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What is a broad definition of pneumonia?
Any infection of the lung parenchyma.
List two common causes of community-acquired acute pneumonia.
Streptococcus pneumoniae and Haemophilus influenzae.
What characterizes aspiration pneumonia?
It is caused by anaerobic oral flora mixed with aerobic bacteria.
Identify one pathological cause of pneumonia in immunocompromised hosts.
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Which type of pneumonia is characterized by high fever and pleuritic chest pain?
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Name a type of pneumonia caused by mycobacterial infection.
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What is the significance of Streptococcus pneumoniae in pneumonia classification?
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What types of infections are most frequently seen in the respiratory tract?
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What underlying factors can lower systemic resistance to pneumonia?
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Cite a leading cause of necrotizing pneumonia.
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What are the three groups of individuals that experience increased frequency of pneumococcal pneumonia?
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Describe the four stages of lobar pneumonia progression in the preantibiotic era.
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What is the primary cause of lobar pneumonia?
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In bronchopneumonia, how is the inflammation typically distributed in the lungs?
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What are some possible complications arising from pneumonia?
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How does the histological appearance differ between congestion and red hepatization stages of lobar pneumonia?
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What is the significance of pleural involvement in pneumonia?
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What characteristic appearance does the lung have during the grey hepatization stage?
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What factors increase the likelihood of complications specifically with serotype 3 pneumococci?
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In what format does the lung typically recover from pneumonia with appropriate therapy?
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What is the Ghon complex and how is it formed in primary TB?
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Describe the typical site and characteristics of secondary TB lesions.
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What are the systemic symptoms associated with localized secondary TB?
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Explain the significance of multinucleated giant cells found in TB granulomas.
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What is miliary TB, and how does it disseminate?
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How does caseous necrosis appear microscopically in TB infections?
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What potential outcomes arise from the foci of scarring in primary TB?
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List at least two factors that can lead to reactivation of dormant primary TB lesions.
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What role do endobronchial and laryngeal TB infections play in disease spread?
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How can intestinal TB occur and what are its typical manifestations?
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What distinguishes atypical pneumonia from typical pneumonia in terms of sputum production?
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Why are mycoplasma infections particularly prevalent among children and young adults?
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What is the typical pattern of lung involvement observed in patients with atypical pneumonia?
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How does the inflammatory infiltrate differ histologically in acute atypical pneumonia compared to chronic cases?
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What are some of the systemic factors that might exacerbate the severity of atypical pneumonia?
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Describe the histological feature characteristic of primary atypical pneumonia.
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In what way does tuberculosis differ from community-acquired atypical pneumonia regarding its pathogen?
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What role do neutrophils play in the histology of acute atypical pneumonia?
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What is a common clinical manifestation of atypical pneumonia aside from cough?
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How does the morphology of the pleura change in atypical pneumonia?
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What morphological feature characterizes cavitary disease in secondary tuberculosis?
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Explain the typical systemic symptoms related to localized secondary tuberculosis.
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How does miliary tuberculosis differ from localized secondary tuberculosis in terms of dissemination?
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What role do multinucleated giant cells play in the granulomatous inflammation seen in tuberculosis?
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Describe how intestinal tuberculosis typically occurs and its primary manifestations.
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What is the primary difference in host response between primary and secondary TB?
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What is the significance of the Ghon complex in diagnosing primary TB?
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Explain the role of caseating and non-caseating granulomas in TB pathology.
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What factors may lead to the progression of primary TB to miliary TB?
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What histological features characterize the granulomas formed in TB infections?
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Study Notes
Lower Respiratory Tract Infections
- Lower respiratory tract infections (LRTIs) are more common than infections of other organs and account for significant workday loss
- The majority of LRTIs are upper respiratory tract infections caused by viruses (common cold, pharyngitis)
- Pneumonia is an infection of the lung parenchyma
- Pneumonia can occur when local defense mechanisms are impaired or the host's systemic resistance is lowered
- Factors affecting systemic resistance include chronic diseases, immunodeficiency, immunosuppressive treatments, and leukopenia
Classifications of Pneumonia
-
Community-acquired acute pneumonia (CAAP)
- Caused by:
- Streptococcus pneumoniae
- Haemophilus influenzae
- Legionella pneumophila
- Caused by:
-
Community-acquired atypical pneumonia
- Caused by:
- Mycoplasma pneumoniae
- Chlamydia spp. (Chlamydia pneumonia)
- Viruses (like respiratory syncytial virus and parainfluenza virus)
- Caused by:
-
Nosocomial Pneumonia
- Caused by:
- Staphylococcus aureus
- Gram-negative rods (Klebsiella spp., E. coli)
- Pseudomonas spp.
- Caused by:
-
Aspiration Pneumonia
- Caused by:
- Anaerobic oral flora like Bacteroides admixed with aerobic bacteria like Streptococcus pneumoniae, Staphylococcus aureus
- Caused by:
-
Chronic Pneumonia
- Caused by:
- Nocardia
- Actinomyces
- Mycobacterium TB
- Fungal infections
- Caused by:
-
Necrotizing Pneumonia and Lung Abscess
- Caused by:
- Staphylococcus aureus
- Klebsiella pneumoniae
- Streptococcus pyogenes
- Caused by:
-
Pneumonia in Immunocompromised Hosts
- Caused by:
- Cytomegalovirus
- Pneumocystis carinii
- Caused by:
Community-Acquired Acute Pneumonia (CAAP)
- Often bacterial in origin, following a viral upper respiratory tract infection
- Streptococcus pneumoniae is the most common cause
Clinical Features of Pneumococcal Pneumonia
- Abrupt onset with high fever, shaking chills, pleuritic chest pain, and productive mucopurulent cough
- Occasional patients may have hemoptysis (coughing up blood)
- Increased frequency in individuals with:
- Underlying chronic diseases (congestive heart failure, COPD, DM)
- Congenital or acquired immunoglobulin deficiency (like AIDS)
- Decreased or absent splenic function (e.g., sickle cell disease)
Morphology of Pneumococcal Pneumonia
- Two morphological patterns:
-
Lobar pneumonia:
- Involves the entire lobe
- Most frequent type
- Caused by Streptococcus pneumoniae
- Consolidation visible on X‑ray
-
Bronchopneumonia:
- More prevalent at extreme ages
- Foci of inflammation and consolidation are distributed in patches throughout one or several lobes
-
Lobar pneumonia:
- Regardless of the pattern, the lower lobes or the right middle lobe are most frequently involved
Lobar Pneumonia Stages
-
Congestion:
- Affected lobe is heavy and red
- Histologically: vascular congestion with proteinaceous fluid, scattered neutrophils, and many bacteria in the alveoli
-
Red Hepatization:
- Lung has a liver-like consistency
- Alveolar spaces packed with neutrophils, red cells, and fibrin
-
Gray Hepatization:
- Lung is dry, gray, and firm
- Red cells become lysed, while fibrinous exudate persists within alveoli
-
Resolution:
- Follows in uncomplicated cases
- Exudates within alveoli are enzymatically digested and either resorbed or expectorated leaving basic architecture intact
- Pleural reaction, leaving fibrous thickening or permanent adhesions
Bronchopneumonia
- Foci of inflammation and consolidation are distributed in patches throughout one or several lobes
- Lung area or substances immediately surrounding areas of consolidation are usually hyperemic and edematous, but the large intervening areas are generally normal
- Pleural involvement is less common than in lobar pneumonia
Histology of Bronchopneumonia
- The reaction consists of focal suppurative exudate that fills the bronchi, bronchioles, and adjacent alveolar spaces
- With appropriate therapy, complete restitution of the lung is the rule for both forms of pneumonia
Complications of Pneumonia
- Tissue destruction and necrosis may lead to abscess formation
- Suppurative material may accumulate in the pleural cavity, producing empyema
- Organization of intra-alveolar exudate may convert areas of the lung into solid fibrous tissue
- Bacteremic dissemination may lead to meningitis, arthritis, or infective endocarditis.
- Complications are more likely with serotype 3 pneumococci
Community-Acquired Atypical Pneumonia
- Characterized by patchy lung inflammation, primarily affecting the alveolar septa and interstitium
- Causes:
- Mycoplasma pneumoniae (most common)
- Viruses, including influenza A and B, respiratory syncytial viruses
- Chlamydia pneumoniae
- Factors impacting severity:
- Extremes of age
- Malnutrition
- Alcoholism
- Underlying debilitating illnesses
- Morphology:
- Lung involvement can be patchy or involve whole lobes
- Affected areas are red-blue and congested
- Pleura is typically smooth, with infrequent pleuritis or effusions
- Predominant interstitial inflammation with widened and edematous alveolar septa
- Infiltrates consist primarily of lymphocytes, macrophages, and occasionally plasma cells
- Neutrophils may be present in acute cases
Tuberculosis
- A communicable chronic granulomatous disease caused by Mycobacterium tuberculosis
- Commonly affects the lungs but can involve any organ or tissue
Primary Tuberculosis
- Develops in previously unexposed individuals
- Elderly and immunosuppressed may lose their sensitivity and experience multiple TB infections
- Source of infection is exogenous
- Only 5% of infected individuals develop significant disease
- Morphology:
- Begins in the lungs, typically in the distal airways of the lower upper lobes or upper lower lobes
- Forms a gray-white consolidation known as a Ghon focus, which undergoes caseous necrosis
- Bacilli drain to regional lymph nodes, also resulting in caseation
- The Ghon focus and regional lymph nodes form the Ghon complex, characteristic of primary TB
- The Ghon complex can fibrose and calcify, detectable by X-ray (Ranke complex)
- Microscopically, displays granulomatous inflammation with both caseating and non-caseating granulomas
- Granulomas contain epithelioid cells, lymphocytes, and multinucleated giant cells
- Epitheloid cells encapsulate the central caseous zone
- Fate of Primary TB:
- Induces hypersensitivity and increased resistance
- Scarred foci may harbor viable bacilli for years
- Can progress to progressive TB in individuals with compromised immunity, like those with AIDS
Secondary Tuberculosis (Reactivation TB)
- Arises in previously sensitized hosts
- Can follow shortly after primary TB or reactivate dormant lesions decades later, often due to weakened immunity
- Classically localized to the apex of one or both upper lobes, possibly due to high oxygen tension
- Morphology:
- Bacilli trigger a strong tissue response, often walling off the focus and preventing lymph node involvement
- Cavitation is common, contributing to dissemination along airways
- Cavitation is a significant source of infectivity, as sputum contains bacilli
- Gross features:
- Localized lesions in the apical or posterior segments of upper lobes
- Cavitary disease, a hallmark of secondary TB
- Caseous necrosis
- Scarring and calcification
- Microscopically:
- Necrotizing granulomatous inflammation with a central necrotic zone surrounded by epithelioid histiocytes, multinucleated giant cells, and lymphocytes
- Multinucleated giant cells may display Langhans type giant cells (nuclei arranged in a horseshoe shape) but are not specific to TB
- Organisms may be present in the central zone of necrosis, detectable by special stains
- Non-necrotizing granulomas can also be present
Spread of Secondary TB
- Miliary TB: disseminated millet seed-like lesions throughout organs via lymphatic and hematogenous routes
- Endobronchial, endotracheal, and laryngeal TB: spread through lymphatic channels or from expectorated infectious material
- Isolated organ TB: hematogenous spread to any organ, most common sites include meninges, kidneys, adrenals, bone, spinal abscess (Pott disease), and fallopian tube
- Lymphadenitis: unifocal lymphadenopathy without ongoing disease, commonly cervical
- Intestinal TB: ingestion of contaminated milk or secondary to swallowing of infected sputum, causing inflammatory enlargement and ulceration, particularly in the ileum
Clinical Features
- Localized secondary TB may be asymptomatic
- Systemic symptoms (related to tumor necrosis factor and interleukin 1):
- Malaise
- Anorexia
- Weight loss
- Fever (remittent, low grade)
- Night sweats
- Localized symptoms (with progressive pulmonary TB):
- Increased sputum, initially mucoid then purulent
- Hemoptysis (in half of patients)
- Pleuritic chest pain
- Extrapulmonary TB symptoms depend on the affected organ, for example:
- Fallopian tube: infertility
- Meninges: neurologic deficit
Tuberculosis (TB)
- TB is a chronic granulomatous disease caused by Mycobacterium tuberculosis.
- It usually affects the lungs, but can affect any organ or tissue.
Types of TB
Primary TB
- Occurs in previously unexposed individuals.
- Elderly and immunocompromised individuals may experience recurrent TB.
- 5% of those exposed develop an active infection.
- Source of organism: Exogenous
-
Morphology:
- Begins in the lungs, typically the distal airways of the lower lobes.
- Gray-white consolidation emerges, called a Ghon focus, which undergoes caseous necrosis
- Bacilli, either free or within phagocytes, drain to the regional lymph nodes (LN) which also caseate.
- Ghon complex: Ghon focus + regional LN complex, which is characteristic of primary TB.
- Ranke complex: The Ghon complex undergoes fibrosis and calcification.
- Microscopic: Granulomatous inflammatory reaction forms both caseating and non-caseating granulomas.
- Epitheloid cells are enclosed within a fibroblastic rim punctuated by lymphocytes.
- Multinucleated giant cells are present in the granuloma.
-
Fate of primary TB:
- Induces hypersensitivity and increased resistance.
- The scar tissue may harbor viable bacilli for years, even a lifetime.
- Uncommonly, the disease may progress without interruption into "progressive TB" because of a weakened immune system, like in AIDS.
- Diagnosis of primary TB in adults is difficult, as it may resemble pneumonia.
- Lymphatohematogenous dissemination may develop resulting in TB meningitis and miliary TB.
Secondary TB (Reactivation TB)
- Arises in a previously sensitized host.
- May follow shortly after primary TB, but typically arises from reactivation of dormant primary lesions many decades after initial infection.
- Reactivation is favored by weakened host resistance.
- Can also result from exogenous reinfection.
- Classically localized to the apex of one or both upper lobes, potentially due to high oxygen tension.
-
Morphology:
- Due to preexisting hypersensitivity, bacilli induce a rapid and marked tissue response that walls off the focus, without LN involvement.
- Cavitation occurs resulting in dissemination along airways in neglected secondary TB.
- Erosion of the airways is a primary source of infectivity as patients produce sputum containing bacilli.
- Gross description: Localized lesions usually in the apical or posterior segments of the upper lobes.
- Cavitary disease (characteristic of secondary TB)
- Caseous necrosis (cheese-like, tan to white grumous material).
- Scarring and calcification.
- Hallmark: Necrotizing granulomatous inflammation, composed of a central necrotic zone surrounded by epithelioid histiocytes with varied numbers of multinucleated giant cells and lymphocytes.
- Multinucleated giant cells may contain Langhans type giant cells (nuclei arranged in a horseshoe shaped pattern at the periphery of the cell), but these are not specific for TB infection.
- Organisms are usually present in the central zone of necrosis, seen on special stains.
- Non-necrotizing granulomas can be present as well.
Spread of Disease with Secondary TB
- Miliary TB: Seeding of distal organs with innumerable small millet-seed like lesions via lymphatic and hematogenous routes. This may be pulmonary miliary TB or systemic.
- Endobronchial, endotracheal and laryngeal TB: Develop via the spread of infective material through lymphatic channels or from expectorated infectious material.
- Isolated organ TB: Occurs by hematogenous spread to any organ and may be the presenting feature. Most common sites include the meninges, kidneys, adrenals, bone, paraspinal abscesses (Pott disease), and fallopian tubes.
- Lymphadenitis: Especially cervical LN. Lymphadenopathy is usually unifocal and the patient does not have ongoing disease.
- Intestinal TB: Due to ingestion of contaminated milk or secondary to swallowing coughed up infective material in secondary TB. Organisms become trapped in mucosal lymphoid aggregations of the small and large bowel which become inflamed, enlarged and ulcerated, especially in the ileum.
Clinical Features
-
Localized secondary TB may be asymptomatic.
-
Symptoms are usually insidious when they appear.
-
Systemic symptoms related to TNF and IL1: Malaise, anorexia, weight loss, fever (remittent low grade), and night sweats.
-
Localized symptoms (with progressive pulmonary TB):
- Increase in sputum volume, initially mucoid then purulent.
- Hemoptysis (in 1/2 of patients).
- Pleuritic chest pain.
-
In extrapulmonary TB, symptoms depend on the organ involved. For example:
- Fallopian tube: Infertility
- Meninges: Neurologic deficit.
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Test your knowledge on lower respiratory tract infections, including their causes and classifications. Learn about pneumonia and the various pathogens responsible for community-acquired pneumonia. This quiz will enhance your understanding of LRTIs and their implications.