told me: “As a public health professional, I see Flu Crew promoting community health through collaboration, and as a student affairs professional, I see student development and growth – this project combines the best of both worlds.”

Rizal and Mediratta’s successors for the two-year director position, Lauren Pischel and Michael Zhang, were also co-authors. Pischel explained that she thinks public health and preventative medicine are incredibly important in medical education.

“Campaigns like this link the individual you see sitting before you in clinic with the health of the population at large,” she said “I would like to see this paper be used to talk about how we can effectively integrate public health teaching and experience into medical school. There is quite a bit of room to grow in this direction.”

Previously: Stanford Medicine grads urged to break out of comfort zoneAn ounce of action is worth a ton of theory: Med student encourages community engagementFrenemies: Chronic cytomegalovirus infection boosts flu vaccination efficacyFlu Near You campaign aims to improve monitoring of flu outbreaks, vaccinations and Student “Flu Crew” brings no-cost flu vaccinations to the community
Related: The Flu Crew: Med students provide vaccinations to the community
Photo, of medical student Lichy Han administering a flu vaccine to Dean Lloyd Minor, MD, in 2012, courtesy of Imee Diego DuBose

Infectious Disease, Medical Education, Medicine and Society, Public Health, Stanford News, Videos

Online curriculum helps students and public learn about influenza

Online curriculum helps students and public learn about influenza

Stanford’s Flu Crew, which administers flu vaccines in and around the Stanford community, has had many successes over the last few years, which we’ll highlight in a post later this week. One achievement I thought deserved special attention is an innovative curriculum on influenza created by former medical student Kelsey Hills-Evans, MD, now an internal medicine resident at Harvard. Her online videos, such as the one above (which is the first in the series), are accessible not only to Flu Crew’s student participants but the public at large.

The videos were produced via a partnership with Khan Academy and built on the flipped classroom model championed by Charles Prober, MD, senior associate dean of medical education. They also received the Shenson Bedside Innovation Award in 2013. Rishi Desai, MD, a Stanford pediatric infectious disease physician and medical fellow at Khan Academy, supervised Hills-Evans’ efforts and told me in an email that Hills-Evans and the Flu Crew “put together some really amazing videos explaining everything from the basics of influenza to common misconceptions and fears that people have about the flu vaccine. They deserve all of the credit for the idea and execution of the project.”

Hills-Evans tried to keep each video under five minutes: “I wanted it to be a quick, high-yield snapshot of information that people could watch in one sitting and not easily forget.” She shared more details with me over email:

What did you aim to convey in these training videos? How did you imagine your audience? 

I wanted our student volunteers to come away from the training with enough general knowledge about influenza to answer nearly any question that patients might have. We equipped them with knowledge about its history, how it genetically changes over time, the clinical symptoms, the vaccine’s risks and benefits, specific patient populations, and even a section on flu shot myths. Our last video was meant for students to become public-health advocates equipped with facts and counter-arguments to some of the most common excuses people have for not protecting themselves with the flu vaccine.

For these general info videos, I was really aiming to be accessible to the general public. The topics are all applicable to the lay person, so I tried my best to stay away from clinical jargon. I wanted people to come away from the training with a better understanding of how dangerous influenza can be – many people shrug at the flu as a bit worse than a winter cold, but it kills tens of thousands of people every year. In addition, there are so many myths generated by popular media and the public about the illness itself (i.e., “I got a stomach flu” which is never actually an influenza virus) and especially about vaccines. It was important to me that we make these videos public so more individuals could be informed.

For the sections meant only for clinical personnel, our priority was to train the members of the Stanford Flu Crew, but I also wanted this component to be exportable to other medical programs. It was meant to teach students to deliver the best intramuscular (IM) injections possible. We’ve been told countless times that our method for IM injections yields extremely high patient satisfaction and nearly pain-free injections (some say “the best flu shot they’ve received”).

Continue Reading »

Infectious Disease, Media, Public Health, Stanford News

Stanford doctor-author brings historic figure Jonas Salk to life

Stanford doctor-author brings historic figure Jonas Salk to life

JacobsStanford professor emerita Charlotte Jacobs, MD, spent the past decade with the ghost of polio vaccine creator Jonas Salk, MD, the subject of her second biography, Jonas Salk: A Life. She dug through archives, conducted over a hundred interviews and read countless first-hand accounts and period news.

But she still had a difficult time choosing the opening scene for her book, the first written biography of the man hailed as an international hero for his role in ending the polio epidemics that ravaged the world during the first half of the 20th century.

Should she start with start with Salk’s humble beginnings as a child born to poor Jewish immigrants in New York City, dive into the life-saving research that propelled him to fame and antagonized his scientific peers, or begin at the end of his life, when he was striving to regain his prestige by seeking an HIV vaccine?

The choice for Jacobs became clear when, during a dinner at a writers’ residency, she described her book and its subject to her fellow participants. As the mostly younger writers quietly nodded, Jacobs realized they not only didn’t know who Salk was, they had no idea of the scope or severity of the polio epidemics. Jacobs, a child during the 1950’s, has chilling memories of this time.

Salk book cover“It was a fear that hovered over us every summer,” Jacobs recalled, “no matter what you did — eat your vegetables go to church, mind your mother — you could be the crippler’s next victim. And it was mostly children who caught the disease.”

Jacobs begins her book, excerpted in the new issue of Stanford Medicine, with a vivid account of the New York City 1916 outbreak. That year, in New York state alone, 8,900 people were infected, 2,400 died and many of the survivors were paralyzed or crippled.

The book has received numerous positive reviews. While Jacobs is happy with the attention, she is most excited for her audience to learn about the remarkable work that Salk and his team did in developing the vaccine and how the American public, through the March of Dimes, funded and carried out the first vaccine trials.

“This trial was run by volunteers; housewives collected the data,” she said. “Never before, and never again, has the public itself conducted a trial of this magnitude.”

Having read the excerpt in Stanford Medicine, I’m eager to read more.

Kim Smuga-Otto is a student in UC Santa Cruz’s science communication program and a writing intern in the medical school’s Office of Communication and Public Affairs.

Previously: This summer’s Stanford Medicine magazine shows some skinHenry Kaplan’s crusade against Hodgkin’s disease, TED Talk discusses the movement to eradicate polio, and Researchers tackle unusual challenge in polio eradication
Photo by Max Aguilera-Hellweg

Global Health, HIV/AIDS, Infectious Disease, Public Health, Research, Rural Health

Drought causes spike in HIV infections in Africa

Drought causes spike in HIV infections in Africa

75148497_50e081cd5b_zHere in California, the drought is plenty serious. Shortages mean short showers, brown lawns, empty reservoirs and fallow fields.

But in sub-Saharan Africa, drought spreads disease, including the still-rampant HIV virus. The phenomenon is more sociological than ecological: Slim harvests slash farmers’ incomes, forcing them to find new ways to earn money. Some turn to sex, according to a new study in The Economic Journal.

As described in a recent article from Stanford’s Center on Food Security and the Environment (FSE):

Analyzing data on more than 200,000 individuals across 19 African countries, the research team finds that by changing sexual behavior, a year of very low rainfall can increase local infection rates by more than 10 percent.

That means condoms and sex education aren’t all that’s needed to thwart the epidemic’s spread, the study’s authors say. Affected farmers also need economic support and alternatives to help them weather the dry period, without sacrificing their health.

“These are the people who really suffer when the rains fail, and who are forced to turn to more desperate measures to make ends meet,” co-author Marshall Burke, PhD, a fellow at the FSE, said in the piece.

Previously: Spread of drug-resistant HIV in Africa and Asia is limited, Stanford research finds, Stanford study: South Africa could save millions of lives through HIV prevention and Changing the prevailing attitude about AIDS, gender and reproductive health in southern Africa 
Photo by Jon Rawlinson

Cancer, Dermatology, Infectious Disease, Stanford News, Transplants

This summer’s Stanford Medicine magazine shows some skin

This summer's Stanford Medicine magazine shows some skin

below surface banner and 1 blogSkin is superficial, literally. But it’s also really deep, as I realized while editing the just-published issue of Stanford Medicine magazine. The summer issue features the special report “Skin deep: The science of the body’s surface.”

I learned from the chair of Stanford’s Department of Dermatology, Paul Khavari, MD, PhD, that thousands of diseases affect the skin. And I learned it’s surprisingly abundant: An average-sized adult is covered with about 20 square feet of skin.

Research on skin is thriving, in part, because skin is so easy to get hold of, Khavari told me. “The accessibility of skin tissue to the application of new technologies, including genomics, proteomics, and metabolomics, make this a watershed moment for progress in alleviating the tremendous suffering caused by the global burden of skin disease,” he said.

The magazine, produced with support from the dermatology department, includes articles not only about new treatments, but also insights into how skin works when it’s healthy and how to keep it that way. In a Q&A and audio interview, actress and playwright Anna Deavere Smith, who is African-American, addresses skin’s social meaning, discussing her relationship to her own skin and how, as a writer and actor, she gets under the skin of her characters. The online version of the magazine includes audio of an interview with Smith.

Also in the issue:

  • The butterfly effect“: A story about two young men coping with one of the world’s most painful diseases — the skin-blistering condition epidermolysis bullosa — including news about an experimental treatment to replace their broken genes. The online version includes a video with a patient at home and interviews with experts on the condition.
  • Surviving melanoma“: A report on progress being made after years of stagnation in treating the most deadly skin cancer: melanoma.
  • The rarest of rashes“:  A look at one of Stanford Medicine’s great accomplishments in dermatology: successful treatment of a rare but dangerous rash — cutaneous lymphoma, a form of blood cancer that spreads to the skin.
  • Take cover“: Tips on keeping skin safe from the sun.
  • Wither youth“: A feature on research seeking to answer the question: Why does skin age?
  • New lungs, new life“: The story of a young woman who lost her smile and had it restored through surgery.

The issue also includes a story considering the rise in number of castoff donor hearts, despite a shortage of the organs for transplants, and an excerpt from Jonas Salk: A Life, a new biography of the polio-vaccine pioneer, written by retired Stanford professor Charlotte Jacobs, MD.

Previously: Stanford Medicine magazine reports on time’s intersection with health, Stanford Medicine magazine traverses the immune system and Stanford Medicine magazine opens up the world of surgery
Photo, from the Summer 2015 issue of Stanford Medicine, by Max Aguilera-Hellweg

Genetics, HIV/AIDS, Infectious Disease, Research, Stanford News

Study shows toothed whales have persisted millions of years without two common antiviral proteins

Study shows toothed whales have persisted millions of years without two common antiviral proteins

1821221135_4a6cd4e8f8_z

Our ability to fend off the flu, HIV and other viruses is enhanced when proteins are produced by two “immune genes,” called MX1 and MX2. Other mammals also have these genes, but little is known about the role they play in the immune responses of these animals.

Now a study comparing the genomes and Mx genes of 60 mammal species has revealed a surprising finding: Every species in the study has functioning Mx1 and Mx2 genes except for dolphins, whales and orcas — species from a lineage of toothed whales that’s persisted for roughly 33 million years.

Gill Bejerano, PhD, a geneticist and developmental biologist, graduate student Benjamin Braun and their team wanted to know more about the status and function of Mx genes in non-human mammals. To do this, they examined and compared the part of the genome that contains the Mx genes in 60 different species including humans, cows, whales, dolphins and orcas.

I think this will open up very exciting research avenues, either to better protect the compromised whales, or to study their different viral defenses, and someday add them to our own arsenal.

The study, published this week in the Proceedings of National Sciences, showed that the Mx1 and Mx2 genes in the toothed whales (bottlenose dolphin, orca, Yangtze river dolphin and sperm whale) they tested were non-functional, and couldn’t produce the proteins that help fight viral infections. Bejerano explained the significance of this finding in our press release:

Given how important the Mx genes seem to be in fighting off disease in humans and other mammals, it’s striking to see a species lose them both and go about its business for millions of years.

To find out when in evolutionary history these genes became inactive the researchers compared the genomes of toothed whales to that of their closest ancestors, the baleen whales and hoofed mammals (ungulates). They found that the Mx genes function in baleen whales and hoofed mammals, but not in toothed whales. This means that some — perhaps all — toothed whales likely lost use of their Mx genes when this lineage split off from these ancestors about 33 million years ago (see Fig. 1).

Continue Reading »

Biomed Bites, Genetics, Infectious Disease, Research, Videos

Why are viruses so wily? One researcher thinks she knows — and is working to thwart them

Why are viruses so wily? One researcher thinks she knows — and is working to thwart them

Welcome to Biomed Bites, a weekly feature that introduces readers to some of Stanford’s most innovative researchers. 

Some of the world’s best known viruses use RNA, rather than DNA, to code for proteins, including polio, measles and hepatitis C. There are a few differences:  RNA uses a component not used in DNA, and RNA is usually single-stranded, rather than the familiar double helix of DNA.

RNA viruses change rapidly, evading efforts to develop vaccines and therapies. But the change is uneven — some genes evolve with nearly every replication, others stay the same for generations. Molecular biologist Karla Kirkegaard, PhD, wondered why. The chair of Stanford’s Department of Microbiology and Immunology explains her discovery in the video above:

The answer was unusual. It turns out that there are different kinds of selective pressures on these regions, and it is very hard for new variants to arise in certain regions because their family members around them poison their advantage.

Alone, for example, a mutated gene might perform better than one that is unaltered. But when it is mixed with other genes, it might make the resultant virus less competitive.

That offers valuable insight for drug development, she said. Consider the interaction of genes and viruses together, rather than aiming to disable a single player, Kirkegaard advises:

My quest right now is to convince people who target antivirals for the common cold, West Nile virus and SARS to think about those processes the viruses have to cooperate on so we won’t have such a big problem with drug resistance.

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.

Previously: Ending enablers: Stanford researcher examines genes to find virus helpers, A conversation on West Nile virus and its recent California surge and Exploring the role of extracellular RNA communication in human disease

Evolution, Genetics, HIV/AIDS, Immunology, Infectious Disease, Research, Stanford News

Study: Chimps teach people a thing or two about HIV resistance

Study: Chimps teach people a thing or two about HIV resistance

I, personally, have never had trouble distinguishing a human being from a chimp. I look, and I know.

But I’m not a molecular biologist. Today’s sophisticated DNA-sequencing technologies show that the genetic materials of the two species, which diverged only 5 million or so years ago (an eye-blink in evolutionary time), are about 98 percent identical. Think about that next time you eat a banana.

One major exception to that parallelism: a set of three genes collectively called the major histocompatibility complex, or MHC. These genes code for proteins that sit on the surfaces of each cell in your body, where they serve as jewel cases that display bits of proteins that were once inside that cell but have since been chopped into pieces by molecular garbage disposals, transported to the cell surface and encased in one or another of the MHC proteins. That makes the protein bits highly visible to roving immune cells patrolling our tissues to see if any of the cells within are harboring any funny-looking proteins. If those roving sentry cells spot a foreign-looking protein bit, they flag the cell on whose surface it’s displayed as possibly having been infected by a virus or begun to become cancerous.

Viruses replicate frequently and furiously, so they evolve super-rapidly. If they can evade immune detection, that’s groovy from their perspective. So our MHC has to evolve rapidly, too, and as a result, different species’ MHC genes  diverge relatively quickly.  To the extent they don’t, there’s probably a good reason.

Stanford immunologist and evolutionary theorist Peter Parham, PhD, pays a lot of attention to the MHC genes. In a new study in PLOS Biology, he and his colleagues have made a discovery that may prove relevant to AIDS research, by analyzing genetic material found in chimp feces. Not zoo chimps. Wild Tanzanian chimps. As I noted in a news release about the study:

The wild chimps inhabit Gombe Stream National Park, a 13.5-square-mile preserve where they have been continuously observed from afar since famed primatologist Jane Goodall, PhD, began monitoring them more than 50 years ago.

One thing that sets the Gombe chimps apart from captive chimps, unfortunately, is a high rate of infection by the simian equivalent of HIV, the virus responsible for AIDS.

The study’s lead author, postdoc Emily Wroblewski, PhD, set up shop in a corner of Parham’s lab and extracted DNA from fecal samples legally obtained by other researchers (close contact with the animals is prohibited). Each sample could be tied to a particular Gombe-resident chimp. RNA extracted from the same sample indicated that chimp’s infection status.

Parham, Wroblewski and their colleagues found that one particular MHC gene came in 11 different varieties – astounding diversity for such a small collection of chimps (fewer than 125 of them in the entire Gombe). Surprisingly, one small part of one of those 11 gene variants was nearly identical to a piece of a protective version of its human counterpart gene, a version that seems to protect HIV- infected people slowing HIV progression to full-blown AIDS.

Why is that important? Because any piece of an MHC gene that has maintained its sequence in the face of 5 million years of intense evolutionary pressure must be worth something.

Sure enough, fecal samples from chimps with that MHC gene variant, so strikingly analogous to the protective human variant, had lower counts of virus that those from infected chimps carrying other versions of the gene.

You can believe that scientists will be closely examining the DNA sequence contained in both the human and chimp gene variant, as well as the part of the MHC protein that DNA sequence codes for. Because it must be doing something right.

Previously: Revealed: Epic evolutionary struggle between reproduction and immunity to infectious disease, Our species’ twisted family tree and Humans share history – and a fair amount of genetic material – with Neanderthals
Photo by Emily Wroblewski

Big data, Emergency Medicine, Genetics, Infectious Disease, Research, Stanford News

Study means an early, accurate, life-saving sepsis diagnosis could be coming soon

Study means an early, accurate, life-saving sepsis diagnosis could be coming soon

image.img.320.highA blood test for quickly and accurately detecting sepsis, a deadly immune-system panic attack set off when our body wildly overreacts to the presence of infectious pathogens, may soon be at hand.

Sepsis is the leading cause of hospital deaths in the United States and is tied to the early deaths of at least 750,000 Americans each year. Usually caused by bacterial rather than viral infections, this intense, dangerous and rapidly progressing whole-body inflammatory syndrome is best treated with antibiotics.

The trouble is, sepsis is exceedingly difficult to distinguish from its non-infectious doppelganger: an outwardly similar but pathogen-free systemic syndrome called sterile inflammation, which can arise in response to traumatic injuries, surgery, blood clots or other noninfectious causes.

In a recent news release, I wrote:

[H]ospital clinicians are pressured to treat anybody showing signs of systemic inflammation with antibiotics. That can encourage bacterial drug resistance and, by killing off harmless bacteria in the gut, lead to colonization by pathogenic bacteria, such as Clostridium difficile.

Not ideal. When a patient has a sterile inflammation, antibiotics not only don’t help but are counterproductive. However, the occasion for my news release was the identification, by Stanford biomedical informatics wizard Purvesh Khatri, PhD, and his colleagues, of a tiny set of genes that act differently under the onslaught of sepsis from they way they behave when a patient is undergoing sterile inflammation instead.

In a study published in Science Translational Medicine, Khatri’s team pulled a needle out of a haystack – activity levels of more than 80 percent of all of a person’s genes change markedly, and in a chaotically fluctuating manner over time, in response to both sepsis and sterile inflammation. To cut through the chaos, the investigators applied some clever analytical logic to a “big data” search of gene-activity results on more than 2,900 blood samples from nearly 1,600 patients in 27 different data sets containing medical information on diverse patient groups: men and women, young and old, some suffering from sterile inflammation and other experiencing sepsis,  and (as a control) healthy people.

The needle that emerged from that 20,000-gene-strong haystack of haywire fluctuations in gene activity consisted of an 11-gene “signature” that, Khatri thinks, could serve up a speedy, sensitive, and specific diagnosis of sepsis in the form of a simple blood test.

The 11-gene blood test still has to be validated by independent researchers, licensed to manufacturers, and approved by the FDA. Let’s hope for smooth sailing. Every hour saved in figuring out a possible sepsis sufferer’s actual condition represents, potentially, thousands of lives saved annually in the United States alone, not to mention billions of dollars in savings to the U.S. health-care system.

Previously: Extracting signal from noise to combat organ rejection and Can battling sepsis in a game improve the odds for material world wins?
Photo by Lightspring/Shutterstock

Stanford Medicine Resources: