Understanding Shigella: Key Features and Clinical Implications

Shigella is a gram-negative rod causing dysentery, reactive arthritis, and hemolytic uremic syndrome.

### Understanding Shigella: Key Features and Clinical Implications
* 🦠 Shigella is a gram-negative rod that is oxidase negative, facultative intracellular, non-lactose fermenting, and **non-motile due to the absence of flagella**, which is a **crucial distinguishing feature from Salmonella**.
* 💧 The transmission of Shigella is fecal-oral, and it produces the **Shiga toxin**, which inactivates the **60S ribosomal subunit**, leading to **decreased protein synthesis** in intestinal cells.
* 🧪 Shigella is **acid stable**, allowing it to **survive gastric acid** and require a **low infectious dose** for infection, contrasting with Salmonella, which is **acid labile** and needs a **higher infectious dose**.
* 🔬 Both Shigella and Salmonella invade the intestinal epithelium via **M cells of Peyer's patches** and utilize a **Type 3 secretion system** to inject toxins into host cells.
* 💩 Clinically, Shigella causes bacillary dysentery (shigellosis), characterized by **bloody, inflammatory, mucusy diarrhea**, and can also lead to **reactive arthritis** and **hemolytic uremic syndrome (HUS)**.
* ⚠ HUS is a triad of **microangiopathic hemolytic anemia**, **thrombocytopenia**, and **acute renal failure**, often associated with schistocytes and abnormal lab findings, including **increased BUN and creatinine levels**.
* 📊 On exams, it’s essential to differentiate between Shigella and Salmonella, especially in cases of HUS, where the causative pathogen might be linked to the **Shiga toxin originally produced by Shigella**.

in this video I'll talk about Shigella. Now I would caution you to first watch the salmonella video because salmonella and Shigella have several overlapping features and what's really important to know for your exams is how to differentiate these two because that often times will show up

so salmonella was the video I published just before I'm going to publish this Shigella video so if you haven't seen salmonella yet stop what you're doing watch my most recent video prior to this one and then come back and watch Shigella

so Shigella is a gram-negative rod that's oxidase negative, facultative intracellular and non-lactose fermenting. It is non-motile because it has no flagella. It also has no production of H2S and both of these features differentiate against salmonella which

does have flagella and does produce H2S. So first high yield point is that Shigella has no flagella. Memorize that. That rhymes, flagella or Shigella has no flagella. Shigella has no flagella. Shigella is transmitted fecal

orally and as we'll see that kind of explains some of the symptoms, pathophysiology. Shigella has an enterotoxin known as the Shiga toxin. What's really high yield to know for exams is the mechanism of the Shiga toxin

and that mechanism is that it inactivates the 60s ribosomal subunit which in turn decreases protein synthesis in the intestinal cells. It also has an endotoxin. It's acid stable which is really important for conveying infection because due to its

acid stability. It's relatively resistant to gastric acid, which is to say a low infectious dose is required because you only need to get a little bit of Shigella into the system because gastric acid won't break it down. And if we contrast that versus Salmonella, in Salmonella it

wasn't acid stable. It was acid labile, and what that meant is that in Salmonella you don't have resistance to gastric acid. It's easily broken down, and so in Salmonella you need a high infectious dose in order to get

infection, whereas in Shigella, because again, I'm repeating myself now to really drive this home, it's resistant to gastric acid, which means that gastric acid won't break it down, which means a smaller infectious dose of this bacteria can go on and cause infection. So that's

another key differentiating feature between Salmonella and Shigella. Just like we saw in Salmonella, Shigella is going to invade the intestinal epithelium via the M cells of the Peyer's patches. So that mechanism is identical, and also like

Salmonella, Shigella has a Type 3 secretion system, which is sort of a way for the bacteria to inject its toxin directly into into a target cell. What's really high yield to know for Shiga toxin, I already mentioned the mechanism, but for

whatever reason, test writers like you to know that the mechanism is identical to the mechanism of EHEC or E. coli. So inactivation of the 60S ribosomal subunit, that's going to be the case for Shiga toxin in Shigella and the mechanism

of the toxin in each E coli and just like we used the pneumonic before, Shigella type 3 secretion system, so I think of the L's in Shigella being the number three, so these are all really high-yield facts, know these for test day, clinically.

Shigella is going to cause three things: one, it's going to cause bacillary dysentery. This is also known as shigellosis, so this is the sort of stereotypical bloody, inflammatory, mucusy diarrhea. This is probably what's showing up on your exam.

So if you have a patient with bloody, inflammatory, mucoid diarrhea, you already are able to sort of narrow that down to just a few different pathogens, Shigella being one of them. It can cause reactive arthritis, so know that, and very importantly, Shigella can cause hemolytic

uremic syndrome or HUS. Now, usually on exams, hemolytic uremic syndrome is going to be caused by that O157:H7 subtype from E coli, but that from E coli is known as a Shiga-like toxin, which is aptly named

because Shigella is the Shiga toxin that can cause it. So E coli got the name of that toxin being Shiga-like because Shigella is where that toxin really originates from. So while on your exam, I would be on the lookout for

the, again, the O157:H7 subtype, you need to know that Shigella itself can cause hemolytic uremic syndrome, and this is a very high-yield disease process for USMLE, COMLEX. So what you need to know is that this is a triad of microangiopathic

hemolytic anemia thrombocytopenia and acute renal failure you'll probably see a picture of what's known as a schistocyte so you see that image here it's sort of like a sheared red blood cell if they give you labs they could give you

increased bleeding time of course because we're dealing with an anemia a decreased hemoglobin of course because we're dealing with a thrombocytopenia they will give you decreased platelet count because the platelets get consumed and look for labs consistent with

intrinsic renal failure because we're dealing with acute renal failure hence the name uremic in the disease name so on your exam if they're going to give you lab printouts look at the BUN and look at the creatinine because remember that in

an intrinsic renal failure the BUN and creatinine ratio is going to be usually less than 15 so all of these clues when taken together will help point you in the direction that you're dealing with hemolytic uremic syndrome and usually on USMLE or COMLEX this tends to be a

third order question where they either give you labs or findings describing HUS and then they ask you what the potential causative pathogen is and again it's probably going to be O157 H7 E. coli however know that that E. coli toxin is called shiga-like because Shigella has

the Shiga toxin which actually does that itself so that's all you need to know again just to sort of summarize here very important to be able to differentiate Shigella versus Salmonella and understand that if you see hemolytic uremic syndrome if you see reactive

arthritis, if you see inflammatory diarrhea, those are the big diseases that they're going to go after. If they want you to pick this bacteria, good luck.

Shigella

Dirty Medicine

Introduction to Shigella and comparison with Salmonella

Video focuses on Shigella, advising viewers to watch the Salmonella video first for comparison.

Emphasizes the importance of differentiating Shigella and Salmonella for exams.

Describes Shigella as a gram-negative rod with key characteristics: oxidase negative, facultative intracellular, non-lactose fermenting, non-motile, and no H2S production.

Highlights the absence of flagella as a key differentiating factor from Salmonella.

Shigella is transmitted fecal-orally; possesses Shiga toxin that inactivates the 60s ribosomal subunit, decreasing protein synthesis.

Shigella's acid stability allows for low infectious dose due to resistance to gastric acid.

Contrasts Shigella's acid stability with Salmonella's acid lability, requiring a high infectious dose for Salmonella.

Reiterates the significance of acid stability as a key differentiating factor between Shigella and Salmonella.

Shigella invades intestinal epithelium via M cells, similar to Salmonella, and possesses a Type 3 secretion system.

Shiga toxin mechanism and clinical presentation

Shiga toxin mechanism is identical to EHEC E. coli, inactivating the 60S ribosomal subunit.

Clinically, Shigella causes bacillary dysentery (shigellosis), reactive arthritis, and hemolytic uremic syndrome (HUS).

HUS is usually associated with E. coli O157:H7, but Shigella can also cause it.

Hemolytic Uremic Syndrome (HUS) in detail

E. coli's Shiga-like toxin is named after Shigella's Shiga toxin.

HUS is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure; lab findings include increased bleeding time, decreased hemoglobin and platelets, and BUN/creatinine ratio <15.

HUS is often a third-order question in exams, requiring identification from lab findings or symptoms.

Differentiating Shigella and Salmonella is crucial; key clinical presentations of Shigella include HUS, reactive arthritis, and inflammatory diarrhea.