*2.6.1 Clinical presentation*

*Advanced Concepts in Endocarditis - 2021*

*2.4.2 Remote origin*

**2.5 Microbiology**

cycle and thus the infection is dispersed.

associated with higher in-hospital mortality.

mia is due to *Staphylococcus aureus* (35–45%) [6].

proposed to increase sensitivity in diagnosis [19].

infected, whatever the mechanism that caused the erosion.

by removing unnecessary intravascular and urinary catheters.

resorption phases of hematomas, from the pacemaker pocket.

• *Dispersion.* In the last step, some cells of the mature biofilm begin to dissociate and disperse again through the environment as planktonic cells to start a new

During the early post-implant period, damage to the vascular wall and the formation of hematomas can favor the settlement of germs from the bloodstream in the implant area; thus, it is very important to avoid the development of bacteremia

The infection can spread to the endovascular structures, during the healing and

Conversely, and generally later, endovascular elements (electrodes) can present

As previously mentioned, between 40 and 50% of patients with CIED have a history of admission, manipulation or invasive procedure in the previous 6 months, potentially responsible for bacteremia. The risk is especially high when the bactere-

In any case, given that many "presumed local" infections can progress to the intravascular components of the device and vice versa, the barrier between local and endovascular infection can be difficult to establish. Once the generator or proximal leads have eroded through the skin, a device should be considered

Gram-positive bacteria are responsible for the vast majority of CIED infections (68–93%). Staphylococci, account for 60–80% of cases. Depending on the series, there is a predominance of infections caused by S Aureus or coagulase-negative staphylococcus (CoNS), although with few differences in their prevalence. Among the CoNS, *Staphylococcus epidermidis* and Staphylococcus Saprophyticus stand out. Methicillin resistance (MR) among Staphylococci varies among studies A high rate of MR in CoNS is associated with a healthcare environment source, reaching 50% in some series. For S aureus the rates of MR range between 2.6% (Germany) and 55% (USA). Gram-negative bacteria (GNB) are also identified in a percentage close to 15%. The higher proportion of GNB may be due to the large rate of different comorbidities, which is associated to more frequent invasive diagnosis or treatment measures. Polymicrobial infection sometimes involves more than one species of CoNS, (2–24% according to series). In a percentage between 8 and 15%, it was not possible to cultivate the responsible germ. Cases related to fungi are anecdotal [5, 6, 17–19].

The diagnosis of IE-CEID, as in valve prostheses, is inconclusive in up to 30% of cases, according to the Duke criteria [20]. For this reason, in the guidelines published by the European Society of Cardiology in 2015, three additional criteria were

fibrin and platelet deposits on erosions produced by friction, deterioration or turbulent flows, on which bacterial colonies can settle and proliferate in a process similar to that of endocarditis, which can also spread to the adjacent endocardium. Concomitant valve involvement is estimated in about 37.2% of cases, most frequently tricuspid valve [11], aortic or mitral valve vegetations are present in 10–15% of patients with CIED endocarditis and valve involvement in CIED infection is

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**2.6 Diagnosis**

The clinical manifestations of IE-CIED can be variable, since it can combine signs and symptoms of local infection, with symptoms and signs of systemic infection.

When there is involvement of the pacemaker pocket, diagnosis can be easier since there will be typical signs of inflammation, such as pain, redness and increased temperature in the implantation area. In addition, there may be an increase in size, either due to the presence of hematoma related to the implant (which should alert to an increased risk of infection) or fluctuation due to the formation of pus, adhesion of the skin as well as spontaneous and sometimes intermittent pus drainage due to dehiscence of the suture or fistulization of the skin (**Figure 2**).

Any exteriorized device should be considered infected (although initial exteriorization was related to aseptic necrosis of the skin due to tension of the device in a small pocket).

Once the pocket is infected, the electrodes are frequently affected in its subcutaneous and extravascular portion, and affect the intravascular portion as well. When there is involvement of the intravascular components, that is, endocarditis of the leads and vascular part of the system, signs and symptoms of systemic infection will appear, with fever, chills, asthenia and anorexia. These data can appear larvae and in the absence of associated involvement of the pacemaker pocket, they can be more difficult to interpret. In a low percentage of patients, signs and symptom of frank sepsis will appear. In case of associated valvular involvement, data of valvular dysfunction and heart failure may also appear.

Clinical manifestations related to septic lung embolism may also appear from vegetations of the PM leads or tricuspid valve.

Among laboratory results data, the acute phase reactants (C-reactive protein, increased sedimentation rate, leukocytosis and procalcitonin) increase. Although these alterations point us towards a systemic infection, acute phase reactants can also appear in local infections.

Regarding the chronology of infections, several aspects must be taken into account:


**Figure 2.** *Exteriorized device.*

the progression to systemic disease faster than in the case of germs such as S Epidermidis or *Propionibacterium acnes*, in which it can be latent and even reactivate late with delayed handling.
