Pulmonary Infections Study Guide PDF

PULMONARY INFECTIONS Dereje G(MD)  The vulnerability of the lung to infection despite these defenses is not surprising because. (1) many microbes are airborne and readily inhaled into the lungs. (2) nasopharyngeal flora are regularly aspirated during sleep, even by healthy...

PULMONARY INFECTIONS Dereje G(MD)  The vulnerability of the lung to infection despite these defenses is not surprising because. (1) many microbes are airborne and readily inhaled into the lungs. (2) nasopharyngeal flora are regularly aspirated during sleep, even by healthy individuals. (3) lung diseases often lower local immune defenses.
 Bacterial pneumonias are classified according to the specific etiologic agent by the clinical setting in which the infection occurs. the area of the lung affected. Type of infection

Community-Acquired Bacterial Pneumonias Introduction Bacterial pneumonias often follow a viral upper-respiratory tract infection. S. pneumoniae (i.e., the pneumococcus) is the most common cause of community-acquired acute pneumonia. Lobar Pneumonia consolidation of a large portion of a lobe or of an entire lobe. Has four stages of the inflammatory response. Initial Stage is Congestion. Characterized by vascular engorgement, intraalveolar fluid with few neutrophils, and often the presence of numerous bacteria. Lung is heavy, boggy, and red.  Red hepatization. characterized by massive confluent exudation, as neutrophils, red cells, and fibrin fill the alveolar spaces. The lobe is red, firm, and airless. Has a liver-like consistency, hence the term hepatization. Gray Hepatization. marked by progressive disintegration of red cells, and persistence of a fibrinosuppurative exudate. Change in lobe color to grayish-brown.  Resolution Final stage. The exudate within the alveolar spaces is broken down by enzymatic digestion. produces granular, semifluid debris that is resorbed, ingested by macrophages, expectorated, or organized by fibroblasts growing into it.





 Pleural fibrinous reaction to the underlying inflammation is often present in the early stages if the consolidation extends to the surface. It may resolve or undergo organization, leaving fibrous thickening or permanent adhesions.

Bronchopneumonia Patchy consolidation of the lung is the dominant characteristic. Foci of Bronchopneumonia are consolidated areas of acute suppurative inflammation. The consolidation is often multi-lobar and frequently bilateral. may be confined to one lobe. Tend to be basal because of the tendency of secretions to gravitate to the lower lobes.  Histologically, a neutrophil-rich exudate fills the bronchi, bronchioles, and adjacent alveolar spaces. elevated, dry, granular, gray-red to yellow, and poorly delimited lesions.


Clinical Features Abrupt onset of high-grade fever, chills, and cough producing mucopurulent sputum. occasionally patients have hemoptysis. When pleuritis is present, it is accompanied by pleuritic pain and pleural friction rub. opacities on radiography. Complications Abscess formation Empyema Bacteremic dissemination Community-Acquired Viral Pneumonias  The most common causes of community-acquired viral pneumonias are Influenza types A and B, The respiratory syncytial viruses, Human metapneumovirus, Adenovirus,rhinoviruses, rubeola virus, and varicella virus. Nearly all of these agents also cause upper-respiratory tract infections.  Causes interstitial inflammation. some outpouring of fluid into alveolar spaces may also occur. mimic bacterial pneumonia on chest films. predisposes to secondary bacterial infections. Often in infants, older adults, malnourished patients, alcoholics, and immunosuppressed individuals. Morphology The process may be patchy, or it may involve whole lobes bilaterally or unilaterally. The affected areas are red-blue, congested, and sub crepitant. The inflammatory reaction is largely confined to the walls of the alveoli. The septa are widened and edematous. contain a mononuclear inflammatory infiltrate of lymphocytes, macrophages and, occasionally, plasma cells.  alveolar spaces in viral pneumonias are free of cellular exudate. In severe cases full-blown diffuse alveolar damage with hyaline membranes may develop. reconstitution of the normal architecture on resolution. Clinical Features The clinical course varies. may go undiagnosed, or manifest as a fulminant, life- threatening infection. fever, headache, and malaise and, later, cough with minimal sputum. ventilation and perfusion mismatch. the degree of respiratory distress often seems out of proportion to the physical and radiographic findings. Hospital-Acquired Pneumonias  pulmonary infections acquired in the course of a hospital stay. severe underlying disease, immunosuppressed, or those on poses risk. prolonged antibiotic regimens. ventilator-associated pneumonia. Gram-negative rods and S. aureus are the most common isolates. Aspiration Pneumonia  Aspiration pneumonia occurs in debilitated patients those who aspirate gastric contents while unconscious or during repeated vomiting. Those affected have abnormal gag and swallowing reflexes that facilitate aspiration. Partly chemical and partly bacterial pneumonia. Typically, more than one organism is recovered on culture, aerobes being more common than anaerobes.  is often necrotizing, pursues a fulminant clinical course, and is a frequent cause of death in individuals predisposed to aspiration Abscess formation is a common complication. Microaspiration, by contrast, occurs in many individuals, especially those with gastroesophageal reflux Lung Abscess  localized area of suppurative necrosis within the pulmonary parenchyma, resulting in the formation of one or more large cavities. The causative organism may be introduced into the lung by Aspiration of infective material
Aspiration of gastric contents
As a complication of necrotizing bacterial pneumonias
Bronchial obstruction
Septic embolism
hematogenous

 Anaerobic bacteria are present in almost all lung abscesses, and they are the exclusive isolates in one-third to two-thirds of cases. The most frequently encountered anaerobes are commensals normally found in the oral cavity. Prevotella, Fusobacterium, Bacteroides, Peptostreptococcus, and microaerophilic streptococci. Morphology few millimeters to large 5 to 6cm cavities. The localization and number of abscesses depend on their mode of development. Abscess due to aspiration of infective material more common on the right most are single. On the right side, the posterior segment of the upper lobe in the apical segments of the lower lobe.  Pneumonia or bronchiectasis commonly are multiple, basal, and diffusely scattered. Septic emboli and abscesses arising from hematogenous seeding are commonly multiple and may affect any region of the lungs. ruptures into airways. air-fluid level on radiographic examination pneumothorax or empyema. meningitis or brain abscess. suppurative focus is surrounded by variable amounts of fibrous scarring and mononuclear infiltration. Clinical Features prominent cough sputum hemoptysis. Spiking fever and malaise are common. Clubbing of the fingers, weight loss, and anemia may all occur. underlying carcinoma must be considered. Secondary amyloidosis may develop in chronic cases.
Tuberculosis  Tuberculosis is chronic granulomatous disease caused by Mycobacterium tuberculosis. Primarily affects the lungs but may affect any organ or tissue in the body. Mycobacteria are are acid-fast bacilli M. tuberculosis hominis is responsible for most cases of tuberculosis. The reservoir of infection typically is found in individuals with active pulmonary disease.  Transmission usually is by inhalation of airborne organisms. by exposure to contaminated secretions of infected individuals. By drinking milk contaminated with Mycobacterium bovis infection. Other mycobacterias are much less virulent than M. tuberculosis and rarely cause disease in immunocompetent individuals. However, they cause disease in 10% to 30% of patients with AIDS.
Pathogenesis Cell-mediated immunity plays significant role in TB pathogenesis. The pathologic features of tuberculosis, such as caseating granulomas and cavitation, are the result of the destructive tissue hypersensitivity that is part and parcel of the host immune response. Because the effector cells for both protective immunity and damaging hypersensitivity are the same, the appearance of tissue hypersensitivity also signals the acquisition of immunity to the organism. The sequence of events from inhalation of the infectious inoculum to containment of the primary occurs as follows;-  Entry into macrophages Replication in macrophages. proliferation of bacilli in alveolar macrophages and air spaces with subsequent bacteremia and bacterial seeding. mostly asymptomatic but can have mild flu like illness. Development of cell-mediated immunity CD4+ T cells that are capable of secreting IFN-γ generated. T cell–mediated macrophage activation and killing of bacteria.
 T cell–mediated macrophage activation and killing of bacteria.
CD4+ T cells, releases IFN-γ, Which activates macrophages. Activated macrophages release a variety of mediators and upregulate expression of including TNF, iNOS, and anti- microbial Peptides. Granulomatous inflammation and tissue damage.


Primary Tuberculosis Is the form of disease that develops in a previously unexposed patient. In the large majority of individuals, the only consequence of primary tuberculosis are the foci of scarring. The foci may harbor viable bacilli and thus serve as a nidus for disease reactivation. About 5% of those newly infected develop progressive primary tuberculosis. Mainly In immunocompromised individuals. Morphology The inhaled bacilli usually implant in the distal air spaces of the lower part of the upper lobe or in the upper part of the lower lobe. They are typically close to the pleura. Ghon focus, a 1-cm to 1.5-cm area of gray-white inflammatory consolidation. In the majority of cases, the center of this focus undergoes caseous necrosis. Ghon complex. Ranke complex Secondary Tuberculosis Secondary tuberculosis is the pattern of disease that arises in a previously sensitized host. Arises from reactivation of dormant primary lesions. It also may result from reinfection. Only a few patients (