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M. pneumoniae causes tracheobroncitis and “primary
atypical pneumonias”, most frequently in children and adolescents.
Infections are world wide and account for about 20% of all cases of
pneumonia in some cities.
Most infections occur in small groups of
people who have frequent close contact, for example, families, military units, and closed institutions.
The organism is
spread by aerosol transmission from person to person over a period of
several months, with an attack rate of greater than 50% within the
group.
The incubation period is 2 to 3 weeks, and the onset is
insidious.
Clinical features are an initial nonproductive cough
followed by the production of watery or mucoid sputum, fever,
rhinorrhea, chest pain, and generalized myalgia.
The diagnosis is made
by culturing M. pneumoniae in special cell-free media after
inoculating specimens of sputum, throat swab, pleural fluids, or
tissues.
Infections commonly involve the oropharynx,
trachea, bronchi, and lungs, usually causing unilateral pneumonia of
the lower lobe.
The radiographic appearance cannot be
distinguished from that of other nonbacterial pneumonias.
The infection is superficial,
with the organisms attaching to ciliated epithelial cells.
Electron microscopy
reveals that the mycoplasma has a specialized tapered, filamentous tip
with a rodlike core, which may attach the mycoplasma to the epithelial
cell.
M. pneumoniae does not produce endotoxin or exotoxin but
does produce hydrogen peroxide and superoxide (O2-).
Microscopically,
there is a patchy interstitial pneumonia with swollen alveolar lining
cells, bronchiolar walls thickened by congestion and edema and an intraluminal exudate of neutrophils, epithelial cells, and
proteinaceous debris.
The initial infiltrate, predominantly a perivascular and peribronchial cuffing by lymphocytes and macrophages.
The pulmonary changes are often complicated by bacterial superinfection.
In rare instances other organs may be involved
(central nervous system, pancreas, joints, skin, heart, and
pericardium), probably as a result of hematogenous spread.
The diagnosis of infection with M. pneumoniae is
made by detecting specific compliment-fixing antibodies.
The symptoms and signs of mycoplasma pneumonia usually
abate within 10 to 14 days, and recovery is hastened by treatment with
broad-spectrum antibiotics.
Patients continue to shed mycoplasmas for
some times after therapy has been discontinued but usually recover
without sequelae.
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