Community acquired acute pneumonia: Morphology Bacterial pneumonia has two patterns of anatomic distribution: lobular bronchopneumonia and lobar pneumonia. Patchy consolidation of the lung is the dominant characteristic of lobular pneumonia. *Lobular pneumonia and bronchopneumonia are similar terms. And fibrinosuppurative consolidation of a large portion of a lobe or of an entire lobe defines lobar pneumonia.
LOBAR PNEUMONIA In lobar pneumonia, four stages of the inflammatory response have classically been described: 1. congestion, 2. red hepatization, 3. gray hepatization, and 4. resolution.
CONGESTION This phase represent the acute inflammatory response to bacterial infection. It lasts for 1-2 days. GROSSLY, the lung is enlarged, heavy, congested, dark red. MICROSCOPICALLY, typical features of acute inflammation are seen. (Dilation and congestion of capillaries, numerous bacteria in the alveolar fluid, eosinophilic edema fluid in the air spaces.)
RED HEPATISATION This phase lasts for 2-4 days. The term hepatisation comes from liver like consistency of affected lobe in cut section. GROSSLY, the affected lobe is red, firm and consolidated. The cut surface reveals airless, granular, red pink liver like consistency. MICROSCOPICALLY, the eosinophilic edema fluid is replaced by fibrin strands and marked cellular exudate of neutrophils and extravasation of red cells is seen.
GREY HEPATISATION This phase lasts for 4-8 days. GROSSLY, affected lobe is firm and heavy. The cut surface is grey, granular and having liver like consistency. The color change begins from hilum and spreads towards the periphery. MICROSCOPICALLY, fibrin strands are more dense; neutrophils and RBC reduce in number; organisms are less numerous and more in degenerative forms.
RESOLUTION It starts at 8 th day and in completed in next 1-3 weeks. But, with antibiotic therapy, resolution begins at 3 rd day. GROSSLY, the affected lobe is gradually restored as a result of liquefaction of fibrin strands by enzymatic action. The process of softening begins centrally and progress peripherally. MICROSCOPICALLY, macrophages are the dominant cells, alveolar capillaries are engorged, progressive removal of cellular exudate, resulting in restoration of normal lung parenchyma with aeration.
BRONCHOPNEUMONIA/ LOBULAR PNEUMONIA It is the infection of terminal bronchioles extending into surrounding alveoli resulting in patchy consolidation of the lung. It is more often multilobar and frequently bilateral and basal because of tendency of secretions accumulating in lower zones due to gravitation. GROSSLY, there are patchy areas of red or grey consolidation affecting as above pattern. MICROSCOPICALLY, 1. Acute bronchiolitis 2. Infiltration by neutrophils in bronchi and bronchioles. 3. Thickening of alveolar septa.
COMPLICATIONS OF CAAcP Tissue destruction and necrosis, causing abscess formation (particularly common with type 3 pneumococci or Klebsiella infections); Spread of infection to the pleural cavity, causing the intrapleural fibrinosuppurative reaction known as empyema; and Bacteremic dissemination to the heart valves, pericardium, brain, kidneys, spleen, or joints, causing metastatic abscesses, endocarditis, meningitis, or suppurative arthritis.
CAAcP: CLINICAL COURSE The major symptoms of community-acquired acute pneumonia are – abrupt onset of high fever, shaking chills, cough productive of mucopurulent sputum; occasional patients may have hemoptysis. The identification of the organism and the determination of its antibiotic sensitivity are the keystones to appropriate therapy. Death may occur as a result of complications or predisposing factors (chronic alcoholism).
COMMUNITY ACQUIRED ATYPICAL PNEUMONIA: CAUSATIVE AGENTS Mycoplasma pneumoniae Chlamydia spp. (C. pneumoniae, C. psittaci, C. trachomatis) Coxiella burnetii (Q fever) Viruses: 1. Respiratory syncytial virus, 2. Parainfluenza virus (children); 3. Influenza A and B (adults); 4. Adenovirus (military recruits); 5. SARS virus
CAAtP: MORPHOLOGY All causal agents produce essentially similar morphologic patterns. The affected areas are red-blue and congested. Predominant is the interstitial nature of the inflammatory reaction, virtually localized within the walls of the alveoli. The alveolar septa are widened and edematous and usually have a mononuclear inflammatory infiltrate of lymphocytes, macrophages, and occasionally plasma cells. In acute cases neutrophils may also be present. Eradication of the infection is followed by reconstitution of the normal architecture of the lung.
CAAtP: CLINICAL COURSE The clinical course of CAAtP is extremely varied, resulting from mild symptoms to severe upper respiratory tract infections. Cough may be absent, and the major manifestations may consist only of - fever, headache, muscle aches, and pains in the legs. The ordinary sporadic form of the disease is usually mild with a low mortality rate, below 1%. But epidemics showed somewhat greater mortality rates.
HOSPITAL ACQUIRED PNEUMONIA DEFINITION: Hospital-acquired pneumonias are defined as pulmonary infections acquired in the course of a hospital stay. INFECTED INDIVIDUALS: They are common in patients with- Severe underlying disease, Immunosuppression, Prolonged antibiotic therapy, or Invasive access devices such as intravascular catheters. Patients on mechanical ventilation are at particularly high risk.
ASPIRATION PNEUMONIA: PATHOGENESIS Aspiration pneumonia occurs in markedly debilitated patients or those who aspirate gastric contents either while unconscious (e.g., after a stroke) or during repeated vomiting. These patients have abnormal gag and swallowing reflexes that predispose to aspiration. The resultant pneumonia is partly chemical because of the extremely irritating effects of the gastric acid, and partly bacterial (from the oral flora). Typically, more than one organism is recovered on culture, aerobes being more common than anaerobes. This type of pneumonia is often necrotizing, pursues a fulminant clinical course, and is a frequent cause of death. In those who survive, lung abscess is a common complication.
LUNG ABSCESS DEFINITION: The term pulmonary abscess describes a local suppurative process within the lung, characterized by necrosis of lung tissue.
LA: CAUSATIVE AGENTS Although under appropriate circumstances any pathogen can produce an abscess, the commonly isolated organisms include aerobic and anaerobic streptococci, S. aureus, and a host of gram-negative organisms. Anaerobic organisms normally found in the oral cavity, including members of the Bacteroides, Fusobacterium, and Peptococcus species, are the exclusive isolates in about 60% of cases.
LA: PATHOGENESIS Aspiration of infective material (the most frequent cause): This is particularly common in acute alcoholism, coma, anesthesia, sinusitis, gingivodental sepsis, and debilitation in which the cough reflexes are depressed. Antecedent primary lung infection: Post-pneumonic abscess formations are usually associated with S. aureus, K. pneumoniae, and the type 3 pneumococcus. Posttransplant or otherwise immunosuppressed individuals are at special risk. Septic embolism: Infected emboli from thrombophlebitis in any portion of the systemic venous circulation or from the vegetations of infective bacterial endocarditis on the right side of the heart are trapped in the lung. Neoplasia: Secondary infection is particularly common in the bronchopulmonary segment obstructed by a primary or secondary malignancy (postobstructive pneumonia).
Miscellaneous: Direct traumatic penetrations of the lungs; spread of infections from a neighboring organ, such as suppuration in the esophagus, spine, subphrenic space, or pleural cavity; and hematogenous seeding of the lung by pyogenic organisms all may lead to lung abscess formation. When all these causes are excluded, there are still cases in which no reasonable basis for the abscess formation can be identified. These are referred to as primary cryptogenic lung abscesses.
LUNG ABSCESS: MORPHOLOGY(1) SIZE: Abscesses vary in diameter from lesions of a few milimeters to large cavities of 5 to 6 cm. DISTRIBUTION: Pulmonary abscesses due to aspiration are more common on the right (because of the more vertical right main bronchus) and are most often single. Abscesses that develop in the course of pneumonia or bronchiectasis are usually multiple, basal, and diffusely scattered. Septic emboli and pyemic abscesses are multiple and may affect any region of the lungs.
LUNG ABSCESS: MORPHOLOGY(2) The cardinal histologic change in all abscesses is suppurative destruction of the lung parenchyma within the central area of cavitation. Continued infection leads to large, green-black, multilocular cavities with poor demarcation of their margins, designated as gangrene of the lung. In chronic cases considerable fibroblastic proliferation produces a fibrous wall.
PYEMIC LUNG ABSCESS WITH TOTAL DESTRUCTION OF UNDERLYING PARENCHYMAL TISSUE
LUNG ABSCESS: CLINICAL COURSE The manifestations of pulmonary abscesses are much like those of bronchiectasis and are characterized principally by cough, fever, and copious amounts of foul-smelling purulent or sanguineous sputum. Fever, chest pain, and weight loss are common. Clubbing of the fingers and toes may appear within a few weeks after the onset of an abscess. Diagnosis of this condition can be only suspected from the clinical findings and must be confirmed radiologically. Whenever an abscess is discovered in older individuals, it is important to rule out an underlying carcinoma, because this is present in 10% to 15% of cases. Complications include extension of the infection into the pleural cavity, hemorrhage, the development of brain abscesses or meningitis from septic emboli, and (rarely) secondary amyloidosis (type AA).
IN SHORT: CHRONIC PNEUMONIAS CAUSED BY FUNGI: HISTOPLASMOSIS In the lungs of otherwise healthy adults, Histoplasma infections produce epithelioid cell granulomas, which usually undergo caseation necrosis and coalesce to produce large areas of consolidation but may also liquefy to form cavities (seen in patients with COPD). With spontaneous or drug control of the infection, these lesions undergo fibrosis and concentric calcification (tree-bark appearance. Histologic differentiation from tuberculosis, sarcoidosis, and coccidioidomycosis requires identification of the 3- to 5-μm thin-walled yeast forms that may persist in tissues for years.
HISTOPLASMOSIS A, Laminated Histoplasma granuloma of the lung B, Histoplasma capsulatum yeast forms fill phagocytes in the lung of a patient with disseminated histoplasmosis (silver stain).
BLASTOMYCOSIS CAUSATIVE AGENT: Blastomyces dermatitidis MORPHOLOGY: In the normal host the lung lesions of blastomycosis are suppurative granulomas. In tissue, B. dermatitidis is a round, 5- to 15-μm yeast cell that divides by broad-based budding. It has a thick, double -contoured cell wall and multiple nuclei.
A, Rounded budding yeasts, larger than neutrophils, are present. Note the characteristic thick wall and nuclei (not seen in other fungi). B, Silver stain.
COCCIDIOIDOMYCOSIS CAUSATIVE AGENT: Coccidioides immitis MORPHOLOGY: C. immitis is present as thick-walled, nonbudding spherules 20 to 60 μm in diameter, often filled with small endospores. A pyogenic reaction is superimposed when the spherules rupture to release the endospores
Coccidioidomycosis with intact and ruptured spherules.
PULMONARY DISEASE IN HIV INFECTION: CLINICAL FEATURES WITH DIAGNOSTIC CRITERIA Despite the emphasis on opportunistic infections, it must be remembered that bacterial lower respiratory tract infection caused by the usual pathogens is one of the most serious pulmonary disorders in HIV infection. The implicated organisms include S. pneumoniae, S. aureus, H. influenzae, and gram-negative rods.
DIAGNOSTIC CRITERIA The CD4+ T-cell count can define the risk of infection with specific organisms. As a rule of thumb, bacterial and tubercular infections are more likely at higher CD4+ counts (>200 cells/mm 3 ). Pneumocystis pneumonia usually strikes at CD4+ counts below 200 cells/mm 3, while cytomegalovirus and Mycobacterium avium complex infections are uncommon until the very late stages of immunosuppression (CD4+ counts <50 cells/mm 3 ).