lung infection and immunity Flashcards

acute vs chronic lung infection: recall the differences in pathogenesis between acute and chronic lung infections e.g. pneumococcal pneumonia vs bronchiectasis

1
Q

bacterial source of acute lung infection pneumoccocal pneumonia

A

Streptococcus pneumoniae

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2
Q

pathogens associated with community acquired pneumonia (CAP)

A

presentation of acute pneuomonia result of cooperative bacteria and viruses

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3
Q

are causes of hospital-acqiured pneumonia same as communtiy acquired pneumonia

A

no

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4
Q

typical community acquired pneumonia pathogens

A

S. pneumoniae, H. influenzae, M. catarrhalis

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5
Q

atypical community acquired pneumonia pathogens

A

M. pneumoniae, C. pneumoniae, L. pneumophilia

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6
Q

risk factors for pneumonia

A

age, smoking, excess alcohol, contact with < 15 years, poverty, overcrowding, some medications, medical history (e.g. COPD, asthma, heart, liver, diabetes), animal contact, geographical variations

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7
Q

diagnosing pneumonia

A

acute lower respiratory tract symptoms (coughing, green (neutrophil)/rusty (dead cell) sputum, dyspnoea as alveoli fill with pus), new focal chest signs, >1 systemic feature (fever, shivers, aches, high temperature), no other explanation for illness, CRB65 (confusion, respiratory rate, blood pressure, age) severity score, stabbing chest pain due to peripheral inflammation, X-ray with dense debris seen in lungs (fibrin, bacteria)

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8
Q

supportive therapy for pneumonia

A

antibiotics, oxygen (hypoxia), fluids (dehydration), analgesia (pain), nebulised saline

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9
Q

pneumonia antibiotic therapy examples

A

amoxicillin, clarithromycin, benzylpenicillin IV

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10
Q

features and outcome of acute antibiotic therapy for pneumonia

A

rapid time of antibiotic administration to reduce septic shock; 1 week treatment leaving airways unscarred and some effort made to clear infections

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11
Q

effect of viral infection on lung

A

mediator release, cellular inflamation, local immune memory; damage to epithelium - loss of cilia, bacterial growth, poor antigen barrier, loss of chemoreceptors

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12
Q

common cold agents

A

many viruses (influenza, respiratory syncytial etc.), atypical bacteria

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13
Q

features of severe viral disease

A

RNA sequence, viral load, DNA, environment - mediators, cell stress, epithelial damage, viral spread

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14
Q

causes of severe flu

A

highly pathogenic strains (zoonotic), absence of prior immunity, predisposing illness/conditions

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15
Q

feature of influenza infection and effect on vaccines

A

no re-infection by same strain; imperfect vaccines

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16
Q

respiratory syncytial virus (RSV) features

A

unstable; recurrent re-infection (filamentous) with similar strains; no vaccine

17
Q

what does RSV cause in neonates

A

bronchiolitis

18
Q

is RSV likely to be present upon hospital admission

A

no

19
Q

viral load: influenza vs RSV

A

influenza - rapid viral load; RSV - delayed viral load

20
Q

why is lung susceptible to infection

A

not sterile - contains many organisms causing pneumonia

21
Q

define bronchiectasis as an example of a chronic lung infection

A

chronic condition where airways become abnormally widened, secondary to chronic inflammation, leading to build-up of excess mucus (more vulnerable to infection)

22
Q

pathogenesis of bronchiectasis

A

inflammation permanently destroying tissue and muscles surrounding bronchi, causing them to widen, become scarred, inflamed and filled with excess mucus; this triggering persistent coughing, SOB, chronic fatigue, and make the lungs more vulnerable to infection as they harbour bacteria

23
Q

causes of bronchiectasis

A

severe pneumonia, whooping cough, TB, measles, immunodeficiency, connective tissue diseases (e.g. rheumatoid arthritis), CF, cilia abnormalities

24
Q

treatment of bronchiecstasis

A

physiotherapy to empty phlegm, antibiotics to clear infection

25
Q

acute inflammation: neutrophils and anti-protease balance

A

neutrophils secrete proteases to destroy microbes during inflammation and infection, and normally this is balanced by anti-proteases in the airways

26
Q

chronic inflammation: neutrophils and anti-protease imbalance

A

number of neutrophils is so large that the anti-proteases are overwhelmed leading to increased free proteases causing damage to the airway epithelia (which in turn makes it easier to be infected, creating a vicious cycle)