Page 504 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster

490 C H A P T E R 12 Lung organisms, Mycoplasma pneumoniae being the most common.
Mycoplasma infections are particularly common among
• Klebsiella-related pneumonia frequently afflicts debili- children and young adults. They occur sporadically or as
tated and malnourished persons, particularly chronic local epidemics in closed communities (schools, military
alcoholics. camps, prisons). Other etiologic agents are viruses, includ-
ing influenza types A and B, the respiratory syncytial
• Thick and gelatinous sputum is characteristic, because viruses, human metapneumovirus, adenovirus, rhinovi-
the organism produces an abundant viscid capsular ruses, rubeola virus, and varicella virus, and Chlamydia
polysaccharide, which the patient may have difficulty pneumoniae and Coxiella burnetii (the agent of Q fever)
coughing up. (Table 12–6). Nearly all of these agents can also cause a
primarily upper respiratory tract infection (“common
Pseudomonas aeruginosa cold”).
• Although discussed here with community-acquired
The common pathogenetic mechanism is attachment of
pathogens because of its association with infections in the organisms to the respiratory epithelium followed by
cystic fibrosis, P. aeruginosa most commonly is seen in necrosis of the cells and an inflammatory response. When
nosocomial settings (discussed later). the process extends to alveoli, there is usually interstitial
• Pseudomonas pneumonia also is common in persons who inflammation, but some outpouring of fluid into alveolar
are neutropenic, usually secondary to chemotherapy; in spaces may also occur, so that on chest films the changes
victims of extensive burns; and in patients requiring may mimic those of bacterial pneumonia. Damage to and
mechanical ventilation. denudation of the respiratory epithelium inhibits mucocili-
• P. aeruginosa has a propensity to invade blood vessels at ary clearance and predisposes to secondary bacterial infec-
the site of infection, with consequent extrapulmonary tions. Viral infections of the respiratory tract are well
spread; Pseudomonas bacteremia is a fulminant disease, known for this complication. More serious lower respira-
with death often occurring within a matter of days. tory tract infection is more likely to occur in infants, elderly
• Histologic examination reveals coagulative necrosis of persons, malnourished patients, alcoholics, and immuno-
the pulmonary parenchyma with organisms invading suppressed persons. Not surprisingly, viruses and myco-
the walls of necrotic blood vessels (Pseudomonas plasmas frequently are involved in outbreaks of infection
vasculitis). in hospitals.

Legionella pneumophila MORPHOLOGY
• L. pneumophila is the agent of Legionnaire disease, an
Regardless of cause, the morphologic patterns in atypical
eponym for the epidemic and sporadic forms of pneu- pneumonias are similar. The process may be patchy, or it may
monia caused by this organism. Pontiac fever is a related involve whole lobes bilaterally or unilaterally. Macroscopi-
self-limited upper respiratory tract infection caused by cally, the affected areas are red-blue, congested, and sub-
L. pneumophila, without pneumonic symptoms. crepitant. On histologic examination, the inflammatory
• L. pneumophila flourishes in artificial aquatic environ- reaction is largely confined within the walls of the
ments, such as water-cooling towers and within the alveoli (Fig. 12–34). The septa are widened and edematous;
tubing system of domestic (potable) water supplies. The they usually contain a mononuclear inflammatory infiltrate of
mode of transmission is thought to be either inhalation lymphocytes, histiocytes, and, occasionally, plasma cells. In
of aerosolized organisms or aspiration of contaminated contrast with bacterial pneumonias, alveolar spaces in atypi-
drinking water. cal pneumonias are remarkably free of cellular exudate. In
• Legionella pneumonia is common in persons with some severe cases, however, full-blown diffuse alveolar damage
predisposing condition such as cardiac, renal, immuno- with hyaline membranes may develop. In less severe, uncom-
logic, or hematologic disease. Organ transplant recipients plicated cases, subsidence of the disease is followed by
are particularly susceptible. reconstitution of the native architecture. Superimposed bac-
• Legionella pneumonia can be quite severe, frequently terial infection, as expected, results in a mixed histologic
requiring hospitalization, and immunosuppressed picture.
persons may have a fatality rate of 30% to 50%.
• Rapid diagnosis is facilitated by demonstration of Le­­ Clinical Features
gionella antigens in the urine or by a positive fluorescent The clinical course of primary atypical pneumonia is
antibody test on sputum samples; culture remains the extremely varied. It may masquerade as a severe upper
standard diagnostic modality. PCR-based tests can be respiratory tract infection or “chest cold” that goes undi-
used on bronchial secretions in atypical cases. agnosed, or it may manifest as a fulminant, life-threatening
infection in immunocompromised patients. The initial pre-
Community-Acquired Atypical Pneumonias sentation usually is that of an acute, nonspecific febrile
illness characterized by fever, headache, and malaise and,
The term primary atypical pneumonia initially was applied later, cough with minimal sputum. Because the edema and
to an acute febrile respiratory disease characterized by exudation are both in a strategic position to cause an alveo-
patchy inflammatory changes in the lungs, largely confined locapillary block, there may be respiratory distress seemingly
to the alveolar septa and pulmonary interstitium. The des- out of proportion to the physical and radiographic findings.
ignation atypical denotes the moderate amounts of sputum,
absence of physical findings of consolidation, only moder-
ate elevation of white cell count, and lack of alveolar
exudates. Atypical pneumonia is caused by a variety of