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Pathogenesis of Salmonella Typhi (Enteric fever/Typhoid fever)
- Enteric fever is usually caused by strains of Salmonella Typhi & Paratyphi A, B, and C.
- Enteric fever is generally characterized by infection of reticuloendothelial system & intestinal lymphoid tissue accompanied by sustained fever & bacteremia.
- The transmission occurs via oral route usually with contaminated foods & water.
- Salmonella Typhi has an Acid tolerance response (ATR) gene that protects them from the acidity of the stomach.
- After escaping from the stomach, S. Typhi passes to ileum & colon.
- It penetrates through the mucosal barrier and is inserted by M-cells (Micro folds-cells of the intestine) or gut epithelial cells through Bacteria mediated endocytosis(BME).
- BME is mediated by the TypeIII secretory system (TTSS) encoded on Salmonella pathogenicity Island-1 (SPI-1).
- The bacilli are resistant to the lysosomal content of M-cells & multiply within them.
- The bacilli are released into underlying lamina propria & presented to the macrophages.
- They evade killing within the macrophage which is accounted to many virulence traits possessed by S. Typhi such as:
- Vi-antigen increases resistance to peroxides of macrophages.
- PhoP & PhoQ gene products modified bacterial LPS.
- ATR gene products
- Spv gene products
- They are then carried by mesenteric lymph nodes to the bloodstream rather than invading adjacent epithelial cells resulting in primary transient bacteremia.
- The bacilli are phagocytosed into the blood stream by phagocytic cells.
- These phagocytic cells carry the bacilli into the liver, spleen & bone marrow and they grow within them.
- After a rapid multiplication, phagocytic cells undergo apoptosis and the bacilli are released into blood stream initiating continuous secondary bacteremia and septicemia.
- Thus, bacteremia and septicemia are manifested by a daily high fever which is a characteristic of enteric fever.
Image Source: Dahab Clinic.
Clinical Manifestation of Salmonella Typhi
Stage I (1st week)
- The slowly rising temperature at 103-104°F.
- Abdominal pain & myalgia
End of 1st week
- Dry cough
- Rose spots may appear on the upper abdomen and on the back of sparse.
- Abdominal distension with tenderness
Stage II (2nd week)
- Signs & symptoms of Stage I progress
End of 2nd week
- The complication and then coma or death (if untreated).
Stage III (3rd week)
- Febrile become toxic and anorexic.
- Weight loss
- Typhoid state ( Apathy, confusion, and psychosis)
- High risk (5-10%) of hemorrhage and perforation may cause death.
Stage IV (4th week) (Recovery period)
- If the individual survives to the 4th week, then the fever, mental state, and abdominal distension slowly improve over a few days.
- Intestinal and neurologic complications may still occur in surviving untreated individuals.
- Weight loss and debilitating weakness last months.
- Greenwood D, Slack RCB, and Peutherer J (2001). Medical Microbiology ELBS,
- Pelczar MJ, Chan ECS, and Krieg NR (1993).Microbiology 5th edition,
- Cheesbrough M (2007). Medical Laboratory Manual for Tropical Countries Vol.2 ELBS London.
- 5% – https://emedicine.medscape.com/article/231135-clinical
- 2% – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2566199/
- 1% – https://www.sciencedirect.com/science/article/pii/0264410X94900310
- 1% – https://quizlet.com/121563421/gi-histology-i-oral-cavity-esophagus-and-stomach-flash-cards/
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