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This document discusses the etiology, pathophysiology, clinical manifestations, and complications of pneumonia acquired in community, hospital, and ventilator settings. It describes the typical and atypical bacterial, viral, and fungal pathogens that can cause community-acquired pneumonia and notes increasing cases of Mycoplasma and Chlamydophila pneumonia. For hospital-acquired and ventilator-associated pneumonia, it outlines the risk of multi-drug resistant pathogens and worse clinical outcomes compared to community-acquired cases. The pathophysiology section overviews the host immune response and factors influencing the lung microbiota and pneumonia development. Clinical features ranging from mild to life-threatening are outlined for the different settings. Potential complications include respiratory

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PNEUMONIA
ETIOLOGY COMMUNITY-ACQUIRED PNEUMONIA:- The list of potential etiologic agents of CAP includes bacteria, fungi, viruses, and protozoa. Newer viral pathogens include metapneumoviruses, the coronaviruses responsible for severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), and the recently discovered coronavirus that is designated SARS-CoV-2.
Separation of potential agents into TYPICAL BACTERIAL PATHOGENS LIKE S. pneumoniae, Haemophilus influenzae, and, in selected patients, S. aureus and gram-negative bacilli such as Klebsiella pneumoniae and P. aeruginosa. ATYPICAL ORGANISMS INCLUDE Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella species respiratory viruses such as influenza virus, adenoviruses, human metapneumoviruses, respiratory syncytial virus, and coronaviruses
With the increasing use of pneumococcal vaccine, the incidence of pneumococcal pneumonia is decreasing. Cases due to M. pneumoniae and C. pneumoniae, however, appear to be increasing, especially among young adults. Earlier literature suggested that aspiration pneumonia was caused primarily by anaerobes, with or without aerobic pathogens. A shift, however, has been noted recently: if aspiration pneumonia is acquired in a community or hospital setting, the likely pathogens are those usually associated with CAP or HAP. Anaerobes may still play a role, especially in patients with poor dentition, lung abscess, necrotizing pneumonia, or empyema.
Epidemiologic Factors Suggesting Possible Causes of Community-Acquired Pneumonia
VENTILATOR-ASSOCIATED PNEUMONIA(VAP):- Potential etiologic agents of VAP include both MDR and non-MDR bacterial pathogens The relative frequency of individual MDR pathogens can vary significantly from hospital to hospital and even between different critical care units within the same institution. Most hospitals have problems with P. aeruginosa and MRSA, but other MDR pathogens are often institution-specific. Less commonly, fungal and viral pathogens cause VAP, usually affecting severely immunocompromised patients. Rarely, community-associated viruses cause mini-epidemics, usually when introduced by ill health care workers.
Microbiologic Causes of Ventilator-Associated Pneumonia
HOSPITAL-ACQUIRED PNEUMONIA (HAP):- HAP in non-intubated patients both inside and outside the ICUis similar to VAP. The main differences are the higher frequency of non-MDR pathogens and the generally better underlying host immunity in non- intubated patients. The bacteriology and outcome of ventilated HAP patients may be very similar to those of patients with VAP.
PATHOPHYSIOLOGY Pneumonia is the result of the proliferation of microbial pathogens at the alveolar level and the hosts response to them. It was thought that the lungs were sterile and that pneumonia resulted from the introduction of potential pathogens into this sterile environment This introduction occurred through microaspiration of oropharyngeal organisms into the lower respiratory tract. Overcoming of innate and adaptive immunity by such microorganisms could result in the clinical syndrome of pneumonia.
Recent use of culture-independent techniques of microbial identification has demonstrated a complex and diverse community of bacteria in the lungs that constitutes the lung microbiota Mechanical factors, such as the hairs and turbinates of the nares, the branching tracheobronchial tree, mucociliary clearance, and gag and cough reflexes, all play a role in host defense but are insufficient to effectively block bacterial access to the lower airways. In the absence of a sufficient barrier, microorganisms may reach the lower respiratory tract by a variety of pathways, including inhalation, microaspiration, and direct mucosal dispersion.
The constitution of the lung microbiota is determined by three factors: microbial entry into the lungs, microbial elimination, and regional growth conditions for bacteria, such as pH, oxygen tension, and temperature. An inflammatory event resulting in epithelial and or endothelial injury results in the release of cytokines, chemokines, and catecholamines, some of which may selectively promote the growth of certain bacteria, such as Streptococcus pneumoniae and P. aeruginosa.
Inflammatory mediators such as interleukin 6 and tumor necrosis factor result in fever, and chemokines such as interleukin 8 and granulocyte colony-stimulating factor increase local neutrophil numbers. Mediators released by macrophages and neutrophils may create an alveolar capillary leak resulting in impaired oxygenation, hypoxemia, and radiographic infiltrates. some bacterial pathogens appear to interfere with the hypoxic vasoconstriction that would normally occur with fluid-filled alveoli, and this interference may result in severe hypoxemia.
Decreased compliance due to capillary leak, hypoxemia, increased respiratory drive, increased secretions, and occasionally infection- related bronchospasm all lead to worsening dyspnea. If severe enough, changes in lung mechanics secondary to reductions in lung volume, compliance, and intrapulmonary shunting of blood may cause respiratory failure.
PATHOLOGY Classic pneumonia evolves through a series of stages. The initial stage is edema with a proteinaceous exudate and often bacteria in the alveoli. Next is a rapid transition to the red hepatization phase. In the third phase, gray hepatization, no new erythrocytes are extravasating, and those already present have been lysed and degraded. The neutrophil is the predominant cell, fibrin deposition is abundant, and bacteria have disappeared. This phase corresponds with the successful containment of the infection and improvement in gas exchange. In the final phase, resolution, the macrophage reappears as the dominant cell in the alveolar space and the debris of neutrophils, and bacteria and fibrin have been cleared, as has the inflammatory response.
CLINICAL MANIFESTATIONS Community-Acquired Pneumonia:- The clinical presentation of pneumonia can vary from indolent to fulminant and from mild to fatal in severity. Manifestations of worsening severity include both constitutional findings and those limited to the lung and associated structures. The patient is frequently febrile and/or tachycardic and may experience chills and/or sweats. Cough may be nonproductive or productive of mucoid, purulent, or blood-tinged sputum. Gross hemoptysis is suggestive of necrotizing pneumonia (e.g., that due to CA-MRSA).
Depending on severity, the patient may be able to speak in full sentences or may be short of breath. With pleural involvement, the patient may experience pleuritic chest pain. Up to 20% of patients may have gastrointestinal symptoms such as nausea, vomiting, or diarrhea. Other symptoms may include fatigue, headache, myalgias, and arthralgias. An increased respiratory rate and use of accessory muscles of respiration are common.
HAP and VAP:- The clinical manifestations of HAP and VAP are nonspecific fever, leukocytosis, increased respiratory secretions, and pulmonary consolidation on physical examination, along with a new or changing radiographic infiltrate. Other clinical features may include tachypnea, tachycardia, worsening oxygenation, and increased minute ventilation. Serial changes in oxygenation may identify pneumonia earlier than other findings and may also be a means to monitor improvement with therapy
COMPLICATIONS CAP:- Complications of severe CAP include respiratory failure, shock multiorgan failure, and exacerbation of comorbid illnesses.
Three particularly noteworthy conditions are metastatic infection, lung abscess, and complicated pleural effusion. Metastatic infection (e.g., brain abscess or endocarditis) is unusual and requires a high degree of suspicion and a detailed workup for proper treatment. Lung abscess may occur in association with aspiration pneumonia or with infection caused by pathogens such as CA-MRSA, P. aeruginosa, or (rarely) S. pneumoniae. A significant pleural effusion should be tapped for both diagnostic and therapeutic purposes. If the fluid has a pH 1000 U/L or if bacteria are seen or cultured, drainage is needed.
CAP:- Apart from death, the major complication of VAP is prolongation of mechanical ventilation, with corresponding increases in the duration of ICU and hospital stay. In rare cases, necrotizing pneumonia (e.g., due to P. aeruginosa or S. aureus) can cause significant pulmonary hemorrhage. Other long-term complications of pneumonia can include long-term oxygen therapy, a catabolic state in a patient already nutritionally at risk, the need for prolonged rehabilitation, andin the elderlyan inability to return to independent function and the need for nursing home placement.

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pneumonia.pptx

  • 2. ETIOLOGY COMMUNITY-ACQUIRED PNEUMONIA:- The list of potential etiologic agents of CAP includes bacteria, fungi, viruses, and protozoa. Newer viral pathogens include metapneumoviruses, the coronaviruses responsible for severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), and the recently discovered coronavirus that is designated SARS-CoV-2.
  • 3. Separation of potential agents into TYPICAL BACTERIAL PATHOGENS LIKE S. pneumoniae, Haemophilus influenzae, and, in selected patients, S. aureus and gram-negative bacilli such as Klebsiella pneumoniae and P. aeruginosa. ATYPICAL ORGANISMS INCLUDE Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella species respiratory viruses such as influenza virus, adenoviruses, human metapneumoviruses, respiratory syncytial virus, and coronaviruses
  • 4. With the increasing use of pneumococcal vaccine, the incidence of pneumococcal pneumonia is decreasing. Cases due to M. pneumoniae and C. pneumoniae, however, appear to be increasing, especially among young adults. Earlier literature suggested that aspiration pneumonia was caused primarily by anaerobes, with or without aerobic pathogens. A shift, however, has been noted recently: if aspiration pneumonia is acquired in a community or hospital setting, the likely pathogens are those usually associated with CAP or HAP. Anaerobes may still play a role, especially in patients with poor dentition, lung abscess, necrotizing pneumonia, or empyema.
  • 5. Epidemiologic Factors Suggesting Possible Causes of Community-Acquired Pneumonia
  • 6. VENTILATOR-ASSOCIATED PNEUMONIA(VAP):- Potential etiologic agents of VAP include both MDR and non-MDR bacterial pathogens The relative frequency of individual MDR pathogens can vary significantly from hospital to hospital and even between different critical care units within the same institution. Most hospitals have problems with P. aeruginosa and MRSA, but other MDR pathogens are often institution-specific. Less commonly, fungal and viral pathogens cause VAP, usually affecting severely immunocompromised patients. Rarely, community-associated viruses cause mini-epidemics, usually when introduced by ill health care workers.
  • 7. Microbiologic Causes of Ventilator-Associated Pneumonia
  • 8. HOSPITAL-ACQUIRED PNEUMONIA (HAP):- HAP in non-intubated patients both inside and outside the ICUis similar to VAP. The main differences are the higher frequency of non-MDR pathogens and the generally better underlying host immunity in non- intubated patients. The bacteriology and outcome of ventilated HAP patients may be very similar to those of patients with VAP.
  • 9. PATHOPHYSIOLOGY Pneumonia is the result of the proliferation of microbial pathogens at the alveolar level and the hosts response to them. It was thought that the lungs were sterile and that pneumonia resulted from the introduction of potential pathogens into this sterile environment This introduction occurred through microaspiration of oropharyngeal organisms into the lower respiratory tract. Overcoming of innate and adaptive immunity by such microorganisms could result in the clinical syndrome of pneumonia.
  • 10. Recent use of culture-independent techniques of microbial identification has demonstrated a complex and diverse community of bacteria in the lungs that constitutes the lung microbiota Mechanical factors, such as the hairs and turbinates of the nares, the branching tracheobronchial tree, mucociliary clearance, and gag and cough reflexes, all play a role in host defense but are insufficient to effectively block bacterial access to the lower airways. In the absence of a sufficient barrier, microorganisms may reach the lower respiratory tract by a variety of pathways, including inhalation, microaspiration, and direct mucosal dispersion.
  • 11. The constitution of the lung microbiota is determined by three factors: microbial entry into the lungs, microbial elimination, and regional growth conditions for bacteria, such as pH, oxygen tension, and temperature. An inflammatory event resulting in epithelial and or endothelial injury results in the release of cytokines, chemokines, and catecholamines, some of which may selectively promote the growth of certain bacteria, such as Streptococcus pneumoniae and P. aeruginosa.
  • 12. Inflammatory mediators such as interleukin 6 and tumor necrosis factor result in fever, and chemokines such as interleukin 8 and granulocyte colony-stimulating factor increase local neutrophil numbers. Mediators released by macrophages and neutrophils may create an alveolar capillary leak resulting in impaired oxygenation, hypoxemia, and radiographic infiltrates. some bacterial pathogens appear to interfere with the hypoxic vasoconstriction that would normally occur with fluid-filled alveoli, and this interference may result in severe hypoxemia.
  • 13. Decreased compliance due to capillary leak, hypoxemia, increased respiratory drive, increased secretions, and occasionally infection- related bronchospasm all lead to worsening dyspnea. If severe enough, changes in lung mechanics secondary to reductions in lung volume, compliance, and intrapulmonary shunting of blood may cause respiratory failure.
  • 14. PATHOLOGY Classic pneumonia evolves through a series of stages. The initial stage is edema with a proteinaceous exudate and often bacteria in the alveoli. Next is a rapid transition to the red hepatization phase. In the third phase, gray hepatization, no new erythrocytes are extravasating, and those already present have been lysed and degraded. The neutrophil is the predominant cell, fibrin deposition is abundant, and bacteria have disappeared. This phase corresponds with the successful containment of the infection and improvement in gas exchange. In the final phase, resolution, the macrophage reappears as the dominant cell in the alveolar space and the debris of neutrophils, and bacteria and fibrin have been cleared, as has the inflammatory response.
  • 15. CLINICAL MANIFESTATIONS Community-Acquired Pneumonia:- The clinical presentation of pneumonia can vary from indolent to fulminant and from mild to fatal in severity. Manifestations of worsening severity include both constitutional findings and those limited to the lung and associated structures. The patient is frequently febrile and/or tachycardic and may experience chills and/or sweats. Cough may be nonproductive or productive of mucoid, purulent, or blood-tinged sputum. Gross hemoptysis is suggestive of necrotizing pneumonia (e.g., that due to CA-MRSA).
  • 16. Depending on severity, the patient may be able to speak in full sentences or may be short of breath. With pleural involvement, the patient may experience pleuritic chest pain. Up to 20% of patients may have gastrointestinal symptoms such as nausea, vomiting, or diarrhea. Other symptoms may include fatigue, headache, myalgias, and arthralgias. An increased respiratory rate and use of accessory muscles of respiration are common.
  • 17. HAP and VAP:- The clinical manifestations of HAP and VAP are nonspecific fever, leukocytosis, increased respiratory secretions, and pulmonary consolidation on physical examination, along with a new or changing radiographic infiltrate. Other clinical features may include tachypnea, tachycardia, worsening oxygenation, and increased minute ventilation. Serial changes in oxygenation may identify pneumonia earlier than other findings and may also be a means to monitor improvement with therapy
  • 18. COMPLICATIONS CAP:- Complications of severe CAP include respiratory failure, shock multiorgan failure, and exacerbation of comorbid illnesses.
  • 19. Three particularly noteworthy conditions are metastatic infection, lung abscess, and complicated pleural effusion. Metastatic infection (e.g., brain abscess or endocarditis) is unusual and requires a high degree of suspicion and a detailed workup for proper treatment. Lung abscess may occur in association with aspiration pneumonia or with infection caused by pathogens such as CA-MRSA, P. aeruginosa, or (rarely) S. pneumoniae. A significant pleural effusion should be tapped for both diagnostic and therapeutic purposes. If the fluid has a pH 1000 U/L or if bacteria are seen or cultured, drainage is needed.
  • 20. CAP:- Apart from death, the major complication of VAP is prolongation of mechanical ventilation, with corresponding increases in the duration of ICU and hospital stay. In rare cases, necrotizing pneumonia (e.g., due to P. aeruginosa or S. aureus) can cause significant pulmonary hemorrhage. Other long-term complications of pneumonia can include long-term oxygen therapy, a catabolic state in a patient already nutritionally at risk, the need for prolonged rehabilitation, andin the elderlyan inability to return to independent function and the need for nursing home placement.