2.respiratory infections
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Transcript of 2.respiratory infections
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Respiratory Infections
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Respiratory tract defences
Ventilatory flow Cough Mucociliary clearance mechanisms Mucosal immune system
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Upper respiratory tract infections
Rhinitis Rhinovirus, coronavirus, influenza/parainfluenza Non-infective (allergic) rhinitis has similar
symptoms (related to asthma) Sinusitis Otitis media
Latter 2 have a risk of bacterial superinfection, mastoiditis, meningitis, brain abscess
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Laryngitis
Most commonly upper respiratory viruses
Diphtheria C. diphtheriae produces a cytotoxic
exotoxin causing tissue necrosis at site of infection with associated acute inflammation. Membrane may narrow airway and/or slough off (asphyxiation)
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Acute epiglottitis
H. influenza type B Another cause of
acute severe airway compromise in childhood
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Pneumonia
Infection of pulmonary parenchyma with consolidation
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Pneumonia
Gr. “disease of the lungs” Infection involving the distal airspaces
usually with inflammatory exudation (“localised oedema”).
Fluid filled spaces lead to consolidation
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Classification of Pneumonia
By clinical setting (e.g. community acquired pneumonia)
By organism (mycoplasma, pneumococcal etc)
By morphology (lobar pneumonia, bronchopneumonia)
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Pathological description of pneumonia
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Organisms
Viruses – influenza, parainfluenza, measles, varicella-zoster, respiratory syncytial virus (RSV). Common, often self limiting but can be complicated
Bacteria Chlamydia, mycoplasma Fungi
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Lobar Pneumonia
Confluent consolidation involving a complete lung lobe
Most often due to Streptococcus pneumoniae (pneumococcus)
Can be seen with other organisms (Klebsiella, Legionella)
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Clinical Setting
Usually community acquired Classically in otherwise healthy young
adults
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Pathology
A classical acute inflammatory response Exudation of fibrin-rich fluid Neutrophil infiltration Macrophage infiltration Resolution
Immune system plays a part antibodies lead to opsonisation, phagocytosis of bacteria
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Macroscopic pathology
Heavy lung Congestion Red hepatisation Grey hepatisation Resolution
The classical pathway
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Lobar pneumonia (upper lobe – grey hepatisation), terminal meningitis
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Pneumonia – fibrinopurulent exudate in alveoli (grossly “red hepatisation”)
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Pneumonia – neutrophil and macrophage exudate (grossly “grey hepatisation”)
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Complications
Organisation (fibrous scarring) Abscess Bronchiectasis Empyema (pus in the pleural cavity)
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Pneumonia – fibrous organisation
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Bronchopneumonia
Infection starting in airways and spreading to adjacent alveolar lung
Most often seen in the context of pre-existing disease
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Bronchopneumonia
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Bronchopneumonia
The consolidation is patchy and not confined by lobar architecture
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Clinical Context
Complication of viral infection (influenza)
Aspiration of gastric contents Cardiac failure COPD
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Organisms
More varied – Strep. Pneumoniae, Haemophilus influenza, Staphylococcus, anaerobes, coliforms
Clinical context may help. Staph/anaerobes/coliforms seen in aspiration
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Complications
Organisation Abscess Bronchiectasis Empyema
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Viral pneumonia
Gives a pattern of acute injury similar to adult respiratory distress syndrome (ARDS)
Acute inflammatory infiltration less obvious
Viral inclusions sometimes seen in epithelial cells
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The immunocompromised host
Virulent infection with common organism (e.g. TB) – the African pattern
Infection with opportunistic pathogen virus (cytomegalovirus - CMV) bacteria (Mycobacterium avium
intracellulare) fungi (aspergillus, candida, pneumocystis) protozoa (cryptosporidia, toxoplasma)
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Diagnosis
High index of suspicion Teamwork (physician, microbiologist,
pathologist) Broncho-alveolar lavage Biopsy (with lots of special stains!)
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Immunosuppressed patient – fatal haemorrhage into Aspergillus-containing cavity
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HIV-positive patient CMV (cytomegalovirus) and “pulmonary oedema” on transbronchial biopsy….
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Special stain also shows Pneumocystis
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Tuberculosis
22 million active cases in the world 1.7 million deaths each year (most
common fatal organism) Incidence has increased with HIV
pandemic
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Tuberculosis
Mycobacterial infection Chronic infection described in many
body sites – lung, gut, kidneys, lymph nodes, skin….
Pathology characterised by delayed (type IV) hypersensitivity (granulomas with necrosis)
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Tuberculosis (pathogenesis of clinical disease)
1. Virulence of organisms
2. Hypersensitivity vs. immunity
3. Tissue destruction and necrosis
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Mycobacterial virulence
Related to ability to resist phagocytosis.
Surface LAM antigen stimulates host tumour necrosis factor (TNF) production (fever, constitutional symptoms)
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Organisms M. tuberculosis/M.bovis main
pathogens in man Others cause atypical infection
especially in immunocompromised host. Pathogenicity due to ability; to avoid phagocytosis to stimulate a host T-cell response
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Immunity and Hypersensitivity
T-cell response to organism enhances macrophage ability to kill mycobacteria this ability constitutes immunity
T-cell response causes granulomatous inflammation, tissue necrosis and scarring this is hypersensitivity (type IV)
Commonly both processes occur together
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Pathology of Tuberculosis (1)
Primary TB (1st exposure) inhaled organism phagocytosed and
carried to hilar lymph nodes. Immune activation (few weeks) leads to a granulomatous response in nodes (and also in lung) usually with killing of organism.
in a few cases infection is overwhelming and spreads
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Pathology of Tuberculosis (2)
Secondary TB reinfection or reactivation of disease in a
person with some immunity disease tends initially to remain localised,
often in apices of lung. can progress to spread by airways and/or
bloodstream
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Tissue changes in TB Primary
Small focus (Ghon focus) in periphery of mid zone of lung
Large hilar nodes (granulomatous) Secondary
Fibrosing and cavitating apical lesion (cancer an important differential diagnosis
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Primary and secondary TB
In primary the site of infection shows non-specific inflammation with developing granulomas in nodes
In secondary there are primed T cells which stimulate a localised granulomatous response
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Primary TB – Ghon Focus
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Secondary TB
Necrosis Fibrosis Cavitation T cell response: CD4
(helper) enhance killing. CD8 (cytotoxic) kill infected cells giving necrosis
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Granulomatous inflammation with caseous necrosis
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Acid fast stain – spot the organism (a red snapper)!
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Complications
Local spread (pleura, lung)
Blood spread. Miliary TB or “end-organ” disease (kidney, adrenal etc.)
Swallowed - intestines
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The host-organism balance
Not all infected get clinical disease Organisms frequently persist following
resolution of clinical disease Any diminished host resistance can
reactivate (thus 33% of HIV positive are co-infected with TB
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Secondary TB – rapid death due to miliary disease
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Miliary white foci – blood spread to lower lobe
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“Galloping consumption” – TB bronchopneumonia
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Decreased immunity – many more organisms on acid fast stain
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Why does disease reactivate?
Decreased T-cell function age coincident disease (HIV) immunosuppressive therapy (steroids,
cancer chemotherapy) Reinfection at high dose or with more
virulent organism
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Lung Abscess
Localised collection of pus. Central tissue destruction. Lined by granulation tissue/fibrosis (attempted healing)
Tumour-like Chronic malaise and fever
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Lung abscess
Organisms: Staphylococcus Anaerobes Gram negatives
Clinical contexts: Aspiration Following pneumonia Fungal infection Bronchiectasis Embolic
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Bronchiectasis
Abnormal fixed dilatation of the bronchi Usually due to fibrous scarring following
infection (pneumonia, tuberculosis, cystic fibrosis)
Also seen with chronic obstruction (tumour)
Dilated airways accumulate purulent secretions
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Bronchiectasis (2)
Affects lower lobes preferentially Chronic recurring infection sometimes
leads to finger clubbing
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Complications of bronchiectasis
Pneumonia Abscess Septicaemia Empyema “Metastatic” abscess Amyloidosis
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Bronchiectasis with chronic suppuration
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Bronchiectasis
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Bronchiectasis distal to an obstructing tumour