I’m currently a sophomore at Stanford. My question is about research experience. I noticed that you have a lot of research/publication experience. How important are they?

It’s difficult to state how “important” research and publications are. Sure, they look good, and if you end up applying to research-oriented medical schools, then having research experience will certainly be an advantage, but even at those schools, research is never the end-all-be-all determinant of how good an applicant is; it’s just one facet. In my case, I didn’t have much clinical experience in terms of shadowing and whatnot, so my application depended heavily on my research, and some might say overly so–I actually got asked quite often on the interview trail why I wasn’t applying M.D./Ph.D. (fortunately, it was a question I was well prepared for, since my mentor and labmates had all asked me the same thing a million times).

The primary question to consider is not how important research is, but rather, how much you enjoy research. Don’t you dare start thinking of research as some sort of achievement you need to check off before applying, because it’s not. If you’ve never done it before, then definitely explore it, but only continue if you find that you enjoy the process. If you force yourself, it’ll only be miserable, and believe me, classwork, other extracurriculars, or hanging out with friends are far better ways to spend your valuable (and limited) time compared to a job you hate.

That said, research is a pretty broad term. If you look hard enough, you will probably find a really cool research topic that jives with your interests, whether it’s rainforest development, ethics, microfinance, etc. If you have trouble with your search, ask upperclassmen, TAs, and professors for help–Stanford is full of resources to help guide undergraduates, as are most other universities.

How can undergraduates get the opportunity to publish?

It’s pretty simple: just find a project you enjoy working on (with a mentor you like and trust), and spend a lot of time working. Oh, and ask about publishing opportunities from the get-go so that your mentor can help guide you along the way–this is part of the art to determining whether a lab/project/mentor is a good fit for you. If you’re looking at research labs and want to get a feel for potential publication opportunities, just find the lab’s website and check out how many publications they produce each year–the more, the better. The slight caveat is that large labs tend to produce more, but large labs also mean less personal time with the mentor, since you have to compete for his/her time. Keep this balance in mind. Also, each subject has a variable rate at which publishable results can be obtained. The nice part is, admissions committees are well aware of the fact that generally speaking, clinical research has a slightly higher publication rate than basic science research.

Overall, if you put in the time and effort and produce results, chances are you’ll find yourself with the opportunity to publish, whether it’s in the local literary journal, scientific magazine, or peer-reviewed journal. Be patient and diligent!

And did you work in the same lab for two years (and published multiple pieces on the same research)?

Yep, I worked in the same lab from sophomore year to senior year, but I did switch projects once, so my publications were technically from 2 different projects.

When is a good time to start research?

Good question. Answer: whenever you’re ready to. Be warned that research will typically take up ~10-15 hours a week, so make sure you’re ready to make that commitment and juggle your schoolwork, other extracurriculars, social life, and sanity. I think the most impressive example I can think of comes from the time I hired Scott–he showed up to the interview with a printout his weekly schedule marked with all the hours each day he could potentially dedicate to our lab–the guy actually gave up his acappella group (Fleet Street) for us. David and I were blown away, and we told our boss that we had to take him even though he was a junior and hence would only be able to give 1 year to the lab (as opposed to sophomore candidates, who can give 1.5-2, which is generally favored for project continuity).

Mind you, don’t go nuts and spend so much time in lab that you don’t have a life. If you find yourself doing this, you’re doing it wrong.

~~~~~

“Hey Jae” is a series that publicly answers questions from pre-med students. I get these from time to time through facebook, e-mail, etc., so I figured if one person’s wondering, more likely are too. Feel free to pose a question of your own through my contact page! As always, best of luck.

“How bad is it, doc?”

I froze, stunned. I had never considered that anyone would ask me, a lowly medical student, a question so critical. Family meetings were the sort of thing attending physicians were supposed to handle. I quickly developed a healthy respect for the power of the white coat.

“Has he got much time left?”

Still frozen. They don’t teach these skills in classes. Rather, they try, but it’s utterly futile, and everyone knows it.

I didn’t want to mess this up. This woman’s face was clearly on the verge of tears. Her concern etched her 86-year-old face deeper than time had ever been able to.

“Just tell me, doc. I can take it. I’ve had this sort of talk before with him multiple times now, and heck, we know we’re a long-living family. We’ve outlived all our friends, and now we’ve just got each other. Honestly, neither of us cares if we go tomorrow or years from now. We’re just waiting to die, and it’s up to God when it happens.”

I finally found my tongue. I began to explain what had brought Mr. K to the hospital: he had become very weak due to anemia and had a fall. Fortunately, there were no broken bones, but he needed a few units of blood transfused so that his body could sufficiently circulate oxygen and nutrients. It was likely that he was continuously losing some blood through his GI tract, since he had a several-month-long history of some blood in his stools, but he didn’t want a colonoscopy since he knew his time was coming anyway. I reassured the sister that after receiving blood, Mr. K was doing much better, and while he may still be bleeding internally, he was, for the time being, stable–we had done everything we could do for him given his wishes.

The sister slowly nodded her understanding, and the concern began to fade from her face…but it didn’t completely disappear. I got the feeling that my job wasn’t done. I asked what was on her mind. She looked back at me, and after a bit of hesitation, admitted that she didn’t actually know the specifics of how things would happen if her brother passed away. She’d made arrangements with a funeral home and knew to call them once her brother passed away, but didn’t know how she herself would be contacted when it happened, or who would do it.

I quickly pulled out my notes and took down her contact information, assuring her several times that I would place it prominently in my hospital note to ensure that she was informed immediately by future doctors if anything happened to Mr. K in the hospital.

I cannot express in words how gratifying it was to watch the look of relief wash over the sister’s face, and how happy I was to see her crack a smile as she shook my hand and said, “Thank you, doc. I really appreciate it.”

She turned around, entered Mr. K’s room, and sat down in the available chair; I heard them begin to chat about childhood memories. As I stood in the hallway looking in, I couldn’t help but think for a moment that all of the hell I’d endured for med school was worth it. I’d just been granted the privilege of trust. I’d just been the person who delivered a bit of peace and comfort. And despite not having “M.D.” after my name, I’d somehow managed to muddle my way through this one.

The most exhilarating part was that for once, what I said had mattered to someone other than myself. As the medical student on the team, it’s rare to feel that anything I say is important. I often feel like I’m just repeating things said by my residents/attending, and honestly, it has yet to actually affect patient care, so I have little stake in anything other than for the sake of my grade/evaluations, which I don’t really care a whole lot about (my philosophy is that I’m here to constantly learn, not just work for a number that “defines” me). But just this once–what I said and how I said it made a real difference.

I think moments like this are what prevent me from becoming jaded. I was talking with my upper-level resident the other day, and she was telling me how frustrating it can be to know that patients frequently have diseases that can’t be reversed. But no matter how grave the medical scenario, there are shining moments where you know you touched someone’s life for the better, and those make up for all the rest of the drudgery. It’s times like this that remind me that medicine is perhaps the field where balancing between science and art is not only conducive to success, but rather, critical.

One of the major influencing factors in me joining medicine was the prolonged illness and death of a close family member, and I still remember all too well how painful it was. I know how horrible it feels to lose someone, no matter how “prepared” you are. I left the hospital on this particular day with my head held just a bit higher, feeling that just maybe, I’d been able to put a bit of positive energy into a family’s medical care.

Do medical students have paid jobs when school is in session? I would think that some would work to help pay off their tuition costs.

Yes and no. Many people do some form of work-study financial aid in school where they find jobs as librarians, TAs, research assistants, manual laborers, etc. Others arrange their own gigs, whether it’s playing in a band or tutoring the local university students or designing web pages. But honestly, many don’t do either, simply because they feel the time investment is either something they cannot afford to make if they wish to maintain their desired level of academic achievement, or they just want to use that time for self-care (social life, cooking, baking, exercise, hobbies, sleep, you get the idea). Here’s a simple decision tree to consider:

• Do you really have time to work? In other words, will you still keep up your academics, social life, sleep schedule, and exercise?
  • If no, stop. Go play some frisbee and enjoy your life as it is.
  • If yes, continue.
• Are you sure? Will you stay sane?
  • If no, stop. Go eat some chocolate and let the soothing effects take place.
  • If yes, continue.
• What are your skills?
  • If research, consider seeking a lab that allows you to work flexibly. Chances are that this will be an extremely difficult job to maintain.
  • If teaching, see if you can find an MCAT program to teach for, or a tutoring arrangement (these often pay $50+/hour), or a TA position.
  • If bartending, look for a bar that doesn’t have you doubling as the bar-back.
  • If music, try to score gigs to play around town.
  • If muscles, then consult with your anatomy lab–chances are they’ll need help from time to time moving bodies and equipment.
  • If programming, let people know you’re into code/web design/etc.
  • If art/photography, consider selling your pieces/work. Chances are you’ll have classmates who get married, and they’ll need a wedding photographer.
  • If something not on this list, be creative and come up with something.
  • If none of the above, look for a simple, non-intensive task, such as librarian. This position has the bonus of giving you study time when people aren’t bugging you about books.

Keep in mind that all of this changes from year to year, particularly once you begin clinical rotations, which are basically a full-time job in and of themselves. I think tutoring is probably the most flexible and gives the best money/hour, but do whatever floats your boat–and remember: not working while in med school is perfectly acceptable, and in many cases, a healthy thing. You really have to weigh whether the (usually minor, in the grand scheme of things) decrease in debt is worth whatever sacrifices the job(s) require.

~~~~~

“Hey Jae” is a series that publicly answers questions from pre-med students. I get these from time to time through facebook, e-mail, etc., so I figured if one person’s wondering, more likely are too. Feel free to pose a question of your own through my contact page! As always, best of luck.

I am a sophomore in college and after one and a half years of being a pre-med, my GPA so far is 3.1, which is very low, I know. I don’t know if I should give up pre-med, since my gpa is too low to get in anywhere. But I always liked to become a doctor, I feel that giving up is not worth it. but on the other hand, my GPA is way too low. I wonder if you have any idea what should I do? I still want to continue but I am afraid that my gpa is too low to get into anywhere.

I think before reading anything that I write, you really need to look at this: Making the Decision to Go To Medical School.

Now, let’s break this down. At the time of this writing, you just completed your first semester of sophomore year. With work, it is perfectly possible to raise your GPA to something more competitive by the time you’re applying–anywhere in the range of 3.5-3.8 is not out of the question, which, when paired with a strong MCAT and extracurriculars, will make for a good application. Based on my personal experience, I’m guessing that overall GPA matters slightly less than science GPA, so start by calculating that to get a feel for where your strengths are. If your science GPA is a 3.8, then there’s less to worry about. On the other hand, if your science is a 2.3, then…you may need to think more carefully about how to improve your science scores.

With regards to classes–where are your grades suffering? Chem? Bio? Physics? If it’s continuously all three, then this may be a problem with regards to your doctoral aspirations. If however, it’s just in your basic introductory classes, then you may just be having a hard time with the learning curve and need to employ a different study strategy. I distinctly recall being miserable in my early organic chem classes until I switched textbooks, at which point my grades skyrocketed to the top of the class and I ended up TAing the subject for 2 years.

So start by analyzing yourself in depth. Take a good long look at where your weaknesses are, come up with a plan to get better (get friends to help you with this!), and then iterate on the plan, adding improvements/tweaks as necessary. There is rarely such a thing as talent–just skills that everyone has taken thousands of hours to hone. I would be saying something considerably different if you were a senior, but now seems a bit early to contemplate the notion of quitting, particularly when you’ve only begun to delve into some of the deeper sciences as a college student. To be blunt, it actually does worry me a bit that you’re thinking of quitting so easily–it only gets harder from here on out. So do whatever it takes to boost your self-confidence–and if, a few years from now, grades are still a problem, then we’ll chat again. Fair?

~~~~~

“Hey Jae” is a series that publicly answers questions from pre-med students. I get these from time to time through facebook, e-mail, etc., so I figured if one person’s wondering, more likely are too. Feel free to pose a question of your own through my contact page! As always, best of luck.

After reading this article, I decided to do some math on the matter…and unless the person into whom the blood is being injected has incredibly low tolerance to heroin, the chances of getting a heroin high by injecting yourself with the blood of someone else who has just used heroin is near nil.

Let’s do some math. Once heroin is introduced into the body, it spreads systemically through blood (timing varies with method). Assuming a 1 gram IV dose and ~5 liters of blood in the average human:

main person’s blood concentration = 0.2 g/L

Now, according to the article, the amount of blood shared is about a teaspoon, or ~5 mL:

0.2 g/L * 5 mL = 0.001 g heroin being transferred

As you can see, the dose from blood is near negligible, as it’s been weakened a thousandfold–for an addict, this amount wouldn’t even be remotely enough to get a high. There are two scenarios in which this technique might be tweaked to work, but both of them will prove fatal to one or both parties:

• Main person takes a particularly heavy dose–they’ll likely suffer respiratory depression to the point of coma/death.
• More blood is used–main person could die if too much blood is drawn or the one accepting blood could suffer an immune response and die.

Why this practice is folly:

• bloodborne diseases
• immune responses from mismatched blood types
• other infections (from normal skin flora or dirty needles, particularly if someone has an immune system weakened by AIDS)
• …it just doesn’t work

Basically, the belief in this practice is due to placebo effect and maybe some residual heroin left over on the needle or in the syringe from the main user.

To understand HIV medication, one must first understand the 6 crucial steps that HIV needs to complete in order to replicate and spread. In order, they are:

1. Binding and fusion: HIV binds to either or both of two cell receptors known as CCR5 (typically in initial stages of infection) and CXCR4 (often in later stages) in order to enter the cell. HIV is surrounded by a lipid envelope that allows it to fuse with the target cell’s membrane, releasing the virus’s core contents into the cytoplasm.
2. Reverse transcription: HIV’s genetic code is RNA-based, so its reverse transcriptase enzyme generates a DNA template.
3. Integration: The DNA template is then integrated into the host cell’s genome.
4. Transcription: The host cell’s protein machinery transcribes and translates mRNA based on the integrated DNA template.
5. Protease cleavage: HIV proteins are initially made in large chains known as poli-proteins, which are cleaved into their functional pieces by proteases.
6. Assembly and release: New virions assemble at the cell membrane and bud from the cell surface.

DRUG CLASS 1: ENTRY INHIBITORS

CCR5 antagonists prevent the first binding step, stopping the virus from entering any cells. The problem is that this is only effective for patients whose variant of HIV solely relies on the CCR5 receptor for virility, so if a tropism test reveals a CXCR4-dependent virus, this option is not used.

• Maraviroc is the only FDA-approved drug in this class.
• Common side effect (CSE): hepatotoxicity (liver problems)

Fusion inhibitors allow the virus to bind initial receptors, but prevent the next step of fusion between the viral and cellular membranes.

• Enfuvirtide is the only FDA-approved drug in this class, and is given through subcutaneous injections.
• CSE: Injection site inflammation/redness in 90% of patients, usually mild.

DRUG CLASS 2: REVERSE TRANSCRIPTASE INHIBITORS

Nucleoside analogue reverse transcriptase inhibitors (NRTIs) compete with natural nucleotides, leading to premature DNA chain termination.

• Drugs: Abacavir, Didanosine, Emtricitabine, Lamivudine, Stavudine, Tenofovir, Zidovudine
• CSE: Mitochondrial toxicity from inhibition of the enzyme responsible for mitochondrial DNA synthesis.

Non-nucleoside reverse transcriptase inhibitors (NNRTIs) bind to the reverse transcriptase enzyme, inhibiting its function.

• Drugs: Delavirdine, Efavirenz, Etravirine, Nevirapine
• CSE: Rash, hepatitis

DRUG CLASS 3: INTEGRASE INHIBITORS

These inhibit incorporation of viral DNA into the host’s genome.

• Raltegravir is the only FDA-approved drug in this class.
• CSE: muscle damage/problems

DRUG CLASS 4: PROTEASE INHIBITORS (PIs)

PIs inhibit viral proteases from cleaving viral poli-proteins into their functional bits, preventing assembly of the virus.

• Drugs: Atazanavir, Fosamprenavir, Darunavir, Indinavir, Lopinavir, Nelfinavir, Saquinavir, Tipranavir
• Ritonavir is a PI that is frequently used in low doses for its interesting effect of preventing metabolism of other PIs–increasing their efficacy.
• CSE: Many possible–nausea, vomiting, diarrhea, hepatitis, etc.

TREATMENT REGIMENS

Treatment regimens vary widely based on the patient, the progression of the disease, the strain of HIV, etc. Broadly speaking, initiation of therapy in treatment-naive patients often begins with one of the following 3-drug combos:

• 2 NRTIs + 1 PI (usually boosted with ritonavir)
• 2 NRTIs + 1 NNRTI
• 2 NRTIs + 1 integrase inhibitor

The idea is to prevent further spread of the virus in the patient with a cocktail to prevent easy resistance mutations. Some of the many things to consider to individualize the treatment for each patient:

• patient preference
• toxicity profile
• child-bearing potential (women)
• strain’s baseline resistance(s)
• does the patient have other conditions that require treatment? (drug interactions)

Key to the regimen are regular check-ups which evaluate adherence to treatment, potential psychological concerns, side effects/complications, resistances, etc. Patients are counseled on prevention of HIV transmission and opportunistic infections, as well as other health changes that might be appropriate.

Nota bene: HIV/AIDS research is a very active field, and the above information could change at any time!

Disease (insect): notes.

1. yellow fever (mosquitoes): Mortality rate is high.
2. dengue fever (mosquitoes): This is the most common insect-borne viral disease in the world. Classic dengue (a.k.a. breakbone fever) is rarely fatal and has few aftereffects, but dengue hemorrhagic fever is much more severe, with ~10% fatality rate.
3. eastern equine encephalitis (mosquitoes): ~50% fatality rate, with usually severe central nervous system problems for survivors.
4. western equine encephalitis (mosquitoes): ~2% fatality rate, but inapparent infections outnumber the apparent ones at least 100:1.
5. St. Louis encephalitis (mosquitoes): ~10% fatality rate, but most infections are inapparent.
6. California encephalitis (mosquitoes): Clinical can be mild to severe, but death is rare.
7. West Nile Virus (mosquitoes): Less than 1% of those infected have symptomatic disease.
8. filariasis (mosquitoes): While the microfilariae (which do not cause symptoms) can be treated with the drug diethylcarbamazine, there is no drug therapy for the adult form of this of this nematode which can cause elephantiasis with repeat infections.
9. Colorado Tick Fever (wood tick)
10. Chagas’ disease (reduviid bug): The acute form can be treated with nifurtimox, but there is no effective drug against the chronic form, which causes myocarditis and megacolon.

All information derived from study of Review of Medical Microbiology and Immunology, authored by Dr. Warren Levinson.

HIV = Human Immunodeficiency Virus
AIDS = Acquired Immunodeficiency Syndrome

In common use, the terms HIV and AIDS are often used interchangeably.

The distinction is made clinically because infection with HIV typically doesn’t immediately cause AIDS, strictly speaking–it can take several years for the presentation of AIDS to become apparent. Because of this, it’s estimated that ~25% of those with HIV/AIDS in the U.S. are unaware that they are infected.

The conundrum is that upon infection with HIV, many of the initial symptoms can be vague: fatigue, low grade fevers, night sweats, weight loss, and intermittent diarrhea are common, but all of these symptoms have many, more frequently seen causes, so unless some risk factors are apparent in a patient’s history, it can be missed*. Hence, many institutions are now adopting the policy that separate written consent is not required for testing, and implementing the highly-recommended opt-out strategy, particularly for pregnant women.

HIV causes a deficiency in an immune cell that is identified by the presence of a marker protein known as CD4, and in 1993 the surveillance case definition came to include that a patient has AIDS if their CD4 count in a lab sample dropped below 200. There are various other tests now in use to confirm infection with the virus, but as far as I know, that was the first clear-cut definition.

* There are also numerous circumstances where the patient may not feel comfortable discussing their sexual history.

If you really feel the need to be saturated with vitamin C “just in case”, your blood level hits maximum at ~400 mg/day; anything above that is peed out, so don’t waste your time and/or money!

Sources:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC55540/
http://lpi.oregonstate.edu/infocenter/vitamins/vitaminC/

Something else to consider that I learned in my renal course: 2000 mg per day of Vitamin C supplement increases urine oxalate (a component of a common variety of kidney stone) by 22%. Men who take 1000 mg or more vs. the RDA of 90 mg have up to 40% higher risk of stone formation. So people who are either at risk of forming calcium oxalate stones or have a history of forming them should be instructed to stop vitamin C supplements.

Mind you, everyone’s risk for forming kidney stones is widely different, so just take the above as a cautionary note of something to keep in mind.

I went to an evolutionary biology talk they had at my school (to celebrate Darwin’s birthday) about the fact that a lot of parasites secrete hormones that suppress a human’s immune system, and that our immune systems, without the parasites, are a lot stronger than they really need to be, as a result of co-evolution.

The point of the talk was that they were experimenting with some kind of parasite (I think pigworm?), chosen for its production of these types of hormones, and its relatively significant safety for humans (can’t reproduce in our systems, have no real ill effects, just kind of hang out and live quotidian parasitic lives secreting these hormones), as a possible treatment for autoimmune diseases.  I seem to remember they had some striking results for Crohn’s disease, but I’m not completely sure.

I think there was a Radiolab episode where they discussed this too.  I think it was called “Parasites.”

~~~ BACKGROUND ~~~
The idea of using parasites to treat autoimmune conditions is a variant of the Hygiene Hypothesis. Put simply, it states that modern industrialized society has become so clean that we’ve disrupted the “natural” balance of cleanliness/dirtiness. Now that we’re all fans of everything being antibacterial/antimicrobial, our immune systems just aren’t constantly under siege. In other words, they’re bored. So without the constant risk of infection keeping them well-disciplined, they start gnawing on the body by mistake.

There is the unfortunate truth that our immune systems, once activated, have absolutely pathetic negative feedback loops. Every other system in the body, from respiration to endocrine to digestive, has signaling pathways in place that, in a healthy individual, allow for surprisingly fine control of homeostasis. The only equivalent that has been elucidated in the immune system is the small quantity of T-regulatory cells, and no one seems to be capable as yet of explaining their origin, what determines who has how many, who has fewer/defective ones, etc. There are a few other factors such as controlled apoptosis/anergy of self-reactive immune cells, but at the moment they’re not too inspiring since they can be overturned. :-/

So it makes sense, then, that with limited endogenous resources to calm down the immune system, an external source may have provided this need for millenia. What better than buggers who evolved to evade the immune system?

~~~ SUPPORT ~~~
A quick scan of clinical trials and pubmed reveals that hookworm species are being used for everything from Celiac to Crohn’s to multiple sclerosis.

http://clinicaltrials.gov/ct2/show/NCT00671138?term=parasite+autoimmune&rank=1
http://clinicaltrials.gov/ct2/show/NCT00630383?term=parasite+autoimmune&rank=4
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856386/
http://www.ncbi.nlm.nih.gov/pubmed/14499784

The current work in the literature appears to be generally in favor of at least trying this approach for those who qualify, and anecdotal evidence, as seen by the gentleman who appeared on the Radiolab episode and told his tale about asthma, is wildly supportive.

In short, it’s possible that for people who simply have environmental (nurture, not nature) causes of autoimmunity, this might well be their miracle “drug”.

~~~ CONCERNS ~~~
One of the main reasons this relatively new approach has been able to make it to clinical trials so quickly is precisely because of its extremely attractive side effect profile. The worms are pretty easy to treat if anything goes wrong or the treatment doesn’t work, so patients aren’t at particularly severe risk for trying it. Hence the question arises–are we just blindly praying for luck and seeing a placebo effect?

I ask because dosing clearly needs work, as you want to give the patient a sufficient load to suppress the immune system, but not enough to cause anemia. How that will be determined for each individual (remember, autoimmunity has various levels of severity) has yet to be properly established, and work is coming out suggesting that the body can tolerate a higher load than initially suspected before therapeutic benefits are viable: http://www.ncbi.nlm.nih.gov/pubmed/20030661

Furthermore, at a more molecular level, parasitic presence isn’t necessarily just about immune suppression–they induce a shift in the immune system’s style from Th1 to Th2 because of the specific cocktail of molecular signaling required to destroy a helminthic parasite. The bizarre conundrum here is that an overactive Th2 response is associated with allergies. Wait. Autoimmunity != being allergic to the body?!? If that’s the case, will treating with parasites cause these people to start developing severe allergies? No one knows–this technique is just too new for any longitudinal studies to be conducted with legitimacy.

This approach also doesn’t really encompass the multifactorial etiology of autoimmunity, and ignores the genetic susceptibilities entirely. For instance, this would do nothing for people with autoimmune polyendocrine syndrome, which is an irreversible defect in the AIRE (autoimmune regulator) gene. Acute infections can also be a cause for autoimmunity, as some bacteria attempt to trick the immune system by presenting proteins similar to those found in the body. It’s all fine and well that our immune systems can tell the fine point differences until the infection is cleared and all these immune cells are seeing endogenous things that look mighty close to to the thing they were killing just days ago (example: infection by Campylobacter jejuni has been associated with Guillain-Barre).

At the end of the day, remember that just because something co-evolved with us doesn’t mean we’re symbiotes. While I suppose from an evolutionary perspective our hygiene has essentially killed off any possibility for such parasitic symbiosis to evolve, the fact remains that plenty of people who aren’t infected with parasites aren’t suffering from autoimmunity, and the advent of modern hygiene came with an overwhelming and undeniable jump in life expectancy. It may be that for this niche population, it’s an efficacious treatment, but I certainly wouldn’t advocate infecting everyone with wormies!