Salmonella Spp Pathogenesis | Essay
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- Goh JiaYeen
The isolation of Salmonella from a swine suffering from hog cholera was first reported in 1885 by Daniel E. Salmon. This isolated bacterium was first named as Bacillus cholerasuis, which is currently known as Salmonella enteric serovar Choleraesuis (Bhunia, 2008; Li et al., 2012).
Salmonella is known to be an important cause of a foodborne illness, known as salmonellosis, in humans globally (Hald, 2013). Salmonellosis ranges from mild to severe food poisoning (gastroenteritis), and even severe typhoid fever, septicaemia, bacteraemia and others. Some of these conditions can be of high morbidity and mortality rates, involving a large population (Bell & Kyriakids, 2009). In the United States, 2 to 4 million cases associated with Salmonella are reported annually, with a death rate of 500 to 1,000 (Bhunia, 2008). Typically, the onset of the symptoms of salmonellosis is 12 to 72 hours after exposure. The common symptoms include abdominal pain, fever, nausea, vomiting, headache, and cramps (Hald, 2013).
In terms of taxonomy, Salmonella spp. are facultatively anaerobic bacteria belonging to the family Enterobacteriaceae (Bhunia, 2008). These bacteria are of gram-negative and rod-shaped. Being a mesophile in nature, these bacteria grow optimally at human body temperature, 37°C, and utilize glucose and other carbohydrates to undergo metabolism, producing acid and gas. However, some of these Salmonella strains are able to adapt and grow at higher temperatures up to 54°C, while some survived and grow under low temperatures at 2°C to 4°C (Li et al., 2012).
In food industry, many preventive measures are taken to prevent the contamination of foods by Salmonella to ensure food safety.
Source and Transmission
The major reservoirs for Salmonella are the intestinal tract of warm-blooded animals, such as birds, turtles, reptiles, insects, farm animals, and humans. Poultry is the most popular source of Salmonella due to the high-density farming operations as salmonellosis can spread quickly to infect the other birds within a flock.This further increases the risk for contamination of the carcasses during slaughter (Bhunia, 2008). If the ovary of the laying hen is colonized by this bacterium, eggs may become infected too via transovarian transmission. In this case, the bacteria are present in the egg before the eggshell is formed (Ricke et al., 2013).
For most cases, the majority of the infections are transmitted to humans via the consumption of contaminated food. The common animal-origin foods that are implicated in the bacteria transmission are beef, poultry, pork, dairy products, fresh produce, and eggs (Hald, 2013). On the other hand, human-to-human and animal-to-human transmission can also occur (Bhunia, 2008).
Salmonella has a broad range of infectious dose, ranging from 30 to 109 CFU g-1 (Blaser & Newman, 1982). Salmonella often enters the host body through oral ingestion. The invasion of Salmonella is mediated by three mechanisms: induced phagocytosis by epithelial cells, phagocytosis by M-cells, and phagocytosis by dendritic cells (Bhunia, 2008; Ricke et al., 2013).
Induced Phagocytosis by Epithelial Cells
Once in the gastrointestinal tract, the Salmonella attaches itself to the intestinal epithelium, facilitated by frimbriae or pili of the bacterial cell (Ricke et al., 2013). It then uses the pathogenicity island 1 (SPI-1) Type III secretion system (Galán, 2001), which is also found in Shigella, and Escherichia coli, to secrete or deliver the proteins through the host membrane surface and into the cytoplasm.This mechanism, also known as “trigger mechanism” (Bhunia, 2008), is able to trigger cytoskeletal rearrangements of the epithelial cells. This then results in cell membrane ‘ruffling’, or an extension of the cell membrane (Liu et al., 2014; Ricke et al., 2013). The bacterium is then engulfed and dragged into the host cell by the actin filaments, in the form of a vacuole.
Phagocytosis by M-Cells
Apart from induced phagocytosis, Salmonella is also able to enter into the basolateral side of the epithelial lining through M-cells. By the expression of several invasion genes, the bacterium is able to attach and invade the M-cells to cross the epithelial barrier (Bhunia, 2008). Here, the bacterium interacts with the host macrophages and become internalized in a vacuole.
Phagocytosis by Dendritic Cells
The dendritic cells, located in the lamina propria, project their dendrites through the epithelial lining and transport the bacterium into the basolateral side of the epithelial lining. Dendritic cells are believed to be the primary phagocytes that are associated with the systemic distribution of bacteria to other sites of the body, such as liver, spleen, and lymph nodes (Bhunia, 2008).
Survival in Phagocytes
However, in the host cells, lysosomes are triggered by the invasion of the foreign body and produce digestive enzymes which degrade the proteins in the bacterium (Luzio et al., 2007). In order to survive in these environments and prevent degradation by the lysosomes, Salmonella again uses the SPI-2 Type III secretion system to inject other bacterial proteins into the surrounding vacuole, altering the vacuole structure and turning it into impermeable to toxic lysosomes (Galán, 2001; Liu et al., 2014).
Intracellular Growth and Infection
In these toxin-proof vacuoles, Salmonella replicates and induces apoptosis of the macrophages and dendritic cells (Bhunia, 2008; Ricke et al., 2013). Velden et al. (2000) suggested that the macrophages cell death is induced by a mechanism associated with the SPI-2 Type III secretion system. However, the macrophage cell death induced by Salmonella is very complicated. Upon apoptosis of the host cells, the Salmonella is then released into the surrounding.
Once the bacterium is released, it colonizes and invades the epithelium cells in the ileum, cecum and proximal colon, inducing inflammation at these sites. These localized inflammations are characterized by neutrophil infiltration, tissue injury and fluid accumulation, leading to abdominal pain, gastroenteritis, and fever, in the infected host. In addition, the damage to the mucosal cells can also result in diarrhea and fluid loss (Bhunia, 2008).
Prevention and Control
The prevention and control of Salmonella is established in the entire chain of the food processing, that is from the raw material to the ready-to-eat-food. Several practices such as facility sanitation, treatments of water and feed, and egg disinfectants, have been extensively used to control the infection of animals or contamination of foods by Salmonella (Ricke et al., 2013).
Preventive biological agents are also used to create barriers to Salmonella from colonizing the gastrointestinal tract. These agents include the probiotics, prebiotics, dietary manipulations, as well as immunological agents. The principle behind the applications of these agents is to enhance the population of the protective gastrointestinal microflora as to prevent the establishment of incoming Salmonella in the pre-harvest stages (Bell & Kyriakids, 2009).
During the post-harvest processes, the food products are avoided from the exposure to the possible contaminants within the plant through the pathways. Chlorine is often used as a decontamination agent by sanitizing the fresh produces. For meat products, several chemical and physical treatments are used. Heat, irradiation, chlorine, and organic acids are the examples of the treatments to alter the food environment which initially nurtures the growth of the bacteria. Upon treatment, the environment becomes unfavourable for the bacteria. In addition, the USDA recommends the consumers to cook all meats and fish to an internal temperature of 62°C and 74°C for poultry (Ricke et al., 2013).
In conclusion, foodborne salmonellosis continues to persist as a public health issue in a majority of countries. It was estimated that there is a considerable number of salmonellosis cases that are not reported. Thus, the true number of cases of salmonellosis is probably much higher than the data we have in hand (Hald, 2013) despite of all the extensive efforts made to suppress and control the contamination of Salmonella. Therefore, all food handlers and consumers should be responsible to ensure the food is handled safely to final consumption. Necessary information such as how to handle and store the foods should be provided through product labelling or government education programmes (Bell & Kyriakids, 2009).
However, as the technology advances, the genetic information analyses achieved in Salmonella gives the scientists a clearer picture of the pathogenesis mechanisms of Salmonella. This allows the design and development of better prevention factors, such as vaccines and antimicrobials that are specifically targeted to affect Salmonella (Ricke et al., 2013). As such, the risk of salmonellosis can be reduced and the public health can be improved.
Bell, C. & Kyriakids, A. 2009, ‘Salmonella’, in Foodborne Pathogens: Hazards, Risk Analysis and Control, eds C. Blackburn, P.J. McClure, Elsevier, pp. 627-674.
Bhunia, A.K. 2008, ‘Salmonella enterica’, in Foodborne microbial pathogens: Mechanisms and pathogenesis, Springer Science, pp. 201-216.
Blaser, M.J. & Newman, L.S. 1982, ‘A review of human salmonellosis: I. Infective dose’, Rev Infect Dis, vol. 4, no. 6, pp. 1096-1106.
Galán, J.E. 2001, ‘Salmonella interactions with host cells: Type III secretion at work’, Annu. Rev. Cell Dev. Biol., vol. 17, pp. 53-86.
Hald, T. 2013, ‘Pathogen updates: Salmonella’, in Foodborne Infections and Intoxications, Academic Press, pp. 67-97.
Li, H.P., Wang, H., D’ Aoust, J.Y. & Maurer, J. 2012, ‘Salmonella species’, in Food Microbiology: Fundamentals and Frontiers, eds. M.P. Doyle, 4th ed., pp. 225-262.
Liu, D., Finlay, B.B., Amagai, S. & Keller, E. 2014, ‘Intracellular infection by Salmonella’, viewed 30 September 2014, <http://www.hhmi.org/biointeractive/intracellular-infection-salmonella>.
Luzio, J.P., Pryor, P.R. & Bright, N.A. 2007, ‘Lysosomes: fusion and function’, Nature Reviews Molecular Cell Biology, vol. 8, pp. 622-632.
Ricke, S.C., Koo, O.K., Foley, S. & Nayak, R. 2013, ‘Salmonella’, in Guide to Foodborne Pathogens, eds R.G. Labbé, S. García, John Wiley & Sons, pp. 112-137.
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