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Author: Michael Barza, M.D.
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1. Pathogenesis

The pathogenesis of pneumonia differs according to the clinical setting.

1.1. Younger patients

In relatively healthy, younger patients, most pneumonias occur by the inhalation of pathogens from the air. These pathogens typically possess “adhesins”, structures in the outer coat of the infecting microbe which allow the microbe to anchor itself to the tracheobronchial epithelium and to avoid being swept away by the mucociliary elevator. Common causes of pneumonia in this population are viruses (especially influenza virus), “atypical pneumonia” pathogens (Mycoplasma pneumoniae in young people, Chlamydia pneumoniae and Legionella pneumophila in others – called “atypical” in contrast to “typical” pneumococcal pneumonia), and Streptococcus pneumoniae. Influenza virus has two adhesins, the hemagglutinin and the neuraminidase. Because of frequent mutations in these adhesins, immunizations must be given every year. The virulence factor of the pneumococcus is not an adhesin but the anti-phagocytic capsule: immunization raises protective anticapsular antibody.

1.2. Elderly patients

By contrast, in elderly, debilitated patients, the pathogenesis is more like that in hospitalized patients, often including gram-negative bacilli, which colonize the nasopharynx and are aspirated into the lung.Nevertheless, the pathogens which affect healthier, younger, people can also affect the elderly.

Frank episodes of gross aspiration tend to result in pneumonia caused by oral anaerobes (“aspiration pneumonia”). Such pneumonias often cavitate and produce putrid empyemas.

2. Two Important Pathogens

In any patient with pneumonia, it is important to keep in the back of one’s mind two unusual but important pathogens, namely, TB and Pneumocystis carinii.

2.1. TB

TB should be considered in patients with a risk of exposure to TB and an apical pulmonary infiltrate

2.2. Pneumocystis carinii

Pneumocystis carinii should be considered in patients with a risk of HIV and a diffuse pulmonary infiltrate (resembling pulmonary edema).

3. Diagnosis

The clinical features of pneumonia are usually cough, fever, and sometimes the production of sputum (especially in bacterial pneumonias, in which sputum tends to be “purulent”) and pleuritic chest pain. However, somewhat similar symptoms may be caused by bronchitis: a chest x-ray can distinguish between bronchitis and pneumonia.

The causative agent can be diagnosed in only about 50% of community-acquired pneumonias, even with sophisticated studies including serology and special cultures. Clinical clues such as lack of sputum, absence of consolidation, and a poor response to beta-lactam antibiotics, are often thought to point to “atypicals” rather than the pneumococcus but prospective studies have not supported this notion. The value of sputum gram-stain (looking for PMNs – to suggest bacterial pneumonia and for characteristic microorganisms) and culture are controversial. Only about 1/3 of patients produce useful sputum and organisms colonizing the mouth but not present in the lung (including the pneumococcus) can confound the interpretation. Blood cultures are also of controversial value because they are positive in only about 10% of patients and usually reveal the pneumococcus (which would be suspected anyway). Nevertheless, these tests are probably useful in sicker patients (fever, elevated WBC) who have not taken antibiotics.

Other types of tests that can be useful are shown on the slide titled Additional Test for Cause.

4. Treatment of community-acquired pneumonia

One of the decisions the physician must make early on is whether or not to admit the patient to hospital. A scoring system was developed by Fine et al to predict the likelihood of death – based on age, comorbidities, clinical and laboratory features. For patients with a low likelihood of death (e.g. younger patients with few comorbidities who are not very “sick”), pneumonia can be treated as an outpatient. Antibiotics are chosen to address the pneumococcus and the “atypicals” primarily, e.g. a macrolide, a quinolone or doxycycline. Quinolones tend to be preferred for elderly patients, who have a higher risk of a gram-negative enteric infection (against which a macrolide would not be effective).

For patients sick enough to require hospitalization, recommended treatments are either the combination of a beta-lactam and a macrolide, or a fluoroquinolone alone.

Currently, about 20-40% of S. pneumoniae are somewhat penicillin-resistant. Most of these strains are also resistant to macrolides but remain susceptible to quinolones. Because the degree of penicillin-resistance is low, the blood levels achieved by intravenous beta-lactams are adequate for treatment and relatively well, younger, outpatients can be treated safely with a macrolide.

5. Prevention of pneumonia

Influenza immunization should be given annually, and pneumococcal immunization once, to elderly patients and those with heart, lung, or metabolic diseases.

6. Nosocomial pneumonia

The pathogenesis has been noted above. In particular, debilitated hospitalized patients are at considerable risk for pneumonia, especially if they have been intubated, had abdominal surgery, or are very elderly. Loss of epithelial fibronectin leads to colonization of the nasopharynx by enteric gram-negatives (including Pseudomonas aeruginosa in patients in the ICU). When these organisms are aspirated by patients whose defense mechanisms (gag reflex, mucociliary elevator, alveolar macrophages) are diminished , pneumonia results(see slide titled Causes of Pneumonia). The main pathogens are gram-negative enterics (in > 50%), and sometimes S. aureus and S. pneumoniae.

A broad-spectrum beta-lactam (penicillin/penicillinase inhibitor; cephalosporin; carbapenem) is a commonly chosen treatment. An aminoglycoside should be added for patients at high risk of P. aeruginosa infection (e.g. in the ICU).

7. Prevention of nosocomial pneumonia

Intubated patients have a high risk of developing pneumonia.Therefore, it seemed a good idea to administer antibiotics prophylactically (either topically to the nasopharynx or systemically or both). However, many trials have shown that this approach does not reduce mortality or length-of-stay in the ICU and does foster antibiotic-resistant organisms. Antacids (traditional or H2 blockers), given to prevent “stress” ulcers in the ICU, have been thought to predispose to pneumonia by reducing gastric acidity and allowing gram-negatives from the intestine to migrate across the stomach to the nasopharynx. It was hypothesized that sucralfate, which works by coating the stomach rather than by diminishing gastric acidity, might be better in this regard. However, comparative trials have yielded conflicting results. One measure that can help is placing the patient in the semirecumbent, rather than the fully recumbent position, in order to reduce aspiration of nasopharyngeal bacteria.

8. Ancillary Material

8.1. Readings

8.1.1. Required

Schaechter Textbook, Chapter 59, pages 549-563.

8.1.2. Recommended

  • Bartlett JG, Dowell SF, Mandell LA, File Jr TM, Musher DM, Fine MJ. Practice guidelines for the management of community-acquired pneumonia in adults. Infectious Diseases Society of America. Clin Infect Dis 2000;31(2):347-82.
  • Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify low-risk patients with community-acquired pneumonia. N Engl J Med 1997;336(4):243-50.
  • Halm EA, Teirstein AS. Clinical practice. Management of community-acquired pneumonia. N Engl J Med 2002;347(25):2039-45.
  • Whitney CG, Farley MM, Hadler J, et al. Increasing prevalence of multidrug-resistant Streptococcus pneumoniae in the United States. N Engl J Med 2000;343(26):1917-24.