Salmonella typhimurium: Entry, Body Barriers, and Immune Response

This report provides a comprehensive overview of Salmonella typhimurium, a gram-negative bacteria causing bacterial gastroenteritis. It details the bacteria's route of entry into the body, primarily through contaminated food and water, and the subsequent infection process. The report metic...Read More

Running head: Salmonella typhimurium 1
Salmonella typhimurium
Name
Institution of Affiliation

Salmonella typhimurium 2
Route of entry into the body
Salmonella typhimurium is a gram-negative bacteria that causes bacterial gastroenteritis.
The bacteria is toxic as a result of having a lipopolysaccharide layer on its outer membrane
protecting it from the external environment, (Arpaia et al., 2011) Gastroenteritis is characterized
by symptoms such as vomiting, abdominal cramps, and diarrhea. The onset of these symptoms
occurs 12 to 72 hours after a Salmonella typhimurium infection. Often this infection can spread
from the gastrointestinal tract to the bloodstream and consequently to other parts of the body
such as the liver and other parts to cause typhoid fever. However, for its infection to be
successful and be clinically manifested in an individual, salmonella has to surpass several
barriers in the body, (Onwuezobe et al., 2012).
Food poisoning is the main entry method for live salmonella into the body. It enters the
body through the mouth by consumption of contaminated food or water that contains the
bacteria. The bacteria then penetrate the intestinal wall, multiply by binary fission in lymphoid
tissue and thereafter it enters the systemic circulation causing Salmonellosis, (Krawiec et al.,
2014). This bacteria is present in polluted water. Animals will get infected by consuming
contaminated feed or water, direct contact with other animals, wild birds or through the grass.
When humans consume contaminated foods such as egg products, poultry, and beef products
they acquire the bacteria. In the kitchen, this bacteria can be cross transferred from raw to cooked
food by hands and contact with kitchen surfaces and equipment, (Varas et al., 2017). Humans
can be carriers as they could have and transmit salmonella without expressing any symptoms.
They do so by shedding the bacteria in their waste matter for up to one year. Salmonella can be
potentially be transferred to other individuals from persons having it up to several months as a
result of limited hand washing after toilet use, (Norton et al., 2012).

Salmonella typhimurium 3
Barriers that Salmonella Encounters
Salmonella typhimurium has to surpass several barriers in the body before causing a
successful infection. These barriers are the body's first line of defense that protects the body from
any external havoc. After ingestion into the body, the bacteria will encounter the acidic
environment of the stomach which it has to survive. Individuals like the old have a high gastric
pH hence there are more susceptible to the bacteria, (Hallstrom & McCormick, 2011). The
Salmonella also has to attach or to colonize intestinal walls of the gastrointestinal tract,
outcompete against the natural micro Bata of the gut. Another hurdle is surviving the body’s
defense mechanisms and crossing the epithelial barrier of the large intestine into the bloodstream
to successfully cause the disease
The Normal Flora that Salmonella has to Interact with
The indigenous intestinal microflora is suggested to interfere with the activity of
Salmonella typhimurium. The normal flora that the Salmonella has to interact with after being
ingested into the human body is mainly the gastrointestinal tract flora, (Swart & Hensel, 2012).
They include Bacteroides spp., Yersinia enterocolitica, Escherichia coli, Achromobacter spp.,
Actinomyces spp., Bacillus spp., Candida albicans, Enterococcus spp. and others. The natural
flora influences the physiology, anatomy, susceptibility to pathogens as well as morbidity of the
host (Gill et al., 2011). The micro-organisms in the stomach are transient and are only kept low
by the high acidity of the stomach. They include Helicobacter pylori which is a potential
pathogen of the stomach hence the Salmonella has to compete against the organism. In the ileum,
there is a moderately mixed flora. Flora of the large bowel is dense which constitutes largely of
anaerobes. The flora protects the body from pathogens such as the Salmonella mostly through
creating high competition for nutrients which starve the pathogens, forming a protective layer

Salmonella typhimurium 4
which denies the pathogen access to the intestinal walls, stimulating the immune system and
through waste product formation which also forms a protective layer (De Jong et al., 2012).
Innate Immune System
Innate immunity; is the immunity that is nonspecific and naturally found in the body.
Acts against all foreign materials in the body with equal measure and does not require prior
sensitization. It includes mechanisms such as chemicals in the blood, physical barriers such as
mucous, epithelial cells of the gastrointestinal tract and immune system cells that attack foreign
cells in the body, (Hurley et al., 2014). This innate immune system provides the initial protection
against the Salmonella especially in the gastrointestinal tract whereby the thick layer of mucous
covering the surface of the gut epithelium acts as an obstacle. This denies Salmonella from
having direct contact with the epithelium temporarily preventing it from getting into the systemic
circulation. The mucus additionally secretes antimicrobial peptides as well as mucins to fight the
bacteria. Different types of immune cells work together to rapidly recognize as well as to
eliminate salmonella through phagocytosis-mediated killing and induction of inflammation.
These in most cases slow down the Salmonella by destroying it but sometimes the Salmonella
profits from the increased synthesis of C-type lectins hence gaining development advantage over
the natural flora; this is because Salmonella typhimurium is well adapted to evade the host
defense mechanisms. (Broz et al., 2012).
Adaptive Immune system
Adaptive immunity is referred to as the acquired immunity. It is an antigen-specific
immune response and stores an immunological memory that it uses to initiate an immunity action
against pathogens. Adaptive immunity is more advanced than the innate immune response
because it involves processing and recognition of the antigen first then followed by the creation

Salmonella typhimurium 5
of immune cells specifically developed to act on the pathogen. The memory created is used to
protect the body against future attacks by the same antigen, (Hotson et al., 2016). The body's
immune system will stimulate the adaptive immune system to protect itself against the
Salmonella; the T cell plays a critical role in this type of immunity. A robust T-cell response is
necessary to get rid of the first infection by Salmonella infection as well as offer protection to
subsequent infections. Several bacteria directed mechanisms such as antigen-presenting cell
function to alter Salmonella’s pathogenic signature to lower or stop the chances of susceptibility
to host immune surveillance. Vaccines also contribute to boosting immunity which consists of an
antibody that protects individuals, usually children, against any bacterial of the blood, (Pastelin-
Palacios et al., 2011). These slow down and stops any infection from taking place but sometimes
especially when the immune system of the host is compromised; salmonella has pathogenic
capabilities that contribute to the success in causing acute or chronic infections, (Tennant et al.,
2016).

Salmonella typhimurium 6
References
Arpaia, N., Godec, J., Lau, L., Sivick, K. E., McLaughlin, L. M., Jones, M. B., Dracheva, T.,
Peterson, S. N., Monack, D. M., & Barton, G. M. (2011). TLR signaling is required
for Salmonella typhimurium virulence. Cell, 144(5), 675-688.
Broz, P., Ohlson, M. B., & Monack, D. M. (2012). Innate immune response toSalmonella
typhimurium, a model enteric pathogen. Gut Microbes, 3(2), 62-70.
De Jong, H. K., Parry, C. M., Van der Poll, T., & Wiersinga, W. J. (2012). Host–pathogen
interaction in invasive salmonellosis. PLoS Pathogens, 8(10), e1002933.
Gill, N., Wlodarska, M., & Finlay, B. B. (2011). Roadblocks in the gut: Barriers to enteric
infection. Cellular Microbiology, 13(5), 660-669.
Hallstrom, K., & McCormick, B. A. (2011). Salmonella interaction with and passage through
the intestinal mucosa: Through the lens of the organism. Frontiers in Microbiology,
2.
Hotson, A. N., Gopinath, S., Nicolau, M., Khasanova, A., Finck, R., Monack, D., &
Nolan, G. P. (2016). Coordinate actions of innate immune responses oppose those of
the adaptive immune system duringSalmonellainfection of mice. Science Signaling,
9(410), ra4-ra4.
Hurley, D., McCusker, M. P., Fanning, S., & Martins, M. (2014). Salmonella–Host
interactions – Modulation of the host innate immune system. Frontiers in
Immunology, 5.
Krawiec, M., Pietkiewicz, M., & Wieliczko, A. (2014). Salmonella spp. as a cause of
mortality and clinical symptoms in free-living garden bird species in Poland. Polish
Journal of Veterinary Sciences, 17(4), 729-731.

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Norton, S., Huhtinen, E., Conaty, S., Hope, K., Campbell, B., Tegel, M., Boyd, R., &
Cullen, B. (2012). A large point-source outbreak of Salmonella Typhirium linked to
chicken, pork and salad rolls from a Vietnamese bakery in Sydney. Western Pacific
Surveillance and Response Journal, 3(2), 1-1.
Onwuezobe, I. A., Oshun, P. O., & Odigwe, C. C. (2012). Antimicrobials for treating
symptomatic non-typhoidal Salmonella infection. Cochrane Database of Systematic
Reviews.
Pastelin-Palacios, R., Gil-Cruz, C., Pérez-Shibayama, C. I., Moreno-Eutimio, M. A.,
Cervantes-Barragán, L., Arriaga-Pizano, L., Ludewig, B., Cunningham, A. F.,
García-Zepeda, E. A., Becker, I., Alpuche-Aranda, C., Bonifaz, L., Gunn, J. S.,
Isibasi, A., & López-Macías, C. (2011). Subversion of innate and adaptive immune
activation induced by structurally modified lipopolysaccharide from Salmonella
typhimurium. Immunology, 133(4), 469-481.
Swart, A. L., & Hensel, M. (2012). Interactions ofSalmonella entericawith dendritic cells.
Virulence, 3(7), 660-667.
Tennant, S. M., MacLennan, C. A., Simon, R., Martin, L. B., & Khan, M. I. (2016).
Nontyphoidal Salmonella disease: Current status of vaccine research and
development. Vaccine, 34(26), 2907-2910.
Varas, M., Ortíz-Severín, J., Marcoleta, A. E., Díaz-Pascual, F., Allende, M. L.,
Santiviago, C. A., & Chávez, F. P. (2017). Salmonella Typhimurium induces
cloacitis-like symptomsin zebrafish larvae. Microbial Pathogenesis, 107, 317-320.