Viral Pneumoni Dari 18

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    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.

    --

    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.

    --

    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 ).

    --

    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.

    --

    The histologic features of infl uenza

    pneumonia are epithelial necrosis of the

    airways with submucosal chronic infl ammation.

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    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

    ( 1214 ). The bronchiolitis may be necrotizing

    and result in a necrotizing bronchopneumonia

    similar to that seen in severe

    herpes simplex infection ( 13 ) ( Fig 2 ).

    --

    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

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    produce giant cell pneumonia with diffuse

    alveolar damage indistinguishable

    from that caused by measles pneumonia.

    --

    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 ).

    ---

    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 ).

    --

    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).

    --

    Pneumonia is also increasingly prevalent

    in patients with specifi c comorbidities

    or risk factors, including smoking,

    chronic obstructive pulmonary disease,

    asthma, diabetes mellitus, malignancy,

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    heart failure, neurologic diseases, narcotic

    and alcohol use, and chronic liver

    disease.

    --

    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.

    --

    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.

    --

    Although most attention traditionally

    focuses on bacterial causes of severe

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    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