17. Respiratory Infections Flashcards
List some respiratory tract infections (upper and lower).
What are some defence mechanisms of the lung?
Sinusitis, tonsilitis, pharyngitis, laryngitis, tracheitis, bronchiolitis, pleurity, bronchitis, pneumonia (infection of alveoli and surrounding lung).
Particles > 10 microns held in upper airways. 3-10 microns trapped in tracheobronchial mucus, 1-5 microns (bacteria) deposited in terminal airways and alveoli. <1 micron suspended in alveolar air, exhaled. Nasal clearance. Tracheobronchial clearance: mucociliary action. Mucus glands sectete thin mucus film. Alveolar clearance: alveolar macrophages.
Give examples of how normal lung defence may be disturbed.
Pneumonia is alveolar inflammation. What are the 3 types?
- Suppression of cough reflex: asthma, anaesthesia, drugs, chest pain, neuromuscular disease
- Injury to mucociliary apparatus: smoking, inhalation of hot/corrosive gases, congenital
- Disturbance of macrophage function: smoking, alcohol, anoxia, O2 toxicity
- Pulmonary congestion and oedema
- Accumulation of secretions
- General immunosuppression + virulent organisms may not need a defence impairment!*
Lobar pneumonia, bronchopneumonia, atypical pneumonia.
What is lobar pneumonia? What is it mostly caused by, and what are some clinical features?
What are the 4 pathologic stages of lobar pneumonia distribution?
Affects large part/entire lobe. Typically afflicts previously healthy males 20-50yo. 90% caused by Streptococcus pneumoniae (pneumococcus). Clinical features: high grade fevers + rigors, productive cough, rusty sputum, pleuritic chest pain, signs of consolidation (auscultation = dull, bronchial breath sounds).
1) Congestion (24hrs) - vessels engorged, alveolar oedema, heavy red lung.
2) Red hepatisation (2-4d) - outpouring of neutrophils and RBC’s into alveoli, red, solid, airless, ‘liver-like’ lung.
3) Gery hepatisation (4-8d) - fibrin and macrophages replace neutrophils and RBC’s, grey, solid airless lung.
4) Resolution (8-10d) - gradual return to normal.
* Classical stages not seen with prompt treatment.*
(pic - upper lobe is bulging and a diff colour, bottom lobe = normal)
What are some complications of lobar pneumonia?
Bronchopneumonia is the commonest type of pneumonia (esp. hosp. acquired). What are the 3 typical clinical settings? How does it begin, and what is it caused by?
What is the pathology of bronchopneumonia?
Most cases resolve. Rarely suppurative complications such as lung abscess or empyema (pus in the pleural cavity), especially with Klebsiella or Staph infections.
Chronic debilitating illness. 2o to viral infections. Extremes of age.
Begins as bronchitis and bronchiolitis, then spreads to alveoli. Caused by low virulence bacteria: typically Staph, Strepto viridans, H. influenzae, Pseudomonas, coliforms.
(pic) - lighter patches are consolidation - can see in all lobes = bilateral. Normal lung is darker.
What are some complications of brochopneumonia?
Compare lobar and bronchopneumonia (lobular) in terms of:
a) Site
b) State of infected person
c) Pathogen
d) XRay/clinical signs
e) Prognosis?
Death b/c usually complicating/terminal event in debilitating illness or extremes of age. Resolution and scarring. Abscess/empyema rare.
NB: distinction not always clearcut; may overlap. More imp = correct ID of causative agent AND determination of disease extent.
Describe interstitial (atypical) pneumonia.
What are the causative agents?
What are some predisposing conditions?
Patchy or extensive. Congested, subcrepitant lungs (no complete solidarity unlike broncho and lobar pneumonia). Inflammation restricted to alveolar septa and interstitial tissues: interstitial pneumonitis. ‘Atypical’ - no/minimal alveolar exudate. Intra-alveolar proteinaceous material forming hyaline mambrane in case of DAD (diffuse alveolar damage). Usual sporadic form usually mild and self-limiting. Epidemic forms = higher mortality. (pic = lots of lymphocytes in aleolar septa). Dry cough b/c no gunge in alveolar spaces.
Agents: Mycoplasma pneumoniae (no peptidoglycan CW), Viruses: influenza A and B, RSV, adeno, rhino, measles, varicella. Chlamydia. Coxiella. Often undetermined.
Predisposing: malnutrition, alcoholism, debilitating illnesses.
NB: clinical course of interstitial (atypical) pneumonia usually self-limiting.
What is pulmonary tuberculosis (TB)? Why is there a UK rise in cases?
What 2 things is pathogenicity in TB due to?
Infection of lungs by Mycobacterium tuberculosis or M.bovis (from unpasteurised milk). Lung = commonest TB site. Major cause of death in developing countries. Infection early in childhood, air-bourne. Clinical disease represents reinfection/reactivation, rarely progressive 1o TB. BCG protects (live, attenuated). UK rise in cases: HIV, immunosuppression, low socioeconomic status, drug resistance.
1) Ability to resist macrophage killing
2) Induction of cell-mediated or delayed type (type IV) hypersensitivity
Why is cell-mediated hypersensitivity central to development of TB pathology?
Describe what happens in T-cell mediated immunity (2-3 weeks after infection).
What is primary TB? What feature may be seen on a CXR?
It is important for the development of characteristic tissue destruction via caseous necrosis and cavitation. Macrophages phagacytose bacilli but cannot kill: multiply, lyse and infect other cells.
CD4 mediated IFN γ secretion: intracellular killing and granuloma formation. CD8 mediated lysis of macrophages and killing. CD4-/CD8- mediated lysis of macrophages and caseation necrosis (wall off infection and kill everything inside); bacilli are killed in anoxic acid environment.
Represents response to 1st contact with tubercle bacilli. Usually asymptomatic and in midzone (top pic). Ghon complex: typically 1cm focus in midzone with draining lymph node. Heals with fibrosis and calcification. (bottom pic - Gohn focus is light spot on L, complex is whole thing)
What is secondary TB?
Microscopic pathology of TB: characteristic changes resulting from type IV hypersensitivity. What can you see in these images?
Reinfection or reactivation, sometimes progressive 1o TB. Bacteria relocate to high O2 areas -> usually apical, Gohn focus about 3cm (larger than 1o) at clinical presentation. (pic)
Top pic: granuloma (collection of activated macrophages) with caseous necrosis in centre.
Bottom pic: Langhan’s giant cells (all nuclei in periphery, horse shoe shape) and epitheloid macrophages (start to connect with each other to wall off infection).
What would a Ziehl-Neelsen stain reveal on microscopic pathology of TB (pic)? How is a definitive diagnosis reached?
What are some complications of pulmonary TB?
Characteristic acid-fast bacilli, red rods against blue background. Definitive dx via sputum culture.
Progressive fibrocavitary TB, gradually destroys lung via necrosis, cavitation and fibrosis.
Miliary TB: bloodborne dissemination within lung or throughout the body; seed-like foci (bottom pic) consisting of granulomas: meninges (may affect cranial nerves), bone marrow, liver, any organ. (pic)
What patients are lung fungal infections most commonly seen in? Give some examples.
What does this show?
Seen with immunocompromised. Examples: HIV: Pneumocystis jirovecii (PCP). Histoplasma, coccidio, candida, aspergillus, mucor, cryptococcus. (pic, L = masses of fungal elements in alveolar space)
Aspiration pneumonia (route of lung infection may also be aspiration (lung infection due to relatively large amount of material from stomach/mouth entering lungs) or blood borne).
What can you see in this blood film? What would the dx be?
Neutrophils filling alveolar space. Alveolar septa = red, capillaries engorged with RBC.
Lobar pneumonia (red hepatisation, 2-4d)
