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Infection of bronchi and bronchioles is most commonly due to viruses.
Adenovirus and measles viruses can cause severe inflammation of bronchioles, which heals by fibrosis leading to permanent damage to lungs (obliterative bronchiolitis).
Bacterial infection of airways is common and precedes development of bronchopneumonia.
Bordetella pertussis causes whooping cough and, in fatal cases, is associated with bronchial and bronchiolar inflammation.

Pneumonia acquired in special environments is associated with unusual organisms
There are three ways of classifying pneumonias,

A clinical classification of pneumonia is best suited for planning investigation and initiating therapy. This is because knowledge of the circumstances in which a person develops a pneumonia is a strong clue as to the likely organism causing infection.
Knowing the pathological pattern, be it bronchopneumonia or lobar pneumonia, gives little clue to the likely cause of infections.

Bronchopneumonia occurs when organisms colonize bronchi and extend into alveoli.
In bronchopneumonia, primary infection centred on bronchi spreads to involve adjacent alveoli, which become filled with an acute inflammatory exudate, and affected areas of lung become consolidated. Initially, consolidation is patchy within the lung (involves lobules) but, if untreated, it becomes confluent (involving lobes).
This pattern of disease, which is most common in infancy and old age, is predisposed by the presence of debility and immobility.
Patients who are immobile develop retention of secretions; these gravitate to the dependent parts of the lungs and become infected, hence bronchopneumonia most commonly involves the lower lobes.
Macroscopically, affected areas of lung are firm, airless and have a dark red or grey appearance. Pus may be present in the peripheral bronchi. Histologically, there is acute inflammation of bronchi, and alveoli contain acute inflammatory exudate.
Involvement of the pleura is common and leads to pleurisy.
If treated, recovery usually involves focal organization of lung by fibrosis.
Common complications include lung abscess, pleural infection (pleurisy), and septicaemia. The causative organisms for this pattern of pneumonia depend on the circumstances predisposing to infection.

In bronchopneumonia, inflammation centred on bronchi spreads out to cause inflammation in the alveoli, which contain acute inflammatory infiltrate. Consolidation is in the dependent parts of the lung.
Hospital-acquired pneumonias are mainly due to Gram-negative bacteria.

Community-acquired pneumonia is usually caused by Gram-positive bacteria Lobar pneumonia occurs when organisms widely colonize alveolar spaces In lobar pneumonia, organisms gain entry to distal air spaces rather than by colonizing bronchi.
Rapid spread through alveolar spaces and bronchioles causes acute inflammatory exudation into air spaces. Macroscopically, the whole of a lobe becomes consolidated and airless.
This pattern of disease is seen in adults.

Vagrants and alcoholics who have poor social and medical care are particularly prone to this pattern of pneumonia, which is often caused by Pneumococcus} or Klebsiella.
Patients with lobar pneumonia are usually severely ill, and there is usually associated bacteraemia. If treated promptly, many patients recover with the lungs returning to normal structure and function by resolution. In other cases the exudate in alveoli is organized, leading to lung scarring and permanent lung dysfunction.
Common complications are development of pleurisy, lung abscess, and septicaemia.
The upper and lower lobes are consolidated compared to the congested but uninvolved middle lobe.
The pleural surfaces over consolidated lobes are covered by a patchy, white, fibrinous
exudate, causing acute pleurisy.
The pleural surfaces over consolidated lobes are covered by a patchy, white,
fibrinous exudate, causing acute pleurisy.

In lobar pneumonia, infection spreads rapidly through air spaces to consolidate a whole lobe. Histologically alveoli are filled with acute inflammatory exudate, which is limited by the pulmonary fissures.
Atypical pneumonia is characterised by inflammation in alveolar septa.
Aspiration pneumonia is caused by chemical and infective damage to lungs
Virus infections of lung cause inflammation of lung interstitium
Most viral infections of the lung cause an interstitial inflammatory response by lymphoid cells (interstitial pneumonitis), which is self-limiting in most cases.
In severe cases, damage to alveolar lining cells leads to alveolar exudation of fibrin similar to that seen in adult respiratory distress syndrome.

Immunosuppressed patients develop opportunistic pneumonias.
The diagnosis and treatment of pneumonia in immunosuppressed patients is becoming increasingly important, particularly with the growing incidence of AIDS.
Infection may be with several types of organism, many being opportunistic infections:
Routine bacterial pathogens responsible for community pneumonias are generally more severe in
immunosuppressed patients.
Mycobacterial infection can be with M. tuberculosis or with atypical mycobacteria.
Viruses, e.g. CMV and herpes simplex.
Fungi, e.g. Candida, Aspergillus
Protozoa, e.g. Pneumocystis carinii
In some instances a diagnosis has to be made on the basis of the invasive techniques of bronchoscopy and analysis of washings, or percutaneous lung aspiration/biopsy.
Lymphocytic interstitial pneumonitis of unknown cause is seen in children with AIDS, but is unusual in adults.

Infection of the lung by Pneumocystis carinii occurs as an opportunistic infection in immunocompromised patients. Histologically, alveoli are filled with a fine, foam-like material, in which the minute bodies of the organism can just be seen as a purple-stained stippling.
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Revised: 02-11-2014.