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Pneumonia
deebya raj mishra
Pneumonia
– … an acute infection of the pulmonary
parenchyma that is associated with at least some
symptoms of acute infection, accompanied by the
presence of an acute infiltrate on a chest
radiograph, or auscultatory findings consistent
with pneumonia
Bartlett. Clin Infect Dis 2000;31:347-82.
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What Causes
Pneumonia?
• infection with bacteria, viruses, fungi, or
parasites
• chemical or physical injury to the lungs
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• Pneumonia can result whenever
these local defense mechanisms are impaired
or
the systemic resistance of the host is lowered
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Lower Systemic Resistance
• chronic diseases,
• immunological deficiency,
• treatment with immunosuppressive agents,
• leukopenia
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Breach of local defenses
Defense Impairment
Loss or suppression of the cough reflex coma, anesthesia, neuromuscular disorders,
drugs, or chest pain
Injury to the mucociliary apparatus cigarette smoke,
inhalation of hot or corrosive gases,
viral diseases, or genetic defects of ciliary
function (e.g., the immotile cilia syndrome)
Accumulation of secretions cystic fibrosis and bronchial obstruction
Interference with the phagocytic or bactericidal
action of alveolar macrophages
alcohol,
tobacco smoke,
anoxia, or oxygen intoxication
deebya raj mishra
Special Character of the Organism
• invade the normal healthy respiratory tract
– by attaching to epithelial cells in the lower respiratory tract and
pharynx
• influenza viruses
– impair ciliary activity
• Haemophilus influenzae and Bordetella pertussis elaborate toxins that
paralyze mucosal cilia
• P. aeruginosa, M. pneumoniae produce ciliostatic substances
– lack specific adherence factors and often gain access after viral
infection causes loss of ciliated epithelium, making individuals with a
viral respiratory infection more susceptible to these secondary
bacterial superinfections
• Streptococcus pneumoniae or Staphylococcus
– avoid phagocytosis or destruction after phagocytosis
• Mycobacterium tuberculosis
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Pneumonia:
deebya raj mishra
MF
MF
Hor Fis
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Hor Fis
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Hor Fis
MF
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NOT ALWAYS LOBAR
Hor Fis
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collection of support tissues within the lung that incluces the alveolar
epithelium, pulmonary capillary endothelium, basement membrane,
perivascular and perilymphatic tissues
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Infiltrate Patterns
Pattern Possible Diagnosis
Lobar S. pneumo, Kleb, H. flu, GN
Patchy Atypicals, viral, Legionella
Interstitial Viral, PCP, Legionella
Cavitary Anaerobes, Kleb, TB, S. aureus,
fungi
Large effusion Staph, anaerobes, Kleb
Pneumatocele
Pneumatocele
Cavity + Air fluid level = LUNG ABSCESS
Clinical Features TYPICAL
Organisms involved
Onset
Cough
Chest pain
Other symptoms
Temp >38
Heart Rate >110
Consolidation signs
WBC count
Chest Xray
S.penumoniae; H.influenzae
Endemic Oral flora
Sudden
Productive
Peluritic
Chills, rigors, sob, diarrhoea
Common
Common
Common
Increased, Neutrophilia
Unilateral, Localized
Atypical Pneumonia
• not caused by one of the more traditional pathogens
(Streptococcus, Haemophilus etc)
– Atypical bacteria, virus
– Bacteria (Mycoplasma, Chlamydia, and Legionella)
• clinical presentation contrasts to that of "typical"
pneumonia
– "atypical" generalized symptoms
fever, headache,sweating and myalgia
– atypical in presentation with only moderate amounts of
sputum, no consolidation, only small increases in white cell
counts, and no alveolar exudate
deebya raj mishra
Clinical Features TYPICAL ATYPICAL
Organisms involved
Onset
Cough
Chest pain
Other symptoms
Temp >38
Heart Rate >110
Consolidation signs
WBC count
Chest Xray
S.penumoniae;
H.influenzae
Endemic Oral flora
Sudden
Productive
Peluritic
Chills, rigors, sob, diarrhoea
Common
Common
Common
Increased, Neutrophilia
Unilateral, Localized
Chlamydiae,
Legionella,
Mycoplasma, Viral
Sub-Acute
Dry
Uncommon
Headache, myalgia
Uncommon
Uncommon
Uncommon
Normal or Slightly
increased
Bilateral, diffuse,
interstitial
Knowing the Names
• HAP: Hospital-acquired pneumonia
– ≥ 48 h from admission
• VAP: Ventilator-associated pneumonia
– ≥ 48 h from endotracheal intubation
• HCAP: Healthcare-associated pneumonia
– Long-term care facility (NH), hemodialysis, outpatient chemo,
wound care, etc.
• CAP: Community-acquired pneumonia
– Outside of hospital or extended-care facility
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Mortality
0.7-2.1%
Mortality
9%
Mortality
>14%
Treatment of CAP
deebya raj mishra
Treatment of CAP
• Mild
– Macrolide (azithromycin, clarithromycin)
– Macrolide + -lactam
– Doxycycline
– Quinolone (moxifloxacin, levofloxacin,
gemifloxacin)
• Severe
– -lactam + macrolide
– -lactam + quinolone
deebya raj mishra
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2,3,4 times:
Duration of Therapy
• Minimum of 5 days
• Afebrile for at least 48 to 72 h
• Longer duration of therapy
– if initial therapy was not active against the
identified pathogen or complicated by extra
pulmonary infection
deebya raj mishra
CAP – Complications
 Hypotension and septic shock
 3-5% Pleural effusion; Clear fluid + pus cells
 1% Empyema thoracis pus in the pleural
space
 Lung abscess – destruction of lung .
 Single (aspiration) anaerobes, Pseudomonas
 Multiple (metastatic) Staphylococcus aureus
 Septicemia – Brain abscess, Liver Abscess
 Multiple Pyemic Abscesses
deebya raj mishra
deebya raj mishra
Prevention
• Smoking cessation
• Vaccination recommendations
– Influenza
• everyone
– Pneumococcal
• Immunocompetent ≥ 65 yo, chronic illness and
immunocompromised ≤ 64 yo
deebya raj mishra
deebya raj mishra

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3. Pneumonia.pptx

  • 2. Pneumonia – … an acute infection of the pulmonary parenchyma that is associated with at least some symptoms of acute infection, accompanied by the presence of an acute infiltrate on a chest radiograph, or auscultatory findings consistent with pneumonia Bartlett. Clin Infect Dis 2000;31:347-82. deebya raj mishra
  • 3. What Causes Pneumonia? • infection with bacteria, viruses, fungi, or parasites • chemical or physical injury to the lungs deebya raj mishra
  • 5. • Pneumonia can result whenever these local defense mechanisms are impaired or the systemic resistance of the host is lowered deebya raj mishra
  • 6. Lower Systemic Resistance • chronic diseases, • immunological deficiency, • treatment with immunosuppressive agents, • leukopenia deebya raj mishra
  • 7. Breach of local defenses Defense Impairment Loss or suppression of the cough reflex coma, anesthesia, neuromuscular disorders, drugs, or chest pain Injury to the mucociliary apparatus cigarette smoke, inhalation of hot or corrosive gases, viral diseases, or genetic defects of ciliary function (e.g., the immotile cilia syndrome) Accumulation of secretions cystic fibrosis and bronchial obstruction Interference with the phagocytic or bactericidal action of alveolar macrophages alcohol, tobacco smoke, anoxia, or oxygen intoxication deebya raj mishra
  • 8. Special Character of the Organism • invade the normal healthy respiratory tract – by attaching to epithelial cells in the lower respiratory tract and pharynx • influenza viruses – impair ciliary activity • Haemophilus influenzae and Bordetella pertussis elaborate toxins that paralyze mucosal cilia • P. aeruginosa, M. pneumoniae produce ciliostatic substances – lack specific adherence factors and often gain access after viral infection causes loss of ciliated epithelium, making individuals with a viral respiratory infection more susceptible to these secondary bacterial superinfections • Streptococcus pneumoniae or Staphylococcus – avoid phagocytosis or destruction after phagocytosis • Mycobacterium tuberculosis deebya raj mishra
  • 19. NOT ALWAYS LOBAR Hor Fis deebya raj mishra
  • 23. collection of support tissues within the lung that incluces the alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues deebya raj mishra
  • 28. Infiltrate Patterns Pattern Possible Diagnosis Lobar S. pneumo, Kleb, H. flu, GN Patchy Atypicals, viral, Legionella Interstitial Viral, PCP, Legionella Cavitary Anaerobes, Kleb, TB, S. aureus, fungi Large effusion Staph, anaerobes, Kleb
  • 31. Cavity + Air fluid level = LUNG ABSCESS
  • 32.
  • 33. Clinical Features TYPICAL Organisms involved Onset Cough Chest pain Other symptoms Temp >38 Heart Rate >110 Consolidation signs WBC count Chest Xray S.penumoniae; H.influenzae Endemic Oral flora Sudden Productive Peluritic Chills, rigors, sob, diarrhoea Common Common Common Increased, Neutrophilia Unilateral, Localized
  • 34. Atypical Pneumonia • not caused by one of the more traditional pathogens (Streptococcus, Haemophilus etc) – Atypical bacteria, virus – Bacteria (Mycoplasma, Chlamydia, and Legionella) • clinical presentation contrasts to that of "typical" pneumonia – "atypical" generalized symptoms fever, headache,sweating and myalgia – atypical in presentation with only moderate amounts of sputum, no consolidation, only small increases in white cell counts, and no alveolar exudate deebya raj mishra
  • 35. Clinical Features TYPICAL ATYPICAL Organisms involved Onset Cough Chest pain Other symptoms Temp >38 Heart Rate >110 Consolidation signs WBC count Chest Xray S.penumoniae; H.influenzae Endemic Oral flora Sudden Productive Peluritic Chills, rigors, sob, diarrhoea Common Common Common Increased, Neutrophilia Unilateral, Localized Chlamydiae, Legionella, Mycoplasma, Viral Sub-Acute Dry Uncommon Headache, myalgia Uncommon Uncommon Uncommon Normal or Slightly increased Bilateral, diffuse, interstitial
  • 36. Knowing the Names • HAP: Hospital-acquired pneumonia – ≥ 48 h from admission • VAP: Ventilator-associated pneumonia – ≥ 48 h from endotracheal intubation • HCAP: Healthcare-associated pneumonia – Long-term care facility (NH), hemodialysis, outpatient chemo, wound care, etc. • CAP: Community-acquired pneumonia – Outside of hospital or extended-care facility deebya raj mishra
  • 42. Treatment of CAP • Mild – Macrolide (azithromycin, clarithromycin) – Macrolide + -lactam – Doxycycline – Quinolone (moxifloxacin, levofloxacin, gemifloxacin) • Severe – -lactam + macrolide – -lactam + quinolone deebya raj mishra
  • 44. Duration of Therapy • Minimum of 5 days • Afebrile for at least 48 to 72 h • Longer duration of therapy – if initial therapy was not active against the identified pathogen or complicated by extra pulmonary infection deebya raj mishra
  • 45. CAP – Complications  Hypotension and septic shock  3-5% Pleural effusion; Clear fluid + pus cells  1% Empyema thoracis pus in the pleural space  Lung abscess – destruction of lung .  Single (aspiration) anaerobes, Pseudomonas  Multiple (metastatic) Staphylococcus aureus  Septicemia – Brain abscess, Liver Abscess  Multiple Pyemic Abscesses deebya raj mishra
  • 47. Prevention • Smoking cessation • Vaccination recommendations – Influenza • everyone – Pneumococcal • Immunocompetent ≥ 65 yo, chronic illness and immunocompromised ≤ 64 yo deebya raj mishra