1 03.09 · ^The common cold (also known as nasopharyngitis, rhinopharyngitis, acute coryza, or a...

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03.09.2014 1

Transcript of 1 03.09 · ^The common cold (also known as nasopharyngitis, rhinopharyngitis, acute coryza, or a...

Page 1: 1 03.09 · ^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

03.09.2014 1

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Lung pathology

Acute pneumonias,

acute viral respiratory infection

Ivan Sakharau, assist. lect.

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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

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“Pneumonia”

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from Ancient Greek πνευμονία (pneumonia, “lung disease”), from πνεύμων (pneumōn, “lung”)

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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

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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

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Classification

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3. Prevalence

unilateral, bilateral

acinar, miliary, lobular, segmental, polysegmentary, lobar, total

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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)

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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

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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

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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)

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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

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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

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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

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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

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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

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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.

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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

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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.

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Lobar pneumonia – spreading of the infection

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Pericarditis Meningitis

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Lobar pneumonia – spreading of the infection

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Sepsis: septicopyemia

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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

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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

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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

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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

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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

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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.

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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

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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

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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

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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

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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

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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”

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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)

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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

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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

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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

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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

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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.

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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)

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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

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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).

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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

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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

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Influenza A1N1

03.09.2014 64

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Influenza A1N1

03.09.2014 65

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Influenza A1N1

03.09.2014 66

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Influenza A1N1

03.09.2014 67

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Influenza A1N1

03.09.2014 68

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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

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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

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Adenovirus infection

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Adenoviruses belong to group of DNA viruses of the family Adenoviridae

can cause respiratory affection, gastroenteritis, conjunctivitis, cystitis

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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

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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

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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

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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)

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Mycoplasma infection

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Mycoplasma infection

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Thank you!