TB , pneumonia and pleural disease Flashcards
TB transmission?
Transmission is airborne - droplet inhalation
pathogen of Primary Pulmonary TB
Develops in a previously unexposed /unsensitised host (ie. first contact with bacillus)
Usually implant in upper lobes
1 – 1.5 cm area of consolidation develops - Ghon focus (inflammation, granulomas and caseous necrosis)
Tubercle bacilli drain into local lymph nodes » Ghon complex (Yellow, necrotic areas in parenchyma & nodes)
consequences of primary pulmonary TB
95% of cases cell mediated immunity controls the infection
Most cases heal by scar formation and eventual calcification
Clinically
Usually asymptomatic
Rarely – fever, pleural effusions
stain used to ID TB?
Organisms
identified using ZN
(Ziehl-Neelsen)
staining
what is Secondary Pulmonary TB
Form of disease that arises in a previously sensitised host.
May follow shortly after 1º TB
Usually arises from reactivation of dormant 1º lesions
May also result from re-infection
Reactivation when host resistance weakened (low prevalence areas)
Re-infection because of waning of the protection offered by the 1º infection (usually in regions of high contagion)
consequences of secondary pulmonary TB
Classically localised to apices of the upper lobes due to high oxygen tension
Pre-existing hypersensitivity » marked tissue response “walling off” infective focus » high risk of cavitation
Clinically:
Asymptomatic
Insidious manifestations (related to cytokine release by activated macrophages)
Elderly or immunosuppressed: Cavitating TB Tuberculous bronchopneumonia Single organ TB Miliary TB
what happens in cavitating TB?
Apical lesion enlarges
Expansion of area of caseation creating a ragged cavity
Clinically:
Erosion of vessels » haemoptysis
Drainage into bronchus / bronchiole » cough / increased amounts of sputum
Fever etc
Adequate tx :
Heal by fibrosis
Inadequate tx +/- debilitation:
Dissemination via airways, lymphatics or vascular channels
Spread into upper airways & gut - open TB
pathogen of Miliary Pulmonary TB
“Galloping consumption”
Haematogenous spread – organisms drain into lymphatics » venous system » right side of heart » pulmonary arteries ….
Scattered small foci (< 2 mm) of consolidation
Foci of consolidation may expand and coalesce
what is tuberculous bronchopneumonia
Rapid spread via airways (open TB)
Extensive parenchymal inflammation
Rare with tx but prognosis poor
pathogen of systemic miliary TB
Infective foci in lungs enter the systemic circulation
Liver, spleen, bone marrow, adrenals, meninges, kidneys, fallopian tubes and epididymis common
Prognosis poor despite treatment
what is Pott’s disease
haematogenous spread of TB to spine, causes erosion and collapse
what is Mycobacterium Avium-Intracellulare Complex
MA and MI (supposed to be MTB?) are different species
Atypical mycobacterium
Opportunistic infection
Uncommon except in AIDS with low CD4 lymphocytes
Organisms proliferate in lungs and GI tract
Clinically
Fever, drenching sweats and weight loss
Abundant acid-fast bacilli within macrophages
Granulomas and necrosis rare in immunodeficient patients
what is pneumonia
Infection of the lung parenchyma (LRTI)
Bacterial, viral, mycoplasmal and fungal. (Usually bacterial)
One type of pneumonia can predispose to another type
Some organisms or patterns termed atypical pneumonia
pathogen of pneumonia
When local defence mechanisms are impaired:
Loss or suppression of cough reflex Impairment of mucociliary apparatus Accumulation of secretions Interference with phagocytic or bactericidal action of alveolar macrophages Pulmonary congestion and oedema Immune suppression
classification of pneumonia
Aetiological agent: (determining treatment)
Type of bacteria
Other organisms
Clinical Setting:
Community-acquired – bacterial or viral/mycoplasma (atypical)
Hospital-acquired – usually bacterial
Pathological – Macroscopic pattern of bacterial pneumonia:
Bronchopneumonia
Lobar pneumonia
what is bronchopneumonia
Patchy
Scattered foci of consolidation
Multilobar and frequently bilateral and basal
= pale areas macroscopically
what is lobar pneumonia
Usually in otherwise healthy adults
Often follows viral URTI
Contiguous consolidation of virtually an entire lobe
Often resolves with or without scarring
Rare now due to antibiotic therapy
Classically due to:
Strep pneumoniae
stages of lobar pneumonia
Characteristic progression, if no treatment:
Congestion and oedema
Few neutrophils, numerous bacteria
Red hepatisation
Massive exudation of neutrophils, red cells and fibrin
Grey hepatisation
Disintegration of red cells and persistence of fibrinosuppurative exudate
Resolution
what is red hepatisation
in lobar pneumonia
Massive exudation of neutrophils, red cells and fibrin
grey hepatisation is then
Disintegration of red cells
Persistence of fibrinosuppurative exudate
can you distinguish lobar and bronchopneumonia histologically
Cannot distinguish broncho and lobar pneumonia histologically
Neutrophils, oedema, rbc & fibrin fill alveolar spaces
pneumonia complications
Respiratory failure Healing by fibrosis / scarring Progressive tissue destruction / necrosis » Abscess formation Spread of infection into pleural cavity » Empyema Septicaemia – bacteraemic dissemination: Heart valves (endocarditis) Meningitis Metastatic abscesses Joints
what is atypical pneumonia
Inflammatory reaction localised to interstitium
Lymphocytes & macrophages
Neutrophils less common unless bronchopneumonia supervenes
what happens in ARDS
severe progression of pneumonia:
Alveoli filled with oedema fluid
ARDS:
Imbalance between pro-inflammatory and anti-inflammatory mediators
Damage to endothelial lining » fibrin exudation
Hyaline membrane formation
Poor prognosis
what happens in aspiration pneumonia
Markedly debilitated patients
Unconscious
Repeated vomiting
Aspirate gastric contents
►Pneumonia
Chemical – gastric acid
Bacterial – oral flora
Necrotising fulminant course
Lung Abscess
Food particles
Foreign body giant cells have engulfed foreign particles.
Haemorrhage and an acute inflammatory infiltrate.
Granulomas later
