Fate Of Listeria Monocytogenes Research Articles

Fate of Listeria monocytogenes on Ready to Serve Lettuce

The ability of Listeria monocytogenes to survive and grow on head lettuce obtained from a retail outlet over a period of 10 months was determined. Lettuce was torn into bite sized pieces, inoculated with L. monocytogenes ATCC 7644, placed into plastic bags, and held under a variety of storage conditions. Samples stored at 5°C and 12°C were subjected to aerobic plate count analysis, and levels of L. monocytogenes were determined immediately after inoculation and after 7 and 14 d of storage. Samples stored at 25°C were sampled after inoculation and after 4 and 8 h storage. Lettuce juice was inoculated, stored at 5°C and sampled as described for head lettuce. Aerobic plate counts on lettuce stored at 5°C and 12°C increased greatly during the 14 d of storage. Behavior of L. monocytogenes was variable. In most trials, numbers increased by several log cycles during 14 d of storage, but in several trials growth never occurred or did not persist for 14 d. The same general growth patterns were observed in lettuce held at 25°C. Aerobic plate counts increased by 1 or 2 log cycles and L. monocytogenes increased by 1 log cycle, except for occasional trials where the organisms did not grow or survive. Lettuce juice held at 5°C was also able to support growth of L. monocytogenes. L. monocytogenes serotype 1 was isolated from some uninoculated samples indicating that the organism was naturally present on some of the lettuce heads purchased from retail outlets.

Fate of Listeria monocytogenes in tissues of experimentally infected cattle and in hard salami.

Muscle, organ, and lymphoid tissues of four Holstein cows experimentally inoculated (intravenously) with Listeria monocytogenes were examined 2, 6, or 54 days postinoculation for the presence of the organism by direct plating and cold enrichment procedures. L. monocytogenes was isolated from 66% of the tissues sampled; 38% of the isolations were attributed to the use of cold enrichment. Isolation of the organism from muscle tissue was possible only with animals inoculated 2 days before slaughter. The fate of L. monocytogenes during the manufacture and storage of fermented hard salami made from this meat also was determined. Three sausage treatments were evaluated: (i) uninoculated control sausage, (ii) "naturally" contaminated sausage (NC) made from meat of an experimentally inoculated cow, and (iii) sausage made from beef inoculated with a laboratory culture of L. monocytogenes (I). Initial Listeria levels in NC and I sausage were 10(3) CFU/g in trial 1 and 10(4) CFU/g in trial 2. Numbers of L. monocytogenes decreased by approximately 1 log10 CFU/g during fermentation and decreased further during drying and refrigerated storage. Small numbers (less than or equal to 20 CFU/g) of L. monocytogenes were present in I and NC sausage at the end of 12 weeks of refrigerated storage; recovery of these organisms generally depended on the use of an enrichment procedure. The results indicate that L. monocytogenes does not multiply during the fermentation and drying processes typical of hard salami manufacture but that survival may occur if the organism is initially present at greater than or equal to 10(3) CFU/g.

Fate of Listeria monocytogenes during manufacture and ripening of semi-hard cheese

Semi-hard cheeses were experimentally elaborated with pasteurized milk from sheep, goat and cow (15: 35: 50) and inoculated to contain 1.9 times 105Listeria monocytogenes/ml in cheeses 1 and 2 and 4 times 103L. monocytogenes/ml in cheeses 3 and 4. Counts of L. monocytogenes were determined by direct surface plating of samples on listeria selective agar medium. The results show the substantial survival of L. monocytogenes present in milk during manufacture and ripening of this type of cheese.

Fate of Listeria monocytogenes During the Manufacture and Ripening of Camembert Cheese

The ability of Listeria monocytogenes to survive the Camembert cheese-making process and grow during ripening of the cheese was examined. Pasteurized whole milk was inoculated to contain about 500 L. monocytogenes [strain Scott A, V7, California, (CA) or Ohio (OH)] CFU/ml and made into Camembert cheese according to standard procedures. All wheels of cheese were ripened at 6°C following 10 d of storage at 15–16°C to allow proper growth of Penicillium camemberti. Duplicate wedge (pie-shaped), surface and interior cheese samples were analyzed for numbers of L. monocytogenes by surface-plating appropriate dilutions made in Tryptose Broth (TB) on McBride Listeria Agar (MLA). Initial TB dilutions were stored at 3°C and surface-plated on MLA after 2, 4, 6 or 8 weeks if the organism was not quantitated in the original sample. Selected Listeria colonies from duplicate samples were confirmed biochemically. Results showed that numbers of Listeria in cheese increased 5- to 10-fold 24 h after its manufacture. Listeria counts for strains Scott A, CA and OH decreased to <10 to 100 CFU/g in all cheese samples taken during the first 18 d of ripening. In contrast, numbers of strain V7 remained unchanged during this period. All L. monocytogenes strains initiated growth in cheese after 18 d of ripening. Maximum Listeria counts of ca. 1 × 106 to 5 × 107 CFU/g were attained after 65 d of ripening. Generally, a 10- to 100-fold increase in numbers of Listeria occurred in wedge or surface as compared to interior cheese samples taken during the latter half of ripening. During this period, Listeria growth paralleled the increase in pH of the cheese during ripening.

Fate of listeria monocytogenes in normal rabbit serum.

Viability of Listeria monocytogenes suspended in either normal rabbit serum or listericidal factor is significantly reduced before cell lysis. In normal serum Listeria populations are initially reduced by clumping of viable bacteria, and the cells within these clumps are morphologically altered and killed by the listericidal factor in serum. This clumping is complement independent and does not occur after suspension in purified listericidal factor. In electron micrographs, densely stained amorphous material was seen surrounding clumped cells suspended in serum. Initial damage to Listeria suspended in either serum or listericidal factor appears to be confined to plasma and mesosomal membranes. The mesosomes are rapidly disorganized, and the plasma membrane becomes crenated and separates from the cell wall. Subsequently, the fibrillar organization of the nuclear region disrupts, and the cytoplasm increases in granularity. Studies utilizing Listeria protoplasts provided evidence in support of the plasma membrane as the site of listericidal action. Cell death may be related to loss in enzyme function after crenation of the plasma membrane and mesosomal dissolution.