Pneumococcal pneumonia is an infection in the lungs caused by bacteria called Streptococcus pneumoniae (also called pneumococcus ). Streptococcus pneumoniae is a Gram-positive coccus that may be found in pairs or in short chains.
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Lobar Pneumonia involves large portion of a lobe or an entire lobe of the lung .
Pneumococcal pneumonia is of diminishing significance because of prompt response to treatment, it is still a significant illness in industrialized nations. In the non-industrialized world it is still a major cause of mortality.
It is commonly a disease of healthy young to middle-aged adults, is rare in infants, and the elderly, and is considerably more common in men than in women.
Alcoholics appear to be particularly vulnerable.
It can infect the upper respiratory tracts of adults and children and can spread to the blood, lungs, middle ear, or nervous system.
Pneumococcal pneumonia is commonly seen in young adults after exposure to cold or after previous respiratory infection. It typically follows a viral infection, often influenza.
The onset of the disease is sudden with fever and chills & ends in crisis after 9-10 days.
Chest pain due to pleural involvement is common, as is hemoptysis, which is characteristically “rusty”, since it is derived from altered blood in alveolar spaces.
Radiologic examination shows alveolar filling in large areas of lung, producing a solid appearance that extend to entire lobes or segments.
Although the symptoms of pneumonia respond rapidly to antibiotic therapy, radiologically the lesion still takes several days to resolve.
Before antibiotic therapy the clinical course was characterized by severe fever, dyspnea, debility, and even loss of consciousness.
The satisfactory resolution of a crisis was the result of a good immune response to the infection. However, often the outcome was not favorable and the patient died.
Sequence of stages is described in 4 phases:
All 4 phases may be seen in different parts of the same lung.
1. Congestion (1-2 days)
2. Red hepatization (2nd-4th day)
3. Gray hepatization (4th-6th day)
4. Resolution (8th-9th day)
In the earliest stage of pneumococcal pneumonia, protein-rich edema fluid containing numerous organisms (Streptococcus pneumoniae) fills the alveoli.
Marked congestion of the capillaries is typical.
Shortly after this congestion occurs there is a massive outpouring of polymorphonuclear leukocytes accompanied by intra-alveolar hemorrhage.
Many of the red blood cells undergo lysis.
These cells, together with polymprphonuclear leukocytes, produce the rusty sputum.
Because the firm consistency of the affected lung is reminiscent of the liver, this stage has been named “red hepatization”.
The next phase, occurring after 2 or more days, depending on the success of treatment, involves the lysis of polymorphonuclear leukocytes and the appearance of macrophages, which phagocytose the fragmented polymorphonuclear leukocytes and other inflammatory debris.
The lung is now no longer congested but still remains firm in this stage of “gray hepatization”.
The alveolar exudates is then removed and the lung gradually returns to normal.
A painful pleuritis is common because the pneumonia often extends to the pleura.
There is usually a small pleural effusion, which resolves.
However, this may occasionally be large and purulent (pyothorax) and may heal with extensive fibrosis.
Rarely, the purulent exudates persists and leads to a loculated collection of pus with fibrous walls (empyema).
Bacteremia is usually present in the early stage and may result in endocarditis or meningitis.
Rarely, the alveolar lesion proceeds to fibrosis, in which case the intra-alveolar exudates becomes organized as fibroblasts leads to a shrunken and firm lobe, a rare complication known as “carnification”.
Another uncommon outcome is a lung abscess.
Little is known about the precise pathogenesis of pneumococcal pneumonia.
The frequency of a previous respiratory tract infection suggests that impairment of airway clearance mechanisms may be important.
It has been suggested that the organisms can multiply rapidly in the increased airway mucus and may then be aspired into the periphery.
The remarkably severe acute inflammation with spreading edema has led to speculation that immunologic mechanisms may be involved
Cause of death: Toxemia with peripheral circulatory failure.
Treatment : Penicillin (penicillin G/amoxicillin) remains the drug of choice for strains that are fully sensitive or have a moderately decreased susceptibility to penicillin, whereas cefotaxime and ceftriaxone are the first-line alternatives in cases with higher levels of resistance.
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