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Image: “All Ready to Go” by Anne Worner. License: CC BY-SA 2.0


Diarrhea is defined as a stool frequency of more than 3 stools per day, which have a high water content of over 75% and increased stool weight, about 250 g. Acute diarrhea usually lasts 2–3 days, and the reason is infections or intoxication. Prolonged diarrhea is chronic and can be caused by food intolerance, inflammatory bowel disease or tumors.


Classification according to the emergence of diarrhea

Diarrhea form Pathomechanism Possible Causes
Secretory diarrhea The mucosa of the intestine releases active water or electrolytes from where water follows osmotically. Chronic inflammatory bowel disease, food poisoning, or intake of laxatives
Osmotic diarrhea Unabsorbed, osmotically active molecules, such as food ingredients or medicines pull water into the intestinal lumen. Lactose intolerance, celiac disease, laxatives, or sorbitol
Exudative diarrhea Inflammation of the intestinal mucosa leads to the accumulation of stool with mucus and blood. Chronic inflammatory bowel diseases, or bacterial/parasitic infections
Hypermotile diarrhea Increased intestinal motility leads to a reduced transit time of the stool, such that not enough water can be withdrawn. Irritable bowel syndrome, hyperthyroidism, or diabetic polyneuropathy
Steatorrhea Decrease in the number of enzymes and bile acids leads to insufficient digestion and absorption of fats. Exocrine pancreatic insufficiency, condition after cholecystectomy


Food poisoning as a cause of diarrhea

Food can have a toxic effect on the human body for various reasons. The most common triggers of food poisoning are caused by toxins produced by bacteria, but even heavy metals such as lead or toxic chemicals can be present in the food and lead to poisoning with symptoms such as diarrhea.

Food poisoning with bacterial toxins

soft serve can be the cause of diarhhoea

Image: Soft serve can be the cause of diarrhea

The disease occurs due to the intake of bacterial toxins, the multiplication of bacteria itself is no trigger. In most cases, there is a contamination of food with Staphylococcus aureus. One reason can be a lack of hand hygiene in the preparation of food. The bacteria are indeed killed by cooking, but not the enterotoxins they release. Very rapid onset of symptoms, about 30 minutes to 2 hours after eating, and an equally short duration of diarrhea symptoms are typical. Classically, several people are affected at the same time. Even Bacillus and Clostridium species can form enterotoxins and cause similar symptoms.

Other food poisonings

Other triggers of food intoxication include toxic metals such as arsenic, lead, zinc, and antimony. Even fungal toxins such as muscarinic (fly agaric) and amatoxin (Amanita phalloides) lead to diarrhea, amongst other symptoms. Saxitoxins, which can be accumulated in steamed mussels and oysters, lead to a disease pattern that is called paralytic shellfish poisoning which results in nausea with vomiting and diarrhea with abdominal cramps.

United States:

  • 179 million cases/year
    • 17 million foodborne
    • ~ 2 million hospitalizations
  • ~ 3,000 deaths
    • 83% elderly
  • $6 billion in medical care and lost productivity

United States: Causes by rate/100K people:

  • Salmonella: 13.6
  • Campylobacter: 13
  • Shiga toxin-producing E. coli: 0.04–0.41
  • Vibrio: 0.45
  • Yersinia: 0.29

Foodborne infections

In foodborne infections, pathogenic germs are absorbed by the food, and the microorganisms multiply in the intestine. Even these often produce toxins, which is why there can be no clear separation of the food poisoning here.


Etiology of salmonellosis

Salmonella enteritis is caused by the consumption of contaminated drinking water or infectious food as a result of insufficient hygiene. The pathogen is Salmonella enteritidis, however out of the more than 2,600 known salmonella serotypes, another 30 pathogens are gastroenteritis pathogens. In 2004, a new subspecies called Salmonella choleraesuis was discovered, which is very resistant against antibiotics and more frequently results in the death of patients.

Different animals can be carriers of the Salmonella pathogen, such as poultry, swine, and reptiles; thus many foods such as eggs, meat, milk, and mussels can be contaminated with salmonella. Even in the case of adequate hygiene by the slaughter staff, who are the chronic carriers of Salmonella, S. enteritidis can be transferred to the meat. In countries with inadequate treatment of water, the feces of infected animals can contaminate the drinking water and thus serve as a source of infection.

Symptoms of S. enteritis

In most cases, infection occurs in the warm season, especially among children and elderly people. It is a matter of invasive gastroenteritis. Typical symptoms of S. enteritis are vomiting and diarrhea after an incubation period of a few hours up to 7 days. Patients also develop spasmodic abdominal pain. The duration of the disease is generally only for a few days.

Diagnosis of salmonellosis

Salmonella species growing on XLD agar

Image: Salmonella species growing on XLD agar. By Nathan Reading, License: CC BY 2.0

The stool and vomit are used for investigation purposes. Onoz- and xylose lysine desoxycholate (XLD) agar in the culture serve as differentiation media. The classification in subtypes is based on the O-antigens and is useful for epidemiological investigations.

Note: The MUCAP test is a quick test for the diagnosis of salmonellosis. Salmonella has a C8-esterase. A substrate is contained in the MUCAP reagent, which is cleaved by the C8-esterase and thus releases a fluorescent dye.

Salmonellosis is notifiable under the Infection Protection Act.

Treatment and prophylaxis of salmonellosis

There should be no antibiotic treatment since this leads to an extension of bacterial elimination. In only about 5% of the patients, systemic infection with fever and massive fluid loss develop, such that hospitalization becomes necessary. Ciprofloxacin and ampicillin are suitable treatments for children.

A small percentage of the patients do not eliminate the Salmonella, such that they are asymptomatic chronic carriers for a long time and receive a prohibition of employment on activities involving food handling.

The prophylactic measures include cooking of poultry, meat, and eggs, as well as the strict separation of cutlery and cutting boards which are used before and after cooking, to avoid cross-contamination.

Typhoid fever

Etiology of typhoid

Salmonella typhi usually spreads by unsanitary conditions during the preparation of food and beverages. Thus, it leads to infections among Europeans, especially during long-distance travel to Africa, Southeast Asia, and Latin America.

Disease pattern of the typhoid fever

The course of the disease can be divided into 3 stages. The incubation period varies, with 10 days being average.

  1. Stadium incrementi during the 1st week after infection: It results in unspecific general symptoms like a headache, fatigue, constipation, and a staircase-shaped increase in fever.
  2. Stadium fastigii in the 2nd–3rd week of infection:
    roseola on a chest of a man with typhus

    Image: Roseola on the chest of a man with typhus. By CDC/Armed Forces Institute of Pathology, Charles N. Farmer, License: Public domain

    After approx. 8 days, a very high fever (up to 41°C) is reached, which continues to persist. Relative bradycardia, leukopenia, and splenomegaly are added to this. A reddish, spotty rash, the so-called roseola, with prominence on the upper body and abdomen is typical, so are disturbances of consciousness, which give the disease its name. One can often notice the typhoid tongue, which is characterized by a white-gray coating in the middle, with reddish tongue tip and edges.

    perforations of the ileum

    Image: Perforation of the ileum with typhoid lesions. By Openi, License: CC BY 2.0

    By destroying the Peyer’s patches of the small intestine, it leads to pea soup diarrhea from the 14th disease day onwards. Other possible symptoms include meningitis, osteomyelitis, and bowel perforation.

  3. Stadium decrementi with stepwise decreasing fever.
Note: In the case of typhoid fever, there are many typical symptoms. These include infectious atypical bradycardia and leukopenia, roseola, typhoid tongue, and pea soup diarrhea.

Diagnosis of typhoid fever

The detection of Salmonella infection is dependent on the week of the disease. One week after infection, the detection in blood cultures can be carried out; an antibody screening of blood serum is possible in the 2nd week. From the 3rd week on, a culture from stool samples can succeed.

Also, the typical leukopenia is found in the blood, often along with a lack of eosinophilic granulocytes.

Treatment of typhoid fever

The antibiotic treatment is carried out with ciprofloxacin or ceftriaxone of the 3rd generation such as cephalosporins.

As is the case of salmonellosis, some of the affected remain chronic carriers for up to 1 year, especially if they have not received antibiotics. Salmonella survives in the gall bladder and the bile ducts, favored by gallstones.

Prophylaxis of the typhoid disease

Particularly in tropical destinations, hygiene is the best protection against infection. Thus, the consumption of insufficiently cooked foods and tap water should be avoided. Also, the vaccination can be done with a dead or non-pathogenic live vaccine, whereby adequate protection is achieved in only about 60% of the vaccinated people.


Yersiniosis is an infectious disease caused by the bacterium Yersinia enterocolitica or Yersinia pseudotuberculosis. The pathogen is spread worldwide, and animals such as pigs or cattle serve as a reservoir. Therefore, the infection can be carried out through contaminated meat, dairy products, and drinking water.

Note: Yersinia can multiply even in the refrigerator at temperatures of 4–8°C.

Symptoms of yersiniosis

Depending on the age of onset, other symptoms occur after an infection with Yersinia.

  • Yersinia gastroenteritis: Occurs mainly in infants. It results in self-limiting bloody diarrhea with exsiccosis.
  • Pseudoappendicitis

    Image: Abdominal and pelvic enhanced computed tomography (CT) scan revealed mucosal thickness of cecum (circle) and enlarged lesional lymph node (arrows). Left panel indicates transverse imaging and right panel indicates coronal imaging. (Pseudoappendizitis). By Openi, License: CC BY 2.0

    Pseudoappendicitis (lymphadenitis of intestinalis) or Morbus Maßhoff:
    In older children and adolescents, it results in inflammation with concomitant swelling of the mesenteric lymph nodes. Typically results in a lymph node conglomerate around the vermiform appendix, such that at the hospital, the misdiagnosed appendicitis is often detected with fever and abdominal pain and mass around the appendix in the sonography.

  • Enterocolitis: The enterocolitis caused by Yersinia is invasive gastroenteritis. The bacterial cells migrate through the mucosa of the intestine and result in inflammation in the Peyer’s patches. Resulting diarrhea continues for 10–14 days and is accompanied by colicky abdominal pain.

After weeks to months following an enteral infection with Yersinia,  inflammatory late-onset diseases such as reactive arthritis, pyomyositis, and persistent ileitis (pseudo-Crohn) are commonly noted. These late effects are very frequently associated with the HLA type B27.

Diagnostics of the Yersinia infection

The aim should be the direct detection of Yersinia from blood culture, stool or infected lymph nodes. The so-called CIN breeding ground (Cefsulodin Irgasan-Novobiocin Agar) serves as the selective agar on which porthole-shaped red colonies grow after 1–2 days.

A namely obligation to notify the authorities exists during the detection of an acute infection with Yersinia.

Treatment of yersiniosis

Usually, only symptomatic treatment for rehydration takes place. Severe gastroenteritis and systemic infections are treated with a combination of ciprofloxacin and ceftriaxone.

Note: Y. enterocolitica forms β-lactamases, such that (amino-) penicillins are not effective.


Shigellosis, or bacterial dysentery, is fecal-oral transmitted dysentery, which mainly affects the colon.

Etiology of the bacterial dysentery

Several Shigella species come into question as pathogens. They are divided into groups from A to D.

Group Species Distribution Symptoms
A S. dysenteriae Tropics Serious disease patterns by the formation of endo- and exotoxin with lethality of 60%
B S. flexneri Worldwide Mild progressive form, since no exotoxin is observed
C S. boydii Middle East, North Africa Mild course
D S. sonnei Central Europe Summer diarrhea in children, no exotoxin, approximately 80% of the shigellosis cases

The only reservoir for pathogens is the human body, such that the fecal-oral transmission occurs via contaminated food and drinking water.

Symptoms of the Shigella dysentery

Diarrhea occurs after an incubation period of 2–10 days. In the mild progressive form this is referred to as white dysentery and in severe, bloody progressive form as red dysentery. Characteristically, the diarrhea is accompanied by abdominal pain and tenesmus with defecation. Even loss of appetite, fever, and consequences of electrolyte loss are common. Gastrointestinal bleeding and intestinal perforation may occur as complications.

Diagnostics of the shigellosis

At the beginning of the disease, one histologically observes catarrhal dysentery, an inflamed, swollen intestinal mucosa. In severe cases, the image changes into pseudomembranous-necrotizing dysentery. The histological image then resembles a chronic inflammatory bowel disease.

The diagnosis is made based on clinical symptoms and a rectum smear since the Shingella dies in the stool sample after a short time.

Treatment of the Shigella dysentery

The treatment should be symptomatic, which means balancing the water and electrolyte losses. Also, a calculated antibiotic treatment can be started with a quinolone. Many Shigella are however affected by an R-plasmid resistant to numerous antibiotics, such that a change of antibiotic treatment after an antibiogram is meaningful.

Treatment of choice: ciprofloxacin or azithromycin.

Note: Motility inhibiting antidiarrheals such as loperamide should be taken only for a short period in most bacterial diarrheal diseases, as although they help against diarrhea, they also prolong the excretion of pathogens.

Infection with Escherichia coli

E. coli

Image: E.coli on endo-Agar. By Lenka M, License: CC BY-SA 1.0

The most well-known bacterium in the world is responsible for about 160 million diarrheal diseases and 1 million cases of death yearly.

Infections with enteropathogenic E. coli

Enteropathogenic E.coli strains, short EPEC, are a common diarrheal pathogen in infants and young children in developing countries. Through the EPEC adhesion factor EAF, the bacteria bind to the epithelial cells of the small intestine and inject toxins in the enterocytes using a type 3 secretion system.

Infections with enterotoxigenic E. coli

The transmission of EPEC occurs in tropical countries through contaminated food and drinking water. For the attachment to the mucosa of the intestine, these strains have specific fimbriae called colonization factors. The pathogenic effect is caused by 1 of the cholera toxins similar to the heat-labile enterotoxin and 2 heat-stable (up to 100°C) toxins. Guanylate cyclase is stimulated through the toxins, among other things, whereby the sodium absorption is inhibited, and more water is extracted from the intestine. It often results in massive watery diarrheas, which are self-limiting in the form of traveler’s diarrhea. In children, it can lead to life-threatening courses through dehydration.

Infections with enteroinvasive E. coli

The infection with EIEC resembles a Shigella infection. The bacteria penetrate the epithelial cells of the colon and lead to a granulocytic inflammation with the discharge of blood and mucus. Even EIEC strains have toxins, which additionally lead to water and electrolyte loss.

Treatment of choice for E. coli (non-Shiga toxin-producing) infections: ciprofloxacin, or trimethoprim/sulfamethoxazole, or azithromycin.

Infections with enterohemorrhagic E. coli

Enterohemorrhagic E. coli, the so-called EHEC, are Shiga toxin-producing E. coli with additional pathogenicity. Even 10—100 bacteria are enough for food poisoning with EHEC. The infection occurs mainly via milk and raw meat, but can also occur during close contact from person to person.

The Vera toxin present in the EHEC bacteria is phage-encoded and like the Shiga toxin is neurotoxic and necrotic. Also, EHEC has a plasmid-encoded hemolysin that triggers the hemorrhagic-uremic syndrome, short HUS. The hemolytic-uremic syndrome, which is also called the Gasser syndrome, is microangiopathic hemolytic anemia with thrombocytopenia and acute renal failure caused by bacterial toxins. If only 2 of these symptoms are present, 1 speaks of incomplete enteropathic HUS. With diarrhea, it is about the typical HUS, which is common in children. The atypical HUS without diarrhea occurs more commonly in adults.

The detection of EHEC is achieved through the polymerase chain reaction (PCR) assay. The treatment should be symptomatic with electrolytes and infusions and plasmapheresis. Loperamide and antibiotics are contraindicated as they do not act against the toxins and there are indications that HUS symptoms occur more frequently among antibiosis. Since 2009, there has been a monoclonal antibody called eculizumab, which inhibits the complement system and reduces the mortality with atypical HUS.

The suspicion or evidence of an EHEC infection is notifiable under the law if a HUS is present, 2 or more people are sick, or the sick person works in the food industry. The suspicion, the illness, and death by a bacterial HUS are also notifiable under the law.

Infections with enteroaggregative E. coli

The attachment to the intestinal epithelium by fimbriae results in diarrhea of secretory type through enterotoxins. Increased mucus production is typical, which delays the elimination of the pathogen, such that the disease can drag on for weeks. In the case of immunosuppressed patients, such as human immunodeficiency virus (HIV) patients, EAEC is the most frequent cause of bacterial enteritis.

Note: EPEC- Pediatrics, ETEC- Tropics, EIEC- like Shigellosis, EHEC-HUS, EAEC-AIDS.



Image: Botulism. By Herbert L. Fred, MD and Hendrik A. van Dijk, License: CC BY 2.0

Clostridium botulinum is the producer of the most potent toxin in the world. Under anaerobic conditions, such as in animal carcasses or insufficiently heated canned food, this bacterium can multiply and produce botulinum toxin. Infants can become infected even by eating contaminated honey, as their intestinal flora has not yet fully developed.

After the intake of poison, there is an inhibition of acetylcholine secretion at the neuromuscular junction. First, the eye muscles are paralyzed; then other facial and pharyngeal muscles. Even vomiting and diarrhea are typical before death due to suffocation or cardiac arrest. The treatment is done with an antiserum, which reduces mortality from about 90% to 10%.

Clostridium difficile infections

C. difficile is an obligate anaerobic spore-former with ubiquitous occurrence. Approx. 80% of infants and < 5% of adults are infected. The infection usually occurs nosocomially (48 hours after hospital admission until 4 weeks after dismissal), through the fecal-oral route. The diarrhea is highly contagious, even indirectly via surfaces.

Risk factors for C. difficile infection:

  • Previous antibiotic therapy (in particular, clindamycin, ampicillin, and cephalosporins)
  • Hospitalization
  • Old age
  • Therapy with proton pump inhibitor (PPI) and/or non-steroidal anti-inflammatory drugs (NSAIDs)
  • Underlying gastrointestinal (GI) disease
  • Immunosuppression

Clinical symptoms are watery, greenish diarrhea with a foul odor, lower abdominal pain, fever, leukocytosis, and hypoalbuminemia.

For the disease definition, 1 or more of the following points must hold:

  • Diarrhea/toxic megacolon with detection of C. difficile enterotoxin A and/or cytotoxin B or cultural evidence of toxin-producing C. difficile in the stool
  • Pseudomembranous colitis in the endoscopy

    Pseudomembranous colitis

    Image: Pseudomembranous Colitis. By Bijhenry, License: CC BY-SA 3.0

  • Histopathologic evidence of a C. difficile infection (CDI) through endoscopy, colectomy or autopsy

The toxin proof is the gold standard for the diagnosis, but it is seldom applied. As a routine, enzyme immunoassay (EIA) is mostly used.

Note: A fast sample transport is essential, as the toxin decomposes within 2 hours at room temperature!

The treatment of C. difficile-associated enterocolitis consists of the completion of the previous antibiotic therapy (if acceptable from a clinical perspective) and an additional antibiotic therapy in case of persistent/severe symptoms, old/critically ill patients or if the current antibiotic therapy needs to be continued. Suitable for this, to avoid the selection of vancomycin-resistant enterococci, are metronidazole in uncomplicated courses and vancomycin in severe courses, during pregnancy or in children below 10 years. The surgical treatment can be necessary for intestinal perforation or toxic megacolon.

In the case of VA (ventilator-associated) CDI, the prophylaxis of an infected patient should be strictly observed with isolation in single rooms for up to 48 hours after cessation of symptoms.

In severe cases, the local health authorities must be notified (e.g. intensive care unit (ICU) requiring/surgery requiring a course, recurrent infection, death from CDI < 30 days after diagnosis).


Vibrio cholerae

Image: Vibrio cholera electron microscopy. By Openi, License: CC BY 2.0

Cholera, or bile diarrhea and vomiting, is caused due to an infection with Vibrio cholerae. The transmission usually occurs through contaminated water in poorer countries without adequate supplies of clean drinking water. Approx. 85% of the infections proceed inapparently; the other 15% are associated with typical symptoms.

rice water stool

Image: Rice-water stool. By F1jmm, License: CC BY-SA 3.0

After an incubation period of 2–3 days, it results in diarrhea and vomiting, whereby the diarrhea is interspersed with flakes of mucus and is therefore called rice-water stool. Due to massive exsiccosis, it then results in subnormal temperature and a typical facial expression with a pointed nose, sunken cheeks, and standing skin folds.


Image: Cholera. By CDC, License: Public domain

This is subsequently followed by general body reactions such as dizziness and coma. The diagnosis can be done quickly through microscopy and stool culture. The definitive diagnosis is done with the help of antiserum. For rehydration, the World Health Organization (WHO)-oral solution consisting of glucose, sodium chloride, sodium citrate, and potassium chloride is recommended. Also, there are several oral cholera vaccines, which are administered in different endemic areas.


Giardia intestinalis

Image: Giardia intestinalis. By CDC/Janice Haney Carr, License: Public domain

Lambliasis or giardiasis is an infection of the intestinal tract caused by the protozoan Giardia intestinalis. Typical symptoms of the lamblia dysentery are diarrhea, flatulence, and malnutrition in case of prolonged illness. The detection of trophozoites or cysts is done using microscopy of stool or from the biopsy of the intestinal tract. Even an antigen detection using ELISA or PCR is possible. It is presumed that a resolved infection can cause lactose intolerance or other food intolerances with persistent GI complaints.

Treatment of choice: metronidazole.

The infection with Giardia is notifiable under the law.

Life cycle of the parasite Giardia lamblia.

Image: The Life cycle of the parasite Giardia lamblia. By LadyofHats, License: Public domain

Amoebic dysentery

Histopathologic image of amoebic dysetery found in endoscopic colonic biopsy

Image: Histological recording of an amoeba infection in the intestinal tissue. By KGH, License: CC BY-SA 3.0

Entamoeba histolytica passes as a cyst in the small intestine and as a 4-core stage thereafter in the colon. There, the amoeba further lives in the form of trophozoites. They form cysts, which are excreted in the stool (up to 50 million per day!). The minuta-form of the E. histolytica causes self-limited diarrhea. The magna-form, on the other hand, penetrates the colonic mucosa and passes from there into the bloodstream. It, then, settles in the form of abscesses in all sorts of organs, including the intestines. Amoebic dysentery, therefore, results in raspberry jelly-like diarrhea with abdominal pain and exsiccosis. Even peritonitis and abscess rupture in the liver is common.

Treatment of choice: metronidazole plus paromomycin.

Note: Often the disease doesn’t break out until many years after the infection.

Important Clues to the Differential Diagnosis of Diarrhea

The clinical presentation of a patient with a foodborne illness can vary, however, some important clues in the clinical history can make the treating doctor suspect an infectious etiology behind the patient’s diarrhea. They are summarized in the following points:

  • Acute abdominal pain that is associated with fever and vomiting is often an indicator of an infectious etiology of diarrhea.
  • A recent change in diet, the ingestion of new foods, or eating undercooked foods are important clues for foodborne illness.
  • Patients with a long duration of symptoms are more likely to be dehydrated. Moreover, chronic diarrhea is unlikely to be infectious in etiology.
  • A history of working in a child-care facility puts the individual at an increased risk of viral diarrhea.
  • History of recent hospitalization in a patient who is presenting with diarrhea raises the suspicion of C. difficile infection.
  • Patients with immunosuppression due to disease or medication who present with diarrhea are more likely to have an atypical infectious cause.
  • History of recent antibiotic use raises the suspicion of C. difficile infection.
  • Travel history puts the individual at an increased risk of acquiring traveling diarrhea, which is infectious in etiology.

Key Recommendations for the Management of Foodborne Illness per the American Family Physician Guidelines

The American Family Physician guidelines that were formulated in 2015 about the management of foodborne illness can be summarized in 4 main points:

  • Stool cultures are the diagnostic standard for bacterial foodborne illness. They must be performed in any patient suspected to have a bacterial etiology behind their diarrhea. They are positive in up to 40% of the cases.
  • A single dose of ondansetron is recommended in children with significant gastroenteritis-related vomiting.
  • Patients with a foodborne illness who have diarrhea that is associated with fever and signs of invasive disease such as leukocytosis should receive empiric antibiotic therapy if their symptoms persist for more than 1 week or if hospitalization is required.
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