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

resistance genes from other GNB via plasmids/transposons, with low permeability for many

*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

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.

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

The prognosis of MRB infections is not good, with an increase in hospital stay, mortality and economic costs [12]. These types of infections are usually resistant to empirical therapies, which implies a delay in starting the correct antibiotic treatment. Also derived from this, the use of second line treatment with lower bactericidal capacity and less favorable pharmodynamic/pharmacokinetic profile contributes to a higher incidence of adverse events. At times,

The difference between these two terms lies in the simple presence (colonization) or clinical involvement (infection). The oropharynx is colonized early by hospital flora, especially GNB, in critically ill patients. The risk of colonization increases with hospital stay and severity. In the same way, the administration of antibiotics systemically increases the risk of acquiring the carrier state. Patients with APACHE II greater than 20 are usually carriers of abnormal flora such as GNB and MRSA. The passage from colonization to infective germs is defined by the rupture of the natural defense mechanisms (neutropenia, immunosuppression), the pathogenicity of the germ itself, alteration of the intestinal flora by antibiotic therapy previously administered. Altered mechanisms of clearance of germs are suggested. A necessary factor for the development of the infection is the overgrowth; 20–40% of carrier patients develop an infection, so those carriers must be actively identified when we want to control an outbreak

antibiotics, constitutive ejection pumps, production of beta-lactamases and so on.

among other GNB.

40 Current Topics in Intensive Care Medicine

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

(through an ineffective environmental containment) [11].

a greater virulence of these germs has been described.

**1.7. Consequences of infection by MRB**

**1.8. Colonization and infection**

of infection by resistant flora.

Infections can be classified according to origin and carrier status:


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 prevented with hygienic measures.
