Listeria Monocytogenes

2 February 2017

The bacterium was named monocytogenes because one distinguish characteristic of infection in rabbits, which was the production of monocytosis in blood (Shuin et al. , 1982). L. monocytogenes is phychrophilic, has a temperature for growth of 0°C to 45°C (Barbosa et al. 1994), and enjoys a competitive advantage against other gram-positive and gram-negative microorganisms in cold environments, such as refrigerators. Recent investigations indicate that the organism can initiate growth at pH values as low as 4. 4. Also, it grows optimally at water activity of 0. 97.

For the majority of strains, the minimum water activity needed for growth is 0. 93 (Lou et al. , 1999); however, some strains may be able to grow at water activity values as low as 0. 90 and survive for long periods of time at 0. 83 (Shahamat et al. , 1980). L. onocytogenes is able to grow in the presence of 10 to 12% sodium chloride; it grows to high populations in moderate salt concentrations (6. 5%).

Listeria Monocytogenes Essay Example

The bacterium survival in high-salt environments is significantly increased by lowering the temperature. Route of Exposure L. monocytogenes is particularly interesting as a foodborne pathogen in that it is ubiquitous in nature. The current understanding of human listeriosis epidemiology suggests that the organism is a common contaminant of food products. This contamination usually takes place on the surface of the products, with up to 15% harboring the organism.

The presence of L. monocytogenes in the food processing chain is evidence by the widespread distribution of the listeriae in processed products. Occurrence of sporadic listeriosis appears to be more common in the spring and summer months. This could be explained by seasonal variations in the type of food products eaten by human populations, with higher-risk products eaten in the warmer months. Some outbreaks investigations suggest that certain ready-to-eat processed foods pose a high risk of contracting listeriosis for susceptible populations.

These foods are usually preserved by refrigeration and offer an ppropriate environment for the multiplication of L. monocytogenes during manufacture, aging, transportation and storage. The entry of L. monocytogenes into food processing plants occurs through soil on clothing or equipments, contaminated hides or surfaces, and possibly healthy human carriers. The humidity and presence of nutrients support the growth of Listeria, which is commonly found in moist areas such as processing equipment, drains, etc (Cox et al. , 1989). In addition, Listeria can attach to different types of surfaces and biofilm formation has been observed in meat and dairy processing environment (Jeong et al. 1994).

Post-processing contamination is the most likely route of contamination of processed foods. Currently, there is no evidence to indicate that L. monocytogenes can survive heat processing protocols. However, because it is a frequent contaminant of raw material used in food processing plants, there are plenty opportunities for reintroduction of listeriae into food processing facilities by cross contamination (Doyle, 1988). If the product is contaminated during its elaboration, the bacteria can survive and multiply throughout storage causing disease when it is consumed.

In conclusion, epidemiologic investigations have repeatedly revealed that the consumption of contaminated food is the primary mode of transmission of listeriosis. Food has been identified as the vehicle of several major outbreaks of listeriosis investigated since 1981. Food Associated Some of the food products associated with L. monocytogenes include unpasteurized milk and products prepared from unpasteurized milk, soft cheeses, frankfurters, delicatessen meats and poultry products, and some seafood. Raw milk is a well-known source of L. monocytogenes. Pasteurization effectively inactivates this organism.

However, fluid milk that is contaminated after pasteurization and stored under refrigeration may achieve very high populations of L. monocytogenes after one week; Furthermore, temperature abuse may enhance the multiplication of bacterial cells. L. monocytogenes can also be found in cheese because of its relative hardiness to temperature fluctuations, ability to multiply at refrigeration temperature and salt tolerance. During manufacturing process, L. monocytogenes is primarily concentrate in the cheese curd, with only a very small portion of cells appearing in the whey.

Then, during ripening of the cheese, the numbers of cells may increase (Camembert), decrease gradually (Colby or cheddar), or decrease rapidly (blue cheese) and then stabilize. In addition, cooked and ready-to-eat meat and poultry products have been implicated as the source of sporadic and epidemic listeriosis on several occasions in North America and Europe (Schwartz et al. , 1989). L. monocytogenes attaches strongly to the surface of raw meats and is difficult to remove or inactivate.

The multiplication in meat and poultry depends on the type of meat, pH, and the type of cell populations of competitive flora (Farber et al. 1999). However, it has been shown that poultry supports the growth of L. monocytogenes better than other meats. Furthermore, the incidence of L. monocytogenes in ready-to-eat products has become a major concern for the meat processing industry. Ready-to-eat meat products that have been received a heat treatment followed by cooling in brine before packaging may provide a particularly conducive environment for multiplication of L. monocytogenes because of the reduction in competitive flora and the high salt tolerance of the organism. L. onocytogenes has also been isolated from domestic and imported, fresh, frozen, and processed seafood products, including crustaceans, molluscan shellfish and finfish (Jinneman et al. , 1999).

However, seafood consumption is still much less when with consumption of meats and cheeses. Also, the production of seafood products is done on a much smaller scale than meat and cheese manufacture. This may be the reason that large outbreaks have not been reported and that case-control studies have not identified this group as a major risk of listeriosis (Rocourt et al. 2000) Characteristics of the disease Human disease usually occurs in high risk groups, who have a predisposing disease that leads to impairment of their T-cell mediated immunity. However, may occasionally occur in individuals with no predisposing conditions. Some of the high risk groups may include pregnant woman, neonates, and immunocompromised adults (Goulet et al. , 1996). On average, there are 0. 7 cases of listeriosis per 100,000 people, but the disease is seen three times higher in the elderly (>70) and 17 times higher in pregnant women.

A wide variety of clinical syndromes have been associated with L. monocytogenes in both humans and animals. In healthy individuals, the disease can take the form of mild to substantial flu-like symptoms, including: fever, fatigue, nausea, cramps, vomiting and diarrhea. More severe complications can include: encephalitis, septicemia, mononucleosis-like syndrome, pneumonia, endocarditis, aortic aneurysm, hepatitis, urethritis, rhombencephalitis, peritonitis, liver abscess, febrile gastroenteritis, CAPD peritonitis, septic arthritis, etc. (Dalton et al. , 1997). Lonocytogenes in pregnant women can lead to an intrauterine infection, resulting in stillbirths and miscarriages. Newborns can develop meningitis after birth via transplacental transmission.

The onset time for serious complications of listeriosis can be anywhere from a couple of days to three weeks. Mortality of untreated infections is among the highest of all foodborne illnesses, 70 percent. The infective dose of L. monocytogenes is not yet known, it is related to variables, including: strain, susceptibility of the victim, type food from which is was consumed, etc.

Mode of Action Listeria monocytogenes is the most invasive bacteria known. The principal site of infection is the liver, but it can invade many cell lines of different types (microphages, fibroblast, hepatocytes and epithelial cells). Listeria monocytogenes infects the host via oral route. Once the bacteria are ingested, they reach the intestine and are translocated between enterocytes and M cells (Pron et al. , 1998); however, the intestinal dendritic cells in the Peyer’s patches appear to be the preferred site for invasion and multiplication (Kolb-Maurer et al. 2000).

Bacteria are then internalized by resident macrophages, in which they can survive and replicate. They are subsequently transported via the blood to regional lymph nodes. When they reach the liver and the spleen, most listeriae are rapidly killed. Depending on the level of T-cell response induced in the first days following initial infection, further dissemination via the blood to the brain or, in the pregnant individuals, the placenta may subsequently occur. In addition, bacteria are internalized in membrane-bound vacuoles, which are lysed within 30 minutes.

Intracellular bacteria are released to the cytosol and begin to multiply with doubling time of about one hour. These intracytoplasmic bacteria become progressively covered by a cloud of cell actin filaments that later rearrange into a polarized comet tail up to 40 ? m in length (Crossart, 1995). The actin comet tail is made of actin microfilaments that are continuously assembled in the vicinity of the bacterium, then realeased and cross-linked. The entire bacteria cycle is completed in about 5 hours.

If cytochalasin D is added after entry, bacteria do not spread within the cytosol. They replicate and form microcolonies in the vicinity of the nucleus. Hence, actin polymerization is essential to intracellular movement and cell-to-cell spreading. In summary, the pathogenic mechanism of L. monocytogenes involves the following steps: adhesion to the host cells, lysis of the phagosome, replication in the host cytoplasm, actin-based intracellular movement and propulsion, and the intercellular spread. Biotransformation

Listeria monocytogenes is of interest to a board range of investigators, including food microbiologist, clinicians, immunologist, medical microbiologist, and even cell biologist because it is developing resistance to most currently used antibiotics. In the past, individuals who develop listeriosis have usually been treated with penicillin or ampicillin in conjunction with an aminoglycoside (Charpentier et al. , 1999), although tetracycline, erythromycin or chloramphenicol, alone or in combination, has also been used (Hof et al. , 1991).

More recently, reports of resistance in Listeria spp. have been published. Such increases in antibiotic resistance have been linked to over-use of antibiotics in animals and humans (Rao, 1998) since these therapeutic compounds were identified nearly 60 years ago. This resistance may arise from a mutation in an intrinsic chromosomal gene, or by acquisition of exogenous genetic material carrying single or multiple resistance determinants (Levy, 1994).

It is now clear that such transfer is possible between unrelated bacterial species (Kruse et al. 1994), and that these interactions are a frequent and important means of genetic exchanges among microorganisms. In conclusion, it is evident that antibiotic resistance is becoming more and more widely reported in all bacteria. Control and Prevention Because L. monocytogenes can grow at refrigerator temperatures, the Center of Disease Control and Prevention (CDC) advise all consumers to reduce the risk of illness by using a refrigerator thermometer to make sure that the refrigerator always stays at 40 °F or below and using perishable items that are precooked or ready-to-eat as soon as possible (CDC, 2005).

For high risk groups it is recommended to not consume hot dogs and luncheon meats, unless they are reheated until steaming hot; not eat soft cheese such as Feta, Brie, and Camembert cheeses, unless it is labeled as made with pasteurized milk; not eat refrigerated smoked seafood, unless it is contained in a cooked dish; and not drink raw (unpasteurized) milk or eat foods that contain unpasteurized milk. Therapy When listeriosis is a likely diagnosis, the use of ampicillin or, in penicillin-allergic patients, vancomycin will provide empiric coverage for L. onocytogenes until the diagnosis is made by culture.

Once listeriosis is confirmed, a combination of ampicillin and gentamicin is the current therapy of choice for all forms of listeriosis. The duration of the treatment for invasive listeriosis has not been studied. Relapses appear to be uncommon, and two to three weeks of therapy with ampicillin and gentamicin is sufficient for most forms of listeriosis. Rhombencephalitis with abscess formation in the central nervous system may require more prolonged therapy, but data are not available that support treatment beyond four weeks (Lorber, 1997).

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