PNEUMONIA

FELISTUS
LEARNING OUTCOMES

1) Identify causes of pulmonary infections

2) Discus predisposing factors to pulmonary
infections
3) Describe the pathology of different types of
pneumonia
INTRODUCTION

Respiratory tract infections are more

frequent than any other infections. Majority
of the upper respiratory tract infections
(URTIs) are caused by viruses (common cold,
pharyngitis) while bacterial, viral,
mycoplasmal and fungal infections of the
lung (pneumonia).
 Acute and chronic pulmonary infections

which are frequent causes of death are

common at all ages and occur when normal
lung or systemic defence mechanisms are
impaired.
Impairment of the defence mechanisms includes -
1. Loss or decreased/suppression of cough reflex
leading to aspiration e.g. In coma, neuromuscular
disorders, anaesthesia, drug effects or chest pain
2. Injury to mucociliary apparatus by cigarette
smoking and gaseous inhalation, genetic disorders,
inhalation of corrosive substances
3. Decreased phagocytic or bactericidal function of
the alveolar macrophages due to smoking, alcohol
and oxygen toxicity.
4. Pulmonary oedema or congestion (congestive
cardiac failure)
5. Accumulation of secretions e.g. Post-operative ,
cystic fibrosis and bronchial obstruction
DEFINITION

 Pneumonia is inflammation of the lung

parenchyma distal to the terminal
bronchioles (respiratory bronchiole, alveolar
ducts, alveolar sacs and alveoli) characterized by
vascular changes and exudation of fluid and
cells.
 The inflammation may reach the pleural surface
causing irritation and inflammation of the pleura
and accumulation of fluid exudate (pleural
effusion).
 The process is influenced by the spongy character
of the lung that allows unimpeded spread of the
inflammatory exudate filling the alveolar and
affected portions of the lung become relatively
solid (consolidation).
ROUTES OF INFECTION

1. Inhalation of microbes present in the air

2. Aspiration – naso and oropharynx
3. Haematogenous spread from a distant foci
of infection
4. Direct spread from an adjacent site of
infection
PATHOGENESIS
 A number of defence mechanisms at
different levels normally protects the lung
and failure of the defence mechanisms and
presence of predisposing factors results in
development of pneumonia. Such situations
include -
 a) Altered consciousness - oropharyngeal

contents can be aspirated into the lungs in

states of unconsciousness e.g. coma, cranial
trauma, seizures, cerebro-vascular accidents,
drug overdose and alcoholism
 b) Depressed cough and gag reflexes - allows aspiration of
gastric contents e.g. in old age, pain from trauma, thoraco-
abdominal surgery, neuromuscular disease, malnutrition,
kyphoscoliosis, severe obstructive pulmonary disease,
endotracheal intubation and tracheostomy
 c) Impaired mucociliary transport - impairment or
destruction of the mucous-covered ciliated epithelium as in
cigarette smoking, respiratory viral infections, immotile
cilia syndrome, inhalation of hot or corrosive gases and old
age.
 d) Impaired alveolar macrophage function - cigarette
smoking, hypoxia, starvation, anaemia, pulmonary oedema
and viral respiratory infections.
 e) Endobronchial obstruction - interferes with effective
clearance of the bronchial tree
 f) Leucocyte dysfunctions - congenital and acquired
immunodeficiency, HIV/AIDS and granulocyte abnormalities
PREDISPOSING FACTORS

How would these factors predispose individuals

to pulmonary infections?
1. Viral infections
2. Hospitalization
3. Cigarette smoking
4. Alcohol excess
5. Bronchiectasis
6. Bronchial obstruction
7. Immunosuppression
8. Intravenous drug use
9. Inhalation
10. Crowding
11. Post operation
CLASSIFICATION
Classification is based on -
1. Aetiologic classification - Bacterial; Viral;
Rickesttsiae; Protozoa; Mycoplasma; Fungal;
Chemical
2. Pathologic classification – how the infection
spreads within the lung
a. Lobar pneumonia
b. Bronchopneumonia
3. Clinical classification – circumstances
surrounding development of disease
a. Community acquired disease
b. Hospital acquired (nosocomial) infections
c. Post-operative pneumonia/hypostatic
pneumonia
d. Aspiration pneumonia
e. Obstructive pneumonia
f. Disease acquired in special environments
g. Disease in immunosuppressed patients
BACTERIAL PNEUMONIA
 Bacterial infection of the lung parenchyma is
the most common cause of pneumonia or
consolidation of one or both lungs.
 There are two types of acute bacterial

pneumonia- lobar pneumonia and

bronchopneumonia, which have distinct
aetiologic agents and morphologic changes.
LOBAR PNEUMONIA

 Lobar pneumonia is an acute bacterial

infection of the lobes of the lungs.
 It may involve a part of the lobe, the entire

lobe or even two lobes of one or both the

lungs.
 Lobar pneumonia is more common in males

that females and allergy plays an important

role in the aetiology and pathogenesis of
lobar pneumonia
AETIOLOGY
 It is based on aetiologic microbes and there are four
types of lobar pneumonia that is: -
 Pneumococcal pneumoniae (Streptococcus
pneumoniae) – 90% of lobar pneumonia and it is mainly
a community acquired infectionStaphylococcus aureus
– haematogenous spread and following viral infection
 Pneumonia by gram negative aerobic bacteria – this is
less common. Organisms include: - H. influenzae
(common in children less than 3 years old and after a
preceding viral infection), Klebsiella pneumoniae
(Frielander’s bacilli), Pseudomonas aeroginosum,
Proteus, Escherichia coli
 Beta haemolytic streptococcus is common in children
after measles or influenza infections, severely
debilitated, elderly and diabetic patients
PATHOGENESIS
 Microbes gain access to the lungs via several routes
because of failure of the lung defence mechanisms and
presence of the relevant predisposing factors.
 Invasion of the lungs results in inflammation of the alveolar
with production of an inflammatory exudate, which spreads
to the adjacent alveoli via the inter-alveolar pores.
 Organisms are destroyed by phagocytosis initially by the
neutrophils and later macrophages. Alveoli are filled up
with the inflammatory exudate with trapped air and then
the whole lobe is converted into a solid mass (air free) – a
process described as consolidation. The lower lobes are
affected most. The infection spreads throughout the entire
lobe and the spread is usually seen on the affected lobe.
 The cells are driven by positive chemotaxis and they
destroy the pneumoniae organisms by first fixing them to
the alveolar wall before they engulf them.
Pathologic Changes
There are four sequential pathologic phases of
lobar pneumonia namely: -
1. Stage of congestion (Initial stage)
2. Stage of red hepatisation (early
consolidation)
3. Stage of grey hepatisation (late
consolidation)
4. Resolution
CONGESTION (INITIAL PHASE)

 Lasts 1 – 2 days and represents the early

acute inflammatory response to bacterial
infection and is characterized by extreme
congestion and excessive serofibrinous
exudation.
 Results from outpouring of protein-rich
exudates into the alveoli. It is usually
associated with dramatic onset of increased
temperature with chills and rigors
Microscopy
 Typical features of acute inflammation

 Dilatation and congestion of capillaries in

alveolar walls
 Oedema fluid

 Few red blood cells and neutrophils

 Numerous bacteria
RED HEPATIZATION

 Lasts from 2nd – 4th day and is characterized

by liver-like consistency of the lung on cut
section due to massive accumulation of
polymorphs in the alveolar spaces.
Macroscopy
 Affected lobe is red, firm and consolidated

 Cut surface is airless, pink, dry, granular and

has liver like consistency

 Accompanied by serofibrinous pleurisy
Microscopy
 Oedema fluid replaced by fibrin strands

 Marked cellular exudates – neutrophils and

extravasations of red blood cells

 Many neutrophils with ingested bacteria

 Less prominent alveolar septa due to cellular

exudation
GREY HEPATISATION

 Lasts from the 4th – 8th day and it occurs due

to accumulation of fibrin in the lung spaces.
Macroscopy
 Lobe is firm, heavy and more friable lung

 Cut surface is dry, granular and grey in

appearance with a liver like consistency

 Change of colour from red to grey begins at

the hilum and spreads towards the periphery

 Fibrinous pleurisy is prominent
Microscopy
 Numerous and dense fibrous strands

 Reduced neutrophils exudation due to

disintegration of neutrophils
 Fewer red blood cells

 Macrophages begin to appear

 Thin clear space separates cellular exudates from

the septa walls

 Polymorph leucocytes present in large numbers

and produce a proteolytic enzyme (substance)

 Vessel congestion is reduced in the inter alveolar

walls
 Exudate in pleural space is partially organized
RESOLUTION
Resolution begins on the 8th or 9th day if no chemotherapy is administered and is
completed in 1 – 3 weeks.
Antibiotic therapy induces resolution on about the 3rd day. Resolution proceeds in
a progressive manner.
Macroscopy
The solid fibrinous constituent is liquefied by enzymatic action restoring normal
aeration in the affected lobe
Softening of the lobe begins centrally and spreads to the periphery
Exudates is removed by coughing/expectoration, phagocytosis and liquefaction
Cut surface is grey-red or dirty brown and frothy and yellow creamy fluid can be
expressed on pressing
Resolution of pleural reaction may undergo organization forming a fibrous
obliteration of pleural cavity
Microscopy
Macrophages are predominant and have engulfed neutrophils and debris
Reduced neutrophils
Granular and fragmented fibrous strands in alveolar spaces
Engorged alveolar capillaries
Progressive removal of fluid content and cellular exudates by expectoration and
lymphatics results in restoration of normal lung parenchyma with aeration
Clinical Features
 Sudden onset

Symptoms - shaking, chills, hotness of the

body, malaise, pleuritic chest pain,
dyspnoea, cough with expectoration –
mucoid, purulent or bloody sputum
Signs
 General – fever, tachycardia, tachypnoea,

cyanosis;
 Respiratory system
Investigations
 Full haemogram – neutrophils leucocytosis,

raised ESR
 Positive blood cultures

 Sputum examination

 Chest X-ray – consolidation

COMPLICATIONS

 Pleural effusion
 Empyema/Lung abscess
 Emphysema
 Lung collapse
 Pneumothorax
 Thromboembolism
 Lobar gangrene
 Metastatic infection(bacteraemia) - pericardium – pericarditis,
myocarditis, endocarditis; otitis media, mastoiditis;
meningitis; brain abscess; purulent arthritis; peritonitis
 Multiple organ failure
 Complications arise as a result of delayed resolution and
spread (local and blood)
 Organization of exudates - occurs in 30% of the cases and
results in lung fibrosis. This post-pneumonic fibrosis is called
carnification
BRONCHOPNEUMONIA

 Bronchopneumonia is inflammation of the

terminal bronchioles that extends into the
surrounding alveoli resulting in patchy
consolidation of the lungs.
 It involves both the right and left lung fields.

It is particularly frequent at extremes of life

(infancy and old age), chronic debilitating
diseases and post operatively.
 The susceptibility in children is due to poor

propulsive power (cough reflex), delicate

mucosa and a short wide bronchiole tree
Pathogenesis
 Organisms gain access to the lungs via the

bronchioles tree where they affect the

bronchioles of both lungs.
 Bronchopneumonia
Aetiology
 Staphylococcus

 Streptococcus

 Pneumococci

 Klebsiella pneumoniae

 Heamophilus influenzae

 Gram negative bacilli – Pseudomonas

 Coliform bacteria
Pathology
Macroscopy
 Patsy areas of red or grey consolidation affecting one or

more lobes
 Involves the lower zones of the lungs due to gravitation

of secretions
 Bronchioles are extensively inflamed and filled with

inflammatory exudates
 Consolidation occurs around the bronchioles

 Slight peribronchiole thickening

 Cut surface shows patchy consolidated lesions with dry,

granular, firm red or grey colour, which are 3 – 4 cm in

diameter. They are slightly elevated above the surface
and can easily be felt by passing fingertips on the cut
surface
Microscopy
 Acute bronchiolitis

 Suppurative exudates containing chiefly of

neutrophils
 Thickening of alveolar septa by congested

capillaries and leucocyte infiltration

 Oedema fluid (less in involved alveolar)

 Alveoli around the bronchioles undergo

absorption, collapse and further out there is

compensatory emphysema
ASPIRATION PNEUMONIA

 Aspiration pneumonia is a pulmonary

sequelae resulting from the abnormal entry
of endogenous secretions or exogenous
substances into the lower airways.
 Occurs because of breakdown in defences

that protect the tracheobronchial tree and

pulmonary complications that result from the
aspiration event
PREDISPOSING FACTORS

 Altered consciousness - alcoholism; seizures;

cerebrovascular accidents; head trauma; general
anaesthesia and drugs
 Dysphagia
 Oesophageal disorder- Stricture, neoplasia, diverticula,
tracheooesophageal fistula and incompetent cardiac
sphincter
 Neurological disorder - Parkinson’s disease, Myaethenia
gravis, Pseudobulbar palsy
 Mechanical disruption of defence barriers - nasogastric
tube, endotracheal intubation and tracheostomy
 Anatomical abnormalities - tracheo-oesophageal
strictures, oesophageal strictures, diverticuli, and gastric
outlet obstruction e.g. pyloric stenosis Pharyngeal
anaesthesia
 Protracted vomiting
Classification
 Aspiration pneumonia refers to three

distinctive syndromes based on the character

of the inoculation, which defines the
pathogenesis of pulmonary complications,
clinical presentation and treatment.
 The three syndromes namely chemical

pneumonitis, bacterial infection and

mechanical obstruction may overlap
Chemical Pneumonitis
 Fluids inherently toxic to the lower airways

and can initiate an inflammatory reaction

that is independent of bacterial infection.
 Examples of such fluids include – acids (e.g.

gastric acid – most common), volatile

hydrocarbons (gasoline, kerosene and animal
fats/milk), mineral oil and alcohol
PATHOGENESIS AND PATHOLOGY

Acids induce an inflammatory reaction, which

is more pronounced at a pH of less than 2.5.
Pathologic changes occur with devastating
rapidity.
 After 48 hours, the lung is grossly oedematous

and haemorrhagic and shows alveolar

consolidation. Resolution begins on the 3rd day
and may be complete or result in parenchymal
scarring.
Macroscopy
 Atelectasis
 Peribronchial haemorrhage
 Pulmonary oedema
 Degeneration of the bronchial epithelium
Microscopy
 Early necrosis of type I alveolar cells

 Fibrin

 Polymorphonuclear infiltration

 Alveolar type II cells degenerate as type I

cells necrose further and detach from the

basement membrane
 Hyaline membrane formation
Natural History
 Chemical pneumonitis may take three

courses namely: -
 Rapid improvement within 4 – 5 days

 Initial improvement but new extending

infiltrations due to pulmonary super

infections
 A fulminant course with death occurring

shortly after aspiration because of adult

respiratory distress syndrome (ARDS
PRESENTATION

 History of aspiration
 Rapid onset of respiratory distress syndrome with cyanosis,
tachycardia and tachypnoea
 Bronchospasms
 Fever
 Chest X-ray shows mottled densities located in one or both
lower lobes
 Lung function - reduced lung compliance; abnormal ventilation-
perfusion ration; reduced diffusing capacity; reduced PO2;
respiratory alkalosis; hypoxaemia
 Metabolic acidosis
 Hypotension - reflex reaction and depletion of intravascular
volume due to fluid aggregation within the lungs.
 Patients with severe aspiration pneumonia progress into adult
respiratory distress syndrome (ARDS(due to pulmonary oedema,
reduced surfactant activity, reflex airway closure, alveolar
haemorrhage and hyaline membrane formation)
BACTERIAL INFECTION

 Bacterial infection is the most common form of

aspiration pneumonia. Bacteria such as
Streptococcus pneumoniae, Heamophilus
influenzae, gram-negative bacilli and
Staphylococcus aureus are relatively virulent
in lower airways and a small inoculation is all
that is required for the infection to take root.
 These pathogens cause pneumonia by
microaspiration (aspiration of small volumes).
Diagnosis is suspected when a susceptible
host develops fever, purulent sputum and a
pulmonary infiltrate in a dependent pulmonary
segment
 Pathology
 The aspirated inoculum is generally

composed of oropharyngeal secretions

habouring bacteria from various sources in
the upper airway.
 The infections are polymicrobial flora with

the principal pathogens being anaerobic

bacteria. Aerobic pathogens are present too
while gram-negative bacilli are common in
patients with hospital acquired aspiration
pneumonia
Presentation
 It takes a variety of pathologic forms
with the initial lesion is pneumonitis,
an inflammatory reaction in the
pulmonary parenchyma.
 After 7 – 14 days from the onset of the

initial episode, there is suppuration,

lung abscess, necrotizing pneumonia
and empyema
Mechanical Obstruction
 Mechanical obstruction is sequelae of aspirating fluids or particulate

matter that are not inherently toxic to the lung but can cause airway
obstruction or reflex airway closure.
Fluids
 Fluids that are not inherently toxic to the lungs include saline,

barium, water and gastric content with a pH exceeding 2.5. Solid

Particles
 The effects and severity of mechanical obstruction depends on the

size the particle and the level of obstruction.

 Large objects obstruct the trachea and larynx causing sudden

respiratory distress, aphonia, cyanosis and death.

 It is very common in children during the oral stage. The particles

involve the usual objects such as peanuts, vegetable particles,

inorganic material, and teeth just to mention a few. The vegetable
materials are bad because they swell due to their hydroscopic
properties and the undigested cellulose cats as a local irritant
causing inflammation.
 What are the complications of aspiration pneumonia
HYPOSTATIC PNEUMONIA

Pneumonia that occurs as a result of

collection of oedema fluid and secretions in
dependent zones of the lungs. The fluid then
gets infected by bacteria from the upper
respiratory tract.
 It is common in severely debilitated, bed-

ridden patients, old and feeble and comatose

patients
NOSOCOMIAL (HOSPITAL-ACQUIRED)
PNEUMONIA

 These are hospital-acquired pulmonary

infections, acquired in the course of stay in
the hospital.
 Nosocomial pneumonia is a new episode of

pneumonia occurring at least 2 days after

admission to hospital. It encompasses post-
operative and certain forms of aspiration
pneumonia.
 They are common in patients with severe

underlying disease, immunosuppression,

prolonged antibiotic therapy or invasive
devices and procedures e.g. intravenous
catheters. They are life-threatening infections
Organisms
 Gram negative rods – Enterobacteriae –

Klebsiella., E. coli, Pseudomonas spp,

Proteus, Serratia
 Staphylococcus aureus

 Pneumococcus

 Legionella
Factors Predisposing to Nosocomial
Pneumonia
1. Reduced Host defence
a. Reduced immune defence (steroid
treatment, malignancy, diabetes)
b. Reduced cough reflex e.g. post-operative
c. Disordered mucociliary clearance e.g.
anaesthetic agents
d. Bulbar or vocal cord palsy
2. Aspiration of nasopharyngeal or gastric
secretions
a. Immobility
b. Reduced consciousness
c. Vomiting, dysphagia, achalasia or severe
reflux
d. Nasogastric intubation
3. Bacteria introduced into the lower respiratory
tract
a. Endotracheal intubation
b. Tracheostomy
c. Infected ventilators/nebulizers/bronchoscopes
d. Dental or sinus infection
4. Bacteraemia
a. Abdominal sepsis
b. Infected emboli
c. Intravenous cannula infection
 Differential Diagnosis of Pneumonia
 Pulmonary infarction
 Pulmonary/pleural tuberculosis

 Pulmonary oedema

 Inflammatory conditions below the diaphragm

THE END
QUESTIONS
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