Community Acquired Pneumonia Flashcards

0
Q

Other than optochin, what is s. pneumonia sensitive to?

A

Bile lysis

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1
Q

What are the different routes of infection of CAP?

A

Microaspiration - s. pneumonia, h. Flu
Massive aspiration - normal flora anaerobes
Inhalation
Hematogenous spread - s. aureus, s. typhi, others

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2
Q

What is the prevalence of s. pneumonia as a cause of CAP?

A

*20-60%

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3
Q

What are common clinical presentations of s. pneumonia?

A
Respiratory tract - upper airway (sinusitis, otitis), lower airway (bronchitis, pneumonia, empyema, bacteremia)
Endocarditis
Meningitis
Arthritis 
Spontaneous bacterial peritonitis
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4
Q

What are the risk factors for s. pneumonia?

A
Younger than 2 or older than 65
A splenic or hyposplenia
Alcoholism
Diabetes 
HIV infection
Antecedent flu
Recent acquisition of new virulent strain
Defects in humoral immunity
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5
Q

What are the virulence factors of s. pneumonia?

A

Capsule - Smooth = encapsulated = virulent
Spontaneous phase variation occurs
High negative charge inhibits complement and Fc interxn with receptor
Pneumolysin - forms pores in host cells
Surface protein A - anti antibodies are protective
Surface antigen A
IgA protease

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6
Q

How does s. pneumonia evade mechanical barriers for aspiration below the larynx?

A

Increased with decreased levels of consciousness
Increased with opiates, alcohol, barbiturates, benzodiazepines
Increased with neurological disease - absence of gag reflex

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7
Q

When does s. pneumonia evade mechanical barriers through lack of mucociliary clearance?

A

Happens in smoking, COPD, bronchiectasis

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8
Q

What are host defenses against s. pneumonia?

A

Colonization - mucosal IgA against capsule
Lungs - alveolar macrophages, PMN recruitment, TH1 cytokines
Blood - igG2, C3, c reactive protein, splenic clearance

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9
Q

What is the pathogenesis of s. pneumonia?

A

Aspiration from nasopharynx
Failure of clearance mechanism
Intra alveolar spread through pores of Kohn and small airways
Congestion
Red hepatization - PMNs, RBCs, fibrin in alveoli
Gray hepatization - degeneration of cellular infiltrate and reabsorption
Resolution

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10
Q

What is the clinical presentation of s. pneumonia?

A

Abrupt onset with shaking fever, chill
Productive cough with *rust colored sputum
Pleuritic chest pain
Referred abdominal pain if lower lobe disease
Atypical presentations in elderly or immunosuppressed

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11
Q

What does the physical exam of a patient with s. pneumonia reveal?

A

Fever
Splinting of affected side
Tactile fremitus
Auscultation - inspiratory crackles, e->a changes, whispered pectoriloquy
Pleural effusion - dullness to percussion, decreased breath sounds
Hypoxemia due to v/q mismatch

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12
Q

How is diagnosis of s. pneumonia made?

A

Cultures from blood or pleural fluid definitive but often negative
Sputum culture not sensitive or specific
Sputum gram stain - *adequate specimen >25 PMNs, <10 SECs
*antigen test - urine for diagnosing pneumonia and CSF for diagnosing meningitis

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13
Q

What is penicillin resistant s. pneumonia (PRSP)?

A

Mutations of penicillin binding proteins
Risk factors are recent antibiotic therapy or hospitalization, children in day care
*highly resistant (MIC>2ug/ml) strains often resistant to other antibiotics

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14
Q

What is macrolide resistance with s. pneumonia?

A

Common in PRSP
Resistance to erythromycin, azithromycin, clarithromycin
Erm (B) gene - ribosomal methylation, MIC >64 high level resistance
Mef (E) gene - efflux pump mechanism, MIC <32 low level resistance

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15
Q

What is the natural history of s. pneumonia with treatment?

A

Fever and tachycardia resolve in 48 hrs

CXR normal after 3 weeks in healthy, may take up to 4 months in chronically ill patients

16
Q

What is the pneumococcal vaccine protective against?

A

Prevents bacteremia, not pneumonia

17
Q

What are the clinical features of aspiration pneumonia?

A

History of reason for impaired consciousness
Insidious onset
Low grade fever, purulent, *foul smelling sputum, weight loss
Poor dental hygiene, cachexia
Often upper lobes, often cavities
Sputum stain and culture has mixed oral flora with PMNs

18
Q

What is the treatment for aspiration pneumonia?

A

*clindamycin or penicillin derivative for several months

19
Q

How does droplet size affect inhalation of infected droplets causing CAP?

A

> 10 micrometers - likely to land in upper respiratory tract
1-5 micrometers - deposits in bronchi, alveoli
<1 micrometer - remains airborne

20
Q

What are the main differences between typical pneumonia and atypical pneumonia?

A
  • typical - abrupt onset, rapid progression, and often lobar distribution
  • atypical - gradual onset, slow progression, patchy distribution
21
Q

What are common causes of atypical pneumonia?

A

Mycoplasma pneumoniae
Clamydophila pneumoniae
Legionella pneumophila

22
Q

How does mycoplasma pneumoniae culture?

A
Difficult 
Slow growth on cell free media
Both aerobic and anaerobic
Mulberry or fried egg colonies
No cell wall
23
Q

How does mycoplasma pneumoniae cause infection?

A

Adheres to respiratory epithelial cells, inhibits ciliary action, induces sloughing of ciliated cells
Attachment via terminal organelle on bacteria and glycoproteins on epithelial cell
Produces hydrogen peroxide which causes damage

24
Q

What are the clinical features of mycoplasma pneumoniae?

A
*ambulatory young persons 
Fever, malaise, headache, cough 
*walking pneumonia - chest clear despite abnormal CXR
Unusual severity: sickle cell
Extra pulmonary manifestations
25
Q

What are extra pulmonary manifestations of mycoplasma pneumoniae?

A

Cold agglutins - IgM antibodies to I antigen on RBCs, reversible
Might cause hemolysis and raynauds
Can cause distal necrosis in patients with sickle cell due to microvascular occlusions
Most commonly neurologic complications

26
Q

How is mycoplasma pneumoniae diagnosed?

A

Culture difficult and not attempted
PCR on throat swab - accurate but not readily available
Direct antigen testing
Cold agglutins titer - > 1:32 is suggestive
Serology - anti mycoplasma IgM and IgG

27
Q

What are the basics of clamydophila and CAP?

A
Obligate intracellular parasite
Elementary bodies are infectious 
Asymptomatic infection is common
Illness often mild and slow progression 
Diagnosed with microimmunofluorescence antibody test
28
Q

What diseases are caused by legionella pneumophila?

A

Legionnaire’s disease - pneumonia, often fatal

Pontiac fever - influenza like illness, rarely fatal

29
Q

Where does legionella live and how is it spread?

A

Lives in fresh water - no human reservoir

Spread via aerosols, not person to person (outbreaks associated with moving water machines)

30
Q

What is legionnaires disease?

A

Incubation 2-10 days
Myalgia, headache, fever, cough
Diarrhea
Bilateral infiltrates

31
Q

What is Pontiac fever?

A

Incubation 20-48 hrs
Fever, myalgia, dry cough
No treatment needed

32
Q

What is the pathogenesis of legionella?

A

Inhalation in droplets reach alveoli and bronchioles
Infection of alveolar macrophages and multiplication inside ER derived sac
Destroy cell and spread

33
Q

How does immunity to legionella work?

A

Cell mediated, not really antibodies

Interferon gamma activates macrophages so they can kill it

34
Q

How is legionella diagnosed?

A

*urine antigen test - for serotype 1 only
Not gram stain
Culture on special media
Serology
Direct FA of sputum, PCR of sputum or bronchoalveolar lavage fluid

35
Q

How is legionella treated?

A

Macrolides like azithromycin
Fluroquinolones
Rifampin with something else
Beta lactams and aminoglycosides don’t work - need something that concentrates in phagolysosome

36
Q

Which causes of CAP are common in AIDs patients depending on cd4 count?

A

CD4 < 400 - m. TB, s. pneumonia (h. Flu, s. aureus)
CD4 < 200 - pneumocystis jiroveci
CD4 < 50-100 - pseudomonas, disseminated m. TB, non-tb myco, cryptococcus neoformans, CMV