Preseason football brought methicillin-resistant staphylococcus aureus (MRSA) back into the limelight with multiple Buccaneers coming down with serious infections. Thanks to Twitter’s unfiltered access to everyone, this news came out via an airing of grievances over missed diagnoses and the team’s subsequent glossing over of Lawrence Tynes’ recovery (interesting aside, he’s filing a grievance over being placed on the non-football injury list, turns out it might not be the best idea to publicly blast the team but at least we get that wonderful header pic). Less recent examples that leap to mind are the string of infections that plagued the Cleveland Browns for half a decade. Professional sports aside, MRSA and its encompassing family of staphylococcus aureus bacteria are a monumental health concern, especially as a source of illness from within the healthcare system.
According to the CDC , data from 2005 shows “an estimated 478,000 hospitalizations with a diagnosis of s.aureus… of those approximately 278,000 hospitalizations were related to MRSA.” This next bit is a little worrisome but I promise it’s not as bad as it sounds. In 2003, 29% of people were colonized with s.aureus and 1.5% with MRSA. Many of you reading this are doing so with s. aureus bacteria happily filling your nose. Don’t panic. It’s often asymptomatic, bacteria is everywhere (literally coating everything), and lots of it is s. aureus. I’ll do my best here to explain what s. aureus and MRSA actually are, why they make us sick, how our bodies defend themselves, and why these bugs are so problematically stubborn. I’d also like to apologize, that’s a lot of very dense ground to cover. I’ll do my best to keep this interesting but micro can get pretty dark.
Anytime you hear about an infection or bacteria with “cocci” or “coccus” in the name, picture something like you see above. That term refers to spherical bacterium, although the clustering shown above is unique to staphylococcus ( staphyle is Greek for “cluster of grapes”). Like I said before, it might be living on you now, a sheet of bacteria with nothing but your skin and immune system standing in its way. Luckily, your skin is really quite good at keeping the outside outside. We’ll assume the worse though, that s. aureus gets past your skin, and start looking at some of the special characteristics contributing to both the bacteria’s continued survival and your growing symptoms.
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This is gratuitously oversimplified, but that’s what we’re going for here. Each of the specific molecules on the diagram above contribute to the virulence (or pathogenecitity/survivability) of staph infections. First, this bug has to protect itself from your immune system. As soon as it’s past the skin, your body’s ubiquitous immune molecules will go to work. One of your major defenses is opsonization . Simply put, a collection of immune system molecules will bind to exterior proteins of a foreign molecule. Their enveloping presence triggers macrophages (think garbage trucks of the immune system) to phagocytize (think eat) the bacteria. This process is pictured below, probably best if you ignore the words and just pay attention to what happens to the red bacterium.
Now back to that diagram with all the molecules on the bacterial cell wall. Protein A extends from the surface of bacteria and will bind the enveloping opsonization molecules (IgG antibodies) in a way that inhibits their pro-phagocytic signalling. In a sense, they use the body’s own signalling molecules as camoflage to hide from the immune system’s search dogs.
Redundancies are lifesavers in every body system, and the immune system is no exception. The diversity in signaling molecules and cellular defenses have driven bacteria to adopt equally impressive countermeasures, including coagulase. Coagulase triggers one of the final steps in our regular clotting cascade (a series of enzymatic reactions that ends with your blood clotting in wounds), and along with clumping factor, surrounds the bacterium with fibrin, a component of blood clots. The picture below is an electron microscope scan of s. aureas surrounded by a protective fibrin meshwork in cow blood. This meshwork serves as a physical barrier inhibiting the binding of your body’s various immune cells.
There are other features helping protect staph from your intrinsic immune defenses, but we’ll move on to how it actually makes you sick. Staph can be expressed as skin infections, endocarditis (infections commonly on the heart valves), osteomyelitis (bone infections), pneumonia, or systemically in bacteremia and sepsis. In systemic cases, infected abscesses can form in any organ, but now we’re just piling on. The horrible illnesses attributed to staph infections largely arise from exotoxins the bacterial colonies will produce and release. It’s worth noting these protective measures and toxins aren’t all expressed by all staph bacteria, which also explains the incredible diversity of staph infection symptoms/locations.
Toxins , , , and are all hemolytic toxins, meaning they disrupt the membranes of blood cells, destroying them in the process. toxin does so by forming an open pore in the blood cell membrane. Passage of water and molecules through cell membranes is incredibly fine-tuned and this deregulated traffic kills the cells.
The remaining toxins deserve their own special designation as superantigens . We’ll think of antigens as any molecule or protein with which your immune system’s antibodies can bind. This binding is often specific, which is why your body can develop unique antibodies to specific illnesses (why you don’t get chicken pox or mono multiple times, why vaccines work safely…WHY VACCINES WORK SAFELY). However, superantigens are capable of non-discriminate activation of your immune system’s T-cells. This activation triggers massive T-cell regulated release of cytokines, molecules that mediate immune and inflammatory responses. Simply put, this is how a bacterial infection causes systemic shock: plummeting blood pressure, high fevers, elevated heart rate, hyperventilation, organ failure, and death. This can be trouble. You need to be in a hospital getting fluids and IV antibiotics right away.
Enterotoxin A is the primary cause of food poisoning and will run your intestines through a gamut of diarrhea, vomiting, and cramping. While it is a superantigen, these reactions will usually be self-limiting to the intestines and GI tract. You’ll be in a rough way for a while and could need some IV fluid management, but the illness should run its course without too much trouble.
Toxin Shock Syndrome Toxin 1 (TSST-1) surprisingly causes toxic shock syndrome. This syndrome will typically present as some collection of a sudden high fever, low blood pressure, confusion, seizures, headaches, etc. Strangely
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