Salmonella: Colonization of gastrointestinal tract by Dra. Liliana Revolledo
Pathogenic and invasion mechanisms
For the presence and evolution of bacterial diseases, an interaction host-agent is needed, where location of bacteria in proper environment, permits adherence, invasion, reply and expression of its virulenceâ€™ factors, as well as the capacity to resist to defense mechanisms of host. When Salmonella comes in hostt, it faces several changes due to its interaction with gastrointestinal ecosystem, and, depending on that, modifies its genetic expression.
The first step to colonize the bacteria is the physical association to the epithelium. The intestinal epithelium represents an interface between the external and the internal environment, considering it the main way of entrance for pathogens.
It does not exist much information about the mechanisms used by Salmonella to colonize digestive tract in birds. One of them is its capacity to multiply itself in the intestinal content, migrate through the mucous, or invade the epithelium.
This interaction can be seen in the next graph. Physical adhesion has been suggested as an intestinal colonization mechanism as there are evidences that fimbrias promote colonization in intestine. Some serotypes colonize more efficiently than others, as well as the activation of some gens that permit alternative mechanisms for colonization. In reproductive tract in birds, fimbria nÂş 1 has been described as the responsible for the adhesion of the bacteria.
Susceptibility of birds to the colonization can be affected by different factors; among them we can mention the following:
1.Â Young birds are more susceptible than adult ones.
2.Â It depends on stump and dose of challenge
3.Â Health condition of birds
4.Â Competence with other bacteria
5.Â Stressing agents increase susceptibility
6.Â Genetic and resistance genetic heritage has been proposed
7.Â Products that may alter normal flora
Adhesion of Salmonella, as well as other intestinal pathogens, to the intestinal surface is the key factor in pathogenic and the central activity in its intestinal colonization.
Despite of bacteria may colonize a healthy host, the risk of infection is linked to stress periods. Epithelial damage that occurs during stress may cause protein secretions of extracellular matrix such as fibronectina that works as a receptor for some adhesion proteins of Salmonella.
In birds, glicosilceramid and gangliosid work as receptors in the surface of intestinal epithelial cells for the adhesion of bacteria, as they act as receptors of Salmonella Enteritidis fimbrias.
Some important pathogenic mechanisms
In birds, salmonella host-specific such as Salmonella enterica serovar gallinarum causes systematic disease after intestinal colonization. On the contrary, salmonella with several hosts such as Salmonella enterica serovar Typhimurium or enteritidis can persist in the digestive tract for many months without obvious clinical signs, apart from young birds where high mortality has been reported.
In case of Salmonella pullorum, survival into macrofags is a crucial event in the persistence of the infection and the island of pathogenicity 2 related to the secretion system type III is necessary for this persistence; characteristics that also can be applied to Salmonella gallinarum due to its genomic similarity.
In mammals, Salmonella oral infection is characterized by initial interaction of bacteria in digestive tract, mainly through cells M and epithelial cells.Â After its entry into the hostâ€™s organism, Salmonella initiates its infection cycle by invading lymphoid tissue.
Its capacity to invade non phagocytic intestinal epithelial cells ensures a protected cellular niche so that microbe replies itself and persists in host, inducing the cells to some readjustments in cytoskeleton that permits its entry.
Salmonella produces cicotoxic effects that result in the destruction of cells M and the invasion of enterocits to be transported to the liver and spleen.Â Salmonella enterica serovar typhimurium can reach the liver and spleen through an alternative route, where intestinal colonization or intestinal epithelial cells are not required, being able to transfer organs by phagocytes that express CD18.
Studies realized in some salmonellas, have permitted to sequence some complete genomes, which has been very useful for epidemiologic studies, host specificity and pathogenesis after detecting the presence of pseudogens, functional profags and secretion systems.
For example, pathogenic isles are constituted by gen group wrapped in codification specific factors of virulence.
There are 17 pathogenic isles (from SPI-1 to SPI-17). The most studied are SPI-1 and SPI-2. It is necessary to indicate that not all of them can be found in the same serovar of Salmonella. Pathogenic 1 and 2 isles are the most determiner of Salmonella enterica virulence, because they codify secretion systems of type III.
The pathogenic isle SPI-1 promotes the invasion of intestinal epithelial cells and the initiation of inflammatory answer in intestinal tract. Furthermore, it is involved in survival and persistence of bacteria at systemic level of host.
Regarding the pathogenic isle SPI-2, the first activity described was the bacterial survival and replication in intracellular compartments of phagocytes that constitute the main reserve for the systemic bacterial dissemination in hostâ€™s organs.
The protein invA dependent on the invasion gen (invA) is considered one of the most important proteins for the assembly of SSTIII. It has been discussed that Salmonella differs from ability to multiply themselves into several kinds of cells, and these cells can choose not to reply in some of them.
In birds, the pathogenic isle SPI-1 in Salmonella typhimurium is related directly to the colonization of the spleen, while the SPI-2 could have a negative effect in its colonization.
Anyway, it has been demonstrated that SPI 1 is more important than SPI 2 in birds (In mice occurs the contrary), confirming that the host and its interactions with agent play a preponderant role in different phases and establishment of infection.