**1.5. Description of the MRB**

*P. aeruginosa* (Pa) has a predilection for humid environments and usually contaminates aqueous solutions such as disinfectants or soaps, mechanical ventilation equipment, fiberoptic bronchoscopes, and so on. Resistance may appear in the course of an antibiotic treatment. Its main mechanism of resistance is the presence of extended-spectrum beta-lactamases (ESBL) and alterations in permeability (porin mutations and expulsion pumps).

*Acinetobacter baumannii* (Ab) contaminates and endemically colonizes the hospital environment. It is capable of surviving and rapidly developing resistance to the main classes of antibiotics, more frequently in summer [7]. Some strains can survive to environmental drying form months, which facilitates transmission via contamination of fómites in the hospital. The health personnel is usually carrier of Gram-negative bacilli (GNB) (30%). Outbreaks have been described in relation to contaminated mechanical ventilation equipment and manual transmission. Infections have also been described in war wounds and in situations of natural disasters. Sixty-three percent of bacterial isolation from war wounds in Iraq and Afghanistan corresponded to this germ [8]. Infections tend to appear in patients with long stay in the ICU and health centers, dependent on mechanical ventilation, central catheter carriers, and with prior treatment with third-generation cephalosporins, fluorquinolones or carbapenemes. Although patients with Ab infection have high mortality, it is not clear whether mortality can be attributed to infection or to life-threatening conditions [9]. Several factors are associated with mortality: isolation in blood cultures, presence of signs of sepsis/septic shock, resistance to imipenem, longer stay in ICU, pneumonia and diabetes mellitus [10]. Cases of community acquisition have been described in situations of chronic obstructive pulmonary disease (COPD), diabetes, alcoholism and cancer [11]. It has great capacity to acquire and accumulate resistance genes from other GNB via plasmids/transposons, with low permeability for many antibiotics, constitutive ejection pumps, production of beta-lactamases and so on.

**1.9. Exogenous-endogenous infections in the ICU**

prevented with hygienic measures.

antibiotics);

Infections can be classified according to origin and carrier status:

ICU. It constitutes 10–15% of the infections acquired in critical care.

infection. They represent 35–40% of infections acquired in critical care.

**1.10. Mechanisms of appearance and extension of resistance**

Some measures aimed at a rational use of antibiotics are the following:

ment educational programs to improve the use of antibiotics;

While some measures of patient-patient transmission control are:

• Exogenous: nonpreceded by digestive colonization. The infective flora is endemic to the

Current Status of Colonization and Infection by Multiresistant Bacteria in the Spanish Intensive…

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• Endogenous: preceded by colonization of the digestive system by potentially pathogenic germs (PPG). It is endogenous primary if the patient already has them at the time of admission. It is usually precocious and represents 50% of registered infections. The endogenous secondary is caused by germs acquired in the ICU and colonizes the patient before causing the

The multimodal prevention of nosocomial pneumonia is based on these concepts. Primary endogenous pneumonias can be prevented with a short course of antibiotics such as cefotaxima that eliminates the colonizing germs of the oropharynx and upper respiratory tract of the carriers. Endogenous pneumonia is treated with the prevention of the carrier state with enteral antibiotics (PPG will not be able to adhere the coated mucosa of antibiotics). Exogenous pneumonia is

The main responsible for the emergence and extension of resistance are the indiscriminate use of antibiotics and the transmission of resistant microorganism between humans (or between human and environment). The antibiotics exert a selective ecological pressure on the bacteria, thus promoting the appearance of resistance germs. Inadequate practices of prevention of the infection along with inadequate hygienic measures will favor the extension of the bacteria. The strategies to avoid these phenomena are aimed at a better use of antibiotics (reducing the selective pressure) and optimizing the infection control measures (reducing the colonization pressure) [13, 14].

• Evaluation committees: formed by clinicians, pharmacists and microbiologists; pursue the effective and safe use of antimicrobials, evaluate and guide decision making; and imple-

• implementation of clinical guidelines and protocols to promote the proper use of antibiotics; • to use a form with pre-authorization for broad-spectrum antibiotics (non-specific restriction);

• personalized audit (mandatory consultation with infectious disease specialists to improve the appropriateness of antibiotic therapy and to reduce the use of broad spectrum

• to use predictive scores for MRB infections can be useful to minimize both the time to initiate appropriate antibiotic treatment and the unnecessary use of broad spectrum antibiotics.

• preferred use of limited spectrum antibiotics (first-generation cephalosporin);

*Klebsiella pneumoniae* (Kp) contaminates the medical material although its main reservoir is the digestive tract and the hands of the health care personnel from where it can give rise to epidemic outbreaks. Its main mechanism of resistance is the production of beta-lactamases. The genes that encode them are transmitted by plasmids, which contribute to their rapid diffusion among other GNB.

MRSA shows resistance to methicillin by means of a protein encoded in the mecA gene and transported in the chromosomal cassette SCCmec. The frequent use of vancomycin has led to the emergence of strains with intermediate or complete resistance to vancomycin by acquisition of the gene through a plasmid. They currently constitute up to 50% of Staphylococcus infections.

### **1.6. Factors that predispose to infections by MRB**

Certain elements as advanced age, functional dependence, cognitive deterioration and comorbidities, prolonged hospital stays, contact with personnel sanitary, intravascular catheters, bladder catheterization, previous antibiotic treatment, and so on, contribute to an increased selective pressure (leading to the emergence of MRB) and increased colonization pressure (through an ineffective environmental containment) [11].
