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Respiratory Infections

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Presentation on theme: "Respiratory Infections"— Presentation transcript:

1 Respiratory Infections
Dr Mulazim Hussain Bukhari

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)


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 Bronchopneumonia 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)

Mycobacterium Environmental contaminant Reservoir M tuberculosis No Human M bovis Human, cattle M leprae Humn M kansasii Rarely Water, cattle M marinum Fish, water M scrofulaceum Possibly Soil, water M avium intracellulare Soil, water, birds M ulcerans Unknown M fortuitum Yes Soil, water, animals M chelonae

Mycobacterium Clinical significance Pigmentation Growth Unclassified M Tuberculosis , M bovis M ulcerans Strict pathogens No No M leprae Strict pathogen Runyon Group 1 M marinum , kansasii Runyon Group 2 Usually pathogenic Photochromogens slow M scrofulaceum Rarely pathogenic Scotochromogens slow Runyon Group 3 M avium intracellulare Pathogenic in immunocompromised No slow Runyon Group 4 M fortuitum, M chelonae No ‘rapid’

37 MYCOBACTERIUM Aerobic bacilli –non spore forming non motile
Cell wall –rich in lipids Acid-fast bacilli Very slow growing

38 Mycobacterium tuberculosis
Causes tuberculosis Classic human disease Pathogenesis Transmission Clinical presentations Diagnosis Treatment Prevention

39 Tuberculosis (pathogenesis of clinical disease)
Virulence of organisms Hypersensitivity vs. immunity Tissue destruction and necrosis

40 Pathogenesis Inhaled aerosols Engulfed by alveolar macrophages Bacilli replicate Macrophages die Infected macrophages migrate local lymph nodes Develop Ghon’s focus Primary complex Cell mediated immune response stops cycle of destruction and spread Viable but non replicating bacilli present in macrophages EVIDENCE OF INFECTION WITH M TUBERCULOSIS Chest x-ray / positive skin test

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

42 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

43 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

44 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

45 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

46 Tissue changes in TB Primary Secondary
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

47 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

Pulmonary tuberculosis Primary complex Asymptomatic HEALS REACTIVATION Post-primary tuberculosis Acute pulmonary disease Systemic spread Aymptomatic /symptomatic LATER DISEASE Renal / CNS etc MILIARY TUBERCULOSIS Pulmonary meningitis

49 DIAGNOSIS Pulmonary tuberculosis Primary complex Asymptomatic 1 1
HEALS 2 3 REACTIVATION Post-primary tuberculosis Acute pulmonary disease Systemic spread Aymptomatic /symptomatic LATER DISEASE Renal / CNS etc MILIARY TUBERCULOSIS Pulmonary meningitis 3 3

50 DIAGNOSIS Evidence of infection Evidence of active disease
Chest x-ray - hilar lymphadenopathy calcification of primary focus/LN Delayed hypersensitivity response to purified protein derivative (PPD) MANTOUX /HEAF TEST Evidence of active disease Sputum for AFB positive Indirect evidence of infection (Mantoux) Direct evidence of infection PCR / culture Histo-pathological evidence

51 Primary TB – Ghon Focus

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

53 Granulomatous inflammation with caseous necrosis

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

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

56 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

57 Secondary TB – rapid death due to miliary disease

58 Miliary white foci – blood spread to lower lobe

59 “Galloping consumption” – TB bronchopneumonia

60 Decreased immunity – many more organisms on acid fast stain

61 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

62 TREATMENT Anti-tuberculous drugs DOT Multi-drug resistant tuberculosis
INAH Rifampicin Ethambutol Pyrazinamide DOT Multi-drug resistant tuberculosis

63 BCG (bacillus Calmette Guerin)
PREVENTION Incidence declined before availability of anti-tuberculous drugs Improved social conditions - housing /nutrition Case detection & treatment Contact tracing Evidence of infection / disease Treatment of infected / diseased contacts ROLE OF IMMUNIZATION BCG (bacillus Calmette Guerin)

64 Bronchiectasis Bronchiectasis is a chronic lung disease that is characterized by permanent dilatation of the bronchi and fibrosis of the lung. It is defined as the pathological, irreversible dilation of bronchi , due to destruction of the bronchilal walls and their supporting tissues It is highly associated with chronic bacterial infection Often looked at, as the final common pathway of many injurious processes

65 Cont. Bronchiectasis , although uncommon,bears the potential to cause severe illness , including repeated respiratory infections , disabling cough, purulent sputum, shortness of breath, chest pain and occasionally hemoptysis, with significant impact on the health and the quality of life of the affected person

66 Causes of 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 Affects lower lobes preferentially Chronic recurring infection sometimes leads to finger clubbing


68 Cont. Repeated or prolonged episodes of pneumonitis,
Inhaled foreign objects or Neoplasms have been known to cause bronchiectasis. When the bronchiectatic process involves most or all of the bronchial tree, whether in one or both lungs, it is believed to be genetic or developmental in origin

69 Types of Bronchiectasis
Bronchiectasis means irreversible dilation and distortion of the bronchi and bronchioles. Pathologically, bronchiectasis can be divided into four types



72 Cylindrical Bronchiectasis
The first type, cylindrical bronchiectasis, is characterized by uniform dilatation of bronchi, that extends into the lung periphery, without tapering. Tubular bronchiectasis is simply the absence of normal bronchial tapering and is usually a manifestation of severe chronic bronchitis rather than of true bronchial wall destruction

73 Bronciectasis Cylindrical Forma uniform dilatation of bronchi, that extends into the lung periphery, without tapering.

74 Varicose Bronchiectasis
The second type is called varicose bronchiectasis and is characterized by irregular and beaded outline of bronchi, with alternating areas of constriction and dilatation.

75 Saccular Bronchiectasis.
The third type is called cystic or saccular bronchiectasis and is the most severe form of the disease. The bronchi dilate, forming large cysts, which are usually filled with air and fluid. Saccular bronchiectasis is the classic advanced form characterized by irregular dilatations and narrowing. The term cystic is used when the dilatations are especially large and numerous

76 Bronchiectasis Saccular Form The bronchi dilate, forming large cysts, which are usually filled with air and fluid.

77 Follicular Bronchiectasis
The fourth type of bronchiectasis is called follicular and is characterized by extensive lymphoid nodules within the bronchial walls. It usually occurs following childhood infections

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

79 Bronchiectasis with chronic suppuration

80 Bronchiectasis

81 Bronchiectasis distal to an obstructing tumour

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