**3.** *E. coli* **antibiotic resistance**

A mature human gut harbors a vast number of bacterial resident microbiota, accounting for more than 1014 individual bacteria. Notably, the composition of the microbiota is individual host specific and the type of species living in the gastrointestinal tract varies with the host age, diet, habits, health, and idiosyncratic status [22]. The intestinal mucosa is a first contact between the immune system and the external environment and plays a central role in a microbe and host cross talk [23]. The indigenous intestinal microbiota provides important protective, metabolic and trophic functions, principally offering resistance to colonization by exogenous microorganisms, and preventing invasion by incoming pathogens.

resistance trends continue, high societal and economic costs can be expected and that better

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

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

105

Work with neonates in a single center concluded that the use of minor antibiotic therapy with reducing preemptive treatment resulted in a moderate reduction of the antibiotic use and did

Another study [36] was conducted to determine the antimicrobial susceptibility patterns among common pathogens in the intensive care unit of a university hospital in Iran between 2006 and 2009. Authors worked with 606 isolates from respiratory, urine, blood, and wound specimens of 456 patients. *E. coli* was present in 8.3% of isolates, and presented high

Scientists worked with 1163 clinical isolates in Taiwan [37]. The frequencies of Gram-positive and Gram-negative bacteria isolates were 30.4 and 56.2%, respectively. *Staphylococcus aureus* was the most common isolate among the Gram-positive organisms, while *Pseudomonas aerugi-*

The antimicrobial resistance in one intensive care unit in Canada was investigated. In 2008, it was found high antibiotic rates to *E. coli*: cefazolin, 20.1%; cefepime, 0.7%; ceftriaxone, 3.7%; gentamicin, 3.0%; fluoroquinolones, 21.1%; piperacillin-tazobactam, 1.9%; and trimethoprimsulfamethoxazole, 24.8%. *E. coli* was the most prevalent Gram-negative bacterium [38].

According to a work conducted in 1975 [39], a hospital acquired urinary tract infection account for approximately 45% of nosocomial infection and 2–4% of the cases may develop septicemia. In this context, it was observed that 40% of the Gram-negative septicemia acquired in hospital originates in the urinary tract. This observation can enhance the *E. coli* importance for acquiring resistance. In 2009 was observed that, Gram-negative bacteria were the most frequent isolates, with *E. coli* being the most common followed by *Pseudomonas aeruginosa* and *Klebsiella* spp. *Candida albicans* accounted for almost 11% of the organisms, followed by

N (%) N (%) N (%)

*nosa, E. coli*, and *Klebsiella pneumoniae* were the leading Gram-negative isolates.

**Bacteria and fungi Total Resistance to all Sensibility**

*Escherichia coli* 27 (49.1) 22 (81.5) 5 (18.5) *Pseudomonas aeruginosa* 7 (12.7) 5 (71.4) 2 (28.6) *Klebsiella* spp. 7 (12.7) 4 (57.1) 3 (42.9) *Candida albicans* 6 (10.9) – – *Acinetobacter baumanni* 3 (5.5) 3 (100) 0 Others 5 (9.1) 2 (40) 3 (60) Total 55 (100) 36 (73.5) 13 (26.5)

**Table 2.** Profile resistance of main microorganisms isolated from hospitals.

management of infections caused by resistant *E. coli* is becoming essential.

not increase mortality [35].

antimicrobial resistance.

*Acinetobacter baumanni* (**Table 2**) [39].

Note: Ref. [39] with modifications.

The intestinal epithelium can resist against microbial invasion, but through evolution mechanisms, potential pathogenic enteric microorganisms developed strategies to circumvent and subvert this strong barrier. As an initial step in the infection process, some pathogens target specific epithelial cell structures, as glycoprotein and glycolipid [24], which act as receptors for attachment, permitting the microorganisms to exploit the underlying signal transduction pathway.

Other strategies utilized by invasive pathogens such as *Salmonella enterica* serovar, *S. thyphimurium, Shigella* spp., and invasive *E. coli* orchestrated their entry into intestinal epithelial cells. This strategy uses the expression of a bacterial type III protein secretion system, to deliver various effectors proteins into the host cell [25]. This effectors protein subverts normal host cell processes by triggering a marked rearrangement of the host cytoskeleton. This procedure facilitates the pathogen to cross the epithelial barrier and induces an inflammatory host response [25].

The latter strategy can be done by direct cytotoxic injury, intracellular migration, disruption of the epithelial tight junctions, or indirectly by inducing neutrophil infiltration. Pathogenic *E. coli* have been shown to increase chloride ion secretion from intestinal epithelia by upregulating the expression of the receptor for the neuropeptide galanin-1 [26].

Enteric pathogens have the propriety to perturb the intestinal epithelial barrier and impact paracellular permeability, most often with an alteration in the arrangement of tight junctional component proteins by mechanisms that are unique for different pathogens. With respect to enteropathogenic *E. coli*, they disrupt the epithelial barrier by the phosphorylation of myosin light chains [27].

*E. coli* isolated from human and animal gut, and as well as from environmental sources presenting antibiotic resistance is a public health problem, especially in developing countries [28]. Work conducted in 2005 [29] showed that extended spectrum lactamase producing *E. coli* (ESBL) strains have spread as a hospital infection. The large plasmid genes coding this resistance also carry genes for resistance to other antibiotics [30]. The frequency of resistance to fluoroquinolone antibiotics (ciprofloxacin, levofloxacin, moxifloxacin, norfloxacin, and nalidixic acid) in *E. coli* has increased worldwide [31].

In one review about *E. coli* producing fimbrial or afimbrial adhesins [32], authors showed that some *E. coli* strains (ETEC STb positive) associated with diarrhea, presented an afimbrial adhesin, named AIDA-I (adhesion involved in diffuse adherence). This adhesin originally found in human *E. coli* isolates showed that the establishment of a persistent and chronic infection could also help the microorganism to resist antimicrobial agents and prevent effective treatment of diseased animals.

In 2010, some authors [33] detected high resistance rates among *E. coli* (up to 30%) to ampicillin, tetracycline, streptomycin, ciprofloxacin, enrofloxacin, and cotrimoxazol. These authors [33] also found lower resistance to gentamicin (6.5%) and chloramphenicol (3.2%).

Also in 2010, one study [34] reported that morbidity and mortality attributable to third -generation-cephalosporin-resistant *E. coli* are significant. They also believe that if prevailing resistance trends continue, high societal and economic costs can be expected and that better management of infections caused by resistant *E. coli* is becoming essential.

microbe and host cross talk [23]. The indigenous intestinal microbiota provides important protective, metabolic and trophic functions, principally offering resistance to colonization by

The intestinal epithelium can resist against microbial invasion, but through evolution mechanisms, potential pathogenic enteric microorganisms developed strategies to circumvent and subvert this strong barrier. As an initial step in the infection process, some pathogens target specific epithelial cell structures, as glycoprotein and glycolipid [24], which act as receptors for attachment, permitting the microorganisms to exploit the underlying signal transduction pathway.

Other strategies utilized by invasive pathogens such as *Salmonella enterica* serovar, *S. thyphimurium, Shigella* spp., and invasive *E. coli* orchestrated their entry into intestinal epithelial cells. This strategy uses the expression of a bacterial type III protein secretion system, to deliver various effectors proteins into the host cell [25]. This effectors protein subverts normal host cell processes by triggering a marked rearrangement of the host cytoskeleton. This procedure facilitates the pathogen to cross the epithelial barrier and induces an inflammatory host response [25]. The latter strategy can be done by direct cytotoxic injury, intracellular migration, disruption of the epithelial tight junctions, or indirectly by inducing neutrophil infiltration. Pathogenic *E. coli* have been shown to increase chloride ion secretion from intestinal epithelia by upregu-

Enteric pathogens have the propriety to perturb the intestinal epithelial barrier and impact paracellular permeability, most often with an alteration in the arrangement of tight junctional component proteins by mechanisms that are unique for different pathogens. With respect to enteropathogenic *E. coli*, they disrupt the epithelial barrier by the phosphorylation of myosin light chains [27]. *E. coli* isolated from human and animal gut, and as well as from environmental sources presenting antibiotic resistance is a public health problem, especially in developing countries [28]. Work conducted in 2005 [29] showed that extended spectrum lactamase producing *E. coli* (ESBL) strains have spread as a hospital infection. The large plasmid genes coding this resistance also carry genes for resistance to other antibiotics [30]. The frequency of resistance to fluoroquinolone antibiotics (ciprofloxacin, levofloxacin, moxifloxacin, norfloxacin, and nali-

In one review about *E. coli* producing fimbrial or afimbrial adhesins [32], authors showed that some *E. coli* strains (ETEC STb positive) associated with diarrhea, presented an afimbrial adhesin, named AIDA-I (adhesion involved in diffuse adherence). This adhesin originally found in human *E. coli* isolates showed that the establishment of a persistent and chronic infection could also help the microorganism to resist antimicrobial agents and prevent effec-

In 2010, some authors [33] detected high resistance rates among *E. coli* (up to 30%) to ampicillin, tetracycline, streptomycin, ciprofloxacin, enrofloxacin, and cotrimoxazol. These authors

Also in 2010, one study [34] reported that morbidity and mortality attributable to third -generation-cephalosporin-resistant *E. coli* are significant. They also believe that if prevailing

[33] also found lower resistance to gentamicin (6.5%) and chloramphenicol (3.2%).

exogenous microorganisms, and preventing invasion by incoming pathogens.

104 *Escherichia coli* Escherichia coli - Recent Advances on Physiology, Pathogenesis and Biotechnological Applications - Recent Advances on Physiology, Pathogenesis and Biotechnological Applications

lating the expression of the receptor for the neuropeptide galanin-1 [26].

dixic acid) in *E. coli* has increased worldwide [31].

tive treatment of diseased animals.

Work with neonates in a single center concluded that the use of minor antibiotic therapy with reducing preemptive treatment resulted in a moderate reduction of the antibiotic use and did not increase mortality [35].

Another study [36] was conducted to determine the antimicrobial susceptibility patterns among common pathogens in the intensive care unit of a university hospital in Iran between 2006 and 2009. Authors worked with 606 isolates from respiratory, urine, blood, and wound specimens of 456 patients. *E. coli* was present in 8.3% of isolates, and presented high antimicrobial resistance.

Scientists worked with 1163 clinical isolates in Taiwan [37]. The frequencies of Gram-positive and Gram-negative bacteria isolates were 30.4 and 56.2%, respectively. *Staphylococcus aureus* was the most common isolate among the Gram-positive organisms, while *Pseudomonas aeruginosa, E. coli*, and *Klebsiella pneumoniae* were the leading Gram-negative isolates.

The antimicrobial resistance in one intensive care unit in Canada was investigated. In 2008, it was found high antibiotic rates to *E. coli*: cefazolin, 20.1%; cefepime, 0.7%; ceftriaxone, 3.7%; gentamicin, 3.0%; fluoroquinolones, 21.1%; piperacillin-tazobactam, 1.9%; and trimethoprimsulfamethoxazole, 24.8%. *E. coli* was the most prevalent Gram-negative bacterium [38].

According to a work conducted in 1975 [39], a hospital acquired urinary tract infection account for approximately 45% of nosocomial infection and 2–4% of the cases may develop septicemia. In this context, it was observed that 40% of the Gram-negative septicemia acquired in hospital originates in the urinary tract. This observation can enhance the *E. coli* importance for acquiring resistance. In 2009 was observed that, Gram-negative bacteria were the most frequent isolates, with *E. coli* being the most common followed by *Pseudomonas aeruginosa* and *Klebsiella* spp. *Candida albicans* accounted for almost 11% of the organisms, followed by *Acinetobacter baumanni* (**Table 2**) [39].


**Table 2.** Profile resistance of main microorganisms isolated from hospitals.
