Can’t tell if we’re agreeing or disagreeing. Companies should totally be able to hire on short-term contracts. But it should be clear that it is a temporary contract from the start, not a bait-and-switch from long-term employment to hire-and-fire.

I mean if the only way they’re gonna have jobs is through predatory hiring practices that could leave them fired and without severance, then yeah. Because if the company is planning on hiring these younger workers for the long-haul, then this shouldn’t be a significant change. I think overall national policy should discourage unnecessary high-turnover and predatory hiring. I’m sure there will be situations this is still unavoidable, but that doesn’t mean we have to endorse it by way of law/policy.

I’m going to digress from the economics a tad and focus on the ethics of this. I feel like companies should be on the hook for this. You should invest in capital (including human labor) based on your confidence in its expected return. Companies should not be able to hire a myriad of workers for funzies and not have to meaningfully consider if that person will be necessary in 6 months. If it is a legitimate business venture, then the cost of potential severance for new hires should be folded into the economics of the decision to pursue that venture. Larger severance pay/worker protections encourage employers to not utilize exploitative hiring practices.

It depends on the half life of the element in question. The most comparable concrete thing we can compare this to with real numbers because we know it works is an RTG. RTGs are solid-state generators, but people could colloquially refer to them as “batteries” and not be terribly wrong. They take a quantity of a radioactive material and allow it to decay, using the heat given off to establish a thermal gradient which is then converted to electricity via thermocouples. Most of these are “fueled” with Pu-238 (at least the ones for spacecraft), which has a half life of 87.7 years. That means in 87.7 years, if you started with 4kg of Pu when you built it, you’d have only 2kg of Plutonium left. If the Pu decayed only into stable isotopes (it doesn’t) then your radioactive emissions/decay would also be exactly halved at this time. If the electrical system is perfectly efficient this would also halve the electrical power produced.

I provide this all as background because to answer your question you have to know three key factors about the device to determine the lifetime of the battery. The half-life of the isotope used, the minimum electrical requirements of the device you’re powering, and the amount of radioactive material in the initial battery. The battery’s lifetime is determined by when decay will decrease the ongoing energy output below the minimum current and voltage requirements needed by the battery. The longer the half life of the isotope, the slower this decrease is and the less initial overpowering that is required.

Ex. If you use an isotope with a 12.5 year half life for a “50-year” battery, you would need to start with 8 times the material needed for your minimum power output requirements. If you use an isotope with a 200 year half life, you only need 19% more starting mass than you minimum requirement. The first battery will produce 8x the power at the very beginning, while the second will only produce 18% more.

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You’ll have to strike a balance between security and ease. Your two major options are reverse proxy and VPN (Tailscale is one option for VPN)

For reverse proxy, you functionally open the app to the internet. Anyone with the correct web address can access the login page. This is inherently less secure than VPN, but not irresponsibly so. Beyond the reverse proxy itself, you’ll also have to learn how to configure an HTTPS certificate to increase security since it will be open to the internet.

For VPN, every user you want to be able to access the service has to be tied into the VPN and have the VPN running throughout their access. Tailscale is arguably the easiest way to configure a VPN right now, as you won’t have to manually deal with VPN configuration files for every device. VPN use will functionally make it like you’re on your home network. VPN access to your network should not be given to tons of people if at all possible.

I would like to point out, the NYT is a reputable news site but cannot even remotely be trusted with medical information/recommendations. I can’t tell you the last time I read a medical news piece from any source (and the NYT is the primary place I get my news) that I couldn’t read it and say “well that’s a gross oversimplification” or worse “this is blatantly misrepresenting the scientific author’s conclusions”. Holding up the NYT as a source of medical/scientific truth is just demonstrating how scientifically illiterate you really are.

You’re citing forum posts to discussions (with some evidence mentioned within) to support this supposition that doctors are horribly informed and out of date. But I’d like to point out that this is being vastly overblown, and even a 5-10 year out-of-date medical professional has immensely more knowledge and safe ability to recommend therapy than a layperson. I can’t pretend to know the credentials of the individual you’re responding to, but they’re clearly well versed in clinical infectious disease based on their comments, and you’re not supporting your position by citing a forum instead of the actual primary literature that supports your position.

Section 2, first paragraph. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6956183/

At their core phages are viruses, there is no reason to expect the host immune system to not recognize them as foreign and attempt to eradicate them outside the GI tract, where most serious infections occur. The GI tract, skin, and to some extent the lower UG tract will likely tolerate these through mechanisms we tolerate colonizing bacterial flora, but colonization, even with antibiotic resistant organisms, is not a primary indication for empiric treatment for eradication. In fact there are some studies that attempting to sterilize the UG tract in colonized asymptomatic women promote symptomatic UTI.

These colonizations become problematic when growth becomes unchecked and infection develops, or they seed infection into another compartment. There is no reason to think something as foreign as a bacteriophage wouldn’t be recognized as foreign in a sterile space (kidneys for pyelonephritis, liver abscess from migrated gut flora, endocarditis, etc) where these serious infections occur.

This ties in nicely with your suggestion of phage cocktail therapy. Yes, that can expedite the delivery of phages, however excessive use of phages could result in anti-phage antibodies, limiting future treatment in a method similar to the development of anti-drug antibodies in epoeitin analogues, insulin therapy, antivenin, and anti-inflammatory antibody therapies like adalimumab (Humira)

No, in fact I believe very heavily in evaluating primary literature to re-evaluate decades-old dogma within medicine. I regularly disagree with my professors when they present outdated information in lecture. I have no income right now, and I have forgone substantial amounts of income by pursuing medical school instead of continuing to practice pharmacy. I’m not in this for the money.

If you would be so kind, I would love to know what evidence you present in contrary to the decades of peer-reviewed cohort, case-control, and RCT data which validate psychiatry as an effective field for managing psychiatric illness. I’d be happy to discuss any scientific data you have that I haven’t seen, and would be happy to change my opinion if it is data-driven.

I can appreciate your skepticism towards medicine and psychiatry, but if you can’t defend your position with anything but accusations and conspiracy, then I don’t think we have much else to discuss.

Thank you for your insightful and well-researched response. I’ll remember that as I continue to provide high-quality evidence based care to all of my psychiatric patients in the future while you bitch about stuff on the internet.

Yup, it’s hard to have a good discussion about the changing tides in ID without feeling like you’re causing a bunch of backsliding and non-compliance. I think being honest with people that the data is generally poor about how we select durations is the moral thing to do. But I do want you to just take your damn antibiotics as prescribed instead of going rouge because you heard “shorter is better” and your pneumonia recurring.

Yes, it covers intestinal colonization with MRSA. Unfortunately Staph aureus is an uncommon GI pathogen, and the majority of detrimental infections secondary to MRSA come from skin-flora translocation to produce surgical site infections/blood stream infections, as well as translocation from the nares into the lungs to produce pneumonia. We thankfully have another method of nares decolonization. While metallobetalactamase producing Pseudomonas is mentioned as well, I have a very low suspicion that FMT would be useful for resistant Pseudomonal pneumonia or diabetic foot infections/osteomyelitis. FMT certainly has a role to play in ID, particularly for enteric gram negatives and VRE within the alimentary canal, but is not a cure-all for antimicrobial resistance.

Hello all, I’m a pharmacist and 4th year medical student with a passion for antimicrobial stewardship and infectious disease. Just wanted to share my overall thoughts on the article.

The author’s point of “finding out if you really need an antibiotic” is honestly one of the central issues in modern antimicrobial resistance coming from two fronts: patients who demand an antimicrobial for a non-indicated reason, and doctors who for various reasons excessively prescribe antibiotics. I could wax on this for hours, but at its core, the single most important thing we can do to decrease antimicrobial resistance is decreasing total antimicrobial exposure. That means fewer prescriptions for shorter courses of narrow-spectrum antibiotics. Unfortunately every bit of this requires more buy-in from patients and more work from clinicians.

To go along with my point above, asking your doctor to make sure you’re getting the shortest possible duration is the single best thing you as a patient can do to help with these issues (other than just not demanding antibiotics if your doctor says no, but that’s a low bar). The key word here is ask though. There’s a huge amount of clinical experience and evidence that is used to determine when it is safe to stop antibiotics. And as much as I believe in patient autonomy and educating my patients, frankly antibiotic selection/course duration is not something the general public is capable of independently making decision on. Ask your doctor, and take what they prescribe for how long they’re prescribed for, and if you have issues then call them to discuss it.

With regards to probiotics, it’s an interesting topic that we don’t have a ton of great data for and physicians are fervently behind or against them in my experience. The fact is we just don’t know enough about them, and most aren’t regulated well enough to give good information about them. Interestingly, there was a recent study which suggested higher rates of central line infections with the organisms in the probiotics in individuals given probiotics while they had a line in place.

Lastly, I think I have to disagree with Dr. Blaser. Medicine doesn’t overvalue antibiotics. We certainly underestimate their risks, but antibiotics are some of the most effective and life-saving medications we as a species have ever developed. Countless lives have been saved solely from their development, and very very few therapies have a NNT as low as appropriate antimicrobial therapy. They truly are astonishingly good medications when they are indicated. The issue is simply prescribing them when they aren’t indicated, which is a big part of why we’re in the mess we’re in, and is in large part driven by underestimating the risks they pose.

The trouble is that, as a whole, antibiotics that work against resistant organisms are inherently more broad. Bacteria develop resistance by either mutating the target site of an antibiotic, decreasing/removing the expression of a target site, increasing removal of the drug from the bacterial cell, or preventing entrance to the cell.

These changes are relatively antibiotic agnostic (in the sense that they do not target one specific antibiotic, they target a general chemical structure which is shared among a class of antibiotics), and in most cases, if you develop a drug which is able to circumvent one of these problems, it will continue to work on the wild-type bacteria of that species (by definition making it broader). I am unaware of any antimicrobial which is effective against drug-resistant organism which has no efficacy against the wild-type of that organism.

I agree with the other poster that phage therapy likely represents a future avenue for antimicrobial resistance. Unfortunately antibiotics will (at least for the foreseeable future) be required as to effectively use phage therapy you must identify the organism and then select appropriate phages which will kill the bacteria, which takes time that a sick patient may not have without antibiotics. We also haven’t quite figured out how to keep our immune system from eradicating the bacteriophages, particularly for infections requiring longer treatment such as endocarditis.

There is a currently existing technology which allows for genetic identification of bacteria and fungi in positive blood cultures approximately 1 day faster than classical methods of culture and biochemical testing. There is active research into changing these tests slightly to be able to function on other body fluids (pus, pulmonary secretions, urine, etc) as well as to be able to function on fresh blood samples instead of waiting 1-2 days for the culture to become positive from bacterial growth, but these technologies are not ready for clinical use, and until they are, broad spectrum antibiotics will be a necessity.

That’s not exactly true. FMT isn’t going to fix your MRSA colonization, and it doesn’t inherently remove resistance genes from the population of bacteria in your gut. If those genes produce a survival disadvantage, they may be selected against and become a minor serotype in your GI tract, but that doesn’t mean that it is eradicated.

Also, you seem to be sharing a lot of links from humanmicrobiome.info, which I would advise against. While I can appreciate the primary author’s dedication to the topic and willingness to cite his sources, his website is not peer reviewed, and he explicitly states he is a proponent of FMT, introducing bias which is not being balanced by a peer review process. Not to mention he admits he is a layperson with no formal medical training/experience. I would direct you to IDSociety.org which is the home of the Infectious Disease Society of America, who publishes the actual guidelines used by infectious disease physicians in North America.

tl;dr - Asking your doctor for the shortest reasonable course is a good thing that will both protect you as a patient as well as minimize your risk of antimicrobial resistance. But the key phrase is ask your doctor, do not take it upon yourself to decide when to stop them. Take whatever course you’re prescribed.

Pharmacist and 4th year medical student with a passion for antimicrobial stewardship and infectious disease.

Historical treatment duration for most infections was truly quite arbitrary. Evidence for most infections, when it is actually tested, have pretty consistently demonstrated shorter treatment durations than were classically taught (10-14 days for pneumonia now generally 5-7, 14 days for Gram Negative Bacteremia now 7, etc). There is a subset of infectious disease doctors that are bucking the trend of historical “you have to complete your course advice” for some infections. In general, what I have seen is recommendations to discontinue antibiotics with significant clinical improvement AND a non-life-threatening infection in a non-sterile body cavity. So nobody is shortening course durations for empyemas or endocarditis.

The issue becomes expecting patients to know what constitutes clinically meaningful recovery and whether or not their infection is one of the “safe” ones to stop antibiotics earlier.

At the end of the day, I totally disagree with your premise, as we should always strive for the minimum safe antimicrobial exposure. However I do agree that telling patients “shorter is better” is bad advice because I don’t want laypeople making these decisions when usually no-ID physicians don’t make them.

You know I felt this way for years. I felt that way through psychopharmacology in pharmacy school, and I felt that way during our psychiatry and behavior lectures in medical school. I felt like psychiatry was minimizing behavior to these boxes was far too reductionist. Then I spent a month in an inpatient psychiatry facility as a third year medical student.

While I completely agree that each individual is unique and people are more than their diagnosis, you’d be absolutely shocked by just how similar patients’ overall stories, maladaptive coping mechanisms, and behaviors are within the same psychiatric illness. I can spot mania from a doorway, and it takes less than five minutes to have a high suspicion for borderline personality disorder. These classifications aren’t some arbitrary grouping of symptoms: they’re an attempt to create standard criteria for a relatively well preserved set of phenotypic behaviors. The hard part is understanding pathology vs culturally appropriate behavior in cultures you don’t belong, and differentiating within illness spectra (Bipolar I vs II; schizophrenia vs bipolar disorder with psychotic features vs schizoaffective)

As I said previously, the process needed to get insurance under these programs can be too complicated for individuals with low literacy or for whom English is a second language, limiting their access to these resources. And believe it or not, there are individuals for whom $15 a month is still not affordable for something they may or may not use that month, like medical insurance.

I’m aware that those costs do not magically disappear and are absorbed into other billing/passed on to society. However that is not why healthcare is so ludicrously expensive in the United States. It is the substantial and unnecessary administrative costs, predominantly driven by for-profit insurance companies, for-profit hospital systems, and pharmacy benefits managers. The continued exploitation of the ill for shareholder benefit is a uniquely American take on health care, and coupled with our incredibly individualistic tendencies bring about a huge fraction of the poor health outcomes we have in comparison to other developed nations, despite spending generally more than double per person.

Some of this is certainly driven by system inefficiencies such as forcing people into a situation where they have to use the ER for primary care. Or where they cannot afford their blood pressure or cholesterol medicine, and instead of our society helping provide these very affordable interventions, we pass the buck. So when those individuals inevitably have a heart attack, we then pay many times more for care that they may not have needed had they simply gotten good preventative care.

I will happily stand up and bash the current US healthcare system. I despise its insistence that human lives and suffering are secondary to wealth-extraction. But as much as I hate it I can’t change it, and while I will advocate for policy to change things, for now all I can do is continue to provide care to the patients presenting as a symptom of an ill society.

I hope others can see that these patients presenting to the ER are simply doing the best they can to take care of themselves and their families, and that the real blame and consternation should be placed on the government, hospital, insurance, and pharmaceutical officials and lobbyists who continue to exploit their illness for profits.