PNEUMONIA - OVERVIEW

P SUKUMARAN
 Pneumonia is defined as inflammation and consolidation of
lung tissue due to an infectious agent . A clinical definition of
pneumonia is two or more of the following symptoms

• Cough
• Purulent Sputum
• Dyspnea or Tachypnea (respiratory rate > 20 /min)
• Rigors or chills
• Pleuritic chest pain
• In conjunction with a new opacity on chest radiograph
 SITE OF ACQUISITION
COMMUNITY ACQUIRED PNEUMONIA
Acute infection of pulmonary parenchyma acquired outside hospital

NOSOCOMIAL PNEUMONIA
HAP – Pneumonia acquired ≥ 48 hrs after hospital admission
VAP – Pneumonia Acquired ≥ 48 hrs after endotracheal intubation

HEALTH CARE ASSOCIATED PNEUMONIA (HCAP)

Pneumonia Acquired
- Health care facilities
- Recent Hospitalisation

Similar to CAP
 RISK FACTORS
• Older age
• Chronic co-morbidities
• Viral respiratory tract infection
• Impaired airway protection
-- Alteration in consciousness
– Dysphagia
• Smoking and alcohol overuse
• Other lifestyle factors
– Crowded living conditions
– Ill-ventilated room
– Exposure to environmental toxins
 .

MICROBIOLOGY

• Potential etiologic agents in CAP includes bacteria, fungi, viruses,

and protozoa.

• Newly identified pathogens include :

 Metapneumoviruses, SARS-CoV-2,SARS and MERS
 Community-acquired strains of MRSA.

• Streptococcus pneumoniae is most common organism along with

Respiratory viruses
 AETIOLOGICAL AGENTS
• Typical bacteria
– S. pneumoniae (most common bacterial cause)
– Haemophilus influenzae
– Moraxella catarrhalis
– Staphylococcus aureus
– Group A streptococci
– Aerobic gram-negative bacteria
– Microaerophilic bacteria and anaerobes
 AETIOLOGICAL AGENTS
• Atypical bacteria
– Legionella spp
– Mycoplasma pneumoniae
– Chlamydia pneumoniae
– Chlamydia psittaci
– Coxiella bumetii
 AETIOLOGICAL AGENTS
• Respiratory viruses
– Influenza A and B viruses
– Severe acute respiratory syndrome coronavirus 2 (SARS-
CoV-2)
– Other coronaviruses ([Link] CoV, SARS CoV, CoV-339E)
– Rhinoviruses
– Parainfluenza viruses
– Adenoviruses
– Respiratory syncytial virus
– Human metapneumovirus
– Human bacaviruses
 IMPORTANT TRENDS
• Decline in S. Pneumonia incidence
– Wide spread use of pneumococcal vaccination
• Decrease in
-individual rates
-Herd immunity
• Str. Pneumonia
– 30 % of cases in Europe
– 10 – 15 % in USA

[Link]. J Med. 2015;373:415

 COVID 19 Pandemic

• SARS – CoV-2
• Increased recognition of other respiratory
viruses (30% of cases) – molecular methods
– Single pathogens
– Cofactors in development of bacterial pneumonia
– Triggers for dysregulated immune response
DISCOVERY OF LUNG MICROBIOME
– Lung was considered sterile
– Culture independent techniques (16S rRNA
sequencing)
– Resident alveolar microbes
• Modulates host immune response
• Direct overgrowth
 ANTI MICROBIAL RESISTANCE
• S. Pneumonia
– May be resistant to one or more antibiotics in the
empiric regimen
– Macrolide > 25 %
– Doxycycline < 20 %
– Beta-lactam
• < 20 % to pencillin
• < 1 % to cephalosporins
– Fluoroquinolone < 2 %

Local antibiogram
METHICILLIN RESISTANT S. AUREUS (MRSA)

Health-care associated
• Risk factors
– Known MRSA prior infection /colonisation
– Recent parenteral antibiotic use
– Recent influenza-like illness
– Presence of empyema
– Cavitary pneumonia
– Immuno suppresson
METHICILLIN RESISTANT S. AUREUS (MRSA)

Community acquired (CAMRSA)

• Younger healthy persons
– H/o of MRSA skin lesions
– Participation in contact sports
– Injection drug use
– Crowded living
– Homosexuals
Pseudomonas
– Uncommon cause of CAP
– More common in
• Known pseudomonas colonization/prior infection
• Recent hospitalization or antibiotic use
• Structural lung disease
• Immunosuppression
 PATHOGENESIS
• Droplet infection/aerosol

• Inhalation

• Colonises naso pharynx

• Micro aspiration to lung

Pathogenesis
• Role of lung Microbiome
– Infecting pathogen compete with resident microbes to replicate
– Resident microbes may influence/ modulate host immune
response to
pathogen

– Alveolar dysbiosis

Uncontrolled replication of lung Microbes

– Anaerobic bacteria
• Prevotella, Veillonella , Micro aerophylic Streptococci
– Viral infection or smoke exposure trigger over growth of
microbes
• Host immune response
Role in determining severity

-Local inflammatory response

-Systemic inflammatory response

 CLINICAL PRESENTATION
• Varies widely Mild pneumonia – severe
• Depends on local and systemic Immune response

Pulmonary signs and symptoms

• Symptoms
– Cough
– Dyspnea
– Pleuritic chest pain

• Signs
– Tachypnea
– Increased work of breathing
– Bronchial breath sounds including crepitations/wheeze
– Tactile fremitus
– egophony
– Dullness to percussion
 Systemic signs and symptoms
• Fever, chills, fatigue, malaise, anorexia
• Tachycardia
• Leukocytosis/ Leukopenia
• Increased inflammatory markers
– ESR, CRP, Procalcitonin
• CAP can present as sepsis
– Hypotension
– Altered mental status
– Other signs of organ dysfunction
• Subtle presentation
– Advanced age
– Impaired immune systems
 DIAGNOSIS
Demonstration of an infiltrate on chest
imaging with clinically compatible syndrome

X RAY
Ultrasonography
C T Chest
 DIAGNOSIS
• Chest radiography

– Routine investigation for evaluation of pneumonia in

adults
– Lung infiltrate is the hallmark finding
– May demonstrate alveolar filling with inflammatory
exudate or interstitial thickening
– Results may be negative, especially with dehydration
– Pleural effusion may be present
 DIAGNOSIS
• Lung ultrasonography

– Accurate alternative to chest radiography that may be

performed at point of care

– May be used as adjunctive means of diagnosing

pneumonia, especially in patients with baseline chest
radiograph abnormalities
 DIAGNOSIS

• CT
– More sensitive than plain radiographs for detecting pneumonia

– Consider if clinical suspicion for pneumonia remains high despite

negative chest radiography findings

– Better at visualizing upper lobes and lingula, necrotizing infection,

multilobar disease, interstitial infiltrates due to atypical pathogens,
empyema, and pleural involvement

– Useful for excluding lung cancer

Pneumococcal pneumonia
Copyrights apply
Copyrights apply
Interstitial pneumonia
Radiological Features:

Air bronchogram sign:

Bulging Fissure Sign
Necrotizing pneumonia
Lung Abscess
 .

ETIOLOGIC DIAGNOSIS
• Except for CAP patients admitted to the ICU,
- no data exist to show that treatment directed at a specific pathogen
is statistically superior to empirical therapy.

• Why should we attempt for an etiologic diagnosis ?

 Identification of an unexpected pathogen

 Pathogens with important public safety implications,

 Without culture and susceptibility data, trends in resistance cannot

be followed and empirical regimens are harder to devise.
 .

GRAM’S STAIN & CULTURE OF SPUTUM

• identify certain pathogens by their characteristic appearance.
• to ensure that a sample is suitable for culture.
• To be adequate for culture, a sputum sample must have >25
neutrophils and <10 squamous epithelial cells per low-power
field.
• Even in cases of proven bacteremic pneumococcal pneumonia,
the yield of positive cultures from sputum samples is ≤50%.

• Inability to produce sputum can result from dehydration, and its

correction may result in increased sputum production
• For patients admitted to the ICU and intubated, a deep-suction
aspirate or bronchoalveolar lavage sample.
 .

 BLOOD CULTURES

• The yield from blood cultures, even when samples are

collected before antibiotic therapy, is disappointingly low.
(5–14% )
• Blood cultures are no longer considered essential for all
hospitalized CAP patients, recommended
• Certain high-risk patients
Neutropenia secondary to pneumonia,
Asplenia,
Complement deficiencies,
CLD
Severe CAP—should have blood cultured.
 .

 URINARY ANTIGEN TESTS

• Two commercially available tests detect pneumococcal

and Legionella antigen in urine.

 The test for Legionella detects only serogroup 1, which

accounts for most cases. The sensitivity and specificity are
as high as 70% and 99%, respectively.
 The pneumococcal urine antigen test is also quite
sensitive and specific (70% and >90%, respectively).

• Both tests can detect antigen even after the initiation of

appropriate antibiotic therapy.
 .

 POLYMERASE CHAIN REACTION

• PCR tests, are available for a number of pathogens.

• PCR of nasopharyngeal swabs, has become the standard for

diagnosis of respiratory viral infection.

• Detect the nucleic acid of Legionella species, M. pneumoniae, C.

pneumoniae, and mycobacteria.

• In patients with pneumococcal pneumonia, an increased

bacterial load documented by PCR is associated with an
increased risk of septic shock, the need for mechanical
ventilation - ICU admission.
 .

 SEROLOGY

• A fourfold rise in specific IgM antibody titer between

acute- and convalescent-phase serum samples is
generally considered diagnostic of infection with the
pathogen in question.

• Time required to obtain a final result for the

convalescent-phase sample and the difficulty of
interpretation.
 .

 BIOMARKERS

C-reactive protein (CRP) and procalcitonin (PCT).

 CRP may be of use in the identification of worsening disease or

treatment failure.

 PCT may play a role in distinguishing bacterial from viral infection,

determining the need for antibacterial therapy, or deciding when
to discontinue treatment.
 Should not be used on their own, but, when interpreted in
conjunction with other findings can result in less antibiotic use in
CAP with no concomitant increase in treatment failure or mortality
risk.
 Differential Diagnosis
• Congestive cardiac failure
• Pulmonary embolism
• Pulmonary hemorrhage
• Atelectasis
• Aspiration or chemical pneumonitis
• Drug reactions
• Lung cancer
• Collagen vascular disease
• Vasculitis
• ILD
 Respiratory illnesses mimicking or
co- occurring with CAP
• AE COPD
• Influenza and other respiratory viral infections
• Acute bronchitis
• Asthma exacerbations
• Presentation as Sepsis
– UTI
– Endocarditis
– Intra abdominal infection
 Treatment
• Most patients aetiology is not known
• Empiric treatment is appropriate
• Pathogens vary with
-Severity of illness
-Local epidemeology
-patient risk factors for drug resistant
org.
Risk stratification
Pneumonia Scoring System

CURB 65 :
SMART – COP
 OUT PATIENT
• Therapy should be directed against St. Pneumoniae and

atypcal pathogens

• Should be stratified according to - Presence or

- Absence of co morbities

• Recommended antibiotics (without co morbidites)Oral macrolides

– Oral Betalactam

• With co morbidities
– Batalactam + Macrolides

• Empiric fluoroquinolones to be avoided

 In Hospital Non -ICU
• Recommended regimen

Beta lactam (co amoxiclavCefotaximCeftraxone)

and
Macrolides

• If hypersensitive to β lactam

– Flucroquinolone (levofloxacin)
(Rule out tuberculosis)
• Can be oral/ parenteral as early as possible

National pneumonia guidelines 2012

 In Hospital ICU
• Without risk for P. Aeruginosa
– Β lactam( cefotaxim ceftriaxone coamoxyclav)+ Macrolide

• With possibility of P Aeruginosa

– Cefepime Ceftazidime

– Cefoperazone Piperacillin Tazobactam

– Imipenam Meropenem

+
– Combination with aminoglycosides/Antipsudomonas fluroquinolone

National pneumonia guidelines 2012

• Antimicrobial therapy to be changed according to pathogen isolated

• Diagnostic interventions should be done

– Thoraco centesis

– Intercostal tube drainage

• If not responding in 48 – 72 hrs look for the cause of non response

– Development of complications

– Presence of atypical org

– Drug resistance
 STEROIDS & CAP
• Controversial
• Not for routine use
• Indicated in
– Patients with exaggerated or dysregulated immune responses

– Septic shock refractory to

• Fluid resuscitation
• Vasopressor administration

– Respiratory failure with FiO2 > 50 %

– Metabolic acidosis < 7.3

– CRP > 150 mg/L

Methyl prednisolone 0.5 mg/kg IV BD

Prednisolone 0.5 – 1 mg/kg (5 days)

 Antibiotic de escalation

• Causative pathogens identified

– Targetted Therapy

• If not, continue empiric treatment for the duration

of therapy if improving
• Duration of therapy
– Patient is afebrile and stable for 48 hrs
– Minimum for 5 days
– Mild infection 5- 7 days
– Severe – 7- 10 days
– Extended course – Immuno compromised
Pathogens (Pseudomonas)
Complications
Discharge

Clinically stable

Can take oral medication

 FOLLOW UP IMAGING

• Usually not recommended in case of clinical

resolution

• To rule out malignancy

 COMPLICATIONS

• Clinical failure
(progress and or develop complications)

• Non resolving pneumonia

(remain symptomatic)
 CLINICAL FAILURE
PROGRESSION OF INITIAL INFECTION
– Dysregulated host immune response

– Infection spreading beyond lung

– Drug resistant pathogen

– Unusual pathogen

– Immune deficiency HIV associated

DEVELOPMENT OF CO MORBID COMPLICATIONS

– Infectious – Nosocomial infection

– Non infectious – Cardio vascular events

 NON RESOLVING CAP

Neither progress nor improve with 7 days of appropriate

empiric antibiotic

-Delayed clinical response

• Multiple co-morbidities

• Severe pneumonia

• Bacteremia

• Certain pathogens
 NON RESOLVING PNEUMONIA
• Loculated infection
• Lung abscess

• Empyema

• Bronchial obstruction

• Pathogens causing sub acute/chronic CAP

• Myco. TB

• Non TB Mycobacterium

• Less common bacteria (Nocardia, Actinomycetes)

• Incorrect initial diagnosis

• Malignancy
DEFINITION OF RECURRENT PNEUMONIA
– > 2 episodes of pneumonia within 6 months
or
– >3 episodes in a life time

– Episodes separated by an asymptomatic interval of at least 1 month

or
– Radiographic clearing of densities between episodes
CAUSES OF RECURRENT PNEUMONIA
– Bronchial Obstructions

– Underlying Lung disease

– Aspiration

– Immuno compromised
 PREVENTION

• Smoking cessation

• Influenza vaccination

• Pneumococcal vaccination
THANK YOU ……