Techniques that help prevent food borne illness in the kitchen are hand washing, rinsing produce, preventing cross-contamination, proper storage, and maintaining cooking temperatures. In general, freezing or refrigerating prevents virtually all bacteria from growing, and heating food sufficiently kills parasites, viruses, and most bacteria. Bacteria grow most rapidly at the range of temperatures between 40 and 140 °F (4 and 60 °C), called the "danger zone". Storing food below or above the "danger zone" can effectively limit the production of toxins. For storing leftovers, the food must be put in shallow containers
for quick cooling and must be refrigerated within two hours. When food is reheated, it must reach an internal temperature of 165 °F (74 °C) or until hot or steaming to kill bacteria. Mycotoxins and alimentary mycotoxicoses
The term alimentary mycotoxicosis refers to the effect of poisoning by mycotoxins through food consumption. The term mycotoxin is usually reserved for the toxic chemical products produced by fungi that readily colonize crops. Mycotoxins sometimes have important effects on human and animal health. For example, an outbreak which occurred in the UK in 1960 caused the death of 100,000 turkeys which had consumed aflatoxin-contaminated peanut meal. In the USSR in World War II, 5,000 people died due to alimentary toxic aleukia (ALA). The common foodborne Mycotoxins include:

Aflatoxins – originating from Aspergillus parasiticus and Aspergillus flavus. They are frequently found in tree nuts, peanuts, maize, sorghum and other oilseeds, including corn and cottonseeds.
This type of softening occurs in areas that continue to be poorly perfused, with little to no blood flow. These are known as "pale" or "anemic infarcts" and are areas that contain dead neuronal tissue, which result in a softening of the cerebrum. Yellow softening
Yellow softening is the third type of cerebral softening. As its name implies, the affected softened areas of the brain have a yellow appearance. This yellow appearance is due to atherosclerotic plaque build-up in interior brain arteries coupled with yellow lymph around the choroid plexus, which occurs in specific instances of brain trauma. Stages
Early life
Newborn cerebral softening has traditionally been attributed to trauma at birth and its effect on brain tissue into adulthood. However, more recent research shows that cerebral softening in newborns and the degeneration of white matter is caused by asphyxia and/or later infection. There is no causal evidence to support the hypothesis that problems in labor contribute to the development of softening in infant white matter. Also, further evidence shows a possible connection between low sugar and high protein levels in cerebral spinal fluid that can contribute to disease or virus susceptibility leading to cerebral softening. Later life
Cases of cerebral softening in infancy versus in adulthood are much more severe due to an infants inability to sufficiently recover brain tissue loss or compensate the loss with other parts of the brain.