Pulmonary Infections Pathology 2024 PDF

Pulmonary infections Pneumonia: any infection in the lung the lung parenchyma is sterile because of defense mechanisms (immune and non- immune) extending from the nasopharynx to the alveolar air spaces  Bacterial pneumonias are classified according to the specific etiologic agent or, if...

Pulmonary infections Pneumonia: any infection in the lung the lung parenchyma is sterile because of defense mechanisms (immune and non- immune) extending from the nasopharynx to the alveolar air spaces  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 Specific clinical settings are associated with a fairly distinct group of pathogens consideration of the clinical setting can be a helpful guide when antimicrobial therapy must be given empirically  MORPHOLOGY Bacterial pneumonia has two patterns of anatomic distribution: lobular bronchopneumonia and lobar pneumonia “consolidation, means “solidification” of the lung due to replacement of the air by exudate in the alveoli Patchy consolidation of the lung is the dominant characteristic of bronchopneumonia consolidation of a large portion of a lobe or of an entire lobe defines lobar pneumonia patterns overlap, patchy involvement may become confluent over time same organism may produce either pattern depending on patient susceptibility Most important from the clinical standpoint : identification of the causative agent and determination of the extent of disease In lobar pneumonia, four stages of the inflammatory response: In the first stage of congestion, the lung is heavy, wet, and red. It is characterized by vascular engorgement, intraalveolar fluid with few neutrophils, and often numerous bacteria The stage of red hepatization: characterized by massive confluent exudation, as neutrophils, red cells, and fibrin fill the alveolar spaces the lobe is red, firm, and airless, with a liverlike consistency, (hepatization)  The stage of gray hepatization: progressive disintegration of red cells and the persistence of a fibrinosuppurative exudate , resulting in a color change to grayish brown stage of 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 Extension of the pneumonia to the lung periphery often produces a pleural fibrinous reaction (pleuritis) This may resolve or undergo organization, leaving fibrous thickening or permanent adhesions  In bronchopneumonia there are focal areas of consolidation The consolidation may be confined to one lobe but more often multilobar and frequently bilateral and basal Well developed lesions are slightly elevated, dry, granular, gray-red to yellow, and poorly delimited at their margins  Histologically, bacterial pneumonia a neutrophil-rich exudate fills the bronchi, bronchioles, and adjacent alveolar spaces Complications of pneumonia: (1) tissue destruction and necrosis, causing abscess formation (2) spread of infection to the pleural cavity, causing pleuritis and empyema (3) bacteremic dissemination to the heart valves, pericardium, brain, kidneys, spleen, or joints, causing abscesses, endocarditis, meningitis, suppurative arthritis  Community-Acquired Viral Pneumonias Prior to COVID-19 pandemic, the most common causes were influenza types A and B, the respiratory syncytial viruses, human metapneumovirus, adenovirus, rhinoviruses During the year 2020, SARS-CoV-2, the agent of COVID- 19 became the leading cause of community-acquired viral pneumonia in most parts of the world All viruses share a propensity to infect and damage respiratory epithelium, producing an inflammatory response When the process extends to alveoli, there is usually interstitial inflammation, some outpouring of fluid into alveolar spaces may occur on chest films the changes may mimic bacterial pneumonia  Community-Acquired Viral Pneumonias it is not possible to distinguish bacterial and viral pneumonia based on radiologic appearance alone damage leading to necrosis of the respiratory epithelium inhibits mucociliary clearance and predisposes to secondary bacterial infections complications of viral infection are more likely in infants, older adults, malnourished patients, immunocompromised patients  MORPHOLOGY The morphologic patterns in viral pneumonias are similar may be patchy or it may involve whole lobes bilaterally or unilaterally Macroscopically, the affected areas are red-blue and congested  MORPHOLOGY On histologic examination: the inflammation is largely confined to the walls of the alveoli The septa are widened and edematous mononuclear inflammatory infiltrate of lymphocytes, macrophages, and, occasionally, plasma cells alveolar spaces in viral pneumonias are free of cellular exudate In severe cases, diffuse alveolar damage with hyaline membranes may develop In less severe, uncomplicated cases, resolution of the disease is followed by reconstitution of the normal architecture Superimposed bacterial infection results in a mixed histologic picture Coronaviruses enveloped, positive-sense RNA viruses that infect humans and several other vertebrate species. Weakly pathogenic coronaviruses cause mild coldlike upper respiratory tract infections, highly pathogenic ones may cause severe, often fatal pneumonia SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), a highly pathogenic strain that is responsible for the first pandemic of the 21st century (COVID-19)  Pathogenesis Highly pathogenic coronaviruses have viral spike proteins that bind the protein angiotensin-converting enzyme 2 (ACE2), which is found on the surface of nasopharyngeal epithelium and type 2 alveolar epithelial cells Following exposure, the virus is taken up into ACE2-expressing cells and replicates rapidly Transmission is mainly through respiratory droplets that are produced by coughing, sneezing, talking, or singing and is most likely to occur indoors in poorly ventilated spaces  The outcome of SARS-CoV-2 infection is variable from asymptomatic infection, particularly in children and younger adults to severe disease that leads to rapid progressive pneumonia The major risk factors for severe disease :  Age. particularly deadly in the elderly, especially those older than 75 years.  Comorbidities. obesity, smoking, diabetes, and chronic cardiac, pulmonary, renal disease  Socioeconomic background, socially defined race, and gender. Males are at higher risk for severe disease,  Laboratory abnormalities. lymphopenia, thrombocytopenia, evidence of coagulopathy or hepatic, cardiac, or renal damage  Genetic factors association between the type A blood group and severe disease germline mutations in genes encoding components of the type I interferon pathway in a subset of patients with severe disease The pathogenesis of COVID-19: Viral infection of type 2 alveolar epithelium cause damage through direct cytopathic effects Individuals who develop severe disease generally have higher viral loads early in the course In some individuals inability to control virus may be due to autoantibodies or genetic variants that interfere with type I interferon signaling alterations in the immune system that occur with aging the presence of comorbid conditions such as obesity and diabetes large numbers of SARSCoV- 2 infected cells elicit an excessive immune response marked by high levels of cytokines such as interferon-g, IL-6, and TNF, setting off an inflammatory cascade referred to as cytokine storm  Cytokine storm produces dysfunction not only in the lung but in multiple other organ systems, including heart and kidneys, similar to the systemic inflammatory response syndrome this pro-inflammatory state persists even after viral loads fall severe COVID-19 has a high propensity for venous and arterial thrombosis thrombosis often occurs in the setting of very high levels of plasma fibrinogen and markedly elevated blood viscosity, a well known risk factor for thrombosis MORPHOLOGY severe cases of COVID-19 show additional findings to viral pneumonia The coagulopathy cause venous thromboembolism and arterial thrombosis, leading to ischemia and stroke Coagulopathy cause microthrombi in the inflamed lung that exacerbate pulmonary dysfunction Myocarditis and inflammatory infiltrates in the CNS have been reported (mechanism not clear yet)  Hospital-Acquired Pneumonias pulmonary infections acquired during a hospital stay. not only have an adverse impact on the clinical course of ill patients but also add considerably to the cost of health care Hospital-acquired infections are common in patients with severe underlying disease and those who are immunosuppressed or are on prolonged antibiotic regimens Patients on mechanical ventilation are a particularly high-risk Gramnegative rods (members of Enterobacteriaceae and Pseudomonas spp.) and S. aureus are the most common isolates , S. pneumoniae is not a common pathogen in the hospital setting  Aspiration Pneumonia Aspiration pneumonia occurs in patients who are debilitated or those who aspirate gastric contents while unconscious (e.g., after a stroke) or during repeated vomiting Those affected typically have abnormal gag and swallowing reflexes Tpneumonia is partly chemical, due to the irritating effects of the gastric acid, and partly bacterial more than one organism is recovered on culture, aerobes being more common than anaerobes Aspiration pneumonia 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  Lung Abscess localized area of suppuration within the pulmonary parenchyma that results in the formation of one or more large cavities The causative organism may be introduced by:  Aspiration of infective material from carious teeth or infected sinuses or tonsils  Aspiration of gastric contents  As a complication of necrotizing bacterial pneumonias, particularly those caused by S. aureus, Streptococcus pyogenes, K. pneumoniae, Pseudomonas spp., Mycotic infections and bronchiectasis also may lead to lung abscesses  Bronchial obstruction, particularly due to lung cancer  Septic embolism, from infective endocarditis  hematogenous spread of bacteria in disseminated pyogenic infection (staphylococcal bacteremia)  selected pathogens can generate or colonize cavitary lesions and radiographically mimic lung abscess fungi , Mycobacterium tuberculosis, nontuberculous mycobacteria, and parasites 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, principally species of Prevotella, Fusobacterium, Bacteroides