10 Lung Infection: Viral and Bacterial Pneumonias Flashcards
Q: What causes pneumonia? (2) Why does it seem that one doesn’t have a cause?
A: Community acquired (CAP)-> large percentage of cases don’t have known cause- maybe not discovered the bacteria yet or we don’t have a test for it yet
Hospital infections (‘nosocomial’)
Q: What can cause community acquired pneumonia that we know about and can do something about? (5- bacteria)
A: Strep. Pneumoniae Mycoplasma pneumoniae Staph. Aureus Chlamydophila pneumoniae Haemophilus influenzae
Q: What can cause hospital acquired pneumonia? (3- bacteria)
A: Staphylococcus aureus (28%) Pseudomonas aeruginosa (21.8%) Klebsiella species (9.8%)
Q: What are atypical bacteria? (2)
A: not covered by standard penicillin antibiotics and require specific antibiotics to treat (usually macrolides- different mechanism of action to penicillins)
Q: Name 3 common ‘typical’ pathogens that cause community acquired pneumonia. 3 atypical ones? (bacteria)
A: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis
Mycoplasma pneumoniae, Chlamydophilia pneumoniae, Legionella pneumophilia
Q: What increases mortality from pneumonia?
A: higher mortality rates with age
Q: Risk factors for pneumonia. Demographic/lifestyle? (3)
A: - age (<2; >65)
- cigarette smoking
- excess alcohol consumption
Q: Risk factors for pneumonia. Social factors? (3)
A: - contact with children <15yrs
- poverty
- overcrowding
Q: Risk factors for pneumonia. Medications? (3)
A: - inhaled corticosteroids (could suppress innate antibacterial responses)
- immunosuppressants
- proton pump inhibitors
Q: Risk factors for pneumonia. Medical history? (9)
A: - COPD (chronic airway disease)
- asthma (chronic airway disease)
- heart disease
- liver disease
- diabetes mellitus
- HIV / complement/Ig deficiencies
- malignancy
- hyposplenism
- previous pneumonia
Q: Risk factors for pneumonia. Specific for certain pathogen. (3)
A: - geographical variation
- animal contact
- healthcare contact (good or bad access)
Q: What is seretide? Salbutamol?
A: steroid and bronchodilator combination
short acting bronchodilator
Q: What are normal oxygen saturation levels (on air)?
A: 94-99% (on 21% oxygen air)
Q: What is a normal respiration rate?
A: 12-20
Q: What are crepitations?
A: crackling or rattling sound
Q: What are the initial investigations performed for possible community acquires pneumonia? (10)
A: - Chest radiograph
- Blood test: Full blood count,
- Blood test: Urea
- Blood test: Electrolytes
- Blood test: Liver function
- Blood test: C reactive Protein
- Arterial Blood gases
- Microbiological investigations – sputum culture
- Microbiological investigations – blood cultures
- Microbiological investigations – urine antigen tests
Q: How does a chest X ray appear in someone with pneumonia?
A: one side/ both are more cloudy
Q: How can you tell it’s pneumonia and not bronchitis or a cold? (6)
A: - New resp. symptoms or signs
- Pleuritic chest pain
- Usually febrile- temperature
- Often hypoxic (can be confused)
- New X ray changes over time eg several days -> inflammation would shift around and progress
- Severe enough to be admitted
Q: How can you tell it’s acute bronchitis and not pneumonia or a cold? (3)
A: Cough +++
Tracheal pain, not pleuritic
No new X ray changes over time
Q: BTS guidelines for diagnosing pneumonia. (4)
A: 1. Acute lower respiratory tract symptoms
- New focal chest signs and, if in hospital, new CXR changes
- > 1 systemic feature (fever, shivers, aches and pains, temperature >38 degrees)
- No other explanation for illness
Q: When should we admit community acquired pneumonia cases to hospital? What is also taken into account?
3 categories?
A: CRB65 severity score
being over 65
0 points: can go home with antibiotics
1-2: can consider hospital
3-4: high severity and needs hospital NEEDS URGENT ANTIBIOTICS
Q: Supportive therapy for pneumonia. (4)
A: Oxygen (for hypoxia) Fluids (for dehydration) Analgesia (for pain) Nebulised saline (may help expectoration of mucous / phlegm) Chest physiotherapy
Q: What do you follow for antibiotic therapy? What’s critical? How long for?
A: local guidelines
time crucial : esp if sepsis has occured
usually for 1 week
Q: What causes community acquired pneumonia in terms of viruses? (2)
A: influenza A or B, respiratory syncytial virus
Q: The effects of viruses on the lung (3). Effect on epithelium? (4)
A: 1. cellular inflammation 2. mediator release 3. local immune memory 4. damage to epithelium o loss of chemoreceptors o poor barrier to antigen o bacterial growth o loss of cilia
Q: Common cold agents. (7)
A: -rhinoviruses (lots of serotypes due to error prone replication)
- coronaviruses
- influenza
- Parainfluenza viruses
- Respiratory syncytial virus
- Adenoviruses
- Enteroviruses
Q: What can cause a more severe disease? (5)
A: -highly pathogenic flu strain (could be better equipped to invade immunity or interfere with host response)
- viral load
- absence of prior immunity -> innate immunodeficiency, B cells, T cells
- co pathogens take advantage of damaged epithelium etc (uncontrolled bacterial infection can kill)
- weakened host immune response: frail elderly, COPD/ asthma, diabetes, pregnancy, heart disease
need to take into account host, pathogen and potential co pathogen
Q: What is RSV bronchiolitis? Who does it mostly affect? Clinical symptoms? (7)
A: Respiratory syncytial virus (acute)
newborns (particularly less than 2yrs)
- chest wall retractions
- nasal flaring
- hypoxemia and cyanosis (bluish tint on skin/lips)
- croupy cough
- expiratory wheezing (prolonged expiration)
- rales and rhonchi (rattling sounds from lung)
- tachypnea with apneic episodes (breathing suspension)
Q: What can RSV predispose you to?
A: asthma
Q: What can happen to someone with rhinovirus infection?
A: even when rhinovirus leaves-> bacterial infection could take over symptoms (opportunistic)
Q: What happens when opportunistic bacteria come into contact with the microbiome in GIT? On the flip side, how can they aid viral function? (3)
A: can compete and eventually remove threat of opportunistic bacteria
- suppression of innate IFN production due to e.g. PRR expression, oxidative stress (CF cells)
- expression of viral entry receptors
- modulation of cytokine expression
Q: Lung microbiome?
A: not sterile environment
Q: Viral-bacterial interactions in respiratory tract (during secondary bacterial infection). (6)
A: -compromised barrier functions -> – mucociliary clearance e.g. loss of ciliated cells, reduction of ciliary beat frequency; loss of epithelial tight junction
- enhanced receptor availability for bacterial binding -> ++ expression of host receptors (e.g. PAFR); display of viral proteins on cell surface
- immunological aberrances: – expression and responsiveness of PRRs; – no. of alveolar macrophages, NK cells, CD4+ and CD8+ T-cells
- impaired immune cell functions: – phagocytosis, cytokine, AMP and antibody production
- immunosuppression by viral components
- changes of microenvironment: ++ nutrient availability for bacterial growth; ++ temperature and extracellular ATP altering bacterial transcriptome Bact
Q: What is a congenital defect that can cause the cilia not to work?
A: There is an inner dynein arm but NO outer dynein arm
This is a DYNEIN ARM DEFECT
Because of this congenital defect, the patient’s cilia does NOT work
