1 03.09 · ^The common cold (also known as nasopharyngitis, rhinopharyngitis, acute coryza, or a...
Transcript of 1 03.09 · ^The common cold (also known as nasopharyngitis, rhinopharyngitis, acute coryza, or a...
03.09.2014 1
Lung pathology
Acute pneumonias,
acute viral respiratory infection
Ivan Sakharau, assist. lect.
Acute pneumonia
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is an inflammatory lung disease affecting alveoli with accumulation of exudate in the alveoli or cellular infiltration in the interstitial tissue
“Pneumonia”
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from Ancient Greek πνευμονία (pneumonia, “lung disease”), from πνεύμων (pneumōn, “lung”)
Classification
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1. Etiology
biological agents: bacteria, viruses, fungi, protozoa, mixed infections
chemical factors: a vapours of chemicals, uremia
physical factors: industrial dust, ionizing radiation
Ways of contamination:
airborne
aspiration from naso- and oropharynx
hematogenous infection of extrapulmonary lesions
from neighbour infected sites
Classification
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2. Pathogenesis Primary: there are laws on its own etiopathogenetic
Secondary: a manifestation of another, as a rule, system or extrapulmonary disease
Risk factors: airway infection (usually viral)
obstructive changes in bronchi
immunodeficiencies, hypothermia, stress
alcohol and tobacco
inhalation of toxic substances and dusts
wounds and injuries, post-operative period
early childhood and old age
Classification
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3. Prevalence
unilateral, bilateral
acinar, miliary, lobular, segmental, polysegmentary, lobar, total
Classification
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4. Clinical and morphological features
lobar pneumonia
bronchopneumonia (focal p.)
interstitial pneumonia
“Older terminology refers to lobar pneumonia or bronchopneumonia, but these terms have little clinical relevance today. In general, lobar pneumonia refers to consolidation of an entire lobe while bronchopneumonia is scattered solid foci in the same or several lobes”
(Rubin's Pathology : Clinicopathologic Foundations of Medicine, 5th Edition)
Differential clinical and morphological characteristics
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Feature Lobar pneumonia Bronchopneumonia
Etiology Pneumococci (Streptococci pneumoniae I, II, III, IV types), Klebsiella pneumoniae
Bacteria, viruses, fungi, mycoplasma, chlamidia, chemical and physical factors
Pathogenesis • Preceding sensibilisation to microbial agent
• Triggering factor (hypothermia, trauma)
After acute bronchitis and bronchiolitis
Clinical signs Acute onset, rapid development
Manifestations increase gradually
Differential clinical and morphological characteristics
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Feature Lobar pneumonia Bronchopneumonia
Exudate Fibrinous or fibrino-purulent Serous, purulent, haemorrhagic, fibrinous, putrid, mixed
Affected lung volume
1 lobe (right lower is most common), 2 lobes, 3 lobes
Acini, lobuli, segment(s)
Prevalent patients age
• Young adults, adults • Always primary
• All ages • Usually secondary
(primary in infants and elderly patients)
Staging 4 stages No
Lobar pneumonia – clinical signs
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Lobar pneumonia – staging
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1. Initial (1st day)
a lobe rapidly becomes red and swollen
protein-rich edema fluid containing numerous bacteria fills the alveoli (“microbial edema”)
some amount of alveolar macrophages and leukocytes is seen
fibrin is seen at the end of the day
as a rule inflammation also develops in the pleura (pleuritis)
bronchi remain intact during all stages (inflammation develops only in alveoli)
Lobar pneumonia – initial stage
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Lobar pneumonia – initial stage
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Lobar pneumonia – staging
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2. Red hepatization (2nd-3rd days)
marked capillary congestion leads to massive outpouring of polymorphonuclear leukocytes and intra-alveolar hemorrhage
affected lobe is of firm consistency and reminiscent of the liver
Lobar pneumonia – red hepatization
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Lobar pneumonia – red hepatization
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Lobar pneumonia – staging
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3. Grey hepatization (4th-6th days)
lysis of polymorphonuclear leukocytes and erythrocytes
macrophages phagocytose the fragmented blood cells
lobe is still firm and grey due to fibrin in alveoli
Lobar pneumonia – grey hepatization
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Lobar pneumonia – grey hepatization
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Lobar pneumonia – grey hepatization
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Lobar pneumonia – staging
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4. Resolution (up to 2 weeks)
fibrinolysis
alveolar exudate is then removed while coughing
lung gradually returns to normal
Lobar pneumonia – complications
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Pleuritis, often painful, is common, because the pneumonia readily extends to the pleura
pleura is usually involved; sometimes “lobar pneumonia” is called “pleuropneumonia”
Pleural effusion occurs frequently, but usually resolves
Pyothorax results from infection of a pleural effusion, and may heal with extensive fibrosis
Lobar pneumonia – pleuritis
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Lobar pneumonia – complications
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Pulmonary fibrosis. The intra-alveolar exudate organizes to form intra-alveolar plugs of granulation tissue. Gradually, increasing alveolar fibrosis leads to a shrunken and firm lobe, a rare complication known as carnification
Lobar pneumonia – pulmonary fibrosis
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Lobar pneumonia – complications
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Lung abscess due to destruction of lung tissue by enzymes of leucocytes and macrophages. A cavity is formed filled with pus and surrounded by fibrous tissue.
Lobar pneumonia – lung abscess
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Lobar pneumonia – complications
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Gangrene due to necrosis of lung tissue.
dark coloration is due to liberation of hemoglobin from hemolyzed red blood cells, which is acted upon by hydrogen sulfide (H2S), resulting in formation of black iron sulfide that remains in the tissues
Lobar pneumonia – gangrene
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Lobar pneumonia – complications
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Spreading of the infection:
Hematogenous: bacteremia occurs in the early stages of pneumococcal pneumonia in more than 25% of patients, and may lead to endocarditis, meningitis, brain abscess, arthritis or sepsis.
Lymphogenous: pericarditis and mediastinitis.
Lobar pneumonia – spreading of the infection
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Pericarditis Meningitis
Lobar pneumonia – spreading of the infection
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Sepsis: septicopyemia
Bronchopneumonia
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Various etiology: bacteria, viruses, fungi, mycoplasma, chlamidia, chemical and physical factors
Affects acini, lobuli, segment(s) (and up to lobes) Develops after acute bronchitis and bronchiolitis
low bronchial drainage leads to penetration of bacteria to respiratory parts of the lung (alveoli)
morphological features differ due to various etiology
Bronchopneumonia
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Bronchopneumonia
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Bronchopneumonia
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Bronchopneumonia
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Can develop as autoinfection:
after aspiration of upper airway content (aspiration p.)
due to blood congestion (hypostatic p.) - confined to the bed or weakened patients
after surgical intervention (postoperative p.) due to secondary immunodeficiency
Bronchopneumonia – streptococcus
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caused by hemolytic streptococci group A and B
very often mixed infection (+ viral infection)
often seen in patients with diabetes
affects the lower lobes
sero-purulent exudate with interstitial component
sometimes abscesses and bronchiectases are formed
Bronchopneumonia – streptococcus
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Bronchopneumonia – pneumococcus
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caused by pneumococci (Streptococci pneumoniae I, II, III, IV types)
exudate contain fibrin and PMN leucocytes
Bronchopneumonia – pneumococcus
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Bronchopneumonia – staphylococcus
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Staphylococcus aureus is a common pulmonary superinfection after influenza and other viral respiratory tract infections.
nosocomial staphylococcal pneumonia typically occurs in chronically ill people who are prone to aspiration, and in intubated patients
characterized by abscess development
abscess can rupture into the pleural cavity and cause a tension pneumothorax and pleural effusions
Bronchopneumonia – Pseudomonas aeruginosa
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most often seen in patients who are immunocompromised
often an infectious vasculitis, in which large numbers of organisms can be seen in blood vessel walls
results in pulmonary infarction.
Bronchopneumonia – fungi
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caused by various fungi (Candida most often)
marked alteration seen as necrosis
proliferative inflammation and granuloma formation
fungi elements in exudate and in the center of granulomas
Bronchopneumonia – fungi
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Bronchopneumonia – viruses
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most often in infants and children
serous, fibrinous, hemorrhagic exudate
hyaline membranes in alveoli
alveolar epithelium contains viral inclusion and often is desquamated
Pneumonias in children
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Etiology: viral, mycoplasma, bacterial, rickettsial, parasitic, fungal, mixed
The most common microbial agents: Klebsiella, Pseudomonas aeruginosa, Proteus, E. coli, Staphylococcus
Mixed viral-bacterial predominate
Predisposing factors: congenital defects of respiratory tract and lungs
congenital and acquired the immunodeficiencies
immaturity of the lung tissue in preterm newborns
aspiration of amniotic fluid in utero or during delivery
mechanical ventilation
surfactant deficiency
Pneumonias in elderly patients
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Etiology: bacterial (Str.pneumoniae, Haemophilus influenzae, Legionella pneumophila, etc.), viral (flu), mycoplasma
Autoinfection is of great value
Predisposing factors: decreased immunity,
impaired mucociliary clearance
cardiopulmonary failure
weakening of the cough reflex
impaired swallowing process
Atypical clinical presentation
Suppurative and destructive complications
Interstitial pneumonia
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= “pneumonitis, alveolitis”
Primary inflammation in the interalveolar and peribronchial stroma
Etiology: viruses, mycoplasma, fungi, Pneumocystis
Develop as hypersensitivity reaction I (immediate) and IV (delayed) types
interstitial fibrosis in outcome
Interstitial pneumonia
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Acute viral respiratory infection (AVRI)
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group of acute inflammatory diseases of the respiratory system, similar in clinical presentation and morphology caused by pneumotropic viruses
“The common cold (also known as nasopharyngitis, rhinopharyngitis, acute coryza, or a cold) is a viral infectious disease of the upper respiratory tract which primarily affects the nose. Symptoms include coughing, sore throat, runny nose, sneezing, and fever which usually resolve in seven to ten days, with some symptoms lasting up to three weeks. Well over 200 viruses are implicated in the cause of the common cold; the rhinoviruses are the most common.”
Wikipedia, “Common cold”
AVRI - pathogenesis
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1. Cytopathic effect:
virus adsorption and penetration
Morphology:
cytoplasmic and/or intranuclear inclusion
giant cell formation
cell degeneration, necrobiosis and necrosis
desquamation
regeneration and proliferation
the formation of multilayered beds
inflammatory infiltration (lymphocytes, plasma cells, macrophages, single neutrophils)
AVRI - pathogenesis
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2. Vasopathic effect:
endothelium of capillaries is affected
Morphology:
vascular paresis and dilatation
hyperemia
an increase in vascular permeability
stasis
thrombosis of capillaries
edema, hemorrhage
AVRI - pathogenesis
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3. Immunosuppressive effect
affect of immune organs, secondary ID
Morphology
reactive hyperplasia of lymphatic tissue
then – accidental transformation and atrophy of the thymus, lymphocyte depletion in peripheral immune organs
4. Spreading and generalization of infection
through airways
haematogenous
Influenza (flu)
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RNA viruses of the family Orthomyxoviridae
According to virion internal proteins (M1 and NP) viruses divided into Influenza virus A, B, C
Surface proteins – hemagglutinin (HA) and neuraminidase (NA) – determ serotypes
Viruses affecting people contain
three subtypes of HA (H1, H2, H3)
two subtypes of NA (N1, N2)
serovariants of A Influenza virus A (less often B) can change Ag-structure in vivo
Known flu pandemics
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Name of
pandemic
Date Deaths Case fatality
rate
Subtype
involved
Pandemic
Severity Index
1889–1890
flu pandemic
(Asiatic or
Russian Flu)
1889–1890 1 million 0.15% possibly H3N8
or H2N2
N/A
1918 flu
pandemic
(Spanish flu)
1918–1920 20 to 100
million
2% H1N1 5
Asian Flu 1957–1958 1 to 1.5
million
0.13% H2N2 2
Hong Kong Flu 1968–1969 0.75 to 1
million
<0.1% H3N2 2
Russian flu 1977–1978 no accurate
count
N/A H1N1 N/A
2009 flu
pandemic
(Swine)
2009–2010 18,000 0.03% H1N1 N/A
Influenza (flu)
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Airborne and transplacental transmission
Incubation period 2-4 days
Local changes are associated with the cytopathic and vasopathic effects of virus
Catarrhal tracheobronchitis
General changes associated with viremia and intoxication
degenerative, inflammatory changes of inner organs, circulatory disorders.
Influenza (flu) – clinical forms
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1. Mild
catarrhal laryngotracheobronchitis (upper airways)
degeneration and desquamation of the respiratory epithelium
hypersecretion of mucus
edema
complete restoration of the epithelium (on 5th day)
Influenza (flu) – clinical forms
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2. Moderate
small bronchi, bronchioles and lung parenchyma
serous-hemorrhagic inflammation
interstitial infiltration in lung
hyaline membranes and giant cells in alveoli
squamous metaplasia of the bronchial epithelium
Influenza (flu) – clinical forms
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3. Severe – two types
with marked intoxication (due to the cytopathic and vasopathic effects of virus).
with pulmonary complications (due to the addition of a secondary infection).
Influenza (flu) – Severe with marked intoxication
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Trachea and bronchi: a pronounced serous-hemorrhagic inflammation and necrosis
Lungs: massive hemorrhage, numerous small foci of serous-hemorrhagic pneumonia, acute emphysema and atelectases
Inner organs: numerous hemorrhages
Serous (serous-hemorrhagic) meningitis, meningoencephalitis, cerebral edema
Influenza (flu) – Severe with pulmonary complications
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Upper respiratory tract: sero-purulent or fibrino-hemorrhagic inflammation
Bronchi: destructive panbronchitis (entire bronchial wall envolved)
Lungs: bronchopneumonia with a tendency to abscess formation, necrosis, hemorrhage, development of atelectasis and emphysema, marked interstitial component
Influenza A1N1
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Influenza A1N1
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Influenza A1N1
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Influenza A1N1
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Influenza A1N1
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Parainfluenza
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group of four distinct serotypes of RNA viruses of the family Paramyxoviridae
common in children under the age of 3 years and is characterized by subglottic swelling
the most common cause of croup, which is characterized by stridor on inspiration and a “barking” cough
Parainfluenza
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infects and kills ciliated epithelial cells of upper respiratory tract
in very young children this process frequently extends into the lower respiratory tract, causing bronchiolitis and pneumonitis
in young children, where the trachea is narrow and the larynx is small, the local edema of laryngotracheitis compresses the upper airway enough to obstruct breathing and cause croup
Adenovirus infection
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Adenoviruses belong to group of DNA viruses of the family Adenoviridae
can cause respiratory affection, gastroenteritis, conjunctivitis, cystitis
Adenovirus infection
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specific presentation of adenovirus infection is “pharyngoconjunctival fever”:
high fever that lasts 4–5 days
pharyngitis
conjunctivitis
enlargement of the lymph nodes of the neck
headache, malaise, and weakness
Adenovirus infection
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Adenovirus infection
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RSV infection
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respiratory syncytial virus (RSV) is RNA viruses of the family Paramyxoviridae
most children have been infected with the virus by age 2
in adults and older, healthy children, the symptoms of RSV are mild and typically mimic the common cold
infection can be severe in some cases, especially in premature babies, transplant patients and other immunocompromised persons
virus causes the cell membranes on nearby cells to merge, forming syncytia
RSV infection
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Mycoplasma infection
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Mycoplasmas refers to a genus of bacteria that lack a cell wall
the smallest self-replicating organisms
at first, they were considered viruses; then intermediate between viruses and bacteria
M. pneumoniae and some other mycoplasmas can cause human infection
tracheobronchitis is most common in children
primary atypical pneumonia can develop
usually it occurs in younger age groups and may be associated with neurological and systemic (e.g. rashes) symptoms
Mycoplasma infection
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alveoli are filled with edematous fluid, macrophages, fewer lymphocytes and detached alveolocytes
alveolocytes have foamy cytoplasm containing PAS positive granules (mycoplasmas)
Mycoplasma infection
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Mycoplasma infection
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