is a Gram-negative, facultative bacillus that
causes a severe form of pneumonia
Legionnaires’ disease. This
species undergoes two growth phases, namely, a
multiplicative phase and an active infective
phase (Vogel & Isberg,
1999). The multiplicative
phase occurs in the early stages of host cell
infection; bacteria are non-motile, long and
filamentous, and are actively multiplying, as
its name suggests (Figure 1). The active
infective phase occurs in the later stages of
infection; cellular morphology in this phase
consists of stout, "fat" bacilli, which is the
case for the vast majority of the organisms
depicted in Figure 2. Recall that the term
bacillus, meaning a rod-shaped bacterium,
should not be confused with the genus of
bacteria known as Bacillus.
This colorized scanning electron micrograph
depicts a large grouping of Gram-negative
Legionella pneumophila bacteria. These
bacteria originated on a one week-old culture
plate (+/- 1 day), which had incubated a single
colony, at 37°C
upon a buffered charcoal yeast extract medium
with no antibiotics.
This scanning electron micrograph depicts a
diffuse group of Gram-negative Legionella
pneumophila bacteria in the active
infective phase [1200 X].
In their natural environment,
infect free-living protozoa
found mostly in aquatic and freshwater
environments (Figure 3), as well as heating, ventilation, and air-conditioning systems,
hot tubs, cooling towers, hot water tanks or
large plumbing systems, which are capable of
transmitting aerosols of the bacteria. However,
they do not seem to grow in car or window
This electron micrograph depicts an amoeba,
Hartmannella vermiformis (orange) as it
entraps a Legionella pneumophila
bacterium (green) with an extended pseudopod.
Lung tissue infection caused by
L. pneumophila begins
after the inhalation
of contaminated water aerosol.
Once this pathogen reaches the alveoli of the lungs, alveolar
macrophages engulf the bacteria. The
macrophage uses coiling
phagocytosis – a long, thin pseudopod engulfs
the bacterium in a coiled vesicle
– to take in L. pneumophila. The
bacterium then alters the endocytic pathway
(Figure 4), and the phagosome
(endosome) that contains the
bacterium associates with small vesicles,
mitochondria, and is eventually surrounded by
the rough endoplasmic reticulum, where the
inside of the vesicle is lined with ribosomes
(Vogel & Isberg, 1999). Fusion of
the phagolysosome is inhibited
because acidification of the vesicle does not
occur, thus the bacteria are able to multiply within the host
cell, lyse the cell and eventually infect other cells
(Figure 4). The ability of L. pneumophila to hinder
the fusion of the phagolysosome,
as well as the ribosome-lined vacuole, are key
features that are unique to this
bacterium (Nash et al., 1984).
Immune evasion strategy used by Legionella
pneumophila to prevent being presented by
MHC class II molecules. This schematic depicts
pneumophila evasion at the cellular level.
The word endosome and phagosome
Motile L. pneumophila are flagellated, which may
be a factor in the
spread of the bacteria in the lungs (Figure 5). The
macrophage infectivity potentiator (Mip) genes are responsible for
increasing L. pneumophila infection in
the host cell. The presence of iron is important
for the pathogenesis of this germ because
without it, replication within the host
mammalian cell is inhibited.
This scanning electron micrograph depicts a
single Legionella pneumophila specimen.
Of particular importance is the presence of
polar flagella, and pili, or long streamers.
Exposure to L. pneumophila results in serious
pneumonia, which can be fatal. Legionnaires'
disease can be very serious and can cause death
in up to 5% to 30% of cases. Most cases can be
treated successfully with antibiotics (drugs
that kill bacteria in the body), and healthy
people usually recover from infection. Immunocompromised
people (individuals with cancer or AIDS) in nursing homes
or hospitalized patients receiving chemotherapy
for organ transplantation or
cancer are more likely to become infected
(Friedman et al., 2007). Fortunately, most normal
individuals are resistant to moderate doses of
Friedman, H., Newton, C., and
Klein, T. Legionella pneumophila: Innate and
Adaptive Immunity. Hoffman, P., Friedman, H.,
and Bendinelli, M. (2007). Legionella
pneumophila: Pathogenesis and Immunity. New
York: Springer. Pg. 151.
Nash, T.W., Libby, D.M., and
Horowitz, M.A. (1984). Interaction between the
Legionnaires’ disease bacterium (Legionella
pneumophila) and human alveolar
macrophages: Influence of
antibody, lymphokines, and hydrocortisone.
The Journal of Clinical Investigation,
Vogel, J.P. & Isberg, R.R.
(1999). Cell biology of Legionella pneumophila.
Current Opinion in Microbiology, 2: