PNEUMOCOCCAL PNEUMONIA

Pneumococus (Streptcoccus pneumoniae)

 90 serotypes
 Serotype 3 – special aggressivity

 The major pathogen in children and adults

 50% - asymptomatic carriers
 Also causes otitis media, meningitis
 !!! Pneumococcus with multiple resistance at ATB
Risk factors for pneumococcus pneumonia

 Smoking
 Alcoholism (↑ Mt if leukopenia)
 COPD
 Chronic disease
 HIV infection – x 40 greater risk
 Splenectomy
Clinical
Consolidation
 Dullness at percussion
 Elderly – frequent insidious onset –
asthenia, confusion, without fever, low   fremitus

cough, without sputum  Bronchial breath sounds

 The fastest evolution – splenectomized  Crackles – like the rain after
patients  death in 24 hours coughing

Pleural effusion
 Unique chill at onset
 Dullness at percussion
 Rust sputum
 ↓ fremitus
 Typical consolidation syndrome  Breath sounds absent
 Pleural effusion – modified clinical
 Pleural friction +/-
picture
Pneumococcal Pneumonia
Bacteriological exam
 Sputum - Gram + cocci; usually found in pairs
(diplococci); encapsulated  

 Blood cultures positive at ~ 25% (rapid positive)

 Urine antigen testing +

 in children and in adults with nonproductive cough
Treatment
As early as possible, before bacteriological results
 Goals
 Treat the infection
 Prevent and treat the complications
 Includes
 Etiological treatment – antibiotics
 Pathogenical treatment – dopamine, corticosterois, noradrenaline in
septic sock
 Supportive measures – O2 supplements, hydration
 Symptomatic treatment – antipyretic, analgesic treatment
 Prophylaxis (in  risk people) - pneumococcal vaccine (23 antigens)
Antibiotics for S pneumoniae
 Beta-lactam: penicillin G, amoxicillin, ceftriaxone
 Fluorquinolone: levofloxacin, moxifloxacin
 Carbapenem: imipenem, meropenem

 In patients who are allergic to penicilin: vancomycin, clindamycin, macrolide

 MDR SP (multidrug resistant):

 Vancomycin  rifampicin
 Lipopeptides – daptomycin
 Oxazolidindiones – linezolid
 Glycylcyclines – tigecycline
 Others beta-lactams – ceftobiprole, ceftaroline
Prognosis
 With antibiotic treatment
 Complete recovery of pulmonary function and architecture
 General mortality ~ 1%
 Patients hospitalization in ICU  Mt ~ 25%

 Without treatment
 Mortality ~ 30%
STAPHYLOCOCCAL
PNEUMONIA
Staphylococcal pneumonia
Staphylococcus aureus
 Gram + cocci
 20 - 40% adults  asymptomatic nasal
carriers
 the most virulent of the staphylococcus
species
 broad spectrum of manifestations: from o Relatively rare ~ 3-5% from bacterial
minor skin infections to systemic life pneumonia
-threating infections o Always severe
o More frequent in young people, after
influenza infections  broncho-
pneumonia post-influenza or in
elderly people
Risk factors

 Chronic disease, pulmonary disease, immunologic disorders

 Chronically i.v. treatment: dialysis, drug addicts

 Frequent admission in hospital, ICU, organ transplantation, cardiac

surgery

2 types of syndromes:
 Through toxins production
cytotoxic, pyrogenic and exfoliative toxins

 Through proliferation, invasion and tissue destruction

Considerations in S. aureus pneumonia

 Progressive dyspnea, tachypnea, cyanosis

 Hypoxemia ~ constantly
 Mucopurulent sputum with blood strips / hemoptysis
 Rarely – typical consolidation syndrome
 Pneumatoceles – hypertransparency areas
 Pleural empyema / pyopneumotorax – frequently
 Defervescence – slow
 There can be a 1-2 weeks period of fever under antibiotic treatment

 Mortality ~ 15% (post-influenza ~ 50%)

Chest X-ray - Necrotizing pneumonia

Focal consolidation in different stages of evolution (consolidation  abcesses); pneumatoceles

Imaging – CT scan
 Treatment
PATHOGENIC
 Correction of respiratory failure with O2 supplements
 Correction of dehydration with intravenous liquids
 Septic shock – noradrenaline if SBP < 70 mmHg
 Correction of mechanical complications: surgical & pleural aspiration
 NB! Early, intense, complex, prolonged, adapted to the complications that
may occur any time
 Etiological treatment / Staphylococcus aureus
NB! The treatment will be initiated considering that there is a MRSA
(80% germs secrete penicillinase)

 Methicillin sensitive SA (MSSA)  Methicillin-resistant (MRSA)

 Oxacillin, nafcillin, cloxacillin  Vancomycin
 Cephalosporins 1st / 2nd generation  Teicoplanin
 Other options:  Linezolid
 Imipenem
 Fluorquinolones  Vancomycin + Rifampicin  Aminoglycoside
 Clindamycin – if there are complications with valvular
prosthesis endocarditis
 Etiologic Treatment
NB! the antibiotic/antibiotic combination to initiate the treatment is/are chosen
regarding the severity of the disease

 Treatment duration
 3  4-6 weeks in septic patients;
 If there will not be septic complications, there is no necessity to
change the antibiotic.
PNEUMONIA WITH GRAM
NEGATIVE BACILLI
Generalities
 3-10% of CAP, but 50% of nosocomial pneumonia
 Necrotizing pneumonia / abscess (hemoptysis)
 Bacteriemia present, but rarely septic metastasis
 Endotoxin-releasing related complications – low BP, septic shock
 Diseminated intravascular coagulation
KLEBSIELLA PNEUMONIAE
Particularities
 Tipically – right upper lobe
 Productive sputum – “chocolate-like”/”currant-jelly”
 Bronchial obstruction by gelatinous sputum
 Empyema/pyopneumothorax
 Laboratory - hyponatremia
 Positive blood culture in ~ 20-50% of cases
Chest X-Radiography

Massive lobar pneumonia Bronchopneumoia

Treatment

Etiological treatment
 Classes:
 3rd /4th generation cephalosporine and/or fluoroquinolone
 aminoglycoside
 piperacillin + tazobactam
 imipenem, meropenem !!! - the most active antibiotics
 Duration:
 2 or more weeks–depending on the presence of septic
complications; inadequate answer extend the duration of treatment
HAEMOPHILUS INFLUENZAE
Particularities

 Gram-negative bacillus – in
patients with COPD

 Pneumonia / broncho-
pneumonia affects more
frequently the lower lobes of
the lungs ± effusion
PSEUDOMONAS AERUGINOSA
Particularities
 < 10% of community-acquired pneumonia (CAP) with Gram-negative;
2nd or 3rd pathogen for nosocomial pneumonia
 Frequent in immune-compromised patients, neutropenia, cystic
fibrosis, bronchiectasis, HIV/AIDS, orotracheal intubated pacients, i.v.
catheter
 > 50% of bacilli  pyocyanin  blue-green pigment which helps at
identification
 Necrotizing bronchopneumonia
Chest X-Ray
Treatment of pseudomonas pneumonia
 An antipseudomonal beta-lactam (piperacillin-tazobactam, ceftazidime,
cefepime) OR a carbapenem (imipenem, or meropenem) PLUS
ciprofloxacin or levofloxacin

OR
 The above beta-lactam PLUS an aminoglycoside PLUS azithromycin 

OR
 The above beta-lactam PLUS an aminoglycoside PLUS a respiratory
fluoroquinolone (moxifloxacin, gemifloxacin, or levofloxacin)

 For penicillin-allergic patients, substitute beta-lactam with

aztreonam (a class of beta-lactams named monobactams)
INTERSTITIAL PNEUMONIA
Physical exam
 Symptoms
 Usually preceded by upper respiratory tract infection
 Dyspnea with tachypnea  respiratory distress
 Signs
 Respiratory - nonspecific:
 ± rales
 ± pleural effusion
 General - with various amplitude according to the etiology:
 Fever
 Cyanosis
 Uncorected hypoxemia at O2 suplimentation
 Tachycardia
Chest X Ray
 bilateral lung involvement, with interstitial infiltrates
MYCOPLASMA PNEUMONIAE
Particularities
 Age 5-20 year
 Incubation: 14-21 days
 Imune mechanisms (CIC ~ 40%; Autoantibodies)
 Insidious onset
 Fever, headache, myalgia
 Conjunctivis
 Physical exam: normal +/- crackels +/- bronchi rales +/- small pleural
effusion transient unilateral (20%)
Interstitial pneumonia
Complications
 Regress in 3-10 days (cough  2-3 weeks)
 Complications:
 Hematological:  Neurological:
 Hemolytic autoimmune anemia  Aseptic meningitis
 Thrombocytopenia  Meningoencefalites
 DIC  Myelitis
 Skin:  Neuropaties
 Rash
 Nodosum erythema  ARDS
 Cardiac:
 Bacterial overlap
 Myocarditis
 Pericardial effusion
Treatment
 Macrolide
 Erythromycin
 Clarythromycin
 Azytromycin

 Tetracycline
 Doxyciclin

 Fluorqouinolone
 Moxifloxacin
 Levofloxacin
INFLUENZA
 Particularities
 Risk factors: extreme age; chronic pulmonary diseases; pulmonary stasis;
pregnancy
 Symptoms:
 Progressive dyspnea, tachypnea, productive cough
 Respiratory distress
 Clinical examination:
 Diffuse roughly vesicular murmur
 Some basal diffuse crackles
Chest X- ray
Treatment

NB! It is especially symptomatic and pathogenic

 O2 therapy:
 by mask
 positive airway pressure assisted therapy
 Antiviral therapy - oseltamivir
 ± corticoids i.v. in high doses
 i.v. fluids, macromolecular solutions, dopamine in case of low BP
 ± an effective antibiotic on staphylococcus, pneumococcus and
haemophylus
PNEUMOCISTIS JIROVECII
Particularities
 In imunosupressed patients
 Variable – subacute/chronic  acute & fatal disease
 Symptoms:
 Sudden onset - fever, cough, progressive dyspnea
 Severe respiratory insufficiency – in 5-7 days
 Gradually onset – in patients with AIDS

 Signs – variable:
 Fever, consolidation, cavitation, pneumothorax, anemia, adenopathies and/or
splenomegaly
Chest X-ray
Differential diagnosis
 In HIV infected patients with:
 Pneumonia with CMV
 TB
 Fungi pneumonia
 Interstitial pneumonitis
 Kaposi sarcoma
 Prophylaxy
• Trimethoprim/
sulfamethoxazole 2tb/12h
• Dapson 100mg/day
Treatment
 Trimethoprim/sulfamethoxazole
po/iv
 Pentamidin:
 Those with intolerance at TMP/SMX
 Duration: 3 weeks
 Dapson/TMP
 Clindamycin/primaquine
LEGIONELLA PNEUMOPHILA
Particularities
 Gram negative aerobic bacillus that do not grow on routine culture
 Source – water; hotels/ boat trips
 Incubation 2-10 days
 “Atypical” pneumonia
 T grd C > 40 degrees
 Varied manifestations: mild non-productive cough  multiple organ failure
 Diarrhea – in 25-50%
 Neurological: headache  confusions  encephalopathy
 Rx – pulmonary infiltration in large area
 Treatment: macrolide, quinolones, tetracycline, others (Rifampicin, Biseptol)
HOSPITAL AQUIRED PNEUMONIA (HAP)
VENTILATOR ASSOCIATED PNEUMONIA (VAP)

HEALTH-CARE ASSOCIATED PNEUMONIA

(HCAP)
Definitions
 Hospital-acquired pneumonia (HAP) or
nosocomial pneumonia is defined by American
Thoracic Society guidelines, a lower respiratory
infection that was not incubating at the time of
hospital admission and that presents clinically
2 or more days after hospitalization.

 Ventilator-associated pneumonia (VAP) is defined

as pneumonia that presents more than
48 hours after endotracheal intubation.

Management of Adults with HAP/VAP; 2016 Clinical Practice Guidelines by IDSA and ATS
HAP & VAP
 The most common cause of death
among all hospital-acquired
infections, with mortality rates of
up to 33%.

 High morbidity and mortality rates,

because these patients are already
critically ill.

Management of Adults with HAP/VAP; 2016 Clinical Practice Guidelines by IDSA and ATS
Hospital mortality
Keep in mind!

 Hospital-acquired pneumonia includes

ventilator-associated pneumonia,
postoperative pneumonia, and
pneumonia that develops in
unventilated patients who have been
hospitalized for at least 48 h.
Do not confuse…
 Health care–associated pneumonia (HCAP)
occurs in non-hospitalized patients who:
 reside in a nursing home or other long-term
care facility;
 have undergone IV therapy (including
chemotherapy) or wound care within the
previous 30 days;
 have been hospitalized in an acute care
hospital for ≥ 2 days within the previous
90 days;
 have attended a hospital or hemodialysis
center within the previous 30 days.
HCAP
 In addition to the usual community-acquired pathogens, HCAP
pathogens include gram-negative bacilli (including  Pseudomonas
aeruginosa) and Staphylococcus aureus (including methicillin-
resistant S. aureus) and various antibiotic-resistant pathogens.

 Symptoms and signs are similar to those of pneumonia that

occurs in other settings, except many elderly patients have less
prominent changes in vital signs.

 Mortality is moderately high, but may be due in part to coexisting

disorders.
Risk factors

 Risk factors in nonintubated patients

 previous antibiotic treatment;
 high gastric pH (due to stress ulcer prophylaxis or therapy
with proton pump inhibitors but not with H2 blockers);
 coexisting cardiac, pulmonary, hepatic, or renal insufficiency.

 Major risk factors for postoperative pneumonia:

 age > 70;
 abdominal or thoracic surgery;
 functional debilitation.
VAP
 Endotracheal  intubation with mechanical ventilation =
the greatest overall risk of hospital-acquired
pneumonia.
 The highest risk of VAP occurs during the first 10 days
after intubation.
 Endotracheal intubation:
 breaches airway defenses;
 impairs cough and mucociliary clearance;
 facilitates microaspiration of bacteria-laden secretions that
pool above the inflated endotracheal tube cuff.
 In addition, bacteria form a biofilm on and within the
endotracheal tube that protects them from antibiotics and
host defenses.
Pathophysiology
 Inhalation
 Primary inhalation pneumonia develops when the organisms bypass
normal respiratory defense mechanisms or when the patient inhales
aerobic gram-negative organisms that colonize the upper respiratory
tract or respiratory support equipment.
 Aspiration
 Is due to the aspiration of colonized upper respiratory tract secretions.
 The stomach appears to be an important reservoir of gram-negative
bacilli that can ascend and colonize the respiratory tract.
 Hematogenous spread 
 Hematogenously acquired infections originate from a distant source and
reach the lungs via the bloodstream.
Pathogens
Pathogens
Patogens Non-MDR Patogens MDR
Streptococcus pneumoniae Pseudomonas aeruginosa
Other Streptococcus spp Acinetobacter spp
Haemophilus influenzae
MSSA MRSA
Antibiotic-sensitive Antibiotic-resistant
Enterobacteriaceae Enterobacteriaceae
Escherichia coli Enterobacter spp
Klebsiella spp Klebsiella pneumoniae
Proteus spp Legionella pneumophila
Enterobacter spp. Burkholderia cepacia
Serratia margescens Aspergillus
Diagnosis
DIAGNOSIS

 Clinical suspicion
 Blood tests
 Leukocytosis (+/- left shift), ESR, fbn
 Procalcitonin
 CRP

 Microbiological tests
 Culture of sputum (spontaneously or by induction of sputum)
 Culture of other fluids (eg, pleural)
 Blood cultures in fever
 Bronchoalveolar lavage
DIAGNOSIS

 Imagistical Dg:
 X ray
 CT scan
 Bronchoscopy

 Other tests for diferential diagnosis

 ECG
 NT proBNP
 Cardiac enzymes
 D-dimers
 Panel of antibodies/anticorps for autoimunity diseases
X Ray
Bronchoscopy
False positive diagnosis
 Colonization of trachea with pathogenic bacteria in
intubated patients

 Other causes of radiological opacity in mechanically

ventilated patients

 Other sources of fever in critically ill patients

Diagnosis diferential
 Congestive heart failure
 Pulmonary embolus or infarction
 Acute respiratory distress syndrome (ARDS)
 Lung hemorrhage
 Bronchiolitis obliterans-organizing pneumonia (BOOP)
 Collagen-vascular diseases (eg, systemic lupus erythematosus)
 Interstitial lung disease
 Bronchogenic / metastatic carcinomas
 Pulmonary drug reactions
Treatment consideration
 Recommend that each hospital generate antibiograms to guide
healthcare professionals with respect to the optimal choice of
antibiotics.
 Reassess patients 2 to 3 days after initiation of treatment, and
change antibiotics based on available culture and clinical data.

 MRSA - vancomycin or linezolid

 P. aeruginosa antibiotic – combination of 2 antibiotics
 Acinetobacter spp. - carbapenem
Antibiotic therapy for VAP
Should Patients Receive 7 Days or 8–15 Days of Antibiotic
Therapy? (HAP & VAP)

 For patients with VAP is recommended a 7-day course of antimicrobial

therapy rather than a longer duration
 There are situations in which a shorter or longer duration of
antibiotics may be indicated, depending upon the rate of improvement
of clinical, radiologic, and laboratory parameters.
 For patients with HAP/VAP, is suggested that antibiotic therapy be de-
escalated rather than fixed.
 De-escalation refers to changing an empiric broadspectrum antibiotic
regimen to a narrower antibiotic regimen by changing the
antimicrobial agent or changing from combination therapy to
monotherapy.
Outcomes

 Usually depend on:

 pre-existing underlying cardiopulmonary function and host
defenses
 risk factors/comorbidities rather than on the initial empiric
therapy

 Complications:
 Multiple organ dysfunction syndrome (MODS)
 Sepsis
 HSV-1 pneumonitis
 Death
Thank you!