Infection with E. coli

Colon bacillus – is considered a typical species of bacteria from the Enterobacteriaceae family (intestinal bacilli). It is the dominant bacterium in the aerobic flora of the healthy human and mammalian colon. As a commensal, it breaks down food debris digested in the higher parts of the digestive tract. E. coli inhabits the gastrointestinal tract of the newborn and constitutes a protective barrier against it being occupied by other species of bacteria that could become a factor in diarrheal diseases.

Types of E. coli infections

Pathogenic properties – E. coli strains with normal intestinal flora are not pathogenic to the host as long as they are within the large intestine.

1. In opportunistic infectionswhich arise under conditions of weakening of the host’s natural immunity are the most frequently detected Gram-negative bacteria. They occur as a factor of bacteremia, blood-borne abscesses, sepsis, even endotoxic shock due to the massive release of the LPS (endotoxin) complex from damaged bacterial cells. They are responsible for causing inflammation in a variety of systems, including wound infections, pneumonia and meningitis, and are the most common cause of residential or hospital-acquired urinary tract infections.

In nosocomial infections (data from 15 countries excluding Poland) E. coli infection ranks third among 15 microorganisms occurring as a factor of nosocomial infections in total and fifth among 16 microorganisms isolated from blood. Based on data from the European Antibiotic Resistance Surveillance System (EARSS) network, the share of blood-isolated E. coli strains resistant to aminopenicillins, fluoroquinolones, third-generation cephalosporins and aminoglycosides increases every year in most countries.

2. Pathogenic varieties of E. coli are equipped with various factors that determine their pathogenic properties. This mainly applies to E. coli strains found in the large intestine. Under appropriate conditions, they can obtain plasmid or chromosomal DNA by recombination or transduction as genetic equipment that determines the pathogenic properties of the strain for humans and animals:

  1. UPEC
  2. NPEC
  3. Diarrhea
  4. EPEC
  5. ETEC

Types of enterotoxins

1. Heat sensitive enterotoxin (LT), biochemically similar to the cholera toxin (CT), exists in two antigenic forms: LT I and LT II. Both of these toxins cause diarrhea without damaging the intestinal epithelial cells – they are inactivated at 60 ° C after 30 minutes of heating. They stimulate the activity of adenylate cyclase, causing active secretion of water by enterocytes into the intestinal lumen.

2. Enterotoxin – warmth (ST) It comes in two forms: ST I and ST II and is not inactivated by heating it to 100 ° C (boiling the infected product). ST I stimulates the activity of guanylate cyclase (cGMP which inhibits Na + absorption and stimulates the secretion of Cl–).

• EHEC (enterohaemorrhagic), enterohemorrhagic E. coli, recently referred to as E. coli (STEC / VTEC), produces a cytotoxin: VTEC because their activity was assayed on Vero lineage, green monkey kidney (rognon) cells, or STEC because it is chemically similar to the so-called the neurotoxin of S. dysenteriae, also known as the Shiga ST toxin. They are heat labile proteins capable of forming pores in the walls of enterocytes.

They belong to the AB toxins, like dysentery toxin, some call them SLT-Shiga-like toxins. The receptor for them is the membrane glycolipid found in the cells of the epithelium of the small intestine. There are two antigenic variants SLTI (VTI) and SLTII (VTII), and the responsible genetic elements are carried by bacteriophages – coliphages.

In addition, in veterinary microbiology, strains of E. coli producing:

  1. necrotic toxins CNF-1 and CNF-2,
  2. cytotoxic factors,
  3. necrotic factors,
  4. degenerative enterocytes of calves and piglets and neurotoxins – heat-labile proteins acting on the intestinal nervous system that release messengers that stimulate the muscles of the gut (diarrhea).

E. coli endotoxin – it is a LPS protein-lipid-polysaccharide complex, released from the disintegrating cells of all gram-negative bacteria, including all strains of E. coli. Once it enters the bloodstream, it may cause a sudden onset of septic shock.

E. coli infection – research

Further strains of E. coli causing intestinal inflammation were identified using biological tests:

  1. EAEC (enteroagregative) E. coli, synthesizes EAST1 toxin (sta A);
  2. NTEC (necrotic) of E. coli, synthesize CNF2 toxin (cnf 2);
  3. EIEC (enteroinvasive) E. coli was detected using the Shigella bioassay described by Sereny as keratoconjunctivitis shigellosa. It demonstrated the ability of bacteria to form ulcerations in conjunctivally infected guinea pigs. It was the equivalent of an invasion into the interior of enterocytes (intestinal epithelial cells). The test used for the detection of virulent Shigella colonies has proved useful in demonstrating the presence of enteroinvasive E. coli (EIEC) strains. It has been proven that the invasive E. coli 0124 serotype (serologically identical to Shigella dysenteriae 3) in 1983 caused a widespread epidemic of red-like diseases developed by employees of the WSSE in Olsztyn.

Dairy products were the carrier of the infection. Molecular genetic research became the basis for the detection of E. coli strains and their pathogenicity related to the presence of genes responsible for the virulence of a bacterial strain isolated from epidemics or food. The following are used: molecular probes and DNA hybridization techniques to identify markers of genes responsible for the synthesis in a bacterial cell of elements determining its virulence, located on plasmids or in chromosomes.

In the study of food contamination, the following are used as a universal genetic determinant for the diagnosis of E. coli (pathogenic and non-pathogenic):

  1. the universal stress protein (uspA) gene;
  2. the gene encoding maleic acid (mdh).

By the PCR method in specialized laboratories the genes of the strains are identified:

• ETEC: factor in piglet diarrhea and diarrheal diseases such as diarrhea in Mexico, the so-called revenge of Moctezumi, and others. These are:

– elt I – LTI heat labile enterotoxin gene;

– est I – STI heat-stable enterotoxin gene;

– est II gene of the heat-stable enterotoxin STII.

• Piglet edema disease and weaning colibacillosis, caused by grafts equipped with:

— fibrie F15- fed A;

– producing a variant of the shiga toxin Stx2e (slt2v).

• Infant diarrhea caused by intimine-producing EPEC strains having a corresponding gene designated (eae A).

The distinguished pathogenic varieties (virotypes) for humans and animals are presented in Table 42.13.

Pathogenesis of E. coli infection

• Parenteral E. coli infections – infection is most often endogenous

– spreading through continuity: E. coli travels ascendingly – in the urinary system from the urethra to the bladder, ureters, renal pelvis, and in the digestive tract in the case of injuries or obstruction from the large intestine through the Bauhin valve to the small intestine;

– blood derivatives: E. coli from the large intestine pass into the blood, causing infection of various systems and organs (opportunistic infection).

• E. coli fecal-oral infections – contact, often associated with primitive sanitation, carried by dirty hands, including in care facilities.

• Digestive E. coli infection with colon It is spread through food or water contaminated with faeces from humans or animals. The hatching period depends on the infectious dose and the individual sensitivity of the infected person. Products of animal origin (meat, milk, cheese), vegetables and fruits washed or sprinkled with contaminated faeces, products eaten raw: lettuce, sprouts, spices can be infected. The infectious dose can vary in size and depends, inter alia, on from the virulence of the strain.

Mechanism of E. coli infection

  1. Colonization of the stomach and intestines (gastroenterocolitis); adherence of bacteria to enterocytes and destruction of their internal structures (EPEC), damage to microvilli, loss of the brush border, loss of digestive and absorbent surfaces, destruction of mucus and induction of local inflammatory reaction.
  2. Colonization and production of enterotoxins (gastroenterocolitis) EHEC, ETEC, EAggEC.
  3. The invasion of the colon epithelial cells and the submucosa tissue causes inflammation and ulceration (colitis) – EIEC.

Source: J. Cianciara, J. Juszczyk, Infectious and parasitic diseases; Czelej Publishing House

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