Causes of Food Poisoning

Many different disease-causing germs can contaminate foods, so there are many different foodborne infections (also called foodborne disease or food poisoning).

• Researchers have identified more than 250 foodborne diseases.
• Most of them are infections, caused by a variety of bacteria, viruses, and parasites.
• Harmful toxins and chemicals also can contaminate foods and cause foodborne illness.

CDC estimates that each year 48 million people get sick from a foodborne illness, 128,000 are hospitalized, and 3,000 die.

Do I Have Food Poisoning?

Common symptoms of foodborne diseases are nausea, vomiting, stomach cramps, and diarrhea. However, symptoms may differ among the different types of foodborne diseases. Symptoms can sometimes be severe, and some foodborne illnesses can even be life-threatening. Although anyone can get a foodborne illness, some people are more likely to develop one. Those groups include:

• Older adults
• Young children
• People with immune systems weakened from medical conditions, such as diabetes, liver disease, kidney disease, organ transplants, or HIV/AIDS, or from receiving chemotherapy or radiation treatment.
• Pregnant women

Most people with a foodborne illness get better without medical treatment, but people with severe symptoms should see their doctor.

Some Common Foodborne Germs

The top five germs that cause illnesses from food eaten in the United States are:

• Norovirus
• Salmonella
• Clostridium perfringens
• Campylobacter
• Staphylococcus aureus (Staph)

Some other germs don’t cause as many illnesses, but when they do, the illnesses are more likely to lead to hospitalization. Those germs include:

• Clostridium botulinum (botulism)
• Listeria
• Escherichia coli (E. coli)
• Vibrio

Some foods are more associated with foodborne illnesses and food poisoning than others. They can carry harmful germs that can make you very sick if the food is contaminated.

• Raw foods of animal origin are the most likely to be contaminated, specifically raw or undercooked meat and poultry, raw or lightly cooked eggs, unpasteurized (raw) milk, and raw shellfish.
• Fruits and vegetables also may get contaminated.
• While certain foods are more likely to make you sick, any food can get contaminated in the field, during processing, or during other stages in the food production chain, including through cross-contamination with raw meat in kitchens.

Viruses

Viruses invade normal cells in your body. Many viruses cause infections that can be spread from person to person.

If water comes into contact with stools of infected people, the water may become contaminated with a virus. The contaminated water can spread the virus to foods. For example, if contaminated water is used to water or wash produce, the virus can spread to the produce. Similarly, shellfish that were living in contaminated water could contain a virus.

If people who are infected with a virus prepare or handle foods, they may spread the virus to the foods.

Common viruses that cause food poisoning include norovirus and hepatitis A.

Bacteria

Bacteria are tiny organisms that can cause infection or disease. Bacteria can enter your body through contaminated food or water.

Bacteria grow quickly when the temperature of food is between 40 and 140 degrees. Keeping food colder than 40 degrees in a refrigerator or freezer can slow or stop the growth of bacteria. Cooking food thoroughly often kills bacteria.

Many types of bacteria can cause food poisoning, including

• certain types of Salmonella
• certain types of Clostridium, including the common C. perfringens and the less common C. botulinum, which causes an illness called botulism
• certain types of Campylobacter, including C. jejuni
• Staphylococcus aureus, also called staph
• Escherichia coli, also called E. coli
• certain types of Vibrio
• Listeria monocytogenes, also called Listeria

Parasites

Parasites are tiny organisms that live inside other organisms. Parasites can enter your body through food or water and settle in your digestive tract. In developed countries such as the United States, parasitic infections are rare.

Parasites that cause food poisoning include

• Toxoplasma gondii, which causes an illness called toxoplasmosis
• Giardia
• Cryptosporidium, which causes an illness called cryptosporidiosis or crypto

Travelers’ diarrhea

People who travel from the United States to developing countries may develop travelers’ diarrhea. Eating food or drinking water contaminated with bacteria, parasites, or viruses causes travelers’ diarrhea. Although travelers’ diarrhea is most often acute, some parasites cause diarrhea that lasts longer.

Bacteria and Viruses

Bacteria and viruses are the most common cause of food poisoning. The symptoms and severity of food poisoning vary, depending on which bacteria or virus has contaminated the food.

To prevent illness, always follow the food safety steps: clean, separate, cook, and chill. Other prevention tips for specific bacteria and viruses are included below.

The bacteria and viruses that cause the most illnesses, hospitalizations, or deaths in the United States are described below and include:

• Campylobacter
• Clostridium perfringens
• E. coli
• Listeria
• Norovirus
• Salmonella

Other important bacteria and viruses that cause foodborne illness include:

• Bacillus cereus
• Botulism
• Hepatitis A
• Shigella
• Staphylococcus aureus (Staphylococcal [Staph] Food Poisoning)
• Vibrio Species Causing Vibriosis

Bacillus cereus

Botulism

Campylobacter

Clostridium perfringens

E. coli

Hepatitis A

Listeria

Norovirus

Salmonella

Shigella

Staphylococcus aureus
Staphylococcal (Staph) Food Poisoning

Vibrio Species Causing Vibriosis

Bacillus cereus, commonly found in soil, is a gram-positive endospore-forming bacterium that can sometimes cause foodborne illness. B. cereus endospores can survive cooking and produce enterotoxins in food after it has been heated; illnesses often occur after eating rice and other prepared foods left at room temperature for too long. The signs and symptoms appear within a few hours of ingestion and include nausea, pain, and abdominal cramps. B. cereus produces two toxins: one causing diarrhea, and the other causing vomiting. More severe signs and symptoms can sometimes develop.

Diagnosis can be accomplished by isolating bacteria from stool samples or vomitus and uneaten infected food. Treatment involves rehydration and supportive therapy. Antibiotics are not typically needed, as the illness is usually relatively mild and is due to toxin activity.

Bacterial infections of the gastrointestinal tract generally occur when bacteria or bacterial toxins are ingested in contaminated food or water. Toxins and other virulence factors can produce gastrointestinal inflammation and general symptoms such as diarrhea and vomiting. Bacterial GI infections can vary widely in terms of severity and treatment. Some can be treated with antibiotics, but in other cases antibiotics may be ineffective in combating toxins or even counterproductive if they compromise the GI microbiota. The key features of common bacterial GI infections.

Campylobacter is a genus of gram-negative, spiral or curved bacteria. They may have one or two flagella. Campylobacter jejuni gastroenteritis, a form of campylobacteriosis, is a widespread illness that is caused by Campylobacter jejuni. The primary route of transmission is through poultry that becomes contaminated during slaughter. Handling of the raw chicken in turn contaminates cooking surfaces, utensils, and other foods. Unpasteurized milk or contaminated water are also potential vehicles of transmission. In most cases, the illness is self-limiting and includes fever, diarrhea, cramps, vomiting, and sometimes dysentery. More serious signs and symptoms, such as bacteremia, meningitis, pancreatitis, cholecystitis, and hepatitis, sometimes occur. It has also been associated with autoimmune conditions such as Guillain-Barré syndrome, a neurological disease that occurs after some infections and results in temporary paralysis. HUS following infection can also occur. The virulence in many strains is the result of hemolysin production and the presence of Campylobacter cytolethal distending toxin (CDT), a powerful deoxyribonuclease (DNase) that irreversibly damages host cell DNA.

Diagnosis involves culture under special conditions, such as elevated temperature, low oxygen tension, and often medium supplemented with antimicrobial agents. These bacteria should be cultured on selective medium (such as Campy CV, charcoal selective medium, or cefaperazone charcoal deoxycholate agar) and incubated under microaerophilic conditions for at least 72 hours at 42 °C. Antibiotic treatment is not usually needed, but erythromycin or ciprofloxacin may be used.

What kind of germ is Campylobacter?

Campylobacter are bacteria that can make people and animals sick. Most human illness is caused by one species, called Campylobacter jejuni, but other species also can cause human illness.

How does food and water get contaminated with Campylobacter?

Many chickens, cows, and other birds and animals that show no signs of illness carry Campylobacter. Campylobacter can be carried in the intestines, liver, and giblets of animals and can be transferred to other edible parts of an animal when it’s slaughtered. In 2014, National Antimicrobial Resistance Monitoring System (NARMS) testing found Campylobacter on 33% of raw chicken bought from retailers.

Milk can become contaminated when a cow has a Campylobacter infection in her udder or when milk is contaminated with manure. Other foods, such as fruits and vegetables, can be can become contaminated through contact with soil containing feces from cows, birds, or other animals. Animal feces can also contaminate lakes and streams. Pasteurization of milk, washing or scrubbing of fruits and vegetables, and disinfection of drinking water helps prevent illness.

How do people get infected with Campylobacter bacteria?

It takes very few Campylobacter germs (fewer than 500) to make someone sick. That means a single drop of juice from raw chicken can have enough Campylobacter in it to infect someone.

Most Campylobacter infections are associated with eating raw or undercooked poultry or from contamination of other foods by these items. People can get infected when a cutting board that has been used to cut and prepare raw chicken isn’t washed before it is used to prepare foods that are served raw or lightly cooked, such as salad or fruit. People also can get infected through contact with the feces of a dog or cat. Campylobacter does not usually spread from one person to another.

Outbreaks of Campylobacter infections have been associated most often with poultry, raw (unpasteurized) dairy products, untreated water, and produce.

Campylobacter infection is common in the developing world, and people who travel abroad have a greater chance of becoming infected. About 1 in 5 Campylobacter infections reported to the Foodborne Diseases Active Surveillance Network (FoodNet) are associated with international travel.

Even more rarely, people may become infected through contaminated blood during a transfusion.

What is the incidence rate?

Active surveillance through the Foodborne Diseases Active Surveillance Network (FoodNet) indicates that about 14 cases per 100,000 people are diagnosed each year. Many more cases go undiagnosed or unreported. CDC estimates that Campylobacter infection affects more than 1.3 million people in the United States every year.

What are the likely outcomes?

Most people who get Campylobacter infection recover completely within two to five days, although recovery can take up to 10 days. Campylobacter infection can result in long-term consequences such as arthritis, irritable bowel syndrome (IBS), or Guillain-Barré syndrome (GBS). CDC estimates about 1 in every 1,000 reported Campylobacter illnesses leads to GBS.

Who is in the Risk Group?

Anyone can become infected with Campylobacter but campylobacteriosis is more common in males, children younger than 5 years, and people 65 years and older.

Botulism is a rare but serious illness caused by a toxin produced by Clostridium botulinum bacteria spores. If the toxin gets into your bloodstream, it can attack your nerves and block signals that control your body’s muscles, most often starting with those in your eyes, face, mouth, and throat. If left untreated, it can paralyze your arms and legs, prevent you from breathing, and even kill you. Find out key facts about botulism and how to prevent it.

Key Facts

• Botulism is a rare but serious paralytic illness that often affects previously healthy people.
• Botulism is caused by botulinum toxin, the most potent known toxin.
• Clostridium botulinum can make spores and, under certain conditions that rarely occur, the spores can grow and make botulinum toxin.
• Even taking a small taste of food containing botulinum toxin can cause botulism.
• Kinds of botulism include foodborne, wound, infant, adult intestinal colonization, and iatrogenic.

Protect Yourself from Botulism

Foodborne botulism is often caused by eating home-canned foods that have not been canned properly. Commercially canned foods are much less likely to be a source of botulism because modern commercial canning processes kill C. botulinum spores.

Botulism in Infants

We don’t know how most babies with infant botulism came into contact with C. botulinum spores, but we do know that these spores can be found in honey. Do not feed honey to children younger than 12 months because it has been linked to some cases of infant botulism.

Foodborne Botulism

Foodborne botulism can be caused by a food that is not prepared or stored properly. In Alaska, foodborne botulism is often caused by traditional Alaska Native foods, including fermented fish, because of the way these foods are sometimes prepared or stored.

Wound Botulism

Sometimes a wound can get infected with C. botulinum. The most common way this happens is when a contaminated illicit drug, such as black tar heroin, is injected into muscle or skin. Wound botulism also has been reported following traumatic injuries, such as motorcycle crashes and surgeries.

Prevention Tips

• If you preserve, can, or ferment your own foods, you can reduce the chance of getting botulism from these foods by:
  • Following safe home canning instructions as recommended by the U.S. Department of Agriculture in the USDA Complete Guide to Home Canning
  • Following all instructions for washing, cleaning, and sterilizing items used in canning
  • Using pressure canners for low-acid foods like potatoes, most other vegetables, and meats
• Everyone can reduce their chances of getting foodborne botulism by:
  • Refrigerating homemade oils infused with garlic or herbs and throwing away any unused oils after 4 days
  • Keeping potatoes that have been baked while wrapped in aluminum foil hot (at temperatures above 140°F) until they are served, or refrigerating them with the foil loosened
• Prevent wound botulism by keeping wounds clean and not injecting illicit drugs. If wounds appear infected, seek medical care quickly.
• Honey can contain the bacteria that causes infant botulism, so do not feed honey to children younger than 12 months.
• If you need an injection of botulinum toxin for a medical condition, your doctor will choose the safest dose. If you get an injection of botulinum toxin for cosmetic reasons, be sure to go to a licensed professional.

Clostridium difficile is a gram-positive rod that can be a commensal bacterium as part of the normal microbiota of healthy individuals. When the normal microbiota is disrupted by long-term antibiotic use, it can allow the overgrowth of this bacterium, resulting in antibiotic-associated diarrhea caused by C. difficile. Antibiotic-associated diarrhea can also be considered a nosocomial disease. Patients at the greatest risk of C. difficile infection are those who are immunocompromised, have been in health-care settings for extended periods, are older, have recently taken antibiotics, have had gastrointestinal procedures done, or use proton pump inhibitors, which reduce stomach acidity and allow proliferation of C. difficile. Because this species can form endospores, it can survive for extended periods of time in the environment under harsh conditions and is a considerable concern in health-care settings.

This bacterium produces two toxins, Clostridium difficile toxin A (TcdA) and Clostridium difficile toxin B (TcdB). These toxins inactivate small GTP-binding proteins, resulting in actin condensation and cell rounding, followed by cell death. Infections begin with focal necrosis, then ulceration with exudate, and can progress to pseudomembranous colitis, which involves inflammation of the colon and the development of a pseudomembrane of fibrin containing dead epithelial cells and leukocytes (Figure). Watery diarrhea, dehydration, fever, loss of appetite, and abdominal pain can result. Perforation of the colon can occur, leading to septicemia, shock, and death. C. difficile is also associated with necrotizing enterocolitis in premature babies and neutropenic enterocolitisassociated with cancer therapies.

Clostridium difficile is able to colonize the mucous membrane of the colon when the normal microbiota is disrupted. The toxins TcdA and TcdB trigger an immune response, with neutrophils and monocytes migrating from the bloodstream to the site of infection. Over time, inflammation and dead cells contribute to the development of a pseudomembrane. (credit micrograph: modification of work by Janice Carr, Centers for Disease Control and Prevention)

Diagnosis is made by considering the patient history (such as exposure to antibiotics), clinical presentation, imaging, endoscopy, lab tests, and other available data. Detecting the toxin in stool samples is used to confirm diagnosis. Although culture is preferred, it is rarely practical in clinical practice because the bacterium is an obligate anaerobe. Nucleic acid amplification tests, including PCR, are considered preferable to ELISA testing for molecular analysis.

The first step of conventional treatment is to stop antibiotic use, and then to provide supportive therapy with electrolyte replacement and fluids. Metronidazole is the preferred treatment if the C. difficile diagnosis has been confirmed. Vancomycin can also be used, but it should be reserved for patients for whom metronidazole was ineffective or who meet other criteria (e.g., under 10 years of age, pregnant, or allergic to metronidazole).

A newer approach to treatment, known as a fecal transplant, focuses on restoring the microbiota of the gut in order to combat the infection. In this procedure, a healthy individual donates a stool sample, which is mixed with saline and transplanted to the recipient via colonoscopy, endoscopy, sigmoidoscopy, or enema. It has been reported that this procedure has greater than 90% success in resolving C. difficile infections.

Clostridium perfringens gastroenteritis is a generally mild foodborne disease that is associated with undercooked meats and other foods. C. perfringens is a gram-positive, rod-shaped, endospore-forming anaerobic bacterium that is tolerant of high and low temperatures. At high temperatures, the bacteria can form endospores that will germinate rapidly in foods or within the intestine. Food poisoning by type A strains is common. This strain always produces an enterotoxin, sometimes also present in other strains, that causes the clinical symptoms of cramps and diarrhea. A more severe form of the illness, called pig-bel or enteritis necroticans, causes hemorrhaging, pain, vomiting, and bloating. Gangrene of the intestines may result. This form has a high mortality rate but is rare in the United States.

Diagnosis involves detecting the C. perfringens toxin in stool samples using either molecular biology techniques (PCR detection of the toxin gene) or immunology techniques (ELISA). The bacteria itself may also be detected in foods or in fecal samples. Treatment includes rehydration therapy, electrolyte replacement, and intravenous fluids. Antibiotics are not recommended because they can damage the balance of the microbiota in the gut, and there are concerns about antibiotic resistance. The illness can be prevented through proper handling and cooking of foods, including prompt refrigeration at sufficiently low temperatures and cooking food to a sufficiently high temperature.

The gram-negative rod Escherichia coli is a common member of the normal microbiota of the colon. Although the vast majority of E. coli strains are helpful commensal bacteria, some can be pathogenic and may cause dangerous diarrheal disease. The pathogenic strains have additional virulence factors such as type 1 fimbriae that promote colonization of the colon or may produce toxins. These virulence factors are acquired through horizontal gene transfer.

Extraintestinal disease can result if the bacteria spread from the gastrointestinal tract. Although these bacteria can be spread from person to person, they are often acquired through contaminated food or water. There are six recognized pathogenic groups of E. coli, but we will focus here on the four that are most commonly transmitted through food and water.

Enterotoxigenic E. coli (ETEC), also known as traveler’s diarrhea, causes diarrheal illness and is common in less developed countries. In Mexico, ETEC infection is called Montezuma’s Revenge. Following ingestion of contaminated food or water, infected individuals develop a watery diarrhea, abdominal cramps, malaise (a feeling of being unwell), and a low fever. ETEC produces a heat-stable enterotoxin similar to cholera toxin, and adhesins called colonization factors that help the bacteria to attach to the intestinal wall. Some strains of ETEC also produce heat-labile toxins. The disease is usually relatively mild and self-limiting. Diagnosis involves culturing and PCR. If needed, antibiotic treatment with fluoroquinolones, doxycycline, rifaximin, and trimethoprim-sulfamethoxazole (TMP/SMZ) may shorten infection duration. However, antibiotic resistance is a problem.

Enteroinvasive E. coli (EIEC) is very similar to shigellosis, including its pathogenesis of intracellular invasion into intestinal epithelial tissue. This bacterium carries a large plasmid that is involved in epithelial cell penetration. The illness is usually self-limiting, with symptoms including watery diarrhea, chills, cramps, malaise, fever, and dysentery. Culturing and PCR testing can be used for diagnosis. Antibiotic treatment is not recommended, so supportive therapy is used if needed.

Enteropathogenic E. coli (EPEC) can cause a potentially fatal diarrhea, especially in infants and those in less developed countries. Fever, vomiting, and diarrhea can lead to severe dehydration. These E. coli inject a protein (Tir) that attaches to the surface of the intestinal epithelial cells and triggers rearrangement of host cell actin from microvilli to pedestals. Tir also happens to be the receptor for Intimin, a surface protein produced by EPEC, thereby allowing E. coli to “sit” on the pedestal. The genes necessary for this pedestal formation are encoded on the locus for enterocyte effacement (LEE) pathogenicity island. As with ETEC, diagnosis involves culturing and PCR. Treatment is similar to that for ETEC.

The most dangerous strains are enterohemorrhagic E. coli (EHEC), which are the strains capable of causing epidemics. In particular, the strain O157:H7 has been responsible for several recent outbreaks. Recall that the O and H refer to surface antigens that contribute to pathogenicity and trigger a host immune response (“O” refers to the O-side chain of the lipopolysaccharide and the “H” refers to the flagella). Similar to EPEC, EHEC also forms pedestals. EHEC also produces a Shiga-like toxin. Because the genome of this bacterium has been sequenced, it is known that the Shiga toxin genes were most likely acquired through transduction (horizontal gene transfer). The Shiga toxin genes originated from Shigelladysenteriae. Prophage from a bacteriophage that previously infected Shigella integrated into the chromosome of E. coli. The Shiga-like toxin is often called verotoxin.

EHEC can cause disease ranging from relatively mild to life-threatening. Symptoms include bloody diarrhea with severe cramping, but no fever. Although it is often self-limiting, it can lead to hemorrhagic colitis and profuse bleeding. One possible complication is HUS. Diagnosis involves culture, often using MacConkey with sorbitol agar to differentiate between E. coli O157:H7, which does not ferment sorbitol, and other less virulent strains of E. coli that can ferment sorbitol.

Serological typing or PCR testing also can be used, as well as genetic testing for Shiga toxin. To distinguish EPEC from EHEC, because they both form pedestals on intestinal epithelial cells, it is necessary to test for genes encoding for both the Shiga-like toxin and for the LEE. Both EPEC and EHEC have LEE, but EPEC lacks the gene for Shiga toxin. Antibiotic therapy is not recommended and may worsen HUS because of the toxins released when the bacteria are killed, so supportive therapies must be used. Table summarizes the characteristics of the four most common pathogenic groups.

The gram-negative bacterium Helicobacter pylori is able to tolerate the acidic environment of the human stomach and has been shown to be a major cause of peptic ulcers, which are ulcers of the stomach or duodenum. The bacterium is also associated with increased risk of stomach cancer (Figure). According to the CDC, approximately two-thirds of the population is infected with H. pylori, but less than 20% have a risk of developing ulcers or stomach cancer. H. pylori is found in approximately 80% of stomach ulcers and in over 90% of duodenal ulcers.

H. pylori colonizes epithelial cells in the stomach using pili for adhesion. These bacteria produce urease, which stimulates an immune response and creates ammonia that neutralizes stomach acids to provide a more hospitable microenvironment. The infection damages the cells of the stomach lining, including those that normally produce the protective mucus that serves as a barrier between the tissue and stomach acid. As a result, inflammation (gastritis) occurs and ulcers may slowly develop. Ulcer formation can also be caused by toxin activity. It has been reported that 50% of clinical isolates of H. pylori have detectable levels of exotoxin activity in vitro. This toxin, VacA, induces vacuole formation in host cells. VacA has no primary sequence homology with other bacterial toxins, and in a mouse model, there is a correlation between the presence of the toxin gene, the activity of the toxin, and gastric epithelial tissue damage.

Signs and symptoms include nausea, lack of appetite, bloating, burping, and weight loss. Bleeding ulcers may produce dark stools. If no treatment is provided, the ulcers can become deeper, more tissues can be involved, and stomach perforation can occur. Because perforation allows digestive enzymes and acid to leak into the body, it is a very serious condition.

Helicobacter infection decreases mucus production and causes peptic ulcers. (credit top left photo: modification of work by "Santhosh Thomas"/YouTube; credit top right photo: modification of work by Moriya M, Uehara A, Okumura T, Miyamoto M, and Kohgo Y)

To diagnose H. pylori infection, multiple methods are available. In a breath test, the patient swallows radiolabeled urea. If H. pylori is present, the bacteria will produce urease to break down the urea. This reaction produces radiolabeled carbon dioxide that can be detected in the patient’s breath. Blood testing can also be used to detect antibodies to H. pylori. The bacteria themselves can be detected using either a stool test or a stomach wall biopsy.

Antibiotics can be used to treat the infection. However, unique to H. pylori, the recommendation from the US Food and Drug Administration is to use a triple therapy. The current protocols are 10 days of treatment with omeprazole, amoxicillin, and clarithromycin (OAC); 14 days of treatment with bismuth subsalicylate, metronidazole, and tetracycline (BMT); or 10 or 14 days of treatment with lansoprazole, amoxicillin, and clarithromycin (LAC). Omeprazole, bismuth subsalicylate, and lansoprazole are not antibiotics but are instead used to decrease acid levels because H. pylori prefers acidic environments.

Although treatment is often valuable, there are also risks to H. pylori eradication. Infection with H. pylori may actually protect against some cancers, such as esophageal adenocarcinoma and gastroesophageal reflux disease.

About Norovirus

Norovirus is a very contagious virus that causes vomiting and diarrhea. Anyone can get infected and sick with norovirus. You can get norovirus from:

• Having direct contact with an infected person
• Consuming contaminated food or water
• Touching contaminated surfaces then putting your unwashed hands in your mouth

Norovirus Symptoms

The most common symptoms are:

• Diarrhea
• Vomiting
• Nausea
• Stomach pain

Prevent Norovirus

Protect yourself and others from norovirus:

• Wash your hands often
• Rinse fruits and vegetables
• Cook shellfish thoroughly
• Stay home when sick and for two days after symptoms stop
• Avoid preparing food for others when sick and for two days after symptoms stop

Trends and Outbreaks

• Outbreaks are common
• The virus spreads very easily and quickly
• Norovirus spreads:
  • From infected people to others
  • Through contaminated foods and surfaces
• Outbreaks can happen anytime, but they occur most often from November to April.

Stomach bug or norovirus?

You may hear norovirus illness be called “food poisoning”, “stomach flu”, or “stomach bug.” Noroviruses are the leading cause of foodborne illness. But, other germs and chemicals can also cause foodborne illness.

Norovirus illness is not related to the flu, which is caused by influenza virus.

Salmonella gastroenteritis, also called salmonellosis, is caused by the rod-shaped, gram-negative bacterium Salmonella. Two species, S. enterica and S. bongori, cause disease in humans, but S. enterica is the most common. The most common serotypes of S. enterica are Enteritidis and Typhi. We will discuss typhoid fever caused by serotypes Typhi and Paratyphi A separately. Here, we will focus on salmonellosis caused by other serotypes.

Salmonella is a part of the normal intestinal microbiota of many individuals. However, salmonellosis is caused by exogenous agents, and infection can occur depending on the serotype, size of the inoculum, and overall health of the host. Infection is caused by ingestion of contaminated food, handling of eggshells, or exposure to certain animals. Salmonella is part of poultry’s microbiota, so exposure to raw eggs and raw poultry can increase the risk of infection. Handwashing and cooking foods thoroughly greatly reduce the risk of transmission. Salmonella bacteria can survive freezing for extended periods but cannot survive high temperatures.

Once the bacteria are ingested, they multiply within the intestines and penetrate the epithelial mucosal cells via M cells where they continue to grow (Figure). They trigger inflammatory processes and the hypersecretion of fluids. Once inside the body, they can persist inside the phagosomes of macrophages. Salmonella can cross the epithelial cell membrane and enter the bloodstream and lymphatic system. Some strains of Salmonella also produce an enterotoxin that can cause an intoxication.

Infected individuals develop fever, nausea, abdominal cramps, vomiting, headache, and diarrhea. These signs and symptoms generally last a few days to a week. According to the Centers for Disease Control and Prevention (CDC), there are 1,000,000 cases annually, with 380 deaths each year. However, because the disease is usually self-limiting, many cases are not reported to doctors and the overall incidence may be underreported. Diagnosis involves culture followed by serotyping and DNA fingerprinting if needed. Positive results are reported to the CDC. When an unusual serotype is detected, samples are sent to the CDC for further analysis. Serotyping is important for determining treatment. Oral rehydration therapy is commonly used. Antibiotics are only recommended for serious cases. When antibiotics are needed, as in immunocompromised patients, fluoroquinolones, third-generation cephalosporins, and ampicillin are recommended. Antibiotic resistance is a serious concern.

Salmonella entering an intestinal epithelial cell by reorganizing the host cell’s cytoskeleton via the trigger mechanism. (credit: modification of work by National Institutes for Health)

Salmonella, the name of a group of bacteria, is one of the most common causes of food poisoning in the United States. Usually, symptoms last 4-7 days and most people get better without treatment. But, Salmonella can cause more serious illness in older adults, infants, and persons with chronic diseases. Salmonella is killed by cooking and pasteurization.

Certain serotypes of S. enterica, primarily serotype Typhi (S. typhi) but also Paratyphi, cause a more severe type of salmonellosis called typhoid fever. This serious illness, which has an untreated mortality rate of 10%, causes high fever, body aches, headache, nausea, lethargy, and a possible rash.

Some individuals carry S. typhi without presenting signs or symptoms (known as asymptomatic carriers) and continually shed them through their feces. These carriers often have the bacteria in the gallbladder or intestinal epithelium. Individuals consuming food or water contaminated with these feces can become infected.

S. typhi penetrate the intestinal mucosa, grow within the macrophages, and are transported through the body, most notably to the liver and gallbladder. Eventually, the macrophages lyse, releasing S. typhi into the bloodstream and lymphatic system. Mortality can result from ulceration and perforation of the intestine. A wide range of complications, such as pneumonia and jaundice, can occur with disseminated disease.

S. typhi have Salmonella pathogenicity islands (SPIs) that contain the genes for many of their virulence factors. Two examples of important typhoid toxins are the Vi antigen, which encodes for capsule production, and chimeric A2B5 toxin, which causes many of the signs and symptoms of the acute phase of typhoid fever.

Clinical examination and culture are used to make the diagnosis. The bacteria can be cultured from feces, urine, blood, or bone marrow. Serology, including ELISA, is used to identify the most pathogenic strains, but confirmation with DNA testing or culture is needed. A PCR test can also be used, but is not widely available.

The recommended antibiotic treatment involves fluoroquinolones, ceftriaxone, and azithromycin. Individuals must be extremely careful to avoid infecting others during treatment. Typhoid fever can be prevented through vaccination for individuals traveling to parts of the world where it is common.

TYPHOID MARY

Mary Mallon was an Irish immigrant who worked as a cook in New York in the early 20^th century. Over seven years, from 1900 to 1907, Mallon worked for a number of different households, unknowingly spreading illness to the people who lived in each one. In 1906, one family hired George Soper, an expert in typhoid fever epidemics, to determine the cause of the illnesses in their household. Eventually, Soper tracked Mallon down and directly linked 22 cases of typhoid fever to her. He discovered that Mallon was a carrier for typhoid but was immune to it herself. Although active carriers had been recognized before, this was the first time that an asymptomatic carrier of infection had been identified.

Because she herself had never been ill, Mallon found it difficult to believe she could be the source of the illness. She fled from Soper and the authorities because she did not want to be quarantined or forced to give up her profession, which was relatively well paid for someone with her background. However, Mallon was eventually caught and kept in an isolation facility in the Bronx, where she remained until 1910, when the New York health department released her under the condition that she never again work with food. Unfortunately, Mallon did not comply, and she soon began working as a cook again. After new cases began to appear that resulted in the death of two individuals, the authorities tracked her down again and returned her to isolation, where she remained for 23 more years until her death in 1938. Epidemiologists were able to trace 51 cases of typhoid fever and three deaths directly to Mallon, who is unflatteringly remembered as “Typhoid Mary.”

The Typhoid Mary case has direct correlations in the health-care industry. Consider Kaci Hickox, an American nurse who treated Ebola patients in West Africa during the 2014 epidemic. After returning to the United States, Hickox was quarantined against her will for three days and later found not to have Ebola. Hickox vehemently opposed the quarantine. In an editorial published in the British newspaper The Guardian, Hickox argued that quarantining asymptomatic health-care workers who had not tested positive for a disease would not only prevent such individuals from practicing their profession, but discourage others from volunteering to work in disease-ridden areas where health-care workers are desperately needed.

What is the responsibility of an individual like Mary Mallon to change her behavior to protect others? What happens when an individual believes that she is not a risk, but others believe that she is? How would you react if you were in Mallon’s shoes and were placed in a quarantine you did not believe was necessary, at the expense of your own freedom and possibly your career? Would it matter if you were definitely infected or not?

When gastrointestinal illness is associated with the rod-shaped, gram-negative bacterium Shigella, it is called bacillary dysentery, or shigellosis. Infections can be caused by S. dysenteriae, S. flexneri, S. boydii, and/or S. sonnei that colonize the GI tract. Shigellosis can be spread from hand to mouth or through contaminated food and water. Most commonly, it is transmitted through the fecal-oral route.

Shigella bacteria invade intestinal epithelial cells. When taken into a phagosome, they can escape and then live within the cytoplasm of the cell or move to adjacent cells. As the organisms multiply, the epithelium and structures with M cells of the Peyer’s patches in the intestine may become ulcerated and cause loss of fluid. Stomach cramps, fever, and watery diarrhea that may also contain pus, mucus, and/or blood often develop. More severe cases may result in ulceration of the mucosa, dehydration, and rectal bleeding. Additionally, patients may later develop hemolytic uremic syndrome (HUS), a serious condition in which damaged blood cells build up in the kidneys and may cause kidney failure, or reactive arthritis, a condition in which arthritis develops in multiple joints following infection. Patients may also develop chronic post-infection irritable bowel syndrome (IBS).

S. dysenteriae type 1 is able to produce Shiga toxin, which targets the endothelial cells of small blood vessels in the small and large intestine by binding to a glycosphingolipid. Once inside the endothelial cells, the toxin targets the large ribosomal subunit, thus affecting protein synthesis of these cells. Hemorrhaging and lesions in the colon can result. The toxin can target the kidney’s glomerulus, the blood vessels where filtration of blood in the kidney begins, thus resulting in HUS.

Stool samples, which should be processed promptly, are analyzed using serological or molecular techniques. One common method is to perform immunoassays for S. dysenteriae. Other methods that can be used to identify Shigella include API test strips, Enterotube systems, or PCR testing. The presence of white blood cells and blood in fecal samples occurs in about 70% of patients. Severe cases may require antibiotics such as ciprofloxacin and azithromycin, but these must be carefully prescribed because resistance is increasingly common.