In bacterial pneumonia, acute inflammation and consolidation (solidification) of the lung are due to a bacterial agent. Clinical signs and symptoms include fever and chills; productive cough with yellow-green (pus) or rusty (bloody) sputum; tachypnea; pleuritic chest pain; and decreased breath sounds, rales, and dullness to percussion.
Studies typically show elevated white blood cell count with a left shift (an increase in immature leukocytes). Chest x-ray for lobar pneumonia typically shows lobar or segmental consolidation (opacification), and for bronchopneumonia typically shows patchy opacification. Pleural effusion may also be picked up on chest x-ray.
In general, the keys to effective therapy are identification of the organism and early treatment with antibiotics.
Lobar pneumonia is characterized by consolidation of an entire lobe. The infect-ing organism is typically Streptococcus pneumoniae (95%) or Klebsiella . The lancet-shaped diplococcus Streptococcus pneumoniae is alpha-hemolytic, bile soluble, and optochin sensitive.
The 4 classic phases of lobar pneumonia are congestion (active hyperemia and edema); red hepatization (neutrophils and hemorrhage); grey hepatization (degra-dation of red blood cells); and resolution (healing). In today’s antibiotic era, these changes are not generally observed in practice.
Bronchopneumonia is characterized by scattered patchy consolidation centered onbronchioles; the inflammation tends to be bilateral, multilobar, and basilar, and particularly susceptible populations include the young, old, and terminally ill. Infecting organisms exhibit more variation than in lobar pneumonia, and include Staphylococci, Streptococci, Haemophilus influenzae, Pseudomonas aeruginosa, etc.Microscopic examination of tissue shows acute inflammation of bronchioles and surrounding alveoli. The diagnosis can often be established with sputum gram stain and sputum culture, but will sometimes require blood cultures.
Complications of pneumonia include fibrous scarring and pleural adhesions, lung abscess, empyema (pus in a body cavity), and sepsis.
Treatment of pneumonia is generally initial empiric antibiotic treatment, modified by the results of cultures and organism sensitivities.
Lung abscess is a localized collection of neutrophils (pus) and necrotic pulmonaryparenchyma. The etiology varies with the clinical setting. Aspiration is the most common cause. It tends to involve right lower lobe and typically has mixed oral flora (often both anaerobic and aerobic) for infecting organisms.
Lung abscess may also occur following a pneumonia, especially one due to S. aureus or Klebsiella . Lung abscesses may also occur following airway obstruction (postob-structive) or deposition of septic emboli in the lung.
Complications of lung abscess include empyema, pulmonary hemorrhage, and sec-ondary amyloidosis.
Atypical pneumonia is the term used for interstitial pneumonitis without consolida-tion. It is more common in children and young adults.
Infecting organisms that can cause atypical pneumonia includeMycoplasmapneumoniae, influenza virus, parainfluenza virus, respiratory syncytial virus (RSV)(which is especially important in young children), adenovirus, cytomegalovirus (CMV) (which is especially important in the immunocompromised), varicella virus, and many others.
Diagnosis.Chest x-ray typically shows diffuse interstitial infiltrates. An elevatedcold agglutinin titer specifically suggests Mycoplasma as a cause, which is important to identify since antibiotic therapy for Mycoplasma exists. Lung biopsy, if performed, typically shows lymphoplasmacytic inflammation within the alveolar septa.
Complications include superimposed bacterial infections and Reye syndrome (potentially triggered by viral illness [influenza/varicella] treated with aspirin).
Tuberculosis (TB).The number of cases of TB is declining in the United States, butthe proportion of cases in people born outside the country is rising. In this clinical setting, a positive PPD skin test may demonstrate that the person has been exposed to the mycobacterial antigens. Individuals who have received the BCG vaccine in some foreign countries may have a positive PPD test without being infected. In such cases chest x-ray and sputum smears and cultures are done.
Infection is usually acquired by inhalation of aerosolized bacilli.
The clinical presentation of Mycobacterium tuberculosis includes fevers and night sweats, weight loss, cough, and hemoptysis.
Primary pulmonary TB develops on initial exposure to the disease. The Ghonfocus of primary TB is characterized by subpleural caseous granuloma formation, either above or below the interlobar fissure. The term Ghon complex refers to the combination of the Ghon focus and secondarily-involved hilar lymph nodes with granulomas. Most primary pulmonary tuberculosis lesions (95%) will undergo fibro-sis and calcification.
Progressive pulmonary TB can take several forms, including cavitary tuberculosis,miliary pulmonary tuberculosis, and tuberculous bronchopneumonia.
Secondary pulmonary TB (also known as postprimary or reactivation TB) occurseither with reactivation of an old, previously quiescent infection or with reinfection secondary to a second exposure to the mycobacteria. In secondary pulmonary TB, the infection often produces a friable nodule at the lung apex (Simon focus) second-ary to the high oxygen concentration present at that site, since the upper parts of the lung typically ventilate more efficiently than the lower parts. Biopsy of affected tissues will typically show AFB-positive caseating granulomas.
Additionally, dissemination to other organ systems can occur in advanced TB via a hematogenous route that often results in a miliary pattern within each affected organ. Sites that may become involved include meninges; cervical lymph nodes (scrofula) and larynx; liver/spleen, kidneys, adrenals, and ileum; lumbar vertebrae bone marrow (Pott disease); and fallopian tubes and epididymis.
Nontuberculous mycobacteria.M. avium complex (MAC) typically occurs in AIDSpatients with CD4 counts <50 cells/mm3 and presents as disseminated disease.
The diagnosis of TB requires identification of the bacilli. Positive sputum smear necessitates culture for species identification. Adequate treatment requires drug susceptibility testing.
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