USMLE® Step 1 style questions USMLE
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A 35-year-old man presents to his primary care physician’s office for evaluation of right knee and ankle pain for the past 2 days. He had similar pain over the left wrist and shoulder joints in the past year that self resolved. The patient has a painless rash on his hands which appeared around the same time. Past medical history is significant for a urinary tract infection 2 months ago which was treated with antibiotics. He has had 7 sexual partners over the past year and is currently sexually active. He uses condoms inconsistently. He denies any recent travel. His temperature is 38.2 °C (100.8°F), pulse is 80/minute, respirations are 16/minute, and blood pressure is 130/80 mmHg. Physical examination shows multiple nontender papulovesicular lesions on his hands. Passive flexion of wrists elicits a sharp pain. Which best describes the route of transmission regarding the causative organism resulting in this patient’s clinical condition?
Content Reviewers:Viviana Popa
The word Neisseria came from Neisser Albert, a German physician who discovered it, while gonorrhea is from the Greek words “gonos” which means "seed", and “rhoe” which means "flow", meaning "flow of seed", an illustration referring to the penile purulent discharge, which was mistakenly thought to be semen in infected males.
Now, a little bit of microbe anatomy and physiology. N. gonorrhoeae is a gram-negative bacterium, because its cell wall has a thin peptidoglycan layer and so it doesn’t retain purple dye used during Gram staining.
Instead, like any other Gram-negative bacteria, N. gonorrhoeae stains pink with safranin dye.
N. gonorrhoeae typically live in pairs called diplococci, stacked side to side, so the pair looks like a coffee bean.
They are also non-motile, non-spore forming, and obligate aerobes, which means that they absolutely need oxygen to grow.
Finally, they’re catalase and oxidase positive - which means they produce both these enzymes.
N. gonorrhoeae grows on a special chocolate medium called Thayer-Martin agar, which mainly consists of sheep blood... err, yum?
Some antimicrobials, like vancomycin and nystatin are usually added to the Thayer-Martin agar, to inhibit the possible growth of undesired bacteria or fungi, and maximize the growth of Neisseria species.
However, other Neisseria species, like N. meningitidis, have the same properties.
So the maltose fermentation test is done to differentiate the two.
The gist of it is that N. gonorrhoeae can’t ferment maltose, whereas N. meningitidis can.
To check for this, a pure sample from the culture of the suspected bacteria, is transferred to a sterile tube containing phenol red-maltose broth, which is then incubated at 36 degrees Celsius for 24 hours.
Since N. gonorrhoeae can’t ferment maltose, the solution stays red, whereas with N. meningitidis, fermentation byproducts make the solution go yellow.
Now, unlike its sister Neisseria meningitidis, Neisseria gonorrhoeae is not an encapsulated bacteria, so it doesn’t have a polysaccharide capsule.
But this bacteria has a ton of other virulence factors, which it uses to attack and destroy host cells, and also to evade the immune system.
First, N. gonorrhoeae has pili, these little thread-like extensions radiating from the bacterial surface.
The pili help N. gonorrhoeae attach to a host’s mucosa surface.
Also, they help bacteria get physically connected with each other, making what’s known as a conjugation pilus, which is a hollow tiny rod, through which bacteria can swap genetic information back and forth - including antibiotic resistance genes.
Interestingly, N. gonorrhoeae pili are made of antigenic proteins which can vary with every infection – what’s known as phase variation.
Ok, so normally, when a certain bacteria causes an infection, the immune system keeps memory of the bacterial antigens configuration.
So if the same bacteria infects again, the immune system remembers it and quickly makes specific antibodies against it.
However, since N. gonorrhoeae changes the antigens on its pili each time it infects a host, the immune system can’t produce a quick specific immune response.
Phase variation is also the reason why there’s no effective vaccine against N. gonorrhoeae.
Pili aside, other virulence factors of N. gonorrhoeae include toxins.
The very important one is IgA protease, a toxic protein that this bacterium uses to destroy Immunoglobulin A – IgA.
IgA helps with bacteria opsonization - meaning it tags the bacteria so that neutrophils can recognize and destroy them.
So IgA protease neutralizes the first line of mucosal defense!
However, not all IgA molecules get neutralized, so some N. gonorrhoeae bacteria are still opsonized, and end up getting attacked by neutrophils.
Inside the neutrophil, N. gonorrhoeae is wrapped in a phagosome, a bubble inside which reactive oxygen species, such as H2O2, are released to kill it.
However, N. gonorrhoeae releases catalase, which breaks down H2O2.
Unfortunately, this translates as a win for N. gonorrhoeae, which now takes over the neutrophil and uses its energetic resources to multiply.
The neutrophil eventually becomes too full, bursting open, and letting out a lot of bacteria in the bloodstream, which is known as gonococcemia.