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INTRODUCTION

Listeria monocytogenes is a ubiquitous environmental saprophyte and an intracellular pathogen in several animals. Humans develop L. monocytogenes infection—listeriosis—primarily through foodborne transmission. The clinical spectrum of listeriosis ranges from febrile gastroenteritis in healthy persons to invasive disease, including bacteremia and meningoencephalitis. Typical risk groups for invasive disease are pregnant women and their neonates, older adults, and immunocompromised persons.

MICROBIOLOGY

L. monocytogenes is a nonsporulating, facultatively anaerobic, short, gram-positive rod that grows well on blood agar, demonstrating small zones of β-hemolysis. Organisms sometimes appear gram-variable and resemble cocci, diplococci, or diphtheroids; this appearance can obscure the diagnosis. On light microscopy, L. monocytogenes demonstrates characteristic tumbling motility. It grows optimally at 30–37oC but can grow at refrigerator temperatures as low as 4oC. Serotypes are usually determined on the basis of somatic (O) and flagellar (H) antigens. Nearly all human illness is caused by serotypes 1/2a, 1/2b, and 4b.

PATHOGENESIS

L. monocytogenes lives in soil and decaying vegetable matter. Numerous bird and mammal species are reservoirs. In addition to its ability to grow at cold temperatures, Listeria’s tolerance to low-pH and high-salt environments facilitates its environmental survival. Human infection typically occurs through ingestion of contaminated food. The infectious dose has not been well established but is likely to be very low for persons with severely impaired cellular immunity. Increased gastric pH, such as that due to proton pump inhibitors, probably promotes the organism’s survival in the gastrointestinal tract. After transcytosis across the intestinal epithelium, the bacteria travel via mesenteric lymph nodes and the bloodstream to the liver and spleen, its target organs; dissemination to other organs can occur. L. monocytogenes can also migrate across the blood–brain barrier and the placenta.

Virulence factors, including a pore-forming cytolysin (listeriolysin O; LLO) and phospholipases, facilitate evasion of intracellular killing by mediating escape from the internalization vacuole; the organism can then enter the host cell cytosol. The surface protein ActA facilitates direct cell-to-cell movement within the cytosol, allowing L. monocytogenes to avoid encountering components of the host immune system, such as antibodies and complement, during dissemination. Iron promotes listerial growth of the organism in vitro, an effect that explains why listeriosis has been associated with iron-overload conditions, including hemochromatosis.

IMMUNE RESPONSE

Although L. monocytogenes is ubiquitous in the environment, infection is rare because of both innate and adaptive host immune responses. Studies of mice have contributed to a detailed understanding of the immune response to infection. Activation of innate immunity is important for host survival. Interferon γ and tumor necrosis factor α (TNF-α) are among the key cytokines involved in this response. T cells are the primary drivers of the adaptive immune response, furthering the clearance of infected cells. Cytotoxic (CD8+) T cells are the main contributors to long-term immunity.

These immune mechanisms explain the ...

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