Chapter 13: Pulmonary infections and tuberculosis Flashcards
What is pulmonary infection?
Pulmonary infections in the form of pneumonia are responsible for one sixth of all deaths in the United States. Pneumonia can be broadly defined as any infection in the lung
Do the lung parenchyma remain sterile during pulmonary infections?
Yes! because of a number of highly effective immune and non-immune defense mechanisms that extend throughout the respiratory system from the nasopharynx to the alveolar space
Despite the immune and non-immune system through the whole respiratory system, the lung is vulnerable. Why?
(1) many microbes are airborne and readily inhaled into the lungs; (2) nasopharyngeal flora are regularly aspirated during sleep, even by healthy individuals; and (3) lung diseases often lower local immune defenses.
The importance of immune defenses in preventing pulmonary infections is emphasized by patients with inherited or acquired defects in innate immunity (including neutrophil and complement defects) or adaptive immunity (e.g., humoral immunodeficiency). What do they all lead to?
An increased incidence of infections with pyogenic bacteria
On this figure, lung defence mechansisms are shown. What is the left (A) and right (B) mechanism? Try to explain steps 1-5 (A) and 1-3 (B). Don’t learn by heart but understand what is happening!
- (A) Innate immune system:
- In the normal lung, removal of microbial organisms depends on entrapment in the mucous blanket and removal by means of the mucociliary elevator;
- Phagocytosis by alveolar macrophages can kill and degrade organisms and remove them from the air spaces by migrating onto the mucociliary elevator, or:
- Phagocytosis and killing by neutrophils recruited by macrophage factors;
- Complement may enter the alveoli and be activated by the alternative pathway to produce the opsonin C3b, which enhances phagocytosis
- Organisms, including those ingested by phagocytes, may reach the draining lymph nodes to initiate immune responses.
- (B) Adaptive immune system:
- Secreted IgA can block attachment of the microorganism to epithelium in the upper-respiratory tract
- 2, In the lower-respiratory tract, serum antibodies (IgM, IgG) are present in the alveolar lining fluid and activate complement more efficiently by the classic pathway, yielding C3b (not shown); In addition, IgG is an opsonin
- The accumulation of immune T cells is important for controlling infections by viruses and other intracellular microorganisms. PMN, neutrophil.
Bacterial pneumonias are classified according to the specific etiologic agent or, if no pathogen can be isolated, by the clinical setting in which the infection occurs. Altogether, seven distinct clinical settings are recognized, each associated with a fairly distinct group of pathogens. What are they?
- Community-Acquired Bacterial Pneumonia 2. Community-Acquired Viral Pneumonia 3. Nosocomial Pneumonia 4. Aspiration Pneumonia 5. Chronic Pneumonia 6. Necrotizing Pneumonia and Lung Abscess 7. Pneumonia in the Immunocompromised Host (this was skipped in the lecture, p520-525 explain all the different types but you don’t have to know them)
In pneumonias, the term “consolidation” refers to “solidification” of the lung. Why?
Due to replacement of the air by exudate in the alvoli
Bacterial pneumonia has two patterns of anatomic distribution: lobular bronchopneumonia and lobar pneumonia. What is the difference between the two?
Patchy consolidation of the lung is the dominant characteristic of bronchopneumonia, while consolidation of a large portion of a lobe or of an entire lobe defines lobar pneumonia
Wat are the four stages of the inflammatory response of lobular pneumonia?
- Congestion: the lung is heavy, boggy, and red. It is characterized by vascular engorgement, intraalveolar fluid with few neutrophils, and often the presence of numerous bacteria. 2. Red hepatization: characterized by massive confluent exudation, as neutrophils, red cells, and fibrin fill the alveolar spaces. On gross examination, the lobe is red, firm, and airless, with a liver-like consistency. 3. Gray hepatization: progressive disintegration of red cells and the persistence of a fibrinosuppurative exudate, resulting in a color change to grayish-brown. 4. Resolution: the exudate within the alveolar spaces is broken down by enzymatic digestion to produce granular, semifluid debris that is resorbed, ingested by macrophages, expectorated, or organized by fibroblasts growing into it
Morphologically explain bronchopneumonia
Foci of bronchopneumonia are consolidated areas of acute suppurative inflammation. The consolidation may be confined to one lobe but is more often multilobar and frequently bilateral and basal because of the tendency of secretions to gravitate to the lower lobes. Well-developed lesions are slightly elevated, dry, granular, gray-red to yellow, and poorly delimited at their margins. Histologically, a neutrophil-rich exudate fills the bronchi, bronchioles, and adjacent alveolar spaces
What is tuberculosis?
A communicable chronic granulomatous disease caused by Mycobacterium tuberculosis
True/false: Although tuberculosis usually involves the lungs, it may affect any organ or tissue in the body
True
True/false: The World Health Organization (WHO) considers tuberculosis to be the most common cause of death resulting from a single infectious agent.
True
True/false: Tuberculosis is seen in every population
False, tuberculosis flourishes under conditions of poverty, crowding, and chronic debilitating illness (older adults, urban poor, AIDS, minority communities, and many more)
Infection with M. tuberculosis typically leads to the development of delayed hypersensitivity. How can this be used in clinical practice?
It can be detected by the tuberculin (Mantoux) test (to diagnose tuberculosis)
What does the histology of tuberculosis look like?
You should be able to recognize this (but pls don’t learn by heart)
The morphologic spectrum of tuberculosis. A characteristic tubercle at low magnification (A) and at higher power (B) shows central granular caseation surrounded by epithelioid and multinucleate giant cells. This is the usual response in individuals who develop cell-mediated immunity to the organism. (C) Occasionally, even in immunocompetent patients, tubercular granulomas may not show central caseation; hence, irrespective of the presence or absence of caseous necrosis, use of special stains for acid-fast organisms is indicated when granulomas are present. (D) In this specimen from an immunosuppressed patient, sheets of macrophages packed with mycobacteria are seen (acid-fast stain).
