30: E. Coli and Salmonella Flashcards
characteristics of escherichia coli
gram-negative bacillus (rod)
many flagella
grows very fast
- 20-minute doubling time
remarkably diverse organism
core genome with 2167 genes
average genome with 4721 genes
total number of possible genes as 10131
constant exchange of genetic material between bacteria
how many pathovars of pathogenic e. coli?
8
variations based on where they infect humans
e. coli statistics
400M infections annually worldwide
EPEC
around a long time
causes childhood diarrhoea
transmits human-human
- not a zoonosis
fecal-oral transmission
no shiga toxin
EHEC/STEC
food/water-borne pathogen in industrialised countries with agriculture
zoonotic from cattle/animals
- not only from eating meat but exposure to cow feces
secreted shiga toxin can lead to haemolytic uremic syndrome (HUS)
- lyses RBC, clogs kidneys, leads to kidney failure
EHEC/STEC statistics
265K illnesses annually in the US
3600 hospitalisations and 30 deaths
where does the shiga toxin come from?
shigella
similarities between EPEC and EHEC/STEC
share virulence determinants
same distinctive mechanism of intestinal colonisation
attachment of EPEC and EHEC/STEC
secrete proteins allowing them to attach through pedestals
bacteria damage microvilli and create their own pedestals
triggers actin production in cells to induce this
inducing pedestal formation
inject an e. coli receptor protein, Tir, into the epithelial cell which allows for attachment
recruits from actin so it’s a solid formation and bacteria stay attached indefinitely
serotyping e. coli antigens
specific polysaccharide and flagellar proteins
polysaccharide side chains (O)
capsular antigen (K)
flagellar protein (H)
many e. coli serotypes and different antigens, so you need a lot of antibodies
main EHEC/STEC serotype
O157H7 causes 90% of the disease
most frequently isolated from people in the US, UK and Japan
EHEC/STEC shiga toxin
forms a pentameter of B subunits that bind and enter host cells, allowing a single A subunit to enter the cell
subunit A inhibits protein synthesis, leading to cell death
attacks epithelial cells, endothelial cells and immune cells
- bacteria allowed outside or into the blood stream
people usually die from kidney failure and systemic inflammation
antibodies are protective against severe disease
EHEC/STEC outbreak at jack in the box in 1992
over 600 people sickened in 6 states (mostly children)
- 4 deaths, 50 cases of kidney failure
cause was knowingly undercooking burgers
USDA began testing beef for O157H7 in 1994
- can’t just test for e. coli because it’s everywhere
how did EHEC come about?
shigella and shiga toxin gene on a plasmid taken up by a bacteriophage (viruses that infect bacteria)
mechanism of turning a commensal into a pathogen
EHEC/STEC transmission in animals
healthy cattle as major reservoirs of O157H7 with no symptoms
- contaminated bovine products and crops as predominant sources for human infections
5% of dairy cows carry EHEC
cow super-shedders exist
- remain infected for long periods of time
- may shed more than 95% of e. coli in a herd of 100
EHEC/STEC human transmission
anything coming into contact with cow feces
undercooked/unpasteurised animal products
contaminated food/water/soil
EHEC/STEC disease in humans
hermorrhagic colitis
- blood diarrhoea from intestinal bleeding
- abdominal cramps
- fever, nausea, vomiting
- mostly self-limiting and resolve in a week
haemolytic uremic syndrome
- most deaths in humans
- kidney failure, anemia, etc.
EHEC/STEC treatment
mainly supportive
antibiotics avoided since they may not reduce symptoms or prevent complications
- doesn’t work against toxins and only bacteria so if bacteria already replicated and produced toxin, too late for antibiotics
salmonella enterica serovars
2 main servovars
s. typhimurium
s. typhi
s. typhimurium
disease - gastroenteritis
duration - short-term infection of GI tract
host range - broad range of humans/animals
global burden - 78M infections and 59K deaths
s. typhi
disease - typhoid fever
- much more severe
duration - life-threatening systemic infection, life-long chronic infection
- 3-5% are carriers shedding high levels
host-range - human specific
global burden - 11M infections and 28K deaths
how does salmonella cause disease?
comes in and lives on the intestinal wall and inside epithelial cells
goes across tissues, lives in RBC
chronic s. typhi and bacterial evasion
inhibits antibody binding and complement
blocks LPS and flagellin binding to TLRs
toxin kills cells and inhibits neutrophils
s. typhi virulence factors
can infect/replicate intracellularly and extracellularly
huge advantage
- evades antibodies inside, produces toxins outside to spread across the body
