General Mechanism of Pathogenesis for Foodborne Pathogens

The diseases caused by foodborne pathogens can be classified into three forms: foodborne infection, foodborne intoxication, and foodborne toxicoinfection and each are discussed below (Fig. 4.1). The principal route of infection for foodborne pathogens is oral and the primary site of action is the intestine. Most foodborne microorganisms cause localized infection and tissue damage but some spread to deeper tissues to induce systemic infection. For successful enteric infection, several factors must work cooperatively in a host. First of all, pathogens must gain access to the host in sufficient numbers to initiate infection. The primary vehicle of transmission is food and water. However, they can be acquired from direct contact with an animal or a human, such as a food handler, from environments (soil, air) or from an arthropod vector. Once inside the host, the pathogens must survive in the changing environment, multiply and propagate. Pathogens must find a suitable niche for colonization, which is facilitated by adhesion factors, invasion factors, and chemotaxis (for example, bacterial affinity for iron allows the organism to reach the liver which has a rich source of iron in the form of transferrin). The microbial cell envelope also helps bacteria to survive in the hostile environment, as the capsule protects the bacteria from being engulfed by phagocytes. In addition, bacterial toxins and enzymes protect cells from elimination by the host immune system. Presence of commensals in the site can assist the invading bacterium to find a niche. For example –in “wound botulism,” aerobic organisms first grow and multiply in the wound, where they utilize oxygen to create an anaerobic microenvironment. Clostridium botulinum, transmitted to wound through sharp object or dust, now have the perfect niche for growth and botulinum toxin production to induce botulism. Pathogens also damage the host tissues and cells by using exotoxins, endotoxins, or enzymes that cause cell death by apoptosis or necrosis and promote bacterial survival and multiplication.