Foodborne illness pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology[edit | edit source]

Incubation Period[edit | edit source]

The delay between consumption of a contaminated food and appearance of the first symptoms of illness is called the incubation period. This ranges from hours to days (and rarely months or even years, such as in the case of Listeriosis or Creutzfeldt-Jacob disease), depending on the agent, and on how much was consumed. If symptoms occur within 1–6 hours after eating the food, it suggests that it is caused by a bacterial toxin or a chemical rather than live bacteria.

During the incubation period, microbes pass through the stomach into the intestine, attach to the cells lining the intestinal walls, and begin to multiply there. Some types of microbes stay in the intestine, some produce a toxin that is absorbed into the bloodstream, and some can directly invade the deeper body tissues. The symptoms produced depend on the type of microbe.

Bacteria[edit | edit source]

Bacteria are a common cause of foodborne illness. Symptoms for bacterial infections are delayed because the bacteria need time to multiply. They are usually not seen until 12–72 hours or more after eating contaminated food.

Exotoxins[edit | edit source]

In addition to disease caused by direct bacterial infection, some foodborne illnesses are caused by exotoxins which are excreted by the cell as the bacterium grows. Exotoxins can produce illness even when the microbes that produced them have been killed. Symptoms typically appear after 1–6 hours depending on the amount of toxin ingested.

Viruses[edit | edit source]

Viral infections make up perhaps one third of cases of food poisoning in developed countries. Foodborne viral infection are usually of intermediate (1–3 days) incubation period, causing illnesses which are self-limited in otherwise healthy individuals, and are similar to the bacterial forms described above.

Infectious Dose[edit | edit source]

The infectious dose is the amount of agent that must be consumed to give rise to symptoms of foodborne illness, and varies according to the agent and the consumer's age and overall health. In the case of Salmonella a relatively large inoculum of 1 million to 1 billion organisms are necessary to produce symptoms in healthy human volunteers, as Salmonellae are very sensitive to acid. An unusually high stomach pH level (low acidity) greatly reduces the number of bacteria required to cause symptoms by a factor of between 10 and 100.

Exotoxins[edit | edit source]

In addition to disease caused by direct bacterial infection, some foodborne illnesses are caused by exotoxins which are excreted by the cell as the bacterium grows. Exotoxins can produce illness even when the microbes that produced them have been killed. Symptoms typically appear after 1–6 hours depending on the amount of toxin ingested.

For example Staphylococcus aureus produces a toxin that causes intense vomiting. The rare but potentially deadly disease botulism occurs when the anaerobic bacterium Clostridium botulinum grows in improperly canned low-acid foods and produces botulin, a powerful paralytic toxin.

Pseudoalteromonas tetraodonis, certain species of Pseudomonas and Vibrio, and some other bacteria, produce the lethal tetrodotoxin, which is present in the tissues of some living animal species rather than being a product of decomposition.

Mycotoxins and Alimentary Mycotoxicoses[edit | edit source]

The term alimentary mycotoxicoses refers to the effect of poisoning by Mycotoxins through food consumption. Mycotoxins have prominently affected on human and animal health such as an outbreak which occurred in the UK in 1960 that caused the death of 100,000 turkeys which had consumed aflatoxin-contaminated peanut meal and the death of 5,000 human lives by Alimentary toxic aleukia (ALA) in the USSR in World War II.^[1] The common foodborne Mycotoxins include:

• Aflatoxins - originated from Aspergillus parasiticus and Aspergillus flavus. They are frequently found in tree nuts, peanuts, maize, sorghum and other oilseeds, including corn and cottonseeds. The pronounced forms of Aflatoxins are those of B1, B2, G1, and G2, amongst which Aflatoxin B1 predominantly targets the liver, which will result in necrosis, cirrhosis, and carcinoma.^{[2] [3]} In the US, the acceptable level of total aflatoxins in foods is less than 20 μg/kg, except for Aflatoxin M1 in milk, which should be less than 0.5 μg/kg.^[4] The official document can be found at FDA's website.^{[5] [6]}

• Altertoxins - are those of Alternariol (AOH), Alternariol methyl ether (AME), Altenuene (ALT), Altertoxin-1 (ATX-1), Tenuazonic acid (TeA) and Radicinin (RAD), originated from Alternaria spp. Some of the toxins can be present in sorghum, ragi, wheat and tomatoes.^{[7] [8] [9]} Some research has shown that the toxins can be easily cross-contaminated between grain commodities, suggesting that manufacturing and storage of grain commodities is a critical practice ^[10].
• Fumonisins - Crop corn can be easily contaminated by the fungi Fusarium moniliforme, and its Fumonisin B1 will cause Leukoencephalomalacia (LEM) in horses, Pulmonary edema syndrome (PES) in pigs, liver cancer in rats and Esophageal cancer in humans.^{[11] [12]} For human and animal health, both the FDA and the EC have regulated the content levels of toxins in food and animal feed.^{[13] [14]}
• Fumonisins - Crop corn can be easily contaminated by the fungi Fusarium moniliforme, and its Fumonisin B1 will cause Leukoencephalomalacia (LEM) in horses, Pulmonary edema syndrome (PES) in pigs, liver cancer in rats and esophageal cancer in humans.^{[11] [12]} For human and animal health, both the FDA and the EC have regulated the content levels of toxins in food and animal feed.^{[13] [14]}
• Trichothecenes - sourced from Cephalosporium, Fusarium, Myrothecium, Stachybotrys and Trichoderma. The toxins are usually found in molded maize, wheat, corn, peanuts and rice, or animal feed of hay and straw.^{[15] [16]} Four trichothecenes, T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) and deoxynivalenol (DON) have been most commonly encountered by humans and animals. The consequences of oral intake of, or dermal exposure to, the toxins will result in Alimentary toxic aleukia, neutropenia, aplastic anemia, thrombocytopenia and/or skin irritaion.^{[17] [18] [19]} In 1993, the FDA issued a document for the content limits of DON in food and animal feed at an advisory level.^[20] In 2003, US published a patent that is very promising for farmers to produce a trichothecene-resistant crop.^[21]

References[edit | edit source]

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