Multistate Outbreak of Listeriosis Associated with Jensen Farms Cantaloupe --- United States, August--September 2011

Multistate Outbreak of Listeriosis Associated with Jensen Farms Cantaloupe --- United States, August--September 2011Early Release
September 30, 2011 / 60(Early Release);1-2

Listeriosis is caused by Listeria monocytogenes, a gram-positive bacillus common in the environment and acquired by humans primarily through consumption of contaminated food. Infection causes a spectrum of illness, ranging from febrile gastroenteritis to invasive disease, including sepsis and meningoencephalitis. Invasive listeriosis occurs predominantly in older adults and persons with impaired immune systems.

Listeriosis in pregnant women is typically a mild "flu-like" illness, but can result in fetal loss, premature labor, or neonatal infection. Listeriosis is treated with antibiotics. On September 2, 2011, the Colorado Department of Public Health and Environment (CDPHE) notified CDC of seven cases of listeriosis reported since August 28. On average, Colorado reports two cases of listeriosis annually in August. By September 6, all seven Colorado patients interviewed with the Listeria Initiative* questionnaire reported eating cantaloupe in the month before illness began, and three reported eating cantaloupe marketed as "Rocky Ford."

A case was defined as illness with one of the outbreak strains isolated on or after August 1. Outbreak strains initially were defined as 1) clinical isolates of L. monocytogenes with specimen collection dates in August 2) with a two-enzyme, pulsed-field gel electrophoresis (PFGE) pattern combination that occurred in two or more persons and 3) that matched any of the three pattern combinations found among Colorado residents in August. Analysis of Listeria Initiative data comparing the first 19 outbreak-associated cases in 2011 with 85 cases among persons aged ≥65 years with sporadic listeriosis identified during August of the years 2004--2010 indicated that cantaloupe consumption was strongly associated with illness caused by the outbreak strains: 19 of 19 (100%) versus 54 of 85 (64%); (odds ratio = 14.9; 95% CI = 2.4--∞). Initial tracebacks of cantaloupe purchased by patients converged on Jensen Farms in Colorado.

After cantaloupe was implicated, PulseNet, the national molecular subtyping network for foodborne bacterial disease surveillance, detected a multistate cluster with a fourth PFGE pattern combination; a sample of cantaloupe collected from the implicated farm yielded L. monocytogenes with this pattern, and interviews with patients revealed that most had consumed cantaloupe. Isolates with this pattern were then also considered to be among the outbreak strains. By September 29, 84 cases with one of the four outbreak PFGE pattern combinations had been reported from 19 states†, including 83 with information on the date of illness onset (Figure). Among the patients, 88% were aged ≥60 years (range: 35--96 years); 55% were female, and two were pregnant. Fifteen deaths were reported. Ninety-two percent (57 of 62 with information on food consumption) reported eating cantaloupe in the month before illness began. All four outbreak strains of L. monocytogenes were isolated from whole and cut cantaloupe samples from patients' homes or from samples of Jensen Farms cantaloupe collected from grocery stores and the farm. On September 14, the farm issued a voluntary recall of its cantaloupe.

This outbreak has several unusual features. First, this is the first listeriosis outbreak associated with melon. Second, four widely differing PFGE pattern combinations and two serotypes (1/2a and 1/2b) have been associated with the outbreak. Third, this outbreak is unusually large; only two U.S. listeriosis outbreaks, one associated with frankfurters (108 cases) and one with Mexican-style cheese (142), have had more cases (1,2). Additional cases likely will be reported because of the long incubation period (usually 1--3 weeks, range: 3--70 days) and the time needed for diagnosis and confirmation. Fourth, this outbreak has the highest number of deaths of any U.S. foodborne outbreak since a listeriosis outbreak in 1998 (1).

CDC recommends that persons do not eat cantaloupes from Jensen Farms. This recommendation is especially important for persons at greater risk for listeriosis, including older adults, persons with weakened immune systems, and pregnant women. Not all of the recalled cantaloupes are individually labeled with stickers to indicate production by Jensen Farms. Consumers should consult the retailer or discard any cantaloupe of uncertain origin. Recommendations for preventing listeriosis from other foods are available at http://www.cdc.gov/listeria.

Reported by
Shaun Cosgrove, Alicia Cronquist, Colorado Dept of Public Health and Environment. Gail Wright, Boulder County Public Health. Tista Ghosh, Richard Vogt, Tri-County Health Department. Paul Teitell, Investigations Br, Food and Drug Administration (FDA) Denver District. Allen Gelfius, Charlotte Spires, Tracy Duvernoy, Sheila Merriweather, FDA Coordinated Outbreak Response and Evaluation (CORE) Network. Molly Freeman, Patricia M. Griffin, Kelly A. Jackson, Lavin A. Joseph, Barbara E. Mahon, Karen Neil, Benjamin J. Silk, Cheryl Tarr, Robert Tauxe, Eija Trees, Div of Foodborne, Waterborne, and Environmental Diseases, National Center for Emerging and Zoonotic Infectious Diseases; Mam Ibraheem, Maho Imanishi, Neena Jain, Jeffrey McCollum, Katherine A. O'Connor, EIS officers, CDC. Corresponding contributor: Kelly A. Jackson, gqv8@cdc.gov, 404-639-4603.


Acknowledgments
State and local health departments in the 19 states with cases.
References
1.Mead, PS, Dunne EF, Graves L, et al. Nationwide outbreak of listeriosis due to contaminated meat. Epidemiol Infect 2006;134:744--51.
2.Linnan, MJ, Mascola L, Lou XD, et al. Epidemic listeriosis associated with Mexican-style cheese. N Engl J Med 1988;319:823--8.

* The Listeria Initiative is a CDC-led, enhanced surveillance system that has routinely collected data on food consumption from all patients with listeriosis since 2004. Additional information is available at http://www.cdc.gov/nationalsurveillance/listeria_surveillance.html.
† Colorado (17 cases), Texas (14), New Mexico (13), Oklahoma (11), Nebraska (6), Kansas (5), Missouri (3), Indiana (2), Wisconsin (2), Wyoming (2), Alabama (1), Arkansas (1), California (1), Illinois (1), Maryland (1), Montana (1), North Dakota (1), Virginia (1), and West Virginia (1).

FIGURE. Number of infections with outbreak-associated strains of Listeria monocytogenes (n = 83), by date of illness onset* --- United States, July--September 2011

* Among persons for whom information on illness onset was reported to CDC by September 29, 2011.
Alternate text: The figure above shows an epidemiologic curve depicting 84 cases of infection with outbreak-asociated strains of Listeria monocytogenes, by date of illness onset, during August September 2011.

full-text:
Multistate Outbreak of Listeriosis Associated with Jensen Farms Cantaloupe --- United States, August--September 2011

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Genes Fact Sheet - National Institute of General Medical Sciences

Genes Fact Sheet

Yesterday
 Scientists knew the structure of DNA and that genes code for proteins, but they did not recognize the complexity of how genes are regulated.

The molecular biology revolution was in its infancy. The first few human genes were cloned, and DNA sequencing was just being developed.

Efforts were just beginning to identify and map genes at the molecular level and to correlate genes with diseases. Only a few human diseases, such as sickle cell disease, were associated with abnormal genes.


Today
The entire human genome and the genomes of hundreds of other species have been sequenced, providing a valuable resource for current and future biomedical advances.

We know that species ranging from microbes to humans have similar genes and genetic pathways. By studying the genes of model organisms and computationally comparing the DNA sequences of different species, researchers discovered the functions of many human genes, including those associated with certain diseases.

We know that most traits and diseases result from a combination of genes acting together and with the environment.

Computational tools allow scientists to analyze how patterns of gene activity are involved in health and disease. The activity patterns of hundreds of genes often reveal more about an organism than do the activities of individual genes.

Using large-scale approaches like genome wide association (GWA) and other statistical tools scientists are beginning to identify the genetic variations associated with some diseases.

The information contained in gene sequences is far more complex than anyone imagined. For example, scientists learned that genes contain large regions of non-coding DNA that regulate gene activity. They also discovered that the body can read the same DNA sequence in different ways to produce different proteins.

Scientists now know that gene regulation is central to an organism's development and to a cell's identity and function.

Researchers are finding that the regulation of gene expression is highly complex and depends upon specific proteins binding to the DNA. These proteins, which include transcription factors and repressors, detect the cell's ever-changing needs and respond by regulating the activity of certain genes.

Scientists continue to discover new roles for RNA, a class of molecule once thought to serve primarily as an intermediate between DNA and proteins during protein synthesis. They now know that RNA molecules can regulate gene expression and catalyze enzymatic reactions, including those that link amino acids together to form proteins.

As scientists have known for more than 100 years, inherited traits are passed from parent to child through genes. But there is a growing appreciation for the many ways not directly tied to DNA sequence that traits can be inherited. These so-called epigenetic processes can profoundly impact the inheritance of traits, including those related to health and disease.

Scientists are continually uncovering the specific patterns of gene expression and epigenetic regulation that determine a cell's identity. Recently, this knowledge was used to achieve a long-sought goal: the reprogramming of adult cells to an embryonic stem cell-like state. These cells are invaluable to studies of the molecular basis of genetic diseases and in understanding the effects of certain drugs. In the future, doctors might be able to use these engineered cells to replace those lost to diseases like Alzheimer's or to traumatic injuries.

The order in which gene mutations occur over millions of years is helping to explain how new molecular structures and functions evolve.

Different populations of people have distinct DNA profiles and possibly different genetic underpinnings of disease.

Genetic tools-such as DNA fingerprinting-are used for a wide variety of purposes, including in criminal forensics, paternity testing, identifying human remains, matching organ donors, studying the inheritance of specific traits in human and animal populations, and understanding the migration patterns of ancient peoples.

Genetics-based biotechnology has grown into a multibillion-dollar industry. It has created new drugs to treat conditions such as diabetes, anemia, growth hormone deficiency, and certain cancers and infectious diseases. It has also led to tests that diagnose rare diseases and predict a person's risk for more common diseases, such as breast cancer.

Biotechnology is creating new research tools to fuel the next generation of discoveries.

Scientists are using computers to analyze publicly available genomic information to predict new uses for existing medicines. The approach could save time and money compared to traditional drug discovery methods. Already, researchers revealed that, based on their effect on the human genome, an anti-ulcer medicine might treat lung cancer and an anticonvulsant might alleviate inflammatory bowel diseases.

Tomorrow
Through improved methods to identify genetic risk factors for common, complex diseases like diabetes, heart disease, and cancer, doctors will be better able to prevent, predict, and treat these diseases.

Doctors will use genetic information to tailor drug prescriptions, screening tests, and lifestyle recommendations for each patient.

Through genetic studies of bacteria, viruses, and other organisms, researchers will better understand how microbes evolve. This will enable them to develop tools to predict and prevent the emergence and spread of infectious diseases.

Using integrative approaches that simultaneously analyze many biological processes, scientists will learn how genes and the environment interact to contribute to disease.

Computer simulations will help investigators understand how regulatory proteins and RNAs target specific genes. This information will facilitate the development of gene therapies and new types of drugs.

Advances in manipulating genes and producing proteins under controlled conditions will improve our ability to produce certain pharmaceuticals, foods, industrial chemicals, agricultural products, and biotechnology tools.

For more information contact the NIGMS Office of Communications and Public Liaison at info@nigms.nih.gov or 301-496-7301.
http://www.nigms.nih.gov/
Content created November 2006; revised August 2011

Genes Fact Sheet - National Institute of General Medical Sciences

CDC Media Relations - Press Release: September 29, 2011

 

CDC takes new steps to combat childhood obesity

Research project will focus on doctors, communities and families to help children make healthy choices

The Centers for Disease Control and Prevention (CDC) today launched a new effort to address childhood obesity using successful elements of both primary care and public health. Funding made available through the Affordable Care Act will support a four year Childhood Obesity Demonstration Project.  Supported by $25 million in funding awards, the project will build on existing community efforts and will work to identify effective health care and community strategies to support children’s healthy eating and active living and help combat childhood obesity. 

The project will target children ages 2–12 years covered by the Children’s Health Insurance Program (CHIP), which provides low cost health insurance to over 7 million children from working families.  Rates of childhood obesity are high overall, but for minority and low–income communities in particular, they are even higher. Using innovative approaches to reach low–income and minority families to tackle childhood obesity prevents the onset of many diseases associated with childhood obesity, including type 2 diabetes, asthma, and heart disease. 

These innovative approaches include combining changes in preventive care at doctor visits with supportive changes in schools, child care centers, and community venues such as retail food stores and parks. Community health workers will provide a bridge between families and resources in their communities in order to inform and educate hard–to–reach, limited English proficiency, and minority communities about disease prevention (including obesity), health insurance enrollment opportunities, and disease management.  Overall, the grantees’ work will focus on strategies that improve children’s health behaviors by involving the children themselves, their parents and other family members and the communities in which they live.

“Over the last three decades, obesity rates among children and adolescents have nearly tripled,” said CDC Director Thomas R. Frieden, MD, MPH.  “Obese children are more likely to have asthma, depression, diabetes, and other serious and costly health problems.  This project will help figure out ways our children can grow up to lead long, healthy and productive lives.”

The project grantees include three research facilities, each of which will receive approximately $6.2 million over four years, to identify effective childhood obesity prevention strategies. The evaluation center will receive about $4.2 million over four years and will determine successful strategies and share lessons and successes.

Research Facilities:

• University of Texas Health Science Center at Houston
• San Diego State University
• Massachusetts State Department of Public Health

Evaluation Center:

• The University of Houston

At the end of the project in September 2015, CDC will disseminate the findings and provide recommendations for successful strategies to prevent obesity among underserved children throughout the United States.
For more information about the Childhood Obesity Demonstration Project visit http://www.cdc.gov/obesity/childhood/researchproject.html
CDC Media Relations - Press Release: September 29, 2011

Abnormal Protein May Explain Loss of Smell With Alzheimer's: MedlinePlus

 

Abnormal Protein May Explain Loss of Smell With Alzheimer's

The protein kills nerve cells in the nose, animal study finds

URL of this page: http://www.nlm.nih.gov/medlineplus/news/fullstory_117006.html
(*this news item will not be available after 12/28/2011)

By Mary Elizabeth Dallas

Thursday, September 29, 2011

Related MedlinePlus Pages

• Alzheimer's Disease
• Taste and Smell Disorders

THURSDAY, Sept. 29 (HealthDay News) -- A loss of a sense of smell can be one of the earliest signs of Alzheimer's disease.

New research suggests that an abnormal form of a protein -- amyloid precursor protein, or APP -- which has been previously associated with the Alzheimer's disease may be to blame.

A study in mice found that animals genetically engineered to produce high levels of the abnormal protein experienced high levels of death in nerve cells in their nose compared to normal mice.

Researchers say the findings may explain why people suffering from the progressive illness often lose their sense of smell while the disease is still in its initial stages. They added this new insight might help doctors detect the condition early on.

"Deficits in odor detection and discrimination are among the earliest symptoms of Alzheimer's disease, suggesting that the sense of smell can potentially serve as a canary in the coal mine for early diagnosis of the disease," study leader Leonardo Belluscio of the U.S. National Institute of Neurological Disorders and Stroke, said in a news release.

"The changes taking place in the olfactory system as a result of Alzheimer's disease may be similar to those in other regions of the brain but appear more rapidly," he added.

APP has been detected in the nose nerve cells of some people with early onset Alzheimer's, a rare form of the disease that runs in families and strikes before age 65.

The researchers found mice making the mutated form of APP had four times as much olfactory nerve cell death at three weeks of age than normal mice.

When researchers blocked the production of high levels of the mutated protein, more olfactory nerve cells survived.

"Reducing APP production suppressed the widespread loss of nerve cells, suggesting that such disease-related death of nerve cells could potentially be stopped," explained Belluscio.

The study, published in the Sept. 28 issue of The Journal of Neuroscience, also found that the cells that died in the nose did not contain amyloid plaques, which are derived from APP. Plaques have long been believed to contribute to the death of nerve cells in the brains of people with Alzheimer's, leading to memory loss.

The researchers say the findings suggest that APP itself may be responsible for the death of nerve cells.
"Together, these results support the hypothesis that amyloid proteins are involved in the degeneration of the brain that occurs with Alzheimer's disease," Donald Wilson of New York University School of Medicine and the Nathan Kline Institute for Psychiatric Research, said in a news release from the journal.

"Further, they provide an exciting opportunity to explore how to prevent or reverse the events that lead to cell death and, ultimately, dementia," added Wilson, an olfactory system expert who was not involved in the study.

While more research is needed, it should be noted that studies involving animals often fail to produce similar results with humans.

SOURCE: Society for Neuroscience, news release, Sept. 27, 2011

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Abnormal Protein May Explain Loss of Smell With Alzheimer's: MedlinePlus