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
