Pathology of Pneumonia POWERPOINT PRESENTATION

PATHOLOGY OF PNEUMONIA

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Introduction:
5000 sq meters
Filters >10,000 L of air / day…!
Normal lungs are sterile.
Delicate, thin resp. mem–gas exch.
Filter, humidify, sterilize, highlysensitive.
RTI –Resp. tract inf. commonest in medical
practice.
Enormous morbidity & mortality.
Pneumonia–inflammation of alveoli.

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Lung defense mechanisms
A, Innate defensesagainst infection:
1, In the normal lung, removal of microbial
organisms depends on entrapment in the mucous
blanket and removal by means of the mucociliary
elevator
2, phagocytosis by alveolar macrophages that can
kill and degrade organisms and remove them from
the air spaces by migrating onto the mucociliary
elevator
.

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3, phagocytosis and killing by neutrophils recruited
by macrophage factors.
4, Serum complement may enter the alveoli and
be activated by the alternative pathway to provide
the opsonin C3b, which enhances phagocytosis
5, Organisms, including those ingested by
phagocytes, may reach the draining lymph nodes
to initiate immune responses

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Additional mechanisms operate after
development of adaptive immunity.
1, Secreted IgA can block attachment of the microorganism
to epithelium in the upper respiratory tract.
2, In the lower respiratory tract, serum antibodies (IgM,
IgG) are present in the alveolar lining fluid. They activate
comple-mentmore efficiently by the classic pathway,
yielding C3b (not shown). In addition, IgGis opsonic.
3, The accumulation of immune T cells is important for
controlling infections by viruses and other intracellular
microorganisms. PMN, polymorphonuclearcell

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Normal Lung

7. Normal
Lung

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Etiology:
Decreased resistance -General/immune
Virulent infection -Lobar pneumonia
Defective Clearing mechanism
Cough/gag Reflex –Coma, paralysis, sick.
Mucosal Injury –smoking, toxin aspiration
Low Alveolar defense -Immunodeficiency
Pulmonary edema –Cardiac failure, emboli.
Obstructions –foreign body, tumors

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Patterns of Lung disorders:
Airway
Bronchitis, Bronchiectasis, Bronchiolitis.
Tumors / Cancer
Parenchyma
Pneumonia.
Lung abscess, TB
Hyaline membrane dis (HMD & ARDS)
Pneumoconiosis
Tumors / Cancer
Pleura:
Pleural effusion (TB)
Tumors / Cancer
* Infections

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PNEUMONIAS
ACUTE INFLAMMATION OF LUNG PARENCHYMA
PATHOGENESIS
•INHALATION OF MICROBES
•HEMATOGENOUS SPREAD
•ASPIRATION
•DIRECT SPREAD
•ALTERED NORMAL DEFENCE MECHANISM
•ALTERED CONSCIOUSNESS
•DEPRESSED COUGH AND GLOTTIC REFLEXES
•IMPAIRED ALVEOLAR MACROPHAGE FUNCTION
•ENDOBRONCHIAL OBSTRUCTION
•LEUCOCYTE DYSFUNCTION

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Classification
Community-Acquired Acute Pneumonia
Streptococcus pneumoniae
Haemophilusinfluenzae
Moraxella catarrhalis
Staphylococcus aureus
Legionella pneumophila
Enterobacteriaceae(Klebsiella
pneumoniae) and Pseudomonas spp.

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Community-Acquired Atypical Pneumonia
Mycoplasma pneumoniae
Chlamydia spp.—Chlamydia pneumoniae,
Chlamydia psittaci, Chlamydia trachomatis
Coxiellaburnetii(Q fever)
Viruses: respiratory syncytial virus,
human metapneumovirus,
parainfluenzavirus (children);
influenza A and B (adults);
adenovirus (military recruits)

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Nosocomial Pneumonia
Gram-negative rods belonging to Enterobacteriaceae
(Klebsiellaspp., Serratiamarcescens, Escherichia coli) and
Pseudomonas spp. S. aureus(usually methicillin-resistant)
Aspiration Pneumonia
Anaerobic oral flora (Bacteroides, Prevotella,
Fusobacterium, Peptostreptococcus), admixed with aerobic
bacteria (S. pneumoniae, S. aureus, H. influenzae, and
Pseudomonas aeruginosa)

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Chronic Pneumonia
NocardiaActinomycesGranulomatous: Mycobacterium
tuberculosis and atypical mycobacteria, Histoplasma
capsulatum, Coccidioidesimmitis, Blastomycesdermatitidis
Necrotizing Pneumonia and Lung Abscess
Anaerobic bacteria (extremely common), with or without
mixed aerobic infection S. aureus, K. pneumoniae,
Streptococcus pyogenes, and type 3 pneumococcus
(uncommon)

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Pneumonia in the Immunocompromised
Host
Cytomegalovirus Pneumocystis jiroveci
Mycobacterium aviumcomplex (MAC)
Invasive aspergillosis
Invasive candidiasis
“Usual” bacterial, viral, and fungal organisms
(listed above)

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Pathogenesis of Pulmonary Infections
Step 1: Entry
Aspiration(ie Pneumococcus)
Inhalation(ie Mtb and viral pathogens)
Inoculation(contaminated equipment)
Colonization(in patients with COPD)
Hematogenousspread (patients with
sepsis)
Direct spread(adjacent abscess)

17. Pathogenesis:

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Pneumonia Types:
Etiologic Types:
Infective
Viral
Bacterial
Fungal
Tuberculosis
Non Infective
Toxins
chemical
Aspiration
Morphologic types:
Lobar
Broncho
Interstitial
Duration:
Acute
Chronic
Clinical:
Primary / secondary.
Typical / Atypical
Community a / hospital a

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ETIOLOGY
BACTERIAL PNEUMONIA
PNEUMOCOCCAL CAUSED BY STREPTOCOCCUS
PNEUMONIAE
STAPHYLOCOCCAL
STREPTOCOCCAL(B HEMOLYTIC STRETOCOCCI)
GRAM NEGATIVE BACTERIA
KLEBSIELLA
HAEMOPHILUS INFLUENZAE
PSEUDOMONAS
PATHOLOGY
ACUTE BRONCHIOLITIS
SUPPURATIVE EXUDATE THICKENING OF ALVEOLAR
SEPTA BY
CONGESTED CAPILLARIES AND
LEUCOCYTE
INFILTERATION.

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VIRAL AND MYCOPLASMAL PNEUMONIA
PATCHY INFLAMMATION CONFINED TO INTERSTITIAL TISSUES OF LUNGS WITHOUT
ALVEOLAR EXUDATE.
ETIOLOGY
RESPIRATORY SYNCYTIAL VIRUS
MYCOPLASMA PNEUMONIAE
ADENO VIRUS
RHINO VIRUS
CMV
CHLAMYDAIA
Q FEVER
PATHOLOGY
INTERSTITAL INFLAMMATION
NECROTISING BRONCHIOLITIS
ALVEOLAR CHANGES
CLINICAL FEATURES
UPPER RESPIRATORY SYMPTOMS,FEVER,HEAD ACHE,NON PRODUCTIVE COUGH.

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CLINICAL FEATURES
CHILLS
FEVER
MALAISE
PLEURITIC CHEST PAIN
DYSPNOEA
COUGH WITH EXPECTORATION
HYPOXAEMIA
BRONCHOPNEUMONIA
INFECTION OF TERMINAL BRONCHIOLES
EXTENDING INTO SURROUNDING
ALVEOLI
RESULTING IN PATCHY CONSOLIDATION.
OCCURS IN EXTREMES OF LIFE .

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Streptococcus pneumoniae Infections
three subsets of patients:
those with underlying chronic diseases such as CHF, COPD, or
diabetes;
those with either congenital or acquired immunoglobulin
defects (e.g., with the acquired immune deficiency syndrome
[AIDS]); and
those with decreased or absent splenic function (e.g., sickle
cell disease or after splenectomy).
spleen contains the largest collection of phagocytes and is there-
fore the major organ responsible for removing pneumo-cocci
from the blood and also produces antibodies against
polysaccharides -against encapsulated bacteria.

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Lobar Pneumonia:
whole lobe, exudation -consolidation
95% -Strep pneum.(Klebsiella in aged, DM,
alcoholics)
High fever, rusty sputum, Pleuritic chest pain.
the lower lobes or the right middle lobe is most
frequently involved

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Four stages:
Congestion–1d –vasodilatation
congestion.
RedHepatization2d Exudation+RBC
GrayHepatizaiton4d neutro& Macrophages.
Resolution–8d few macrophages, normal.

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congestion
the affected lobe(s) is
(are) heavy, red, and
boggy;
histologically,vascular
congestion can be seen,
with proteinaceous fluid,
scattered neutrophils,
and many bacteria in
the alveoli

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red hepatization–
lung lobe has a liver-like
consistency; the
alveolar spaces are
packed with neutrophils,
red cells, and fibrin

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gray
hepatization-
lung is dry, gray, and
firm, because the red
cells are lysed and
fibrinosuppurative
exudate persists
within the alveoli
Resolution -uncomplicated
cases, as exudates within the alveoli
are enzymatically digested to
produce granular, semifluid debris
that is resorbed, ingested by
macrophages, coughed up, or
organized by fibroblasts growing
into it
The pleural reaction (fibrinous or
fibrinopurulent pleuritis) may
similarly resolve or under-go
organization, leaving fibrous
thickening or permanent adhesions.

28. Congestion
Red Hepatisation
Grey Hepatization
Resolution
Pathogenesis of Pneumonia

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Lobar
Pneumonia:

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Lobar
Pneumonia:

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Lobar Pneumonia –Gray hep…

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Lobar Pneumonia:

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Complications of Pneumonia
Abscesses
Localized tissue destruction and necrosis may lead to
abscess
Right side often in aspiration.
Staphylococcus; Klebsiella; Pneudomonas
Pleuritis / Pleural effusion.
Inflammation of the pleura ( Streptococcus pneumoniae)
Blood rich exudate (esp. rickettsial diseases)
Empyema
Pus in the pleural space.

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Septicemia
bacteremicdissemination may lead to meningitis,
arthritis, or infective endocarditis. Complications are
much more likely with serotype 3 pneumococci
organizationof the intra-alveolar exudate may
convert areas of the lung into solid fibrous tissue

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Bronchopneumonia (patchy)
Extremes of age. (infancy and old age)
Staph, Strep, Pneumo & H. influenza
Patchy consolidation –distributed in patches not limited to
lobes.
Suppurative inflammation
Usually bilateral
Lower lobes common

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Broncho-
pneumonia
GROSS-Well-developed
lesions up to 3 or 4 cm in
diameter are slightly elevated
and are gray-red to yellow;
lung substance immediately
surrounding areas of
consolidation is usually
hyperemicand edematous, but
the large intervening areas are
generally normal.
Pleural involvement is less
common than in lobar
pneumonia.
Histologically, the
reaction consists
of focal sup-
purative exudate
that fills the
bronchi,
bronchioles, and
adja-cent
alveolar spaces.

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Broncho-pneumonia

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Bronchopneumonia:

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Broncho–Pneumonia-Lobar
Extremes of age.
Secondary.
Both genders.
Staph, Strep, H.infl.
Patchy consolidation
Around Small airway
Not limited by
anatomic boundaries.
Usually bilateral.
Middle age –20-50
Primary in a healthy
males common.
95% pneumoc (Klebs.)
Entire lobe consolidation
Diffuse
Limited by anatomic
boundaries.
Usually unilateral

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Interstitial / atypical Pneumonia
Primary atypical pneumonia in the
immunocompetant host (Mycoplasma or
Chlamydia)
Interstitial pneumonitis
immunocompromised host : Pneumocystic carinii; CMV
Immunocompetant host: Influenza A
Gross features:
Lungs are heavy but not firmly consolidated
Microscopic features:
Septal mononuclear infiltrate
Alveolar air spaces either ‘empty’ or filled with
proteinaceous fluid with few or no inflammatory cells

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Interstitial Pneumonia:
Lymphocyte
Infiltrate in
alveloar wall

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Chronic Pneumonia
Chronic, lymphoid infiltrate,
No classic stages.
Lung destruction –cavity, abscess etc.
Organisms
Mycobacterium tuberculosis
Histoplasma capsulatum
Aspergillosis
Actinomyces

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FibrocavitatingTuberculosis

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45Dr.D.Gomathinayagam, M.D.,
TB Granuloma with caseation

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Langhans’ Giant cell

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candida -psuedohyphae

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Cryptococci

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Aspergillosis

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Mucormycosis

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Actinomycotic colony

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Histoplasmosis

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Comm–Pneumonia-Nosoc
In healthy adults
Gram positive.
Streptococcus
pneumoniae (90%)
Strep. Pyogenes,
Staph, H.
influenzae and
Klebsiella in elderly
or with COPD.
In *sick patients.
gram-negative bacilli
Pseudomonas
aeruginosa, Escherichia
coli, Enterobacter,
Proteus, and Klebsiella.

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Pathogenesis of Clinical features:
*Alveolar inflammation.
Tachypnoea, Dyspnoea, Resp Acidosis
Solid/airless lungs –decreased
oxygenation.
Dull percussion-Consolidation –
Exudation
Rusty sputum-RBC & Inflammatory cells.
Fever –Inflammatory mediators.

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LUNG ABSCESS
LOCALISED AREA OF NECROSIS WITH
SUPPURATION.MORE COMMON IN RIGHT LUNG,
RIGHT APEX OF LOWER LOBE.
PRIMARY
SECONDARY
ETIOPATHOGENSIS
STAPHYLOCOCCUS,STREPTOCOCCUS ETC.
ASPIRATION
SECONDARY TO PNEUMONIA
BRONCHIAL OBSTRUCTION
SEPTIC EMBOLI
DIRECT EXTENSION

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GROSS –ABSCESS WALL SURROUNDED
BY ACUTE PNEUMONIA
CLINICAL FEATURES
•FEVER
•MALAISE
•LOSS OF WEIGHT
•COUGH
•PURULENT EXPECTORATION
•HAEMOPTYSIS
•CLUBBING OF FINGERS AND TOES.

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Lung Abscess:

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Lung Fungal Abscess: Candida