Chicken Salmonella Enteritidis IgY ELISA Kit

Salmonella is a facultative anaerobic bacterium of the Enterobacteriaceae family. The genus Salmonella can be divided into Salmonella enterica and Salmonella bongore. So far, more than 2,500 serotypes have been identified. Salmonella enterica is a subspecies of Salmonella enterica. It can infect poultry and is the main pathogen in poultry farming. Salmonella enterica can also infect humans and cause foodborne diseases. It usually spreads during food processing and can adhere to solid surfaces such as refrigerators and processing lathes. It can also infect eggs and meat products, posing a serious threat to public health. Poultry is the natural target of Salmonella enterica. Chicks under 1 week old show high pathogenicity. Infected chicks often show lethargy, decreased appetite, white feces, and often have a sticky anus. Acute infection can cause the death of chicks. The hearts of infected chicks show varying degrees of damage, and the liver shows punctate hemorrhage or local necrosis. The ovaries and follicles of laying hens will also be damaged and deformed after infection. However, Enteritidis Salmonella rarely causes death in chickens over one month old, and adult chickens usually do not show clinical symptoms, and there is no significant change in the egg production of chickens. However, meat or egg products from latently infected chickens can become carriers of Enteritidis Salmonella, which can spread through the food chain and infect humans, thus endangering public health. Enteritidis Salmonella is currently the only Salmonella that can cause human disease and is associated with egg contamination, indicating that it poses a "unique" threat to food safety. There are two possible ways for eggs to be contaminated with Salmonella. The first is horizontal transmission from colonized intestines or contaminated feces through the eggshell during or after egg laying. The intestinal infection route is usually that Salmonella enters the intestine from the hen's mouth, then invades the intestinal epithelial cells and colonizes in the intestine. Subsequently, macrophages are attracted to the invasion site and surround the Salmonella. Finally, Salmonella enters the internal organs with the migration of macrophages. Enteritidis Salmonella can be isolated from the cecum, liver, spleen and ovary. The eggshell contamination route is that Enteritidis Salmonella attaches to the eggshell and eggshell membrane. This surface contamination may be the result of vaginal infection or fecal contamination of the hen. The second possible route is vertical transmission from infected hens, directly contaminating the yolk, yolk membrane, albumen, shell membrane and eggshell. Although the Salmonella deposited on the albumen and yolk membrane are inhibited from growing in the antibacterial environment inside the egg, once they penetrate the yolk membrane to reach the yolk, they will grow extensively in this nutrient-rich environment.

Figure 1. Overview of the various transmission routes of Salmonella. (Sources: Shaji S, et al.; 2023)

Many virulence factors have been shown to play multiple roles in the pathogenesis of Salmonella infection. These factors include flagella, capsules, plasmids, adhesion systems, and virulence islands. The virulence of Salmonella is closely related to its virulence islands (SPIs), which are gene clusters located in specific regions of the bacterial cell chromosome and are responsible for encoding various virulence factors. These gene clusters or SPIs can be located on plasmids or chromosomes, and they often have a variable G/C composition compared to the surrounding regions, with repetitive sequences on both sides. SPIs are often associated with transfer RNA (tRNA) and mobile genetic elements, and their base composition is often completely different from the core genome. Different SPIs play different roles in the pathogenesis and virulence of Salmonella. At present, 23 SPIs have been found in Salmonella, and SPI-1, SPI-2, SPI-3, SPI-4, and SPI-5 are present in all Salmonella enteritidis. After entering the intestine, Salmonella enteritidis attaches to intestinal epithelial cells and M cells. The T3SS system encoded by SPI-1 can form a needle-like complex to connect with the host cell. At the tip of the needle, the SipB protein is inserted into the cell membrane to form a channel to the inside of the cell. The effector of T3SS can enter the host cell through the channel. The T3SS system in SPI-1 can secrete more than 20 effector proteins, among which SipA and SptP can bind to actin and improve the efficiency of Salmonella entering the host cell by affecting the formation of membrane ruffles and the rearrangement of the actin cell skeleton. AvrA and Sptp proteins can promote the replication of Salmonella in cells and increase the invasive ability and translocation of bacteria. When bacteria pass through the cell membrane, they can bind to the cell membrane to form a vesicle structure (SCV). Salmonella enteritidis expresses the effector protein of SPI-2 in the vesicle and migrates to the periphery of the cell with the SCV, promoting intracellular replication and systemic spread. During this period, SpiA can exist continuously, which helps to maintain the vesicle and synergize with the effector of SPI-2. The SPI-3 gene is involved in the intestinal colonization of MisL-dependent fibronectin binding and the intracellular survival of the high-affinity magnesium transport encoded by mgtCB, which is essential for the intestinal disease stage. SPI-4 encodes a specific type I secretion system, which is related to the pathogenicity of bacteria. SPI-5 is co-regulated with SP-1 or SPI-2 genes and is involved in the secretion of intestinal mucosal fluid and the activation of inflammatory factors.

S. enteritidis
Salmonella enterica serovar Enteritidis
Salmonella serotype Enteritidis
Enteritidis