Enteroinvasive E. coli (EIEC)
E. coli (Escherichia coli) and Shigella are two types of bacteria that belong to the same family of Enterobacteriaceae. They are both gram-negative, rod-shaped, facultative anaerobes that can cause intestinal infections in humans and animals.
E. coli is a diverse group of bacteria that normally lives in the intestines of healthy people and animals. Most strains of E. coli are harmless or beneficial, but some can cause diarrhea, urinary tract infections, respiratory illness, bloodstream infections, and other diseases. E. coli strains are classified into different pathotypes based on their virulence factors and mechanisms of infection. Some of the most common pathotypes are enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), enteroinvasive E. coli (EIEC), and enteroaggregative E. coli (EAEC).
Shigella is a group of bacteria that causes shigellosis, a severe form of dysentery characterized by bloody diarrhea, fever, abdominal cramps, and dehydration. Shigella is divided into four species: Shigella dysenteriae, Shigella flexneri, Shigella boydii, and Shigella sonnei. Each species has different serotypes based on the antigenic structure of its lipopolysaccharide (LPS) and other surface proteins. Shigella is highly infectious and can be transmitted by direct or indirect contact with fecal matter from infected people or animals.
E. coli and Shigella are closely related genetically and biochemically, but they have distinct epidemiological and clinical features. E. coli is more widespread and diverse than Shigella and can be found in various environmental sources such as water, soil, food, and animals. Shigella is more restricted to humans and primates and is mainly associated with poor sanitation and hygiene conditions. E. coli causes a range of intestinal and extraintestinal diseases depending on the pathotype, while Shigella causes a more severe and invasive form of dysentery that can lead to complications such as hemolytic uremic syndrome (HUS) and reactive arthritis. E. coli and Shigella can be differentiated by several biochemical tests such as lactose fermentation, motility, lysine decarboxylase activity, indole production, gas production from glucose, and urease activity. Additionally, molecular methods such as polymerase chain reaction (PCR), serotyping, multilocus sequence typing (MLST), and whole genome sequencing (WGS) can be used to identify and characterize E. coli and Shigella strains at the genetic level.
In summary, E. coli and Shigella are two related but distinct groups of bacteria that cause intestinal infections in humans and animals. They have different epidemiology, pathogenesis, clinical manifestations, diagnosis, and treatment options. Understanding their similarities and differences is important for preventing and controlling their spread and impact on public health.
Enteroinvasive E. coli (EIEC) is a type of pathogenic bacteria that causes a syndrome similar to shigellosis, a severe form of dysentery. Dysentery is an infection of the intestines that results in diarrhea with mucus and blood, along with abdominal pain, fever, and dehydration.
EIEC infects the colonic epithelium, the inner lining of the large intestine, by using adhesin proteins to bind to and enter the intestinal cells. Once inside the cells, EIEC lyses the endocytic vacuole, a membrane-bound compartment that contains the bacteria and replicates in the cytoplasm. EIEC then moves from cell to cell by forming actin tails, which are structures made of protein filaments that propel the bacteria through the cytoplasm. This process of epithelial cell destruction and inflammatory infiltration can lead to colonic ulceration, which is a loss of tissue in the intestinal wall.
EIEC does not produce any toxins but relies on its invasive ability to cause disease. The infection usually occurs within 12 to 72 hours after ingestion of contaminated food or water, although person-to-person transmission can also occur. The disease can range from mild to severe, depending on the strain of EIEC and the host factors. Some patients may experience only watery diarrhea, while others may develop dysentery with fever, chills, malaise, abdominal cramps, and blood and leukocytes (white blood cells) in stool specimens. The disease is usually self-limiting, meaning that it resolves without complications within a few days. However, some patients may develop dehydration or electrolyte imbalance due to fluid loss, which may require rehydration therapy.
EIEC is one of several diarrheagenic strains of E. coli that can cause gastroenteritis in humans. Other strains include enterohemorrhagic E. coli (EHEC), which can cause bloody diarrhea and hemolytic uremic syndrome (a serious condition that affects the blood and kidneys); enterotoxigenic E. coli (ETEC), which produces toxins that cause traveler`s diarrhea; enteropathogenic E. coli (EPEC), which can cause diarrhea outbreaks in newborns; and enteroaggregative E. coli (EAEC), which can cause acute and chronic diarrhea in children.
: Disease Caused
EIEC infections are usually caused by consuming contaminated food or water, although person-to-person transmission can also occur. Some common sources of EIEC outbreaks include leafy greens, raw milk, and undercooked meat. The bacteria can survive in acidic environments and low temperatures, making them difficult to eliminate.
The infective dose of EIEC is higher than that of Shigella spp., which means that a larger number of bacteria are needed to cause illness. This reduces the potential for person-to-person transmission, but it does not eliminate it completely. EIEC can spread through fecal-oral contact, especially among children, elderly people, and immunocompromised individuals.
To prevent EIEC infections, it is important to practice good hygiene and sanitation, avoid drinking untreated water, and cook food thoroughly. EIEC outbreaks should be reported to public health authorities and investigated promptly to identify the source and prevent further cases.
Enteroinvasive E. coli (EIEC) is a type of pathogenic bacteria that causes a syndrome similar to shigellosis, with profuse diarrhea and high fever. EIECs are highly invasive, and they use adhesin proteins to bind to and enter intestinal cells. They produce no toxins but severely damage the intestinal wall through mechanical cell destruction. The pathogenesis of EIEC involves the following steps:
- Epithelial cell penetration: EIEC uses a type III secretion system (T3SS) to inject effector proteins into the host cell cytoplasm, which triggers actin rearrangements and membrane ruffling that facilitate bacterial uptake. A plasmid-encoded antigen called virulence marker antigen (VMA) is also important for bacterial invasion.
- Lysis of endocytic vacuole: After entering the host cell, EIEC escapes from the endocytic vacuole by secreting another set of effector proteins that disrupt the vacuolar membrane and activate host cell death pathways.
- Intracellular multiplication: EIEC replicates in the host cell cytoplasm using the host cell machinery. The bacteria can reach high numbers within a single cell, causing cytoplasmic distension and eventual cell lysis.
- Directional movement through cytoplasm: EIEC uses actin-based motility to move within the cytoplasm and spread to adjacent cells. The bacteria recruit host actin filaments to form a tail-like structure that propels them forward. This process is similar to that observed with Listeria and Shigella.
- Extension into adjacent epithelial cells: EIEC can move from one cell to another by forming membrane protrusions that are engulfed by neighboring cells. This allows the bacteria to avoid exposure to the extracellular environment and evade immune responses.
This process of epithelial cell destruction with inflammatory infiltration can progress to colonic ulceration and dysentery. EIEC is not toxigenic, but invasive.
EIEC infection causes a spectrum of symptoms ranging from mild to severe. The incubation period is usually 1 to 3 days but can be longer in some cases. The onset of symptoms is typically abrupt and may include:
- Watery diarrhea progressing to dysentery with fever, chills, malaise, abdominal cramps, and blood and leukocytes in stool specimens. Dysentery is more common in children and immunocompromised individuals.
- Dehydration and electrolyte imbalance due to fluid loss. This can lead to complications such as hypovolemic shock, renal failure, and death if not treated promptly.
- Extraintestinal manifestations such as septicemia, arthritis, conjunctivitis, and hemolytic uremic syndrome (HUS) are rare but possible.
The duration of illness is usually 3 to 7 days but can be longer in some cases. Most patients recover without sequelae, but some may develop chronic intestinal inflammation or post-infectious irritable bowel syndrome (IBS).
The severity of EIEC infection depends on several factors, such as:
- The virulence of the strain. Some strains have more invasive or cytotoxic properties than others.
- The host`s immune status. Immunocompromised individuals, such as those with HIV/AIDS, cancer, or malnutrition, are more susceptible to severe infection and complications.
- The host`s genetic factors. Some individuals may have genetic variations that affect their susceptibility or resistance to EIEC infection.
- The environmental factors. Poor sanitation, overcrowding, and lack of access to safe water and food increase the risk of exposure and transmission of EIEC.
EIEC infection can be prevented by practicing good hygiene, avoiding contaminated food and water, and washing hands before eating and after using the toilet. There is no vaccine available for EIEC infection.
EIEC strains can be difficult to distinguish from Shigella spp and from other E. coli strains, including nonpathogenic strains. In general, identification of EIEC entails demonstrating that the organism possesses the biochemical profile of E. coli yet with the genotypic or phenotypic characteristics of Shigella spp.
Some of the methods that can be used to diagnose EIEC infection are:
- Detection of VMA by ELISA: VMA (virulence marker antigen) is a plasmid-encoded protein that mediates bacterial invasion into epithelial cells. It can be detected by enzyme-linked immunosorbent assay (ELISA) in stool samples or bacterial isolates.
- HeLa cell invasion assay: This is a cell culture-based method that measures the ability of EIEC to invade and multiply within HeLa cells, a human cervical cancer cell line. The assay requires incubation of bacteria with HeLa cells, followed by lysis of extracellular bacteria and enumeration of intracellular bacteria by plating on selective media.
- Sereny test: This is an animal model-based method that involves inoculation of bacterial suspension into guinea pig eyes, producing conjunctivitis. This test mimics the human infection and can differentiate EIEC from other E. coli strains based on their ability to cause inflammation and ulceration in the conjunctiva.
- Biochemical profile: Compared with other E. coli strains, EIEC are biochemically atypical, being non-motile, lactose non-fermenters, and negative for lysine decarboxylase. These features can be tested by conventional biochemical tests or automated systems. However, some EIEC strains may show atypical results or overlap with Shigella spp, so the biochemical profile alone is not sufficient for diagnosis.
- Molecular methods: Several molecular methods have been developed to detect specific genes or sequences associated with EIEC virulence, such as pInv genes (plasmid invasion genes), ipaH gene (invasion plasmid antigen H gene), or ial gene (invasion-associated locus gene). These methods include polymerase chain reaction (PCR), multiplex PCR, real-time PCR, loop-mediated isothermal amplification (LAMP), and DNA microarray. Molecular methods offer high sensitivity and specificity but may require specialized equipment and expertise.
The main goal of treatment for EIEC infection is to rehydrate the patient and prevent complications such as dehydration, electrolyte imbalance, and hemolytic uremic syndrome (HUS). Rehydration can be achieved by drinking fluids that contain water, salt, and sugar, such as oral rehydration solutions (ORS) or broth. In severe cases, intravenous fluids may be needed to restore fluid and electrolyte balance.
Antibiotics are not routinely recommended for EIEC infection, as they may not shorten the duration of symptoms or reduce the risk of HUS. However, antibiotics may be considered for patients with severe disease (such as high fever, bloody stools, or signs of sepsis), immunocompromised hosts, or those with risk factors for complicated disease (such as valvular or endovascular cardiac disease, atherosclerosis, inflammatory bowel disease, or pregnancy). Antibiotics may also be indicated for patients with persistent symptoms (>1 week) or public health concerns (such as outbreaks or travelers).
The choice of antibiotic depends on the susceptibility of the EIEC strain and the clinical scenario. Some possible options include fluoroquinolones (such as ciprofloxacin), macrolides (such as azithromycin), and rifaximin. These antibiotics have activity against both E. coli and Shigella spp., which can be difficult to distinguish from EIEC. However, resistance to these antibiotics may vary by geographic region and should be guided by local epidemiology and culture results.
Patients with EIEC infection should avoid anti-diarrheal agents (such as loperamide or bismuth subsalicylate), as they may worsen the inflammation and increase the risk of HUS. Patients should also avoid nonsteroidal anti-inflammatory drugs (NSAIDs), as they may increase the bleeding tendency.
Patients with EIEC infection should be monitored for signs of complications, such as worsening diarrhea, dehydration, abdominal pain, blood in stools, fever, confusion, or decreased urine output. These may indicate the development of HUS, which is a serious condition that can cause kidney failure, anemia, and thrombocytopenia. HUS requires prompt hospitalization and supportive care, which may include blood transfusions and kidney dialysis.
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