Retail Meat Linked to Urinary Tract

Infections: Strong New Evidence

ScienceDaily (Jan. 21, 2010) — Chicken sold in supermarkets, restaurants and other
outlets may place young women at risk of urinary tract infections (UTI), McGill
researcher Amee Manges has discovered. Samples taken in the Montreal area between
2005 and 2007, in collaboration with the Public Health Agency of Canada and the
University of Guelph, provide strong new evidence that E. coli (Escherichia coli) bacteria
originating from these food sources can cause common urinary tract infections.

Eating contaminated meat or food does not directly lead to a UTI. While some E. coli
such as O157:H7 can cause serious intestinal disease, these E. coli bacteria can live in the
intestine without causing problems. In women however, the bacteria can travel from the
anus to the vagina and urethra during sex, which can lead to the infection.

The research team is also investigating whether livestock may be passing antimicrobial-
resistant bacteria on to humans. This is due to the use of antibiotics to treat or prevent
disease in the animals and to enhance their growth, which may lead them to develop
resistance to the medication. When animals are slaughtered and their meat is processed
for sale, the meat can be contaminated with these bacteria.

"These studies might open the door to discussions with policymakers," Manges said,
"about how antibiotics are used in agriculture in Canada. It's certainly something we need
to continue studying."

The public should not be alarmed. Manges advises that consumers should cook meat
thoroughly and prevent contamination of other foods in the kitchen. Although some
infections caused by these E. coli are resistant to some antibiotics, the infections can still
be treated. Manges hopes that understanding how these bacteria are transmitted will help
reduce infections. She also hopes more attention will be focused on how meat is
produced in Canada. Her research is part of a broader study concerning food safety and is
financed through funding by the Government of Canada, Public Health Agency of
Canada, in collaboration with the Laboratory for Foodborne Zoonoses, specifically the
Canadian Integrated Program for Antimicrobial Resistance Surveillance, and also the
Division de l'inspection des aliments, Ville de Montréal.
Cardiologists Discover 'Pouch' in Heart
That May Raise Stroke Risk
ScienceDaily (Jan. 20, 2010) — UC Irvine cardiologists have found a pouchlike structure
inside the heart's left atrial chamber that may be a potent source of stroke-causing blood
clots.

About 80 percent of the 700,000-plus strokes that occur annually in the U.S. are due to
blood clots blocking a brain artery. In up to a third of these cases, the clots' origin cannot
be determined. Study co-author Dr. Subramaniam Krishnan said the discovery of this left
atrial pouch could provide answers and inform neurologists' efforts to prevent stroke
recurrences.

Krishnan and Dr. Miguel Salazar of UCI first spotted the pouch during autopsy research.
Subsequent ultrasound and CT scans of patients' hearts confirmed the finding. The
researchers estimate that the anatomical feature, which Krishnan likened to a kangaroo
pouch, is present in 30 percent to 35 percent of individuals. Study results appear in the
January issue of Journal of the American College of Cardiology: Cardiovascular
Interventions.

"The cul-de-sac nature of the heart pouch can promote stagnation of the blood, forming
clots that can travel into the brain and cause a stroke," Krishnan said. "It was thought that
the body of the left atrium was largely smooth and unlikely to be a source of blood clots,
but we have found that not to be true for roughly one in three people."

Krishnan and UCI neurologist Dr. Mark Fisher are currently studying the prevalence of
the left atrial pouch in patients who have already had strokes. "This finding points to a
potentially important cause of strokes," Fisher said. "The presence of this pouch could
change how neurologists treat these patients and lead to new therapeutic strategies for
preventing strokes."
Common Stomach Pathogen May Protect
Against Tuberculosis, Researchers Find
ScienceDaily (Jan. 20, 2010) — It's been implicated as the bacterium that causes ulcers
and the majority of stomach cancers, but studies by researchers at Stanford University,
UC Davis, and the University of Pittsburgh have found that Helicobacter pylori (H.
pylori) also may play a protective role -- against the worldwide killer, tuberculosis (TB).

In an article appearing online in PLoS ONE, Jay Solnick, UC Davis professor of medicine
and microbiology, and his co-authors report that H. pylori infection may enhance
immunity against tuberculosis, a disease endemic in many parts of the world, and for
which there is no effective vaccine.

"Here is a bacterium that we know is sometimes harmful and that is clearly associated
with cancer," Solnick said. "But it's not that simple."

Solnick explains that up until the 20th century, when public health improved and
antibiotic use was widespread, virtually everyone was infected with H. pylori. That
remains the case today in most developing countries, implying that H. pylori may have
evolved with its human host because it confers some selective benefit.

"These new findings suggest that one such benefit may that H. pylori provides protection
against tuberculosis, and perhaps other infectious diseases as well," he said.

Tuberculosis is second only to HIV as a cause of death due to a single infectious agent;
an estimated one third of the world population has latent TB infection. But only 30
percent of people exposed to TB ever become infected, and only 10 percent of those
infected will develop active tuberculosis disease.

"One explanation may be the presence of chronic infection of the stomach with H.
pylori," Solnick said. The findings also may eventually aid in managing TB, since H.
pylori infection may help determine whether someone infected with TB gets a latent,
asymptomatic infection or active disease.

The collaborative research effort began with the hypothesis that a person's immune
responses to individual infections are modified by the existence of other infections, said
Sharon Perry, an epidemiologist at Stanford University, and the study's lead author.

Early studies funded by the National Institutes of Health showed that a patient infected
with H. pylori had elevated immune responses to TB antigens. Perry's work expanded to
test the hypothesis in patients from immigrant populations in Santa Clara County, then in
households in Gambia and Pakistan, where TB is prevalent. In the two-year study, they
found that individuals exposed to TB who then progressed to active disease were less
likely to be infected with H. pylori than those who were not infected with H. pylori.
Protection against tuberculosis may have been a result of enhanced immune responses to
TB antigens in those infected with H. pylori, since H. pylori induces expression of
interferon gamma and other cytokines, which are important for immunity against viral
and bacterial infections.

At this point, Perry and Stanford University professor Julie Parsonnet wanted to test the
theory in non-human primates. They enlisted Solnick at UC Davis, in conjunction with
JoAnne Flynn of the Department of Microbiology and Molecular Genetics and
Immunology at the University of Pittsburgh School of Medicine.

With a grant from the Bill and Melinda Gates Foundation, Solnick, Parsonnet, and Flynn
looked at the role of H. pylori in 41 monkeys challenged with TB. Again, the findings
were striking. Of the 30 monkeys that tested positive for H. pylori, only 5 developed
active TB, but 6 of 11 monkeys that were negative for H. pylori developed active disease.

"The one-disease, one-pathogen paradigm doesn't tell the whole story," said Perry. "It is
incomplete as an explanation of the clinical outcomes of chronic infection. In fact, the
thousands of organisms that live with us play a role in shaping our immune response to
specific infections."

Solnick cites the "hygiene hypothesis" as one possible explanation. That theory suggests
that a reduction in exposure to infectious diseases can make the immune system less able
to fight other challenges. Conversely, exposure to certain pathogens may aid immune
response to other infections.

The authors acknowledge the findings are preliminary and propose several follow-up
studies. First, Solnick, Parsonnet and Flynn have proposed research to test whether
experimental infection of H. pylori will protect monkeys from TB, and whether it will
enhance the protective effect of immunization. If successful, they will test a recombinant
H. pylori strain that expresses TB antigens for possible immunization against TB. These
studies will be performed in collaboration with Ondek Ltd, founded by Barry Marshall,
who was awarded the Nobel Prize in 2005 for the discovery of H. pylori.
COPD, Even When Mild, Limits Heart
Function
ScienceDaily (Jan. 20, 2010) — A common lung condition, COPD (chronic obstructive
pulmonary disease) diminishes the heart's ability to pump effectively even when the
disease has no or mild symptoms, according to research published in the Jan. 21 issue of
the New England Journal of Medicine.

The study is the first time researchers have shown strong links between heart function
and mild COPD. The research was funded by the National Heart, Lung, and Blood
Institute (NHLBI) of the National Institutes of Health.

Researchers have long known that severe cases of COPD have harmful effects on the
heart, decreasing its ability to pump blood effectively. The new results suggest that these
changes in the heart occur much earlier than previously believed, in mild cases and even
before symptoms appear. One in five Americans over the age of 45 has COPD, but as
many as half of them may not even be aware of it.

"This study shows that COPD, even in its mildest form, is associated with diminished
heart function," said NHLBI Acting Director Susan B. Shurin, M.D. "We now have
evidence that the presence of even mild COPD may have important health implications
beyond the lungs."

COPD is the fourth leading cause of death in the United States, and it is strongly
associated with smoking. COPD often involves destruction of lung tissue, called
emphysema, as well as narrowed airways, persistent cough, and mucus production,
known as chronic obstructive bronchitis. These abnormalities impair the flow of air in the
lungs and make breathing more difficult.

Although damage to the airways from COPD is not fully reversible, treatments can
substantially improve a patient's daily life. "COPD is one of the big killers in the United
States, yet it is unknown to many," said James P. Kiley, Ph.D., director of the NHLBI
Division of Lung Diseases. "Unfortunately, many people with COPD don't recognize
common symptoms such as having shortness of breath while doing activities they used to
be able to do. It's important that we continue to increase awareness of the signs of COPD
and available treatments."

Using breathing tests and imaging studies of the chest, researchers measured heart and
lung structure and function in 2,816 generally healthy adults (average age of 61 years).
Study participants were part of the MESA Lung Study, an extension of the Multi-Ethnic
Study of Atherosclerosis (MESA), a large, NHLBI-supported study focused on finding
early signs of heart, lung, and blood diseases before symptoms appear.
Sensitive magnetic resonance imaging (MRI) and computed tomography (CT) scans
uncovered mild abnormalities in heart and lung function in many participants. They
discovered that the link between lung and heart function was strongest in current
smokers, who are at risk for both diseases, and especially in those with emphysema. The
findings also appeared, to a lesser extent, in people with mild COPD who had never
smoked.

"These results raise the intriguing possibility that treating lung disease may, in the future,
improve heart function," said Graham Barr, M.D., Dr. P.H., assistant professor of
medicine and epidemiology at Columbia University Medical Center in New York City,
principal investigator of the MESA Lung Study, and lead author of the paper. "Further
research is needed to prove whether treating mild COPD will help the heart work better."

The larger MESA project involves more than 6,000 middle-aged and older men and
women from six urban communities across the United States. Participants in MESA
come from diverse races and ethnic groups, including African Americans, Latinos,
Asians and whites. They have been tracked since enrollment began in 2000.

Because the MESA study population is ethnically mixed and covers a broad age range of
apparently healthy people, the results of this study may be widely applicable to the
general U.S. population.

The NHLBI also supports a national campaign, COPD Learn More Breathe Better, to
help people with COPD and those at risk to become more aware of COPD, get diagnosed
early, better understand this disease and live better with it.
Appendicitis May Be Related to Viral
Infections
ScienceDaily (Jan. 19, 2010) — Can you catch appendicitis? And if you do, is it
necessarily an emergency that demands immediate surgery?

Yes and no, according to a new study by UT Southwestern Medical Center surgeons and
physicians.

The researchers evaluated data over a 36-year period from the National Hospital
Discharge Survey and concluded in a paper appearing in the January issue of Archives of
Surgery that appendicitis may be caused by undetermined viral infection or infections,
said Dr. Edward Livingston, chief of GI/endocrine surgery at UT Southwestern and
senior author of the report.

The review of hospital discharge data runs counter to traditional thought, suggesting that
appendicitis doesn't necessarily lead to a burst appendix if the organ is not removed
quickly, Dr. Livingston said.

"Just as the traditional appendix scar across the abdomen is fast becoming history, thanks
to new single-incision surgery techniques that hide a tiny scar in the bellybutton, so too
may the conventional wisdom that patients with appendicitis need to be operated on as
soon as they enter the hospital," said Dr. Livingston. "Patients still need to be seen
quickly by a physician, but emergency surgery is now in question."

Appendicitis is the most common reason for emergency general surgery, leading to some
280,000 appendectomies being performed annually.

Appendicitis was first identified in 1886. Since then, doctors have presumed quick
removal of the appendix was a necessity to avoid a subsequent bursting, which can be an
emergency. Because removing the appendix solves the problems and is generally safe,
removal became the standard medical practice in the early 20th century.

But this latest research studying appendicitis trends from 1970 to 2006 suggests
immediate removal may not be necessary. Evidence from sailors at sea without access to
immediate surgery and from some children's hospitals, whose practice did not call for
emergency surgery, hinted that non-perforated appendicitis may resolve without surgery,
said Dr. Livingston.

In undertaking the study, the researchers screened the diagnosis codes for admissions for
appendicitis, influenza, rotavirus and enteric infections. They found that seasonal
variations and clustering of appendicitis cases support the theory that appendicitis may be
a viral disease, like the flu, Dr. Livingston said.
Statistical data revealed peaks, which may be outbreaks of appendicitis, in the years
1977, 1981, 1984, 1987, 1994 and 1998. In addition, researchers uncovered some
seasonal trends for appendicitis, documenting a slight increase in appendicitis cases
during the summer.

"The peaks and valleys of appendicitis cases generally matched up over time, suggesting
it is possible that these disorders share common etiologic determinates, pathogenetic
mechanisms or environmental factors that similarly affect their incidence," Dr.
Livingston said.

Researchers have been able to rule out flu and several other common infections as a
direct cause. They also were able to rule out several types of intestinal viruses.

Appendicitis afflicts about one in 10 people during their lifetime. The condition occurs
when the appendix becomes obstructed, but doctors are unsure why. Dr. Livingston and
other UT Southwestern researchers in 1995 identified an unexpected rise in appendicitis
cases, reversing a downward trend throughout the previous 25 years.

"Though appendicitis is fairly common, it still remains a frustrating medical mystery,"

Dr. Livingston said. "While we know surgical removal is an effective treatment, we still
don't know the purpose of the appendix, nor what causes it to become obstructed."

Other UT Southwestern researchers involved in the Archives of Surgery paper were Dr.
Robert W. Haley, chief of epidemiology, and Dr. Adam Alder, a resident and lead author.
The team also collaborated with economists at Southern Methodist University on novel
statistical methodologies to uncover the associations.
Sharing a Hospital Room Increases Risk
of 'Super Bugs'
ScienceDaily (Jan. 8, 2010) — Staying in a multi-bed hospital room dramatically
increases the risk of acquiring a serious infectious disease, Queen's University researchers
have discovered.

A new study led by infectious diseases expert Dr. Dick Zoutman says the chance of
acquiring serious infections like C. difficile (Clostridium difficile) rises with the addition
of every hospital roommate.

"If you're in a two, three or four-bedded room, each time you get a new roommate your
risk of acquiring these serious infections increases by 10 per cent," says Dr. Zoutman,
professor of Community Health and Epidemiology at Queen's. "That's a substantial risk,
particularly for longer hospital stays when you can expect to have many different
roommates."

Dr. Zoutman suggests hospitals need to consider more private rooms in their planning.
"Despite other advances, multi-bedded rooms are still part of hospital design in the 21st
century. Building hospitals with all private rooms is not yet the standard in Ontario or
Canada -- but it should be."

Also on the Queen's team are master's student Meghan Hamel and Associate Professor
Christopher O'Callaghan. The findings are published on-line in the American Journal of
Infection Control.

The researchers argue that it's cheaper in the long run to build more private rooms
because of the high costs of treating people with superbugs. For facilities with multi-bed
rooms that are unable to take on major redesign, Dr. Zoutman suggests converting four-
bed rooms to two-bed semi-privates, and changing semi-private rooms in high-risk areas
to private rooms, as much as possible.

"One important way to improve patient safety in our hospitals is to reduce the number of
roommates that patients are exposed to during their hospital stay," he stresses.
"Especially in acute care hospitals, where the risks are highest, we need to change our
room configurations as much as current resources will allow, and strive to design and
build new hospital facilities with entirely private rooms."
Double Trouble: Bacterial Super-
Infection After the Flu
ScienceDaily (Jan. 22, 2010) — Current research suggests that the flu may predispose to
secondary bacterial infections, which account for a significant proportion of mortality
during flu pandemics.

The report by Lee et al. appears in the February 2010 issue of The American Journal of
Pathology.

Influenza affects between three and five million people annually, causing up to 500,000
deaths worldwide. While most people will recover in one to two weeks, others will
develop life-threatening conditions such as pneumonia or bronchitis. High-risk groups for
seasonal influenza include the very young and old, people with compromised immune
systems, and pregnant women. However, during influenza pandemics, mortality may be
significant in previously healthy young adults.

A common complication of flu infection is a secondary "super-infection" by bacteria,

which greatly increases the morbidity and mortality of the disease. The most common
bacterial agents found following flu pandemics have been Streptococcus pneumoniae,
Haemophilus influenzae, Group A Streptococcus, and Staphylococcus aureus.
Furthermore, reports of infection with antibiotic-resistant strains have been increasing in
recent years.

To explore the mechanisms governing the increased pathogenesis of flu upon super-
infection, a group led by Dr. Sally R. Sarawar of the Torrey Pines Institute for Molecular
Studies, San Diego, California confirmed that otherwise nonlethal influenza and H.
influenzae infections cause high mortality rates in mice when flu infection precedes H.
influenzae infection. Their data confirm a restricted time period for this heightened
susceptibility and highlight that excessive bacterial, and not viral, growth is associated
with increased lethality. The fact that this increased mortality was observed in both
immunocompromised and immunocompetent mice suggests that even normal healthy
people are at increased risk for complications following bacterial super-infection.

Lee et al. suggest that the "lethal synergy between influenza virus and the bacterial
respiratory pathogen, H. influenzae, is mediated by innate immunity. They observed that
severe damage to the airways was an early event in the co-infected mice, eventually
leading to death. This underscores the need for early antiviral and antibiotic treatment to
combat severe disease in human patients and highlights the importance of vaccination
and effective hygiene measures to prevent secondary bacterial infections during influenza
infection.

This new model will be useful for further investigating the mechanisms underlying severe
disease caused by the interaction between influenza virus and bacteria, which may have
resulted in numerous deaths during influenza pandemics and continues to constitute a
significant clinical problem in susceptible individuals." Currently ongoing studies suggest
that this model may also be useful for identifying target molecules for the development of
novel therapeutic agents and strategies.