Page 505 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster
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Figure 12–34 Viral pneumonia. The thickened alveolar walls are infil- Pulmonary Infections 491
trated with lymphocytes and some plasma cells, which are spilling over
into alveolar spaces. Note focal alveolar edema in the center and early Influenza Virus Type A/H1N1 Infection
fibrosis at upper right.
In March 2009, a novel swine-origin influenza A virus,
Identifying the causative agent can be difficult. Tests for strain H1N1, was identified, which spread in the United
Mycoplasma antigens and polymerase chain reaction (PCR) States and worldwide, leading to a pandemic affecting
testing for Mycoplasma DNA are available. As a practical more than half a million patients, with more than 6200
matter, patients with community-acquired pneumonia for deaths by November 2009.
which a bacterial agent seems unlikely are treated with a
macrolide antibiotic effective against Mycoplasma and Chla- Most patients have only a self-limiting illness, with viral
mydia pneumoniae, because these are the most common replication limited to pharynx and tracheobronchial tree.
pathogens producing treatable disease. Pneumonia occurs in severe disease. Comorbid conditions
such as obesity, heart disease, and COPD are seen in fatal
Influenza Infections cases. Unlike the usual seasonal influenza in which older
patients are more at risk of dying, the H1N1 pandemic
Perhaps no other communicable disorder causes as much killed only a few patients over 60 years of age, suggesting
public distress in the developed world as the threat of an that immunity is achieved with previous exposure. Patho-
influenza epidemic. The influenza virus is a single-stranded logic findings at autopsy include acute tracheobronchitis,
RNA virus, bound by a nucleoprotein that determines the bronchiolitis, diffuse alveolar damage, pulmonary throm-
virus type—A, B, or C. The spherical surface of the virus is bosis, and alveolar hemorrhage. In addition, approximately
a lipid bilayer containing the viral hemagglutinin and half have bacterial superinfection.
neuraminidase, which determine the subtype (e.g., H1N1,
H3N2). Host antibodies to the hemagglutinin and neur- S U M M A RY
aminidase prevent and ameliorate, respectively, future Acute Pneumonias
infection with the influenza virus. The type A viruses infect
humans, pigs, horses, and birds and are the major cause of • S. pneumoniae (the pneumococcus) is the most common
pandemic and epidemic influenza infections. Epidemics of cause of community-acquired acute pneumonia, and the
influenza occur through mutations of the hemagglutinin distribution of inflammation is usually lobar.
and neuraminidase antigens that allow the virus to escape
most host antibodies (antigenic drift). Pandemics, which last • Morphologically, lobar pneumonias evolve through four
longer and are more widespread than epidemics, may stages: congestion, red hepatization, gray hepatization, and
occur when both the hemagglutinin and neuraminidase are resolution.
replaced through recombination of RNA segments with
those of animal viruses, making all animals susceptible to • Other common causes of acute pneumonias in the com-
the new influenza virus (antigenic shift). Commercially munity include H. influenzae and M. catarrhalis (both associ-
available influenza vaccines provide reasonable protection ated with acute exacerbations of COPD), S. aureus (usually
against the disease, especially in vulnerable infants and secondary to viral respiratory infections), K. pneumoniae
elderly persons. A particular subtype of avian influenza— (observed in patients who are chronic alcoholics), P. aeru-
“bird flu,” caused by strain H5N1—has caused massive ginosa (seen in persons with cystic fibrosis, in burn victims,
outbreaks in domesticated poultry in parts of Southeast and in patients with neutropenia), and L. pneumophila, seen
Asia in the last several years; this strain is particularly particularly in organ transplant recipients.
dangerous, since it has the potential to “jump” to humans
and thereby cause a worldwide influenza pandemic. • In contrast with acute pneumonias, atypical pneumonias are
characterized by respiratory distress out of proportion
to the clinical and radiologic signs, and by inflammation
that is predominantly confined to alveolar septa, with
generally clear alveoli.
• The most common causes of atypical pneumonias include
those caused by M. pneumoniae, viruses including influenza
viruses types A and B, human metapneumovirus, C. pneu-
moniae, and C. burnetii (agent of Q fever).
Hospital-Acquired Pneumonias
Nosocomial, or hospital-acquired, pneumonias are defined
as pulmonary infections acquired in the course of a hospi-
tal stay. The specter of nosocomial pneumonia places an
immense burden on the burgeoning costs of health care, in
addition to the expected adverse impact on illness outcome.
Nosocomial infections are common in hospitalized persons
with severe underlying disease, those who are immuno-
suppressed, or those on prolonged antibiotic regimens.
Those on mechanical ventilation represent a particularly
high-risk group, and infections acquired in this setting
