LEGIONELLA - World Health Organization

Typing
Helbig et al. (1995) suggested that differences in the virulence of Legionella species or serogroups
are associated with different epitopes within the bacterial cell wall (epitopes are parts of a
foreign organism or its proteins that are recognized by the immune system and targeted by
antibodies, cytotoxic T cells or both). Tests using monoclonal subtyping show that the strains of
L. pneumophila serogroup 1 most commonly associated with disease in humans share a common
epitope (Watkins et al., 1985; Ehret, von Specht & Ruckdeschel, 1986; Dournon et al., 1988).
Depending on the typing scheme used, these strains may be referred to as Pontiac (Watkins
et al., 1985); monoclonal antibody (MAb) 2-reactive (Joly et al., 1986) or MAb 3/1-positive
(Dresden Panel, 2002; Helbig et al., 2002).
In a European-wide study of L. pneumophila, 1335 cases of Legionnaires’ disease were serotyped,
and monoclonal types of serogroup 1 were grouped according to the presence of the epitope
recognized by MAb 3/1 (Dresden Panel, 2002). Approximately 66.8% of cases were MAb
3/1-positive, and 11.7% of the overall isolates belonged to the MAb 3/1-negative serogroup 1
subgroups. Monoclonal subtype Philadelphia was the most frequently recognized. Most of
the MAb 3/1-negative strains were from nosocomial infections (53.5%), with 27.3% from
community-acquired cases and 14.2% from travel-associated cases (Helbig et al., 2002). The
proportion of MAb 3/1-negative strains was significantly higher in the Scandinavian region
than in Mediterranean countries or the United Kingdom, for both community-acquired and
nosocomial cases.
1.5 Virulence and pathogenicity
Various studies have shown that the pathogenesis and ecology of Legionella are inherently
related. Rowbotham first demonstrated that L. pneumophila could infect amoeba, and characterized
the life cycle of Legionella in amoeba (Rowbotham, 1980). Horwitz’s classical experiments
demonstrated that L. pneumophila multiplied intracellularly in human macrophages by
avoiding phagosome–lysosome fusion (Horwitz, 1983). There are striking similarities in the
processes by which legionella infect protozoa and mammalian phagocytic cells (Bozue &
Johnson 1996; Horwitz 1984, Garduno et al., 2002). The abilities of Legionella to infect mammalian
and protozoan cells are related, using common genes and gene products.
1.5.1 Overview and life-cycle
The virulence mechanisms of L. pneumophila are complex and not fully understood. Virulence
is an important factor in the ability of L. pneumophila to infect and subsequently multiply
within amoebae (Fields et al., 1986; Moffat & Tompkins, 1992). However, some strains with low
virulence can multiply within certain host cells (Tully, Williams & Fitzgeorge, 1992). Studies
contrasting the role that different virulence factors play in host populations may help to show
how the bacteria develop an ability to infect humans, without the need for a protozoan host.
LEGIONELLA AND THE PREVENTION OF LEGIONELLOSIS