New Evidence Supports Prostate Cancer Screening

My regular readers know that prostate cancer screening has been an active research topic recently.  (My not-so-regular readers who are interested are invited to catch up on the topic by reading my most recent post on the subject.  See the link below.)  Whether testing men for prostate cancer saves lives is still an open question.  Large trials are currently underway that should provide a definitive answer in the next few years.

In the meantime, preliminary results from a Swedish trial give prostate screening a boost.  The study, published in The Lancet, randomized 20,000 men between 50 and 64 years of age to a group that was invited to undergo PSA testing every 2 years, and another group that was not.  The men in the screening group were offered PSA tests until they reached age 70.  Men with elevated PSAs were offered further testing such as digital rectal examinations and prostate biopsies.

As expected, more prostate cancer was diagnosed in the screening group than in the control group.  12.7% of the men in the screening group were diagnosed with prostate cancer compared to 8.2% in the control group.  Also as expected, the mortality rate from prostate cancer was quite low, as prostate cancer typically grows quite slowly and takes many years to cause harm.  Nevertheless, the screening group showed a survival advantage.  The risk of death from prostate cancer was 0.90% for the control group and only 0.50% in the screening group.

This means that (at least in this study) screening for prostate cancer saved lives.  For each life saved, 293 men needed to be invited for screening and followed for an average of 14 years and 12 men were diagnosed with prostate cancer.  Similar to mammography screening for breast cancer, the vast majority of people screened were not helped, and some were certainly harmed by surgery for cancer that would not have shortened their lives.  Others died of prostate cancer despite being screened.

This is the first glimmer suggesting that routine PSAs may indeed be life-saving, with benefits in the same numerical ball-park as mammograms for breast cancer.  Definitive answers are expected in the next few years as larger studies are completed.

Learn more:

The Lancet article:  Mortality results from the Göteborg randomised population-based prostate-cancer screening trial

Wall Street Journal Health Blog post:  Swedish Trial Finds Prostate-Cancer Screening Saves Lives

Reuters article:  Study finds prostate screening cuts cancer deaths

My last post about prostate cancer screening:  American Cancer Society Revises its Guidelines for Prostate Cancer Screening

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Doctors to Deal with Distracted Drivers

Doctors are expected not just to diagnose and treat diseases but to prevent disease by counseling patients about behaviors that expose them to risk.  We are expected to ask patients about smoking, alcohol use, high-risk sexual behavior, failure to use seatbelts and dancing on windowsills.  We are expected to counsel our patients to refrain from behaviors that may lead to injury or disease.

“Mrs. Jones, I’m very worried about the fact that you grease your stairs with motor oil.  I advise that you stop.”

To the list of dangerous behaviors we should be asking our patients about, we now must add distracted driving.  A perspective article in this week’s New England Journal of Medicine argues eloquently that distracted driving due to cell phone use is a major cause of preventable injury and death, and that physicians have a duty to warn and educate patients about it.

It’s important to note that this is a perspective article, similar to an op-ed piece, and not a scientific paper.  The science here is quite thin, but no ethical randomized trial can be imagined in which drivers are assigned to an attentive or a distracted group and then broken bones are tallied.  The few observational studies available suggest that distracted driving impairs drivers about as much as alcohol intoxication.

Though texting while driving is obviously dangerous, the author argues that even talking on the phone hands-free is distracting and keeps drivers from focusing all their attention on the task at hand.  She argues that talking on a cell phone is much more impairing than listening to the radio or talking with a passenger.

The data, though, is fuzzier.  A study from Virginia Tech (see link below) used video cameras in actual cars and trucks and observed drivers over more than 6 million miles.  They correlated driver behavior with the risk of a crash or a near crash.  They conclude that

Driving is a visual task and non-driving activities that draw the driver’s eyes away from the roadway, such as texting and dialing, should always be avoided.  “Headset” cell phone use is not substantially safer than “hand-held” use, because the primary risk associated with both tasks is answering, dialing, and other tasks that require your eyes to be off the road.  In contrast, “true hands-free” phone use, such as voice activated systems, are less risky if they are designed well enough so the driver does not have to take their eyes off the road often or for long periods.

So just don’t text while driving, and don’t read that text that you just received.  And if you have to dial to make a call, consider waiting until you arrive at your destination.  And remind me to ask you about this at your next annual exam.

Fortunately, I ride my bike to work.  But maybe I should find a different time to do Sudoku.

Learn more:

Reuters article:  Doctors urged to warn against cellphone use in cars

US Department of Transportation official website for distracted driving:  www.distraction.gov

New England Journal of Medicine perspective article:  The Most Primary of Care — Talking about Driving and Distraction

Virginia Tech Transportation Institute article:  New Data from VTTI Provides Insight into Cell Phone Use and driving Distraction

Tangential miscellany:

In the interests of full disclosure, this is a shameless plug for my esteemed colleague, friend and neighbor, Dr. Jonathan Corren, who is also a terrific allergist.  His new book 100 Questions & Answers about Allergies was just published and offers a comprehensive guide to allergy diagnosis and management written for patients.  I haven’t read it yet, but when I do, I’ll review it here.

Finally, medical news posting will be on hiatus for two weeks and will resume July 2.

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Heavy Coffee Drinkers May not be Getting any Boost from their Caffeine Fix

Everyone knows that caffeine is useful on occasion if we need to stay alert, especially when we’re sleepy.  Is there any college graduate who hasn’t had a caffeine-fueled all-night study session before an exam?  I certainly remember several nights in which I drank coffee to the point of inability to blink, much less sleep.

But for those who drink a lot of coffee daily, how much of a boost in alertness are they getting?  A study in this issue of Neuropsychopharmacology offers an interesting insight.

Over 300 subjects were randomized to receive either caffeine tablets or placebo tablets.  They all had to abstain from caffeine for 16 hours before the experiment.  The caffeine group then received a 100 mg caffeine tablet and 90 minutes later a 150 mg caffeine tablet.  (These doses are roughly the amount in a cup of coffee.  See the Mayo Clinic link below for an interesting review of the amounts of caffeine in different beverages.)  The placebo group received a placebo tablet and 90 minutes later a second placebo tablet.  The subjects were asked about headache and alertness before and after each dose.

The responses varied depending on the subjects’ usual caffeine use.  Those who normally were moderate to heavy users of caffeine reported an increase in headache and a decrease in alertness after placebo but not after caffeine.  So after caffeine they were feeling normal and without it they were having withdrawal symptoms – headache and sleepiness.  Surprisingly, even those who normally use little or no caffeine didn’t report any more alertness after caffeine than after placebo.  But at least they weren’t having withdrawal symptoms with placebo.

So it sounds like heavy coffee drinkers aren’t getting a boost from their coffee.  They’re just avoiding withdrawal.  They should probably slowly decrease their use of caffeine to more reasonable ammounts.

And those of us who drink little coffee are probably experiencing a boost from psychological conditioning as much as from caffeine.  We expect the hot fluid that we know so well to make us more alert, so it does.  If someone slipped us decaf without our knowledge it would likely work almost as well.

To celebrate this new-found wisdom, I’m going to go home and drink Diet Coke until I have palpitations.

Learn more:

BBC News article:  ‘People become immune to coffee boost’, experts believe

Mayo Clinic article:  Caffeine content for coffee, tea, soda and more

Neuropsychopharmacology article abstract:  Association of the Anxiogenic and Alerting Effects of Caffeine with ADORA2A and ADORA1 Polymorphisms and Habitual Level of Caffeine Consumption

Tangential miscellany:

I’m happy to report that US Airways Magazine has reprinted my post Erroneous Evidence About Enough Exercise in their current issue.  So if you’re flying US Airways this month please grab a copy and brag to your friends that you were reading my posts years before I was cool.

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Carotid Artery Stenting Almost Ready for Prime Time

Three months ago I wrote about carotid artery narrowing, which is one of a number of causes of stroke.  There are currently two alternative treatments for severe carotid artery narrowing:  surgery, called endarterectomy, to open the artery, and a newer procedure called carotid artery stenting.  (Read my previous post, link below, for some background about these procedures and their role in stroke prevention.)

Thus far, carotid artery stenting has not been shown to be as safe as endarterectomy.  So endarterectomy has remained the proven standard.

This week stenting finally gains some credibility in the largest study to compare the two treatments, published in this week’s New England Journal of Medicine.  Over 2,500 patients with carotid artery narrowing were randomized to stenting or endarterectomy.  They were followed for serious complications immediately after the procedure or for strokes in the subsequent years.

Surprisingly, the patients receiving stenting did overall as well as the patients undergoing endarterectomy, making this the first study in which endarterectomy was not clearly superior.  Stenting carried a slightly higher risk of stroke after the procedure, but endarterectomy had a higher risk of heart attack.  Interestingly, patients younger than 70 tended to do better with surgery, while older patients did better with stenting.

So stenting is finally finding some role in treating carotid artery narrowing.  Training and experience in the physician performing either procedure is vital.

An editorial in the same issue of the New England Journal of Medicine concludes

… until more data are available, carotid endarterectomy remains the preferred treatment for most patients with symptomatic carotid stenosis; treatment for asymptomatic stenosis remains controversial. However, given the lack of significant difference in the rate of long-term outcomes, the individualization of treatment choices is appropriate.

Learn more:

New England Journal of Medicine article:  Stenting versus Endarterectomy for Treatment of Carotid-Artery Stenosis

New England Journal of Medicine editorial:  Carotid-Artery Stenting in Stroke Prevention

LA Times Booster Shots:  Angioplasty plus stents is as good as surgery for clearing neck arteries, study finds

My previous post about carotid artery stenting:  Carotid Stenting Still Controversial

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A Brief History of Unnatural Selection

Indulge me as I digress from writing about health this week to write about an important scientific breakthrough.

People have been altering the living things around us as long as we have been around.  We domesticated wild wolves into tame dogs and kept them for protection and as pets.  Eventually humans began to farm, and raise livestock.  We then began selecting the best animals to breed for the next generation, and we selected seeds from the best plants to sow.  Generation after generation, we changed the animals and plants that we had domesticated by allowing only those with characteristics we valued to reproduce.  We had no idea what made wheat grain larger or why some sheep grew more wool, we just knew that these traits are inherited, and by breeding the right specimens we could get more of what we wanted.  Through this simple repetitive selective breeding all human crops and domesticated livestock eventually became unrecognizable from their wild origins.  The wheat we eat today has about as much resemblance to pre-human wheat as my neighbor’s yippy dachshund has to a wolf.

So millennia before any people were rigorously studying living things (engaged in what we now call biology) people were progressively modifying many animal and plant species.  In 1859 Charles Darwin published “On the Origin of Species” his landmark work which argued that just as people select the pet cats and tomatoes and carrots that form the next generation, nature selects the survivors of every species to reproduce.  He proposed that it is this selection by nature (i.e. natural selection) that explains how all species change over time and how new species arise from older forms.

At about the same time Gregor Mendel showed that inheritance follows certain predictable patterns.  The offspring are not simply a blend of the traits of the parents.  Rather the parents’ traits are somehow transmitted in distinct indivisible packages (now called genes) which are inherited and expressed according to simple rules he described.

In the 1940s and 50s the molecule carrying genetic information was found to be deoxyribonucleic acid, DNA.  And in 1953 James Watson and Francis Crick discovered the shape of the DNA molecule – the double spiral staircase – that allowed it to serve as a molecular information storehouse.

Since then the fields of molecular biology and genetic engineering have exploded, with the development of techniques to identify, isolate and sequence genes.  In 1977 the entire set of genes (genome) of a virus was sequenced, meaning its entire DNA code was deduced.  Since then the genomes of many species, including humans, have been sequenced.  Genes have been inserted into crops to make them more resistant to disease and the molecular mechanisms of some genetic diseases have been discovered.

(By the way, those who object to genetically modified organisms in their food should not eat any crops at all since all modern crops have been modified through human selection since prehistory.  Genetic modification is just a finer tool for continuing the work of millennia.  Now that I think about it, these critics should also only keep wild tigers and wolves for pets.)

This week another threshold has been crossed.  Investigators synthesized an entire genome from scratch, inserted it into cells that had their original DNA removed, and formed cells that reproduced and expressed their new synthetic genes.  The effort took 15 years.  The achievement has no immediate practical uses.  It was simply a demonstration of the technologies required for such a feat.  Potential practical uses are myriad, but are likely far off in the future.  Their discovery was published in the journal Science and has received much press attention.

Though we have much more to learn, the pace of discovery is accelerating.

Learn more:

Wall Street Journal article:  Scientists Create Synthetic Organism

Science article:  Creation of a Bacterial Cell Controlled by a Chemically Synthesized Genome

The Ancestor’s Tale by Richard Dawkins is a fascinating tour through the history of life on Earth.

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Maybe You Have Food Allergies, But Probably Not

A lot of people who believe they have food allergies don’t.  What’s worse, a lot of people who were told by their doctor they have food allergies don’t.

An article in the current issue of the Journal of the American Medical Association tried to review the existing literature on food allergies to standardize how food allergies are diagnosed.  What the study found was an inconsistent jumble of unreliable test results and methods.

First, to clear up some of the confusion, we have to understand the difference between food allergy and food intolerance. A food allergy is a reproducible adverse reaction to a specific food that is mediated by a specific antibody that your body makes.  It usually results in a rash or difficulty breathing and can be life-threatening.  The article estimates that more than 1% or 2% of the population (but less than 10%) have true food allergies.

Food intolerance is any other adverse effect from food.  Lactose intolerance, for example, is the inability to digest lactose, the carbohydrate in dairy products.  It leads to abdominal discomfort and diarrhea whenever dairy foods are ingested.  It is not an allergy.  Neither is acid reflux, which can be exacerbated by certain foods, or gustatory rhinitis, in which spicy foods cause a runny nose.  These are all food intolerances.  So if you get heartburn every time you eat mint, you’re not allergic.  You just have acid reflux that is exacerbated by mint.

But we doctors are a more important source of the confusion.  Unfortunately, there is no easy way to accurately test for food allergies.  The most common tests are skin prick tests, in which small amounts of the food proteins are injected into the skin, and blood tests which look for antibodies to certain food proteins.  The problem with both tests is that they are very inaccurate and yield many false positives – the tests can be abnormal even when the person is not allergic.  So based on these tests many patients have been incorrectly told that they have a food allergy.

The most accurate way to diagnose a food allergy is a food challenge – a patient is given the test food in a disguised form so that she doesn’t know if it is the suspected allergen or a placebo.  Then the patient is observed.  This is accurate but impractical.  The patient must be under observation for a prolonged time in a facility that is equipped to handle a potentially life-threatening allergic reaction.

So the current state of the field is disorganized.  There is no standardized accepted way to accurately test for food allergies, and without that foundation, no way to study them.  The authors conclude

“There is voluminous literature related to food allergy, but high-quality studies are few. Prime needs for advancement of the field are uniformity in the criteria for what constitutes a food allergy and a set of evidence-based guidelines on which to make this diagnosis.”

Learn more:

Los Angeles Times Booster Shots:  With food allergies, much is said but little is known, conclude researchers

New York Times article:  Doubt Is Cast on Many Reports of Food Allergies

Journal of the American Medical Association article:  Diagnosing and Managing Common Food Allergies

Tangential miscellany:

An article in the current issue of Annals of Internal Medicine reviews the experience of the Israeli Field Hospital that responded to the Haiti earthquake. The field hospital had 121 medical staff and 109 support personnel. They arrived 89 hours after the earthquake with a mobile hospital that had operating rooms, intensive care units, equipment for radiology and laboratory testing, and medications. In 10 days they triaged 1,111 patients, hospitalized 737 of them and performed 244 surgeries – an impressive demonstration of logistical, medical and humanitarian preparedness.

Annals of Internal Medicine article:  Early Disaster Response in Haiti: The Israeli Field Hospital Experience

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Zostavax is Safe, Effective, and Not Free

Varicella zoster virus (VZV) is the virus that causes chicken pox, usually a relatively minor childhood illness.  Unlike other viruses that are cleared from our bodies after infection, VZV stays in our sensory nerve cells forever.  Over the subsequent decades our immunity to VZV wanes.  When our immunity falls too low, VZV can reactivate and cause shingles.  Shingles is a painful blistering rash along the distribution of one sensory nerve.  The rash resolves in a few weeks, but in some older patients the effected patch of skin can remain painful for months or even permanently.  This painful condition after shingles is called postherpetic neuralgia and it can be quite debilitating.

In 2006 a vaccine to prevent shingles, Zostavax, became available.  It is recommended for everyone over 60 who has had chicken pox.  It has been proven effective in preventing shingles, and therefore in preventing postherpetic neuralgia.

But is Zostavax safe?  A large study in the current issue of Annals of Internal Medicine answered that question.  The study randomized over 38,000 patients to receive Zostavax or a placebo injection.  The side effects from Zostavax were not worse than from placebo.  Most of the side effects (like most vaccines) involved inflammation at the site of injection.

So to summarize, Zostavax is safe, and it effectively prevents a very painful potentially disabling condition. Recall also that all children are now being vaccinated against chicken pox, so that in 60 years Zostavax will not even be necessary since a generation will have grown up uninfected with VZV.

In anything resembling a rational healthcare delivery system champagne corks would fly, the makers of Zostavax would get a pat on the back (and well-deserved profits) and we would all shift our attention to more pressing matters.  Some patients would decide to buy Zostavax; some would not.  Private or government charity programs would pay for the vaccine for indigent patients.  Joy and health would reign.

But instead, there is gnashing of teeth and wringing of hands.  Why?  Because only about 7% of eligible patients have received the vaccine.  It turns out Zostavax is the most expensive vaccine recommended for adults (about $200) and the first to be covered by Medicare part D, the Medicare drug “benefit”.  That means pharmacists are paid to dispense it to patients, not doctors.

To sort out why more patients aren’t receiving Zostavax, another study in the same issue of Annals of Internal Medicine surveyed hundreds of primary care doctors about the barriers that might be preventing them from recommending and administering Zostavax to their patients.  The results: the biggest barrier was financial.  Many patients without coverage don’t want to pay for it, and doctors aren’t being paid by insurance companies to administer it.

This was such a staggeringly shocking finding, that it merited an editorial in the very same issue of Annals.  That’s three articles about a vaccine that works as intended and is safe.  The editorial opines that reimbursement should be revised to promote increased utilization of the vaccine.  In other words, we should take more money from other people to assure that patients who don’t want to pay for their own Zostavax can get it for free.

Now don’t get me wrong, I’m all for charity care for indigent patients.  (I volunteer at a clinic that serves indigent patients two afternoons a month.)  But the vast majority of patients who aren’t getting Zostavax aren’t poor; they just have better things to do with $200.

What the editorial didn’t say is that you can’t do much better than a product or service in which the main barrier to obtaining more is the price.  After all, that’s the only reason we don’t get twice as many clothes or cars or homes.  If the price was lower, we would.  If Zostavax was free, some other barrier to its use would necessarily arise, perhaps a lengthy wait, or a difficult to navigate bureaucracy, or rationing by some other means.

So perhaps each patient should shoulder the cost of his or her own Zostavax.  We should also all donate a little time or money for those who truly can’t afford it.  And some of us may rationally choose to accept the risk of shingles.  Alternatively, we could riot in Athens until the EU pays to keep us all shingles-free.

Learn more:

Annals of Internal Medicine Summary for Patients:  Safety of the Vaccine to Prevent Shingles

Annals of Internal Medicine article:  Safety of Herpes Zoster Vaccine in the Shingles Prevention Study

Annals of Internal Medicine article:  Barriers to the Use of Herpes Zoster Vaccine

Annals of Internal Medicine editorial:  The Looming Rash of Herpes Zoster and the Challenge of Adult Immunization

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Vitamin E is Effective for Fatty Liver

My regular readers know my skepticism about vitamin supplements.  I leap at the chance to bring you news that some vitamin has been tested for some disease and found useless.  So for balance, I have to also report when a well-designed study finds that a vitamin actually helps something.

This week’s New England Journal of medicine published a study about the treatment of nonalcoholic steatohepatitis (NASH).  NASH, also known informally as fatty liver, is a condition in which fat is deposited in the liver, causing liver inflammation.  It is more common in overweight patients, and those with diabetes and elevated triglycerides.  Fatty liver may eventually progress to liver failure.

Weight loss is the mainstay of treatment for fatty liver, and though some medications have been used for NASH, none have been proven to be effective.

The study randomized patients with fatty liver to placebo or 800 IU of vitamin E daily.  (There was a third group randomized to Actos, a diabetes medication, but that’s for another post.)  The patients were followed for about two years.  Improvement in their fatty liver was assessed by liver biopsy at the beginning and end of the study.

The patients taking vitamin E did quite a bit better than the patients taking placebo, with significantly more of the vitamin E patients having improvement or resolution of their fatty liver.  The authors of the study caution that the trial was too short to test the long-term safety of vitamin E, especially at this high dose.  They cite a worrisome study from 2005 that suggests that vitamin E at high doses may actually be associated with higher mortality.  (See second article, below.)

So if you have NASH talk to your doctor about starting vitamin E, and keep working on losing weight.  If you don’t have NASH and are taking vitamin E, consider donating your vitamin E to someone with NASH and taking a daily dose of nothing.

Learn more:

New England Journal of Medicine article: Pioglitazone, Vitamin E, or Placebo for Nonalcoholic Steatohepatitis

Annals of Internal Medicine Articles:  Meta-Analysis: High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality

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A Dietitian’s Thoughts on Diet Sodas

Two weeks ago I wrote a post about the mistake we make when we think of some medicine or food as generally “good for you” or “bad for you” as opposed to having specific benefits and harms.  I started with an anecdote in which a friend asked me whether diet sodas or regular sodas were better for you.

Susan Dopart, a terrific dietitian who I’ve known for over a decade, emailed me to bend my thinking about diet sodas and about non-nutritive sweeteners (i.e. artificial sweeteners) in general.  With her permission, I thought I’d share her thoughts with you.

She shared with me an article reviewing studies that link the use of artificial sweeteners with various adverse health outcomes, like obesity and insulin resistance.  The studies were all observational, that is, not randomized.  For example, one study showed that people who drink more diet sodas tend to weigh more than people who drink fewer diet sodas.  That’s exactly the kind of study that makes me want to pour lemon juice on my paper cuts.  The media misunderstands this kind of study and reports that diet sodas cause obesity.  But an equally likely possibility is that people who have stronger cravings for sweets will be overweight (by eating actual sweets) and will also drink more diet sodas (because they’re sweet).  It’s like noticing that my lawn wilts on the same days that the beaches are crowded and blaming the crowds for my wilting lawn.  But both are caused by a third phenomenon – hot days.

So, fancying myself the Defender of Science Against Confusing Nonsense, I emailed Susan that the studies were completely unconvincing and that artificial sweeteners haven’t been proven to have any adverse health effects.  Susan agreed that there is no solid science on the subject, but said that in the absence of good science the best guide we have is our professional experience.  She certainly has lots of experience, and she believes that sweeteners, whether natural or artificial, increase cravings for more sweets.  In her experience patients who have stopped drinking any kind of soda have noticed their cravings for sweets decrease.

That’s a potentially important lesson, and someone should test it rigorously.  In the meantime, I appreciate Susan sharing her expertise with us.

Learn more:

There is a mechanism that could explain how sweets cause increased cravings for sweets.  It’s a theory by psychologist Seth Roberts that weight gain is mediated by a learned association between tasty foods and calorie content.  This hasn’t been tested in a good study (yet) but I found his paper intriguing and easy to read.  (I have no idea what Susan Dopart thinks about it.)

What Makes Food Fattening?  A Pavlovian Theory of Weight Control by Seth Roberts

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Your Food Is Pretty Safe, But it’s Not Getting Safer

In a world where journalism was free of hype the above headline would have been atop the many stories this week relating to a press release by the CDC about food-borne illness.  The numbers are far less sensational than the headlines.

The CDC report reviewed statistics about food-borne illnesses in 2009.  Overall there were 17,468 laboratory-confirmed food-borne infections in 2009.  What the CDC press release doesn’t mention is that this number has stayed about the same for several years.  (It was 17,883 in 2007.)  But rather than putting out a press release that declares “We’re Doing About the Same!” they focused on the bacteria that seem to have caused fewer infections this year, like a toxic strain of E. coli.  (See the link below.)

The bottom line is that you’re about twice as likely to die in a car accident in the US than to get sick from contaminated food.  (There were 39,800 fatalities related to motor vehicles in 2008.)  The CDC may in fact deserve some credit for that.

But the last several years suggest that the easy improvements have already been made and that further progress will be more difficult and incremental.  The bacteria, after all, will continue doing their best to contaminate our food.

Learn more:

CDC Press Release:  CDC Report Shows Success in Fighting E. coli O157:H7

Wall Street Journal article:  E. Coli Infections Dropped Last Year

Reuters article:  U.S. sees big drop in 6 food poisoning bugs: CDC

LA Times Booster Shots:  Early signs of progress against E. coli and shigella, but listeria, salmonella …?

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