Gambaran radiologis pneumonia virus secara umum

Clinically, viral pneumonia in adults can be divided into two groups: so-called atypical
pneumonia in otherwise healthy hosts and viral pneumonia in immunocompromised hosts ( 5 )
Infl uenza virus types A and B account for most viral pneumonias in immunocompetent
adults ( 5 ). It has been considered that clinical history,
results of physical examination,
and imaging features cannot enable the
prediction of the etiologic agent.
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Various histopathologic patterns of
lung injury have been described in viral
pneumonia. Although some of these
patterns may be relatively unique to a
specifi c clinical context, others are nonspecifi
c with respect to either the cause
or pathogenesis.
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Viruses can result in several pathologic
forms of lower respiratory tract
infection, including tracheobronchitis,
bronchiolitis, and pneumonia.
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Most respiratory viruses damage cells
directly through cytopathic effects mediated
by means of either viral-directed
cell lysis or the inhibition of host cell
RNA, protein, and DNA synthesis. Other
viruses (eg, cytomegalovirus [CMV], adenovirus,
or herpesvirus) may produce
specifi c nuclear changes or characteristic
cytoplasmic inclusions ( 11 ) ( Fig 1 ).
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Cytopathic respiratory viruses (eg,
infl uenza, adenovirus, and herpesvirus
group) cause a virus-specifi c lung injury
pattern. Infl uenza virus affects the epithelium
diffusely and, in severe cases, results
in necrotizing bronchitis and/or bronchiolitis
and diffuse alveolar damage.
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The histologic features of infl uenza
pneumonia are epithelial necrosis of the
airways with submucosal chronic infl ammation.
Fatal infl uenza pneumonia represents
a necrotizing bronchiolitis with
diffuse alveolar damage, which can be
hemorrhagic.
Adenovirus has its greatest effect in
the terminal bronchioles and may produce
bronchiolitis or even bronchiectasis
( 12 14 ). The bronchiolitis may be necrotizing
and result in a necrotizing bronchopneumonia
similar to that seen in severe
herpes simplex infection ( 13 ) ( Fig 2 ).
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In immunocompetent individuals,
RSV and parainfl uenza viruses may produce
necrotizing bronchiolitis characterized
by exudates within bronchiolar
lumen, infl ammatory cells in the wall
of bronchioles, a peribronchiolar reaction
with chronic infl ammatory cells, and
exudate in alveoli. In immunocompromised
patients, parainfl uenza viruses
produce giant cell pneumonia with diffuse
alveolar damage indistinguishable
from that caused by measles pneumonia.
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The predominant pathologic process
of hantavirus pulmonary syndrome and
severe acute respiratory syndrome (SARS)
is diffuse alveolar damage and diffuse
lung disease characterized histologically
by interstitial edema and central alveolar
fi lling ( 18 , 19 ) ( Fig 5 ).
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The radiologic fi ndings refl ect the
variable extent of the histopathologic
features, which include diffuse alveolar
damage (intraalveolar edema, fi brin,
and variable cellular infi ltrates with a
hyaline membrane), intraalveolar hemorrhage,
and interstitial (intrapulmonary
or airway) infl ammatory cell infi ltration
( 20 ).
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Manifestasi klinik infeksi virus
The clinical signs and symptoms of viral
pneumonia are often nonspecifi c, and
the clinical course of infection will be
highly dependent on the overall immune
status of the host ( 3 ).
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The possibility of pneumonia should
be considered in any patient who has new
respiratory symptoms (including cough,
sputum, or dyspnea), particularly when
these symptoms are accompanied by fever
or abnormalities at physical examination
of the chest (eg, rhonchi and rales).
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Pneumonia is also increasingly prevalent
in patients with specifi c comorbidities
or risk factors, including smoking,
chronic obstructive pulmonary disease,
asthma, diabetes mellitus, malignancy,
heart failure, neurologic diseases, narcotic
and alcohol use, and chronic liver
disease.
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A thorough physical examination, posteroanterior
and lateral chest radiography,
and a blood leukocyte count with
a differential cell count should be performed
when pneumonia is suspected.
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Even with intensive laboratory investigation,
the specifi c microbiologic cause can be established with certainty
only in approximately 50% of patients
with pneumonia. The probable predominant
organism varies with the hosts epidemiologic
factors, the severity of illness,
and the laboratory approach used to establish
the diagnosis.
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Although most attention traditionally
focuses on bacterial causes of severe
community-acquired pneumonia, viruses
can also cause serious lower respiratory
tract infections. The predominant respiratory
viruses that can cause severe
pneumonia include infl uenza and RSV