Studies suggest that up to 10% of human gastrointestinal tracts may be colonized by L. monocytogenes.
Due to its frequent pathogenicity causing meningitis in newborns (acquired transvaginally), pregnant mothers are often advised not to eat soft cheeses such as Brie, Camembert, feta and queso blanco fresco, which may be contaminated with and permit growth of L. monocytogenes . It is the third most common cause of meningitis in newborns.
More recently, L. monocytogenes has been used as the model organism to illustrate the Patho-biotechnology concept.
L. monocytogenes was first described by E.G.D.Murray in 1926 based on six cases of sudden death in young rabbits. Murray referred to the organism as Bacterium monocytogenes before J.H. Harvey Pirie changed the genus name to Listeria in 1940.. Although clinical descriptions of L. monocyotogenes infection in both animals and humans were published in the 1920s, not until 1952 in East Germany was it recognized as a significant cause of neonatal sepsis and meningitis. Listeriosis in adults would later be associated with patients living with compromised immune systems, such as individuals taking immunosuppressant drugs and corticosteroids for malignancies or organ transplants, and those with HIV infection.
It wasn't until 1981 however that L. monocytogenes was identified as a cause of foodborne illness. An outbreak of listeriosis in Halifax, Nova Scotia involving 41 cases and 18 deaths, mostly in pregnant women and neonates, was epidemiologically linked to the consumption of coleslaw containing cabbage that had been treated with L. monocytogenes contaminated raw sheep manure. Since then a number of cases of foodborne listeriosis have been reported, and L. monocytogenes is now widely recognized as an important hazard in the food industry.
The infective dose of L. monocytogenes varies with the strain and with the susceptibility of the victim. From cases contracted through raw or supposedly pasteurized milk, one may safely assume that in susceptible persons, fewer than 1,000 total organisms may cause disease. L. monocytogenes may invade the gastrointestinal epithelium. Once the bacterium enters the host's monocytes, macrophages, or polymorphonuclear leukocytes, it becomes blood-borne (septicemic) and can grow. Its presence intracellularly in phagocytic cells also permits access to the brain and probably transplacental migration to the fetus in pregnant women. The pathogenesis of L. monocytogenes centers on its ability to survive and multiply in phagocytic host cells.
Bacteriophage treatments have been developed by several companies. EBI Food Safety and Intralytix both have products suitable for treatment of the bacteria. The FDA of the United States approved a cocktail of six bacteriophages from Intralytix, and a one type phage product from EBI Food Safety designed to kill the bacteria L. monocytogenes. Uses would potentially include spraying it on fruits and ready-to-eat meat such as sliced ham and turkey.
The methods for analysis of food are complex and time-consuming. The present U.S. Food and Drug Administration (FDA) method, revised in September, 1990, requires 24 and 48 hours of enrichment, followed by a variety of other tests. Total time to identification takes from 5 to 7 days, but the announcement of specific nonradiolabled DNA probes should soon allow a simpler and faster confirmation of suspect isolates.
Recombinant DNA technology may even permit 2-to-3 day positive analysis in the future. Currently, the FDA is collaborating in adapting its methodology to quantitate very low numbers of the organisms in foods.
Bio-Rad Laboratories (www.bio-rad.com) have come up with media called Rapid'L.Mono Medium which cut short time to 48 hours
Following internalisation, the bacterium must escape from the vacuole/phagosome before fusion with a lysosome can occur. Two main virulence factors which allow the bacterium to escape are listeriolysin O (LLO - encoded by hly) and phospholipase C B (plcB). Secretion of LLO and PlcB disrupts the vacuolar membrane and allows the bacterium to escape into the cytoplasm where it may proliferate.
Once in the cytoplasm, L. monocytogenes exploits host actin for the second time. ActA proteins associated with the old bacterial cell pole (being a bacilli, L. monocytogenes septates in the middle of the cell and thus has one new pole and one old pole) are capable of binding the Arp2/3 complex and thus induce actin nucleation at a specific area of the bacterial cell surface. Actin polymerization then propels the bacterium unidirectionally into the host cell membrane. The protrusion which is formed may then be internalised by a neighbouring cell, forming a double-membrane vacuole from which the bacterium must escape using LLO and PlcB.