When a doctor suspects that their patient has a bacterial infection, they can do one of two things. The first is order diagnostic tests—blood, wound, or stool cultures, gram stains, and urinalyses are most common—to check for bacteria and, if present, their type. They then prescribe a course of antibiotic therapy best suited to destroy the specific infection the patient has. Antibiotics should be targeted in this way to decrease systemic effects as much as possible.
Alternatively, the doctor may choose to skip the testing process, which is often expensive and time-consuming, and use an empiric therapy: their best guess based on their medical judgment. Uncomplicated UTIs, for example, usually have readily identifiable symptomatology, and in the absence of co-occurring health problems, a doctor may skip a urinalysis and prescribe a broad-spectrum antibiotic. This is common for ear infections, bacterial infections of the integumentary system like Staphylococcus aureus and Streptococcus pyogenes, and conjunctivitis assumed to be pinkeye.
Sometimes, broad-spectrum antibiotics are ordered for a suspected bacterial infection while diagnostic tests are processed. This is usually the case for acutely-ill patients whose infections are unstable and who will receive more targeted therapies once the type of bacteria is determined. Another occasion for prescribing broad-spectrum antibiotics is prophylactically: patients with some cardiac abnormalities and those with recent joint replacements are often prescribed broad-spectrums before dental procedures, so that oral bacteria do not invade the bloodstream. It should be mentioned that the American Dental Association believes far fewer patients require prophylactic antibiotics than the patients's physicians think they need. The ADA has been working with physicians to find evidence-based solutions for their differences in opinion.
Antibiotic resistance occurs when some portion of bacteria survive antibiotic therapy and proliferate. Reasons for a strain’s resistance are as diverse as the individuals carrying it, but two main contributors stand out. One is the over-prescription or misuse of antibiotics, particularly for conditions that aren’t bacterial, such as the flu, conditions that would be self-limiting without antibiotics, and conditions that would be better treated with highly-targeted antibiotic therapies. When antibiotics are used frequently in a population, the bacteria the population comes into contact with will learn to adapt to the treatments.
This ties into the other main contributor to antibiotic resistance: compliance. There is a reason doctors and pharmacists insist that an entire course of antibiotics is finished, even if symptoms improve before the antibiotics run out. They want to make sure all of the bacteria have been killed. It makes sense that the weakest would die earliest and easiest. If treatment ends prematurely, the strongest bacteria survive and proliferate, and the infection itself becomes stronger and more resistant to further treatment. If the infection is then transferred to another person, the new host receives only the fittest, most damaging bacteria. Their body will not be able to build an immune response against the weak bacteria before dealing with the strong, and they will be less able to fight their infection.
In a way, on the humans’s end, you could argue that this is artificial selection. It is pharmaceutical meddling that selectively breeds antibiotic-resistant bacteria. Antibiotics used in livestock processing and agriculture—human technologies—contribute to the problem. On the other hand, the bacteria themselves are experiencing natural selection. Some members of their population are weaker than others: their cell membranes are more easily pierced and their proteins and DNA strands are more readily torn apart. While the weak die, the strong adapt and, over time, evolve. When they reproduce, they favor the fittest. Eventually, the new generation's average member becomes as deadly as the old generations's strongest.
No comments:
Post a Comment