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Bacterial food poisoning

Foodborne illness or food poisoning is caused by consuming food contaminated with pathogenic bacteria, toxins, viruses, prions or parasites. Such contamination usually arises from improper handling, preparation or storage of food. Foodborne illness can also be caused by adding pesticides or medicines to food, or by accidentally consuming naturally poisonous substances like poisonous mushrooms or reef fish. Contact between food and pests, especially flies, rodents and cockroaches, is a further cause of contamination of food. more...

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Some common diseases are occasionally foodborne mainly through the water vector, even though they are usually transmitted by other routes. These include infections caused by Shigella, Hepatitis A, and the parasites Giardia lamblia and Cryptosporidium parvum.

The World Health Organization defines it as diseases, usually either infectious or toxic in nature, caused by agents that enter the body through the ingestion of food. Every person is at risk of foodborne illness.

Good hygiene practices before, during, and after food preparation can reduce the chances of contracting an illness.

Symptoms and mortality

Symptoms typically begin several hours after ingestion and depending on the agent involved, can include one or more of the following: nausea, abdominal pain, vomiting, diarrhea, fever, headache or tiredness. In most cases the body is able to permanently recover after a short period of acute discomfort and illness. However, foodborne illness can result in permanent health problems or even death, especially in babies, pregnant women (and their fetuses), elderly people, sick people and others with weak immune systems. Similarly, people with liver disease are especially susceptible to infections from Vibrio vulnificus, which can be found in oysters.

Incubation period

The delay between consumption of a contaminated food and appearance of the first symptoms of illness is called the incubation period. This ranges from hours to days (and rarely months or even years), depending on the agent, and on how much was consumed. If symptoms occur within 1-6 hours after eating the food, it suggests that it is caused by a bacterial toxin rather than live bacteria.

During the incubation period, microbes pass through the stomach into the intestine, attach to the cells lining the intestinal walls, and begin to multiply there. Some types of microbes stay in the intestine, some produce a toxin that is absorbed into the bloodstream, and some can directly invade the deeper body tissues. The symptoms produced depend on the type of microbe.

Infectious dose

The infectious dose is the amount of agent that must be consumed to give rise to symptoms of foodborne illness. The infective dose varies according to the agent and consumer's age and health. In the case of Salmonella, as few as 15-20 cells may suffice .

Pathogenic agents

An early theory on the causes of food poisoning involved ptomaines, alkaloids found in decaying animal and vegetable matter. While some poisonous alkaloids are the cause of poisoning, the discovery of bacteria left the ptomaine theory obsolete.


Bacterial infection is the most common cause of food poisoning. In the United Kingdom during 2000 the individual bacteria involved were as follows: Campylobacter jejuni 77.3%, Salmonella 20.9%, Escherichia coli O157:H7 1.4%, and all others less than 0.1% .


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Campylobacter: unmasking the secret genes of a food-poisoning culprit
From Agricultural Research, 10/1/04 by Marcia Wood

Microarrays, or gene chips, enable scientists to get a quick look at thousands of genes in a single experiment. Here, technician Sharon Horn monitors robotic equipment as it imprints Campylobacter microarrays on glass slides. Photo by Peggy Greb. (K11465-1)

The "juice" that always seems to leak out of those packages of fresh chicken you bring home from the supermarket can make a big mess on your kitchen counter. But more importantly, the juice can pose a hazard to your health. Nasty microbes called Campylobacter jejuni can live in that liquid and on the skin of fresh, uncooked poultry.

Thoroughly cooking chicken--by grilling, frying, roasting, or baking--kills this food-poisoning microbe. But if you accidentally splash some of the raw juice on food that you'd planned to eat uncooked, such as leafy greens for a fresh salad, you'd be wise to throw them out. Here's why: If the microbe takes hold on those greens, as it is very adept at doing, you might be in for a case of campylobacteriosis food poisoning that you won't soon forget.

Campylobacter is thought to be the leading cause of bacterial food poisoning in humans and is likely the perpetrator of more than 400 million cases of diarrhea every year. Though being careful when you handle raw poultry should help keep you safe, ARS researchers want to do more to zap this microbial menace before it reaches your home.

At Albany, California, scientists in the ARS Produce Safety and Microbiology Research Unit are making key advances in the international effort to clobber Campylobacter. The California team, based at the Western Regional Research Center, is focusing on Campylobacter's genes.

Why the interest in the microbe's genetic makeup? Because investigating genes may lead to discovery of faster, more reliable ways to detect the microbe in samples from humans and other animals, food, and water.

In addition, gene-based research opens the door to simpler, less-expensive tactics for distinguishing look-alike species and strains of Campylobacter and its close relatives, such as the Arcobacters. This will enable experts to quickly finger culprit microbes in food poisoning outbreaks.

Finally, the studies may lead to innovative, environmentally friendly techniques to circumvent the genes that make C. jejuni strains so successful in causing human gastrointestinal upset and in some cases paralysis or even death.

Working with the Institute for Genomic Research, Rockville, Maryland, the Albany scientists have decoded the makeup, or sequence, of all the genes and other genetic material in a specially selected strain of C. jejuni.

This research represents the first time that a C. jejuni strain from a farm animal--this case, a market chicken--has been sequenced. That's important, notes research leader Robert E. Mandrell, because chicken is the leading source of the bacterium in food. Earlier C. jejuni genome sequencing, performed elsewhere, was based on a specimen from a gastroenteritis patient and was lacking key features, such as the ability to colonize chickens, Mandrell says.

The next step: Zero in on specific genes. "We're particularly interested in the genes that make Campylobacter so viable and virulent," says ARS molecular biologist William G. Miller. They're targeting, for instance, genes that carry the code for making oligosaccharides. These compounds likely enable the microbe to stick like glue to chicken skin in the poultry processing plant even though the birds are bathed and rinsed with chlorinated water. The oligosaccharides might be important in invading and colonizing the human body, as well, Miller notes.

With this genome sequence information in hand, the scientists are developing microarrays, or gene chips, that make possible a quick look at thousands of genes in a single experiment. For these analyses, robotic equipment precisely places pieces of the pathogen's DNA in an array of infinitesimally small droplets on glass microscope slides.

"We build and use these microarrays to compare and contrast DNA of various Campylobacter samples," explains microbiologist Craig T. Parker. "We're also using microarrays to get a snapshot of genes in action so that we can see when genes are turned on or off." For example, Parker is pinpointing the genes that are active in helping Campylobacter overcome our bodies' protective actions. By tracking the action of the microbes' genes, Parker and co-investigators may be able to determine a way to derail them.

Though C. jejuni has grabbed center stage because of its known virulence, its relatives are also of interest. The Albany studies of C. coli, C. lari, and C. upsaliensis, for example, are attracting the attention of member nations in a three-continent collaboration called "Campycheck," formed to evaluate the importance of these lesser-known or newly emerging species. The Albany scientists and colleagues from the ARS Richard B. Russell Agricultural Research Center, Athens, Georgia, are advisors to Campycheck.

In clinical laboratories, these less-studied pathogens may inadvertently be killed by the antibiotics used to identify the better-known ones. The likely result? An inaccurate picture of their prevalence and virulence. Campycheck may yield a detailed, accurate picture.

The Campylobacter studies in the United States and abroad might never completely eliminate the need for careful handling of raw poultry in our homes or the kitchens of school cafeterias, fine restaurants, and other eateries. But the research can reduce our chances of ever encountering this unruly microbe.

This research is part of Food Safety, an ARS National Program (#108) described on the World Wide Web at

To reach scientists mentioned in this story, contact Marcia Wood, USDA-ARS Information Staff, 5601 Sunnyside Ave., Beltsville, MD 20705-5129; phone (301) 504-1662, fax (301) 504-1641, e-mail

What Makes a Campylobacter Strain Virulent?

Here's the puzzle: You have two samples of what seem to be the food-poisoning microbe Campylobacter jejuni. A quick look at the specimens with a microarray assay (see main story) shows no immediately apparent differences in their genes. But when you expose piglets--animals susceptible to this microbe--to the bacteria, one strain makes the animals ill, while the other affects them only mildly.

Why the difference?

ARS food safety researchers Craig T. Parker, at Albany, California, and colleague Michael E. Konkel at Washington State University in Pullman, are designing a series of experiments that should enable them to find out. What's more, their work may help other scientists who are investigating the virulence of other major foodborne pathogens.

Even though their preliminary microarray scan failed to reveal significant differences in the C. jejuni specimens' DNA, this technology offers another option--one that allows them to delve more deeply.

Instead of beginning with the microbe's DNA, these followup assays begin with RNA--genetic material that's formed when the DNA, or genes, becomes active.

In these tests, the scientists will place the two strains in petri dishes with colonies of a type of human intestinal cell. Called epithelial cells, they're the target of real-life Campylobacter attacks. The researchers will take samples of the two strains at successive intervals, looking for changes in RNA that occur over time. RNA extracted from the strains provides tell-tale evidence of genes that went into action. The work is much like that of police detectives who analyze evidence to reconstruct what really happened at a crime scene. The scientists use an enzyme called reverse transcriptase to match up the RNA to a version of the DNA from which it originated. Then, they use the microarray assay to discern the differences between that DNA and the microbe's DNA as it existed at the outset of the experiment. The comparison should reveal genes that were activated in the attack and genes that remained silent.

In earlier work at Pullman, collaborator Konkel uncovered one such C. jejuni gene. Named ciaB, short for Campylobacter invasion antigen B, it cues the microbe to secrete a similarly named protein, CiaB, which apparently plays a crucial role in enabling the bacterium to penetrate epithelial cells. Though undoubtedly key to C. jejuni's invasions, it is unlikely to act alone. The West Coast scientists expect to uncover other genes that will lead them into the dark heart of Campylobacter's virulence.--By Marcia Wood, ARS.

COPYRIGHT 2004 U.S. Government Printing Office
COPYRIGHT 2005 Gale Group

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