You are on page 1of 33

Pulmonary infections

Pulmonary Infections
Respiratory tract infections are more frequent
than infections of any other organ and account
for the largest number of workdays lost in the
general population.
The vast majority are upper respiratory tract
infections caused by viruses (common cold,
pharyngitis) but bacterial, viral, mycoplasmal, and
fungal infections of the lung (pneumonia) still
account for an enormous amount of morbidity
and mortality
Pneumonia can be very broadly defined as any
infection of the lung parenchyma
pneumonia can result whenever these defense
mechanisms are impaired or whenever the
resistance of the host in general is lowered
Factors that affect resistance in general
chronic diseases,
immunologic deficiency,
treatment with immunosuppressive agents,
leukopenia, and
unusually virulent infections
The clearing mechanisms can be interfered with
by many factors, such as the following:
Loss or suppression of the cough reflex
Injury to the mucociliary apparatus
Interference with the phagocytic or bactericidal
action of alveolar macrophages
Pulmonary congestion and edema
Accumulation of secretions in conditions such as
cystic fibrosis and bronchial obstruction
Pneumonias are classified by the specific
etiologic agent, which determines the
if no pathogen can be isolated, by the clinical
setting in which the infection occurs
Classifying by the clinical setting
Community-Acquired Acute Pneumonia
Community-Acquired Atypical Pneumonia
Nosocomial Pneumonia
Aspiration Pneumonia
Chronic Pneumonia
Necrotizing Pneumonia and Lung Abscess
Pneumonia in the Immunocompromised Host
Community-acquired pneumonias may be
bacterial or viral
Bacterial invasion of the lung parenchyma
causes the alveoli to be filled with an
inflammatory exudate, thus causing
consolidation ("solidification") of the
pulmonary tissue
Clinical course and severity determined by
etiologic agent
the host reaction
the extent of involvement
Risk factors;. extremes of age, chronic diseases
(congestive heart failure, COPD, and diabetes),
congenital or acquired immune deficiencies,
decreased or absent splenic function, and
indoor smoke
Streptococcus Pneumoniae-
the most common cause of community-acquired
acute pneumonia
It is capsulated,Gram positve ,lancet shaped
Can be isolated from sputum,but blood culure is
more specific
Pneumococcal vaccines containing capsular
polysaccharides from the common serotypes are
available for use in patients at high risk.
Haemophilus Influenzae
It is a pleomorphic, Gram-negative organism ,and a
very common cause of CAP
it exists in two forms: encapsulated (5%) and
unencapsulated (95%)
the encapsulated form dominates the unencapsulated
(producing haemocin)
six serotypes of the encapsulated form (types a to f),
type b, which has a polyribosephosphate capsule, used
to be the most frequent cause of severe invasive
H. influenzae is the most common bacterial cause of
acute exacerbation of COPD
Moraxella Catarrhalis
it is being increasingly recognized as a cause of
bacterial pneumonia, especially in the elderly.
It is the second most common bacterial cause
of acute exacerbation of COPD.
Along with S. pneumoniae and H. influenzae,
M. catarrhalis constitutes one of the three
most common causes of otitis media in
Staphylococcus Aureus
Klebsiella Pneumoniae
Pseudomonas Aeruginosa
Legionella Pneumophila
Bacterial pneumonia has two gross patterns of
anatomic distribution: lobular
bronchopneumonia and lobar pneumonia
Bronchopneumonia Patchy consolidation of
the lung
Lobar pneumonia is an acute bacterial
infection resulting in fibrinosuppurative
consolidation of a large portion of a lobe or of
an entire lobe
In lobar pneumonia, four stages of the
inflammatory response have classically been
red hepatization,
gray hepatization, and
congestion, the lung is heavy, boggy, and red.
It is characterized by vascular engorgement,
intra-alveolar fluid with few neutrophils, and
often the presence of numerous bacteria.
red hepatization that follows is characterized
by massive confluent exudation with red cells
(congestion), neutrophils, and fibrin filling the
alveolar spaces
gray hepatization follows with progressive
disintegration of red cells and the persistence
of a fibrinosuppurative exudate giving the
gross appearance of a grayish brown, dry
resolution, the consolidated exudate within
the alveolar spaces undergoes progressive
enzymatic digestion to produce a granular,
semifluid, debris
Foci of bronchopneumonia are consolidated
areas of acute suppurative inflammation.
The consolidation may be patchy through one
lobe but is more often multilobar and
frequently bilateral and basal because of the
tendency of secretions to gravitate into the
lower lobes.
Well-developed lesions are usually 3 to 4 cm
in diameter
tissue destruction and necrosis, causing
abscess formation
spread of infection to the pleural cavity
bacteremic dissemination
Clinical Course
brupt onset of high fever,
shaking chills, and
cough productive of mucopurulent sputum;
occasional hemoptysis
Ches pain
Radiologic finding-opacities
Asthma is a chronic inflammatory disorder of
the airways that causes recurrent episodes of
wheezing, breathlessness, chest tightness, and
cough, particularly at night and/or in the early
These symptoms are usually associated with
widespread but variable bronchoconstriction
and airflow limitation that is at least partly
reversible, either spontaneously or with
It is thought that inflammation causes an
increase in airway responsiveness
(bronchospasm) to a variety of stimuli
based on the frequency and severity of
symptoms classified in to;.
mild intermittent,
moderate, and
severe persistent asthma
Useful to guide therapy
The major etiologic factors of asthma are
genetic predisposition to type I
hypersensitivity ("atopy"), acute and chronic
airway inflammation, and bronchial
Many cells play a role in the inflammatory
response, in particular eosinophils, mast cells,
macrophages, T lymphocytes, neutrophils, and
epithelial cells
Atopic Asthma
Nonatopic Asthma
Drug-Induced Asthma
Occupational Asthma
overdistended lungs because of overinflation
areas of atelectasis
Mucous plugs
Microscopic findings
called air way remodeling
Thickening of the basement membrane of the
bronchial epithelium
Edema and an inflammatory infiltrate in the
bronchial walls, with a prominence of
eosinophils and mast cells
An increase in size of the submucosal glands
Hypertrophy of the bronchial wall muscle
Hemodynamic Edema Edema Due to Undetermined Origin
Microvascular Injury
Left-sided heart failure (common) Infections: pneumonia, septicemia High altitude

Volume overload Inhaled gases: oxygen, smoke Neurogenic (central nervous system trauma

Liquid aspiration: gastric contents, near-

Pulmonary vein obstruction

Hypoalbuminemia Drugs and chemicals

Nephrotic syndrome Shock, trauma

Liver disease Radiation

Protein-losing enteropathies Transfusion related

Lymphatic obstruction (rare)

Hemodynamic Pulmonary Edema
The most common hemodynamic mechanism
of pulmonary edema is that attributable to
increased hydrostatic pressure
pulmonary congestion and edema are
characterized by heavy, wet lungs
the alveolar capillaries are engorged,
an intra-alveolar granular pink precipitate is
Alveolar microhemorrhages and hemosiderin-
laden macrophages ("heart failure" cells) may
be present
Edema Caused by Microvascular
injury to the capillaries of the alveolar septa
The edema results from primary injury to the
vascular endothelium or damage to alveolar
epithelial cells
This results in leakage of fluids and proteins
first into the interstitial space and, in more
severe cases, into the alveoli