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Pneumonia
Figure 1: Evolution of the Potentially Pathogenic Micro-organisms Present in the Oropharyngeal Flora
Related to the Co-morbidity, Antibiotic Treatment and Colonisation Pressure
1 2 3 4
Acute (3–5 days) or
Idem + antibiotic
chronic co-morbidity,
Idem + antibiotic
Normal
treatment or ICU
including advanced
treatment for
person
admission/tracheal
age with functional
3–5 days
intubation for
incapacity
>7–10 days
S. pneumoniae
Enterobacteria-
S. pneumoniae* H. influenzae
producing ESBL**
N. meningitidis* Enterobacterias
P. aeruginosa
Idem + non-fermenting
S. pyogenes* Methicillin-susceptible
Methicillin-resistant
MR GNB***
S. aureus
S. aureus
Candida spp.
ESBL = extended-spectrum β-lactams; GNB = Gram-negative bacilli; ICU = intensive care unit; MR = multiresistent; *Transitorily present in healthy carriers; **Producers of ESBL or with type
ampC chromosomal β-lactamases; ***P. aeruginosa, Stenotrophomonas spp., Acinetobacter spp., Burkholderia spp.
Figure 2: Empirical Antibiotic Treatment Schedules for Figure 3: Empirical Antibiotic Treatment Schedules of
Ventilator-assisted Pneumonia Indicated in Patients Ventilator-assisted Pneumonia Indicated in Settings of
without Risk Factors for Infection by P. aeruginosa Risk of Infection by P. aeruginosa or by Micro-organisms
with Resistance to the Most Common Antibiotics
None (previously
Acute (3–5 days) or chronic
Risk factors
healthy person)
co-morbidity, including advanced Acute (5 days) or chronic Idem + antiobiotic treatment
age with functional incapacity
Risk factors
co-morbidity + antibiotic or ICU admission/tracheal
treatment for 5 days intubation for >7–10 days
Micro-organisms
most probably
Micro-organisms
causing
S. pneumoniae
most probably
pneumonia
S. pneumoniae
H. influenzae
causing
Enterobacteria-producing ESBL
Enterobacterias
pneumonia
P. aeruginosa
Idem + non-fermenting
Methicillin-susceptible Methicillin-resistant S. aureus
MR GNB*
S .aureus
Antibiotic Monotherapy with a third-generation cephalosporin
β-lactam active against P. aeruginosa**
treatment (ceftriaxona or cefotaxima), ertapenem or amoxicillin–clavulanic
Antibiotic
±
schedules or with a fluorquinolone (levofloxacin or moxifloxacin)
treatment
amikacin, ciprofloxacin or levofloxacin***
schedules
±
linezolid or a glycopeptide
Empirical Antibiotic Treatment
ESBL = extended-spectrum β-lactams; GNB = Gram-negative bacilli; ICU = intensive care unit;
for Hospital-acquired Pneumonia MR = multiresistent; *P. aeruginosa, Stenotrophomonas spp., Acinetobacter spp.,
The choice of empirical antibiotic treatment in any infectious
Burkholderia spp.; **Piperacilin–tazobactam, meropenem, imipenem, ceftazidim or
cefepime; ***Cotrimoxazol, colymycin, phosphomicin or tigecyclin may eventually be added
disease, including VAP and ICU pneumonia, should take the according to the patterns of sensitivity of the predominant flora in the unit. Tigecyclin may be
following points into consideration:
substituted for the aminoglycoside, the fluoroquinolon, the glycopeptide and linezolid.
• the most likely aetiological micro-organisms; Generally, the micro-organisms causing VAP originate from the
• the antibiotics likely to be active against these micro-organisms; and oropharyngeal flora of the patient. The bacterial flora of the
• the pharmacokinetics/pharmacodynamics of these antibiotics. oropharynx is maintained by mechanisms responsible for colonisation
immunity. Chronic diseases
81
and acute inflammatory processes lower
The Most Likely Aetiological Micro-organisms the resistance of the oropharynx, allowing it to be colonised by Gram-
The micro-organisms isolated most frequently from the bronchial negative bacilli.
82,83
As a result, within three to five days of admission to
secretions of patients with VAP are S. aureus and P. aeruginosa, the ICU, enterobacteria can colonise the oropharynx following the
comprising around 50% of the isolates. These are followed, in order of onset of an acute inflammation. The enterobacteria originate from
frequency, by: enterobacteria (Escherichia coli, Klebsiella spp., colonic flora of the patients themselves or – to a lesser degree – via
Enterobacter spp., Citrobacter spp., Serratia spp. and Proteus spp.) the hands of their carers. Colonisation of the oropharynx by Gram-
accounting for 15%; non-fermentative Gram-negative bacilli other than negative bacilli occurs predominantly in patients with an underlying
P. aeruginosa (Acinetobacter, Stenotrophomonas and Burkholderia) in co-morbidity. Therefore, a healthy person (e.g. a carer) rarely has
10%; and Haemophilus influenzae and Streptococcus pneumoniae significant colonisation of Gram-negative bacilli in the oropharynx
in the remainder.
79-80
even after prolonged exposure in the hospital or in the ICU.
62 EUROPEAN RESPIRATORY DISEASE
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