Transcript PNEUMONIA

•TYPES
COMMUNITY ACQUIRED ACUTE
PNEUMONIA
• CAUSATIVE AGENTS
• MORPHOLOGY
 COMPLICATIONS
 CLINICAL COURSE
COMMUNITY ACQUIRED ATYPICAL
PNEUMONIA
• CAUSATIVE AGENTS
• MORPHOLOGY
 COMPLICATIONS
 CLINICAL COURSE
HOSPITAL ACQUIRED PNEUMONIA
 DEFINITION
 CAUSATIVE AGENTS
ASPIRATION PNEUMONIA
 PATHOGENESIS (WITH CLINICAL PICTURE)
 CAUSATIVE AGENTS
LUNG ABSCESS
 DEFINITION
 CAUSATIVE AGENTS
 PATHOGENESIS
 MORPHOLOGY
 CLINICAL COURSE
CHRONIC PNEUMONIA
 HISTOPLASMOSIS
 BLASTOMYCOSIS
 COCCI-DIODO-MYCOSIS
PULMONARY DISEASE IN HIV
INFECTION
 CLINICAL FEATURES AND DIAGNOSTIC CRITERIA
PNEUMONIA
 TYPES:
There are mainly two types of pneumonia1. COMMUNITY ACQUIRED ACUTE PNEUMONIA
2. COMMUNITY ACQUIRED ATYPICAL PNEUMINIA
Other types are:
1. HOSPITAL ACQUIRED PNEUMONIA
2. ASPIRATION PNEUMONIA
3. CHRONIC PNEUMONIA
4. PNEUMONIA IN IMMUNOCOMPROMIZED HOST
5. LUNG ABSCESS
Community acquired acute
pneumonia: Causative Agents
 Streptococcus pneumoniae
 Haemophilus influenzae
 Moraxella catarrhalis
 Staphylococcus aureus
 Legionella pneumophila
 Enterobacteriaceae (Klebsiella pneumoniae) and
Pseudomonas spp.
Community acquired acute
pneumonia: Morphology
 Bacterial pneumonia has two patterns of
anatomic distribution: lobular
bronchopneumonia and lobar pneumonia.
 Patchy consolidation of the lung is the dominant
characteristic of lobular pneumonia.
*Lobular pneumonia and bronchopneumonia are
similar terms.
 And fibrinosuppurative consolidation of a large
portion of a lobe or of an entire lobe defines lobar
pneumonia.
LOBAR PNEUMONIA
 In lobar pneumonia, four stages of the
inflammatory response have classically been
described:
1. congestion,
2. red hepatization,
3. gray hepatization, and
4. resolution.
CONGESTION
 This phase represent the acute inflammatory response
to bacterial infection.
 It lasts for 1-2 days.
 GROSSLY, the lung is enlarged, heavy, congested, dark
red.
 MICROSCOPICALLY, typical features of acute
inflammation are seen. (Dilation and congestion of
capillaries, numerous bacteria in the alveolar fluid,
eosinophilic edema fluid in the air spaces.)
RED HEPATISATION
 This phase lasts for 2-4 days.
 The term hepatisation comes from liver like
consistency of affected lobe in cut section.
 GROSSLY, the affected lobe is red, firm and
consolidated.
 The cut surface reveals airless, granular, red pink liver
like consistency.
 MICROSCOPICALLY, the eosinophilic edema fluid is
replaced by fibrin strands and marked cellular exudate
of neutrophils and extravasation of red cells is seen.
GREY HEPATISATION
 This phase lasts for 4-8 days.
 GROSSLY, affected lobe is firm and heavy.
 The cut surface is grey, granular and having liver like
consistency .
 The color change begins from hilum and spreads
towards the periphery.
 MICROSCOPICALLY, fibrin strands are more dense;
neutrophils and RBC reduce in number; organisms are
less numerous and more in degenerative forms.
RESOLUTION
 It starts at 8th day and in completed in next 1-3 weeks.
 But, with antibiotic therapy, resolution begins at 3rd day.
 GROSSLY, the affected lobe is gradually restored as a
result of liquefaction of fibrin strands by enzymatic
action.
 The process of softening begins centrally and progress
peripherally.
 MICROSCOPICALLY, macrophages are the dominant
cells, alveolar capillaries are engorged, progressive
removal of cellular exudate, resulting in restoration of
normal lung parenchyma with aeration.
BRONCHOPNEUMONIA/ LOBULAR
PNEUMONIA
 It is the infection of terminal bronchioles extending into
surrounding alveoli resulting in patchy consolidation of the
lung.
 It is more often multilobar and frequently bilateral and
basal because of tendency of secretions accumulating in
lower zones due to gravitation.
 GROSSLY, there are patchy areas of red or grey
consolidation affecting as above pattern.
 MICROSCOPICALLY,
1. Acute bronchiolitis
2. Infiltration by neutrophils in bronchi and bronchioles.
3. Thickening of alveolar septa.
COMPLICATIONS OF CAAcP
 Tissue destruction and necrosis, causing abscess
formation (particularly common with type 3
pneumococci or Klebsiella infections);
 Spread of infection to the pleural cavity, causing the
intrapleural fibrinosuppurative reaction known as
empyema; and
 Bacteremic dissemination to the heart valves,
pericardium, brain, kidneys, spleen, or joints, causing
metastatic abscesses, endocarditis, meningitis, or
suppurative arthritis.
CAAcP: CLINICAL COURSE
 The major symptoms of community-acquired acute
pneumonia are –
abrupt onset of high fever,
 shaking chills,
cough productive of mucopurulent sputum;
occasional patients may have hemoptysis.
• The identification of the organism and the
determination of its antibiotic sensitivity are the
keystones to appropriate therapy.
• Death may occur as a result of complications or
predisposing factors (chronic alcoholism).
COMMUNITY ACQUIRED ATYPICAL
PNEUMONIA: CAUSATIVE AGENTS
 Mycoplasma pneumoniae
 Chlamydia spp. (C. pneumoniae, C. psittaci, C.
trachomatis)
 Coxiella burnetii (Q fever)
 Viruses:
1. Respiratory syncytial virus,
2. Parainfluenza virus (children);
3. Influenza A and B (adults);
4. Adenovirus (military recruits);
5. SARS virus
CAAtP: MORPHOLOGY
 All causal agents produce essentially similar morphologic
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patterns.
The affected areas are red-blue and congested.
Predominant is the interstitial nature of the
inflammatory reaction, virtually localized within the
walls of the alveoli.
The alveolar septa are widened and edematous and usually
have a mononuclear inflammatory infiltrate of
lymphocytes, macrophages, and occasionally plasma cells.
In acute cases neutrophils may also be present.
Eradication of the infection is followed by reconstitution of
the normal architecture of the lung.
CAAtP: CLINICAL COURSE
 The clinical course of CAAtP is extremely varied,
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resulting from mild symptoms to severe upper
respiratory tract infections.
Cough may be absent, and the major manifestations may
consist only of fever,
headache,
muscle aches,
and pains in the legs.
The ordinary sporadic form of the disease is usually mild
with a low mortality rate, below 1%. But epidemics
showed somewhat greater mortality rates.
HOSPITAL ACQUIRED PNEUMONIA
 DEFINITION: Hospital-acquired pneumonias are
defined as pulmonary infections acquired in the
course of a hospital stay.
 INFECTED INDIVIDUALS: They are common in
patients with Severe underlying disease,
 Immunosuppression,
 Prolonged antibiotic therapy, or
 Invasive access devices such as intravascular catheters.
 Patients on mechanical ventilation are at particularly
high risk.
HAP: CAUSATIVE AGENTS
 Pseudomonus
 Staphylococcus
 Enterobacteriacae
ASPIRATION PNEUMONIA:
PATHOGENESIS
 Aspiration pneumonia occurs in markedly debilitated
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patients or those who aspirate gastric contents either while
unconscious (e.g., after a stroke) or during repeated
vomiting.
These patients have abnormal gag and swallowing reflexes
that predispose to aspiration.
The resultant pneumonia is partly chemical because of the
extremely irritating effects of the gastric acid, and partly
bacterial (from the oral flora).
Typically, more than one organism is recovered on culture,
aerobes being more common than anaerobes.
This type of pneumonia is often necrotizing, pursues a
fulminant clinical course, and is a frequent cause of death.
In those who survive, lung abscess is a common
complication.
ASPIRATION PNEUMONIA:
CAUSATIVE AGENTS
 Anaerobic oral flora
 Bacteroides,
 Prevotella,
 Fusobacterium,
 Peptostreptococcus,
 Admixed with aerobic bacteria
 Streptococcus pneumoniae,
 Staphylococcus aureus,
 Haemophilus influenzae, and
 Pseudomonas aeruginosa
LUNG ABSCESS
 DEFINITION:
 The term “pulmonary abscess” describes a local
suppurative process within the lung,
characterized by necrosis of lung tissue.
LA: CAUSATIVE AGENTS
 Although under appropriate circumstances any
pathogen can produce an abscess, the commonly
isolated organisms include aerobic and anaerobic
streptococci, S. aureus, and a host of gram-negative
organisms.
 Anaerobic organisms normally found in the oral cavity,
including members of the Bacteroides, Fusobacterium,
and Peptococcus species, are the exclusive isolates in
about 60% of cases.
LA: PATHOGENESIS
 Aspiration of infective material (the most frequent cause):
This is particularly common in acute alcoholism, coma,
anesthesia, sinusitis, gingivodental sepsis, and debilitation in
which the cough reflexes are depressed.
 Antecedent primary lung infection: Post-pneumonic abscess
formations are usually associated with S. aureus, K. pneumoniae,
and the type 3 pneumococcus. Posttransplant or otherwise
immunosuppressed individuals are at special risk.
 Septic embolism: Infected emboli from thrombophlebitis in
any portion of the systemic venous circulation or from the
vegetations of infective bacterial endocarditis on the right
side of the heart are trapped in the lung.
 Neoplasia: Secondary infection is particularly common in the
bronchopulmonary segment obstructed by a primary or
secondary malignancy (postobstructive pneumonia).
 Miscellaneous: Direct traumatic penetrations of the lungs;
spread of infections from a neighboring organ, such as
suppuration in the esophagus, spine, subphrenic space, or
pleural cavity; and hematogenous seeding of the lung by
pyogenic organisms all may lead to lung abscess formation.
 When all these causes are excluded, there are still cases in which
no reasonable basis for the abscess formation can be identified.
These are referred to as primary cryptogenic lung abscesses.
LUNG ABSCESS: MORPHOLOGY(1)
 SIZE: Abscesses vary in diameter from lesions of a few
milimeters to large cavities of 5 to 6 cm.
 DISTRIBUTION:
 Pulmonary abscesses due to aspiration are more
common on the right (because of the more vertical
right main bronchus) and are most often single.
 Abscesses that develop in the course of pneumonia or
bronchiectasis are usually multiple, basal, and
diffusely scattered.
 Septic emboli and pyemic abscesses are multiple and
may affect any region of the lungs.
LUNG ABSCESS: MORPHOLOGY(2)
 The cardinal histologic change in all abscesses is
suppurative destruction of the lung parenchyma within
the central area of cavitation.
 Continued infection leads to large, green-black,
multilocular cavities with poor demarcation of their
margins, designated as “gangrene of the lung”.
 In chronic cases considerable fibroblastic proliferation
produces a fibrous wall.
PYEMIC LUNG
ABSCESS WITH TOTAL
DESTRUCTION OF
UNDERLYING
PARENCHYMAL
TISSUE
LUNG ABSCESS: CLINICAL COURSE
 The manifestations of pulmonary abscesses are much like those
of bronchiectasis and are characterized principally by cough,
fever, and copious amounts of foul-smelling purulent or
sanguineous sputum. Fever, chest pain, and weight loss are
common. Clubbing of the fingers and toes may appear
within a few weeks after the onset of an abscess.
 Diagnosis of this condition can be only suspected from the
clinical findings and must be confirmed radiologically.
 Whenever an abscess is discovered in older individuals, it is
important to rule out an underlying carcinoma, because this is
present in 10% to 15% of cases.
 Complications include extension of the infection into the pleural
cavity, hemorrhage, the development of brain abscesses or
meningitis from septic emboli, and (rarely) secondary
amyloidosis (type AA).
CHRONIC PNEUMONIA
 CAUSATIVE AGENTS:
 Nocardia
 Actinomyces
 Granulomatous:
 Mycobacterium tuberculosis and atypical
mycobacteria,
 Histoplasma capsulatum,
 Coccidioides immitis,
 Blastomyces dermatitidis
IN SHORT: CHRONIC PNEUMONIAS
CAUSED BY FUNGI: HISTOPLASMOSIS
 In the lungs of otherwise healthy adults, Histoplasma
infections produce epithelioid cell granulomas, which
usually undergo caseation necrosis and coalesce to
produce large areas of consolidation but may also
liquefy to form cavities (seen in patients with COPD).
 With spontaneous or drug control of the infection, these
lesions undergo fibrosis and concentric calcification
(tree-bark appearance.
 Histologic differentiation from tuberculosis,
sarcoidosis, and coccidioidomycosis requires
identification of the 3- to 5-μm thin-walled yeast forms
that may persist in tissues for years.
HISTOPLASMOSIS
A, Laminated Histoplasma
granuloma of the lung
B, Histoplasma capsulatum yeast
forms fill phagocytes in the lung of
a patient with disseminated
histoplasmosis (silver stain).
BLASTOMYCOSIS
 CAUSATIVE AGENT: Blastomyces dermatitidis
 MORPHOLOGY:
 In the normal host the lung lesions of blastomycosis
are suppurative granulomas.
 In tissue, B. dermatitidis is a round, 5- to 15-μm yeast
cell that divides by broad-based budding. It has a
thick, double -contoured cell wall and multiple nuclei.
A, Rounded budding yeasts, larger than neutrophils, are present.
Note the characteristic thick wall and nuclei (not seen in other
fungi).
B, Silver stain.
COCCIDIOIDOMYCOSIS
 CAUSATIVE AGENT: Coccidioides immitis
 MORPHOLOGY:
 C. immitis is present as thick-walled, nonbudding
spherules 20 to 60 μm in diameter, often filled with
small endospores.
 A pyogenic reaction is superimposed when the
spherules rupture to release the endospores
Coccidioidomycosis with intact and ruptured spherules.
PULMONARY DISEASE IN HIV
INFECTION: CLINICAL FEATURES WITH
DIAGNOSTIC CRITERIA
 Despite the emphasis on “opportunistic” infections, it
must be remembered that bacterial lower respiratory
tract infection caused by the “usual” pathogens is one
of the most serious pulmonary disorders in HIV
infection.
 The implicated organisms include S. pneumoniae, S.
aureus, H. influenzae, and gram-negative rods.
DIAGNOSTIC CRITERIA
 The CD4+ T-cell count can define the risk of
infection with specific organisms. As a rule of
thumb, bacterial and tubercular infections are
more likely at higher CD4+ counts (>200
cells/mm3).
 Pneumocystis pneumonia usually strikes at CD4+
counts below 200 cells/mm3,
 while cytomegalovirus and Mycobacterium avium
complex infections are uncommon until the very
late stages of immunosuppression (CD4+ counts
<50 cells/mm3).