Legionella pneumophila is a thin, ærobic, pleomorphic, flagellated, non-spore forming, Gram-negative bacterium of the genus Legionella.^[1][2] L. pneumophila is the primary human pathogenic bacterium in this group and is the causative agent of legionellosis or Legionnaires' disease.

Characterization

L. pneumophila is an acid-fast, non-sporulating, and morphologically a non-capsulated rod-like bacteria, often characterized as being a coccobacillus. Ærobic and unable to hydrolyse gelatin or produce urease, they are also non-fermentative. L. pneumophila is neither pigmented nor does it autofluoresce. It is oxidase- and catalase-positive, and produces beta-lactamase. L. pneumophila has a colony morphology that is gray-white with textured cut-glass appearance; it also requires cysteine and iron to thrive.

Cell membrane structure

While L. pneumophila is categorized as a Gram-negative organism, it stains poorly due to its unique lipopolysaccharide-content in the outer leaflet of the outer cell membrane.^[3] The bases for the somatic antigen specificity of these organisms are located on the side-chains of its cell wall. The chemical composition of these side chains both with respect to components as well as arrangement of the different sugars determines the nature of the somatic or O-antigen determinants, which are important means of serologically classifying many Gram-negative bacteria. At least 35 different serovars of L. pneumophila have been described as well as several other species being subdivided into a number of serovars.

Detection

Sera have been used both for slide agglutination studies as well as for direct detection of bacteria in tissues using fluorescent-labelled antibody. Specific antibody in patients can be determined by the indirect fluorescent antibody test. ELISA and microagglutination tests have also been successfully applied.

Reservoir

L. pneumophila is a facultative intracellular bacterium that can invade and replicate inside amoebae in the environment. Ameoba can thus serve as a reservoir for L. pneumophila as well as provide protection from environmental stresses such as chlorination.^[4]

Frequency of occurrence

In the USA about 30 infections with L. pneumophila appear per 100.000 residents per year. The infections peak within the summer months. Within endemic regions, about 4% to 5% of Pneumonia are caused by L. pneumophila. ^[5]

Pathogenesis

In humans, L. pneumophila invades and replicates in macrophages. The internalisation of the bacteria can be enhanced by the presence of antibody and complement but is not absolutely required. A pseudopod coils around the bacterium in this unique form of phagocytosis. Once internalized, the bacteria surround themselves in a membrane-bound vacuole that does not fuse with lysosomes that would otherwise degrade the bacteria. In this protected compartment the bacteria multiply. The bacteria use a Type IVB secretion system known as Icm/Dot to inject effector proteins into the host. These effectors are involved in increasing the bacteria's ability to survive inside the host cell. Survival is enhanced by these effector proteins (Ank proteins) because they interfere with fusion of the Legionella-containing vacuole with the host's degradation endosomes.^[6]

Genomics

The determination and publication of the complete genome sequences of three clinical L. pneumophila isolates in 2004 paved the way for the understanding of the molecular biology of L. pneumophila in particular and Legionella in general. In depth comparative genome analysis using DNA arrays to study the gene content of 180 Legionella strains revealed the high genome plasticity and frequent horizontal gene transfer. Further insight in the L. pneumophila life cycle was gained by investigating the gene expression profile of L. pneumophila in Acanthamoeba castellanii, its natural host. L. pneumophila exhibits a biphasic life cycle and defines transmissive and replicative traits according to gene expression profiles.^[2]

Treatment

Macrolides (azithromycin) or fluoroquinolones (moxifloxacin) are the standard treatment for Legionella pneumonia in humans.

References