Legionellaceae are facultative intracellular parasites that cause primarily respiratory tract infections. In nature, Legionella cells are unencapsulated, relatively slender rods, whereas in clinical material, they appear coccobacillary in shape (see Figure1). Members of the Legionellaceae family are aerobic and fastidious, with a particular requirement for L-cysteine.

Fig1. Summary of Legionella disease. 1 Indicates first-line drugs.

A. Epidemiology

 The Legionellaceae family includes 34 species whose normal habitat is within environmental protozoa and amebae in soil and water, including water in cooling towers and distribution systems. About 85 to 90 percent of human disease is caused by a single species, Legionella pneumophila. Most infections result from inhalation of aerosolized organisms within amebas or within environmental biofilm but, occasionally, may follow other exposures (for example, swimming in contaminated water). Both sporadic cases and localized outbreaks may occur. One famous outbreak occurred in 1976 during a convention of American Legion members (hence the name, Legionella). Cases of legionellosis in the United States nearly tripled from 2000 to 2009. The organism is chlorine tolerant and, thus, sur vives water treatment procedures. There is no person-to-person spread of the disease. Growth within the environmental ameba induces the expression of key virulence factors that make the Legionellae more fit for infection of human macrophages.

B. Pathogenesis

 The organism gains entry to the upper respiratory tract by aspiration of water containing the organism or by inhalation of a contaminated aerosol. Failure to clear the organisms permits them to reach the lungs. Alveolar macrophages in the lung bed normally constitute an important line of defense for clearing invading organisms. Although the macrophages do phagocytose L. pneumophila, the resulting phagosome fails to fuse with a lysosome. Instead, the organisms multiply within the protected environment of the phagosome until the cell ruptures, releasing a new crop of bacteria.

C. Clinical significance

Legionellaceae primarily cause respiratory tract infections. There are two distinctly different presentations: Legionnaires disease (LD) and Pontiac fever. The state of the host's cell-mediated immunity plays a critical role in determining which manifestation will occur. Immunosuppressed patients are more likely to develop severe pneumonia when infected with Legionella while Pontiac fever is almost always seen in otherwise healthy individuals.

1. Legionnaires disease: This is an atypical, acute lobar pneumonia with multisystem symptoms. It may occur sporadically or in out breaks (for example, nosocomial outbreaks have occurred). LD typically develops in only 1 to 5 percent of individuals exposed to a common source. Legionellae are estimated to cause 1 to 5 percent of the cases of community-acquired pneumonias in adults (Figure 2). The case fatality rate for LD ranges from 5 to 30 percent, a high rate that may reflect the fact that many LD patients have additional contributing factors, such as pulmonary disease or immunocompromising factors. Symptoms develop after an incubation period ranging from 2 to 10 days. Early symptoms may be relatively nonspecific: fever, malaise, myalgia, anorexia, and/or headache. The severity and range of symptoms associated with LD vary substantially. A cough that is only slightly productive then occurs, sometimes with respiratory compromise. Diarrhea (watery rather than bloody stools) occurs in 25 to 50 percent of cases. Nausea, vomiting, and neurologic symptoms may also occur. Risk factors associated with a presentation of LD include advanced age, smoking or chronic lung disease, immune sup pression due to cancer or its treatment, kidney disease, and diabetes.

Fig2. Common pathogens causing community-acquired pneumonia.

 2. Pontiac fever: This is an influenza-like illness that characteristically infects otherwise healthy individuals. The attack rate among those exposed to a common source is typically 90 percent or more. Recovery is usually complete within 1 week. No specific therapy is required.

D. Laboratory identification

LD cannot be diagnosed unambiguously on the basis of clinical presentation or radiologic appearance of lungs. Although the organism can be Gram stained, the Gimenez stain is more useful for visualization. The definitive method of diagnosis involves the culturing of Legionella from respiratory secretions, using buffered (pH 6.9) char coal yeast extract (Figure 1) enriched with L-cysteine, iron, and α-ketoglutarate. Visible colonies form in 3 to 5 days. A urinary anti gen test using an enzyme immunoassay is available and has several advantages over culture. For example, the test positivity can persist for days even during administration of antibiotic therapy, making it useful in patients who receive empiric anti-Legionella therapy. Further, the results of the urinary antigen test can be available within hours, whereas culture results require 3 to 5 days. However, it is important to note that the urinary tract antigen test only detects infection with serogroup A L. pneumophila. Therefore, a negative antigen test does not rule out infection with all Legionellae. When LD is suspected, both a urinary antigen test and Legionella culture of a respiratory specimen should be ordered.

E. Treatment

 Macrolides, such as erythromycin or azithromycin, are the drugs of choice for LD. Fluoroquinolones are also effective (see Figure 1). Pontiac fever is usually treated symptomatically, without antibiotics

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