Legionella Infection And Immunity

N Cary Engleberg, Departments of Internal Medicine and Microbiology and Immunology, Division of Infectious Diseases, University of Michigan Medical School, Ann Arbor, Michigan, USA

Joan K Brieland, Unit for Laboratory Animal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA

Copyright © 1998 Elsevier Ltd. All Rights Reserved.

Legionella pneumophila is a facultative intracellular pathogen that causes Legionnaires' disease in humans. In nature, this organism is commonly present in aquatic habitats, often growing as an intracellular parasite of free-living protozoa. Occasionally, L. pneumophila contaminates water distribution systems, resulting in inoculation of humans by inhalation of infectious aerosols or microaspiration of potable water. In susceptible hosts, a fibrin-opurulent pneumonia with infiltration of mononuclear and polymorphonuclear phagocytes develops. The infection is progressive and may be fatal, particularly in immunocompromised hosts.

Although L. pneumophila is not an obligate intracellular pathogen, progressive disease occurs only when host mononuclear phagocytic cells (MPCs) are permissive to intracellular replication of the organism. In 1980, Horwitz and colleagues demonstrated that L. pneumophila replicates in unactivated human MPCs. Subsequent in vitro studies demonstrated that L. pneumophila also replicates in unactivated MPCs from other animal species, including guinea pigs, rats, nonhuman primates and A/J mice. These species, like humans, develop replicative /,. pneumophila infections following experimental inoculation. In contrast, other mouse strains, including BDF1, DBA/2, C3H/HeN, C57B1/6, BALB/c and outbred mice, have nonpermissive MPCs; these animals do not support intrapulmonary growth of L. pneumophila. Recently, a single autosomal, dominant gene on murine chromosome 13 (designated Lgn-1) was linked to the permissiveness of murine MPCs for L. pneumophila replication.

The primacy of intracellular infection in the development of progressive disease has been confirmed by numerous experiments with L. pneumophila mutants that are unable to grow in MPCs in vitro. Predictably, these mutant bacteria cannot cause progressive infection in animals. The ability of a susceptible host to survive replicative L. pneumophila lung infection is dependent on a complex interaction between host MPCs, cytokines and effector cells which facilitate MPC activation and elimination of the pathogen.

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