Detailed practice guidelines have been published for the management of both community- and hospital-acquired pneumonia (1,2). The following will briefly summarize important aspects of treatment.

The approach to the management of community-acquired pneumonia (CAP) has evolved over the last several years. The focus of management is now empiric treatment according to the patient’s age and underlying conditions. This shift is based on several factors. First, there has been no convincing association demonstrated between individual symptoms, physical findings or laboratory results, and specific etiology. Specifically, the findings considered classical for "atypical" pneumonia occur no more frequently in patients with bacterial pneumonia than they do with mycoplasma, chlamydial, or viral pneumonia. Second, prospective studies evaluating the causes of CAP in adults have failed to identify the cause in 40%-60% of cases. Third, the laboratory diagnosis of pneumonia is imperfect. The referenced guidelines suggest that establishing an etiologic diagnosis has value for patients requiring hospitalization but this is controversial.

The most common and important etiologic agent identified in virtually all studies is Streptococcus pneumoniae. There is even some evidence that pneumonia of unknown etiology may often be secondary to S. pneumoniae (3). Other pathogens include Haemophilus influenzae, Mycoplasma pneumoniae, Chlamydia pneumoniae, Staphylococcus aureus, Moraxella catarrhalis, Klebsiella pneumoniae and other gram-negative rods, Legionella species, influenza virus, respiratory syncytial virus, adenovirus, parainfluenza virus. Although not absolute, certain pathogens cause pneumonia more commonly among persons with specific risk factors. Important examples include COPD and smoking where S. pneumoniae, H. influenzae, M. catarrhalis, and Legionella spp. are commonly encountered; alcoholism in which S. pneumoniae, anaerobes, and gram-negative bacilli are common; and nursing-home residents where frequent pathogens include S. pneumoniae, H. influenzae, S aureus, and Legionella spp. Despite the belief that gram negatives are more common in nurisng home residents, there is no good data to support that belief. In young, previously healthy, ambulatory patients S. pneumoniae, M. pneumoniae, and C. pneumoniae are common.

The empirical therapy outlined in the referenced guidelines divides those with CAP into outpatients and hospitalized patients. For outpatients the recommended antibiotics are macrolides (azithromycin, clarithromycin, or erythromycin), fluoroquinolones with enhanced activity against S. pneumoniae (levofloxacin or grepafloxacin), or doxycycline. For hospitalized patients a second or third-generation cephalosporin (cefuroxime, cefotaxime, or ceftriaxone) or a fluoroquinolone with enhanced activity against S. pneumoniae is recommended. For those hospitalized patients with overwhelming pneumonia, a macrolide should be added to cover Legionella spp. Therapy should be modified and directed at specific pathogens when accurate microbiologic data is available. Issues of antibiotic resistance are also important. As S. pneumoniae resistance to macrolides and penicillin has increased, guidelines have changed as evidenced by the strong representation of the newer fluoroquinolones in the present guidelines. However, there is no clinical data to suggest that patients infected with macrolide or penicillin resistant S. pneumoniae cannot be treated with either of these agents. The reason for this is likely explained by the pharmacokinetics of the macrolides and the levels of resistance to the penicillins. Macrolides are concentrated in the lung at levels about ten times those found in blood. Although the breakpoints for penicillin resistance to S. pneumoniae are 2 mg/L, these were chosen to reflect levels obtainable in the CSF. Much higher concentrations are achieved in the lung so that it would not be unreasonable to expect pneumococcal pneumonia due to strains with MICs of < 4 mg/L to be successfully treated with a b-lactam. Currently in North America ~ 99% of isolates of S. pneumoniae have MICs of < 4 mg/L. A recent article in the New England Journal of Medicine (4) by investigators from our department has documented the rise in fluoroquinolone resistance in S. pneumoniae isolates in Canada over the last ten years. This increase in resistance was significantly correlated with an increase in fluoroquinolone prescriptions over the same time period. What this means clinically is not yet known.

The approach to hospital-acquired pneumonia (HAP) relies on assessments of disease severity, the presence of risk factors for specific organisms, and the time of onset of HAP. An important concept to the understanding of HAP is that the most common route of entry of organisms into the lungs is by microaspiration of oropharyngeal secretions. The more virulent the organism aspirated the more likely pneumonia is to develop. Oropharyngeal colonization with enteric gram-negative bacilli increases with increasing duration of hospitalization and increasing severity of illness. In patients with severe HAP who have been hospitalized for 5 or more days (late onset), Pseudomonas aeruginosa, Enterobacter spp., and Acinetobacter spp. are of increased significance. Other risk factors for P. aeruginosa include prolonged ICU stay, mechanical ventilation, steroids, previous antibiotics, and structural lung disease.

Recommendations for the treatment of mild-to-moderate HAP or early onset severe HAP includes either a second generation cephalosporin, a third generation nonpseudomonal cephalosporin or a b-lactam/b-lactamase inhibitor combination. One of the newer fluoroquinolones would also be acceptable. For late onset severe HAP, coverage for P. aeruginosa and Acinetobacter spp. is required. Recommended therapy includes an aminoglycoside or fluoroquinolone plus one of: antipseudomonal penicillin, b-lactam/b-lactamase inhibitor, ceftazidime, or imipenem.

1. Bartlett J.G., Breiman R.F., Mandell L.A., Thomas, M.F. 811 Community –Acquired Pneumonia in Adults; Guidelines for Management. Clin Infect Dis 1998;26:811-38.

2. A consensus statement, American Thoracic Society. Hospital-acquired pneumonia in adults: diagnosis, assessment of severity, initial antimicrobial therapy, and preventive strategies. Am J Respir Crit Care Med 1995;153:1711-25.

3. Ruiz-Gonzalez A, Falguera M, Nogues A, Rubio-Caballero M. Is Streptococcus pneumoniae the leading cause of pneumonia of unknown etiology? A microbiologic study of lung aspirates in ocnsecutive patients with community-acquired pneumonia. Am J Med 1999;106:385-90.

4. Chen D.K, McGeer A, de Azavedo J.C., Low D.E., for the Canadian Bacterial Surveillance Network. Decreased susceptibility of Streptococcus pneumoniae. NEJM 1999; 341(4):233-9.