Bacterial Gastroenteritis 

Updated: Jul 17, 2018
Author: Jennifer Lynn Bonheur, MD; Chief Editor: BS Anand, MD 

Overview

Practice Essentials

Bacterial gastroenteritis has many causes, can range from mild to severe, and typically manifests with symptoms of vomiting, diarrhea, and abdominal discomfort. It is usually self-limited, but improper management of an acute infection can lead to a protracted course.

Signs and symptoms

An index of suspicion can be generated for a specific set of potential causative pathogens by considering the following stool characteristics:

  • Appearance

  • Volume

  • Frequency

  • Presence or absence of blood

  • pH

  • Presence or absence of reducing substances

  • White blood cell (WBC) count

  • Serum WBC count

Diarrhea is defined as daily stools with a mass greater than 15 g/kg for children younger than 2 years and greater than 200 g for children 2 years or older. Adult stool patterns vary from 1 stool every 3 days to 3 stools per day; therefore, consider individual stool patterns.

Systemic features that can guide empiric therapy and help narrow the differential diagnosis of the causative organism include the following:

  • Onset and duration of symptoms

  • Presence or absence of vomiting

  • Presence or absence of fever

  • Presence or absence of abdominal pain

Specific bacterial pathogens may be associated with the following:

  • Ingestion of particular foods

  • Exposure to water

  • Exposure to animals

  • Travel to particular countries

  • Preexisting conditions

Physical findings may include the following:

  • Dehydration (primary cause of morbidity and mortality)

  • Malnutrition (typically a sign of a chronic process)

  • Abdominal pain

  • Borborygmi

  • Perianal erythema

See Clinical Presentation for more details.

Diagnosis

Diagnostic approaches may include the following assessments:

  • Stool pH

  • Presence of reducing substances in stool

  • Fecal leukocytes

  • Antilisteriolysin O (ALLO)

  • Identification of pseudomembranes in the colon by direct visualization (diagnostic for C difficile)

  • Stool culture

A high index of suspicion is needed to choose the appropriate culture medium. Media used to isolate bacteria responsible for gastroenteritis include the following:

  • Blood agar: All aerobic bacteria and yeast; detects cytochrome oxidase production

  • MacConkey EMB agar: Inhibits gram-positive organisms; permits lactose fermentation

  • XLD agar and HE agar: Inhibit gram-positive organisms and nonpathogenic gram-negative bacilli; permit lactose fermentation and H2S production

  • Skirrow agar: Selective for Campylobacter species

  • SM agar: Selective for enterohemorrhagic E coli

  • CIN agar: Selective for Yersinia enterocolitica

  • Thiosulfate-citrate-bile-sucrose (TCBS) agar: Selective for Vibrio species

  • CCFE agar: Selective for C difficile

See Workup for more detail.

Management

Because most infectious diarrheas are self-limited, medical care is primarily supportive and may include the following:

  • Oral rehydration: Live Lactobacillus GG and heat-killed Lactobacillus LB reduce the duration of diarrhea in children when added to oral rehydration solution[1, 2]

  • When oral rehydration is unsuccessful, intravenous (IV) rehydration should be provided

  • Close monitoring for secondary complications

  • For some bacterial gastroenteritis infections, antimicrobial therapy is required

  • For refractory cases of Cryptosporidium infection, antimotility agents are useful

Standard antimicrobial therapies for bacterial gastroenteritis include the following:

  • Aeromonas species: Cefixime and most third- and fourth-generation cephalosporins

  • Bacillus species: None necessary for self-limited gastroenteritis; vancomycin and clindamycin for severe disease

  • Campylobacter species: Erythromycin; therapy started more than 4 days after onset of symptoms appears to produce no clinical benefit

  • C difficile: Discontinuance of the potential causative antibiotics; if this is impossible or ineffective, oral metronidazole or (in seriously ill patients who do not respond to metronidazole) vancomycin

  • Clostridium perfringens: None

  • Listeria species: None necessary unless invasive disease occurs; ampicillin and trimethoprim-sulfamethoxazole (TMP-SMX) for invasive disease

  • Plesiomonas species: TMP-SMX or any cephalosporin

  • Vibrio cholerae: Tetracycline; in resistant cases, TMP-SMX, erythromycin, doxycycline, chloramphenicol, or furazolidone

  • Yersinia species: TMP-SMX, fluoroquinolones, or aminoglycosides; reserved for complicated cases

  • E coli: TMP-SMX if diarrhea is moderate or severe; for systemic complications, a parenteral second-generation or third-generation cephalosporin

  • Salmonella species: None necessary for nontyphoid, uncomplicated diarrhea but may be considered for infants younger than 3 months and for high-risk patients (eg, those who are immunocompromised or have sickle cell disease); for drug-sensitive strains, ampicillin or, alternatively, TMP-SMX, fluoroquinolones, or third-generation cephalosporins

  • Shigella species: None necessary for most mild infections; for moderate-to-severe cases, ampicillin for drug-sensitive strains and TMP-SMX for ampicillin-resistant strains or in cases of penicillin allergy; fluoroquinolones may be considered in patients with highly resistant organisms

Dietary measures include the following:

  • Begin with the BRAT diet (ie, bananas, rice, applesauce, toast)

  • Introduce lean meats and clear fluids as soon as possible[3]

  • When giving lactose-containing dairy products, be alert for signs of malabsorption

  • For infants, continue breastfeeding throughout the illness

See Treatment and Medication for more detail.

Background

Bacterial gastroenteritis is a very common disorder. It has many causes, can range from mild to severe, and usually manifests with symptoms of vomiting, diarrhea, and abdominal discomfort. Other causes of some of these symptoms include viral infections, improper diet, malabsorption syndromes, various enteropathies, and inflammatory bowel disease. (See Etiology,Presentation, Workup, and Treatment.)

Bacterial gastroenteritis is usually self-limited, but improper management of an acute infection can lead to a protracted course. By far, the most common complication is dehydration. (See Prognosis and Presentation.)[4, 5, 6, 7]

Etiology

Salmonella, Shigella, and Campylobacter species are the top three leading causes of bacterial diarrhea worldwide, followed closely by Aeromonas species.

Aeromonas and Shigella infection have a higher incidence in summer and fall, and Campylobacter infection usually occurs in summer months. Yersinia infection occurs most frequently in winter months and in colder climates.

Bacteria employ several mechanisms to invoke a pathologic response. Invasive bacteria cause mucosal ulceration and abscess formation with a subsequent inflammatory cascade. Bacterial toxins control enteral and extraenteral cellular processes. For example, the heat-labile and heat-stable enterotoxins of Escherichia coli activate enteral adenylate cyclase and guanylate cyclase signaling systems.

Verotoxin, which enterohemorrhagic E coli and Shigella species produce, causes systemic disorders such as seizures and hemolytic-uremic syndrome (HUS). Other noninvasive bacteria adhere to the gut wall, causing inflammation.

Organisms such as E coli and Clostridium species are normal enteric flora, pathogenic strains of which can cause gastroenteritis.

Vibrio parahaemolyticus, a seafood-transmitted bacterium, appears to be an emerging foodborne pathogen in North America, with over 45,000 cases every year in the United States alone.[8]  The rise in incidence may be attributed in part to the climate change effects on the quantity and distribution of this pathogen. A new lineage of V parahaemolyticus has been identified (sequence type 631) that may rapidly become the predominant type endemic to the Atlantic coast of North America.[8]

Risk factors

Studies have suggested that the use of acid-suppressing medications (proton pump inhibitors [PPIs], although not H2 receptor antagonists [H2RAs]) may increase the risk of developing gastroenteritis by reducing the acidic environment that serves as an initial defense mechanism against gastrointestinal infections. This effect has also been noted to be dose dependent (ie, an increased dose of PPI therapy is associated with an increased risk of infection). PPI use has also been associated with a higher risk of gastroenteritis hospitalization.[49]

PPI therapy has also been suggested to be an independent risk factor for the development and recurrence of C difficilecolitis[9]  as well as increases the risk Campylobacter gastroenteritis.[10]

Epidemiology

Occurrence in the United States

Bacterial gastroenteritis is a very common problem in primary care and emergency department settings, especially in children younger than 5 years.[6, 7] Diarrhea accounts for as many as 5% of pediatric office visits and 10% of hospitalizations in this age group.

Very often, gastroenteritis is underreported in the adult population. Each year, gastroenteritis in adults accounts for 8 million doctor visits and 250,000 hospitalizations. Episodes of gastroenteritis do not occur at random but usually take place in outbreaks. Traveler's diarrhea affects 20-50% of people traveling from industrialized to developing countries.[7, 11, 12]

From 2000 to 2009, the number of hospitalized patients with any Clostridium difficile infection (CDI) discharge diagnoses more than doubled, from approximately 139,000 to 336,600, and the number with a primary CDI diagnosis more than tripled, from 33,000 to 111,000.[13]

Among CDIs identified in the Center for Disease Control and Prevention’s (CDC’s) Emerging Infections Program data in 2010, 94% were associated with receiving health care; of these, 75% had onset among persons not currently hospitalized, including recently discharged patients, outpatients, and nursing home residents.[13]

International occurrence

Worldwide, millions of children and adults are affected by diarrhea each year. In developing countries, where sanitation is suboptimal, epidemics of bacterial gastroenteritis can develop and cause significant mortality.[5, 7, 11, 12, 14]

In a retrospective Australian study (2001-2013), investigators analyzing bacterial toxin-mediated foodborne outbreaks found that Clostridium perfringens was the most common cause (76%), and that the most common settings were commercial preparation food services (48%) and elderly care facilities (39%).[15] The main contributing factor across all outbreaks was inadequate temperature control of the food.

Race-, sex-, and age-related demographics

Most infectious diarrheas do not affect one sex more than the other.[39]  Aeromonas species are a significant cause of bacterial gastroenteritis in young children. Very young children are particularly susceptible to secondary dehydration and malabsorption. Yersinia species infect children younger than 1 year almost exclusively, though it has been reported that the preparation and ingestion of chitterlings (the small intestine of pigs) may pose an increased risk of infection with Yersinia enterocolitica serotype O:3.[16, 17]

Prognosis

With proper management, the prognosis for bacterial gastroenteritis is very good, especially in industrialized countries. Mortality predominantly is due to dehydration and secondary malnutrition from a protracted course. Treat severe dehydration with parenteral fluids.

Once malnutrition from secondary malabsorption begins, prognosis becomes grim unless the patient is hospitalized and supplemental parenteral nutrition is started. Neonates and young infants are at particular risk for dehydration, malnutrition, and malabsorption syndromes.

Even though the mortality rate from bacterial gastroenteritis is low in industrialized countries, people can, and do, die from complications. Prognosis in countries without modern medical care or for patients with serious preexisting medical conditions is more guarded.

Morbidity and mortality

Diarrhea and vomiting are so commonplace that nonphysicians usually underappreciate the potential mortality and morbidity of bacterial gastroenteritis. In the United States each year, several hundred people die from complications of bacterial gastroenteritis; the majority are elderly persons.

The CDC reported that enteritis deaths more than doubled in the United States between 1999 and 2007, from about 7,000 to 17,000. Adults older than 65 years accounted for 83% of deaths. C difficile was the most common bacterial infectious cause of gastroenteritis-associated deaths, being tied to 14,500 of them (up from 2700 in 1999).[18]

Gastroenteritis-causing pathogens are the second leading cause of morbidity and mortality worldwide. Many developing countries do not have the resources to properly treat diarrhea and vomiting associated with bacterial gastroenteritis, leading to a disproportionately high mortality rate.

Complications

Common complications that can occur with various organisms in cases of bacterial gastroenteritis are as follows:

  • Aeromonas caviae - Intussusception, gram-negative sepsis, and hemolytic uremic syndrome (HUS)

  • Bacillus species - Fulminant liver failure (very rare) and rhabdomyolysis (very rare)

  • Campylobacter species - Bacteremia, meningitis, cholecystitis, urinary tract infection, pancreatitis, and Reiter syndrome

  • C difficile - Chronic diarrhea, toxic megacolon, and ileus

  • C perfringens serotype C - Enteritis necroticans

  • Enterohemorrhagic E coli - Hemorrhagic colitis

  • Enterohemorrhagic E coli O157:H7 - HUS

  • Listeria species - Bacteremia and meningitis

  • Plesiomonas species - Septicemia

  • Salmonella species - Enteric fever, bacteremia, meningitis, osteomyelitis, myocarditis, and Reiter syndrome

  • Shigella species - Seizures, HUS, bowel perforation, and Reiter syndrome

  • Vibrio species - Rapid dehydration

  • Yersinia enterocolitica - Appendicitis, bowel perforation, intussusception, peritonitis, toxic megacolon, cholangitis, bacteremia, and Reiter syndrome

Enteric fever

S typhi causes enteric fever. This syndrome has an insidious onset of malaise, fever, abdominal pain, and bradycardia. Diarrhea and rash (rose spots) appear after 1 week of symptoms. Bacteria may have disseminated at that time, and treatment is required to prevent systemic complications such as hepatitis, myocarditis, cholecystitis, and gastrointestinal bleeding.

HUS

Damage to the vascular endothelial cells by verotoxin causes HUS. Thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure are characteristic of HUS. Symptoms usually develop 1 week after the onset of diarrhea, when organisms may be absent.

Reiter syndrome

Reiter syndrome can complicate acute infections. Arthritis, urethritis, conjunctivitis, and mucocutaneous lesions are characteristic. Affected individuals usually do not demonstrate all the features.

Dehydration

Dehydration is the most common complication from gastroenteritis in the United States. Continuing fluid losses without compensatory intake can result in severe dehydration. Hyponatremic seizures can be avoided by rehydrating with oral rehydration solution instead of free water.

Inflammatory bowel disease

A study suggested that infectious gastroenteritis may play a role in the initiation and/or exacerbation of inflammatory bowel disease.[19] Similarly, irritable bowel syndrome may develop more often following bacterial gastroenteritis. This topic is highly controversial, and no conclusive evidence currently exists to support or refute this hypothesis.

Carrier states

Carrier states are observed after some bacterial gastroenteritis infections. After Salmonella diarrhea, 1-4% of individuals with nontyphoid and enteric fever infections become carriers. The carrier stage for Salmonella species is more likely to develop in females, infants, and individuals with biliary tract disease. Asymptomatic C difficile carriage may be seen in many hospitalized patients receiving antibiotics and in 50% of infants.

Patient Education

Education is most important for the prevention and treatment of bacterial gastroenteritis. Proper oral rehydration therapy helps to prevent dehydration and hastens recovery of the intestinal mucosa.

Diet restrictions that prevent secondary malabsorption are extremely important; relapse typically occurs due to dietary noncompliance.

Emphasize proper hygiene and food preparation practices to caretakers in order to prevent future infections and spread of bacterial gastroenteritis.

For patient education information, see Gastroenteritis (Stomach Flu) and Foreign Travel.

 

Presentation

History

Stool characteristics

Diarrhea is defined as daily stools with a mass greater than 15g/kg for children younger than 2 years and greater than 200 g for children 2 years or older. Adult stool patterns vary from 1 stool every 3 days to 3 stools per day; therefore, consider individual stool patterns.

Consistency, color, volume, and frequency are very important in determining whether the stool source is from the small or large bowel. Table 1, below, outlines these characteristics and demonstrates that an index of suspicion can be generated easily for a specific set of organisms.

Table 1. Stool Characteristics and Sources (Open Table in a new window)

Stool Characteristics

Small Bowel

Large Bowel

Appearance

Watery

Mucus and/or blood

Volume

Large

Small

Frequency

Increased

Increased

Blood

Possibly heme-positive but never gross blood

Possibly grossly bloody

pH

Possibly < 5.5

>5.5

Reducing substances

Possibly positive

Negative

White blood cell (WBC) count

< 5/high-power field (HPF)

Possibly >10/HPF

Serum WBC count

Normal

Possible leukocytosis, bandemia

Organisms

Preformed toxins:

Bacillus species, Staphylococcus aureus

Invasive bacteria:

E coli and Shigella, Salmonella, Campylobacter, Yersinia, Aeromonas, and Plesiomonas species

Toxic bacteria:

E coli, cholera, C perfringens, Vibrio species, Listeria monocytogenes

Toxic bacteria:

C difficile

Other causes:

rotavirus, adenovirus, calicivirus, astrovirus, Norwalk virus, and Giardia and Cryptosporidium species

Other causes:

Entamoeba species

Systemic symptoms

Associated systemic symptoms can guide empiric therapy. Some enteric infections have characteristic systemic symptoms, whereas the associated systemic features of others do not occur reliably. Table 2, below, outlines the frequency of these symptoms with various organisms.

The characteristics of symptom onset and symptom duration can narrow the differential diagnosis of the organism. The onset of symptoms within 6 hours of exposure to the bacterial source indicates a preformed toxin, probably produced by a species of Staphylococcus or Bacillus. Table 2 outlines the incubation periods and duration of common bacteria.

Table 2. Symptoms and Their Characteristics (Open Table in a new window)

Organism

Incubation

Duration

Vomiting

Fever

Abdominal Pain

Aeromonas species

None

0-2 weeks

+/-

+/-

No

Bacillus species

1-16 hours

1-2 days

Yes

No

Yes

Campylobacter species

2-4 days

5-7 days

No

Yes

Yes

C difficile

Variable

Variable

No

Few

Few

C perfringens

0-1

1 day

Mild

No

Yes

Enterohemorrhagic E coli

1-8 days

3-6 days

No

+/-

Yes

Enterotoxigenic E coli

1-3 days

3-5 days

Yes

Low

Yes

Listeria species

20 hours

2 days

Few

Yes

+/-

Plesiomonas species

None

0-2 weeks

+/-

+/-

+/-

Salmonella species

0-3 days

2-7 days

Yes

Yes

Yes

Shigella species

0-2 days

2-7 days

No

High

Yes

S aureus

2-6 hours

1 day

Yes

No

Yes

Vibrio species

0-1 days

5-7 days

Yes

No

Yes

Y enterocolitica

0-6

1-46 days

Yes

Yes

Yes

Food-borne bacteria

Particular foods are associated with certain bacterial infections. Ingestion of raw or contaminated food, particularly raw milk and meat, is a common cause of bacterial gastroenteritis. The following list outlines organisms that cause food poisoning:

  • Dairy - Campylobacter, Salmonella, Listeria, and Staphylococcus species

  • Eggs - Salmonella species

  • Meats - C perfringens and Salmonella, Aeromonas, Campylobacter, and Staphylococcus species

  • Ground beef - Enterohemorrhagic E coli

  • Poultry - Campylobacter species

  • Pork - C perfringens and Y enterocolitica

  • Seafood - Aeromonas, Plesiomonas, Vibrio species, and astrovirus

  • Oysters - Plesiomonas and Vibrio species and calicivirus

  • Vegetables - Aeromonas species and C perfringens

  • Alfalfa sprouts - Enterohemorrhagic E coli and Salmonella species

  • Fried rice - Bacillus species

  • Custards, mayonnaise - Staphylococcus species

A study by Calbo et al reported a foodborne nosocomial outbreak due to extended-spectrum β-lactamase (ESBL)–producing Klebsiella pneumoniae.[20] This may be the first reported hospital outbreak that provides evidence that food can be a transmission vector for ESBL K pneumoniae.

Water-borne bacteria

Water is a major reservoir for many organisms that cause diarrhea. Swimming pools have been associated with outbreaks of Shigella organisms, and Aeromonas species are associated with exposure to the marine environment.

Animal-borne bacteria

Animals can transmit particular bacteria. Exposure to young dogs or cats is associated with Campylobacter transmission. Exposure to turtles is associated with Salmonella transmission.

Travel-associated infections

Travel history is an important and a useful clue in determining bacterial etiology. Enterotoxigenic E coli is the leading cause of traveler's diarrhea. Rotavirus, Shigella, Salmonella, and Campylobacter species are prevalent worldwide and need to be considered, regardless of specific travel history.

The risk of contracting diarrhea while traveling is the highest in Africa. Travel to Portugal, Spain, and Eastern European countries is also associated with a relatively high risk. Organisms associated with travel to particular locations are as follows:

  • Nonspecific - Enterotoxigenic E coli and Aeromonas, Giardia, Plesiomonas, Salmonella, and Shigella species

  • Developing tropics -C perfringens

  • Africa - Entamoeba species and Vibrio cholerae

  • Americas (South and Central) - Entamoeba species and V cholerae

  • Asia - V cholerae

  • Australia, Canada, Europe -Yersinia species

  • India - Entamoeba species and V cholerae

  • Japan, North America (Atlantic coast[8] ) - V parahaemolyticus

  • Mexico - Aeromonas, Entamoeba, Plesiomonas, and Yersinia species

  • New Guinea - Clostridium species

Bacteria associated with preexisting conditions

Preexisting medical conditions can predispose patients to infections with particular organisms. The following list outlines such medical conditions and their associated organisms:

  • C difficile - Hospitalization with antibiotic administration

  • Plesiomonas species - Liver diseases or malignancy

  • Salmonella species - Intestinal dysmotility, malnutrition, achlorhydria, hemolytic anemia (especially sickle cell disease), immunosuppression, and malaria

  • Rotavirus - Hospitalization

  • Giardia species - Agammaglobulinemia, chronic pancreatitis, achlorhydria, and cystic fibrosis

  • Cryptosporidia - Immunocompromise and immunosuppression

Outbreaks

Outbreaks are caused by particular bacteria, including enterohemorrhagic E coli O157:H7, Listeria monocytogenes, C perfringens, and Salmonella species.

Physical Examination

Dehydration is the primary cause of morbidity and mortality in cases of gastroenteritis. Assess every patient for signs, symptoms, and severity of dehydration. Lethargy, depressed consciousness, dry mucous membranes, sunken eyes, poor skin turgor, and delayed capillary refill should raise the suspicion for dehydration.

Malnutrition is typically a sign of a chronic process. Reduced muscle and fat mass is found. This is usually due to the development of secondary carbohydrate intolerance.

Abdominal pain is a common symptom in gastroenteritis. Nonspecific, nonfocal abdominal pain and cramping are common with some organisms. This pain usually does not increase with palpation. Focal abdominal pain worsened by palpation, rebound tenderness, or guarding should alert the clinician to possible complications or to another noninfectious gastrointestinal diagnosis.

Borborygmi, defined as a significant increase in peristaltic activity with small bowel diarrhea, can cause an audible and/or palpable increase in bowel activity.

Perianal erythema results from the passage of many stools causing a constantly wet area. Failure to properly dry the buttocks and perianal area results in erythema and skin breakdown.

 

DDx

Diagnostic Considerations

Conditions to consider in the differential diagnosis of bacterial gastroenteritis include the following:

  • Colovesical fistula

  • Cholera

  • Diverticulitis

  • Food allergies

  • Food poisoning

  • Gardnerella (bacterial vaginosis)

  • Viral gastroenteritis

  • Giardiasis

  • Isosporiasis

  • Lower gastrointestinal bleeding

  • Meckel diverticulum

  • Microsporidiosis

  • Salmonellosis

  • Shigellosis

  • Short-bowel syndrome

  • Ulcerative colitis

Differential Diagnoses

 

Workup

Approach Considerations

A stool pH of 5.5 or below or the presence of reducing substances indicates carbohydrate intolerance. This is usually transient in nature.

Enteroinvasive infections of the large bowel cause leukocytes, predominantly neutrophils, to accumulate in the lumen which are then shed into stool. The absence of fecal leukocytes does not eliminate the possibility of enteroinvasive organisms; however, the presence of fecal leukocytes eliminates consideration of enterotoxigenic E coli, Vibrio species, and viruses. Shigella characteristically causes marked bandemia with variable total white blood cell (WBC) count.

Examine any exudate found in the stool for leukocytes. Such exudates are highly suggestive of inflammatory bowel disease, which could be infectious or of another origin.

Antilisteriolysin O (ALLO) is positive during the convalescent phase of bacterial gastroenteritis and when invasive disease has occurred.

Commercially available multiplex molecular panels may be more sensitive and provide more rapid results (< 3 hours) than stool cultures, which are labor intensive and whose results may take longer than 1 day (66.5 hours).[21, 44]

Procedures

Identification of pseudomembranes in the colon by direct visualization is diagnostic for C difficile; however, the yield may be low.

Bacterial Cultures

Identifying the causative agent underlying the gastroenteritis is important in the management of patients with severe or prolonged diarrhea, symptoms consistent with invasive disease, or a history that may predict a complicated disease course.[22] Moreover, stool culture findings are a means for public health officials to identify and track outbreaks of bacterial gastroenteritis.

Table 3, below, lists common bacteria and the optimal culture media for their growth.

Table 3. Common Bacteria and Optimum Culture Media (Open Table in a new window)

Organism

Detection Method

Microbiologic Characteristics

Aeromonas species

Blood agar

Oxidase-positive, flagellated GNB

Bacillus species

Blood agar

Facultatively aerobic, spore-forming GPR; beta hemolytic; reduces nitrates; ferments carbohydrates

Campylobacter species

Skirrow agar

Rapidly motile, curved GNR; Campylobacter jejuni 90% of infections, Campylobacter coli 5% of infections

C difficile

CCFE agar, EIA for toxin, LA for protein

Anaerobic, spore-forming GPR; toxin-mediated diarrhea; produces pseudomembranous colitis

C perfringens

None available

Anaerobic, spore-forming GPR; toxin-mediated diarrhea

E coli

MacConkey, EMB, or SM agar

Lactose-producing GNR

Listeria species

Blood agar

Flagellated GPB

Plesiomonas species

Blood agar

Oxidase-positive GNR

Salmonella species

Blood, MacConkey, EMB, XLD, or HE agar

Nonlactose, non–H2S-producing GNR

Shigella species

Blood, MacConkey, EMB, XLD, or HE agar

Nonlactose and H2S-producing GNR; verotoxin (neurotoxin)

Staphylococcus species

Blood agar

Heat-stable, preformed toxin-mediated GPC

Vibrio species

Blood or TCBS agar

Oxidase-positive, motile, curved GNB

Y enterocolitica

CIN agar

Nonlactose-producing, oval GNR

CCFE = cycloserine-cefoxitin-fructose-egg; CIN = cefsulodin-irgasan-novobiocin; EIA= enzyme immunoassay; EMB = e-methylene blue; GNB = gram-negative bacillus; GNR = gram-negative rod; GPB = gram-positive bacillus; GPC = gram-positive cocci; GPR = gram-positive rod; H2S = hydrogen sulfide; HE = Hektoen enteric; LA = latex agglutination; SM = Sorbitol-MacConkey; TCBS = thiosulfate-citrate-bile-sucrose; XLD = xylose-lysine-deoxycholate.

The following is a list of the different culture media used to isolate bacteria. A high index of suspicion is needed to choose the appropriate medium.

  • Blood agar - All aerobic bacteria and yeast; detects cytochrome oxidase production

  • MacConkey EMB agar - Inhibits gram-positive organisms; permits lactose fermentation

  • XLD agar and HE agar - Inhibit gram-positive organisms and nonpathogenic gram-negative bacilli; permit lactose fermentation and H2S production

  • Skirrow agar - Selective for Campylobacter species

  • SM agar - Selective for enterohemorrhagic E coli

  • CIN agar - Selective for Y enterocolitica

  • Thiosulfate-citrate-bile-sucrose agar - Selective for Vibrio species

  • CCFE agar - Selective for C difficile

Stool cultures are useful when positive, but the yield is usually low. Refrigerate stool that is not cultured at 4°C within 2 hours of collection, or place it in a transport medium. Always culture stool for Campylobacter, Salmonella, and Shigella species, especially if stool leukocytes or gross blood is found in the stool.

Serotype Salmonella for S typhimurium DT104, particularly if the gastroenteritis is associated with raw milk or cheese ingestion. S typhimurium DT104 is a multidrug-resistant organism, and antibiotic sensitivities are crucial to guide therapy.[23, 24]  

Preformed toxin from Bacillus or Staphylococcus species may cause rapid-onset gastroenteritis. In such cases, the bacteria may not exist in the gastrointestinal tract; therefore, culture the food ingested by the person.

Bloody diarrhea with a history of ground beef ingestion should raise the suspicion for enterohemorrhagic E coli. If E coli is found in the stool, type it to determine if it is O157:H7. Report cases of E coli O157:E7 gastroenteritis (and other infectious problems) to the state health department. Shiga toxin-producing Escherichia coli (STEC) O103:H2 has also been detected in raw cow milk and dairy farm cattle.[43]

History of raw seafood ingestion or foreign travel should prompt additional screening for Vibrio and Plesiomonas species.

 

Treatment

Approach Considerations

Because most infectious diarrhea is self-limited, medical care is primarily supportive in nature. Oral rehydration therapy is the cornerstone of diarrhea treatment, especially for small bowel infections that produce a large volume of watery stool output. Studies confirm that early refeeding hastens recovery. Many commercial oral rehydration formulas are available and have been designed to promote optimal absorption of nutrients.

Young infants and neonates are at a high risk for secondary complications and require close monitoring, as do older individuals.

Consider intravenous rehydration when oral rehydration is unsuccessful. Particular attention must be paid to repletion of potassium as needed.

Administer maintenance fluids plus replacement of losses to ill children. Administer small amounts of fluid at frequent intervals in order to minimize discomfort and vomiting. A 5 or 10cc syringe without a needle is a very useful tool. The syringe can be used to place small amounts of fluid in the mouth quickly. Once the patient becomes better hydrated, cooperation improves enough for the patient to take small sips from a cup. This method is time intensive and requires dedication. Encouragement from the physician is necessary to promote compliance.

Live Lactobacillus GG and heat-killed Lactobacillus LB reduce the duration of diarrhea in children when they are added to oral rehydration solution.[1, 2]  A systematic review and meta-analysis of 31 randomized-controlled trials comprising 8672 children and adults suggests with moderate certainty that probiotics are effective for preventing C difficile-associated diarrhea and that short-term use of probiotics in conjunction with antibiotics appears to be safe in those who are immunocompetent and those who aren't severely debilitated.[45] Adverse effects appeared in 32 trials assessed, but they were more common in the control groups.

Antimicrobial therapy is indicated for some bacterial gastroenteritis infections. However, many conditions are self-limited and do not require therapy.

Antimotility agents are not indicated routinely for infectious diarrhea (except for refractory cases of Cryptosporidium infection).

Inpatient care

Admit neonates or young infants with moderate dehydration, suspected infection with enterohemorrhagic E coli, or bloody diarrhea.

Oral rehydration in cases of gastroenteritis is a time-consuming task that requires vigilance. Evaluate the caretaker of a child who requires oral rehydration for compliance. Consider admission if any doubt exists regarding potential compliance.

Older patients, often with other illnesses, require careful observation and consideration for admission.

Consultations

Certain organisms cause abdominal pain and bloody stools. Symptoms resembling appendicitis, hemorrhagic colitis, intussusception, or toxic megacolon may be observed. In such cases, obtain a consultation with a surgeon.

Consider consultation with an infectious disease specialist, especially for any patient who is immunocompromised due to human immunodeficiency virus (HIV) infection, chemotherapy, or immunosuppressive drugs, because atypical organisms are more likely and complications can be more serious and can fulminate.

Diet

Although some claim that changes in dietary regimen are not necessary, improper diet can result in prolonged recovery or development of carbohydrate malabsorption, especially if the acute episode is overshadowed by an undiagnosed chronic bacterial or malabsorption syndrome.

Thus, a prolonged course of diarrhea should prompt investigation of complicating factors. Results from tests such as stool acidity and reducing substances can indicate carbohydrate malabsorption. Failure to recognize this complication can result in significant rapid weight loss with wasting of fat and muscle mass.

Dietary considerations

The BRAT diet (ie, bananas, rice, applesauce, toast) has been recommended for years in cases of gastroenteritis. This diet is adequate during early convalescence, but, as the patient tolerates solid food, advance the diet to provide adequate protein and caloric intake.[3, 25, 26]

Introduce lean meats and clear fluids as soon as possible.[3] Dairy products are said to be better absorbed when given with proteins or complex carbohydrates.

When feeding lactose-containing dairy products, carefully monitor the patient for signs of malabsorption.

Breast milk contains many substances that promote bowel growth and antagonize bacteria; thus, continue breastfeeding throughout the illness for infants.

Follow-Up

Follow-up care in cases of bacterial gastroenteritis depends on the severity of the infection and the age of the patient. Uncomplicated diarrhea may not require follow-up if the patient or caretaker is reliable and has adequate access to medical care if needed.

Monitor young children, elderly patients, and debilitated individuals closely to ensure that complications do not occur. Monitor patients requiring labor-intensive oral rehydration to ensure that the proper diet has been reintroduced.

Neonates require strict follow-up care within a few days of the illness to ensure that malabsorption and dehydration do not occur.

Deterrence and Prevention

Avoidance of undercooked meats and seafood, as well as contaminated water supplies, when traveling may help to reduce the risk of transmission of food and water-borne infectious causes of gastroenteritis and associated symptoms.

Vaccines

Salmonella typhi vaccine is recommended for travelers to countries with a high incidence of this infection, persons with intimate exposure to a documented typhoid fever carrier, and workers with frequent exposure to these bacteria. Live attenuated, killed whole-cell, and capsular polysaccharide vaccines are available.

Vibrio vaccine is available but only protects 50% of immunized persons for 3-6 months. It is not indicated for widespread use.

In February 2006, the US Food and Drug Administration (FDA) approved an oral vaccine for rotavirus (RotaTeq) for use in infants. On Feb 21, 2006, the American Academy of Pediatrics (AAP) and the Advisory Committee on Immunization Practices (ACIP) recommended that RotaTeq be part of regularly scheduled childhood immunizations. The vaccine is administered in a 3-dose series starting between ages 6 and 12 weeks and ending before age 32 weeks.

Clinical trials of RotaTeq demonstrated prevention of 74% of all rotavirus gastroenteritis cases, of nearly all severe rotavirus gastroenteritis cases, and of nearly all hospitalizations. A previously marketed rotavirus vaccine (RotaShield) was associated with intussusception, but RotaTeq did not show an increased risk compared with placebo in clinical trials.

In April 2008, the FDA approved Rotarix, another oral vaccine, for prevention of rotavirus gastroenteritis. It is currently recommended that Rotarix be administered in 2 separate doses to patients between ages 6 and 24 weeks. Rotarix was efficacious in a large study, which showed that it protected patients with severe rotavirus gastroenteritis and also decreased the rate of severe diarrhea or gastroenteritis from any cause.[27]

 

Medication

Medication Summary

The goals of pharmacotherapy in cases of gastroenteritis are to reduce morbidity and to prevent complications. The following is a list of standard antimicrobial therapies for bacterial gastroenteritis (although, as previously stated, many conditions are self-limited and require no therapy):

  • Aeromonas species - Use cefixime and most third-generation and fourth-generation cephalosporins

  • Bacillus species - No antibiotics are necessary for self-limited gastroenteritis, but vancomycin and clindamycin are first-line drugs for severe disease

  • Campylobacter species - Erythromycin may shorten the illness duration and shedding; delaying therapy beyond 4 days from the onset of symptoms appears to produce no clinical benefit

  • C difficile - Discontinue potential causative antibiotics; if antibiotics cannot be stopped or this does not resolve the diarrhea, use oral metronidazole or vancomycin (vancomycin is reserved for seriously ill patients whose condition does not respond to metronidazole)

  • C perfringens - Do not treat with antibiotics

  • Listeria species - No antibiotics are needed unless invasive disease occurs; ampicillin and Bactrim are first-line drugs for invasive disease

  • Plesiomonas species - Use trimethoprim-sulfamethoxazole or any cephalosporin

  • V cholerae - Tetracycline is the usual antibiotic of choice, but resistance to it is increasing; other antibiotics that are effective when V cholerae is sensitive to tetracycline include cotrimoxazole, erythromycin, doxycycline, chloramphenicol, and furazolidone

  • Yersinia species - Treatment (ie, trimethoprim-sulfamethoxazole, fluoroquinolones,* aminoglycosides) does not shorten the disease duration and should be reserved for complicated cases

* Note that fluoroquinolone resistance in Salmonella is increasingly being reported worldwide, with several molecular mechanisms described.[40]

E coli

Antibiotic treatment appears to increase the likelihood of developing HUS. Consider antibiotics if diarrhea is moderate or severe. Trimethoprim-sulfamethoxazole is a first-line drug, but a parenteral second-generation or third-generation cephalosporin for systemic complications should be used.

Salmonella species

Antibiotic treatment prolongs the carrier state and is associated with relapse; thus, treatment is not indicated for nontyphoid, uncomplicated diarrhea. Consider treatment for infants younger than 3 months and for high-risk patients, such as patients who are immunocompromised or who have sickle cell disease.

Ampicillin is recommended for drug-sensitive strains. Trimethoprim-sulfamethoxazole, fluoroquinolones,* or third-generation cephalosporins (fluoroquinolones are not recommended for use in children) are also acceptable alternatives. S typhimurium T104 is a multidrug-resistant organism. Sensitivities from the cultured specimens are important to guide therapy.

In July 2018, the FDA ordered ordered label changes for fluoroquinolones to strengthen warnings about the antibiotics' risks for mental health side effects and serious blood sugar disturbances.[41, 42]

Shigella species

Antibiotic treatment may shorten illness duration and shedding but does not prevent complications. Most mild infections will recover without antibiotics. Moderate to severe cases should be treated with antibiotics. Ampicillin is preferred for drug-sensitive strains. For ampicillin-resistant strains or in cases of penicillin allergy, trimethoprim-sulfamethoxazole is the drug of choice, although resistance does occur. Fluoroquinolones* may be considered in patients with highly resistant organisms.

Antibiotics

Class Summary

Along with the immune system, antibiotics help to destroy offending organisms.

Cefixime (Suprax)

Cefixime is a potent, long-acting oral cephalosporin with increased gram-negative coverage. It arrests bacterial growth by binding to 1 or more penicillin-binding proteins.

Ceftriaxone (Rocephin)

Ceftriaxone is a third-generation parenteral antibiotic with wide coverage, including of gram-negative bacilli. It arrests bacterial growth by binding to 1 or more penicillin-binding proteins.

Cefotaxime (Claforan)

Cefotaxime is a third-generation parenteral antibiotic with wide coverage, including of gram-negative bacilli. It arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth.

Erythromycin (E.E.S., EryPed, Erythrocin, Ery-Tab)

Erythromycin is an old bacteriostatic macrolide with activity against most gram-positive organisms and atypical respiratory organisms. It is useful for Campylobacter and Vibrio enteritis. Nausea is a common adverse effect and may be tolerated poorly by some patients. Enteric-coated tablets are associated with less nausea.

Trimethoprim-sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

This is a folate synthesis blocker that has wide antibiotic coverage.

Vancomycin (Vancocin)

Vancomycin therapy is a powerful treatment for antibiotic-associated colitis. Vancomycin is indicated for patients who cannot receive or whose condition has not responded to penicillins and cephalosporins or who are infected with resistant staphylococci.

To avoid toxicity, the current recommendation is to assay trough levels after the third dose drawn 0.5 hour before the next dosing. Use creatinine clearance to adjust the dose in patients diagnosed with renal impairment.

Vancomycin is used in conjunction with gentamicin for prophylaxis in patients allergic to penicillin who are undergoing a gastrointestinal or genitourinary procedure.

Rifaximin (Xifaxan)

Rifaximin is a nonabsorbed (< 0.4%), broad-spectrum antibiotic specific for enteric pathogens of the gastrointestinal tract (ie, gram-positive, gram-negative, aerobic, anaerobic). Rifampin is a structural analogue. It binds to the beta subunit of bacterial deoxyribonucleic acid (DNA)-dependent ribonucleic acid (RNA) polymerase, thereby inhibiting RNA synthesis. It is indicated for E coli (enterotoxigenic and enteroaggregative strains) associated with travelers' diarrhea.

Rifamycin (Aemcolo, Rifamycin SV MMX)

Oral nonabsorbable antibiotic which can be used for the treatment of bacterial infections of the colon. Belongs to the ansamycin antibacterial drug class and acts by inhibiting the beta-subunit of bacterial DNA-dependent RNA polymerase, blocking 1 of the DNA transcription steps, which results in bacterial synthesis inhibition and consequently bacterial growth. It is indicated for traveler’s diarrhea caused by noninvasive strains of E coli, not complicated by fever or blood in the stool.

 

Questions & Answers

Overview

What is bacterial gastroenteritis?

What stool characteristics should be considered in the evaluation of suspected bacterial gastroenteritis?

How is diarrhea defined in bacterial gastroenteritis?

Which systemic features should be considered in the evaluation of bacterial gastroenteritis?

Which factors are associated with specific pathogens in bacterial gastroenteritis?

Which physical findings are characteristic of bacterial gastroenteritis?

Which assessments may be included in the workup of bacterial gastroenteritis?

How are culture media selected in the workup of bacterial gastroenteritis?

What is included in medical care for bacterial gastroenteritis?

What are antimicrobial treatment options for bacterial gastroenteritis?

What are dietary modifications for management of bacterial gastroenteritis?

What is the manifestation of bacterial gastroenteritis?

What are the leading causes of bacterial gastroenteritis?

How does the season influence the likely etiology of bacterial gastroenteritis?

What is the pathophysiology of bacterial gastroenteritis?

What is the role of verotoxin in the etiology of bacterial gastroenteritis?

Which normal enteric flora have pathogenic strains that cause gastroenteritis?

What is the role of Vibrio parahaemolyticus in the etiology of bacterial gastroenteritis?

What are the risk factors for bacterial gastroenteritis?

What is the prevalence of bacterial gastroenteritis in the US?

What is the global prevalence of bacterial gastroenteritis?

How does the prevalence of bacterial gastroenteritis vary by sex?

How does the prevalence of bacterial gastroenteritis vary by age?

What is the prognosis of bacterial gastroenteritis?

What is the morbidity and mortality of bacterial gastroenteritis?

What are common complications of bacterial gastroenteritis?

What is enteric fever in bacterial gastroenteritis?

What causes HUS in bacterial gastroenteritis?

What is Reiter syndrome in bacterial gastroenteritis?

How does dehydration occur in bacterial gastroenteritis?

What is the role of bacterial gastroenteritis in the etiology of inflammatory bowel disease (IBD)?

What is the prevalence of carrier states in bacterial gastroenteritis?

What information about bacterial gastroenteritis should patients be given?

Presentation

How is diarrhea defined and stool assessed in the evaluation of bacterial gastroenteritis?

What are systemic symptoms of bacterial gastroenteritis?

Which food-borne pathogens cause bacterial gastroenteritis?

Which water-borne pathogens cause bacterial gastroenteritis?

Which animal-borne pathogens cause bacterial gastroenteritis?

What is the role of travel history in determining etiology in bacterial gastroenteritis?

Which pathogens are associated with particular locations in the etiology of bacterial gastroenteritis?

Which medical conditions can predispose patients to bacterial infections causing gastroenteritis?

What pathogens are associated with outbreaks of bacterial gastroenteritis?

What are the physical findings characteristic of bacterial gastroenteritis?

What are the physical findings of malnutrition in bacterial gastroenteritis and what do they signify?

How is abdominal pain characterized in bacterial gastroenteritis?

What is borborygmi in bacterial gastroenteritis?

What causes perianal erythema in bacterial gastroenteritis?

DDX

Which conditions should be considered in the differential diagnoses of bacterial gastroenteritis?

What are the differential diagnoses for Bacterial Gastroenteritis?

Workup

What is the initial approach to the workup for bacterial gastroenteritis?

How is C difficile infection diagnosed in bacterial gastroenteritis?

What is the role of bacterial cultures in the diagnostic assessment of bacterial gastroenteritis?

Which culture media are used in the workup of bacterial gastroenteritis?

What is the role of stool cultures in the diagnosis of bacterial gastroenteritis?

Why is it important to test for S typhimurium DT104 in bacterial gastroenteritis?

When is ingested food cultured for bacteria in the workup of gastroenteritis?

What raises the suspicion of enterohemorrhagic E coli in bacterial gastroenteritis?

What should prompt additional screening for Vibrio and Plesiomonas in the workup of bacterial gastroenteritis?

Treatment

What are the treatment options for bacterial gastroenteritis?

When is inpatient care indicated for the treatment of bacterial gastroenteritis?

Which specialist consultations are needed for the treatment of bacterial gastroenteritis?

When are dietary modifications indicated in the treatment of bacterial gastroenteritis?

Which dietary modifications are used in the treatment of bacterial gastroenteritis?

What is included in follow-up care for bacterial gastroenteritis?

What may reduce the risk of transmission of food and water-borne infections causing bacterial gastroenteritis?

Which vaccines are used to prevent bacterial gastroenteritis?

Which vaccines should infants receive to prevent bacterial gastroenteritis?

What is the role of RotaTeq in the prevention of bacterial gastroenteritis?

What is the role of Rotarix in the prevention of bacterial gastroenteritis?

Medications

What are the goals of drug treatment for bacterial gastroenteritis?

What are the risks and benefits of antibiotic treatment for bacterial gastroenteritis?

Which medications in the drug class Antibiotics are used in the treatment of Bacterial Gastroenteritis?