Emerging Threat of Salmonella typhi Epidemiological Trends and Local Impact

Emerging Threat of Salmonella typhi Epidemiological Trends and Local Impact

Structure and Cell-type

Salmonella typhi (S. typhi) belongs to the Kingdom Bacteria, Phylum Proteobacteria, Class Gammaproteobacteria, Order Enterobacteriales, family Enterobacteriaceae, Genus Salmonella, Species Salmonella enterica, Subspecies Salmonella enterica enterica, and Serovar Salmonella enterica serovar Typhi. It is a flagellated bacteria, gram-negative, non-spore-forming, anaerobic, bacillus, and facultative (utilizes organic substrates and redox reactions for energy). It has a diameter of between 0.7 to 1.5 mm and a length between 2 to 5 mm. Additionally, S. Typhi is characterized by three antigens: the flagellar (H), somatic (O), and capsule (Vi) antigens. The H antigen follows two forms known as phase one and phase two. Generally, the microorganism changes from one state to another. Antigens O are characterized by definite sequences and occur on the cell’s surface. Further, Vi antigens are superficial antigens that overlap the O antigens and are crucial in distinguishing S. typhi from other Salmonellae.

Virulence Factors

typhi expresses a combination of particular characteristics that are effective in the bacterium’s pathogenicity. Firstly, it contains endotoxin and a Vi antigen that are associated with an increase in virulence. The Vi antigen facilitates the survival and replication of the bacterium by blocking the activity of the C3b complementary system. Furthermore, virulence depends on the organism’s ability to invade cells by forming a protective coat, the lipopolysaccharide (LPS), and the production of invasion genes (inv genes). LPS are highly glycosylated and are produced as integral parts of the outer cell membrane. Inv genes are proteins that invade the non-phagocytic cells, allowing the bacterium to survive and reproduce intracellularly (Jaroni, 2014). Inv genes also block the action of leukocytes by inhibiting oxidative bursts, rendering innate immunity response ineffectual.

History, Natural Reservoir, Disease Caused, and Epidemiology

According to Song et al. (2010), humans are the only natural reservoir of S.typhi. Accordingly, S. typhi is a highly invasive intracellular pathogen that causes typhoid fever. Typhoid fever is a life-threatening systemic infection and atypical gastrointestinal human syndrome. It is an ancient disease that affected humans through outbreaks like the plague of Athens. Currently, the disease is rare in developed countries and is often related to tourists returning from affected areas. Nonetheless, typhoid fever is still widespread in developing countries with poor sanitary methods, especially in Southeast Asia and sub-Saharan Africa (Spanò, 2016). Studies have also reported that in tropical areas, the fever is more common when the season is hot and dry, such that the concentration of the bacteria accumulates more in rivers and streams or during the rainy seasons when floods lead to contamination of water sources (Ugboko & Nandita, 2014).

Pathogenesis and Clinical Manifestations

The infection by S.typhi follows a fecal-oral transmission route via contaminated foods and drinking water. Infection begins in the small intestines, where the ingested organisms invade the epithelial cells. The microorganisms then colonize the mucosa and penetrate the bloodstream. Consequently, transient bacteremia occurs, where the bacteria invades the reticular-endothelial system (the bone marrow, spleen, and liver), kidneys, and gall bladder. At this point, the macrophages are destroyed. The bacteria then re-invades the intestines from the gall bladder, which is characterized by Peyer’s patches (PP), ulceration, and inflammation. Also, this re-invasion marks the first clinical manifestation of the disease.

Symptoms include a high fever, headache, loss of appetite, nausea, constipation, anorexia, malaise, myalgia, enlargement of the spleen (depending on its location), and the formation of red spots on the abdominal skin. Progression to this first clinical manifestation of the infection is slow, usually from 3 to 56 days, with 10 to 20 days being typical. Further, the re-invasion into the intestinal tract, usually within the third week of infection and between 39°C and 41°C (“Salmonella Typhi,” 2014), leads to inflammation and necrosis. These conditions lead to watery and bloody diarrhea. Subsequently, intestinal perforation also causes peritonitis and septicemia, the leading cause of death in typhoid fever. Other complications associated with S.typhi infection include meningitis, hepatic failure, thyroid abscess, neonatal encephalopathy, and reactive arthritis, especially in persons with certain histocompatibility types, such as human leukocyte antigen.

Interaction with Host Cells

As the pathogens invade the lymphatic tissue in the intestinal mucosa, they encounter various host phagocytic cells like macrophages. Nonetheless, the pathogen often survives and multiplies within the macrophages. They do this by establishing a support Salmonella-containing vacuole (a specialized compartment derived from the endolysosomal system). The vacuole and the endolysosomal system are usually in a close dynamic relationship. Microscopy studies have revealed that the membrane system connects the vacuole with other intracellular compartments. In addition to Salmonella-containing vacuole, S. typhi is characterized by type III secretion systems. These systems deliver bacterial proteins (bacterial effectors) directly into the cell’s cytoplasm, hence, manipulating the functions of the host cells for their benefit.

Treatment and Prevention

Traditional drugs for the treatment of S.typhi infection include chloramphenicol, amoxicillin ampicillin, sulfamethoxazole, and trimethoprim. However, the effectiveness of these drugs has been put into question due to the emergence of strains conveying multidrug-resistant (MDR) features. Mechanisms of drug resistance by S. typhi include inactivating the drug, modifying the drug’s target sites, reducing drug-membrane permeability, and rapid extrusion of the drug. Therefore, selecting suitable antibiotics requires knowledge of the drug’s susceptibility or the resistance of the identified strains.

Note: Mechanisms of Antibiotic Resistance in Salmonella typhi. (p. 472), by Ugboko, H., & Nandita, D. (2014). International Journal of Current Microbiology and Applied Sciences.

Moreover, treating the infection also involves the application of vaccines to reduce the predisposition of hosts to the disease. Available vaccines include the Ty21a vaccine and the parenteral Vi vaccine. The Ty21a vaccine contains the S. typhi strain Ty21a, while the parenteral Vi vaccine contains the Vi antigen of S. typhi (Ugboko, H., & Nandita, D. 2014). Prevention and control measures include improved sanitary systems, identifying and vaccinating carriers, and ensuring the safety of foods and drinking water, for example, through pasteurization of dairy products and boiling drinking water.

In conclusion, S. typhi is a bacterium that causes systemic and typhoid fever in humans, the only natural reservoirs. Some of its virulence factors include secretion of toxins and disruption of the innate immune response. Infection by this bacterium is treated with the appropriate antibiotics and vaccines. Finally, since contaminated foods and water are the primary sources of infection, proper sanitation practices are key prevention measures.

References

Jaroni, D. (2014). SALMONELLA | Salmonella typhi. Encyclopedia of Food Microbiology, 349-352. https://doi.org/10.1016/b978-0-12-384730-0.00296-2

Salmonella Typhi. Salmonellatyphi.org. (2014). Retrieved 7 February 2022, from https://www.salmonellatyphi.org/.

Song, J., Willinger, T., Rongvaux, A., Eynon, E., Stevens, S., & Manz, M. et al. (2010). A Mouse Model for the Human Pathogen Salmonella Typhi. Cell Host & Microbe, 8(4), 369. https://doi.org/10.1016/j.chom.2010.09.003

Spanò, S. (2016). Mechanisms of Salmonella Typhi Host Restriction. Advances in Experimental Medicine and Biology, 283-285. https://doi.org/10.1007/978-3-319-32189-9_17

Ugboko, H., & Nandita, D. (2014). Mechanisms of Antibiotic Resistance in Salmonella typhi. International Journal of Current Microbiology and Applied Sciences, 3(12), 461-476. Retrieved 7 February 2022, from https://www.researchgate.net/profile/Harriet-Ugboko/publication/321491731_Mechanisms_of_Antibiotic_resistance_in_Salmonella_typhi/links/5a256dbb4585155dd41fdf2d/Mechanisms-of-Antibiotic-resistance-in-Salmonella-typhi.pdf.

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For your paper on pathology or microbe-environment interactions, you will pick a microorganism. The organism can not be one of the ones your instructor goes over during the lecture listed in the syllabus. Select a pathogen/microbe from current events that is an emerging or reemerging concern to you or people in your area. Provide local epidemiological data/statistics for the organism.

Emerging Threat of Salmonella typhi Epidemiological Trends and Local Impact

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Introduction to the organism (structure, cell type, morphology, metabolic requirements, natural reservoir, history, etc.)

Introduction to the disease(s) caused by the organism (epidemiology, signs, symptoms, etc.) OR an introduction to the environmental impact of the organism

List and describe factors employed by the organism to assist in its growth, reproduction, culture conditions, host/pathogen interactions and/or virulence. (e.g., nitrogen fixation, symbiotic interactions etc.) Categorize virulence factors by mechanisms of action (Immunity Avoidance, Tissue/Cell Lysis, Colonization/Spread)

Discussion of treatment/prevention options for the disease(s) caused by the organism (Antibiotics or other chemotherapeutics given as part of treatment and their mechanisms of action, Vaccines available and type)

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