is the type of pneumonia that Staphylococcus aureus causes.
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A 32-year-old man comes to the office because he noticed a painful lump in his buttock. His medical history is noncontributory, except that he currently works as a fitness trainer. Physical exam shows increased local temperature, tenderness, and induration in his right buttock. A surgical drainage is scheduled and 40cc of pus are collected. A few days after, the patient's condition deteriorates despite antibiotic therapy with dicloxacillin and surgical drainage. His temperature is 38.6°C (103.1°F), pulse is 100/min, respirations are 18/min, blood pressure is 120/70 mmHg. A gram stain is obtained and shown below.
At this point, which of the following is the most likely mechanism of drug resistance in this organism?
In fact, its name, broken down, means “golden cluster of grapes”.
It sorta starts making sense if you look at it under a microscope - it tends to grow in sticky clusters, and it stains purple when Gram-stained due to its peptidoglycan cell wall, so it’s Gram positive and it resembles grapes.
As for its “golden” color, when it’s grown on blood agar plates, the colonies have a distinctive golden-yellow color.
Staphylococcus aureus are Gram positive and facultative anaerobes, meaning that they can survive in aerobic and anaerobic environments.
They’re non-motile and don’t form spores.
Staphylococci produce an enzyme called catalase which converts hydrogen peroxide to water and oxygen.
Other common cocci, such as streptococci and enterococci, are catalase negative so they don’t have this ability and we can use a few drops of hydrogen peroxide to differentiate them.
Catalase positive bacteria will foam up, while in catalase negative bacteria, nothing happens.
Now, a couple of other staphylococci species, like Staph epidermidis and Staph saprophyticus are also catalase positive, so to distinguish between them we can look for another enzyme that’s made by Staph aureus, called coagulase.
Coagulase converts fibrinogen into fibrin.
So let’s say that we stir up some Staph aureus bacteria in a liquid “emulsion”, and then add a few drops of plasma which contains fibrinogen. The coagulase positive staph aureus will convert the soluble fibrinogen to sticky fibrin, which then visibly clumps up, whereas coagulase negative bacteria won’t.
Staph aureus is extremely common and about a quarter of the population is colonized by it, usually in their nostrils, groin, armpits, and other parts of their skin.
But, most of the time it’s a normal part of our skin flora, and doesn’t cause trouble.
The skin flora is a complex ecosystem of different bacterial species and occasionally, Staph aureus can begin to dominate that ecosystem.
In individuals that have staph aureus colonization, a number of factors like the pH, humidity, sweat levels of the skin, as well as presence of other bacteria on our skin, all affect the amount of staph aureus that’s present.
If more and more Staph aureus is around on the skin, it begins to penetrate through tiny microfissures in the skin, like you get with eczema, as well as larger breaks in the skin like you might get after shaving.
In fact, it’s particularly troublesome in terms of causing wound infections where there is a large break in the skin either from trauma or after a surgery.
A bunch of furuncles clustered together make a carbuncle.
There can also be diffuse skin infections, like superficial impetigo which is an infection of the epidermis, or deeper-reaching cellulitis, which is an infection of the dermis and can spread over larger surfaces rapidly.
If the infection goes deeper, it can develop into a subcutaneous abscess - a collection of pus that’s walled off and sometimes develops thin walls within it - called septations.
Now if the infection is overlying a muscle, it can spread into the muscle causing a pyomyositis.
In addition, bacteria in the blood is called bacteremia, and it can lead to a number of serious problems.
There’s typically a widespread immune reaction that causes the blood vessels to expand and the blood pressure to fall. The result is hypotension and poor perfusion to various organs - a process called sepsis.
Once it’s in the blood, Staph aureus can also get to various parts of the body.
It can get into the central nervous system - causing bacterial meningitis or an epidural abscess in the spine.
It can get into the lungs causing a severe pneumonia.
It can start to grow on the heart valves in clumps called vegetations - damaging the valves - a process called infective endocarditis.
Bits of the vegetations can then chip off and embolize further causing other local infections around the body.
Now, in addition to invading the body through the skin, Staph aureus can also enter directly into the bloodstream when a person is getting surgery or having dental work done. These events occur infrequently, but when they do come up it’s important to take precautions.
For example, individuals at high risk of getting serious disease with Staph aureus - like immunocompromised individuals or those that are at risk for infective endocarditis - should be given antibiotic prophylaxis.
Another property of our golden staph is its ability to create biofilm on medical implants like indwelling intravenous catheters, prosthetic heart valves, and artificial joints.
The biofilm is, essentially, a layer of “slime” within which the Staph aureus live. It forms when a cluster of Staph aureus adheres to a surface either a natural one like the surface of a valve or an artificial one like the surface of a catheter.
The bacteria start to produce extracellular matrix made of exopolysaccharides, or EPS, and over time the cells get completely surrounded by it.
The cells that are surrounded by the gel-like layer of exopolysaccharides, can communicate with one other through biochemical signals and can even swap genetic information back and forth - including antibiotic resistance genes.
In addition, Staph aureus thrives but doesn’t divide rapidly within these biofilms, and it’s relatively hard for antibiotics to penetrate into the biofilms.
Combined that makes it much harder to get rid of these biofilm infections, and often requires simply removing the surface that they’re growing on, if possible.
If all of this wasn’t enough, S. aureus can also release superantigens or toxins.
In fact, there are five major toxins related to S. aureus - toxic shock syndrome toxin 1, or TSST-1, Panton-Valentine leukocidin toxin, hemolysin, exfoliatin, and enterotoxin… toxin.