Escherichia coli

In 1885, Theodor Escherich described the bacterium later named after him as the first specific intestinal bacterium

Escherichia coli (E. coli for short) - also known as coliform bacteria - is a gram-negative, sporeless, acid-forming and peritrichous flagellated and therefore mobile bacterium. It ferments with gas formation, glucose, lactose, mannitol and forms indole. Escherichia coli is normally found in the human and animal intestines. Within the family Enterobaceriaceae in the order Enterobacteriales, E. coli belongs to the important genus Escherichia and is its type species. E.coli plays a major role in intestinal and extraintestinal infections (Hof H et al. 2019). E.coli is the most common sepsis pathogen (Hof H et al. 2019)!

In addition to E. coli, other Escherichia species exist, such as E. fergusonii and E. hermanii. Most members of these species are not pathogenic, but there are also numerous different pathogenic strains. Escherichia coli is one of the most common causative agents of human infectious diseases.

• DAEC (diffusely adherent E.coli): formation of special fimbriae (Afa-Dr), bind to enterocytes of the small intestine; abolition of microvilli.
• EPEC (enteropythogenic E.coi - dyspepsia coli): special ability of the pathogens to adhere to the intestinal mucosa cell by "bundle forming pili" -bfp- with abolition of microvilli. The pathogen factor EAF (EPEC-adhesion factor) can be detected.
• ETEC (enterotoxin-forming E.coli): heat-labile enterotxins (LT I and LT II). Less commonly, a heat-stable enterotxin (ST). Widely distributed in tropical countries. Causes traveler's diarrhea.
• EIEC (enteroinvasive E.coli): carry a plasmid (pINV) that allows them to invade and destroy the intestinal mucosal cell of the colon. Mimic bacterial (shigella) dysentery.
• EAEC (enteroaggregative E.coli): Adherence fimbriae (AAF) bind to mucosal cells and stimulate mucus production. Watery diarrhea. Immunosuppressed more frequently affected.
• EHEC (enterohemorrhagic E.coli/ verotoxin-producing E.coli = VTEC/ Shiga-like toxin-producing E.coli = STEC): carry a chromosomal gene whose product (eae) mediates adhesion to epithelial cells. A shiga toxin (Stx, also verotoxin or shiga-like toxin) can be produced in a phage-encoded manner, inhibit protein synthesis of human cells. This has similarities to the neurotoxic toxin of Shiga-dysenterica. A hemolysin can be produced in a plasmid-encoded manner. Hemorrhagic colitis; possible occurrence of "hemolytic uremic syndrome (HUS).

In the human intestinal flora, E. coli is known as a vitamin producer, especially for vitamin K, in addition to Bacteroides fragilis and Lactobacillus acidophilus. The bacterium is the classic faecal indicator. I.e. its detection always testifies to contamination with human or animal faeces and signals contamination with other pathogens (bacteria, protozoa, viruses, worms). In 100 ml. No E.coli may be detectable in 100 ml. of water (drinking water hygiene).

Route of infection: Infection with E. coli usually occurs by the following routes:

• By eating contaminated ground beef that is undercooked (one of the most common sources) or unpasteurized milk, by visiting petting zoos, by eating prepared foods (such as those in salad bars) that have been prepared with contaminated water or are themselves contaminated (manure), by swallowing inadequately chlorinated water in swimming or wading pools contaminated with the stool of infected persons, by inadequate hygiene, especially in the case of small, diaper-wearing children, the bacteria can easily spread from person to person. Cattle are common carriers of EHEG (enteropathogenic E.coli). The infectious dose can be low. Only 10-100 EHEC on meat or vegetables are sufficient.

E. coli infections can occur in people at any age. Severe infections occur more frequently in children and older people (Robert Koch Institute 2018).

Intraintestinal infections: digestive tract: gastroenteritis, haemorrhagic colitis, travellers' diarrhoea.

Extraintestinal infections due to pathogenic Escherichia coli (ExPEC):

• Urinary tract: cystitis in women, urethritis, urethrocystitis, cystopyelitis, pyelonephritis,
• Prostate: Prostatitis
• Gall bladder: cholecystitis
• Wound infections
• Infections of pressure sores
• Gram-negative foot infection (e.g. in diabetics)
• Lung: Pneumonia
• CNS: meningitis in newborns
• Sepsis (e.g. urosepsis, cholangiosepsis): E.coli is the most common sepsis pathogen - especially in the elderly.

Germs are detected exclusively by culture. The cultures grow easily on solid selective culture media (e.g. Endo Agar or McConkey Agar). The final assignment is done by "colorful series" or MALDI_TOF mass spectrometry. Serological typing can detect at least 170 O antigens, 50 H antigens, and 70-K antigens (Johnson JR et al. 2018). These detections are significant for certain epidemiologic questions but have no relevance to routine practice (Johnson JR et al. 2018). Detection of individual pathogenicity factors such as shiga toxins and enterotoxins is achieved by ELISA and PCR.

See below the individual clinical pictures. Resistance to aminopenicillins, cephalosporins, cotrimoxazole and quinolones (often as multi-resistance: 3MGN, 4MGN) must be expected.

Prophylaxis see below. Intestinal infections with EPEC, ETEC, EIEC, EHEC are always exogenous.

For further information see: EHEC, infection control and hygiene measures

Every person harbours a large number of different strains and variants in their intestine, most of which are harmless commensals. Some variants of E. coli are due to a special equipment e.g. urpathogenic, while others are intestinal pathogenic. They can cause extraintestinal and intraintestinal infections:

Pathogenesis of intestinal infections: the pathogenesis of intestinal infections caused by E.coli varies and depends on the particular mosaic of virulence factors. Specific EHEC strains encode an enterohemolysin that supplies iron to the bacterium after lysis of erythrocytes. Another gene (LEE gene) codes for a protein of the same name (locus enterocytes effacement), which ensures firm binding after the bacterium has bound to the enterocyte. The binding itself is mediated by a surface protein (intimin). Furthermore, E. coli can produce toxins in a certain phage population. Phagenbesatz toxins form (Shigatoxin I and II). These toxins have a high homology with the shigatoxin of Shigella dysenterica. Their formation is dependent on external factors. If the bacterium is irritated by certain factors, e.g. antibiotics that attack the genome (e.g. quinolones), the phages begin to reproduce, whereby the gene for toxin formation is also activated. When the bacteria decay, these intracellular toxins are released and cause systemic damage. The toxins bind to specific receptors (neutral glycolipids) that are found not only on enterocytes but also on endothelia in kidney and brain vessels. Shiga toxins can cause hemolytic uremic syndrome (HUS), a feared complication.

Molecular mechanisms for the development of virulence factors: The molecular mechanisms by which non-pathogenic intestinal E coli bacteria acquire virulence functions are only partially understood. One possible cause is mutations in lipopolysaccharide (LPS) transporter genes (7 LPS transporters have been described so far: LptA-G -Dong H et al. 2017-). Mutations in the transporter proteins LptD (G580S) and LptE (T95I) that translocate LPS from the inner to the outer membrane which is essential for E. coli growth (Dong H et al. 2017) lead to resistance to various antibiotics, to antimicrobial peptides and host complement. These results suggest that non-pathogenic bacteria can acquire virulence properties by altering the functions of essential genes (Kaito C et al. 2020).

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