The respiratory tract is the most typical site of infection by pathogenic microorganisms. Pneumonia accounts for 1.2 million hospitalizations every year in the United States, with an estimated 58,000 deaths. Pneumonia, together with influenza, is the leading cause of death from an infectious illness within the United States.
Diagnosis and management of pneumonia need knowledge of host risk elements, potential infectious agents, and environmental exposures. Pneumonia is an infection from the lung tissue caused by a number of different bacteria, viruses, parasites, and fungi, resulting in inflammation of the lung parenchyma and accumulation of an inflammatory exudate within the airways.
Infection usually begins in the alveoli, with secondary spread towards the interstitium, resulting in consolidation and impaired gas exchange. Infection can also extend towards the pleural space, causing pleurisy (inflammation of the pleura, characterized by pain on inspiration). The exudative response from the pleura to pneumonia is termed parapneumonic effusion, which itself can become infected and develop into frank pus (empyema).
Despite technologic advances in diagnosis, a particular causative agent isn’t identified in as numerous as 50% of instances of community-acquired pneumonia. Even in instances in which a microbiologic diagnosis is made, there’s generally a delay of several days before the pathogen can be identified and antibiotic susceptibility determined.
Symptoms are nonspecific and do not reliably differentiate the various causes of pneumonia. Therefore, knowledge of one of the most common etiologic organisms is crucial in determining rational empiric antibiotic regimens. Bacterial causes of community pneumonia vary by comorbid illness and severity of pulmonary infection S pneumoniae may be the most typical organism isolated in community-acquired pneumonia in both immunocompetent and immunocompromised people.
A number of additional organisms require special consideration in specific hosts or simply because of public wellness significance. Understanding and identifying affected person chance factors (eg, smoking, HIV infection) and host defense mechanisms (cough reflex, cell-mediated immunity) focuses attention on the most likely etiologic agents, guides empiric therapy, and suggests possible interventions to reduce further chance.
For instance, sufferers who have suffered strokes and have impaired ability to protect their airways are at risk for aspirating oropharyngeal secretions. Precautions for example avoiding thin liquids in these patients might reduce the chance of future lung infections. Likewise, an HIV-infected affected person with a low CD4 lymphocyte count is at chance for pneumocystic pneumonia and should be given prophylactic antibiotics.
Even though pneumonia is really a relatively common illness, it occurs infrequently in immunocompetent people. This can be attributed towards the effectiveness of host defenses, such as anatomic barriers and cleansing mechanisms within the nasopharynx and upper airways and local humoral and cellular factors within the alveoli.
Normal lungs are sterile below the very first major bronchial divisions. Pulmonary pathogens reach the lungs by one of four routes: (1) direct inhalation of infectious respiratory droplets, (2) aspiration of oropharyngeal contents, (three) direct spread along the mucosal membrane surface from the upper towards the lower respiratory system, and (4) hematogenous spread.
Incoming air with suspended particulate matter is subjected to turbulence within the nasal passages and then to abrupt changes in direction as the airstream is diverted through the pharynx and along the branches from the tracheobronchial tree. Particles larger than 10 mm are trapped within the nose or pharynx;
those with diameters of 2-9 mm are deposited about the mucociliary blanket; only smaller particles achieve the alveoli. M tuberculosis and Legionella pneumophila are examples of bacteria that are deposited directly within the lower airways through inhalation of small airborne particles.
Bacteria trapped in the upper airways can colonize the oropharynx and subsequently be transported into the lungs either by “microaspiration” or by overt aspiration via an open epiglottis (eg, in sufferers who lose consciousness after excessive alcohol intake).
The respiratory epithelium has unique properties for fighting off infection. Epithelial cells are covered with beating cilia blanketed by a layer of mucus. Every cell has about 200 cilia that beat up to 500 times/min, moving the mucus layer upward toward the larynx. The mucus itself contains antimicrobial compounds such as lysozyme and secretory IgA antibodies.
Chronic cigarette smokers have decreased mucociliary clearance secondary to damage of cilia and should, therefore, rely a lot more heavily on the cough reflex to clear aspirated material, excess secretions, and foreign bodies. Bacteria that achieve the terminal bronchioles, alveolar ducts, and alveoli are inactivated primarily by alveolar macrophages and neutrophils.
Opsonization from the microorganism by complement and antibodies enhances phagocytosis by these cells. Impairment at any level of host defenses increases the chance of developing pneumonia. Children with cystic fibrosis have defective ciliary activity and are prone to develop recurrent sinopulmonary infections, particularly with S aureus and P aeruginosa.
Sufferers with neutropenia, whether acquired or congenital, are also susceptible to lung infections with gram-negative bacteria and fungi. Antigenic stimulation of T cells leads towards the production of lymphokines that activate macrophages with enhanced bactericidal activity. HIV-infected sufferers have depleted CD4 T lymphocyte counts and are pre-disposed to a variety of bacterial (including mycobacterial) and fungal infections.
Most patients with pneumonia have fever, cough, tachypnea, tachycardia, and an infiltrate on chest x-ray film. Extrapulmonary manifestations that might supply clues to the etiologic agents consist of pharyngitis (Chlamydia pneumoniae), erythema nodosum rash (fungal and mycobacterial infections), and diarrhea (Legionella).
The following questions aid in guiding empiric therapy for a affected person who presents with signs or symptoms consistent with pneumonia: (1) Is this pneumonia community acquired or healthcare acquired (eg, hospital, nursing house)? (2) Is this affected person immunocompromised (HIV infected, a transplant recipient)? (three) Is this affected person an injection drug user?
(4) Has this patient had a recent alteration in consciousness (suggestive of aspiration)? (5) Are the symptoms acute (days) or chronic (weeks to months)? (6) Has this patient lived in or traveled through geographic areas associated with particular endemic infections (histoplasmosis, coccidioidomycosis)?
(7) Has this affected person had recent zoonotic exposures related to pulmonary infections (psittacosis, Q fever)? (8) Could this affected person have a contagious infection of public wellness significance (tuberculosis)? (9) Could this patient’s pulmonary virus be associated with a common source exposure (Legionella or influenza outbreak)?