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Chapter: Medical Microbiology: An Introduction to Infectious Diseases: Mycoplasma and Ureaplasma

Mycoplasmal Pneumonia - Mycoplasma Pneumoniae

M. pneumoniae produces a common form of pneumonia, which tends to occur inany season and has a predilection for younger individuals.

MYCOPLASMA PNEUMONIAE

MYCOPLASMAL PNEUMONIA

M. pneumoniae produces a common form of pneumonia, which tends to occur inany season and has a predilection for younger individuals. The illness is charac-terized by a nonproductive cough, fever, and headache, with radiologic and clini-cal evidence of scattered areas of pneumonia. The course is almost always be-nign, but improvement is accelerated by treatment with non – cell wall – active antimicrobials.

EPIDEMIOLOGY

M. pneumoniae accounts for approximately 10% of all cases of pneumonia. Infection isacquired by droplet spread. Experimental challenges indicate that the human infectious dose is very low, possibly less than 100 colony-forming units. Endemic infections with M. pneumoniae occur worldwide, but they are especially prominent in temperate cli-mates. Epidemics at 4- to 6-year intervals have been noted in both civilian and military populations. The most common age for symptomatic M. pneumoniaeinfection is between 5 and 15 years, and the disease accounts for more than one third of all cases of pneumonia in teenagers, but is also seen in older persons. Infections in children less than 6 months of age are uncommon. 

The disease often appears as a sporadic, endemic illness in families or closed communities because its incubation period is relatively long (2 to 15 days) and because prolonged shedding in nasal secretions may cause infections to be spread over time. In families, attack rates in susceptible individuals approach 60%. Asymptomatic in-fections occur, but most studies have suggested that more than two thirds of infected cases develop some evidence of respiratory tract illness.

PATHOGENESIS

M. pneumoniae infection involves the trachea, bronchi, bronchioles, and peribronchial tis-sues, and may extend to the alveoli and alveolar walls. Initially, the organism attaches to the cilia and microvilli of the cells lining the bronchial epithelium. This attachment is me-diated by a surface mycoplasmal cytadhesin (P1) protein that binds to complex oligosac-charides containing sialic acid found in the apical regions of bronchial epithelial cells. The oligosaccharide receptors are chemically similar to the I antigen on the surface of erythrocytes and are not found on the nonciliated goblet cells or mucus, to which M.pneumoniae does not bind. The organisms interfere with ciliary action and initiate aprocess that leads to desquamation of the involved mucosa and a subsequent inflamma-tory reaction and exudate. The inflammatory response is at first most pronounced in the bronchial and peribronchial tissue and is composed of lymphocytes, plasma cells, and macrophages, which may infiltrate and thicken the walls of the bronchioles and alveoli. Organisms are shed in upper respiratory secretions for 2 to 8 days before the onset of symptoms, and shedding continues for as long as 14 weeks after infection.

IMMUNITY

Both local and systemic specific immune responses occur. Local IgA antibody is pro-duced but disappears 2 to 4 weeks after the onset of the infection. Complement-fixing serum antibody titers reach a peak 2 to 4 weeks after infection and gradually disappear over 6 to 12 months. Nonspecific immune responses to the glycolipids of the outer membrane of the organism often also develop, which can be detrimental to the host. For example, cold hemagglutinins are IgM antibodies that react with the I antigen of human RBCs and are seen in about two thirds of symptomatic patients infected withM. pneumoniae.

Immunity is not complete, and reinfection with M. pneumoniae is common. Clinical dis-ease appears to be more severe in older than in younger children, which has led to the sug-gestion that many of the clinical manifestations of disease are the result of immune re-sponses rather than invasion by the organism. High titers of cold agglutinations may be associated with hemolysis and Raynaud’s phenomena. Antibodies may develop in response to an alteration of the I antigen by the organism or may represent cross-reacting antibodies.


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Medical Microbiology: An Introduction to Infectious Diseases: Mycoplasma and Ureaplasma : Mycoplasmal Pneumonia - Mycoplasma Pneumoniae |


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