Escherichia coli enteritis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.
Overview
E. coli enteritis is an infectious cause of acute gastroenteritis caused by a pathogenic strain of the Gram-negative rod, Escherichia coli. 'It is one of the most common causes of diarrhea worldwide and is responsible for 20% to 50% of all infectious diarrhea, with an incidence in the USA of approximately 20-30 cases per 100,000 individuals. E. coli enteritis may be classified according to the causative E. coli strain into Enterotoxigenic E. coli (ETEC), Enteropathogenic E. coli (EPEC), Enterohemorrhagic E. coli (EHEC), Enteroinvasive E. coli (EIEC), and Enteroaggressive E. coli (EIEC). Transmission of pathogenic E. coli strains is usually by the fecal-oral route in contaminated foods and water. The pathogenesis by which each E. coli strain causes clinical manifestations is unique: ETEC, EHEC, and EAEC secrete toxins, EIEC invades the host colonocytes and migrates within cells, whereas EPEC uses EPEC-elongation factor (EAF) to cause "attachment and effacing". Risk factors in the development of E. coli enteritis include young and old age, immunocompromised status, pregnancy, recent ingestion of uncooked or poorly handled vegetables, meat (e.g. hamburgers), poultry, raw milk, or poorly stored foods that require refrigeration (e.g. mayonnaise), drinking from untreated water, recent travel to developing countries, exposure to infected individuals, daycare, and healthcare settings, and recent sexual history of receptive anal or oral-anal contact. Following transmission, the incubation period of pathogenic E. coli strains is approximately 1-10 days, during which the infected patient remains asymptomatic. Early manifestations of E. coli enteritis include diffuse abdominal pain, vomiting, and severe, acute watery diarrhea, which may be followed by episodes of bloody diarrhea (in EHEC and EIEC infections). The majority of patients report resolution of symptoms within 5-10 days of symptom-onset. Common complications of E. coli enteritis include hemolytic uremic syndrome (in EHEC infection), thrombotic thrombocytopenic purpura (in EHEC infection), and acute kidney injury. Prognosis of E. coli enteritis is generally excellent, and the majority of cases resolve without any long-term sequelae. Identification of the causative strain is usually not necessary for diagnosis and treatment. Diagnostic laboratory tests may include either stool culture, ELISA, or polymerase chain reaction (PCR). Rehydration is the mainstay of therapy of E. coli enteritis. Oral rehydration fluids (e.g. oral rehydration solutions) are indicated among patients who can tolerate oral intake, otherwise IV rehydration is indicated. Since the majority of cases of E. coli enteritis are self-limited and the exact infective strain is often not identified, empiric antimicrobial therapy is generally not recommended. Antimicrobial therapy using either fluoroquinolone or TMP-SMX may be administered (but is not required) in ETEC infection, EPEC infection, and EIEC infection, but not in EHEC infection. Effective preventive measures include hand washing using soap and water and proper food handling.
Historical Perspective
Theodor Escherich, a German physician, was the first to grow cultures of E. coli in 1885. The first pathogenic E. coli strain described was enteropathogenic E. coli (EPEC). The infection was reported in 1945 following outbreaks of infant diarrhea in the United Kingdom.[1]
Classification
E. coli enteritis may be classified according to the causative E. coli strain into Enterotoxigenic E. coli (ETEC), Enteropathogenic E. coli (EPEC), Enterohemorrhagic E. coli (EHEC), Enteroinvasive E. coli (EIEC), and Enteroaggressive E. coli (EIEC).
Pathophysiology
E. coli normally colonizes the human GI tract shortly following birth. However, the colonizing E.coli strains are different from the pathogenic strains. Transmission of pathogenic E. coli strains is usually by the fecal-oral route via infected food products (e.g. undercooked beef, vegetables, unpasteurized milk products or juice), contaminated water, infected cattle, or human fecal material (e.g. oral-anal contact). Only enteroinvasive E. coli (EIEC) has true replication within the host cell, whereas all other types of E. coli replicate outside the host cell. The small intestine is the primary site of action of ETEC and EPEC, whereas the colon is the primary site of action of EHEC and EIEC. EAEC may act on either enterocytes or colonocytes. The pathogenesis by which each E. coli strain causes manifestations is unique: ETEC, EHEC, and EAEC secrete toxins, EIEC invades the host colonocytes and migrates within cells, whereas EPEC uses EPEC-elongation factor (EAF) to cause "attachment and effacing". Finally, the diffusely adherent E. coli strain (DAEC) is a subtype of EPEC that utilizes unique patterns of adherence.
Causes
E. coli enteritis is caused by pathogenic strains of the bacterium Escherichia coli, a Gram-negative rod.
Differential Diagnosis
E. coli enteritis must be differentiated from other causes of abdominal pain, diarrhea, and fever (less common), such as other infectious causes, including bacterial, viral, fungal, and parasitic causes, in addition to non-infectious causes, including acute pancreatitis, appendicitis, bowel obstruction, diverticulitis, drug reaction, hyperthyroidism, inflammatory bowel disease, mesenteric ischemia, peritonitis, and pneumonia.
Epidemiology and Demographics
E. coli is one of the most common causes of diarrhea worldwide and is responsible for 20% to 50% of all infectious diarrhea. The exact incidence of E. coli enteritis is difficult to estimate, but it is thought that E. coli causes more than 500-700 million cases of enteritis and is responsible for approximately 700,000 deaths each year. In the USA, the incidence of E. coli enteritis is estimated to be approximately 20-30 cases per 100,000 individuals. Young children < 5 years of age and elderly individuals are more commonly affected with E. coli enteritis. There is no gender or racial predilection to the development of E. coli enteritis. E. coli enteritis is more common in developing countries than in developed countries.
Risk Factors
Risk factors in the development of E. coli enteritis include young and old age, immunocompromised status, pregnancy, recent ingestion of uncooked or poorly handled vegetables, meat (e.g. hamburgers), poultry, raw milk, or poorly stored foods that require refrigeration (e.g. mayonnaise), drinking from untreated water, recent travel to developing countries, exposure to infected individuals, daycare, and healthcare settings, and recent sexual history of receptive anal or oral-anal contact.
Screening
Screening asymptomatic individuals for the presence of enteritis-causing E. coli strains is not recommended.
Natural History, Complications and Prognosis
Following transmission, the incubation period of pathogenic E. coli strains is approximately 1-10 days, during which the infected patient remains asymptomatic. Early manifestations of E. coli enteritis include severe, acute watery diarrhea, diffuse abdominal pain, and vomiting, which may be followed by episodes of bloody diarrhea (in EHEC and EIEC infections). The majority of patients report resolution of symptoms within 5-10 days of symptom-onset. Common complications of E. coli enteritis include hemolytic uremic syndrome (in EHEC infection), thrombotic thrombocytopenic purpura (in EHEC infections), and acute kidney injury. Prognosis of E. coli enteritis is generally excellent, and the majority of cases resolve without any long-term sequelae.
Diagnosis
History and Symptoms
Symptoms of E. coli enteritis include diarrhea (either watery or bloody), nausea, vomiting, abdominal pain, and bloating with or without fever (fever is characteristically absent in EHEC enteritis, but may be present in enteritis caused by other E. coli strains). Less common symptoms may be related to complications of E. coli enteritis, such as hemolytic uremic syndrome, and may include spontaneous bruising, oliguria/anuria, and painless gross hematuria.
Physical Examination
Physical examination of patients with E. coli enteritis may be remarkable for abdominal tenderness, fever (occasionally), and signs of dehydration, such as abnormal orthostatic vital signs, reduced skin turgor, slow capillary refill, and dry mucous membranes. Physical examination among patients with severe dehydration may be remarkable for altered mental status. Physical examination may also be remarkable for findings suggestive of complications of the E. coli enteritis (e.g. hemolytic uremic syndrome), such as skin pallor, petechiae, and bruises.
Laboratory Findings
Identification of the causative strain is usually not necessary for diagnosis and treatment. Diagnostic laboratory tests for E. coli enteritis usually include either stool culture, ELISA, or polymerase chain reaction (PCR). Other laboratory findings in E. coli enteritis are usually non-specific and may include increased white blood cell count and elevated inflammatory markers. Laboratory findings suggestive of dehydration may include relative polycythemia, metabolic alkalosis, elevated BUN and serum creatinine (suggestive of pre-renal acute kidney injury). When hospitalized, patients should also be monitored for laboratory findings that may suggest development of hemolytic uremic syndrome, such as hemolytic anemia, elevated serum creatinine, and thrombocytopenia.
Treatment
Medical Therapy
Rehydration is the mainstay of therapy of E. coli enteritis. Oral rehydration fluids (e.g. oral rehydration solutions) are indicated among patients who can tolerate oral intake, otherwise IV rehydration is indicated. Since the majority of cases of E. coli enteritis are self-limited and the exact infective strain is often not identified, empiric antimicrobial therapy is generally not recommended. Antimicrobial therapy using either fluoroquinolone or TMP-SMX may be administered (but is not required) in ETEC infection (traveler's diarrhea), EPEC infection, and EIEC infection, but not in EHEC infection (due to increased risk of hemolytic uremic syndrome and prolonged shedding). In adults, additional pharmacologic therapies may include antiemetic agents (not recommended in pediatric patients). Antidiarrheal agents are generally not recommended during the acute infection phase.
Surgery
Surgery is not recommended to treat E. coli enteritis.
Prevention
According to the Centers for Disease Control and Prevention (CDC), preventive measures against development of E. coli enteritis include applying proper hand hygiene using soap and water, cooking meat thoroughly (to a temperature of at least 160°F / 70˚C), avoiding consumption of raw and unpasteurized products (e.g. milk, other dairy products, and juices), and avoiding swallowing water when swimming.[2]
References
- ↑ Bray, J (1945). "Isolation of antigenically homogeneous strains of Bacterium coli neapolitanum from summer diarrhoea of infants". J of Pathol Bacteriol. 57 (2): 239–47.
|access-date=requires|url=(help) - ↑ "E coli infection". www.cdc.gov. Centers for Disease Control and Prevention. May 20 2014. Retrieved December 19 2015. Check date values in:
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