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Respiratory Infections. Respiratory tract defences Ventilatory flow Cough Mucociliary clearance mechanisms Mucosal immune system.

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Presentation on theme: "Respiratory Infections. Respiratory tract defences Ventilatory flow Cough Mucociliary clearance mechanisms Mucosal immune system."— Presentation transcript:

1 Respiratory Infections

2 Respiratory tract defences Ventilatory flow Cough Mucociliary clearance mechanisms Mucosal immune system

3 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

4 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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6 Acute epiglottitis H. influenza type B Another cause of acute severe airway compromise in childhood

7 Pneumonia Infection of pulmonary parenchyma with consolidation

8 Pneumonia Gr. “disease of the lungs” Infection involving the distal airspaces usually with inflammatory exudation (“localised oedema”). Fluid filled spaces lead to consolidation

9 Classification of Pneumonia By clinical setting (e.g. community acquired pneumonia) By organism (mycoplasma, pneumococcal etc) By morphology (lobar pneumonia, bronchopneumonia)

10 Pathological description of pneumonia

11 Organisms Viruses – influenza, parainfluenza, measles, varicella-zoster, respiratory syncytial virus (RSV). Common, often self limiting but can be complicated Bacteria Chlamydia, mycoplasma Fungi

12 Lobar Pneumonia Confluent consolidation involving a complete lung lobe Most often due to Streptococcus pneumoniae (pneumococcus) Can be seen with other organisms (Klebsiella, Legionella)

13 Clinical Setting Usually community acquired Classically in otherwise healthy young adults

14 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

15 Macroscopic pathology Heavy lung  Congestion  Red hepatisation  Grey hepatisation  Resolution The classical pathway

16 Lobar pneumonia (upper lobe – grey hepatisation), terminal meningitis

17 Pneumonia – fibrinopurulent exudate in alveoli (grossly “red hepatisation”)

18 Pneumonia – neutrophil and macrophage exudate (grossly “grey hepatisation”)

19 Complications Organisation (fibrous scarring) Abscess Bronchiectasis Empyema (pus in the pleural cavity)

20 Pneumonia – fibrous organisation

21 Bronchopneumonia Infection starting in airways and spreading to adjacent alveolar lung Most often seen in the context of pre- existing disease

22 Bronchopneumonia

23 The consolidation is patchy and not confined by lobar architecture

24 Clinical Context Complication of viral infection (influenza) Aspiration of gastric contents Cardiac failure COPD

25 Organisms More varied – Strep. Pneumoniae, Haemophilus influenza, Staphylococcus, anaerobes, coliforms Clinical context may help. Staph/anaerobes/coliforms seen in aspiration

26 Complications Organisation Abscess Bronchiectasis Empyema

27 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

28 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)

29 Diagnosis High index of suspicion Teamwork (physician, microbiologist, pathologist) Broncho-alveolar lavage Biopsy (with lots of special stains!)

30 Immunosuppressed patient – fatal haemorrhage into Aspergillus-containing cavity

31 HIV-positive patient CMV (cytomegalovirus) and “pulmonary oedema” on transbronchial biopsy….

32 Special stain also shows Pneumocystis

33 Tuberculosis 22 million active cases in the world 1.7 million deaths each year (most common fatal organism) Incidence has increased with HIV pandemic

34 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)

35 Tuberculosis (pathogenesis of clinical disease) 1. Virulence of organisms 2. Hypersensitivity vs. immunity 3. Tissue destruction and necrosis

36 Mycobacterial virulence Related to ability to resist phagocytosis. Surface LAM antigen stimulates host tumour necrosis factor (TNF)  production (fever, constitutional symptoms)

37 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

38 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

39 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

40 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

41 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

42 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

43 Primary TB – Ghon Focus

44 Secondary TB Necrosis Fibrosis Cavitation T cell response: CD4 (helper) enhance killing. CD8 (cytotoxic) kill infected cells giving necrosis

45 Granulomatous inflammation with caseous necrosis

46 Acid fast stain – spot the organism (a red snapper)!

47 Complications Local spread (pleura, lung) Blood spread. Miliary TB or “end- organ” disease (kidney, adrenal etc.) Swallowed - intestines

48 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

49 Secondary TB – rapid death due to miliary disease

50 Miliary white foci – blood spread to lower lobe

51 “Galloping consumption” – TB bronchopneumonia

52 Decreased immunity – many more organisms on acid fast stain

53 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

54 Lung Abscess Localised collection of pus. Central tissue destruction. Lined by granulation tissue/fibrosis (attempted healing) Tumour-like Chronic malaise and fever

55 Lung abscess Organisms:  Staphylococcus  Anaerobes  Gram negatives Clinical contexts:  Aspiration  Following pneumonia  Fungal infection  Bronchiectasis  Embolic

56 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

57 Bronchiectasis (2) Affects lower lobes preferentially Chronic recurring infection sometimes leads to finger clubbing

58 Complications of bronchiectasis Pneumonia Abscess Septicaemia Empyema “Metastatic” abscess Amyloidosis

59 Bronchiectasis with chronic suppuration

60 Bronchiectasis

61 Bronchiectasis distal to an obstructing tumour


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