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Listeria which grows between 0-50°C functions as a facultatively anaerobic foodborne pathogen with Gram-positive characteristics and demonstrates significant abilities to invade host cells while existing broadly in nature. Listeria organisms show resistance to environmental changes by surviving both acidic conditions and high salt concentrations. The food industry considers Listeria monocytogenes a major threat because it possesses distinctive properties. Listeriosis caused by this pathogen poses great danger to pregnant women newborns older adults and immunocompromised individuals.
Bacteria affect meat and vegetable surfaces frequently because they contaminate up to 15% of these food products. This bacteria lives temporarily inside both animal and human digestive systems which indicates that humans encounter it regularly.
The psychrophilic bacterium possesses a competitive advantage against both Gram-positive and Gram-negative microorganisms when stored at refrigerated temperatures. The organism proliferates extensively in spoiled foods when food decay causes an increase in alkalinity. The patterns seen in widespread human listeriosis outbreaks resemble what happens during animal listeriosis epidemics. The first documented instance of foodborne listeriosis in Canada emerged between 1980 and 1981 through contaminated coleslaw consumption. Multiple food products beyond coleslaw have been identified as sources of outbreaks of different magnitudes including both unpasteurized and pasteurized cheese varieties as well as pasteurized milk, butter, a range of fruits and vegetables and multiple types of meat products.
Table 1. Some foods implicated in published reports of foodborne listeriosis
| Dairy products | Fruits and vegetables | Meat products | Fish products |
| Pasteurized whole milk Chocolate milk Mexican-style cheese Soft cheese (different types) Hard cheese Goat cheese Ice cream Fresh cream | Coleslaw (cabbage) Lettuce Corn Rice salad Strawberries Cantaloupes Nectarines Salted mushrooms Alfalfa tablets Apples Blueberries Stone fruit Sprouts | Delicatessen foods (deli meats) Uncooked hot dogs Turkey franks Pork tongue in aspic Pork pie Beef Jellied pork Cooked ham Foie gras Ox tongue Undercooked chicken | Tuna salad Smoked fish Shrimp salad |
(Source: Schlech WF. 2019)
Scientists established that the genus Listeria consisted of eight species and two subspecies until the most recent studies. Scientists have discovered 17 species within the Listeria genus today. Only L. monocytogenes and L. ivanovii among the Listeria genus demonstrate pathogenic traits for humans. The bacterium shows narrow beta-hemolytic zones on blood agar plates and umbrella-shaped growth patterns in semi-solid media and requires catalase and CAMP tests for its identification from other genera. Its pathogenicity stems from a unique intracellular lifecycle: The bacterium binds to host cells using internalin proteins and escapes phagosomes by producing Listeriolysin O (LLO), afterward exploiting actin polymerization to move between cells. The microorganism penetration through the intestinal barrier leads to widespread infections including septicemia as well as meningitis and maternal-fetal transmission. Invasive Listeria infections can be classified into three main clinical categories: Human listeriosis cases consist of pregnancy-related and neonatal infections which make up 14% of cases alongside bacteremia or septicemic listeriosis which represents 52% and central nervous system infections such as meningitis or meningoencephalitis known as neurolisteriosis which comprise 31% of cases.
Figure 1. Schematic of Listeria monocytogenes infection of a human host
(Source: Radoshevich L, et al. 2018)
The incubation period for Listeria infection ranges from 3 to 70 days, with clinical presentations varying significantly depending on the host's immune status. When healthy people contract infection, they develop self-limiting gastroenteritis which manifests as fever combined with diarrhea and vomiting. Invasive infections typically progress to meningitis which manifests through headaches and neck stiffness accompanied by altered consciousness and complications such as septicemia and endocarditis with mortality rates that can reach 30%. Pregnant women face an infection risk that is between 13 and 100 times higher than non-pregnant women with maximum infection rates appearing during the last stages of pregnancy. The placenta functions as a bacterial "sanctuary" which can lead to chorioamnionitis and other serious outcomes including miscarriage and premature birth and may cause neonatal septicemia or meningitis with mortality rates between 27-33%. Even though pregnant women can exhibit just mild symptoms like low-grade fever, the fetal outcomes often turn out to be extremely poor which underscores the need for early diagnosis.
Pregnant women experience a risk of Listeria infection that exceeds the general population's by a factor of 13 to 100 times. More than 65% of all pregnancy-related cases result from infections that occur during the late stages of pregnancy. This susceptibility stems from the physiological immunosuppressive state during pregnancy: Fetal tolerance requires the downregulation of maternal Th1 immune responses including IL-12 and IFN-γ as well as dominant Th2 responses which consist of IL-4 and IL-10 thereby reducing maternal capability to destroy intracellular pathogens. The interaction between E-cadherin on placental trophoblast cells and the Listeria internalin InlA molecule establishes the molecular foundation of the bacteria's placentotropism. Mutated inlA genes in bacterial strains lead to decreased invasiveness yet enable infection of the fetus via placental transmission.
Listeria initially arrives at the small intestinal mucosa after oral entry into the human body and then travels to other organs through both the circulatory system and lymph nodes. The ability of this intracellular bacterium to hide within host cells poses diagnostic challenges because of its uncommon nature. Listeria secretes listeriolysins and phospholipases that break down the vacuole membrane after cellular entry which helps it survive inside cells. Upon reaching the cytoplasm Listeria monocytogenes begins to multiply and triggers actin filament formation which facilitates its travel through the cytoplasm to the plasma membrane. The bacterium reaches neighboring cells by forming plasma membrane protrusions followed by intercellular spread. The circulation mechanism allows Listeria to bypass the extracellular space which helps it to evade human T cell immunity by transferring directly between cells while remaining infectious across multiple organs and tissues.
Empirical studies have revealed that Listeria monocytogenes can invade both extravillous trophoblast cells (EVT) and syncytiotrophoblast (SYN). Immunohistochemistry indicates that LM entered the SYN of the placenta in patients with listeriosis. Most infections occurred in the third trimester of pregnancy, further indicating that SYN could be where the bacteria enter the placenta. The bacteria cross the placental barrier to enter the fetus through the umbilical vein and then target the liver and central nervous system. The bacteria's phospholipase PlcB enables them to destroy tight junctions between brain microvascular endothelial cells which allows them to penetrate the blood-brain barrier and cause neonatal meningitis.
Figure 2. The schematic diagram of Listeria penetrating the placental barrier
(Source: Wang Z, et al. 2021)
Pregnant women with Listeria infection exhibit highly heterogeneous clinical signs which sharply differ between mild maternal symptoms and severe impacts on the fetus. Infections in pregnant women typically produce low-grade fevers below 38.5°C and mild gastrointestinal symptoms such as diarrhea and nausea in 68% of cases while 30% of infected individuals remain asymptomatic. The vague signs in pregnant women often resemble common cold symptoms or regular pregnancy discomforts which results in postponed diagnoses. Research indicates that patients typically wait 7-14 days between symptom emergence and diagnosis confirmation and diagnostic processes that extend beyond 48 hours triple the fetal death risk.
Listeria infection during pregnancy leads to devastating results for pregnancy outcomes. The likelihood of spontaneous miscarriage rises to 20-29% when infections occur early in pregnancy before 12 weeks which represents a 21 times greater risk compared to pregnancies without infection. Mid to late pregnancy infections predominantly lead to chorioamnionitis which occurs in 65% of cases and also result in preterm birth with rates between 40-60% and stillbirth at a rate of 14.3%. Between 15% and 30% of fetuses develop an intrauterine infection even when their mothers show no symptoms.
Neonatal infections receive classification into early-onset types that present within 72 hours of birth and late-onset types that show up between 7 to 60 days after birth. Early-onset neonatal infections usually develop into septicemia leading to a death rate between 27-33%, whereas late-onset infections most commonly result in meningitis which makes up 55% of all neonatal infections. Around 30% of surviving patients develop neurological sequelae including epilepsy along with intellectual disability and motor dysfunction. Examining the infected placentas through pathological analysis shows focal necrotic chorionitis accompanied by significant neutrophil infiltration as typical features. Bacteria tend to aggregate within the intervillous spaces as well as inside trophoblast cells. Placental perfusion insufficiency directly produces these pathological changes which might explain how fetal growth restriction develops.
To prevent complications and death as well as long-term sequelae in human listeriosis patients it is essential to promptly provide adequate antimicrobial treatment. Penicillin together with ampicillin and amoxicillin represent primary treatments among β-lactam antibiotics. Research demonstrates that at sub-inhibitory concentrations β-lactam antibiotics reduce LLO production but achieve complete bactericidal effectiveness at levels 16 times above the minimum inhibitory concentration. The successful elimination of Listeria depends on the use of β-lactam drugs to target penicillin-binding proteins (PBPs). The response of Listeria to β-lactam antibiotics varies across different PBPs with PBP3 emerging as the main target. Listeria naturally resists antibiotics that bind poorly to PBP3 like cephalosporins regardless of other PBPs being fully blocked. During peptidoglycan synthesis Listeria uses PBP3 in its final stages and blocking this protein reduces Listeria's ability to survive.
Patients should receive intravenous ampicillin or penicillin G combined with gentamicin for better bacterial elimination as the first treatment while trimethoprim-sulfamethoxazole works as a substitute for individuals who cannot tolerate penicillin. The duration of treatment needs to be adjusted according to the site of infection: The typical treatment period for meningitis lasts between 4 and 6 weeks although pregnant women need only 2 weeks of treatment. Monitoring of antimicrobial resistance highlights the necessity for careful monitoring of nephrotoxic risks when combining aminoglycosides with β-lactams.
References
| Target | Cat. No. | Product Name | Expression System | Tag/Conjugate | Application | |
| L. monocytogenes | DAGP0192 | Recombinant Listeria monocytogenes p60 [His] | E. coli | His | ELISA, LF | Inquiry |
| DAG4326 | Recombinant L. monocytogenes Internalin [His] | E. coli | His | N/A | Inquiry | |
| DAG-P2903 | Active Listeriolysin (aa 60 - 529) | E. coli | Unconjugated | SDS-PAGE | Inquiry | |
| DAG-P2785 | Active Listeriolysin (aa 26 - 529) | E. coli | Unconjugated | SDS-PAGE | Inquiry | |
| L. monocytogenes FliC | DAG-H10322 | L. monocytogenes Flagellin [His] | E. coli | His | N/A | Inquiry |
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