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PNEUMONIAS

By
Dr Bashir Ahmed Dar
Chinkipora Sopore
Kashmir
Associate Professor
Medicine
Email
drbashir123@gmail.com
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
have 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 but 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
and dental procedures.
 3.Ineffective coughing as in post-traumatic,post-
operatiive,paralysis of larynx or pharynx.
 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
Re transcriptase

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
 Viral pneumonia often goes unrecognized
because the person may not appear very ill.
 Disease 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
Occurs primarily in the cold and winter and
tends to be more serious in people with
cardiovascular or lung disease.
* Leucocyte count is usually normal or low
* The x ray may show features of interstitial or.
atypical pneumonia
* 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
 Streptococcus Pneumoniae generally
resides in the nasopharynx and is found in
approximately 50% of healthy individuals.
 Pneumococci infect type II alveolar cells.
 As the pneumococci reach the alveolar
spaces they come in contact with epithelium
of alveolus and produce alveolar lesions..
BACTERIA THAT CAUSE
PNEUMONIA
 The pneumonic lesion progresses as
pneumococci multiply in the alveolus and
invade further alveolar epithelium. and start
spreading from alveolus to alveolus
through the pores of Kohn, thereby
producing inflammation and consolidation
along larger areas of the lung.The damage
may result in rust coloured sputum.
BACTERIA THAT CAUSE
PNEUMONIA
 Streptococcus agalactiae bacterium is
usually found in genital tract of females 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
 Abcess formation is very common.in
staphylococcal infection.
 The abcesses are thin walled,multiple and
commonly bilateral giving rise to patchy
bronchopneumonia.
BACTERIA THAT CAUSE
PNEUMONIA
 Sincemultiple sites are involved bilaterally
simultaneously a scattered appearance of
heterogeneous opacities is the usual result.
 Eventually more and more alveoli may be
affected and ultimately a homogeneous
opacification simulating lobar pneumonia
may be observed.
BACTERIA THAT CAUSE
PNEUMONIA
 Due to these small abcesses the staphylococcus
aureus produces purulent (pus-laden) sputum that
often appears creamy and may be bloodstained.
BACTERIA THAT CAUSE
PNEUMONIA
 Staphylococcal organism can also cause
 Boils
 Abscesses
 Styes
 Carbuncles
 Cellulitis
 Impetigo
BACTERIA THAT CAUSE
PNEUMONIA
 Septic shock.
 septic arthritis
 osteomyelitis
 Internal abscesses anywhere within the
body
 meningitis
 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
2. Bacillus anthracis is Anthrax or Wool-Sorters
disease Associated with wool sorting, with
animal handlers, and veterinarians, and produces
eschar on skin.
BACTERIA THAT CAUSE
PNEUMONIA
2. Nocardia & Actinomyces
Beaded filamentous rod shaped bacteria,
causing rib destruction, cutaneous sinuses,
cavitation, and spreads to pleura and chest
wall.
BACTERIA THAT CAUSE
PNEUMONIA
 Actinomyces israeli ,an anaerobic organism
occuring in mouth as commensal
 When local defences break then can cause
 three forms of disease.
 1.Cervicofacial with discharging sinuses
 Abdominal actinomycosis with discharging
sinuses.
BACTERIA THAT CAUSE
PNEUMONIA
 And pulmonary actinomycosis with
widespread suppurative pneumonia with
discharging chest wall sinuses.
 The pus from sinuses contain sulphur
granules.
BACTERIA THAT CAUSE
PNEUMONIA
 Bacteria Gram Negative cocci
2. Neisseria meningitidis (meningococci)
cause epidemics in military
recruits,schools,young adults,overcrowded
places.

5. Moraxella catarrhalis
BACTERIA THAT CAUSE
PNEUMONIA
 Bacteria gram negative rods
2. Klebsiella pneumoniae (friedlanders
bacillus) produces blood stained Current
Jelly sputum.
3. Upper lobes being most affected with
massive lobar consolidation.
BACTERIA THAT CAUSE
PNEUMONIA

 Bulgingof interlobar fissure is a


characteristic finding in Klebsiella
pneumoniae
BACTERIA THAT CAUSE
PNEUMONIA
2.Pseudomonas aeruginosa produces green
sputum as well as Haemophilus.
3. Acinetobacter often found on respiratory
therapy equipment and on human skin
very difficult to treat due to multiple drug
resistance.
4. Burkholderia pseudomallei occurs with
exposure to contaminated soil
BACTERIA THAT CAUSE
PNEUMONIA
6. Yersinia Pestis,causes
three forms of Plague Disease
– Pneumonic
– Bubonic
– Septicemic
via flea bites and ticks due to animal
contacts like rats,rodents.
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 is Whooping cough
common in children.
TULARAEMIA SKIN &
GLANDULAR
BACTERIA THAT CAUSE
PNEUMONIA
There are other bacteria or Bacteroides that
are anaerobes and usually found in
aspirationn pneumonia and are as follows.
11.Fusobacterium
12.Porphyromonas
13.Prevotella
14.Proteus
15.Serratia
ANAEROBIC BACTERIA
 Other anaerobic bacteria are
 •Actinomyces
 •Bifidobacterium
 •Clostridium
 •Peptostreptococcus
 •Propionibacterium
 These are bacteria that do not live or grow in the
presence of oxygen.
Gram-Negative Bacteria
 Thereare many Gram-Negative bacteria
such as Cyanobacteria, Spirochaetes, E-coli,
Salmonella, Pseudomonas, Moraxella,
Helicobacter, Stenotrophomonas,
Legionella,Hemophilus influenzae,
Neisseria Meningitidis, Moraxella
Catarrhalis, Neisseria Gonorrhoeae,
Acinetobacter Baumanii .
Gram-Negative Bacteria
 People most likely to get sick with Gram-negative germs
are those who:
 • are seriously ill
 • are in the hospital for a long time
 • have taken many antibiotics or drugs
 • 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
 Old,alcoholic, and in diabetic
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 preceding viral infection may
predispose to bacterial pneumonia, by
damaging some of the lung's defenses
against infection or may occur without
preceding viral 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
 Fungi that can cause pneumonia are
– Histoplasmosis
– Blastomycosis
– Cryptococcosis
– Sporotrichosis - primarily a lymphocutaneous disease,
but can involve the lungs as well
 Aspergillus
 Candida
 Coccidiodomycosis
Fungal Pneumonia
 Histoplasmosis H/O of contact with
Chickens, bats, river valleys and excavation.
 Coccidioidomycosis may occur after
exposure to a wind or rain storm in an
endemic area.
 HISTOPLASMOSIS
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.
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 that
spreads rapidly in cows, sheep, and goats,
slaughter houses, research facilities, where
handling of animals or their birth products
is a source of exposure.
Hepatosplenomegaly is a common finding.
Rickettsial Pneumonia
 Rickettsia pneumonia usually gives rise to atypical
pneumonia.Vasculitis of small vessels is basic
underlying pathology in rickettsial infections.
 Rickettsial infections usually present with fever,
skin rash and eschar.
 Common fleas such as cat and dogs fleas and rat
fleas are reported worldwide, as are their
transmitted rickettsial diseases.
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.Poor environmental hygiene conditions
 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 entry commonly skin the organisms
localize in endothelial cells and enter into the cells.
It proliferates intracelluarly. A papule may be
formed that 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.
ATYPICAL BACTERIA
 Are organisms that do not fit in virus,bacteria
or fungus.
 Thus these bacteria are called atypical and
produce atypical pneumonia.
 These organisms also do not stain with gram
stain.
ATYPICAL BACTERIA
 Following organisms constitute atypical bacteria.
 Legionella
 Mycoplasma
 Chlamydia trachomatis an afebrile pneumonia, usually seen in 2 wk to
6 months of age
 Chlamydia psittaci
 Chlamydia pneumoniae
 Chlamydia trachomatis is a sexually transmitted disease that may also
cause pneumonia and bronchitis and conjuctivitis in early infancy by
passing through contaminated genital tract, but it may occur in adults
too.
ATYPICAL BACTERIA
 Other organisms that cause atypical pneumonia
are
 Coxiella burnetii (Q-fever) ingestion of
comtaminated milk, or inhalation of contaminated
aerosols from barnyard animals
 Mycobacterium tuberculosis and other
Mycobacterium
 And some species of fungi ,viruses and protozoa
Classification of Pneumonias

BY SITE

 LOBAR PNEUMONIA
 BRONCHOPNEUMONIA
 INTERSTITIAL OR ATYPICAL
PNEUMONIA
Lobar Pneumonia
 Consolidation or pneumonia of whole lobe
of lung is called lobar pneumonia.
Broncho-Pneumonia

 Bronchopneumonia is characterized first by


inflammation of small bronchioles then of alveoli there
by resulting in patchy bilaterial consolidation of lung.
b
Pathogenesis of
Bronchopneumonia
 There is initial terminal bronchiolitis that then spreads to 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,infilfamatory cells, collapse and emphysema.
 Resolution of the exudate usually restores normal lung
structure.Organization may occur and result in fibrous scarring in some
cases or Aggressive disease may produce abscesses.
Broncho-Pneumonia

 Lesions may be more extensive that often fuses together


resembling lobar pneumonia (confluent
bronchopneumonia).
These are the lungs from a cow with severe
bronchopneumonia and fibrinous pleuritis.

Liver

Diaphragm

Abomasum
This is the same lung cut open showing deposits of fibrin between
sections of lung with bronchopneumonia.
These are lungs from a cow with severe Pasteurella
bronchopneumonia.
This is severe bacterial bronchopneumonia and pleuritis in a pig caused by
Actinobacillus pleuropneumonia.
This is a closer look at the same lung.
Again, note the black line. The
darker red tissue has severe Pasteurella
bronchopneumonia. The white spots
are abscesses.
Here is the same lung cut open to show
The severe bronchopneumonia and numerous
abscesses (white spots)
Bacterial pneumonia in a pig. Areas with inflammation are dark
pink. Normal lung is light pink.
This is the same lung cut open showing areas of inflammation (dark pink)
and Normal tissue (light pink)
These are the lungs from a cow
with chronic
bronchopneumonia. The
areas with
inflammation
are to the right of the
black lines. Within the
areas of inflammation
are numerous
abscesses
(white spots).
This is the same lung cut open to show
areas of inflammation and abscess
formation (white spots). The
normal lung is the white
colored region to the
far right.
This is severe fibrinous pleuritis
and pneumonia caused by aspirating
foreign material into the lung.
This is the same lung cut open to show regions
of the lung with severe inflammation
and necrosis.
These are the lungs of a horse with chronic, fibrous pleuritis. Note
how the fibrous material appears organized and is stuck to the
surface of the lung.
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. Most
of viruses produce this type of pneumonia
also.The inflammation is confined to interalveolar
septa or interstitial spaces between alveoli and
radiologically gives appearance of reticulonodular
pattern.linear thread like opacities here and there
in lungs.
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,typical of interstitial pneumonia.
CAUSES OF ATYPICAL
PNEUMONIA
 Following organisms constitute atypical bacteria and cause atypical
pneumonia
 Mycoplasma
 Legionella
 Chlamydia trachomatis
 Chlamydia psittaci
 Chlamydia pneumoniae
 Q-fever
 Tularemia
 Anthrax
 Viruses
 Fungi
CAUSES OF ATYPICAL
PNEUMONIA
 Others like
 Histoplasmosis
 Coccidiodomycosis
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
 EXTRA PULMONARY MANIFESTATIONS
 gastrointestinal
 musculoskeletal
 dermatologic
 cardiac
 neurologic symptoms
 The most common pathogen of atypical pneumonia is
Mycoplasma pneumoniae. It ranks second only to S.
pneumoniae
LEGIONELLA
 Occurred first in military personnel called
legionnairs while using tank water etc.
LEGIONELLA
 So in legionella pneumonia there will be
history of contact with Cooling towers,
condensers,Water tanks,AC
coolers,washings etc.
 There is also history of GIT disturbances.
Chlamydial infection
 Due to
 Chlamydia trachomatis
 Chlamydia psittaci
 Chlamydia pneumoniae
 Chlamydia trachomatis is a sexually transmitted
disease that may also cause pneumonia and
bronchitis and conjuctivitis in early infancy by
passing through contaminated genital tract, but it
may occur in adults too.
Chlamydial infection
 Chlamydia psittaci infection will have
history of contact with pigions,pet shops
and zoo.
Q- FEVER
Q fever is common rickettsial disease that
gives rise to pneumonia.In Q fever there
will be history of contact with cattle, sheep,
goats, contaminated milk, birthing various
livestock


TULAREMIA--ANTHRAX
 Tularemia will have history of contact
with Rabbits, ticks
 Tularemia also causes lymph gland
involvement.
 Anthrax has contact with Goat hair/skin,
wool, bone meal fertilizer and causes black
spot on skin due to ulcer surrounded by
edema called eschar.
TULARAEMIA SKIN &
GLANDULAR
ANTHRAX ESCHAR
HISTOPLASMOSIS
 People with atypical pneumonia due
histoplasmosis will have history of contact
with Chickens, bats, river valleys .It also
produces skin leisions.

 Coccidioidomycos
 foundin people residing in
California,Southwest USA.
 HISTOPLASMOSIS
COXIELLA BURNETII

 Coxiella burnetii: This is related to


exposure to infected parturient cats, cattle,
sheep, or goats.
 Burkholderia (Pseudomonas) pseudomallei
(melioidosis): This infection may result
from travel to Thailand or other countries in
Southeast Asia.
Atypical or Interstitial or viral
Pneumonia
 In atypical pneumonia extrapulmonary
symptoms, most often give some clue to
the causative organism.
 The symptoms are generally more than the
sings in the chest or x-ray as already said.
so this type of setting is called occult
pneumonia.
CHEMICAL 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.
 Aspiration of gastric contents in pts with gastro-
esophageal reflux disease(HCL may directly and
quickly cause lung damage resulting in chemical
pneumonia.
Serological tests for atypical
pneumonia
 1.Mycoplasma pneumoniae
 complement fixation test, IgM by latex
agglutination or ELISA test.
 cold agglutinin test.
 2.Legionella pneumophila
 rapid microagglutination test
 Test for Legionella antigen in the urine.
Serological tests for atypical
pneumonia
 3.Chlamydia
 Microimmunofluorescence
 ELISA
 4.Coxiella burnetii
 complement fixation test.
 Serologic tests. A four fold or greater rise in
titer is confirmatory of an acute infection
Serological tests for atypical
pneumonia

 Skintesting for
histoplasmosis,coccidioidomycosis.
.
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 pneumonia

◆ new cough
◆ new infiltrate or progressive
infiltrate on
chest radiograph.
 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
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.
RISK FACTORS
 Hypogammaglubolinemia
 Sever Neutrogena
 Corticosteroid therapy
 Environmental risk factors.
– Obstructions – foreign body, tumors
- Prolonged mechanical ventilation
- extremes of age
RISK FACTORS THAT FORM BASIS OF
SECONDARY PNEUMONIAS
* Partial bronchial obstruction by tumour
causes stasis of secretions and secondary
infection distal to site of obstruction
 Vomiting and aspiration during
anaesthesia,sleep,coma,alcholism
 Inhalation of septic matter during
tonsillectomy,dental procedure,or general
anaesthesia
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.
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
 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.
Route of Entry

 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
 Keep everything sprayed with antibacterial
agent of some sort, strict hand
washing,face masks and gloves for you and
your children until another person is no
longer contagious.
Pathogenesis and 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 (6th day onwards)
 The alveolar exudates is then removed and
the lung gradually returns to normal.
Diagramatic pathogenesis
Pathogenesis how organism
reaches alveoli
Grey
Hepatization
Resolution

Congestion
Red Hepatisation
Summary of Stages of
Lobar Pneumonia:
 Four stages:
 Congestion – vasodilatation
– Red Hepatization - Exudation+RBC
– Gray Hepatization - 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
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
TREATMENT OF
PNEUMONIA
 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
 Rickettsialinfections respond promptly to
early treatment with the antibiotics like
 Doxycycline
 Chloramphenicol
 Tetracycline
Treatment for fungal infections
 Firstgive 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
 Olderchildren: 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 fungal 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.
Treatment for fungal infections
 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
Afebrile Pneumonia Syndrome
 Afebrile pneumonia syndrome (APS) is a
relatively uncommon disease of neonates
and infants younger than 6 months.
Transmitted in female genital tract to baby
by pathogens Chlamydia trachomatis,
cytomegalovirus (CMV), and Ureaplasma
urealyticum during delivery.
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.
 Typically, infants are afebrile or have only
a very little fever.
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
RADIOLOGY

 X-RAYS
ON VARIOUS TYPES OF
PNEUMONIA
Anatomy
Normal
Chest
Radiograph
Anatomy
Lobes
 Right upper lobe:
Lobes (continued)
 Right middle lobe:
Lobes (continued)
 Right lower lobe:
Lobes (continued)
 Left lower lobe:
Lobes (continued)
 Left upper lobe with Lingula:
Lobes (continued)
 Lingula:
Lobes (continued)
 Left upper lobe - upper division:
RUL pneumonia
RML pneumonia
RLL pneumonia
LUL pneumonia
LLL pneumonia
What’s happened here?

Right upper
lobe collapse
Bulging Fissure Sign

Consolidation spreading rapidly, causing lobar expansion


and bulging of the adjacent fissure inferiorly .

Historically Klebsiella pneumoniae involving the right


upper lobe . Friedlander pneumonia.
ATYPICAL PNEUMONIA
 In next slides you will thread like linear
striations extending here and there in the
lungs forming sort of a network.you may
also see very small patchy spots nodules
over or along these lines giving reticulo-
nodular appearance characteristic of
atypical or viral pneumonias.
INTERSTITIAL / ATYPICAL
PNEUMONIA
ATYPICAL
PNEUMONIA
Bronchopneumonia
 Progressive

disease showing
Bilateral patchy
opacification
with consolidation
 Patchy broncho
pneumonia more on
left side.
Thank you.
Always take proper detailed history
of a patient.

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