AssessmentsStreptococcus pyogenes (Group A Strep)
Streptococcus pyogenes (Group A Strep)
USMLE® Step 1 style questions USMLE
USMLE® Step 2 style questions USMLE
A 36-year-old man presents to the emergency department for evaluation of a rash on the right forearm. The patient was recently admitted to the hospital for pain-control in the setting of nephrolithiasis. He recalls, “After I left, I was feeling fine, then the next day my arm started hurting, and I noticed a red rash near the site where I had my IV.” He is otherwise healthy and does not take any medications daily. Temperature is 38.0°C (100.4°F), pulse is 110/min, respirations are 14/min, and blood pressure is 119/77 mmHg. Physical examination demonstrates a well demarcated erythematous, warm, and painful rash over the anterior aspect of the right forearm without fluctuance. Infection with which of the following organisms is most likely responsible for this patient’s cutaneous findings?
Content Reviewers:Viviana Popa, MD
Streptococcus pyogenes, sometimes called Strep pyogenes, can be broken down into “strepto” which means chain, “coccus”, which refers to round shape, “pyo” which means pus, and “genes” which refers to forming.
So, Strep pyogenes are round bacteria that grow in chains, responsible for a number of infections that often present with pus. Strep pyogenes are also called Group A Strep – GAS - in Lancefield classification developed by American microbiologist Rebecca Lancefield.
Ok now, Strep pyogenes has a thick peptidoglycan cell wall, which takes in purple dye when Gram-stained - so this is a gram-positive bacteria.
It’s non-motile and doesn’t form spores, and it’s also a facultative anaerobe, meaning it can survive in both aerobic and anaerobic environments.
Finally, Strep pyogenes is catalase negative, meaning it doesn’t make an enzyme called catalase.
However, unlike other common cocci like Enterococci, Strep pyogenes is pyrrolidonyl arylamidase positive, because it makes an enzyme called L-pyrrolidonyl arylamidase.
To test for this, a small sample is taken from a suspected bacterial colony, and then inoculated to a disk pad that’s embedded with pyrrolidonyl beta naphthylamide - another joy of a word.
With Strep pyogenes, pyrrolidonyl arylamidase hydrolyzes pyrrolidonyl beta—naphthylamide to produce beta-naphthylamide.
Try saying that 3 times fast! Finally, another reagent called N-methylamino-cinnamaldehyde is added to the disk, and it reacts with beta—naphthylamide, resulting in a bright red color that confirms Strep pyogenes is pyrrolidonyl arylamidase positive.
When cultivated on a medium called blood agar, Strep pyogenes colonies cause beta-hemolysis, also called complete hemolysis. That’s because Strep pyogenes makes toxins known as streptolysins, which hydrolyze the hemoglobin in red blood cells to transparent yellow color byproducts.
But some other Streptococcus species, like Strep agalactiae, are also beta-hemolytic. So a bacitracin test is done to distinguish Strep pyogenes.
Now, Strep pyogenes has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system.
So first, Strep pyogenes is encapsulated, meaning it’s covered by a polysaccharide layer called a capsule.
And on the capsule, there are adherence proteins such as lipoteichoic acid, Streptococcus fibronectin binding protein - or Sfbl for short, and M protein, which help Strep pyogenes attach to the host cells, like those in the skin or the pharyngeal mucosa.
Then, Strep pyogenes uses toxins like hyaluronidase, which destroys hyaluronic acid, a cement substance that keeps cells of the connective tissues and blood vessels tightly linked.
Destruction of hyaluronic acid results in local inflammation, and enables the bacteria to spread to the bloodstream.
In the bloodstream, Strep pyogenes uses streptolysin O and S, which are toxins that cause hemolysis, or red blood cell destruction.
It also uses erythrogenic toxins, that are also called Streptococcal Pyrogenic Exotoxins, or Spe for short, which come in 3 flavors: SpeA, SpeB, and SpeC.
This leads to increased hemolysis in the dermal and submucosal blood capillaries. What is more, SpeA and SpeC are superantigens, meaning they don’t need to be eaten up and processed by an antigen-presenting cell such as a macrophage to generate an immune response from T-cells.
Instead, they interact immediately with the class II MHC molecule on the surface of the macrophage, forming a superantigen-MHC complex, which then interacts with the T-cell receptor and stimulates up to 30% of the entire T- cell population.
This is 300 times powerful the conventional antigens, and it stimulates the release of a whole bunch of inflammatory cytokines.
Specifically, this is called a cytokine storm, and it can result in toxic shock syndrome or TSS, which happens when a such cytokine storm triggers widespread systemic vasodilation, making blood pressure drop, which leads to poor perfusion of vital organs.
From the bloodstream, strep pyogenes bacteria can spread to other organs, like the lungs, causing pneumonia or lung abscesses, or the heart, where they form clumps called vegetations on the heart valves, causing infective endocarditis.
In these cases, Strep pyogenes usually gets in the bloodstream through a breach on the skin, a mucosal laceration, or following surgery.
When Strep pyogenes infects the epidermis, it causes impetigo, which are superficial skin lesions that look like honey clusters.