pneumoniasbydrbashirahmeddar-090819135701-phpapp01.ppt

yohannesfetene2 37 views 238 slides Jul 04, 2024
Slide 1
Slide 1 of 269
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48
Slide 49
49
Slide 50
50
Slide 51
51
Slide 52
52
Slide 53
53
Slide 54
54
Slide 55
55
Slide 56
56
Slide 57
57
Slide 58
58
Slide 59
59
Slide 60
60
Slide 61
61
Slide 62
62
Slide 63
63
Slide 64
64
Slide 65
65
Slide 66
66
Slide 67
67
Slide 68
68
Slide 69
69
Slide 70
70
Slide 71
71
Slide 72
72
Slide 73
73
Slide 74
74
Slide 75
75
Slide 76
76
Slide 77
77
Slide 78
78
Slide 79
79
Slide 80
80
Slide 81
81
Slide 82
82
Slide 83
83
Slide 84
84
Slide 85
85
Slide 86
86
Slide 87
87
Slide 88
88
Slide 89
89
Slide 90
90
Slide 91
91
Slide 92
92
Slide 93
93
Slide 94
94
Slide 95
95
Slide 96
96
Slide 97
97
Slide 98
98
Slide 99
99
Slide 100
100
Slide 101
101
Slide 102
102
Slide 103
103
Slide 104
104
Slide 105
105
Slide 106
106
Slide 107
107
Slide 108
108
Slide 109
109
Slide 110
110
Slide 111
111
Slide 112
112
Slide 113
113
Slide 114
114
Slide 115
115
Slide 116
116
Slide 117
117
Slide 118
118
Slide 119
119
Slide 120
120
Slide 121
121
Slide 122
122
Slide 123
123
Slide 124
124
Slide 125
125
Slide 126
126
Slide 127
127
Slide 128
128
Slide 129
129
Slide 130
130
Slide 131
131
Slide 132
132
Slide 133
133
Slide 134
134
Slide 135
135
Slide 136
136
Slide 137
137
Slide 138
138
Slide 139
139
Slide 140
140
Slide 141
141
Slide 142
142
Slide 143
143
Slide 144
144
Slide 145
145
Slide 146
146
Slide 147
147
Slide 148
148
Slide 149
149
Slide 150
150
Slide 151
151
Slide 152
152
Slide 153
153
Slide 154
154
Slide 155
155
Slide 156
156
Slide 157
157
Slide 158
158
Slide 159
159
Slide 160
160
Slide 161
161
Slide 162
162
Slide 163
163
Slide 164
164
Slide 165
165
Slide 166
166
Slide 167
167
Slide 168
168
Slide 169
169
Slide 170
170
Slide 171
171
Slide 172
172
Slide 173
173
Slide 174
174
Slide 175
175
Slide 176
176
Slide 177
177
Slide 178
178
Slide 179
179
Slide 180
180
Slide 181
181
Slide 182
182
Slide 183
183
Slide 184
184
Slide 185
185
Slide 186
186
Slide 187
187
Slide 188
188
Slide 189
189
Slide 190
190
Slide 191
191
Slide 192
192
Slide 193
193
Slide 194
194
Slide 195
195
Slide 196
196
Slide 197
197
Slide 198
198
Slide 199
199
Slide 200
200
Slide 201
201
Slide 202
202
Slide 203
203
Slide 204
204
Slide 205
205
Slide 206
206
Slide 207
207
Slide 208
208
Slide 209
209
Slide 210
210
Slide 211
211
Slide 212
212
Slide 213
213
Slide 214
214
Slide 215
215
Slide 216
216
Slide 217
217
Slide 218
218
Slide 219
219
Slide 220
220
Slide 221
221
Slide 222
222
Slide 223
223
Slide 224
224
Slide 225
225
Slide 226
226
Slide 227
227
Slide 228
228
Slide 229
229
Slide 230
230
Slide 231
231
Slide 232
232
Slide 233
233
Slide 234
234
Slide 235
235
Slide 236
236
Slide 237
237
Slide 238
238
Slide 239
239
Slide 240
240
Slide 241
241
Slide 242
242
Slide 243
243
Slide 244
244
Slide 245
245
Slide 246
246
Slide 247
247
Slide 248
248
Slide 249
249
Slide 250
250
Slide 251
251
Slide 252
252
Slide 253
253
Slide 254
254
Slide 255
255
Slide 256
256
Slide 257
257
Slide 258
258
Slide 259
259
Slide 260
260
Slide 261
261
Slide 262
262
Slide 263
263
Slide 264
264
Slide 265
265
Slide 266
266
Slide 267
267
Slide 268
268
Slide 269
269

About This Presentation

this is about pneumoniasbydrbashirahmeddar-090819135701-phpapp01.ppt share


Slide Content

PNEUMONIAS
By
Dr Bashir Ahmed Dar
Chinkipora Sopore
Kashmir
Associate Professor
Medicine
Email
[email protected]

NOTE
The purpose of this presentation is to take
full detailed history in case of pneumonia to
arrive at correct diagnosis.
The presentation has been made very easy
for undergraduate as well as for post
graduate medical students.
Description of various organisms and x-rays
has made the task very simple.

Definition of Pneumonia
Pneumonia is defined as inflammation of
lung parenchyma
The term pneumonitis is synonymous but is
best avoided
During the process of inflammation of
alveoli there occurs inflammatory exudate
that fill up air spaces and result in
consolidation of lung.

Primary Pneumonia
There is no pre-existing abnormality of
respiratory system.

Secondary Pneumonia
is characterized by
absence of specific pathogenic organism in
the sputum and presence of some pre-
existing abnormality of respiratory system.

Secondary Pneumonia
Examples are
1.Aspiration of pus from any foci,vomitus,gastric
contents
2.Inhalation of septic matter during
tonsilectomy,dental procedures.
3.Ineffective coughing as in post-traumatic,post-
operatiive,paralysis laryngeal or phyrangeal.
4.Partial bronchial obstruction

Classifications by (causative
agents) Pneumonia
Classifications by (causative agents)
Viral pneumonia
Bacterial Pneumonia
Fungal pneumonia
Rickettsial pneumonia
Protozoal pneumonia
Radiation pneumonia
Chemical pneumonia
Aspiration pneumonia
Hypostatic pneumonia

Viruses that cause acute
pneumonia

Rev Tran&Protease

Retranscriptase
Protease

Viruses that cause acute pneumonia
Adenovirus
Coronavirus
influenza A and B viruses
parainfluenza virus
respiratory syncytial virus
coxsackievirus A21
Rhinovirus
viruses that cause rubella and measles
often self limiting but can be complicated

Features of viral Pneumonias
The clinical features differ from that of
bacterial pneumonia.
Symptoms are more than the chest signs and
x-ray signs
Course is mild and self limiting and
resolves by 7-10 days time.

Features of viral Pneumonias
It usually starts with a dry (nonproductive)
cough
Characteristic features or constitutional symptoms
like fever ,headache,sore throat,dry
cough,malaise,running nose,common cold,aches
and pains precedes several days before viral
pneumonia occurs than in bacterial pneumonia
which is more abrupt in onset.

Features of viral Pneumonias
Strikes primarily in the fall and winter and
tends to be more serious in people with
cardiovascularor lung disease.
*Leucocyte count is usually normal or low
* On x ray may show features of interstitial or of
atypical pneumonia

Features of viral Pneumonias
Viral pneumonia often goes unrecognized
because the person may not appear very ill.
The symptoms vary with age and whether
the person has other health problems.
Diagnosis confirmed by isolation of virus
and serological tests

BACTERIA THAT CAUSE
PNEUMONIA
GRAM POSITIVE COCCI
1.Streptococcus Pneumoniae
the most common
2. Streptococcus Pyogenes
3. Streptococcus Agalactiae

BACTERIA THAT CAUSE
PNEUMONIA
S-Pneumoniae generally resides in the
nasopharynx and is carried asymptomatic in
approximately 50% of healthy individuals.
A strong association exists with viral
illnesses, such as influenza. Viral infections
increase Pneumococcal attachment to the
receptors on activated respiratory
epithelium. Once aerosolized from the
nasopharynx to the alveolus,

BACTERIA THAT CAUSE
PNEUMONIA
Pneumococci infect type II alveolar cells.
The pneumonic lesion progresses as
pneumococci multiply in the alveolus and
invade alveolar epithelium. Pneumococci
spread from alveolus to alveolus through
the pores of Kohn, thereby producing
inflammation and consolidation along lobar
compartments

BACTERIA THAT CAUSE
PNEUMONIA
Patients with pneumococcal pneumonia
may produce bloody or rust-colored
sputum.

BACTERIA THAT CAUSE
PNEUMONIA
Streptococcus agalactiae bacterium is a
commensal organism in the genital tract and
it can cause pneumonia in newborn babies.
It does not happen too often, but the baby
sometimes inhales fluid containing the
bacteria during its journey down the birth
canal and develops pneumonia soon after
birth.

BACTERIA THAT CAUSE
PNEUMONIA
4. Staphylococcus aureus is gram positive
organism,affecting children and old people.
as well as extreme ages.it can produce thin
walled air filled cavities ("pneumatoceles"),

BACTERIA THAT CAUSE
PNEUMONIA
Commonly following influenza in
debilitated patients and in those with cystic
fibrosis.
Abcess formation is very common.
The abcesses are thin walled,multiple and
commonly bilateral giving rise to patchy
bronchopneumonia.

BACTERIA THAT CAUSE
PNEUMONIA
As opposed to other acute bacterial or lobar
pneumonias which begin in alveoli,
bronchopneumonia originates in small
bronchioles. Typical bacteria causing this form of
infection include Staphylococcus aureusand
Gram-negative organisms such as Pseudomonas
aeruginosa.

BACTERIA THAT CAUSE
PNEUMONIA
Since multiple sites are involved
simultaneously a scattered appearance of
heterogeneous opacities is the usual
Eventually more and more alveoli are
affected and ultimately a homogeneous
opacification simulating lobar pneumonia
may be observed.

BACTERIA THAT CAUSE
PNEUMONIA
Staphylococcal pneumoniais diagnosed
by finding typical clusters of Gram-
positive cocciby microscopy and
subsequently a heavy growthof
Staphylococcus aureusin a purulent(pus-
laden) sputumthat often appears creamy
and bloodstained.

BACTERIA THAT CAUSE
PNEUMONIA
Staphylococcal organism can also cause
Boils (pus-filled infections of hair follicles).
Abscesses (collections of pus in pockets under the skin).
Styes (infection of glands in the eyelid).
Carbuncles (infections larger than an abscess, usually with
several openings to the skin).
Cellulitis (infection of the skin and the fat and tissues that
lie immediately beneath it).
Impetigo (a skin infection that produces pus-filled blisters).

BACTERIA THAT CAUSE
PNEUMONIA
Septic shock.
Severe joint problems (septic arthritis).
Bone marrow infection (osteomyelitis).
Internal abscesses anywhere within the body.
Inflammation of the tissues that surround the brain
and spinal cord (meningitis).
Lung infection (pneumonia).
Infection of the heart lining (endocarditis).

BACTERIA THAT CAUSE
PNEUMONIA
Some strains of staphylococcal bacteria
produce toxins (poisons) when they grow
and reproduce on food. If you eat food
contaminated with staphylococcal bacteria,
these toxins can cause staphylococcal food
poisoning. The toxins can also cause
scalded skin syndrome and, very
occasionally, toxic shock syndrome.

BACTERIA THAT CAUSE
PNEUMONIA
Bacteria gram positive rods
1.Bacillus anthracis is Anthrax or Wool-Sorters
disease Associated with wool sorting, with
animal handlers, and veterinarians,produces
eschar

BACTERIA THAT CAUSE
PNEUMONIA
2. Nocardia sp
Beaded filamentous rod shaped bacteria,
Pleura and chest wall involvment
3.Actinomyces sp.
Beaded filamentous rod shaped bacteria,
causing rib destruction, cutaneous sinuses,
cavitation, spreads to pleura and chest
wall.

BACTERIA THAT CAUSE
PNEUMONIA
Caused by actinomyces israeli ,an anaerobic
organism occuring in mouth as commensal
When local defences break then can occur
Three forms recognised
Cervicofacial actinomycosis with
discharging sinuses
Abdominal actinomycosis with discharging
sinuses

BACTERIA THAT CAUSE
PNEUMONIA
Then lastly pulmonary actinomycosis with
widespread suppurative pneumonia with
empyema often bilateral and persistent
discharging chest wall sinuses
The pus from sinuses contains sulphur
granules

BACTERIA THAT CAUSE
PNEUMONIA
Bacteria Gram Negative cocci
1.Neisseria meningitidis (meningococci)
cause epidemics in military
recruits,schools,young adults,overcrowded
places.
2.Moraxella catarrhalis

BACTERIA THAT CAUSE
PNEUMONIA
Bacteria gram negative rods
1. Klebsiella pneumoniae produces Current
Jelly sputum, more commonly seen in
patients with COPD, alcoholics, and the
elderly.

BACTERIA THAT CAUSE
PNEUMONIA)
Also called (friedlanders bacillus)
Severe form of pneumonia with high
mortality
Upper lobes being most affected with
massive lobar consolidation
Sputum is jelly like and blood stained
producing (current jelly sputum).

BACTERIA THAT CAUSE
PNEUMONIA
On x-ray there is consolidation and bulging
of interlobar fissure characteristic finding.
Sputum smear shows gram negative bacilli

BACTERIA THAT CAUSE
PNEUMONIA
2.Pseudomonas aeruginosa produces green sputum,
abscess formation, Common cause of pneumonia
in cystic fibrosis and those with severely
compromised respiratory defenses.
3. Acinetobacter sp.often found on respiratory
therapy equipment and on human skin
very difficult to treat due to multiple drug
resistance.
4. Burkholderia pseudomallei exposure with
contaminated soil

BACTERIA THAT CAUSE
PNEUMONIA
6. Yersinia Pestis,causes Pneumonic plague
Initial plague patients acquire this disease
via flea bites and animal contacts like
rats,rodents. Plague has three forms .

BACTERIA THAT CAUSE
PNEUMONIA
Forms of Plague Disease
–Pneumonic
–Bubonic
–Septicemic

BACTERIA THAT CAUSE
PNEUMONIA
7. Francisella tularensis ,Tularemia Infection
is via tick bite or contact with contaminated
rabbits.
8. Hemophilus influenzae more commonly
seen in patients with COPD, alcoholics, and
the elderly.
9. Bordetella pertussis Whooping cough

TULARAEMIA SKIN &
GLANDULAR

BACTERIA THAT CAUSE
PNEUMONIA
10. Bacteroides melaninogenicus anaerobe
aspirationn
11.Fusobacterium sp.anaerobe Aspiration
12.Porphyromonas sp.anaerobe Aspiration
13.Prevotella sp.anaerobe
14.Proteus sp Aspiration
15.Serratia sp.

ANAEROBIC BACTERIA
Following are anaerobic bacteria
•Bacteroides
•Fusobacterium
•Porphyromonas
•Prevotella
•Actinomyces
•Bifidobacterium
•Clostridium
•Peptostreptococcus
•Propionibacterium

ANAEROBIC BACTERIA
Are bacteria that do not live or grow in the
presence of oxygen.
Anaerobic bacteria can cause an infection
when a normal barrier (such as skin, gums,
or intestinal wall) is damaged due to
surgery, injury, or disease.
Usually produce small abcesses and cause
foul smelling breath.

BACTERIA THAT CAUSE
PNEUMONIA
Infections with Pseudomonas,
Haemophilus, and pneumococcal species
are known to expectorate green sputum.

Gram-Negative Bacteria
There are many groups of Gram-Negative bacteria
such as Cyanobacteria, Spirochaetes, Green-
Sulphur and Green Non-Sulphur Bacteria and
Proteobacteria etc. Out of which, proteobacteria is
one of the major group of known Gram-Negative
bacteria (it includes bacteria like E-coli,
Salmonella, Pseudomonas, Moraxella,
Helicobacter, Stenotrophomonas, Legionella,
Acetic Acid Bacteria etc.).

Gram-Negative Bacteria
Along with the above mentioned bacteria,
there are several other type of Gram-
Negative bacteria such as Hemophilus
influenzae (also known as Bacillus
influenzae), Neisseria Meningitidis,
Moraxella Catarrhalis, Neisseria
Gonorrhoeae, Acinetobacter Baumanii
(which comes under Nosocomical Gram-
Negative bacteria group).

Gram-Negative Bacteria
People most likely to get sick with resistant
Gram-negative germs are those who:
• are seriously ill
• are in the hospital for a long time
• have taken many antibiotics or drugs used
to destroy bacteria
• have a disease that prevents the body
from fighting infection
• have been in a nursing home or long-term
care setting
• are on a ventilator or breathing machine

Clinical Features of Bacterial
Pneumonia
Onset is often sudden
High grade fever
Rigors and chills
Sputum is rusty coloured or blood stained

Features of Bacterial
Pneumonias
In fact, the viral infection predisposes to
bacterial pneumonia, by damaging some of
the lung's defenses against infection. One
important clue to this diagnosis is
deterioration after initial improvement

Signs of Pneumonia
Decreased chest movements
Dull on percussion
VF/VR increased
Bronchial breathing
Bronchophoney,aegophony and whispering
pectoriloquy may be present
Crepitations

Fungal Pneumonia
Endemic fungi
–Histoplasmosis
–Blastomycosis
–Cryptococcosis
–Sporotrichosis -primarily a lymphocutaneous disease,
but can involve the lungs as well
Aspergillus
Candida
Coccidiodomycosis

Fungal Pneumonia
Histoplasmosis All Chickens, bats, river
valleys
Coccidioidomycos All California,
Southwest USA

Fungal Pneumonia
Histoplasma capsulatum: Infection can
result from exposure to contaminated bat
caves or from excavation in endemic areas

HISTOPLASMOSIS

Fungal Pneumonia
Coccidioides immitis: Pneumonia may
develop after travel to the southwestern
United States and after exposure to a wind
or rain storm in an endemic area.

Fungal Pneumonia
Blastomyces dermatitidis: Patients may
have traveled to the midwestern United
States or the Canadian Shield.

Clinical features of fungal
Pneumonias
Occurs in a particular setting
History of immunosupression like in
AIDS,malignancy,Corticosteroid
theraphy,radiation theraphy,antimalignant
drugs.
Debilitated bed ridden people,malnutrition.
Has chronic serious pre-existing disease.

Clinical features of fungal
Pneumonias
People working in agriculture
lands,caves,old buildings,places of bird
droppings,soil.
The disease runs a chronic course.

Fungal Pneumonia
Diagnostic efforts must be escalated,
progressing to more aggressive measures
(fiberoptic bronchoscopy, fine needle
aspiration, and rarely thoracoscopic or
traditional open lung biopsy) until a specific
diagnosis is reached.
Skin tests

Protozoal Pneumonia
Parasites causing pneumonia are
1.Toxoplasma gondii
2.Strongyloides stercoralis
3.Ascariasis.
4.Cryptosporidia
5.Hookworms

Protozoal or Parasitic
Pneumonia
A variety of parasites can affect the lungs.
These parasites typically enter the body
through the skin or by being swallowed.
Once inside, they travel to the lungs, usually
through the blood. One type of white blood
cell, the eosinophil, responds vigorously to
parasite infection. Eosinophils in the lungs
can lead to eosinophilic pneumonia.

Rickettsial Pneumonia
Typhus fevers (epidemic and endemic)
Rocky mountain spotted fever,scrub typhus,
rickettsialpox
Louse-borne
flea-borne through rats and mouse fleas

Rickettsial Pneumonia
Q fever
Acute, self-limited, systemic disease caused by the
rickettsia Coxiella burnetii. Q fever spreads
rapidly in cows, sheep, and goats, and in humans it
tends to occur in localized outbreaks. Q fever
common in slaughterhouses, research facilities,
and plants, where handling of animals or their
birth products is a source of exposure.

Rickettsial Pneumonia
Q fever ranging from multiple segmental
opacities to pleural effusion, lobar
consolidation, or linear
atelectasis.Hepatosplenomegaly is a
common finding; it usually is accompanied
with elevation of liver enzymes

Rickettsial Pneumonia
Rickettsia pneumonia cannot be
distinguished clinically, radiologically, or
histologically from atypical pneumonia.

Features of Rickettsial
infection
Rickettsiae are small bacteria that are obligate
intracellular parasites. They are maintained in
nature through cycle involving reservoir mammals
and arthropod vectors except louse borne
typhus. Humans are incidental hosts via arthropod
vector. Vasculitis of small vessels is basic
underlying pathology. The severity of disease can
range from mild to multi-organ failure and
even fatal outcome. Patients usually present with
fever, skin rash/eschar and headache

Features of Rickettsial
infection
The geographic and temporal distribution of
rickettsioses is mainly determined by their vectors.
Louse-transmitted diseases occur worldwide. Lice
parasitize in poor people, preferentially in cold
places and during wars. Common fleas such as cat
and dogs fleas and rat fleas are reported
worldwide, as are their transmitted diseases.

Features of Rickettsial
infection
For tick species, they are highly dependent on
their environment. Thus, tick-transmitted
rickettsial diseases are usually restricted to parts of
the world where they can be transmitted by the
local fauna. Pet dogs and cat may act as transport
hosts which carry the infected ticks from its
original habitats to home, where the humans may
be exposed to the ticks.

Features of Rickettsial
infection
Scrub typhus occurs over a wide area of
Asia and Pacific region. Chiggers (larval-
stage of trombiculid mites) are vectors for
scrub typhus. Chiggers prefer warm,
moist,and shady places.

Features of Rickettsial
infection
In Hong Kong, majority of the reported cases
contracted the diseases locally,in which half of the
spotted fever and scrub typhus cases were related
to outdoor activities,such as hiking or camping in
rural areas. In contrast, poor environmental
hygiene condition
such as inadequately managed rubbish collection
points and wet markets was a risk factor for
contracting murine typhus.

Features of Rickettsial
infection
In Hong Kong, majority of the reported cases
contracted the diseases locally,in which half of the
spotted fever and scrub typhus cases were related
to outdoor activities,such as hiking or camping in
rural areas. In contrast, poor environmental
hygiene condition
such as inadequately managed rubbish collection
points and wet markets was a risk factor for
contracting murine typhus.

Features of Rickettsial
infection
At the site of inoculation organisms localize in
endothelial cells and entry into the cells by
receptor mediated mechanism and phagocytosis. It
proliferates intracelluarly. A papule may be
formed and later ulcerates in the central. It is
called eschar. The organisms released from the
infected cells can infect endothelial cells in the
blood vessels throughout the body via lymphatic
vessels. The rickettsemia causes generalized
vasculitis affecting every organs in the body.

Features of Rickettsial
infection
Diagnosis of rickettsial infection relies upon
a combination of clinical, epidemiology and
laboratory findings

ATYPICAL BACTERIA
Are organisms that do not fit in
virus,bacteria or fungus.
Thus bacteria are called atypical and
produce atypical pneumonia.
These organisms do not stain with gram
stain and do not follow any common
morphological pattern.

ATYPICAL BACTERIA
These are the bacteria's that will be called as atypical bacteria and
causing also atypical pneumonias like other viral agents etc.and
constitute following organisms
Legionella
Mycoplasma pneumoniae
Chlamydia trachomatis an afebrile pneumonia, usually seen in 2 wk to
6 months of age
Chlamydia psittaci
Chlamydia pneumoniae , Chlamydia trachomatis
This is a sexually transmitted disease that may also cause pneumonia
and bronchitis. It usually is a subacute infection of early infancy
producing a sudden cough and eosinophilia without fever that lasts
from 1-3 weeks, but it may occur in adults too.

ATYPICAL BACTERIA
Chlamydia pneumoniae , Chlamydia trachomatis
Are transmitted to infants at birth from the cervix of an
infected mother. Adults having chlamydial pneumonia are
usually immunocompromised with the infection spreading
from the eye (conjunctival) to the respiratory tract via the
nasolacrimal duct.
Coxiella burnetii (Q-fever) ingestion of comtaminated
milk, or inhalation of contaminated aerosols from barnyard
animals
Mycobacterium tuberculosis and other Mycobacterium

Classification of Pneumonias
BY SITE
LOBAR PNEUMONIA
INTERSTITIAL PNEUMONIA
BRONCHOPNEUMONIA

Lobar Pneumonia
Organisms cause inflammatory exudate that
fill up air spaces and result in consolidation
of whole lobe of lung

Broncho-Pneumonia
Common cause is satphylococcal infection.
Bronchopneumonia is characterized by patchy
exudative consolidation of lung parenchyma due
to terminal bronchiolitis with consolidation of
peribronchial alveoli.
Common also with gram negative organisms

Pathogenesis of
Bronchopneumonia
There is initial terminal bronchiolitis with patchy consolidation of
peribronchial lung tissue.
Bronchioles are plugged by the swollen mucosa and their secretion. As
a result, the air cannot enter the alveoli.
The imprisoned air in the alveoli is absorbed causing collapse of the
alveoli.
Collapsed areas are surrounded by areas of compensatory emphysema.
Consolidated areas are surrounded, from inside outwards, by areas of
congestion, collapse and emphysema .
Resolution of the exudate usually restores normal lung structure.
Organization may occur and result in fibrous scarringin some cases.
Aggressive disease may produce abscesses.

Broncho-Pneumonia
Bronchopneumonia may occur as a complicationof some
disease.
E.g. In children -Diphtheria , Measles , Whooping Cough
In adult -Influenza, typhoid & Paratyphoid fever etc
It is often seen in two extremes of life (in infants & old
age).

Broncho-Pneumonia
1.Bilateral (less often unilateral), patchy consolidation
with intervening normal lung tissue.
3.Lesion is more extensive at the base of the lung and
often fuses together resembling lobar pneumonia
(confluent bronchopneumonia).
4.Range from red to gray depending on age of the lesion.

Atypical or Interstitial or viral
Pneumonia
Atypical pneumonia as already said is
caused by atypical bacteria that do not gram
stain or do not fit in any category like in
virus or bacteria.some special fungi and
rickettsia and most of viruses can also cause
this type of pneumonia .The inflammation is
confined to interalveolar septa or interstitial
spaces between alveoli and radiologically
gives appearance of reticulonodular pattern.

Atypical or Interstitial or viral
Pneumonia
In the next slide you will see white spaces
that are alveolar spaces and are empty and
clear.but surrounded by swollen interstitial
tissue infiltrated with inflammatory cells.

Atypical or Interstitial or viral
Pneumonia
Causes
Mycoplasma
Legionella
Chlamydia
Pneumocystis carinni
. coxiella
Viruses

Atypical or Interstitial or viral
Pneumonia
Fungi
Histoplasma capsulatum (histoplasmosis)
Coccidioides immitis (coccidioidomycosis)

Atypical or Interstitial or viral
Pneumonia

Causes of Interstitial &
atypical pneumonia
Mycoplasma pneumonia occurs in
Adolescents and young adults
Legionnaire's disease (summer peak) Adult
Cooling towers, condensers, excavation
sites
Water tanks
Psittacosis Adult Psittacine birds, pigeons,
turkeys, pet shops, zoos

Causes of Interstitial &
atypical pneumonia
Q fever Adult Cattle, sheep, goats,
contaminated milk, birthing various
livestock
Tularemia Adult Rabbits, ticks
Anthrax Adult Goat hair/skin, wool,
bonemeal fertilizer
Viral pneumonia Winter All

Causes of Interstitial &
atypical pneumonia
Histoplasmosis All Chickens, bats, river
valleys
Coccidioidomycos All California,
Southwest USA

HISTOPLASMOSIS

TULARAEMIA SKIN &
GLANDULAR

LEGIONELLA
Occurred first in military personnel called
legionnairs while using tank water etc.

Legionella
pneumonia(legionnairs
disease)
Caused by legionella pneumophila
Transmitted in water droplets orginating in
infected humidifier ,cooling systems and from
stagnant water in cisterns and shower heads
Cough with mucoid scanty sputum
Gastrointestinal symptoms like nausea,abdominal
pain and diarrhoea and mental confusion or
delirium are common

PSITTACOSIS

Atypical or Interstitial or viral
Pneumonia
As the conditions caused by these agents
have different courses and respond to
different treatments, the identification of the
specific causative pathogen is important

Atypical or Interstitial or viral
Pneumonia
In atypical pneumonia the x ray finding usually do
not show lobar type of picture but meaning that
the affection is restricted to small areas that is
interstitial spaces between alveoli, rather than
involving a whole lobe. As the disease progresses,
however, the look can tend to be lobar pneumonia.
There is also absence of leukocytosis.
Extrapulmonary symptoms, give some clue to the
causing organism.

Atypical or Interstitial or viral
Pneumonia
In atypical pneumonia the symptoms are
generally more but if you look for chest
sings they are very little or absent even the
x-ray may not show any thing. Though the
patient looks worse.so this type of setting is
called occult pneumonia.

Atypical or Interstitial or viral
Pneumonia
In atypical pneumonia if you look at x ray chest
you will find infiltration(white haziness)
commonly begins in the perihilar region (where
the bronchus begins) and spreads in a wedge-or
fan-shaped fashion toward the periphery of the
lung field.
Or u may find network of reticular shadows as
small linear striations running in all directions on
which may be small white nodular appearance.
Or may be small patchy.

Atypical or Interstitial or viral
Pneumonia
The most common pathogen of this group is
Mycoplasma pneumoniae. It ranks second
only to S. pneumoniae.
onset is usually more insidious.

Atypical or Interstitial or viral
Pneumonia
A combination of the clinical,
epidemiologic, radiographic, and laboratory
features can specify a certain etiology so
that empiric treatment can begin.

Atypical or Interstitial or viral
Pneumonia

Mycoplasma
Mycoplasmosis is a collective term for
infectious diseases caused by the micro-
organisms called mycoplasmas. There are a
number of mycoplasmas that can infect
poultry, number of bird species including
chickens, turkeys, gamebirds and pigeons.
Mycoplasma pneumonia occurs in
Adolescents and young adults

Mycoplasma
Mycoplasma pneumoniae can be communicated
through close personal contact via respiratory
droplets or contact with poultry or birds chicken
etc.
EXTRAPULMONARY MANIFESTATIONS:
gastrointestinal
musculoskeletal
dermatologic
cardiac
neurologic symptoms

Mycoplasma
Depending on the severity of illness, additional
studies may be done, include:
Complete blood count (CBC)
Blood cultures
Blood tests for antibodies to mycoplasma
Bronchoscopy
Open lung biopsy (only done in very serious
illnesses when the diagnosis cannot be made from
other sources)

Mycoplasma
Sputum culture to check for mycoplasma bacteria
A urine test or a throat swab may also be done.
Individuals working or living in crowded areas
including homeless shelters or schools are at a
greater risk of developing mycoplasma
pneumonia.
Patients may report exposure to overcrowded
institutions such as jails, shelters for homeless
persons, or military training camps.

Mycoplasma
The symptoms associated with this
condition include chest pain, cough and
excessive sweating. The cough is not
bloody and is usually dry. Those suffering
from this condition may also get fever,
headache and sore throat.

Legionnaire's disease (summer peak) Adult
Cooling towers, condensers, excavation
sites,water tanks.
Interstitial / atypical Pneumonia
Legionella pneumophila: Patients may report
exposure to contaminated air-conditioning cooling
towers, exposure to a grocery store mist machine,
or a visit or recent stay in a hospital with a
contaminated water system.

LEGIONELLA
Occurred first in military personnel called
legionnairs while using tank water etc.

Psittacosis
Has three species
Chlamydia psittaci
C. trachomatis
C. pneumoniae
Transmission occurs person to person via
respiratory secretions in case of
C.pneumoniae

PSITTACOSIS

Interstitial / atypical Pneumonia
Coxiella burnetii: This is related to
exposure to infected parturient cats, cattle,
sheep, or goats.
Chlamydia psittaci: Patients may report
exposure to turkeys, chickens, ducks, or
psittacine birds.
•Travel history

Interstitial / atypical Pneumonia
Burkholderia (Pseudomonas) pseudomallei
(melioidosis): This infection may result
from travel to Thailand or other countries in
Southeast Asia.
M tuberculosis: Pneumonia may develop in
immigrants from Asia or Africa.

Interstitial / atypical Pneumonia
Chemical pneumonia (usually called
chemical pneumonitis) is caused by
chemical toxicants such as pesticides, which
may enter the body by inhalation or by skin
contact. When the toxic substance is an oil,
the pneumonia may be called lipoid
pneumonia

Serological tests for atypical
pneumonia
Mycoplasma pneumoniae > complement fixation
test, IgM by latex agglutination or ELISA, cold
agglutinins
Legionella pneumophila >rapid
microagglutination test, test for Legionella antigen
in the urine.
Chlamydia spp >microimmunofluorescence,
ELISA
Coxiella burnetii >complement fixation test.

Serological tests for atypical
pneumonia
Skin testing for
histoplasmosis,coccidioidomycosis.
serologic tests. A four fold or greater rise in
titer is confirmatory of an acute infection.

SOME OTHER FORMS OF
PNEUMONIA
Eosinophilic pneumonia is invasion of the
lung by eosinophils, a particular kind of
white blood cell. Eosinophilic pneumonia
often occurs in response to infection with a
parasite or after exposure to certain

SOME OTHER FORMS OF
PNEUMONIA
Chemical pneumonia (usually called
chemical pneumonitis) is caused by
chemical toxicants such as pesticides, which
may enter the body by inhalation or by skin
contact. When the toxic substance is an oil,
the pneumonia may be called lipoid
pneumonia

Classification by mode of acquiring
pneumonia
1.Community acquired pneumonia
2.Nosocomial pneumonia

Community acquired
pneumonia
This indicates pneumonia occuring in a person
in a community outside hospital .
Common organisms responsible are
Streptocccus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
.

Nosocomial pneumonia
Acquired by a patient in the following
settings:
in a hospital after being admitted for >48 hours
or
<7 days after a patient is discharged from
hospital.

Nosocomial Bacterial
Pneumonia -Etiology
Gram-negative enteric bacilli
(predominant)
Gram-positive cocci, including:
Staphylococcus aureus ( e.g.,MRSA ),
Streptococcus pneumoniae
Anaerobes
Others

Nosocomial pneumonia
new cough
new infiltrate or progressive infiltrate on
chest radiograph, accompanied by:
fever or hypothermia, leukocytosis, sputum
production
Etiology: polymicrobial
In wards,icu,and in patients on mechanical
vetillation

ASPIRATION PNEUMONIA
OCCUR IN FOLLOWING SETTINGS
Altered Level of Consciousness
Alcoholism
Seizures
Drugs
Anesthesia
Central nervous system disorders
Trauma
Dysphagia
Esophageal disorders
Neurological disorders
Mechanical Disruption of Functional Barriers
Nasogastric tubes

Coliforms" -bacteria related to Escherichia
colifrom GIT etc-and Pseudomonas
aeruginosacan also cause
bronchopneumonia in ICU patients who
require assisted ventilation to support their
breathing

RISK FACTORS THAT FORM BASIS OF
SECONDARY PNEUMONIAS
Pre existing disease like Partial bronchial
obstruction by tumour causes stasis of
secretions and secondary infection distal to
site of obstruction
In acute bronchitis,bronchietasis and lung
abcess ,the pus may be carried to alveoli

RISK FACTORS
Ineffective coughing post surgery,laryngeal
paralysis,bulbar paralysis
Vomitting and aspiration during
anaesthesia,sleep,coma,alcholism
Aspiration
Inhalation of septic matter during
tonsillectomy,dental procedure,or general
anaesthesia

RISK FACTORS
Aspiration of gastric contents in pts with
gastro-oesophageal reflux disease(HCL may
directly and quickly cause lung damage
resulting in chemical pneumonia

RISK FACTORS
Infection with opportunistic pathogen in
immunocompromised host
(AIDS,Malignancy).TB,Fungal,and
cryptosporidia, toxoplasma infection can
take over

RISK FACTORS
-Asplenia
–HIV/AIDS
–Elderly
Defective Clearing mechanism
–Cough/gag Reflex –Coma, paralysis, sick.
–Mucosal Injury –smoking, toxin aspiration
–Low Alveolar defense -Immunodeficiency
–Pulmonary edema –Cardiac failure, embol.
–Obstructions –foreign body, tumors
-Prolonged mechanical ventilation
-extremes of age

RISK FACTORS
Hypogammaglubolinemia
Sever Neutrogena
Corticosteroid therapy
Environmental risk factors Aspergillosis (air, water)
Legionella (water) Histoplasmosis (bird droppings &
bat caves) Psittacosis (pet birds) Anthrax (soil)

Route of Entry
Aspiration
Inhalation
Inoculation
Colonization (in patients with COPD)
Hematogenous spread (patients with
sepsis)
Direct spread

Route of Entry
Typical pneumonia is usually acquired by
droplet spread of the pathogen through
sneezing,coughing etc. The organism may
also manifest itself as a suprainfection in
patients previously infected by an upper or
lower respiratory viral infection. There is no
age-specific predisposition

Route of Entry
So the most common way you catch
pneumonia bacterial or viral is to breathe
infected air droplets from someone who has
pneumonia or common cold,running
nose,sneezing etc. Another cause is an
improperly cleaned air conditioner. Yet
another source of infection in your lungs is
spread by an infection from somewhere else
in your body, such as your kidney.

Route of Entry
Germs are spread both by aerosolized droplets that
you breathe in (such as from a sneeze), and
through body fluids left on surfaces like counter
tops and door handles. If you avoid people who
are coughing or sneezing, and wash your hands
frequently, you can reduce your chances of
catching a virus or bacterial infection.

Route of Entry
I would suggest keeping everything sprayed
with a antibacterial agent of some sort,
strict hand washing, You could also buy
face masks and gloves for you and your
children until another person is no longer
contagious.

Route of Entry
Spread is common in industrialized cities,
lower socioeconomic groups or in cases of
crowded living quarters. The incidence of
bacterial pneumonia increases in winter and
spring in temperate zones.

Pathogenesis how organism
reaches alveoli

Pathogenesis how organism
reaches alveoli

Congestion
Red Hepatisation
Grey Hepatization
Resolution
Pathogenesis of Pneumonia

Four phases of pneumonia
are
1. Congestion (1-2 days)
2. Red hepatization (2nd-4th day)
3. Gray hepatization (4th-6th day)
4. Resolution (6th day onwards)

Congestion (1-2 days)
Organism after entry from various routes
Come in contact with alveolar walls
The capillaries in alveolar walls in response
increase their blood supply by dilatation so
that inflammatory cells reach there quickly
for defense, increased blood flow and
dilatation result thus in congestion of that
turns lung into mild reddish colour.

Red hepatization
(2nd-4th day)
Because of this congestion
and dilatation there is
outpouring of red cells and
hemorrhage into alveoli as
well as some polymorphs
the consistency of the
affected lung thus
becomes like a liver and
very red in colour, this
stage therefore has been
named “red hepatization”.

Gray hepatization
(4th-6th day)
In this stage the
macrophages appear
which phagocytose the
fragmented
polymorphonuclear
leukocytes and red cells
and other inflammatory
debris.The lung now no
longer remains congested
but still remains firm in
this stage of “gray
hepatization”. Its due to
WBCs,lymphocytes
,macrophages that colour
is grey.

Gray hepatization (4th-6th
day)
Polymorphonuclear leukocytes, at this stage
produce the rusty sputum since RBCs are
broken down and release haemosidren
mixed with sputum is rusty.

Resolution (6
th
day onwards)
The alveolar exudates is then removed and
the lung gradually returns to normal.

Summary of Stages of
Lobar Pneumonia:
Four stages:
Congestion–vasodilatation
–RedHepatization-Exudation+RBC
–GrayHepatization-neutro & Macrophages.
–Resolution–few macrophages, normal.

Complications of Pneumonia
A painful pleuritis
pleural effusion
Pyothorax
Empyema
Fibrosis due to laying down of fibroblasts in
non resolving pneumonia called
carnification of lung.
Necrotizing lung & lung abcess

The pleural surface at the
lower left demonstrates areas
of yellow-tan purulent exudate.
Pneumonia may be
complicated by a pleuritis.
Initially, there may just be an
effusion into the pleural space.
There may also be a fibrinous
pleuritis. However, bacterial
infections of lung can spread
to the pleura to produce a
purulent pleuritis.
A collection of pus in the
pleural space is known as
empyema.

Complications of Pneumonia
1. Pulmonary fibrosis.
2. Bronchiectasis
3. Lung abscess
4. Empyema
5. Bacteraemia with abscess in other organs
6.ARDS
7.Bacteremia
8.Collapse of lung
9.Hemoptysis

Complications of Pneumonia
Parapneumonic effusions
Septic arthritis
Endocarditis
Pericarditis
Respiratory failure
Mental symptoms

Investigations of Pneumonia
Total and differential count
PBF
Blood ,urine,sputum culture/sensitivity
Gram staining/stain for AFB
Fiberoptic bronchoscopy with bronchial
washing/ brushing /biopsy

Investigations of Pneumonia
X-ray chest
CT chest
Serological tests
ABG
Other all routine basic tests

TREATMENT OF
PNEUMONIA
Uncomplicated pneumonia
Erythromycin 250-500mg 6 hrly or with
combination with cefuroxime or Amoxycillin or
Ampicillin 500 mg 6-8 hrly x 7-10 days.
Azithromycin 500mg x3-5 days if pt intolerant to
erythromycin
Consider levofloxacin 500 mg once a day if pt
elderly

TREATMENT OF
PNEUMONIA
Moderately sick
Ceftriaxone 1-2 gram once or BD iv and
erythromycin or azithromycin 500 mg daily
Ampicillin –clauvulanic acid plus
erythromycin or azithromycin

TREATMENT OF
PNEUMONIA
Severely sick
Ceftriaxone 1-2 gram once or twice a day
plus either azithromycin 500 mg a day or
levofloxacin 500 once a day x 7-10days

TREATMENT OF
PNEUMONIA
In multiresistant cases and in staphylococcal
or gram negative infection can give
multiresistant strains give Vancomycin
500mg to 1 gram I/V twice daily.

TREATMENT OF
PNEUMONIA
For klebsiella,legionella,actinomycosis
Gentamycin, ceftriaxone for two weeks even
Azithromycin.
Rifampicin be given in legionella also
For actinomycosis also Benzyle penicillin 10-20
million units iv 6 hrly day.
In severe cases piperacillin plus tazobactam or
Meropenem.
Clindamycin 800mg 8 hrly followed by 300 mg
orally 8hrly in aspiration pneumonia.

Treatment for rickettsial
infection
Rickettsial infections respond promptly to
early treatment with the antibiotics
doxycycline
chloramphenicol
tetracycline

Treatment for fungal infections
First give test dose as follows: 1 mg in 20
ml of D5W over 30 minutes to 1 hour;
monitor vital signs every 30 minutes for
next 2 hours.if no untoward reaction occurs
then do as follows.

Treatment for fungal infections
Amphotericin B comes in a vial that
contains 50mg of powder. Each vial needs
to be mixed with 10ml of Water for
Injection. The dose is then drawn up and
again mixed with 500mL of dextrose and
shaken.

Treatment for fungal infections
then give 0.25 to 0.5 mg/kg daily by slow
I.V. infusion (0.1 mg/ml over 2 to 6 hours)
or 1mg/10mL. with or without flucytosine
for two weeks to several months.even on
alternate days.
fatal infections may require higher dosages
(1 to 1.5 mg/kg daily).

Treatment for fungal infections
The Amphotericin B should NEVER be
mixed with Normal Saline or Half Normal
Saline as it will precipitate.
Flush I.V. line with 5% dextrose injection
before and after infusion.
Pretreat with antihistamines, antipyretics, or
corticosteroids, as prescribed.

Treatment for fungal infections
What to Monitor in Patients Receiving
Amphotericin B
The following should be monitored more
aggressively during the initial 2 weeks of therapy.
1.The patient's temperature, pulse, respiration, and
blood pressure should be recorded every 30
minutes for 2 to 4 hours.and keep eye on

Treatment for fungal infections
2. BUN, SCr
3. Potassium, magnesium, sodium, and other
electrolytes
4. CBC
Since patient tolerance varies greatly, the dosage
of amphotericin B must be individualized and
adjusted according to the patient's clinical status
(e.g., site and severity of infection, etiologic agent,
cardio-renal function, etc.).

Treatment for fungal infections
The efficacy and safety of 2 weeks of
intravenous itraconazole (200 mg twice
daily for 2 days, then 200 mg once daily for
12 days) followed by 12 weeks of oral
itraconazole capsules 200 mg twice daily
were also evaluated in a multicentre, open
trial in 31 immunocompromised patients
with invasive pulmonary aspergillosis .

Treatment for fungal infections
FLUCYTOSINE
Older children: A dose of 50 mg/kg every 6
or 8 hours is normally used in older
children. Always check the blood level after
1–2 days if a dose as high as this is used in
a young baby.

Treatment for viral infections
flucytosine 250,250mg capsules are also available
and given as 50-150mg/kg/day 6-8 hrly x 4-6
weeks.
or may be 2 weeks followed by fluconazole.
so is with amphotericin x 10days or 4-6 weeks.
amphotericin B alone (0.5 mg/kg/day; or
amphotericin B (0.5 mg/kg/day) plus 5-flucytosine
(150 mg/kg/day; intravenously. Therapy was
given for an average duration of 10 days in some
groups.

Treatment for viral infections
Acyclovir
The duration of intravenous therapy with
Acyclovir is usually 5 days.
The doses recommended above (5 or
10mg/kg bodyweight or 500mg/m2 ) should
be given every 12 hours.

Treatment for viral infections
Adults: 5 mg/kg infused at a constant rate over at
least 1 hour, every 8 hours for 7 days in adult
patients with normal renal function.
oral dose
800mg 4 hrly x7-10days
Chronic Suppressive Therapy for Recurrent
Disease: 400 mg 2 times daily for up to 12 months

SOME X-RAYS ON
PNEUMONIAS

BULGING FISSURE
KILEBSILLA PNEUMONIA

INTERSTITIAL PNEUMONIA

LOWER LOBE PNEUMONIA

MIDDLE LOBE
COSOLIDATION

PNEUMATOCELE

RIKETESSIAL TICKS

UPPER LOBE
CONSOLIDATION

Afebrile Pneumonia Syndrome

Afebrile Pneumonia Syndrome
Afebrile pneumonia syndrome (APS) is a
relatively uncommon disease of neonates
and infants younger than 6 months. APS
was first described as a vertically
transmitted infection of newborns and
young infants by the female genital tract
pathogens Chlamydia trachomatis,
cytomegalovirus (CMV), and Ureaplasma
urealyticum

Afebrile Pneumonia Syndrome
More recently, other potential causes of the
syndrome have been recognized, including
respiratory syncytial virus (RSV),
parainfluenza virus, adenovirus, and
Pneumocystis jiroveci.

Afebrile Pneumonia Syndrome
Early symptoms of respiratory disease in
neonates and infants are frequently
nonspecific and include changes in feeding
status, listlessness, irritability, and poor
color. Onset may be acute or subacute.
Typically, infants are afebrile or have only a
low-grade fever (<102°F).

Afebrile Pneumonia Syndrome
Viral afebrile pneumonia syndrome (APS)
typically has a more rapid onset, with a 1-
to 2-day history of rhinorrhea and, often, a
brassy cough. Nonspecific findings of poor
feeding, lethargy, and irritability may be
accompanied by congestion, apnea
(uncommon), and cyanosis (rare). Fever is
often absent in very young infants.

Factors that are associated with increased risk
of contracting APS in infants include the
following:
Low socioeconomic status
Young maternal age
Multiple maternal sex partners
Unmarried maternal status
Exposure to other children at home or in
daycare
Exposure to secondhand smoke

Pneumocystis carinii

Pneumocystis carinii pneumonitis (PCP) is a
common opportunistic disease that occurs
almost exclusively in persons who have
profound immunodeficiency.
PCP was and still is the most common life-
threatening opportunistic infection occurring in
patients with HIV disease.

The taxonomy of P cariniihas not been established.
If it is either a protozoan or a fungus. Recent studies
show P cariniimore closely resemble fungi than
protozoa.
Eriksson places P cariniiin a new
family, Pneumocystidaceae, and in
a new order, Pneumocystidales
(Ascomycota).

The mode of replication of P cariniihas not
been established. However, the stages in its life
cycle have been characterized. Sporozoites
excyst through breaks in the cyst wall and then
are termed trophozoites. The means by which
the trophozoite form progresses to the cyst
phase is not known.

The portal of entry for P cariniihas not been
firmly established; however, because with rare
exceptions the organism has been found only in
the lung, inhalation is a likely mode of
transmission. Airborne transmission has been
demonstrated in animals. In most individuals,
the organism is dormant and sparsely dispersed
in the lung, with no apparent host response
(latent infection). In susceptible
(immunocompromised) hosts, the organism
occurs in massive numbers.

With rare exceptions, P carinni causes disease
only when natural mechanisms of host defense
are compromised.

Pneumocystis cariniihas been found in the
lungs of rats, rabbits, mice, dogs, sheep, goats,
ferrets, chimpanzees, guinea pigs, horses, and
monkeys. The organism has been reported in
lower animals and humans from all continents.
Animal to animal transmission by the airborne
route has been demonstrated. Because about
70 percent of healthy individuals may have
humoral antibody to P carinii, subclinical
infection must be highly prevalent.

Tachypnea and fever are consistent features of
the pneumonitis, and diffuse bilateral alveolar
disease can be observed by radiography.
Diagnosis requires the identification of P carinii
in pulmonary tissue or lower airway fluids.
Such specimens may be obtained by lung
biopsy, inducement of sputum, bronchoalveolar
lavage, or needle aspiration of the lung. The
Gomori, Giemsa, fluorescence-labelled
antibody, or toluidine blue O stains may be
used to identify the organism.

Pneumo Pneumocystis carinii

•Four drugs currently available for therapy of
P cariniipneumonitis are:
Pentamidine isethionate
Trimethoprim-Sulfamethoxazole
atovaquone
trimetrevate
Trimethoprim-sulfamethoxazole is
preferred because of its low toxicity
and greater efficacy.

BACTRIM-DS
Bactrim DS tablet contains. 160 mg of
trimethoprim and 800 mg of
Sulfamethoxazole.
21 days course

Prednisolone40 mg bid x 5 days, then 40
mg/day x 5 days, then 20 mg/day to
completion of treatment

Alternative Treatments:
–TMP15 mg/kg/day PO + dapsone100
mg/day x 21 days
–Pentamidine4 mg/kg/day IV x 21 days
-Atovaquone750 mg PO bid with meal x 21
days
PCP is the most frequently identified serious
in HIV disease

PCP
Site of Infection:
–Attaches to and damages type I pneumocytes.
Results in interstitial inflammation with
infiltration of lymphocytes and
macrophages in interstitial tissue of lungs.

PCP: Extrapulmonary
Infection
Extrapulmonary sites of infection:
–Reticuloendothelial system (liver, spleen, bone
marrow)
–Sinuses, middle ear, eye, and dermis around
head.

Patients at Risk
AIDS at CD4 < 200.
Congenital and acquired defects in cellular
immunity.
Organ transplantation recipients.
Chemotherapy.
Corticosteroids.
Malnutrition.
Premature birth.

PCP: Clinical Features
Cough
–Usually nonproductive, occasionally whitish sputum.
Dyspnea
Fever
May be accompanied by night sweats, but not
rigors.
 Rales
–May be present, but are often absent.

PCP: Pearls
Similar to atypical pneumonias.
Physical examination is often less severe
than x-ray findings.
Gradual onset

PCP: CXR Findings
90-95% have pulmonary infiltrates.
Combined interstitial & alveolar infiltrates.
Predominantly at bases and centrally.
Pneumothorax can be present.
Lace like appearance.

Histologic Diagnosis
Sputum (induced if necessary):
–Diagnostic
–Flexible Bronchoscopy with Bronchoalveolar
lavage to find pnuemocytis carinii in sputum
and secretions.
.

Histological Diagnosis
Transbronchial biopsy:
Percutaneous Lung aspiration:
Open lung biopsy:
–Only in rapidly deteriorating patients with a
negative bronchoscopy.

Histologic Diagnosis
Future techniques: Serum PCR?
Stains:
–Gram and Giemsa stain both cyst and
trophozoites.
–Gomori’s silver and Toluidine stains for cysts.

Pathophysiology
Pneumocystis infection is specific to the lung
Trophozoites bind tightly to alveolar epithelium,
but do not invade cells
CD4 T cells recognize pathogen and recruit
macrophages
Macrophages release TNF-αwhich propagates
immune response through further recruitment and
cytokine release

Pathophysiology continued
Results in a large
inflammatory response
which can lead to
diffuse alveolar
damage, impaired gas
exchange, and
respiratory failure

Diagnosis continued
Gomori methenamine silver (GMS) stain from
BAL specimen showing “crushed ping-pong
ball” appearance of cyst wall

Diagnosis continued
Calcofluor white stains the fungal cyst wall for
rapid diagnosis

Diagnosis continued
Immunofluorescence showing trophozoites
(arrowheads) and cysts (arrows)

Radiographic Findings
Typically see bilateral, ground glass opacities that
progress over time to become homogenous and
diffuse
10% of HIV patients will show upper lobe cysts
Less common to see solitary or multiple nodules,
upper lobe predominance, or pneumothorax
Rare to see pleural effusion or lymphadenopathy
(search for another cause)
HRCT is more sensitive during early stages when
CXR will likely appear normal

PA Chest Radiograph
Demonstrates
bilateral, perihilar,
R > L, ground glass
opacities

PA Chest Radiograph
Progressive
disease showing
extensive ground
glass opacification
with consolidation

PA Chest Radiograph
Diffuse ground
glass opacity with
reticular pattern
indicating cyst
formation

PA Chest Radiograph
Diffuse, ground
glass opacities with
large left sided
pneumothorax
Cysts predispose
patients to pneumo-
thorax

PA Chest Radiograph
Patchy, ground
glass opacities in the
apices in an
AIDS patient on
pentamidine
prophylaxis