Wikipedia

Listeria monocytogenes

Listeria monocytogenesis the species ofpathogenic bacteriathat causes the infectionlisteriosis.It is afacultative anaerobicbacterium, capable of surviving in the presence or absence of oxygen. It can grow and reproduce inside the host's cells and is one of the mostvirulentfoodborne pathogens. Twenty to thirty percent of foodborne listeriosis infections in high-risk individuals may be fatal.[1][2][3]In theEuropean Union,listeriosis continues an upward trend that began in 2008, causing 2,161 confirmed cases and 210 reported deaths in 2014, 16% more than in 2013. In the EU, listeriosis mortality rates also are higher than those of other foodborne pathogens.[4][5]Responsible for an estimated 1,600 illnesses and 260 deaths in theUnited Statesannually,listeriosisranks third in total number of deaths among foodborne bacterial pathogens, with fatality rates exceeding evenSalmonellaspp.andClostridium botulinum.

Listeria monocytogenes
Scanning electron micrographofListeria monocytogenes.
Scientific classificationEdit this classification
Domain: Bacteria
Phylum: Bacillota
Class: Bacilli
Order: Caryophanales
Family: Listeriaceae
Genus: Listeria
Species:
L. monocytogenes
Binomial name
Listeria monocytogenes
(E. Murray et al. 1926) Pirie 1940

Named forJoseph Lister,Listeria monocytogenesis aGram-positivebacterium,in the phylumBacillota.Its ability to grow at temperatures as low as 0 °C permits multiplication at typical refrigeration temperatures, greatly increasing its ability to evade control in human foodstuffs.Motileviaflagellaat 30 °C and below, but usually not at 37 °C,[6]L. monocytogenescan instead move withineukaryoticcells by explosivepolymerizationofactinfilaments (known as comet tails or actin rockets).[3]OnceListeria monocytogenesenters the hostcytoplasm,multiple changes in bacterial metabolism and gene expression help to complete its metamorphosis from soil dweller to intracellular pathogen.[7]

Studies suggest that up to 10% of humangastrointestinal tractsmay be colonized byL. monocytogenes.[1]Nevertheless, clinical diseases due toL. monocytogenesare more frequently recognized byveterinarians,especially asmeningoencephalitisinruminants.See:listeriosis in animals.

Due to its frequentpathogenicity,causingmeningitisin newborns (acquired transvaginally), pregnant women are often advised not to eat soft cheeses such asBrie,Camembert,feta,andqueso blanco fresco,which may be contaminated with and permit growth ofL. monocytogenes.[8]It is the third most common cause of meningitis in newborns.Listeria monocytogenescan infect the brain, spinal-cord membranes and bloodstream of the host[9]through the ingestion of contaminated food such as unpasteurized dairy or raw foods.[10]

Classification

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L. monocytogenesis aGram-positive,non-spore-forming,motile, facultatively anaerobic, rod-shaped bacterium. It iscatalase-positive andoxidase-negative, and expresses a betahemolysin,which causes destruction of red blood cells. This bacterium exhibits characteristic tumbling motility when viewed with light microscopy.[11]AlthoughL. monocytogenesis actively motile by means of peritrichousflagellaat room temperature (20−25 °C), the organism does not synthesize flagella at body temperatures (37 °C).[12]

The genusListeriabelongs to the class Bacilli and the order Bacillales, which also includesBacillusandStaphylococcus.Listeriacurrently contains 27 species:Listeria aquatica, Listeria booriae, Listeria cornellensis, Listeria cossartiae, Listeria costaricensis, Listeria farberi, Listeria fleischmannii, Listeria floridensis, Listeria goaensis, Listeria grandensis, Listeria grayi, Listeria immobilis, Listeria innocua, Listeria ivanovii, Listeria marthii, Listeria monocytogenes, Listeria murrayi, Listeria newyorkensis, Listeria portnoyi, Listeria riparia, Listeria rocourtiae, Listeria rustica, Listeria seeligeri, Listeria thailandensis, Listeria valentina, Listeria weihenstephanensis, Listeria welshimeri.L. denitrificans,previously thought to be part of the genusListeria,was reclassified into the new genusJonesia.[13]BothL. ivanoviiandL. monocytogenesare pathogenic in mice, but onlyL. monocytogenesis consistently associated with human illness.[14]The 13serotypesofL. monocytogenescan cause disease, but more than 90% of human isolates belong to only three serotypes: 1/2a, 1/2b, and 4b.L. monocytogenesserotype 4b strains are responsible for 33 to 35% of sporadic human cases worldwide and for all major foodborne outbreaks in Europe and North America since the 1980s.[15]

History

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L. monocytogeneswas first described by E.G.D. Murray (Everitt George Dunne Murray) in 1924 based on six cases of sudden death in young rabbits, and published a description with his colleagues in 1926.[16] Murray referred to the organism asBacterium monocytogenesbeforeHarvey Piriechanged the genus name toListeriain 1940.[17]Although clinical descriptions ofL. monocytogenesinfection in both animals and humans were published in the 1920s, it was not recognized as a significant cause ofneonatal infection,sepsis,andmeningitisuntil 1952 inEast Germany.[18]Listeriosisin adults was later associated with patients living with compromised immune systems, such as individuals takingimmunosuppressant drugsandcorticosteroidsformalignanciesor organ transplants, and those with HIV infection.[19]

L. monocytogeneswas not identified as a cause of foodborne illness until 1981, however. An outbreak of listeriosis inHalifax,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 contaminated withL. monocytogenes-contaminated sheep manure.[20]Since then, a number of cases of foodborne listeriosis have been reported, andL. monocytogenesis now widely recognized as an important hazard in the food industry.[21]

Pathogenesis

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Stages in the intracellular lifecycle ofL. monocytogenes:(Center) Cartoon depicting entry, escape from a vacuole, actin nucleation, actin-based motility, and cell-to-cell spread. (Outside) Representative electron micrographs from which the cartoon was derived. LLO, PLCs, and ActA are all described in the text. The cartoon and micrographs were adapted from Tilney and Portnoy (1989).
Main article:Listeriosis
See also:2008 Canada listeriosis outbreak,2008–2009 Chile listeriosis outbreak,and2011 United States listeriosis outbreak
See also:2014 Macedonia listeriosis outbreak,2017–2018 South African listeriosis outbreak,and2018 Australian rockmelon listeriosis outbreak

InvasiveinfectionbyL. monocytogenescauses the disease listeriosis. When the infection is not invasive, any illness as a consequence of infection is termed febrile gastroenteritis. The manifestations of listeriosis include sepsis,[22]meningitis(ormeningoencephalitis),[22]encephalitis,[23]corneal ulcer,[24]pneumonia,[25]myocarditis,[26]andintrauterineorcervicalinfections in pregnant women, which may result inspontaneous abortion(second to third trimester) orstillbirth.Surviving neonates of fetomaternal listeriosis may suffer granulomatosis infantiseptica —pyogenicgranulomasdistributed over the whole body — and may suffer from physical retardation.Influenza-like symptoms, including persistent fever, usually precede the onset of the aforementioned disorders. Gastrointestinal symptoms, such as nausea, vomiting, anddiarrhea,may precede more serious forms of listeriosis or may be the only symptoms expressed. Gastrointestinal symptoms were epidemiologically associated with use ofantacidsorcimetidine.The onset time to serious forms of listeriosis is unknown, but may range from a few days to 3 weeks. The onset time to gastrointestinal symptoms is unknown, but probably exceeds 12 hours. An early study suggested thatL. monocytogenesis unique among Gram-positive bacteria in that it might possesslipopolysaccharide,[27]which serves as anendotoxin.Later, it was found to not be a true endotoxin.Listeriacell walls consistently containlipoteichoic acids,in which a glycolipid moiety, such as a galactosyl-glucosyl-diglyceride, is covalently linked to the terminal phosphomonoester of the teichoic acid. This lipid region anchors the polymer chain to the cytoplasmic membrane. These lipoteichoic acids resemble the lipopolysaccharides of Gram-negative bacteria in both structure and function, being the onlyamphipathicpolymers at the cell surface.[28][29]

L. monocytogeneshas D-galactose residues on its surface that can attach to D-galactose receptors on the host cell walls. These host cells are generallyM cellsandPeyer's patchesof the intestinal mucosa. Once attached to these cells,L. monocytogenescan translocate past the intestinal membrane and into the body.[citation needed].Alternatively, losses of structural integrity (such as small lacerations) in the gastrointestinal epithelium could allow the microorganism to penetrate from the gastrointestinal tract to the bloodstream.

The infectious dose ofL. monocytogenesvaries 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. monocytogenesmay invade the gastrointestinal epithelium. Once the bacterium enters the host'smonocytes,macrophages,orpolymorphonuclear leukocytes,it becomes bloodborne (sepsis) and can grow. Its presence intracellularly inphagocyticcells also permits access to the brain and probably transplacental migration to the fetus in pregnant women. This process is known as the "Trojan Horse mechanism". The pathogenesis ofL. monocytogenescenters on its ability to survive and multiply in phagocytic host cells. It seems thatListeriaoriginally evolved to invade membranes of the intestines, as an intracellular infection, and developed a chemical mechanism to do so. This involves a bacterial proteininternalin(InlA/InlB), which attaches to a protein on the intestinal cell membrane "cadherin" and allows the bacteria to invade the cells through a zipper mechanism. These adhesion molecules are also to be found in two other unusually tough barriers in humans — the blood-brain barrier and the fetal–placental barrier, and this may explain the apparent affinity thatL. monocytogeneshas for causing meningitis and affecting babiesin utero.Once inside the cell,L. monocytogenesrapidly acidifies the lumen of the vacuole formed around it during cell entry to activate listeriolysin O, acholesterol-dependent cytolysincapable of disrupting the vacuolar membrane. This frees the pathogen and gives it access to the cytosol of the cell, where it continues its pathogenesis.[30]Motility in the intracellular space is provided by actin assembly-inducing protein, which allows the bacteria to use the host cell's actin polymerization machinery to polymerize the cytoskeleton to give a "boost" to the bacterial cell so it can move in the cell. The same mechanism also allows the bacteria to travel from cell to cell.[31]

Regulation of pathogenesis

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L. monocytogenescan act as asaprophyteor apathogen,depending on its environment. When this bacterium is present within a host organism,quorum sensingand other signals cause the up-regulation of severalvirulencegenes. Depending on the location of the bacterium within the host organism, different activators up-regulate the virulence genes. SigB, an alternativesigma factor,up-regulatesVirgenes in the intestines, whereasPrfAup-regulates gene expression when the bacterium is present in blood.[32][33][34][35]L. monocytogenesalso senses the entry to host by examining available nutrient sources. For exampleL-glutamine,an abundant nitrogen source in the host, induces the expression of virulence genes inL. monocytogenes.[36]Little is known about how this bacterium switches between acting as a saprophyte and a pathogen; however, severalnoncoding RNAsare thought to be required to induce this change.[citation needed]

Pathogenicity of lineages

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L. monocytogeneshas three distinct lineages, with differing evolutionary histories and pathogenic potentials.[37]Lineage I strains contain the majority of human clinical isolates and all human epidemic clones, but are underrepresented in animal clinical isolates.[37]Lineage II strains are overrepresented in animal cases and underrepresented in human clinical cases, and are more prevalent in environmental andfood samples.[38]Lineage III isolates are very rare, but significantly more common in animal than human isolates.[37]

Detection

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Colonies of typicalL. monocytogenesas they appear when grown onListeria-selectiveagar

The Anton test is used in the identification ofL. monocytogenes;instillation of a culture into the conjunctival sac of a rabbit or guinea pig causes severe keratoconjunctivitis within 24 hours.[39][40]

Listeriaspecies grow on media such as Mueller-Hinton agar. Identification is enhanced if the primary cultures are done on agar containing sheep blood, because the characteristic small zone of hemolysis can be observed around and under colonies. Isolation can be enhanced if the tissue is kept at 4 °C for some days before inoculation into bacteriologic media. The organism is a facultative anaerobe and is catalase-positive and motile.Listeriaproduces acid, but not gas, when fermenting a variety of carbohydrates.[41] The motility at room temperature and hemolysin production are primary findings that help differentiate Listeria fromCorynebacterium.[42]

The methods for analysis of food are complex and time-consuming. The present U.S. 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 five to seven days, but the announcement of specific non-radiolabelledDNA probesshould soon allow a simpler and faster confirmation of suspect isolates.[43]

Recombinant DNA technology may even permit two- to three-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.[citation needed]

Treatment

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When listeric meningitis occurs, the overallmortalitymay reach 70%, fromsepsis50%, and from perinatal/neonatal infections greater than 80%. In infections during pregnancy, the mother usually survives. Reports of successful treatment with parenteralpenicillinorampicillinexist.[44]Trimethoprim-sulfamethoxazolehas been shown effective in patients allergic to penicillin.[44]

A bacteriophage,Listeria phage P100,has been proposed asfood additiveto controlL. monocytogenes.[45]Bacteriophage treatments have been developed by several companies. EBI Food Safety and Intralytix both have products suitable for treatment of the bacterium. The U.S.Food and Drug Administration(FDA) approved a cocktail of sixbacteriophagesfrom Intralytix, and a one-type phage product from EBI Food Safety designed to killL. monocytogenes.Uses would potentially include spraying it on fruits and ready-to-eat meat such as sliced ham and turkey.[46]

Use as a transfection vector

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BecauseL. monocytogenesis an intracellular bacterium, some studies have used this bacterium as a vector to deliver genesin vitro.Currenttransfectionefficiency remains poor. One example of the successful use ofL. monocytogenesinin vitrotransfer technologies is in the delivery of gene therapies for cystic fibrosis cases.[47]

Cancer treatment

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Listeria monocytogenesis being investigated as acancer immunotherapyfor several types of cancer.[48][49]

A live attenuatedListeria monocytogenescancer vaccine,ADXS11-001,is under development as a possible treatment forcervical carcinoma.[50]

Epidemiology

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Researchers have foundListeria monocytogenesin at least 37mammalian species,both domesticated and feral, as well as in at least 17 species ofbirdsand possibly in some species offishandshellfish.Laboratories can isolateListeria monocytogenesfromsoil,silage,and other environmental sources.Listeria monocytogenesis quite hardy and resists the deleterious effects of freezing, drying, and heat remarkably well for a bacterium that does not form spores. MostListeria monocytogenesstrains are pathogenic to some degree.[citation needed]

Routes of infection

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Listeria monocytogeneshas been associated with such foods as rawmilk,pasteurized fluid milk,[51]cheeses(particularly soft-ripened varieties), hard-boiled eggs,[52]ice cream,rawvegetables,fermented raw-meatsausages,raw and cookedpoultry,raw meats (of all types), and raw and smokedfish.Most bacteria can survive near freezing temperatures, but cannot absorb nutrients, grow or replicate; however,L. monocytogeneshas the ability to grow at temperatures as low as 0 °C which permits exponential multiplication in refrigerated foods. At refrigeration temperature, such as 4 °C, the amount of ferric iron can affect the growth ofL. monocytogenes.[53]

Infectious cycle

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The primary site of infection is the intestinal epithelium, where the bacteria invade nonphagocytic cells via the "zipper" mechanism. Uptake is stimulated by the binding of listerial internalins (Inl) toE-cadherin,a host cell adhesion factor, or Met (c-Met), hepatocyte growth factor. This binding activates certain Rho-GTPases, which subsequently bind and stabilizeWiskott–Aldrich syndrome protein(WASp). WASp can then bind theArp2/3 complexand serve as anactinnucleation point. Subsequent actin polymerization creates a "phagocytic cup", an actin-based structure normally formed around foreign materials by phagocytes prior to endocytosis. The net effect of internalin binding is to exploit the junction-forming apparatus of the host into internalizing the bacterium.L. monocytogenescan also invade phagocytic cells (e.g.,macrophages), but requires only internalins for invasion of nonphagocytic cells.[citation needed]

Following internalization, the bacterium must escape from the vacuole/phagosomebefore fusion with alysosomecan occur. Three main virulence factors that allow the bacterium to escape arelisteriolysin O(LLO encoded byhly) phospholipase A (encoded byplcA) andphospholipase B(plcB).[54][55]Secretion of LLO and PlcA disrupts the vacuolar membrane and allows the bacterium to escape into the cytoplasm, where it may proliferate.[citation needed]

Once in the cytoplasm,L. monocytogenesexploits hostactinfor the second time.ActA proteinsassociated with the old bacterial cell pole (being a bacillus,L. monocytogenesseptates in the middle of the cell, thus has one new pole and one old pole) are capable of binding theArp2/3 complex,thereby inducing 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 formed may then be internalized by a neighboring cell, forming a double-membrane vacuole from which the bacterium must escape using LLO and PlcB. This mode of direct cell-to-cell spread involves a cellular mechanism known asparacytophagy.[56]

The ability of L. monocytogenes to successfully infect depends on its resistance to the high concentrations ofbileencountered throughout thegastrointestinaltract.[57]This resistance is due, in part, to thenucleotide excision repairprotein UvrAthat is necessary forrepair of DNA damagescaused bybile salts.[58]

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