Listeriosis pathophysiology

Overview
Most human infections follow consumption of contaminated food. Rare cases of nosocomial transmission have been reported.

When Listeria bacteria get into a food processing factory, they can live there for years, sometimes contaminating food products. The bacterium has been found in a variety of raw foods, such as uncooked meats and vegetables, as well as in foods that become contaminated after cooking or processing, such as soft cheeses, processed meats such as hot dogs and deli meat (both products in factory-sealed packages and products sold at deli counters), and smoked seafood. Unpasteurized (raw) milk and cheeses and other foods made from unpasteurized milk are particularly likely to contain the bacterium.

Listeria is killed by pasteurization and cooking; however, in some ready-to-eat foods, such as hot dogs and deli meats, contamination may occur after factory cooking but before packaging. Unlike most bacteria, Listeria can grow and multiply in some foods in the refrigerator.

Microbiology: Listeria Monocytogenes
Listeria uses the cellular machinery to move around inside the host cell: it induces directed polymerization of actin by the ActA transmembrane protein, thus pushing the bacterial cell around.

Listeria monocytogenes for example, encodes virulence genes which are thermoregulated. The expression of virulence factor is optimal at 37 degrees Celsius and is controlled by a transcriptional activator, PrfA, whose expression is thermoregulated by the PrfA thermoregulator UTR element. At low temperatures, the PrfA transcript is not translated due to structural elements near the ribosome binding site. As the bacteria infects the host, the temperature of the host melts the structure and allows translation initiation for the virulent genes.

Pathogenesis: Mechanism of Infection
The majority of Listeria bacteria are targeted by the immune system before they are able to cause infection. Those that escape the immune system's initial response, however, spread though intracellular mechanisms and are therefore guarded against circulating immune factors (AMI).

To invade, Listeria induces macrophage phagocytic uptake by displaying D-galactose receptors that are then bound by the macrophage's polysaccharide receptors (Notably, in most bacterial infections it is the host cell, not the bacteria, that displays the polysaccharide). Once phagocytosed, the bacteria is encapsulated by the host cell's acidic phagolysosome organelle. Listeria, however, escapes the phagolysosome by lysing the vacuole's entire membrane with secreted hemolysin, now characterized as the exotoxin listeriolysin O. The bacteria then replicate inside the host cell's cytoplasm.

Listeria must then navigate to the cell's periphery to spread the infection to other cells. Outside of the body, Listeria has flagellar-driven motility. However, at 37°C, flagella cease to develop and the bacteria instead usurps the host cell's cytoskeleton to move. Listeria, inventively, polymerizes an actin tail or "comet", using host-produced actin filaments with the promotion of virulence factor ActA. The comet forms in a polar manner and aids the bacteria's migration to the host cell's outer membrane. Gelsolin, an actin filament severing protein, localizes at the tail of Listeria and accelerates the bacterium's motility. Once at the cell surface, the actin-propelled Listeria pushes against the cell's membrane to form protrusions called filopods or "rockets". The protrusions are guided by the cell's leading edge to contact adjacent cells which subsequently engulf the Listeria rocket and the process is repeated, perpetuating the infection. Once phagocytosed, the Listeria is never again extracellular: it is an intracytoplasmic parasite like Shigella flexneri and Rickettsia.

Resources
CDC Listeriosis