shigella and salmonella Flashcards
vaccine for shigella
no
difference between shigella and salmonella
shigella is more likely to cause bloody diarrhoea, sheigella does not have a capsule, shigella is non motile unlike salmonella, shigella only needs a few organism 10-100 to cause disease as not destroyed by stomach acid like salmonella is, so salmonella you need many microbrew to be I infected also we get shiegalla by contact with human faces whereas salmonella is via animal faces(but can be human faces as well)
tx shigella
macrolide or fluroquinolones (ciprofloxacin)
shiegalla symptoms
abdominal cramps
bloody diarrhoea
tenesmus
fever
how do we catch shigella
fecal oral route
how to we catch salmonella
via contamination of animal droppings inf food as salmonella lives in the gIT of animals such as birds or by the faces of humans as the bacteria lives in the GI of humans too, contaminated vegetables etc contaminated surfaces
culture of shigella
macokeys agar both salmonella snd sheigella are lactose non fermenting so grow as colourless colonies
types of shiegella
s. boudin
s. flexnerri
s.sonnei
s.dystenery
virulence factors of shigella
endotoxin
exotoxin - some strains have the shigag toxin which is very similar to the EHEC , binds to the 60 s subunit of ribosomes and damages glomeruli and hence why can lead to HUS
complications of shigella
HUS
toxic megacoln
Reuters
seziures!!!! NB in young children
rectal prolaps due to the tensusmus
prevention of shigella
eating packaged food and water
chlorinated water
personal hygiene
diagnosis of shiegella
stools- will see polymorpho luekpcyets (neutrophils) and rbc
culture on maconkeys agar
target of shiegella
the colon, M cells of Peters patchers they invade cause inflammation and necrosis and ulcers
what group do salmonella and shigella fall under
family enterobactericae - they are primary organisms as they always cause disease unlike secondary where they are commensals
types of diarrhoea
No cell invasion: The bacteria bind to the in- testinal epithelial cells but do not enter the cell. Diar- rhea is caused by the release of exotoxins (called enterotoxins in the GI tract), which causes electrolyte
and fluid loss from intestinal epithelial cells or epithelial cell death. Watery diarrhea without systemic symp- toms (such as fever) is the usual picture. Enterotoxi- genic Escherichia coli and Vibrio cholera are examples.
2) Invasion of the intestinal epithelial cells: The bacteria have virulence factors that allow binding and invasion into cells. Toxins are then released that de- stroy the cells. The cell penetration results in a systemic immune response with local white blood cell infiltration (leukocytes in the stool) as well as fever. The cell death results in red blood cell leakage into the stool. Exam- ples: Enteroinvasive Escherichia coli, Shigella, and Sal- monella enteritidis.
taining white and red cells, this deeper invasion results in systemic symptoms of fever, headache, and white
blood cell count elevation. The deeper invasion can also result in mesenteric lymph node enlargement, bactere- mia, and sepsis. Examples: Salmonella typhi, Yersinia enterocolitica, and Campylobacter jejuni.
salmonella virulence factors
has h antigens meaning its motile and it constantly changes its antigens evading the immune system
has a polysaccharide capsule
what is shigella similar to
IEC) in that they both invade intestinal epithelial cells and release Shiga toxin, which causes cell de- struction. White cells arrive in an inflammatory reac- tion. The colon, when viewed via colonoscopy, has shallow ulcers where cells have sloughed off. The illness begins with fever (unlike ETEC and cholera, which do not invade epithelial cells and therefore do not induce a fever), abdominal pain, and diarrhea. The diarrhea may contains flecks of bright-red blood and pus (white cells). Patients develop diarrhea because the inflamed colon, damaged by the Shiga toxin, is unable to reabsorb fluids and electrolytes.
shiga toxin
This is the same toxin as in EHEC and EIEC, and its mechanism is the same. has an A subunit and b subunit (binding) to allow the a toxin to enter and inactivate the 60 s ribosome stopping protein synthesis