Escherichia coli (E. coli) is a Gram-negative bacterium common to the digestive tract of humans and other mammals, as well as the soil and water. While most E. coli are a non-pathogenic, normal component of the human microbiome, some strains produce enterotoxins which cause diarrheal illnesses. The notorious O157:H7 strain is the best known of the Shiga toxin producing strains, which can cause hemorrhagic colitis and life-threating hemolytic uremic syndrome (HUS).
Both live and heat-killed E. coli are often used as a non-pathogenic challenge to the fly's immune system, to contrast to entomopathogenic bacteria such as Photorhabdus luminescens or Erwinia caratovora. Live Drosophila larvae and adults can be infected orally or via septic injury (injection). Priming flies with exposure to heat-killed E. coli can increase their immune response to subsequent infections with other Gram-negative bacteria or entomopathogenic bacteria. Drosophila respond to E. coli by upregulating several antimicrobial peptides (FBgg0001101, FBgg0001102) and accumulating lipids in the gut.
E. coli infection in flies has been used as a general model of bacterial sepsis.
[updated Jul. 2021 by FlyBase; FBrf0222196]
Symptoms of Shiga toxin-producing E. coli (STEC) infection vary for each person, but often include severe stomach cramps, diarrhea (often bloody), and vomiting. Some people may have a fever, which usually is not very high (less than 101 degrees F or 38.5 degrees C). Most people get better within 5 to 7 days. Some infections are very mild, but others are severe or even life-threatening. About 5 to 10% of people who are diagnosed with STEC infection develop a potentially life-threatening complication known as hemolytic uremic syndrome (HUS). HUS develops about 7 days after symptoms first appear, when diarrhea is improving. Clues that someone is developing HUS include decreased frequency of urination, feeling very tired, and losing pink color in cheeks and inside the lower eyelids. People with HUS should be hospitalized because their kidneys may stop working and they may develop other serious problems. Most people with HUS recover within a few weeks, but some suffer permanent damage or die. (https://www.cdc.gov/ecoli/ecoli-symptoms.html)
E coli O157 can produce two different Shiga toxins encoded by bacteriophage. Stx1 is very similar to the type 1 toxin of Shigella dysenteriae; Stx2 is genetically and immunologically distinct with 55–60% similarity in genetic and amino acid sequences. The possession and expression of the Stx2 gene and the variant Stx2c (which often occurs with Stx2) correlate strongly with the causation of bloody diarrhoea and haemolytic uraemic syndrome. Shiga toxins bind to glycosphingolipid globotriaosylceramide (Gb3), a cell surface receptor. They are then internalised by clathrin-dependent endocytosis, and go on to specifically depurinate 28S eukaryotic rRNA, inhibiting protein synthesis. This step induces a ribotoxic-stress response that can lead to cytokine release and apoptotic cell death. (Pennington 2010 and references therein, pubmed:20971366)