**4. Mechanisms of antibiotic resistance in Gram-negative bacteria**

**5. Diarrheagenic and extra intestinal** *E. coli* **pathotypes**

logical features of the disease they cause [44].

**Pathotype Common genotype Most common** 

EPEC eae +, bfp +, EAF + Non-specific

ETEC LT, ST, (STa, STb

toxins)

EHEC eae +, stx + Bloody diarrhea

EAEC AA +, aaa −/aaa + Persistent diarrhea

A-EPEC eae +, bfp (−/+), EAF − Nonspecific

**Table 3.** Key virulence determinants of diarrheagenic *E. coli*.

Note: Ref. [44] with modifications.

EIEC Inv Bacillary dysentery Inflammation and

Several distinct pathogenic categories (i.e., pathotypes or virotypes) of diarrheagenic *E. coli* strains are recognized. Each pathotype is defined by a characteristic set of virulence-associated determinants that act in a concert to determine the clinical, pathological, and epidemio-

Antibiotic Resistance among *Escherichia coli*: Isolates and Novel Approaches to the Control of *E. coli* Infections

By definition, the virulence determinants of each *E. coli* pathotype are distinct. However, they can generally be categorized as either colonization factors (adhesins), which enable the bacteria to bind closely to the intestinal mucosa and resist removal by peristalsis, or secreted toxins, which interfere with the normal physiological processes of host cells. The key virulence determinants of the primary pathotypes of diarrheagenic *E. coli* are summarized in **Table 3**.

**Intestinal pathology Susceptibile groups**

Children under 2 years of age in developing countries

http://dx.doi.org/10.5772/67400

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Children in developing countries;

Children and the elderly in industrialized countries

All ages; more common in lessdeveloped countries

Children in lessdeveloped countries; travelers to those countries

Children and adults; reservoir for human

infection

travelers

Intimate adhesion, attaching–effacing lesions throughout the intestine, loss of brush border enterocyte

No notable change, adhesion to small intestinal mucosa

attaching–effacing lesions confined to the large intestine; necrosis in severe cases; HUS, hemorrhagic colitis

disruption of the mucosa, mostly of the large intestine; necrosis and blood

cytotoxic changes in enterocytes

Some lesions throughout the intestine; toxin production as EAST1

loss

**presentation**

gastroenteritis, noninflammatory diarrhea

Watery, choleralike diarrhea, noninflammatory diarrhea

'Hemorrhagic colitis';

Inflammation;

gastroenteritis

Bacterial antimicrobial resistance in both the medical and agricultural fields has become a serious problem worldwide. Resistant bacteria isolated from agriculture, farm or hospital can transfer the resistance genes to human pathogens [40]. The selection pressure applied by the antibiotics that are used in clinical and agricultural settings has promoted the evolution and spread of genes that confer resistance, regardless of their origins. Several factors can be implicated with resistance, sensibility, and antibiotic resistance dissemination such as: (i) impermeable barriers [6]; in this case, some bacteria are intrinsically resistant to certain antibiotics because they have an impermeable membrane or lack the target of the antibiotic; (ii) multidrug resistance efflux pumps; these pumps protect the bacterial cell against toxic molecules. It is an active transport mechanism for outside the cell. Some transporters, such as those of the resistance-nodulation cell division family, can pump antibiotics directly outside the cell, whereas others, such as those of the major facilitator superfamily, secrete them into the bacterial periplasm; (iii) resistance mutations; these mutations can cause a modification in the target protein, for example, by disabling the antibiotic-binding without changing the protein functionality. Specific examples include mutations in the gyrase, which cause resistance to fluoroquinolones, in RNA polymerase subunit B, which cause resistance to rifampicin, and in the 30S ribosomal subunit protein S12 (encoded by *rpsL*), which cause resistance to streptomycin; and (iv) antibiotic inactivation; inactivation can occur by covalent modification of the antibiotic, such as that catalyzed by acetyltransferases acting on aminoglycoside antibiotics, or by degradation of the antibiotic, such as the hydrolytic degradation of the β-lactam ring on antibiotics by the β-lactamases. The emergence of drug resistance among diarrheagenic *E. coli* is important, and in infant, is a cause of morbidity and mortality principally in developing countries. Analyzing stools of infants in India was verified that about 90% of *E. coli* strains presented resistance to the most antibiotics tested [41]. All isolates were resistant to ampicillin, imipenem, cotrimoxazole, and sensitive to amikacin, and presented 29 different antibiotic profiles. Most of the isolated *E. coli* harbored plasmids (64%) and up to 76% could transfer their plasmids. The transconjugant strains were carrying plasmids and presented resistance to ampicillin, imipenem, and cotrimoxazole. The authors found an increase in the prevalence of drug resistance among *E. coli* isolates, and conjugation transfer of plasmids contributed to a rapid spread of an antibiotic resistance.

Cyclomodulins are a growing functional family of toxins, which hijack eukaryotic cell cycle. Four cyclomodulin types are actually known in *E. coli*: cytotoxic necrotizing factors (CNFs), cycle inhibiting factor (Cif), cytolethal distending toxins (CDTs), and the pks-encoded toxin.

One interesting work [42] isolated ceftriaxone-resistant *E. coli* from 1.5% of participants in Maryland and Michigan, United States. One *E. coli* isolate collected from an apparently healthy person, presented resistance to eight antibiotics, and the resistance genes were contained on an incompatibility plasmid. These plasmid types are common among *Enterobacteriaceae* and can carry multiple resistance genes, generating multidrug resistance [43]. In Krueger's work [42], the source of the extensively resistant *E. coli* is not known, but the isolated strain may have been acquired from food.
