LUNG ABSCESS  Lung abscess is a localised area of necrosis of lung tissue with suppuration.

 It is of 2 types:

 - Primary lung abscess that develops in an otherwise normal lung. The commonest cause is aspiration of infected material.

 - Secondary lung abscess that develops as a complication of some other disease of the lung or from another site


 The microorganisms commonly isolated from the lungs in lung abscess are streptococci, staphylococci and various gram-negative organisms. These are introduced into the lungs from one of the following mechanisms:

 1.   Aspiration of infected foreign material.

 2. Preceding bacterial infection.

 3.  Bronchial obstruction.

 4. Septic embolism.

 5. Miscellaneous (i) Infection in pulmonary infarcts, (ii) Amoebic abscesses, (iii) Trauma to the lungs. (iv) Direct extension from a suppurative focus.

Abscesses may be of variable size from a few millimeters to large cavities, 5 to 6 cm in diameter. The cavity often contains exudate. An acute lung abscess is initially surrounded by acute pneumonia and has poorly-defined ragged wall. With passage of time, the abscess becomes chronic and develops fibrous wall.

Microscopic Examination

The characteristic feature is the destruction of lung parenchyma with suppurative exudate in the lung cavity. The cavity is initially surrounded by acute inflammation in the wall but later there is replacement by exudate of lymphocytes, plasma cells and macrophages. In more chronic cases, there is considerable fibroblastic proliferation forming a fibrocollagenic wall.

Related Questions Respiratory System


Causative organism

-Mycobacterium tuberculosis 
-Strict aerobe 
-Pathogenic strains
-hominis, bovis, avium, murine& cold blooded vertebrate strain 

Koch’s bacillus
-small slender, rod like bacillus, 4umnon-motile, aerobic -high lipid content 
-divides every 16 to 20 hours, an extremely slow rate 
-stains very weakly Gram-positive or does not retain dye due to the high lipid & mycolicacid content of its cell wall 
-can withstand weak disinfectant and survive in a dry state for weeks. 

Demonstrated by 
-Fluorescent dye method 
-Culture in LJ media 
-Guinea pig inoculation

Modes of transmission

Inhalation , Ingestion, Inoculation , Transplacental

Route Spread 
Local , Lymphatic , Haematogenous , By natural passages, 


- Anti‐mycobacterial CMI, confers resistance to bacteria → dev. of HS to tubercular Ag 
- Bacilli enters macrophages 
- Replicates in phagosomeby blocking fusion of phagosome&  lysosome, continues for 3 weeks →bacteremiabut  asymptomatic 
- After 3 wks, T helper response is mounted by  IL‐12 produced  by macrophages 
- T cells produce IFN, activates macrophages → bactericidal  activity, structural changes 
- Macrophages secrete TNF→ macrophage recruitment,  granuloma& necrosis

Fate of granuloma 
- Caseousmaterial undergo liquefaction---cold abscess 
- Bones, joints, lymph nodes & epididymis---sinuses are formed & sinus tract lined by tuberculousgranulation tissue 
- Dystrophic calcification

Types of TB

1. Primary Pulmonary TB 
2. secondary TB (miliary, fibrocaseous, cavitary) 
3. Extra-pulmonary TB (bone, joints, renal, adrenal, skin… )

Primary TB
Infection in an individual who has not been previously infected or immunised 
Primary complex 
    -lungs, hilarlymph nodes 
    -tonsils, cervical lymph nodes 
    -small intestine, mesenteric lymph nodes

Primary TB
In the lung, Ghon’scomplex has 3 components: 
1. Pulmonary component -Inhalation of airborne droplet ~ 3 microns. 
    -Bacilli locate in the subpleuralmid zone of lung 
    -Brief acute inflammation –neutrophils. 
    -5-6 days-invoke granulomaformation. 
    -2 to 8 weeks –healing –single round ;1-1.5 cm-Ghon focus. 
2. Lymphatic vessel component 
3. Lymph node component

Fate of primary tuberculosis

- Lesions heal by fibrosis, may undergo calcification, ossification 
    -a few viable bacilli may remain in these areas  
    -bacteria goes into a dormant state, as long as the person's immune system remains active 
- Progressive primary tuberculosis: primary focus continues to grow & caseousmaterial disseminated to other parts of lung 
- Primary miliarytuberculosis: bacilli may enter circulation through erosion of blood vessel 
- Progressive secondary tuberculosis: healed lesions are reactivated, in children & in lower resistance

Secondary tuberculosis

-Post-primary/ reinfection/ chronic TB 
-Occurs in immunized individuals. 
-Infection acquired from 

    -endogenous source/ reactivation 
    -exogenous source/ reinfection 

-when immune system is depressed 
-Common in low prevalence areas. 
-Occurs in 10-15% of patients 
-Slowly progressive (several months) 

-when large innoculum of bacteria occurs 
-In areas with increased personal contact

Secondary TB

-Sites-Lungs 1-2 cm apical consolidation with caseation 
-Other sites -tonsils, pharynx, larynx, small intestine & skin

Fate of secondary tuberculosis

•Heal with fibrous scarring & calcification 
•Progressive secondary pulmonary tuberculosis: 

a) aneurysm of arteries–hemoptysis 
b) bronchopleuralfistula 
c) tuberculousempyema 


• Millet like, yellowish, firm areas without caseation 
• Extensive spread through lympho-hematogenousroute 
• Low immunity 
• Pulmonary involvement via pulmonary artery 
• Systemic through pulmonary vein: 
    -LN: scrofula, most common 
    -kidney, spleen, adrenal, brain, bone marrow

Signs and Symptoms of Active TB

• Pulmonary-cough, hemoptysis, dyspnea 
• Systemic: 
• fever 
• night sweats 
• loss of appetite 
• weight loss 
• chest pain,fatigue 

•If symptoms persist for at least 2 weeks, evaluate for possible TB infection


•Sputum-Ziehl Neelsen stain –10,000 bacilli, 60% sensitivity 
    -release of acid-fast bacilli from cavities intermittent. 
    -3 negative smears : low infectivity 

•Culture most sensitive and specific test.
     -Conventional Lowenstein Jensen media-10 wks. 
     -Liquid culture: 2 weeks 

•Automated techniques within days 
    should only be performed by experienced laboratories (10 bacilli) 

•PPD for clinical activity / exposure sometime in life 
•X-ray chest 

PPD Tuberculin Testing

- Read after 72 hours. 
- Indurationsize -5-10 mm 
- Does not d/s b/w active and latent infection 
- False +: atypical mycobacterium 
- False -: malnutrition, HD, viral, overwhelming infection, immunosuppression 
- BCG gives + result.

Tuberculosis Atypical mycobacteria 

- Photochromogens---M.kansasii 
- Scotochromogens---M.scrofulaceum 
- Non-chromogens---M.avium-intracellulare 
- Rapid growers---M.fortuitum, M.chelonei

5 patterns of disease 

- Pulmonary—M.kansasii, M.avium-intracellulare 
- Lymphadenitis----M.avium-intracellulare, M.scrofulaceum 
- Ulcerated skin lesions----M.ulcerans, M.marinum 
- Abscess----M.fortuitum, M.chelonei 
- Bacteraemias----M.avium-intracellulare as in AIDS

Other lung diseases


1. Sarcoidosis

a. More common in African-Americans.

b. Associated with the presence of noncaseating granulomas.

Sarcoidosis is an immune system disorder characterised by non-necrotising granulomas (small inflammatory nodules). Virtually any organ can be affected, however, granulomas most often appear in the lungs or the lymph nodes.

Signs and symptoms

  • Sarcoidosis is a systemic disease that can affect any organ. Common symptoms are vague, such as fatigue unchanged by sleep, lack of energy, aches and pains, dry eyes, blurry vision, shortness of breath, a dry hacking cough or skin lesions. The cutaneous symptoms are protean, and range from rashes and noduli (small bumps) to erythema nodosum or lupus pernio
  • Renal, liver, heart or brain involvement may cause further symptoms and altered functioning. Manifestations in the eye include uveitis and retinal inflammation
  • Sarcoidosis affecting the brain or nerves is known as neurosarcoidosis.
  • Hypercalcemia (high calcium levels) and its symptoms may be the result of excessive vitamin D production
  • Sarcoidosis most often manifests as a restrictive disease of the lungs, causing a decrease in lung volume and decreased compliance (the ability to stretch). The vital capacity (full breath in, to full breath out) is decreased, and most of this air can be blown out in the first second. This means the FEV1/FVC ratio is increased from the normal of about 80%, to 90%.


Corticosteroids, most commonly prednisone

2. Cystic fibrosis

a. Transmission: caused by a genetic mutation (nucleotide deletion) on chromosome 7, resulting in abnormal chloride channels.

b. The most common hereditary disease in Caucasians.

c. Genetic transmission: autosomal recessive.

d. Affects all exocrine glands. Organs affected include lungs, pancreas, salivary glands, and intestines. Thick secretions or mucous plugs are

seen to obstruct the pulmonary airways and intestinal tracts.

e. Is ultimately fatal.

f. Diagnostic test: sweat test—sweat contains increased amounts of chloride.

3. Atelectasis

a. Characterized by collapse of the alveoli.

b. May be caused by a deficiency of surfactant and/or hypoventilation of alveoli.

Pulmonary Hypertension 

Sustained elevation of mean pulmonary arterial pressure.

Elevated pressure, through endothelial cell dysfunction, produces structural changes in the pulmonary vasculature. These changes ultimately decrease pulmonary blood flow and stress the heart to the point of failure. Based on etiology, pulmonary hypertension is divided into two categories.

Primary (idiopathic): The cause is unknown.
Secondary: The hypertension is secondary to a variety of conditions which increase pulmonary blood flow or increase resistance to blood flow. Example: Interstitial fibrosis.
The changes involve large and small pulmonary blood vessels and range from mild to severe. The major changes include atherosclerosis, striking medial hypertrophy and intimal fibrosis of small arteries and arterioles, and plexogenic arteriopathy. Refer to Figure 15-7 in your textbook.

Dyspnea and fatigue eventually give way to irreversible respiratory insufficiency, cyanosis and cor pulmonale.

Pulmonary embolism

A pulmonary embolism (thromboembolism) occurs when a blood clot, generally a venous thrombus, becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs.

Clinical presentation

Signs of PE are sudden-onset dyspnea (shortness of breath, 73%), tachypnea (rapid breathing, 70%), chest pain of "pleuritic" nature (worsened by breathing, 66%), cough (37%), hemoptysis (coughing up blood, 13%), and in severe cases, cyanosis, tachycardia (rapid heart rate), hypotension, shock, loss of consciousness, and death. Although most cases have no clinical evidence of deep venous thrombosis in the legs, findings that indicate this may aid in the diagnosis.


The gold standard for diagnosing pulmonary embolism (PE) is pulmonary angiography

An electrocardiogram may show signs of right heart strain or acute cor pulmonale in cases of large PEs

In massive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the heart is unable to match the pressure.


Acutely, supportive treatments, such as oxygen or analgesia

In most cases, anticoagulant therapy is the mainstay of treatment. Heparin or low molecular weight heparins are administered initially, while warfarin therapy is given

Pulmonary edema

Pulmonary edema is swelling and/or fluid accumulation in the lungs. It leads to impaired gas exchange and may cause respiratory failure.

Signs and symptoms

Symptoms of pulmonary edema include difficulty breathing, coughing up blood, excessive sweating, anxiety and pale skin. If left untreated, it can lead to death, generally due to its main complication of acute respiratory distress syndrome.


physical examination: end-inspiratory crackles during auscultation (listening to the breathing through a stethoscope) can be due to pulmonary edema. The diagnosis is confirmed on X-ray of the lungs, which shows increased vascular filling and fluid in the alveolar walls.

Low oxygen saturation and disturbed arterial blood gas readings may strengthen the diagnosis


Cardiogenic causes:

  1. Heart failure
  2. Tachy- or bradyarrhythmias
  3. Severe heart attack
  4. Hypertensive crisis
  5. Excess body fluids, e.g. from kidney failure
  6. Pericardial effusion with tamponade

Non-cardiogenic causes, or ARDS (acute respiratory distress syndrome):

  1. Inhalation of toxic gases
  2. Multiple blood transfusions
  3. Severe infection
  4. Pulmonary contusion, i.e. high-energy trauma
  5. Multitrauma, i.e. severe car accident
  6. Neurogenic, i.e. cerebrovascular accident (CVA)
  7. Aspiration, i.e. gastric fluid or in case of drowning
  8. Certain types of medication
  9. Upper airway obstruction
  10. Reexpansion, i.e. postpneumonectomy or large volume thoracentesis
  11. Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
  12. Lack of proper altitude acclimatization.


When circulatory causes have led to pulmonary edema, treatment with loop diuretics, such as furosemide or bumetanide, is the mainstay of therapy. Secondly, one can start with noninvasive ventilation. Other useful treatments include glyceryl trinitrate, CPAP and oxygen.