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Inflammation of the pulmonary parenchyma
terminal airway
alveolar space
Other pathogen:parasite, chlamydia , pneumocystis carinii , Legionella
physicochemical factor:radioactive ray,allergy
Community-Acquired pneumonia (CAP)
Streptococcus pneumoniae(40%)
G-(20%):Klebsiella pneumoniae
Hospital-acquired pneumonia (HAP)
G-(50%:aeruginosus Bacillus, Klebsiella pneumoniae, hemophilies influenzae
etc. )
Pneumococcus 30% Staphylococcus aureus 10%
lobar pneumonia
lobular pneumonia
interstitial pneumonia
lobar pneumonia
bronchus are not involved
staphylococci aureus pneumonia
Klebsiella pneumoniae can develop cavity
X-ray:consolidation Extremes of age.
lobular pneumonia
Secondary to other disease
Both genders.
Pe: moist rales
Staph, Strep, H.infl.
X-ray: irregular patch along lung markings
Patchy consolidation
Lobe lobular
Middle age – 20-50 Around Small airway

Primary in a healthy Not limited by

males common. anatomic boundaries.
95% pneumoc (Klebs.) Usually bilateral.
Entire lobe consolidation
Limited by anatomic boundaries.
Usually unilateral
interstitial pneumonia
Secondary to other disease
Mild symptom and sign
Irregular straps stretch from hilum , reticulate
Pneumococcal Pneumonia
Streptococcus pneumoniae
normal flora of upper respiratory tract
Without tocxin:never cause necrosis or cavitate
Inhalation---proliferate spread---- often involve pleura
Congestion : extensive serous exudation, vascular engorgement, and rapid bacterial
red hepatization: Airspaces are filled with polymorphonuclear cells, vascular
congestion occurs, and extravasation of RBCs
gray hepatization: accumulation of fibrin is associated with inflammatory WBCs and
RBCs in various stages of disintegration, and alveolar spaces are packed with an
inflammatory exudate.
resolution: resorption of the exudate.
Without alveolar wall and structure damage
organized pneumonia are rare

5-10%empyema 15-20%inflamation outside lung

Clinical manifestation
predisposing cause:defense of respiratory tract is damaged
General symptom: sudden onset,chill,high fever, myalgia
Respiratory symptom:rusty sputum, chest pain, dyspnea
gastrointestinal tract symptom
General:cyanosis, perioral herpes,
Respiratory:Consolidation of lung
course of disease1-2weeks
Pleurisy, empyema
Blood routine test:wbc N
Sputum smear,culture
•blurred lobe
•consolidation with air bronchogram
• pleurisy
• pericarditis
differential diagnosis
caseous pneumonia;
tuberculosis toxic symptom
Smear :tubercle bacillus in sputum
Apex or upper or lower part of clavicle, with nonuniform density, absorbed slowly
Cavitate or scatered in the lung
Other pneumonia
acute lung abscess\
acute lung abscess
occur rapidly, obvious toxic symptoms
large amount of purulent sputum
blood white cell and neutrophile increase
x-ray: thin walled cavity with air fluid level, infectious lesion around it
lung carcinoma
Obstructive pneumonia
Tumor appear after antibiotic
Hilar lymph node enlarge or atelectasis after antibiotic
Inflammation do not absorb or recurrent pneumonia after antibiotic esp. old
CT,MRI, bronchoscope OR cytology
Mild /moderate:penicillin
Allergy to penicillin: erythromycin, lincomycin, quinolones
Severe:first or second generation of cephalosporins
penicillin-resistant strain :high doses of penicillin or cephalosporins,
quinolones , Vancomycin
Supportive measures:
bed rest
analgesics for pleuritic pain
O2 : cyanosis, significant hypoxemia
Acute purulent infection of lung caused by Staphylococcus
susceptible population:immune deficiency or bronchus lung disease
Skin infection---- blood ------ lung----- consolidation and purulent -------destruct
-------- lung abscess
Produce toxin and enzyme
Clinical manifestation
General symptom: sudden onset,chill,high fever
Respiratory symptom:blood-streaked sputum or pink milky, chest pain, dyspnea
Blood routine test
X-ray:segment or lobe consolidation,lobular infiltration
single or multiple cavity with air fluid level
inconstant lesion
small develop large one
Drainage focus
penicillin-resistant:cephalosporins, quinolones , Vancomycin
Severe:3rd cephalosporins, quinolones
MRSA(methicillin resistant staphylococcus aureus ): Vancomycin
General introduction
less than 1% of CAP , more than 10% of HAP
Main pathogen of HAP
often occur in old,bronchus-lung disease or multiple organ failure
ESBL extended spectrum β lactamases--drug fast
Normal flora of upper respiratory and intestinal tract

Lobar or lobular consolidation---esp upper lobe

interlobar fissure descending

Single or multiple abscess

Fibroplasia of focus is quiet obvious,tend to organized

most common in men >= 40 and alcoholics
predisposing factors: heart or lung disease, diabetes and malignancy
Onset: sudden with severe systemic upset (high fever, rigors) and pleuritic pain
sputum is purulent, brick red, gelatinous or blood-stained
consolidation is usually seen in the upper lobes accompany bulging of the fissures
marked necrosis and cavitation multiple honeycomb abscess
lung abscess and empyema are common
mortality is 20-50%
2nd or 3rd cephalosporin +aminoglycoside antibiotic
Piperacillin +aminoglycoside antibiotic
antibiotics + enzyme inhibitor or Tienam
account for < 2% of CAP, but for most HAP
mortality is about 25 to 50% despite the availability of effective antibiotics
usual pathogens Klebsiella pneumoniae Pseudomonas aeruginosa, Escherichia coli,
Enterobacter sp, Proteus sp, Serratia marcescens, and Acinetobacter sp.
usually occur in infants, the elderly, alcoholics, and debilitated or
immunocompromised hosts, especially those with neutropenia.
Main route of infection is aspiration
Consolidation or fused lesion
Multiple abscess
Pleurisy or empyema
2nd or 3rd generation cephalosporin +aminoglycoside
semisynthetic penicillin +aminoglycoside
Pseudomonas aeruginosa
β- lactam antibiotics, aminoglycoside, quinolones
 β- lactam antibiotics+ aminoglycoside
Enterobacter sp
Carbenicillin or piperacillin+ aminoglycoside,
3rd Cephalosporin
identified cases of legionellosis as early as 1943
1976 led to the discovery of the bacterium Legionella pneumophila
> 30 species. 19 species are pathogen of human
accounts for 1 to 8% of CAP that result in hospitalization and about 4% of lethal
Hospital pneumonias.
late summer and early fall.
water supply and evaporative condensers of air conditioning systems or
contaminated showerheads.
•incubation period is 2 to 10 days
•prodromal phase:malaise, fever, headache, and myalgias
•initially nonproductive and subsequently productive of mucoid sputum
•high fever, sometimes with relative bradycardia, and diarrhea is common
•mental status with confusion, lethargy,
•a unilateral, patchy segmental or lobar alveolar infiltrate
•Consolidation esp. lower lobe
•Cavity or lung abscess in severe
•Lesion is still aggravate while clinical treatment is effective.
•Absorb slowly 1-4months


WBC bad prognosis

50-70% hyponatremia
hypophosphatemia, and abnormal liver function tests.

Giemsa stain


Erythromycin +rifampin
course of treatment :2-3weeks