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Chapter 200 Legionella
Lucy S. Tompkins
Legionellosis comprises Legionnaires disease (Legionella pneumonia), other invasive extrapulmonary Legionella infections, and an acute flulike illness known as Pontiac fever. In contrast to the syndromes associated with invasive disease, Pontiac fever is a self-limiting illness that develops after aerosol exposure and may represent a toxic or hypersensitivity response to Legionella.
Legionellaceae are aerobic, non–spore-forming, unencapsulated gram-negative bacilli that stain poorly with Gram stain when performed on smears from clinical specimens. Microorganisms in tissue can be better visualized with the Gimenez or silver stains (Dieterle or Warthin-Starry). Stained smears of Legionella pneumophila taken from colonial growth resemble Pseudomonas. Unlike other Legionella species, L. micdadei stains acid fast. Although >30 species of the genus have now been identified, the majority (90%) of clinical infections are caused by L. pneumophila, and most of the remainder are caused by L. micdadei, L. bozemanii, L. dumoffii, and L. longbeachae.
The organisms are fastidious and require L-cysteine, ferric ion, and α-keto acids for growth. Colonies develop within 3-5 days on buffered charcoal yeast extract agar, which may contain selected antibiotics to inhibit overgrowth by other microorganisms; Legionella rarely grows on routine laboratory media.
The environmental reservoir of Legionella in nature is fresh water (lakes, streams, thermally polluted waters, potable water), and invasive pneumonia (Legionnaires disease) is related to exposure to potable water or to aerosols containing the bacteria. Growth of Legionella occurs more readily in warm water, and exposure to warm water sources is an important risk factor for disease. Legionella organisms are facultative intracellular parasites and grow inside protozoans present in biofilms consisting of organic and inorganic material found in plumbing and water storage tanks and various other bacterial species. Epidemic and sporadic cases of community-acquired Legionnaires disease can be attributed to potable water in the local environment of the patient. Risk factors for acquisition of sporadic community-acquired pneumonia include exposure to cooling towers, nonmunicipal water supply, residential plumbing repairs, and lower water heater temperatures, which facilitate growth of bacteria or lead to release of a bolus of biofilm containing Legionella into potable water. The mode of transmission may be by way of inhalation of aerosols or by microaspiration. Outbreaks of Legionnaires disease have been associated with protozoans in the implicated water source; replication within these eukaryotic cells presumably amplifies and maintains Legionella within the potable water distribution system or in cooling towers. Outbreaks of community-acquired pneumonia and some nosocomial outbreaks have been linked to common sources, including potable hot water heaters, evaporative condensers cooling towers, whirlpool baths, humidifiers, and nebulizers. Travel-associated Legionnaires disease and Pontiac fever are increasingly recognized in major outbreaks.
Hospital-acquired infections are most often linked to potable water. Exposure may occur through 3 general mechanisms: (1) inhalation of contaminated water vapor through artificial ventilation; (2) aspiration of ingested microorganisms, including those in gastric feedings, that are mixed with contaminated tap water; and (3) inhalation of aerosols from showers and sinks. Extrapulmonary legionellosis may occur through topical application of contaminated tap water into surgical or traumatic wounds. In contrast to Legionnaires disease, Pontiac fever outbreaks have occurred through exposure to aerosols from whirlpool baths, ultrasonic humidifiers, and ventilation systems.
The incidence of community-acquired Legionnaires disease caused by L. pneumophila occurring sporadically in adults is estimated at 7-20 cases/100,000 per year and demonstrates geographic differences. Legionella infections are reported most frequently in fall and summer, and recent studies show an association with total monthly rainfall and humidity. Approximately 0.5-5.0% of those exposed to a common source develop pneumonia, whereas the attack rate in Pontiac fever outbreaks is very high (85-100%). In 1 large community-based study of adults, Legionella was associated with 3% of pneumonia cases. Taken together, Mycoplasma pneumoniae, Chlamydophila pneumoniae, and L. pneumophila account for 10-38% of all community-acquired pneumonia, and therefore the current clinical guidelines for community-acquired pneumonia in adults recommend empirical therapy with macrolides or quinolones. Acquisition of antibodies to L. pneumophila in healthy children occurs progressively over time, although these antibodies presumably reflect subclinical infection or mild respiratory disease or antibodies that cross react with other bacterial species. Community-acquired Legionnaires disease in children is increasingly reported (1.7% of reported cases), and most cases occur in children age 15-19 yr, followed by infants age <1 yr. The incidence in infants is reported to be 0.11/100,000. It is likely that legionellosis is significantly underreported, both in children and adults.
As estimated by seroconversion to L. pneumophila among children hospitalized with pneumonia, the Legionnaires disease rate is quite low. Most nosocomial infections have been reported as case reports; therefore, the true incidence of disease in children is unknown. Nosocomial infection rates in adults are difficult to determine, because many hospital laboratories do not attempt to isolate Legionella by culture. Hospital-acquired legionellosis in children is associated with clinical risk factors and with environmental exposure.
Although Legionella can be grown on artificial media, the intracellular environment of eukaryotic cells provides the definitive site of growth. Legionella organisms are facultative intracellular parasites of eukaryotic cells. In nature, Legionella
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