What Is Eiec

[Xena Donovan]

EnteroinvasiveEscherichia coli (EIEC) is a type of pathogenic bacteria whose infection causes a syndrome that is identical to shigellosis, with profuse diarrhea and high fever. EIEC 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.

EIEC are closely related to Shigella, like all E. coli are.[1][2] Their similarity in disease phenotype come from a homologous large virulence plasmid pINV. They also have in common in their loss of cadaverine synthesis, of ompT, and of curli formation. These features are probably acquired independently, as the two lost cadaverine synthesis in different ways.[3] Moreover, the "EIEC" does not form a monophyletic group in E. coli.[4]

After the E. coli strain penetrates through the epithelial wall, the endocytosis vacuole gets lysed, the strain multiplies using the host cell machinery, and extends to the adjacent epithelial cell. In addition, the plasmid of the strain carries genes for a type III secretion system that is used as the virulent factor. Although it is an invasive disease, the invasion usually does not pass the submucosal layer. The similar pathology to shigellosis may be because both strains of bacteria share some virulent factors. The invasion of the cells can trigger a mild form of diarrhea or dysentery, often mistaken for dysentery caused by Shigella species. The illness is characterized by the appearance of blood and mucus in the stools of infected individuals or a condition called colitis.[citation needed]

Dysentery caused by EIEC usually occurs within 12 to 72 hours following the ingestion of contaminated food. The illness is characterized by abdominal cramps, diarrhea, vomiting, fever, chills, and a generalized malaise. Dysentery caused by this organism is generally self-limiting with no known complications.[5]

It is currently unknown what foods may harbor EIEC, but any food contaminated with human feces from an ill individual, either directly or via contaminated water, could cause disease in others. Outbreaks have been associated with hamburger meat and unpasteurized milk.[6]

The genus Escherichia is named after Theodor Escherich, the individual who isolated the type species of the genus. These organisms are gram-negative facultatively anaerobic bacilli, may exist singly or in pairs, utilize both fermentative and respiratory metabolism for energy, and either are nonmotile or motile by peritrichous flagella.E coli has a rapid reproduction time as low as 20 minutes in laboratory conditions and virulence depends on what types of capsular antigens, flagellar antigens, and somatic polysaccharides each strain possesses. [1]

Most cases of neonatal meningitis cases are caused by group B streptococcal infections and E coli (50% and 20% respectively). Pregnant individuals are at a higher risk for colonization with the K1 capsular antigen strain of E coli. Approximately 80% of the E coli strains that cause neonatal meningitis feature the K1 capsular antigen. This K1 capsular antigen is similar to the group B Neisseria meningitidis capsule, which provides protection from phagocytosis. [2] This strain commonly is observed in neonatal sepsis, which carries a mortality rate of up to 50% if untreated and up to 10% if treated. Some 25-50% of survivors have subsequent neurologic deficits and up to 20% demonstrated developmental abnormalities at 5 years post infection. Low birth weight and a positive cerebrospinal fluid (CSF) culture result portend a poor outcome. [3] In adults, E colimeningitis is rare but occasionally can be seen in those with neurosurgical trauma or complications of neurosurgical procedures with prosthetic device infections. E coli meningitis in an individual with no significant medical comorbidities or those receiving immunosuppression, particularly steroids, should raise suspicion of Strongyloides stercoralis hyperinfection involving the central nervous system. E coli and other enteric bacteria enter the bloodstream attached to the parasite as it migrates through the gut wall toward the lungs as part of its reproductive cycle. While this can occur occasionally, steroids cause alteration in immune regulation and upregulate the generation of filariform larva, which is the stage of the parasite that undergoes this migration. [4]

Recognize that not all cases of aspiration will lead to pneumonia. Many cases of acute aspiration lead to aspiration pneumonitis, an inflammatory reaction within the lungs, that may present with many of the similar symptoms of pneumonia but not require antimicrobial therapy.

A parapneumonic effusion and empyema may be secondary to an untreated E coli pneumonia. Lung abscesses from septic emboli may develop from an E coli bacteremia. This mechanism is different from a pneumonia, as the primary route of infection is seeding the lungs through the blood stream and not an infection through the alveoli as seen in pneumonia. The primary etiology of the bacteremia generally is pyelonephritis or intraabdominal infection.

Unless from a sputum culture isolated during pneumonia, blood culture during bacteremia, or wound culture aspirated from a lung abscess that identifies E coli, it is impossible to distinguish lung pathology caused by this organism from other enteric gram-negative organisms.

E coli intra-abdominal infections often result from damage to the gut mucosal barrier. This leads to localized infections (eg, diverticulitis, appendicitis) or geographically distant infections (transient splanchnic vein bacteremia leading to pyogenic liver abscesses) (see image below). Complete disruption of the gastrointestinal tract can be spontaneous, traumatic, or anastomotic (prior surgical reconnection site of bowel with failure to heal) in origin with subsequent spillage of gastrointestinal contents, subsequent peritonitis, and complicated by abscess formation. Intra-abdominal abscesses often are polymicrobial as they derive mainly from the gastrointestinal tract that harbors millions of different gram-positive, gram-negative, and anaerobic species. Therefore, E coli plays a component role in these infections but is not the sole cause unless isolated via culture from a sterile space.

Despite naming conventions, there are no differences in antimicrobial susceptibilities of these different E coli bacteria. Thus, antibiotics that target E coli would treat all these organisms if they were identified in the same patient. Care must be given in identifying hematochezia or gross blood in the stool, as this may be secondary to dysentery caused by ETEC or EHEC, with lysis of these bacteria though antibiotic treatment potentially leading to release of their toxins and clinical deterioration of the patient.

As a cause of enteric infections, 6 different mechanisms of action of 6 different varieties of E coli have been reported. Enterotoxigenic E coli (ETEC) is a cause of traveler's diarrhea; enteropathogenic E coli (EPEC) is a cause of childhood diarrhea; enteroinvasive E coli (EIEC) causes a Shigella -like dysentery; enterohemorrhagic E coli (EHEC) causes hemorrhagic colitis that can lead to a diffuse systemic illness of hemolytic-uremic syndrome (HUS); enteroaggregative E coli (EAggEC) primarily is associated with persistent diarrhea in children in developing countries, and enteroadherent E coli (EAEC) is a cause of childhood diarrhea and traveler's diarrhea in Mexico and North Africa. ETEC, EPEC, EAggEC, and EAEC colonize the small bowel, and EIEC and EHEC preferentially colonize the large bowel prior to causing diarrhea.

Kappeli et al looked at 97 non-O157 STECstrains in patients with diarrhea and found that HUS developed in 40% of patients; serotype O26:H11/H most often was associated with this syndrome. [1] Although strains associated with HUS were more likely to harbor STX 2 and EAE compared with those associated with bloody diarrhea, only 5 of the 8 patients with HUS had the STX2 gene; among the 3 patients with EAE -negative, STX2 -negative strains, only STX1 or STX1 and EHXA caused the HUS.

The urinary tract is the most common site of E coli infection, and more than 90% of all uncomplicated UTIs are caused by E coli infection. The recurrence rate after a first E coli infection is 44% over 12 months. E coli UTIs are caused by uropathogenic strains of E coli. E coli causes a wide range of UTIs, including uncomplicated urethritis cystitis, symptomatic cystitis, pyelonephritis, acute prostatitis, prostatic abscess, and sepsis from an ascending urinary tract infection. Uncomplicated cystitis occurs primarily in females who are sexually active and are colonized by a uropathogenic strain of E coli. Subsequently, the periurethral region is colonized from contamination of the colon, and the organism reaches the bladder during sexual intercourse.

Uropathogenic strains of E coli have an adherence factor called P fimbriae, or pili, which binds to the P blood group antigen. These P fimbriae mediate the attachment of E coli to uroepithelial cells. Thus, patients with intestinal carriage of E coli that contains P fimbriae are at greater risk of developing UTI than the general population. Complicated UTI and pyelonephritis are observed in elderly patients with structural abnormalities or obstruction such as prostatic hypertrophy or neurogenic bladders or in patients with indwelling urinary catheters. Escherichia coli right sided pyelonephritis is visualized in the image below.

E coli bacteremia usually is associated with UTIs, especially in cases of urinary tract obstruction of any cause. The systemic reaction to endotoxin (cytokines) or lipopolysaccharides can lead to disseminated intravascular coagulation and death. E coli is a leading cause of nosocomial bacteremia from a GI or genitourinary source.

Other miscellaneous E coli infections include septic arthritis, endophthalmitis, suppurative thyroiditis, sinusitis, osteomyelitis, endocarditis, and skin and soft-tissue infections (especially in patients with diabetes).

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