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Internal Medicine

Salmonella gastroenteritis (food poisoning)

  • Worldwide: One of the M/C causes of diarrhoea
  • Europe: 2nd M/C foodborne disease after campylobacteriosis

Aetiopathology

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Pathogenesis of salmonellosis | Giannella RA. Salmonella. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 21. Available from: https://www.ncbi.nlm.nih.gov/books/NBK8435/
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Invasion of intestinal mucosa by Salmonella. | Giannella RA. Salmonella. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 21. Available from: https://www.ncbi.nlm.nih.gov/books/NBK8435/

 

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Proliferation of Salmonella with Severe Gastroenteritis | Nucleus Medical Media Inc/Alamy Stock Photo

 


Cilnical features

12-36 hours after exposure, bacteria multiply in the small intestine, causing an intestinal inflammation (enteritis) with symptoms lasting from 2-7 days

  • Diarrhoea (watery and non-bloody but may be mucoid and bloody)
  • Fever
  • Abdominal cramps
  • Vomiting
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Course of S. enteritidis in C57Bl/6-Bcgr (Slc11a1+/+), a resistant mouse model. Salmonella rapidly reaches the cecum in the early stage of the infection between 12 and 48 h postinoculation (PI) and remains in this organ as an important reservoir for 5 days PI, with increasing bacteria multiplication. The presence of bacteria in the cecum seems to be associated with its extracellular multiplication in the intestinal content and intermittent shedding in the feces. The colonization of the small intestine occurs during the first 4 days PI. In this period, Salmonella penetrates the intestinal mucosa, causing different degrees of degeneration of the microvilli, which is reversible (membrane ruffling). This mechanism is mediated by effector proteins translocated by T3SS encoded in SPI-1. Intracellular multiplication of the bacteria in mononuclear phagocyte system (MPS) occurs from 3 days PI. The exact route of Salmonella dissemination from intestine to MPS is unclear, but from the moment that bacteria reach the MPS, they remain in spleen, causing splenomegaly by 10 days PI. The intracellular multiplication in MPS coincides with the production of IFNγ, which restricts the replication of intracellular Salmonella. | Maciel, B. M. (2017). Salmonella enterica: Latency. In R. P. Rezende (Ed.) (p. Ch. 3). Rijeka: IntechOpen. https://doi.org/10.5772/67173

Complications

Enteritis:

  • Severe disease: Dehydrationsevere toxicity (infants)
  • Immunocompromise: Sepsis
  • Extraintestinal localizations: Salmonella meningitis (children), osteitis, osteomyelitis (coexisting sickle-cell anaemia in children), etc
journal.ppat.1002933.g001
Dissemination of S. Typhi during systemic infection: Typhoid is usually contracted by ingestion of food or water contaminated by fecal or urinary carriers excreting S. Typhi. The incubation period is usually 7 to 14 d. In the small intestine the bacteria adhere to the mucosa and then invade the epithelial cells. The Peyer’s patches, which are aggregrated lymphoid nodules of the terminal ileum, play an important role in the transport to the underlying lymphoid tissue. Specialized epithelial cells such as M cells overlying these Peyer’s patches are probably the site of internalization of S. Typhi. Once the bacteria have penetrated the mucosal barrier, the invading organism translocates to the intestinal lymphoid follicles and the draining mesenteric lymph nodes, and some pass on to the reticuloendothelial cells of the liver and spleen. During the bacteremic phase, the bacteria are widely disseminated throughout the body. Secondary infection can occur with liver, spleen, bone-marrow, gallbladder, and Peyer’s patches as the most preferred sites. The gallbladder is the main reservoir during a chronic infection with S. Typhi and invasion occurs either directly from the blood or by retrograde spread from the bile. Of interest, the ability of Salmonella to form biofilms on gallstones is likely to be a critical factor in establishment of chronic carriage and shedding of S. Typhi. The bacteria that are excreted in the bile can then reinvade the intestinal wall by the mechanism previously described or are excreted by feces. Typical clinical symptoms are fever, malaise, and abdominal discomfort. Clinical features such as a tender abdomen, hepatomegaly, splenomegaly, and a relative bradycardia are common. Rose spots, the classical skin lesions associated with typhoid fever, are relatively uncommon and occur in 5%–30% of cases. The most severe manifestations of typhoid leading to sepsis and death are either necrosis of the Peyer’s patches resulting in gut perforation and peritonitis or a toxic encephalopathy associated with myocarditis and haemodynamic shock. |

Other long-term complications:

  • Irritable bowel syndrome (IBS)
  • Inflammatory bowel disease (IBD)

Diagnosis

Histopathology

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Electron photomicrograph demonstrating invasion of guinea pig ileal epithelial cells by Salmonella typhimurium. Arrows point to invading Salmonella organisms. (Courtesy Akio Takeuchi, Walter Reed Army Institute of Research, Washington, D.C.). | Giannella RA. Salmonella. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 21. Available from: https://www.ncbi.nlm.nih.gov/books/NBK8435/

 

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Current model of the series of events leading to an inflammatory diarrhea during Salmonella serotype Typhimurium infection of calves. (A) Transmission electron micrograph of bovine Peyer’s patch at 15 min after infection of a ligated ileal loop with Salmonella serotype Typhimurium strain ATCC 14028 (109 CFU/loop). Ruffling of the brush border of an enterocyte and bacterial internalization into membrane-bound vacuoles can be seen (bar = 2.5 μm). (B) Transmission electron micrograph of bovine Peyer’s patch at 15 min after infection of a ligated ileal loop with Salmonella serotype Typhimurium strain ATCC 14028 (109 CFU/loop). An M cell in the follicle-associated epithelium containing an internalized bacterium is shown (bar = 2.5 μm). (C) Focal infiltration of neutrophils in the lamina propria (LP) of an absorptive villus in bovine Peyer’s patches at 1 h after infection of a ligated ileal loop with Salmonella serotype Typhimurium strain ATCC 14028 (109 CFU/loop) (bar = 20 μm). (D) Blunting of absorptive villus 3 h after infection of a ligated ileal loop with Salmonella serotype Typhimurium strain ATCC 14028 (109 CFU/loop). Note the hemorrhage and infiltration of the lamina propria with neutrophils. Arrows indicate areas where neutrophils transmigrate into the intestinal lumen (L). The arrowhead indicates the detachment of surface epithelial cells at the tip of an absorptive villus (bar = 20 μm). (E) Presence of a large number of neutrophils in the intestinal lumen (L) at 8 h postinfection of a ligated ileal loop with Salmonella serotype Typhimurium strain ATCC 14028 (109 CFU/loop). Note the hemorrhage, injury to the intestinal epithelium, and detached enterocytes (bar = 20 μm). (F) Gross pathology of the terminal ileum of a calf at 48 h after oral infection with Salmonella serotype Typhimurium strain ATCC 14028 (1010 CFU). Note the pseudomembrane formation over a bovine Peyer’s patch (bar = 1 cm). | Zhang, S., Kingsley, R. A., Santos, R. L., Andrews-Polymenis, H., Raffatellu, M., Figueiredo, J., … Bäumler, A. J. (2003). Molecular Pathogenesis of <em>Salmonella enterica</em> Serotype Typhimurium-Induced Diarrhea. Infection and Immunity, 71(1), 1 LP-12. https://doi.org/10.1128/IAI.71.1.1-12.2003

 


Management

Prevention:

  • Hygienic slaughtering practices
  • Thorough cooking and refrigeration of food

Treatment:

  • Oral rehydration supplements (typically containing salts NaCl and KCl)
  • Antibiotics (if required):
      • Ceftriaxone
    • Azithromycin (resistant populations)

 

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