RESPIRATORY PATHOLOGY

1. MBChB
Y3
RESPIRATORY PATHOLOGY
- PNEUMONIA
SAMOEI – EGERTON UNIVERSITY

2. RESPIRATORY
PATHOLOGY
2
1. Paediatric lung disease
2. Pulmonary vascular disease
3. Pulmonary infections
4. Chronic obstructive pulmonary
disease
5. Chronic restrictive pulmonary
disease
6. Tumours of lungs
7. Pleura and diseases

3. CONTENTS
1. ANATOMY OF LUNGS REVIEW
2. PULMONARY INFECTIONS
3. DEFINITION OF PNEUMONIA
4. ETIOPATHOGENESIS
5. CLASSIFICATION
6. MORPHOLOGICAL FEATURES
7. CLINICAL FEATURES
8. DIAGNOSIS/TESTS
9. TREATMENT AND PREVENTION
10.MANAGEMENT
3

4. 4
• Acute and chronic pulmonary infections are common at all ages and
are a frequent cause of death.
• They are generally caused by a wide variety of microorganisms such
as bacteria, viruses, fungi and mycoplasma.
• Important and common examples of acute pulmonary infections are:
• Pneumonias
• Fungal infections
• Lung abscess
• Pulmonary tuberculosis
PULMONARY INFECTIONS

5. PNEUMONIA
5
GENERAL CONSIDERATIONS

6. 6
• Is acute inflammation of the lung parenchyma distal to the terminal
bronchioles (consisting of the respiratory bronchiole, alveolar ducts,
alveolar sacs and alveoli).
• The terms ‘pneumonia’ and ‘pneumonitis’ are often used
synonymously for inflammation of the lungs, while ‘consolidation’
(meaning solidification) is the term used for gross and radiologic
appearance of the lungs in pneumonia.
DEFINITION - PNEUMONIA

7. 7
PATHOGENESIS
Microorganisms gain entry into the lungs
by one of the following four routes:
1. Inhalation of the microbes present in
the air.
2. Aspiration of organisms from
nasopharynx or oropharynx.
3. Hematogenous spread from a distant
focus of infection.
4. Direct spread from an adjoining site
of infection.
The normal lung is free of bacteria because
of the presence of a number of lung defense
mechanisms at different levels such as:
1. Nasopharyngeal filtering action
2. Mucociliary action of the lower
respiratory airways
3. Presence of phagocytosing alveolar
macrophages
4. IgAs.
Failure of these defense mechanisms and
presence of certain predisposing factors
result in pneumonias. These conditions are:
1. Altered consciousness
2. Depressed cough and glottic reflexes
3. Impaired mucociliary transport
4. Impaired alveolar macrophage function
5. Endobronchial obstruction
6. Immunocompromised states

8. 8
CONT…
Altered consciousness
Oropharyngeal contents may be aspirated in
states causing unconsciousness e.g. in coma,
cranial trauma, seizures, CVAs, drug overdose,
alcoholism etc.
Depressed cough and glottic reflexes
May allow aspiration of gastric contents e.g. in
old age, pain from trauma or thoracoabdominal
surgery, neuromuscular disease, weakness d/t
malnutrition, kyphoscoliosis, severe OPDs,
endotracheal intubation and tracheostomy.
Endobronchial obstruction
Interferes with effective clearance mechanism
e.g in tumor, foreign body, cystic fibrosis and
chronic bronchitis.
Impaired mucociliary transport
• Normal protection offered by mucus-covered
ciliated epithelium is impaired or destroyed in
many conditions, favouring passage of bacteria
into the lung parenchyma.
• The conditions are cigarette smoking, viral
respiratory infections, immotile cilia syndrome,
inhalation of hot or corrosive gases and old
age.
Impaired alveolar macrophage function
Permits growth of microorganisms e.g. by
cigarette smoke, hypoxia, starvation, anemia,
pulmonary edema and viral respiratory
infections.
Immunocompromised states
• In congenital and acquired immunodeficiencies
(e.g. AIDS, debility, senility,
immunosuppressive therapy) and granulocyte
abnormalities may predispose to pneumonia.

9. 9
CLASSIFICATION
BASED ON:
Anatomical classification:
-Anatomic region of the lung
parenchyma involved
1. Lobar pneumonia
2. Bronchopneumonia (Lobular
pneumonia)
3. Interstitial pneumonia.
Clinical settings in which infection
occurred:
1. Community-acquired pneumonia
2. Health care-associated pneumonia
(including hospital acquired pneumonia)
3. Ventilator-associated pneumonia
Etiological classification:
1. Bacterial pneumonia
2. Viral pneumonia
3. Pneumonias from other etiologies.
• In the present discussion, a combined
approach of etiologic and morphologic
classification will be followed.

10. CLASSIFICATION
10

11. 11
General signs and symptoms
Main symptoms:
• Cough with greenish or yellow
mucus;
• Bloody sputum happens on
occasion
• Fever with shaking chills
• Sharp or stabbing chest pain
worsened by deep breathing or
coughing
• Rapid, shallow breathing
• Shortness of breath
Additional symptoms:
• Headache
• Excessive sweating and clammy
skin
• Loss of appetite
• Excessive fatigue
• Confusion in older people

12. 12
Diagnosis
Medical history
Emphysema, tobacco abuse,
Physical examination
Listen to lungs with a stethoscope to
check for bubbling or crackling sounds
and for rumblings, which means
there’s thick liquid in your lungs. Both
these sounds could mean there is
inflammation caused by an infection.
CXR; will show whether or not you
have pneumonia and if so, how severe
the infection is and where it’s located.
CT scan; If the x-rays aren't clear
CBC; to check your WCC or to
look for viruses, bacteria, or other
organisms; If WCC is high, this
suggests bacterial infection
Examination of phlegm or blood;
to help identify microorganism
that's causing the pneumonia.
ABGs; to check how well you are
oxygenating your blood
Bronchoscopy; in more advanced
pneumonia
Once the organism causing the
pneumonia is identified, a treatment
plan is developed

13. 13
Treatment
• If the cause is bacterial, cure the infection
with antibiotics - Doxycycline
• Respiratory treatments to remove
secretions may be necessary.
• Occasionally, steroid medications may be
used to reduce wheezing if there is an
underlying lung disease.
• Antiviral medications can reduce the
severity of the viral infection if taken 1 to
2 days after symptoms begin.
• In some cases it is difficult to distinguish
between viral and bacterial pneumonia, so
antibiotics may be prescribed.
• If you have an underlying chronic disease,
severe symptoms, or low oxygen levels,
you will likely require hospitalization for
IV antibiotics and oxygen therapy.
• Infants and the elderly are more
commonly admitted for treatment of
pneumonia.
• Many people can be treated at home with
antibiotics.
Home remedies:
• Drink plenty of fluids to help loosen
secretions and bring up phlegm.
• Get lots of rest.
• Have someone else do household chores.
• Control your fever with aspirin or
acetaminophen.
• DO NOT give aspirin to children.

14. 14
• With treatment, most patients will improve within two weeks.
• Elderly or debilitated patients who fail to respond to treatment may die
from respiratory failure.
Prognosis

15. 15
ADD A FOOTER
1. Organization
2. Empyema
3. Lung abscess
4. Metastatic infection
5. Pleural effusion
Complications
O/E

16. 16
Prevention
Germs that cause pneumonia can be
contagious and are spread through coughing
and sneezing. You can prevent pneumonia
by following good hygiene habits.
Cough or sneeze into a tissue.
Use separate drinking glasses and eating
utensils.
Wash your hands often with warm soapy
water.
Use alcohol based gel for hand washing
when soap and water are not available.
Avoid smoking. Tobacco damages your
lung's ability to ward off infection.
Wear a mask when cleaning dusty or
moldy areas
Vaccination of children, the elderly, and
people with diabetes, asthma, emphysema,
HIV, cancer, or other chronic conditions:
-Pneumococcal vaccine (Pneumovax,
Prevnar) prevents Streptococcus
pneumoniae.
-Flu vaccine prevents pneumonia and other
infections caused by influenza viruses. It
must be given yearly to protect against new
viral strains.
-Hib vaccine prevents pneumonia in
children from Hemophilus influenzae type b.

17. 17
ADD A FOOTER
Lobar pneumonia
Lobular pneumonia (bronchopneumonia)
Legionella pneumonia
1. BACTERIAL PNEUMONIA

18. 18
• Bacterial infection of the lung parenchyma
• Is the most common cause of pneumonia or consolidation of one or
both the lungs.
Types:
1. Lobar pneumonia
2. Bronchopneumonia (lobular pneumonia)
3. Legionella pneumonia
Confluent pneumonia combines the features of both lobar and lobular
and involves larger (confluent) areas in both lungs irregularly, others
consider this as a variant of bronchopneumonia.
BACTERIAL PNEUMONIA

19. 19
Lobar pneumonia
Acute bacterial infection of part of a lobe,
the entire lobe, or even two lobes of one or
both lungs.
ETIOLOGY
• There are 4 types based on causative
microbial agent
Pneumococcal pneumonia
Most common form of lobar pneumonias
(>90% of all lobar pneumonias)
Caused by Streptococcus pneumoniae
Type 3 S. pneumoniae causes particularly
virulent form of lobar pneumonia.
Is community-acquired infection.
Staphylococcal pneumonia
Staphylococcus aureus causes pneumonia
by hematogenous spread of infection from
another focus or after viral infections.
Streptococcal pneumonia
Hemolytic streptococci may rarely cause
pneumonia such as in children after
measles or influenza, in severely
debilitated elderly patients and in
diabetics.
Pneumonia by gram -ve aerobic bacteria
Gram –ve bacteria less likely cause lobar
pneumonia.
Hemophilus influenzae, Klebsiella
pneumoniae (Friedlander’s bacillus),
Pseudomonas, Proteus and Escherichia
coli, H. influenzae commonly causes
pneumonia in children below 3 years of
age after a preceding viral infection.

20. 20
Morphologic
features
Laennec’s description divides lobar
pneumonia into 4 sequential pathologic
phases:
1. Stage of congestion (initial phase)
2. Red hepatisation (early consolidation)
3. Grey hepatisation (late consolidation)
4. Resolution.
These stages seen in untreated cases are found
much less often nowadays d/t early institution
of abx therapy and improved medical care.
In lobar pneumonia, as the name suggests,
part of a lobe, a whole lobe, or two lobes are
involved, some times bilaterally.
The lower lobes are affected most commonly.
STAGE OF CONGESTION: INITIAL
PHASE
• Represents the early acute inflammatory
response to bacterial infection that lasts for
1 to 2 days.
Grossly,
The affected lobe is enlarged, heavy, dark
red and congested.
Cut surface exudes blood-stained frothy
fluid.
Histologically,
1. Dilatation and congestion of the
capillaries in the alveolar walls.
2. Pale eosinophilic edema fluid in the air
spaces.
3. A few red cells and neutrophils in the
intra-alveolar fluid.
4. Numerous bacteria demonstrated in the
alveolar fluid by Gram’s staining.

21. 21
Cont…
RED HEPATISATION: EARLY CONSOLI
DATION
This phase lasts for 2 to 4 days.
Hepatisation refers to liver-like consistency of the
affected lobe on cut section.
Grossly,
Affected lobe is red, firm and consolidated.
The cut surface of the involved lobe is airless, red-
pink, dry, granular and has liver-like consistency.
This stage of red is accompanied by serofibrinous
pleurisy.
Histologically,
1. Edema fluid of the preceding stage is replaced
by strands of fibrin.
2. There is marked cellular exudate of neutrophils
and extravasation of red cells.
3. Many neutrophils show ingested bacteria
4. The alveolar septa are less prominent than in the first
stage due to cellular exudation.
GREY HEPATISATION: LATE CONSOLI DATION
This phase lasts for 4 to 8 days.
Grossly,
The affected lobe is firm and heavy.
The cut surface is dry, granular and grey in appearance
with liver-like consistency.
The change in colour from red to grey begins at the hilum
and spreads towards the periphery.
Fibrinous pleurisy is prominent.
Histologically,
1. Fibrin strands are dense and more numerous.
2. Cellular exudate of neutrophils is reduced due to
disintegration of many inflammatory cells as
evidenced by their pyknotic nuclei. Red cells are also
fewer. Macrophages begin to appear in the exudate.
3. Cellular exudate is often separated from the septal
walls by a thin clear space.
4. Organisms are less numerous and appear as
degenerated forms.

22. 22
Cont…
RESOLUTION
This stage begins by 8th to 9th day if no
chemotherapy is administered and is completed in
1 to 3 weeks.
However, antibiotic therapy induces resolution on
about 3rd day.
Resolution proceeds in a progressive manner.
Grossly,
Previously solid fibrinous constituent is liquefied
by enzymatic action, eventually restoring the
normal aeration in the affected lobe.
The process of softening begins centrally and
spreads to the periphery.
Cut surface is grey-red or dirty brown and frothy,
yellow, creamy fluid can be expressed on pressing.
The pleural reaction may also show resolution
but may undergo organisation leading to
fibrous obliteration of pleural cavity.
Histologically,
1. Macrophages are the predominant cells in
the alveolar spaces, while neutrophils
diminish in number. Many of the
macrophages contain engulfed neutrophils
and debris.
2. Granular and fragmented strands of fibrin
in the alveolar spaces are seen due to
progressive enzymatic digestion.
3. Alveolar capillaries are engorged.
4. There is progressive removal of fluid
content as well as cellular exudate from the
air spaces, partly by expectoration but
mainly by lymphatics, resulting in
restoration of normal lung parenchyma with
aeration.

23. 23
Complications
Since the advent of antibiotics, serious
complications of lobar pneumonia are
uncommon.
May develop in neglected cases and in patients
with impaired immunologic defenses.
Include:
Organisation
In about 3% of cases, resolution of the exudate
does not occur but instead it undergoes
organisation.
There is ingrowth of fibroblasts from the
alveolar septa resulting in fibrosed, tough, airless
leathery lung tissue.
This type of post-pneumonic fibrosis is called
carnification.
Pleural effusion
About 5% of treated cases of lobar pneumonia develop
inflammation of the pleura with effusion.
The pleural effusion usually resolves but sometimes
may undergo organisation with fibrous adhesions
between visceral and parietal pleura.
Empyema
Less than 1% of treated cases of lobar pneumonia
develop encysted pus in the pleural cavity termed
empyema.
Lung abscess
A rare complication of lobar pneumonia is formation
of lung abscess, especially when there is secondary
infection by other organisms.
Metastatic infection
Occasionally, infection in the lungs and pleural cavity
in lobar pneumonia may extend into the pericardium
and the heart causing purulent pericarditis, bacterial
endocarditis and myocarditis.
Other forms of metastatic infection encountered rarely
in lobar pneumonias are otitis media, mastoiditis,
meningitis, brain abscess and purulent arthritis.

24. 24
1. Shaking chills,
2. Fever,
3. Malaise with pleuritic chest pain
4. Dyspnea
5. Cough with expectoration which is mucoid, purulent or even bloody.
6. Tachycardia and tachypnea
7. Cyanosis if the patient is severely hypoxemic.
8. Marked neutrophilic leucocytosis.
9. Blood cultures are positive in about 30% of cases.
10. Chest radio graph may reveal consolidation.
Clinical features

25. 25
• Is infection of the terminal bronchioles
• Extends into the surrounding alveoli
• Resulting in patchy consolidation of the lung.
• The condition is frequent at the extremes of life (in infancy & old age)
Bronchopneumonia/Lobular
pneumonia

26. 26
Morphologic
features
Grossly,
• Patchy areas of red or grey
consolidation often involving the
lower zones of the lungs due to
gravitation of the secretions.
• On cut surface, these patchy
consolidated lesions are dry,
granular, firm, red or grey in colour,
3 to 4 cm in diameter, slightly
elevated over the surface and are
often centered around a bronchiole
• These patchy areas are best
picked up by passing the
fingertips on the cut surface.
Histologically,
1. Acute bronchiolitis.
2. Suppurative exudate,
consisting chiefly of
neutrophils, in the
peribronchiolar alveoli.
3. Thickening of the alveolar
septa by congested capillaries
and leucocytic infiltration.
4. Less involved alveoli contain
edema fluid.

27. 27
• The complications of lobar pneumonia may occur in
bronchopneumonia as well.
• However, complete resolution of bronchopneumonia is uncommon.
• There is generally some degree of destruction of the bronchioles
resulting in foci of bronchiolar fibrosis that may eventually cause
bronchiectasis.
Complications

28. 28
• The patients of bronchopneumonia are generally infants or elderly
individuals.
• There may be history of preceding bed-ridden illness, chronic debility,
aspiration of gastric contents or upper respiratory infection.
• For initial 2 to 3 days, there are features of acute bronchitis but
subsequently signs and symptoms similar to those of lobar pneumonia
appear.
• Blood examination usually shows a neutrophilic leucocytosis.
• Chest radiograph shows mottled, focal opacities in both the lungs,
chiefly in the lower zones.
Clinical features

29. 29
• Legionella pneumonia or Legionnaire’s disease is an epidemic illness
caused by gram-negative bacilli, Legionella pneumophila that thrives in
aquatic environment.
• It was first recognized following investigation into high mortality among
those attending American Legion Convention in Philadelphia in July 1976
and hence the name.
• The epidemic occurs in summer months by spread of organisms through
contaminated drinking water or in air-conditioning cooling towers.
• Impaired host defenses in the form of immunodeficiency, corticosteroid
therapy, old age and cigarette smoking play important roles.
Legionella Pneumonia

30. 30
Grossly,
• There are changes of widespread bronchopneumonia involving many lobes and there may
be consolidation of the entire lung.
• Pleural effusion is frequently present.
Histologically,
• The changes are not distinctive.
• Common features are as under:
i) Intra-alveolar exudate, initially of neutrophils but later composed mainly of macrophages.
ii) Alveolar septa show foci of hyperplasia of the lining epithelium and thrombosis of
vessels in the septa.
iii) The organisms may be demonstrated in the macro phages by special stains or by
immunofluores cent techniques.
Morphologic features

31. 31
Clinical features
The disease begins with;
Malaise
Headache
Muscle-aches
High fever
Chills
Cough
Tachypnea.
Systemic manifestations unrelated
to pathologic changes in the lungs
are seen due to bacteremia and
include;
Abdominal pain
Watery diarrhea
Proteinuria
Mild hepatic dysfunction.

32. 32
ADD A FOOTER
(PRIMARY ATYPICAL PNEUMONIA)
2. VIRAL AND MYCOPLASMAL
PNEUMONIA

33. 33
• Characterised by patchy inflammatory changes, largely confined to
interstitial tissue of the lungs, without any alveolar exudate.
• Other terms used for these respiratory tract infections are interstitial
pneumonitis, reflecting the interstitial location of the infl ammation,
and primary atypical pneumonia, atypicality being the absence of
alveolar exudate commonly present in other pneumonias.
• Interstitial pneumonitis may occur in all ages.
• Most of the cases are mild and transient; exceptionally it may be
severe and fulminant.
VIRAL & MYCOPLASMAL PNEUMONIA

34. 34
• Interstitial pneumonitis is caused by a wide variety of agents, the most common
being respiratory syncytial virus (RSV).
• Others are Mycoplasma pneumoniae and many viruses such as influenza and para
infl uenza viruses, adenoviruses, rhinoviruses, coxsackieviruses and cyto
megaloviruses (CMV).
• Occasionally, psittacosis (Chlamydia) and Q fever (Coxiella) are associated with
interstitial pneumonitis.
• Infections of the respiratory tract with these organisms are quite common.
• In most cases, the infec tion remains confined to the upper respiratory tract
presenting as common cold.
• Occasionally, it may extend lower down to involve the interstitium of the lungs.
• The circumstances favouring such extension of infection are malnutrition, chronic
debilitating diseases and alcoholism.
Etiology

35. 35
Morphologic
features
• Irrespective of the etiologic agent, the pathologic changes are
similar in all cases.
Grossly,
• Depending upon the severity of infection, the involvement
may be patchy to massive and widespread consolidation of
one or both the lungs.
• The lungs are heavy, congested and subcrepitant.
• Sectioned surface of the lung exudes small amount of frothy
or bloody fluid.
• The pleural reaction is usually infrequent and mild.
Histologically,
• Hallmark of viral pneumonias is the interstitial nature of the
infl ammatory reaction.
• The microscopic features are as under:
i) Interstitial infl ammation There is thickening of alveolar
walls due to congestion, oedema and mononuclear inflammatory
infi ltrate comprised by lympho cytes, macrophages and some
plasma cells.
ii) Necrotising bronchiolitis This is
characterised by foci of necrosis of the
bronchiolar epithelium, inspissated
secretions in the lumina and mononuclear
infiltrate in the walls and lumina.
iii) Reactive changes The lining epithelial
cells of the bronchioles and alveoli
proliferate in the presence of virus and may
form multinucleate giant cells and syncytia
in the bronchiolar and alveolar walls.
Occasionally, viral inclusions (intranuclear
and/or intra cytoplasmic) are found,
especially in pneumonitis caused by CMV.
iv) Alveolar changes In severe cases, the
alveolar lumina may contain oedema fluid,
fibrin, scanty infl amatory exudate and
coating of alveolar walls by pink, hyaline
membrane similar to the one seen in
respiratory distress syndrome. Alveolar
changes are prominent if bacterial infection
supervenes.

36. 36
The major complication of interstitial pneumonitis is superimposed
bacterial infection and its complications.
Most cases of interstitial pneumonitis recover completely.
In more severe cases, there may be interstitial fibrosis and permanent
damage.
Complications

37. 37
• Majority of cases of interstitial pneumonitis initially have upper
respiratory symptoms with fever, headache and muscle-aches.
• A few days later, dry, hacking, non-productive cough with retrosternal
burning appears due to tracheitis and bronchitis.
• Blood fi lm shows characteristic neutrophilic leucocytosis.
• Chest radiograph may show patchy or diff use consolidation.
• Cold agglutinin titres in the serum are elevated in almost half the cases
of mycoplasmalpneumonia, 20% cases of adenovirus infection but
absent in other forms of viral pneumonia.
• Isolation of the etiologic agent, otherwise, is difficult.
Clinical features

38. 3. FUNGAL PNEUMONIAS
38
(FUNGAL INFECTIONS OF THE LUNG)
Pneumocystis pneumonia
Other fungal infections of the lung

39. 39
• Fungal infections of the lung are more common than tuberculosis in the US.
• These infections in healthy individuals are rarely serious but in
immunosuppressed individuals may prove fatal.
• General aspects of mycotic infections are covered in Chapter 6.
• Here, some common examples of fungal infections of the lung are briefly
given:
Pneumocystis pneumonia
Aspergillosis
Mucormycosis
Candidiasis
FUNGAL PNEUMONIAS
 Histoplasmosis
 Cryptococcosis
 Coccidioidomycosis
 Blastomycosis

40. 40
• Pneumocystis is an opportunistic fungal infection of the lungs.
• The original species P. carinii infects rats while P. jirovecii causes
pneumonia by inhalation of the organisms in neonates and
immunosuppressed people.
• Almost 100% cases of HIV/AIDS develop opportunistic infection
during the course of disease, most commonly Pneumocystis
pneumonia.
• Other immunosuppressed groups are patients on chemotherapy for
organ transplant and tumours, malnutrition, agammaglobulinemia etc.
Pneumocystis Pneumonia

41. 41
Grossly,
• The affected parts of the lung are consolidated, dry and grey.
Microscopically, the features are as under:
1. Interstitial pneumonitis with thickening and mononuclear infiltration of
the alveolar walls.
2. Alveolar lumina contain pink frothy fluid having the organisms.
3. By Grocott’s methenamine-silver (GMS) stain, the characteristic oval or
crescentic cysts, about 5μm in diameter and surrounded by numerous tiny
black dot-like organism P. jirovecii are demonstrable in the frothy fluid.
4. No significant inflammatory exudate is seen in the air spaces.
Morphologic features

42. 42
ADD A FOOTER
Rapid onset of;
Dyspnea
Tachycardia
Cyanosis
Non-productive cough.
If untreated;
t causes death in one or two weeks.
Chest radiograph shows diffuse alveolar and interstitial infiltrate.
Clinical features

43. 43
Other Fungal Infections of Lung
Aspergillosis
• Aspergillosis is the most common fungal
infection of the lung caused by Aspergillus
fumigatus that grows best in cool, wet climate.
• The infection may result in allergic
bronchopulmonary aspergillosis, aspergilloma
and necrotising bronchitis.
• Immunocompromised persons develop more
serious manifestations of aspergillus infection,
especially in leukemic patients on cytotoxic
drug therapy and HIV/AIDS.
• Extensive hematogenous spread of aspergillus
infection may result in widespread changes in
lung tissue due to arterial occlusion, thrombosis
and infarction.
MORPHOLOGIC FEATURES
Grossly, pulmonary aspergillosis may occur
within preexisting pulmonary cavities or in
bronchiectasis as fungal ball.
Microscopically,
 The fungus may appear as a tangled mass
within the cavity.
 The organisms are identified by their
characteristic morphology—thin septate
hyphae with dichotomous branching at
acute angles which stain positive for
fungal stains such as PAS and silver
impregnation technique.
 The wall of the cavity shows chronic
inflammatory cells.

44. 44
Cont…
Mucormycosis
 Mucormycosis or phycomycosis is caused
by Mucor and Rhizopus.
 The infection in the lung occurs in a
similar way as in aspergillosis.
 The pulmonary lesions are especially
common in patients of diabetic
ketoacidosis.
 Mucor is distinguished by its broad, non-
parallel, nonseptate hyphae which branch
at an obtuse angle.
 Mucormycosis is more often
angioinvasive, and disseminates; hence it
is more destructive than aspergillosis.
Candidiasis
 Candidiasis or moniliasis caused by
Candida albicans is a normal
commensal in oral cavity, gut and
vagina but attains pathologic form in
Immunocompromised host.
 Angioinvasive growth of the organism
may occur in the airways.
Histoplasmosis
 It is caused by oval organism,
Histoplasma capsulatum, by inhalation
of infected dust or bird droppings.
 The condition may remain
asymptomatic or may produce lesions
similar to the Ghon’s complex.

45. 45
Cont…
Cryptococcosis
• It is caused by Cryptococcus neofor
mans which is round yeast having a
halo around it due to shrinkage in
tissue sections.
• The infection occurs from infection
by inhalation of pigeon droppings.
• The lesions in the body may range
from a small parenchymal
granuloma in the lung to
cryptococcal meningitis.
Coccidioidomycosis
 Coccidioidomycosis is caused by
Coccidioides immitis which are spherical
spores.
 The infection in human beings is acquired
by close contact with infected dogs.
 The lesions consist of peripheral
parenchymal granuloma in the lung.
Blastomycosis
 It is an uncommon condition caused by
Blastomyces dermatitidis.
 The lesions result from inhalation of
spores in the ground.
 Pathological features may present as
Ghon’s complex-like lesion, as a
pneumonic consolidation and as multiple
skin nodules.

46. 4. NON-INFECTIVE PNEUMONIAS
46
Aspiration (Inhalation) Pneumonia
Hypostatic Pneumonia
Lipid Pneumonia

47. 47
• Aspiration or inhalation pneumonia results from inhalation of different
agents into the lungs.
• These substances include food, gastric contents, foreign body and
infected material from oral cavity.
• A number of factors predispose to inhalation pneumonia which
include: unconsciousness, drunkenness, neurological disorders
affecting swallowing, drowning, necrotic oropharyngeal tumours, in
premature infants and congenital tracheoesophageal fistula.
• Some patients die immediately from asphyxiation or laryngospasm
without developing pneumonia.
Aspiration (Inhalation) Pneumonia

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• Pathologic changes vary depending upon the aspirated particulate matter but
in general right lung is affected more often due to direct path from the main
bronchus:
• 1. Aspiration of small amount of sterile foreign matter such as acidic
gastric contents produces chemical pneumonitis. It is characterised by
hemorrhagic pulmonary edema with presence of particles in the
bronchioles. Patients rapidly develop cyanosis, dyspnea, shock and bloody
sputum and are often likely to die of cardiac failure. If the patient survives
the acute episode, secondary bacterial infection is likely to occur.
• 2. Non-sterile aspirate causes widespread bronchopneumonia with
multiple areas of necrosis and suppuration. A granulomatous reaction with
foreign body giant cells may surround the aspirated vegetable matter.
Morphologic features

49. 49
• Hypostatic pneumonia is the term used for collection of edema fluid
and secretions in the dependent parts of the lungs in severely
debilitated, bed-ridden patients.
• The accumulated fluid in the basal zone and posterior part of lungs
gets infected by bacteria from the upper respiratory tract and sets in
bacterial pneumonia.
• Hypostatic pneumonia is a common terminal event in the old, feeble,
comatose patients.
Hypostatic Pneumonia

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• Another variety of non-infective pneumonia is lipid pneumonia which is of
2 types: exogenous and endogenous.
Exogenous lipid pneumonia
This is caused by aspiration of a variety of oily materials.
These are: inhalation of oily nasal drops, regurgitation of oily medicines
from stomach (e.g. liquid paraffin), administration of oily vitamin
preparation to reluctant children or to debilitated old patients.
Endogenous lipid pneumonia
Endogenous origin of lipids causing pneumonic consolidation is more
common.
The sources of origin are tissue breakdown following obstruction to airways
e.g. obstruction by bronchogenic cancer, tuberculosis and bronchiectasis.
Lipid Pneumonia

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Grossly,
 The exogenous lipid pneumonia affects the right lung more frequently due to direct path
from the main bronchus.
 Quite often, the lesions are bilateral.
 The affected part of the lungs is consolidated.
• Cut surface is characteristically ‘golden yellow’.
Microscopically, the features are as under:
• i) Lipid is finely dispersed in the cytoplasm of macrophages forming foamy macrophages
within the alveolar spaces.
• ii) There may be formation of cholesterol clefts due to liberation of cholesterol and other
lipids.
• iii) Formation of granulomas with foreign body giant cells may be seen around the large
lipid droplets.
Morphologic features

52. THANK YOU!
SAMOEI KIPLETING
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