Shigella
Definitions & Key takeaways
Shigella is a genus of bacteria known to cause a contagious form of gastroenteritis known as shigellosis. Shigellosis is characterized by an inflammation of the gastrointestinal tract, which causes destruction and inflammation of the epithelium, leading to dysentery with symptoms like severe abdominal and rectal cramping and pain, a fever, and watery diarrhea with mucous with or without blood or pus. Shigella is transmitted through the fecal-to-oral route, mainly through fingers, food, and flies. It's diagnosed with a fecal sample and treatment centers around fluid and electrolyte replenishment and antibiotics.
Shigella is a gram negative bacterium that belongs to the Enterobacter Ieae family. There are four species of Shigella shigella dysentery.
Shigella flexneri shigella boi and Shigella Soni and each has its own serotypes in humans. These species can all cause shigellosis which is a contagious infection of the intestines, particularly the colon and shigellosis can progress to dysentery which is when the infection causes inflammation of the colon, resulting in severe abdominal pain and diarrhea.
Now, shigella is a gram negative rod shaped bacterium, meaning it looks like a little red or pink stick on a gram stain.
And it's a facultative anaerobe. So it can survive with or without oxygen in the environment.
It has no flagellum making it non modal and it does not form spores. It's also a non lactose fermentor.
So it doesn't ferment lactose and it's urease and oxidase negative, meaning it does not produce these enzymes. Finally, it doesn't produce hydrogen sulfide gas either.
And this can be used to selectively identify shigella on special culture mediums like Macconkey auger on this medium. Shigella mostly forms white, non lactose, fermenting non hydrogen sulfide producing colonies.
Now, once shigella is ingested, it multiplies in the small intestine and then passes into the colon there. It targets the epithelial layer of the mucosal lining or it infects colonic enterocytes in microfold cells or M cells.
And these M cells phagocytose which means they eat the bacteria from the intestinal lumen and then spit it out into the underlying mucosa associated lymphoid tissues.
Or malts. Malts are a type of mucosal immune tissue that extends into the submucosa and contains plenty of immune cells like macrophages.
The macrophages gobble up shigella to neutralize the pathogen. But the bacterium induces apoptosis or programmed cell death in the macrophage.
Now, when a macrophage dies, it releases a variety of cytokines, including interleukin one beta, which activates an intense inflammatory process that recruits additional immune cells to wage war at the site of the infection.
And this results in the death of epithelial cells which damages the colonic mucosa resulting in and abscesses all the damage and migration of immune cells, particularly polymorphonuclear leukocytes through the epithelium disrupts the cellular junctions between neighboring epithelial cells, allowing shigella from the intestinal lumen to enter enterocytes through the lateral sides of the cell.
And actually, that's not the only way Shigella can infect enterocytes after the initial infection. After shigella kills the macrophage and is released into the immune tissue under the epithelium.
It can access and infect colonic enterocytes from their basal side. Shigella uses its type three secretory system which acts almost like a syringe to puncture and inject proteins into the enterocyte and makes the enterocytes phagocytose sulla.
So that means shigella is slowly engulfed by the cell membrane forming a membrane bound compartment that eventually pinches off from the cell membrane and ends up inside the cell or it's called a pheo.
Then shigella can use a number of effector proteins which slice the phagosome and release shigella into the cytoplasm in the cytoplasm effector proteins also induce shigella s actin base motility.
This starts by recruiting the host cells, small actin filaments to one end of the bacteria. And as more and more actin filaments get recruited and polymerized behind the bacteria's end pole that propels the bacteria forward like a rocket that helps shigella blast through the lateral sides of both the host Andy.
And after the neighboring enterocyte further spreading the infection. Finally, one particular species of Shigella shigella dysentery serotype, one also produces shigatoxin shigatoxin similar to the shiga like toxin, producing pathotype of E coli is an A B toxin.
So it has two main subunits A and B that are joined by a disulfide bond. Each subunit plays a specific role in the invasion and destruction of a host cell.
The B subunit helps bind the toxin to the host cell's membrane where the toxin is ultimately engulfed into a phagosome within the host cells, cytoplasm, the inside of the phagosome becomes more acidic.
And as a consequence, the disulfide bond holding the two subunits together becomes weak and eventually breaks separating the subunits at this point.
The A subunit can then diffuse through the phagosome membrane into the cytoplasm where it targets the ribosomes. In eukaryotic cells, ribosomes are made of two main subunits.
The larger of the two is the 60 S subunit and it contains a 28 SR RNA protein that's important for the initiation of polypeptide synthesis.
The shigatoxin A subunit cleaves 28 SR RNA. And the end results is an arrest of protein synthesis, followed by cell death.
If shigatoxin reaches the endothelial cells, that line the mucosal blood vessels, it can damage them which allows the toxin to enter the bloodstream causing complications like hemolytic uremic syndrome.
So that means from the bloodstream, the toxin can get to the kidneys and bind to the endothelial cells lining the glomerulus, making them die by apoptosis.
Consequently, a dead endothelial cell leaves a gap in the capillary wall. And as more gaps keep forming, it results in holes big enough to allow large molecules like proteins to start leaking out of the capillaries, resulting in proteinuria.
The destruction of endothelial cells triggers an inflammatory process in which inflammatory molecules like cytokines and chemokines are released cytokines and chemokines activate blood platelets and initiate the clot formation.
As these platelets are used to form these clots, their number in the blood decreases resulting in low platelets or thrombocytopenia.
Also, these clots can be big enough to obstruct small arterioles. So as red blood cells are forced to pass through obstructed micro vessels, they can get sliced into fragments called schistocytes in a process known as microangiopathic hemolysis.
So as more red blood cells get destroyed in the process, their number reduces, which can cause anemia. Alternatively, if clots obstruct too many arterioles organs that depend on high blood flow.
This is how too much of metabolic waste like urea start accumulating in the blood leading to uremia. Then hus is a combination of hemolytic anemia.
When red blood cells are being overly destroyed, kidney failure due to destroyed glomerular cells that results in uremia or high levels of blood urea and thrombocytopenia, meaning low platelets.
All right. Now, shigella can survive the acidic stomach ph making it extremely virulent where as few as 10 bacteria can cause an infection.
And shigella is typically transmitted through the fecal oral route. So, this can include consuming contaminated water or food, particularly if prepared with unwashed hands.
Flies that carry stool particles from one place to food as well as contact with contaminated objects or hands that reach the mouth.
Sometimes shigella can be transmitted through forms of sexual contact. Typical symptoms of shigellosis are related to the resulting dysentery and last for approximately seven days.
They include severe abdominal and rectal cramping and pain, high fever, vomiting, loss of appetite, fecal incontinence and watery mucus like diarrhea, which can contain blood or pus.
In extreme cases, particularly in Children, tonic clonic seizures might happen. That's when consciousness is lost in involuntary phases of muscle activity, progress from a rigid or tonic phase to a clonic phase of rhythmic contractions and relaxations and even sepsis can happen.
But most often in neonates, malnourished Children and people with a shigella dysentery serotype one infection and finally reactive arthritis also called Reiter syndrome.
Can rarely occur in the weeks following an infection and it usually affects the knee joints causing pain and swelling. A definitive diagnosis of shigellosis can be made with a fecal sample cultured on selective media like mcconkey auger where again, white, non lactose fermenting non hydrogen sulfide, producing colonies of shigella form stool stains with methylene blue, might also show polymorphonuclear leukocytes polymerase chain reaction or PCR testing, which directly identifies shigella DNA can also be done.
Treatment of shigellosis involves fluid and electrolyte replenishment and commonly the use of antibiotics including beta lactams, both penicillins and cephalosporins, macrolides and quinolones.
Finally, an infected person can be a carrier for infection up to four weeks after onset of symptoms. So, an important part of treatment is practicing good hygiene and sanitation to limit the spread to uninfected individuals.
All right, as a quick recap shigellosis is a contagious infection caused by the bacteria. Shigella that targets M cells and enterocytes in the colonic mucosa shigella causes destruction and inflammation of the epithelium that can lead to dysentery with hallmark symptoms like severe abdominal and rectal cramping and pain.
A fever and watery diarrhea with mucus with or without blood or pus. Its route of transmission is fecal to oral, mainly through fingers, food flies and feces.
It's diagnosed with a fecal sample in treatment centers around fluid and electrolyte replenishment and antibiotics.
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