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PATHOPHYSIOLOGY OF ENTERIC
FEVER
TEJAS D
ROLL NO 122
• All pathogenic salmonella species, when
present in the gut are engulfed by phagocytic
cells, which then pass them through the
mucosa and present them to the macrophages
in the lamina propria.
• Nontyphoidal salmonellae are phagocytized
throughout the distal ileum and colon. With
toll-like receptor (TLR)–5 and TLR-4/MD2/CD-14
complex, macrophages recognize pathogen-
associated molecular patterns (PAMPs) such as
flagella and lipopolysaccharides.
• Macrophages and intestinal epithelial cells then
attract T cells and neutrophils with interleukin 8
(IL-8), causing inflammation and suppressing the
infection
• In contrast to the nontyphoidal salmonellae, S
typhi and paratyphi enter the host's system
primarily through the distal ileum. They have
specialized fimbriae that adhere to the epithelium
over clusters of lymphoid tissue in the ileum (Peyer
patches), the main relay point for macrophages
traveling from the gut into the lymphatic system.
The bacteria then induce their host macrophages
to attract more macrophages.
• S typhi has a Vi capsular antigen that masks
PAMPs, avoiding neutrophil-based
inflammation.
• Typhoidal salmonella co-opt the macrophages'
cellular machinery for their own
reproduction as they are carried through the
mesenteric lymph nodes to the thoracic duct
and the lymphatics and then through to the
reticuloendothelial tissues of the liver, spleen,
bone marrow, and lymph nodes.
• Once there, they pause and continue to
multiply until some critical density is reached.
Afterward, the bacteria induce macrophage
apoptosis, breaking out into the bloodstream
to invade the rest of the body.
• The bacteria then infect the gallbladder via
either bacteremia or direct extension of
infected bile. The result is that the organism re-
enters the gastrointestinal tract in the bile and
reinfects Peyer patches. Bacteria that do not
reinfect the host are typically shed in the stool
and are then available to infect other hosts.
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pathophysiology of enteric fever

  • 2. • All pathogenic salmonella species, when present in the gut are engulfed by phagocytic cells, which then pass them through the mucosa and present them to the macrophages in the lamina propria. • Nontyphoidal salmonellae are phagocytized throughout the distal ileum and colon. With toll-like receptor (TLR)–5 and TLR-4/MD2/CD-14 complex, macrophages recognize pathogen- associated molecular patterns (PAMPs) such as flagella and lipopolysaccharides.
  • 3. • Macrophages and intestinal epithelial cells then attract T cells and neutrophils with interleukin 8 (IL-8), causing inflammation and suppressing the infection • In contrast to the nontyphoidal salmonellae, S typhi and paratyphi enter the host's system primarily through the distal ileum. They have specialized fimbriae that adhere to the epithelium over clusters of lymphoid tissue in the ileum (Peyer patches), the main relay point for macrophages traveling from the gut into the lymphatic system. The bacteria then induce their host macrophages to attract more macrophages.
  • 4. • S typhi has a Vi capsular antigen that masks PAMPs, avoiding neutrophil-based inflammation. • Typhoidal salmonella co-opt the macrophages' cellular machinery for their own reproduction as they are carried through the mesenteric lymph nodes to the thoracic duct and the lymphatics and then through to the reticuloendothelial tissues of the liver, spleen, bone marrow, and lymph nodes.
  • 5. • Once there, they pause and continue to multiply until some critical density is reached. Afterward, the bacteria induce macrophage apoptosis, breaking out into the bloodstream to invade the rest of the body. • The bacteria then infect the gallbladder via either bacteremia or direct extension of infected bile. The result is that the organism re- enters the gastrointestinal tract in the bile and reinfects Peyer patches. Bacteria that do not reinfect the host are typically shed in the stool and are then available to infect other hosts.
  • 6.