USMLE® Step 1 style questions USMLE
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A 7-year-old boy is brought to the emergency department by his parent due to 3 days of fatigue, malaise, decreased urine output, and gingival bleeding. The parent states that the patient had abdominal pain and bloody diarrhea one week earlier, which resolved without treatment. The patient has no prior medical diagnoses. Family history is also non-contributory. Temperature is 37.0°C (98.6° F), pulse is 94/min, respirations are 22/min, and blood pressure is 106/68. Physical exam shows petechiae on the arms and in the mouth. Laboratory testing and urinalysis are obtained and shown below.
|Blood, plasma, serum|
|Total bilirubin||5 mg/dL|
|Direct bilirubin||0.3 mg/dL|
|Blood Urea Nitrogen (BUN)||32 mg/dL|
|Lactate dehydrogenase (LDH)||370 U/L|
Alright, now E. Coli is gram-negative because its cell wall has a thin peptidoglycan layer so it cannot retain the crystal violet stain, but instead, it stains pink with Safranin dye used during Gram staining.
So it looks like a little pink rod under the microscope.
Also, E. Coli is a catalase positive bacteria, and that means it produces an enzyme called catalase.
This can be tested by adding a few drops of hydrogen peroxide to a colony of bacteria, and catalase makes hydrogen peroxide dissociate into water and oxygen, making the mixture foam.
E. Coli is also a lactose fermenter, because it can produce an enzyme called beta B-galactosidase that cleaves lactose into glucose and galactose monomers.
To test this, E. Coli can be cultivated on lactose-containing media such as Phenol lactose, and as it ferments it, the fermentation results in the production of acids that turn the red of phenol to yellow.
It is also a facultative anaerobe, meaning it lives in environments with or without oxygen.
Now, taking a closer look to this bacteria, E. Coli is encapsulated, meaning it’s covered by a polysaccharide layer called a capsule.
E. Coli is a motile bacteria, because it has helical whip-like threads called flagella that it can use to move around.
When E coli is cultivated on eosin methylene blue agar, it grows into black colonies with a greenish-black metallic sheen.
Alright, most of E. Coli are harmless, and they can peacefully colonize the human gut without causing any trouble.
However, some strains of E. Coli are pathogenic, meaning they can cause illness. It starts with this bacteria using little thread-like extensions called fimbriae to attach to the host cell surface.
E coli has many different strains that can do that, and they cause different diseases. These strains can be classified by two systems.
The first system uses serotypes, and it groups E. Coli strains based on their antigens.
Antigens are elements that the host’s immunity considers foreign and mount an immune reaction as a response.
So, bacteria within a given serotype, trigger a similar immune response.
Alright, E. Coli has a number of antigens, and among them we have somatic antigens located just on the cell membrane, and these ones are abridged with the letter “O”.
There are also capsular – “K” antigens located on the capsule, fimbrial – “F” antigens located on the fimbria, and flagellar – “H” antigens located on the bacterial flagella.
Usually after this letter that tells on what part of the bacteria where the antigen is found, it follows a designation number in case there are more antigens of the same kind, such as K1, K2, and so forth… E. Coli antigens, influence its power to cause diseases, so that’s why they can alternatively be referred to as virulence factors.
For example, E. Coli with capsular antigen one, or K1, are the ones that cause neonatal meningitis, while an E. Coli that has an O157, and an H7 – designated as O157:H7, is associated with hemorrhagic colitis, hemolytic uremic syndrome and diarrheal outbreaks.
Other E. Coli serotypes include E. Coli SE15, E. Coli F11, E. Coli O25:H and so on… but in fact, these serotypes are so numerous and they can go up to 200 serotypes.
Thankfully, there’s a much simpler classification, and that is based on pathotypes.
A pathotype is a group of organisms of the same species, that cause disease in the same way - meaning they use the same virulence factors.
And there are 5 E.Coli pathotypes: Shiga-like toxin-producing E.Coli, or STEC for short, enterotoxigenic E. Coli or ETEC, enteroinvasive E. Coli, or EIEC, enteropathogenic E. Coli, or EPEC, and uropathogenic E. coli or UPEC/
So first, Shiga-like toxin-producing E. Coli, or STEC is called that because it makes a toxin similar to the one called Shiga toxin produced by Shigella.
STEC attaches to the host’s intestinal cells, and then start releasing toxins that cause injury to intestinal epithelium and underlying blood vessels, resulting in inflammation.
This makes fluid and blood leak into the intestinal lumen, resulting in bloody diarrhea.
That’s why some people refer to it as enterohemorrhagic E. Coli, or EHEC.
But STECs can also affect the urinary tract, causing hemolytic uremic syndrome or HUS. Hemolytic uremic syndrome usually develops after STEC have released their toxin into the bloodstream.
From the bloodstream, the toxin can get to the kidneys, and bind to the endothelial cells lining the glomerulus, making them die by apoptosis, or programmed cell death.
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 such as proteins to start leaking out of the capillaries, resulting in proteinuria.
The destruction of endothelial cells triggers an inflammatory process in which inflammatory molecules such as cytokines and chemokines are released.
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 force to pass through obstructed micro-vessels, they can get sliced into fragments called schistocytes in this 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, like the kidney, may lack blood and die by ischemia.
Now, an ischemic kidney is unable to filter blood. This is how too much of metabolic wastes such as urea, start accumulating in the blood, leading to uremia.