Flashcards in Pneumonia and Tuberculosis Deck (27):
Factors which predispose to a lung infection
Factors which predispose to a lung infection include
- loss or suppression of the cough reflex (immobility, unconsciousness, neuromuscular disorders etc) leading to aspiration.
- ciliary defects (e.g. smokers, squamous metaplasia, immotile cilia syndromes)
- accumulation of secretions (eg. cystic fibrosis, chronic bronchitis)
- immune deficiency local (alveolar macrophage inhibition) or systemic (IgA deficiency, HIV/AIDS).
Remember asplenic patients are particularly at risk of infection with encapsulated bacteria such as S. pneumoniae.
Inflammation of the large airways. Usually viral (RSV) can get superimposed bacterial infection (H. influenzae, S. pneumoniae). Characterised by cough, dyspnoea, tachypnoea and increased sputum production. Tests may reveal elevated white cell count (sensitive but non-specific) and there are rarely x-ray changes.
Inflammation of the smaller airways. Almost always in infants and almost always viral (RSV, parainfluenza). Can lead to a severe bronchopneumonia. Again, WCC is usually elevated and there may be changed in xray.
Alveolar inflammation with exudation of fluid into the alveoli and interstitium, leading to consolidation.
Classification of pneumonias
1. Community acquired (including community acquired atypical pneumonia)
2. Health care associated (hospital acquired or nosocomial pneumonia)
3. Aspiration pneumonia
4. Pneumonia in immunocompromised
Community acquired pneumonia
90% are Streptococcus Pneumoniae, remainder are mostly gram negative organisms (including Haemophilus influenzae).
Gastric contents aspirated, often associated with an impaired conscious state (including intoxication, anaesthesia, stroke, seizure), during vomiting or those with a poor gag reflex (stroke) - always protect your patients airways.
Pneumonia in immunocompromised
Usually bacterial, may also be viral, fungal or other.
2. Lobar pneumonia
Diffuse, patchy consolidation, usually centred on bronchi or bronchioles, may affect more than one lobe (tends to occur in the very young and old).
Affects most or all of a lobe, tends to occur in adults.
What are the most important factors in determining the prognosis of pneumonia?
1. The extent of the disease
2. The causative agent
3. The co-morbidities of the patient
Phases of lobar pneumonia
1. Congestion: occurs within the first 24 hours, outpouring of protein rich fluid into the intra-alveolar fluid associated with the presence of a few neutrophils and venous congestion.
2. Red hepatisation: last a few days, massive accumulation of neutrophils, fibrin, and extravasated red cells within the alveoli. Red, firm and airless - the lung appears like liver.
3. Grey hepatisation: accumulation of fibrin with destruction of red and white cells, leading to grey, solid lung.
4. Resolution: 8-10 days after onset, resorption of exudates and debris by macrophages or coughed up and restoration of the underlying lung architecture.
Microscopic features of pneumonia
Neutrophils (early) and lymphocytes/macrophages (later) found.
Clinical presentation of pneumonia
Patient present unwell, with fever, productive cough with purulent sputum. Modified by the administration of abx.
1. Pulmonary abscess
3. Organisation of the exudate leading to scarring
4. Bacterial dissemination to other organs and joints
Complication of severe pneumonia due to pyogenic organisms (e.g. Staph. aureus) can result in a florid inflammatory response that leads to the formation of an abscess cavity filled with dead bacteria and inflammatory cells. Abscesses heal by repair (scar) rather than resolution and may persist despite antibiotics due to the poor penetration of antibiotics into the cavity.
Spread of infection to the pleural cavity causing an inflammatory fibrosuppurative reaction (ie pus in the pleural cavity and organisms may be seen on gram stain). May see a deterioration in patient recovery, spiking fevers, despite appropriate abc therapy. Drainage may be required
Infective agent in tuberculosis
Tubercle bacilli (Mycobacterium tuberculosis) however lung diseases can also occur with other 'atypical' mycobacterium.
Stages of tuberculosis
Tuberculosis has two main stages:
1. Primary TB
2. Post-primary TB (many different terms used)
Most people may be asymptomatic, develop a fever and/or pleural effusion. The patient breathes in droplets containing tubercle bacilli and the bacillus enters the alveolar macrophages, replicating within the macrophages phagosomes.
In about 3-4 weeks a Th1 type immune response occurs, stimulated by APC expressing MHC-II associated mycobacterial antigens in the draining lymph node. Mature Th1 cells secrete IFN-gamma which drives the macrophages to kill the mycobacteria and the formation of granulomas ad caseous necrosis. Mantoux test becomes positive. The activated macrophages also secrete TND which recruits further monocytes from the blood, these monocytes differentiate into epitheloid histocytes present in the granulomatous response.
In most cases infection of a healthy individual is subclinical - indicated only by a tuberculin hypersensitivity reaction in a previously negative individual. Occasionally some patients do not contain the infe ction and they may go on immediately to post-primary TB. Lymphohaematogenous dissemination may result in the development of tuberculous meningitis.
Primary tuberculosis lesion - 10mm round lesion with a central zone of caseous necrosis surrounded by palisaded epitheloid histocytes, giant cells and lymphocytes. This is a caseating granuloma and is usually found in the mid zone of the lung. Usually this lesion will organise leaving a fibrocalcific nodule.
Usually the nodule contains living bacilli that may persist and cause post-primary TB.
Ghon focus with involvement of the hilar lymph nodes.
May occur soon after primary infection or when the latent infection has been reactivated (tends to occur when the patient is relatively immunocompromised). Pulmonary TB is the most frequent form of post-primary disease. This tends to be clasically located in the apex of the upper lobes, maybe secondary to the high oxygen tension. A florid inflammatory response occurs, leading to a larger (1-2cm), cavitating lesion with a central area of caseous necrosis. The patient may be asymptomatic or have systemic symptoms including malaise, anorexia, weight loss, fever, night sweats and haemoptysis. The patient may be coughing up sputum that contains bacilli (therefore the patient needs to be isolated).
Ongoing and greater lung involvement may occur if the infection is not contained. May spread lymphohaematogenously throughout the lung and other parts of the body.
The spread of blood borne TB. Multiple small granulomas (about the size of millet seeds) are seen in the lungs and potentially other organs.
Diagnosis of TB
Relies on recognition of acid-fast bacilli on microscopy or recognition of the patterns of cavitation and caseous necrosis either radiologically, biopsy or at autopsy.
Mantoux or tuberculin test, in which a small quantity of tuberculin protein is injected subcutaneously. An individual who has previously been exposed to TB will generate a stronger response than a non-exposed individual.