Wake Forest School of Medicine Section on Infectious Diseases

Why Dog Rabies Persists—and What It Takes to Eliminate It

Brinkley Bellotti — Mon, 26 Jan 2026 00:00:00 GMT

This month, two MMWR reports highlighted three human rabies deaths in the United States. Two individuals were infected after encounters with bats(Ireland et al. 2026). In the third case, the exposure was never identified, but genetic sequencing revealed a strain associated with dogs in Haiti (Barger et al. 2026). Globally, more than 99% of human rabies cases result from bites by rabid dogs, causing approximately 60,000 deaths every year (Organization 2018).

This is particularly sobering because rabies is entirely preventable. Dog owners know that vaccines for canine rabies are highly effective, and for humans, post exposure prophylaxis saves lives when administered promptly. In fact, modeling studies show that vaccinating just 70% of dogs in a community can eliminate dog mediated rabies transmission (Organization 2018). So why, if we know how to eliminate dog rabies, does it remain a persistent threat in so many parts of the world?

Dog rabies is concentrated primarily in low and middle income countries where dog populations include free roaming owned dogs, community dogs, and strays. Vaccinating these diverse and mobile populations is both logistically difficult and economically demanding. The main global strategy is mass dog vaccination campaigns: large, usually annual efforts aiming to vaccinate as many dogs as possible over a short time (Organization 2018).

Photo of a free-roaming dog in Arequipa. Photo credit Brinkley Bellotti.

Beginning during my graduate work in the Castillo Lab at the University of Pennsylvania, and continuing today, I conduct research focusing on an ongoing dog rabies outbreak in Arequipa, Peru. Our goal is to identify strategies that maximize vaccination coverage given the city’s limited resources. Arequipa has an enormous dog population (roughly 250,000 animals!) many of which spend part of their time roaming the streets. Mass vaccination in the city relies on temporary vaccination points, where trained vaccinators set up stations and dog owners bring their pets.

In one study I contributed to, we applied algorithms traditionally used to solve “facility location problems.”(Castillo-Neyra et al. 2024) Companies like Amazon use these models to choose optimal warehouse locations. We used the same principles to determine where to place vaccination points so that the average distance residents must travel is minimized. These algorithms help ensure that logistical barriers don’t prevent people from vaccinating their dogs.

Predicted vaccination campaign participation. Panel A shows tent locations (white triangles) used in the 2016 MDVC, while panel B shows the optimized placement of tents obtained using the p-probability method. Houses (colored dots) are shaded according to their probability of participating in the MDVC, which was determined using our mixed-effects Poisson regression function with the random-effects coefficient for 2016 that related participation probability to distance to the nearest vaccination tent. These maps were created using R package ggmap version 4.0.0 from Castillo-Neyra et al. (2024)

Another study examined the timing of vaccination drives. (Bellotti et al. 2025) Historically, campaigns in Arequipa were conducted in a single day or weekend, an almost impossibly compressed timeline for vaccinating a quarter million dogs. We modeled an alternative strategy: staggering the campaign so that different districts are vaccinated on successive weekends over several months. Officials worried that because dogs move freely throughout the city,(Raynor et al. 2020) infected animals from unvaccinated districts might reintroduce the virus into districts that had already completed their campaign. The model confirmed that some re-seeding would occur. However, the overall effect was still positive: staggering the campaign increased the total number of vaccinated dogs, ultimately improving rabies control despite the added complexity.

These examples represent just a few of the obstacles involved in controlling canine rabies in one city with minimal wildlife reservoirs complicating transmission. Rabies control illustrates how seemingly straightforward public health interventions can actually involve deeply complex social, biological, and logistical systems. It also demonstrates how disruptions, such as the COVID 19 pandemic (Raynor et al. 2021), can ripple through these systems, causing lasting setbacks.

Map of Arequipa Department. Arequipa Department consists of 8 provinces. Prior to February 2021, rabies cases were contained in Arequipa province (the province containing Arequipa city). In February 2021, cases spread to the neighboring province of Caylloma, primarily in the city of El Pedregal. Seven cases have since been detected in El Pedregal. Shapefiles used to create maps are from Peru’s National Geo-referenced Data Platform Geo Peru. Figure from Raynor et al. (2021).

References

Barger, Alexandra, Sara F. Margrey, Allison W. Siu, et al. 2026. “Imported Human Rabies — Kentucky and Ohio, 2024.” MMWR. Morbidity and Mortality Weekly Report 75 (2). https://doi.org/10.15585/mmwr.mm7502a3.

Bellotti, Brinkley Raynor, Elvis W. Díaz, Micaela De La Puente-León, et al. 2025. “Challenging a Paradigm: Staggered Versus Single-Pulse Mass Dog Vaccination Strategy for Rabies Elimination.” PLOS Computational Biology 21 (2). https://doi.org/10.1371/journal.pcbi.1012780.

Castillo-Neyra, Ricardo, Sherrie Xie, Brinkley Raynor Bellotti, et al. 2024. “Optimizing the Location of Vaccination Sites to Stop a Zoonotic Epidemic.” Scientific Reports 14 (1). https://doi.org/10.1038/s41598-024-66674-x.

Ireland, Malia, Curtis L. Fritz, Stacy Holzbauer, et al. 2026. “Human Rabies Deaths — Minnesota and California, 2024.” MMWR. Morbidity and Mortality Weekly Report 75 (2). https://doi.org/10.15585/mmwr.mm7502a4.

Organization, World Health. 2018. WHO Expert Consultation on Rabies: Third Report. World Health Organization.

Raynor, Brinkley, Micaela De La Puente-León, Andrew Johnson, et al. 2020. “Movement Patterns of Free-Roaming Dogs on Heterogeneous Urban Landscapes: Implications for Rabies Control.” Preventive Veterinary Medicine 178 (May). https://doi.org/10.1016/j.prevetmed.2020.104978.

Raynor, Brinkley, Elvis W. Díaz, Julianna Shinnick, et al. 2021. “The Impact of the COVID-19 Pandemic on Rabies Reemergence in Latin America: The Case of Arequipa, Peru.” PLOS Neglected Tropical Diseases 15 (5). https://doi.org/10.1371/journal.pntd.0009414.

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@online{bellotti2026,
  author = {Bellotti, Brinkley},
  title = {Why {Dog} {Rabies} {Persists—and} {What} {It} {Takes} to
    {Eliminate} {It}},
  date = {2026-01-26},
  url = {https://wakeforestid.com/posts/2026-01-26-why-dog-rabies-persists/},
  doi = {10.59350/p4swp-ba751},
  langid = {en}
}

For attribution, please cite this work as:

Bellotti, Brinkley. 2026. “Why Dog Rabies Persists—and What It Takes to Eliminate It.” January 26. https://doi.org/10.59350/p4swp-ba751.

Why Is Getting on Buprenorphine So HARD These Days?! : Part 2

Erin Barnes — Fri, 21 Nov 2025 00:00:00 GMT

A lot of people have been working on the fentanyl problem for a few years now. There are different strategies that can be taken and different ones work for different people. Here are some of the options that are used most often.

Option 1: Go Inpatient

Inpatient detoxification programs have the ability to do EXTREMELY low dose inductions (sometimes referred to as microdosing). They can use patches or IV versions of the buprenorphine so that you are getting only a fraction of a milligram of buprenorphine to start. You can then increase the amount by a couple tenths of a milligram as well. These amounts are so low that it does not trigger the withdrawal. It will take about 5-14 days, though, to get the buprenorphine to full strength.

It may be difficult in some areas to find inpatient settings that do this type of induction or that take your insurance. Even if your detox does not do this type of medication, if you can last a few days in the more supported environment of an inpatient detox so that most of the medication is out of your system when you leave, you can then start the full dose of your buprenorphine medication once you leave- the fentanyl is then mostly out of your system.

Option 2: Methadone

Methadone does not have the same problems that buprenorphine does- it will not make you sick when you take it. It is then very easy to get on methadone from fentanyl. Methadone can start at about 30-40 milligrams a day and increase you by 5-10 mg every couple of days. People may need >100mg to feel completely ok. The methadone clinics are trying to increase people’s methadone doses more quickly than they did in the past but still are limited by safety and some federal restrictions.

Many methadone clinics now offer buprenorphine as well as methadone. It can be tricky to get form methadone to buprenorphine similar to how it is tricky with fentanyl but there are techniques and ways. Some people may start on methadone to help them stabilize and then transition to buprenorphine with the help of their clinic later.

Option 3: High Dose Induction: Pedal to the Metal

This method is now well studied in the emergency room (ER) setting¹. Persons would come into the ER in severe withdrawal. ER doctors start by giving 16-24 mg of buprenorphine all at once, right off of the bat. The rationale here is that the person feels very bad and we are already behind treating their withdrawal. So we are going to push the last of the fentanyl out of their system as quickly as possible and replace it all with buprenorphine all at once- none of this slow trickling in and out. People may get 32-64 mg of buprenorphine on the first day. Studies show this is very effective and in one major study <1% of people had any precipitated withdrawal with this approach.

This technique can still be challenging to do in a regular outpatient clinic setting. It is hard for someone to wait long enough to go into severe withdrawal. Anxiety in particular tends to cause people to jump the gun. Supportive medications to help relieve anxiety, cramping, diarrhea, and restlessness are prescribed with the buprenorphine to help the person wait as long as possible before taking their first dose- ideally at least 24 hours. It is also helpful to have friends and loved ones support you during this time in a calm environment.

Option 4: A Variation on the Old Way

Some providers have still found some strategies similar to how we used to do it that can work. You would wait until you have had about 6 hours from last dose and a few physical signs of withdrawal. Then you build up the medication over time. You would use 0.5 mg (a 2 mg suboxone film cut into 4 pieces) at first and then increase to 1mg at time then 2 mg at a time and finally 8 mg at a time. You would be at 16-24 mg by the end of the day. In this method you are going lower and slower than we would have in the past but not quite as slow as some of the inpatient detox clinics can go. It helps to have people support you, keep you occupied, and help you keep track of the medicine. You would be given medicines to help keep you more comfortable.

Option 5: The Long-Acting Shot

This technique is newer and has fewer reports than some of these other options but is very exciting²³. Sublocade is the tradename for a long-acting version of buprenorphine- it lasts about 1 month.

It is injected into the body and then slowly releases into the blood stream. It will not reach its full strength in your blood stream until 24 hours after the shot- it is slowly releasing in. There are also week long versions of the medication. The theory is that this slowly leaks into your blood stream from the injection site. This slow leak into the blood stream is similar to the very slow, low dose inductions done in an inpatient detox. The other benefit is that once the shot is given you can’t take it back- even if you use, the shot is going to continue to release the medication and slowly take its place. This means you don’t have to ‘start over’ and try again to get on the medication.

In the largest study so far of this technique with Sublocade, people were brought into the ER after an overdose reversal and were then given the shot after tolerating 4 mg of buprenorphine. In the clinic, people are experimenting with having people prove they can tolerate much lower doses to show they are not allergic and the timing for how long to wait from last use before the shot is still being worked out.

Footnotes

AA H, AA V, J L, et al. High-Dose Buprenorphine Induction in the Emergency Department for Treatment of Opioid Use Disorder. JAMA network open. 07/01/2021 2021;4(7)doi:10.1001/jamanetworkopen.2021.17128↩︎
TA O, KJ R, TT D, et al. Rapid induction onto extended-release injectable buprenorphine following opioid overdose: A case series. Drug and alcohol dependence reports. 03/16/2023 2023;7doi:10.1016/j.dadr.2023.100144↩︎
KW L, A M, I G, B H, M D, JM K. Initiation and Dosing of Extended-Release Buprenorphine: A Narrative Review of Emerging Approaches for Patients Who Use Fentanyl. Substance abuse and rehabilitation. 03/25/2025 2025;16doi:10.2147/SAR.S516138↩︎

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@online{barnes2025,
  author = {Barnes, Erin},
  title = {Why {Is} {Getting} on {Buprenorphine} {So} {HARD} {These}
    {Days?!} : {Part} 2},
  date = {2025-11-21},
  url = {https://wakeforestid.com/posts/2025-11-20-why-is-getting-bup-so-hard-2/},
  doi = {10.59350/dfzn3-grg82},
  langid = {en}
}

For attribution, please cite this work as:

Barnes, Erin. 2025. “Why Is Getting on Buprenorphine So HARD These Days?! : Part 2.” November 21. https://doi.org/10.59350/dfzn3-grg82.

Why Is Getting on Buprenorphine So HARD These Days?! : Part 1

Erin Barnes — Thu, 13 Nov 2025 00:00:00 GMT

The Rise of Fentanyl

We speak of the US opioid epidemic as if it is one single thing, but it is actually a rapidly shifting, regionally variable wave of different events. We are currently in what many consider to be the 4th wave of the opioid epidemic: use of high potency synthetic opiates (i.e. fentanyl and its friends) + stimulants (methamphetamine or cocaine) along with some special flourishes like Xylazine. The reason I say this is regional is because new drugs do not hit all areas of the US at once. They tend to enter in one area and sort of spread/diffuse into others. For example, fentanyl came in first to the Northeast US. This is because the Northeast long sourced heroin from areas that supplied it in the white powder form compared with places like the West Coast which tended to be more frequently supplied with black tar heroin. It was easier to mix the white powder fentanyl into the white powder heroin. For this reason, graphs of the overdose deaths of the US tend to show fentanyl hitting around 2013/2014 but in my area in North Carolina we didn’t start seeing it as much until a few years later. The amount of additives like xylazine will also vary place to place; nearly all of the fentanyl in Philadelphia is laced with xylazine but it is much less in other areas. Why does fentanyl matter? Fentanyl is more potent than heroin so less drug is needed to get the same effect. Fentanyl is also supposed to have a very short ‘half-life’ meaning its effects should wear off and the drug leave your system fairly quickly. This is somewhat true-persons who use fentanyl do tend to feel that the effect wears off quickly and have to use more often. BUT. We have found that when persons use large amounts of fentanyl regularly that something interesting happens. Fentanyl loves fat and it seems that with a lot of use the fentanyl can sort of deposit into your body’s fat stores. Then when you stop using the fentanyl it can slowly release from the fat into your system at low levels. Case reports show urines testing positive for fentanyl weeks after last use.

How We Used To Do It

In order to understand why fentanyl is making buprenorphine inductions harder, that we have to look at how we used to do inductions and why.¹ Remember: buprenorphine always wins. It will push any other opioid that is present in your system out of the way, off of the opioid receptor. But even though buprenorphine is stronger in THIS way, once it takes the place of the old opioid it turns the ‘volume’ down from 100% to 50%. This drop from 100% to 50% is withdrawal which we have caused (‘precipitated’) by giving you the buprenorphine. In order to avoid precipitated withdrawal in the past we would have you wait a few hours after your last use of prescription opioids/heroin until you felt moderately unwell, give you a small amount of buprenorphine, and slowly increase the buprenorphine over 2-3 days. People got on buprenorphine after experiencing only a few hours of mild-moderate withdrawal symptoms. Why did this work?

Well Imagine your brain opioid receptors are like the seats in a movie theater-each chair is an opioid receptor in your brain. Imagine when I give you hydromorphone, heroin, methadone, etc. it is putting a person in the chair. In advanced addiction, the person feels ‘normal’ and not sick when the receptors (chairs) are filled. Buprenorphine is different. It only turns the receptor on halfway. So to visualize that lets imagine that each time a buprenorphine sits down it causes the neighboring chair to go empty.

So. Imagine you just used a full opioid like heroin. Your theater looks like the picture on the left above and you feel pretty good/normal. As time goes by the drug wears off: these guys get up and leave their seats empty. More empty seats= more withdrawal. Different drugs have different speeds at which people leave the seats. Heroin and hydromorphone leave their seats faster than morphine which leaves faster than methadone. In the cycle of addiction the person uses every time enough drug has left enough ‘seats’ empty that withdrawal is kicking in.

Now. Let’s think about what happens if we add buprenorphine to the mix. REMEMBER: Buprenorphine always wins: if there are no empty seats, buprenorphine will grab the seat, kick the other guy out, and take its place. And for each seat the buprenorphine takes it leaves a seat empty. So what does this look like if we take buprenorphine (Bup) at each of these stages above.

So now we see why this approach worked: people would wait until they were in moderate withdrawal and take a small amount of buprenorphine. They would then feel BETTER with the buprenorphine and more comfortable. They then felt well enough to wait another hour or 2 for more seats to empty and would then take more buprenorphine. By the end of 2-3 days all of the seats were filled with buprenorphine and the person did not have any withdrawal symptoms. It is all about keeping the balance: wait just long enough for open seats to become available so taking buprenorphine helps us feel better rather than worse but not waiting so long that someone is in severe withdrawal feeling awful.

Fentanyl Gumming Up The Works

Fentanyl throws off the balance because it is more potent than heroin. You need a lot less fentanyl (maybe 100 times less) to get the same effect as heroin. That is why drug cartels like it: they can make it cheap and don’t need to use as much of it= more profit for them. People aren’t that exact though – they are using more than they would need to get the ‘exact same effect’ as heroin. It’s why overdoses are so much more common when fentanyl is present. So in our thought experiment it is almost like we have 2 fentanyls sitting in each chair where we would have had only 1 heroin. Our theater now looks like this:

You can see the problem. Even in severe withdrawal there are not a lot of open seats for buprenorphine to sit in! It is going to have to push some fentanyl out of the way even though the person ALREADY feels AWFUL. Also remember that in heavy users some fentanyl will be slowly leaking back in from the fat stores. So some fentanyl people just keep wandering back in and sitting in the chairs you are trying to empty out. CURSES!

Stimulants and Xylazine

The use of stimulants and xylazine with a lot of fentanyl products further complicates the picture. Stimulant withdrawal can be kind of sneaky. Withdrawal in severe opioid addiction has a lot of symptoms: restlessness, anxiety, yawning, cramping, goosebumps, vomiting, diarrhea.

But stimulant withdrawal may not have as many physical symptoms. What it DOES do is mess with your mood and mind. A lot. I like to imagine that your brain is a tube of toothpaste where the toothpaste is made of the chemicals that help you feel ok/good. Methamphetamine forces your brain to release a lot more of those chemicals at once- it squeezes all the toothpaste out in one go. So, the next day you drop into depression/ irritability/anxiety and have no ‘toothpaste’ to help- you have to make more feel good chemicals and this takes some time (the worst withdrawal is the first 3-14 days). What this means is that if someone is withdrawing from fentanyl AND stimulants, their anxiety and irritability and feeling BAD is going to be EVEN WORSE. It was already hard enough to deal with ‘just’ bad opioid withdrawal and now we add on this extra weight?!

Xylazine has a similar problem. Xylazine is something mixed into opioids that many persons may not even know they are getting, much less how much they are getting. Withdrawal from xylazine results in high levels of agitation, anxiety, and possibly blood pressure changes. Furthermore, the buprenorphine is not going to help this part- buprenorphine doesn’t affect the same receptors that xylazine does. People withdrawing from these additional substances are going to have an even more difficult time waiting out the time between last use of the full opioid and beginning buprenorphine. They are more likely to jump the gun or to start taking other stuff (meth, coke, benzos) in addition to the buprenorphine that can affect the induction.

So, What Do We Do? See Part 2.

Footnotes

Note: Pharmacokinetics and pharmacodynamics which describe how drugs interact with receptors and the body processes is cool but complicated stuff. It is a lot more complicated and weird than I have described it here.↩︎

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@online{barnes2025,
  author = {Barnes, Erin},
  title = {Why {Is} {Getting} on {Buprenorphine} {So} {HARD} {These}
    {Days?!} : {Part} 1},
  date = {2025-11-13},
  url = {https://wakeforestid.com/posts/2025-11-13-why-is-getting-bup-so-hard-1/},
  doi = {10.59350/b7psw-sn910},
  langid = {en}
}

For attribution, please cite this work as:

Barnes, Erin. 2025. “Why Is Getting on Buprenorphine So HARD These Days?! : Part 1.” November 13. https://doi.org/10.59350/b7psw-sn910.

Farewell to Dr. Phil Lackey

Michael DeWitt — Fri, 03 Jan 2025 00:00:00 GMT

Dr. Phil Lackey is retiring from Wake Forest University School of Medicine after many years of service to the school and the community. True to his amazing character, he was on service during his final week of work. Dr. Lackey has been an instrumental part of expanding our activities in High Resolution Anoscopy(HRA) and has been a great mentor to many of our students, residents, and fellows. He completed his medical education at the University of North Carolina at Chapel Hill and completed his residency and fellowship in infectious diseases at the University of Alabama at Birmingham.

Thank you, Phil!

Dr. Phil Lackey

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@online{dewitt2025,
  author = {DeWitt, Michael},
  title = {Farewell to {Dr.} {Phil} {Lackey}},
  date = {2025-01-03},
  url = {https://wakeforestid.com/posts/2025-01-03-lackey-retire/},
  langid = {en}
}

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DeWitt, M. Farewell to Dr. Phil Lackey. (2025). at <https://wakeforestid.com/posts/2025-01-03-lackey-retire/>

In the news: Wake Forest faculty discusses H5N1 and ongoing research

Michael DeWitt — Tue, 10 Dec 2024 00:00:00 GMT

Dr Brinkley Bellotti was recently interviewed by the MIT Technology Review on the topic of H5N1 and its continued spread in dairy cows and poultry. In her interview, Dr Bellotti mentions that unmitigated spread of H5N1 in animals could lead to recombination events of the influenza virus which could allow for strains that could more easily infect humans.

Members of the Section on Infectious Diseases including the Infectious Disease Epidemiology and Applied Statistics Group (IDEAS) and their collaborators are working on a number of projects to help understand the spread of H5N1 and its impact on animal and human health and have published several preprints on the topic.

In the first preprint, they provide the first estimates of the basic reproduction number (R0) and other epidemiologic parameters for H5N1 in dairy cows and show that the virus can spread rapidly within herds¹. As part of this work, they developed a web application that allows users to simulate the spread of H5N1 in dairy herd.

Example of the H5N1 web application outputs allowing simulation of the spread of H5N1 in a dairy herd

In the second preprint, IDEAS members Michael DeWitt and Brinkley Bellotti along with Wake Forest University Biology Professor Nicholas Kortessis show that the time farms have to mobilize interventions is extremely limited, with outbreaks often being essential over by the time of detection². These findings have important implications for the design of effective surveillance and intervention strategies to control the spread of H5N1, suggesting that sensitive and frequent testing is likely needed to stop on-farm outbreaks and institute effective control measures to prevent farm to farm spread.

Figure 2 from DeWitt et al. (2024) showing the estimates values of the basic reproduction number (R0) and epidemic speed for H5N1 in dairy cows compared to other pathogens. Panel B shows the different surveillance strategies for detecting an ongoing outbreak within a farm.

Figure 3 from DeWitt et al. (2024) showing the results from the modeling study showing the time to detection of an outbreak and the time to control an outbreak for different surveillance strategies.

link photo credit: Cynthia Goldsmith/ Jackie Katz

References

Bellotti, B. R., DeWitt, M. E., Wenner, J. J., Lombard, J. E., McCluskey, B. J. & Kortessis, N. Challenges and lessons learned from preliminary modeling of with-in herd transmission of highly pathogenic avian influenza H5N1 in dairy cattle. 2024.08.06.606397 (2024). doi:10.1101/2024.08.06.606397

DeWitt, M. E., Bellotti, B. R. & Kortessis, N. Time is of the essence: Effectiveness of dairy farm control of H5N1 is limited by fast spread. 2024.11.15.623774 (2024). doi:10.1101/2024.11.15.623774

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@online{dewitt2024,
  author = {DeWitt, Michael},
  title = {In the News: {Wake} {Forest} Faculty Discusses {H5N1} and
    Ongoing Research},
  date = {2024-12-10},
  url = {https://wakeforestid.com/posts/2024-12-10-h5n1-updates/},
  langid = {en}
}

For attribution, please cite this work as:

DeWitt, M. In the news: Wake Forest faculty discusses H5N1 and ongoing research. (2024). at <https://wakeforestid.com/posts/2024-12-10-h5n1-updates/>

Antimicrobial Awareness Week 2024

Michael DeWitt — Mon, 09 Dec 2024 00:00:00 GMT

Antimicrobial Awareness Week 2024

U.S. Antibiotic Awareness Week (AAW) is observed each year from November 18-24. The purpose of AAW is to raise awareness of the importance of appropriate antibiotic and antifungal use and the threat antimicrobial resistance poses to people, animals, plants and in our environment. See the CDC for more at here. Based on a recent study, between 1990 and 2021, deaths from AMR decreased by more than 50% among children younger than 5 years but increased by over 80% for adults 70 years and older (see the study here).

The Wake Forest University School of Medicine Section on Infectious Diseases is dedicated to antimicrobial stewardship and we’re proud that our medical students are involved in communicating this message to the public. Antimicrobial stewardship is a key component of infectious disease control and prevention and part of the research mission of the Center for Microbial Ecology and Emerging Diseases.

Educational Materials

Check out the series of educational materials to help raise awareness about antimicrobial stewardship and resistance for Antimicrobial Awareness Week 2024. Check them out!

How does antimicrobial resistance spread?

What is one thing you wish more people knew about antimicrobial resistance?

How do animals contribute to antimicrobial resistance?

How can AMR awareness be included in medical student interactions with patients?

What are things in my everyday life to combat antimicrobial resistance?

How do we make smart decisions about antimicrobial use in resource-limited settings?

What are some of the things being done internationally to combat antimicrobial resistance?

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@online{dewitt2024,
  author = {DeWitt, Michael},
  title = {Antimicrobial {Awareness} {Week} 2024},
  date = {2024-12-09},
  url = {https://wakeforestid.com/posts/2024-12-09-aaw/},
  doi = {10.59350/8zyab-nm406},
  langid = {en}
}

For attribution, please cite this work as:

DeWitt, Michael. 2024. “Antimicrobial Awareness Week 2024.” December 9. https://doi.org/10.59350/8zyab-nm406.

Collabathon on Estimating Real-Time Epidemic Growth Rates

Michael DeWitt — Mon, 28 Oct 2024 00:00:00 GMT

Image credit: Epistorm

In September, Wake Forest University School of Medicine researchers Michael DeWitt and Brinkley Bellotti from the Section on Infectious Diseases attended the 2024 Epistorm Rt-Estimate Collabathon in Boston hosted by Northeastern University and the Network Science Institute. A collabathon (combination of “collaboration” and “hackathon”) is a multi-day event where practitioners and researchers come together to build software and form collaborations around one main idea. This collabathon included experts from public health agencies, industry, academia, and NGOs brought together to address a key challenge in public health: estimating real-time epidemic growth rates. Supported by the Centers for Disease Control and Prevention CFA Insight Net initiative, the collabathon focused on improving tools for estimating the real-time reproduction number: a key epidemiologic parameter that drives infectious disease control and prevention measures. Some of the major outputs of this workshop included new frameworks for testing modelling methods as well as new software packages to improve estimations.

Image credit: Epistorm

“I worked primarily in the Julia programming language to implement a package to handle primary censoring and truncation,” said Michael DeWitt. “This phenomenon occurs because we don’t know the precise moment when someone is infected and similarly delays in our detection lead to both censoring and truncation. Outbreak and forecasts that don’t take this phenomenon into account will be biased. By developing modular software in Julia, we can allow researchers and infectious disease modelers better, plug and play tools to forecast outbreaks.”

“Though many methods and tools to estimate Rt exist, techniques to evaluate model performance are still needed. Because the goal of real-time epidemic growth rate epidemics is prediction, the team I worked with began developing methods to validate Rt estimation methods with short-term prediction performance,” said Brinkley Bellotti.

Additional package development included summRt to help provide summary statistics for Rt estimates and RtEval to help evaluate the performance of Rt estimation methods.

This work continues to underline Wake Forest University’s School of Medicine’s commitment to research and innovation in microbial ecology and emerging infectious diseases.

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@online{dewitt2024,
  author = {DeWitt, Michael and Bellotti, Brinkley},
  title = {Collabathon on {Estimating} {Real-Time} {Epidemic} {Growth}
    {Rates}},
  date = {2024-10-28},
  url = {https://wakeforestid.com/posts/2024-10-28-epistorm-rt-collabathon/},
  doi = {10.59350/mcqh1-nvd03},
  langid = {en}
}

For attribution, please cite this work as:

DeWitt, Michael, and Brinkley Bellotti. 2024. “Collabathon on Estimating Real-Time Epidemic Growth Rates.” October 28. https://doi.org/10.59350/mcqh1-nvd03.

Medical Student 2024

Michael E. DeWitt — Thu, 24 Oct 2024 00:00:00 GMT

2024 was a busy summer for research in the Section on Infectious Diseases with medical students attending conferences in Australia, Atlanta, and participating in the summer Medical Student Research Program. Faculty and staff mentors are grateful for the hard work and dedication of the students and are looking forward continuing to support our students in their research endeavors.

Josh Manuel presents his project on resistance profiles for Neisseria gonorrhoeae

Mathieu Norcross presents his project on the evolutionary dynamics of Marbug virus

Jaden Seman presents his project on the evolutionary dynamics of Monkeypox virus and Mpox

Abson Mandola presents his project on assessing the impact of bot infliltration on an STI surveys

CDC’s STI Conference

Emily Ye and Taylor Ellis presented their poster titled “Campus Confidential: Decoding Sexual Health Education for College Students” at the CDC’s STI Conference in Atlanta, GA mentored by Dr. Candice J. McNeil with statistical support from Jennifer J. Wenner.

International Conference on Emerging Infectious Diseases

Abson Mandola presented his poster titled “Attack of the Bots: When an STI Survey Goes Viral” at the International Union Against Sexually Transmitted Infections Conference in Sydney, Australia mentored by Dr. Candice J. McNeil, Michael E. DeWitt, and Jennifer J. Wenner. Abson was also awarded a travel grant from the International Union Against Sexually Transmitted Infections to attend the conference.

Medical Student Research Program

The Medical Student Research Program is a compensated, 9 week, full-time summer research experience for rising 2nd year Wake Forest School of Medicine students. This program requires the students to select a mentor and a project from a list of approved projects or develop their own project with the support of a mentor. It includes authoring an NIH-style grant application and presenting their research at the Medical Student Research Day.

As part of the research experience in Infectious Diseases, members of the Section on Infectious Diseases mentor students in program and also held weekly “lunch and learn” style seminars which included discussions of their research along with talks conducted by invited speakers. These discussions included topics in:

biosecurity and biosurveillance
biostatistics that you should know
ecology and evolotion in infectious diseases
use of Artificial Intelligence in infectious disease research
rabies dynamics
vaccine field trials
and more!

Josh Manuel presented his poster “Patient Population-Specific Analysis of Neisseria gonorrhoeae Antibiotic Resistance Markers in Guilford County, North Carolina Using Whole Genome Sequencing” at the Medical Student Research day. This work was mentored by Jennifer J Wenner, Thomas F. Wierzba, John W. Sanders, Candice J. McNeil, and Michael E. DeWitt.

Musa Malik presented his posted “Epidemiological Trends and Bio-Surveillance of Tularemia: A Systematic Review” at the Medical Student Research day. This work was mentored by Michael E. DeWitt, John W. Sanders, and Thomas F. Wierzba.

Jaden Seman presented his poster “Apoxalypse: Evaluating the evolution and transmission dynamics of Mpox and its pandemic potential” at the Medical Student Research day. This work was mentored by Michael E. DeWitt, John W. Sanders, and Thomas F. Wierzba.

Mathieu Norcross presented his poster “Epidemic evolution: The changing epidemiological parameters of the highly virulent Marburg Virus” at the Medical Student Research day. This work was mentored by Michael E. DeWitt, John W. Sanders, and Thomas F. Wierzba.

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@online{e._dewitt2024,
  author = {E. DeWitt, Michael},
  title = {Medical {Student} {Research} in 2024},
  date = {2024-10-24},
  url = {https://wakeforestid.com/posts/2024-10-17-msrp2024/},
  doi = {10.59350/weysd-wwf85},
  langid = {en}
}

For attribution, please cite this work as:

E. DeWitt, Michael. 2024. “Medical Student Research in 2024.” October 24. https://doi.org/10.59350/weysd-wwf85.

IDWeek 2024

Michael E. DeWitt — Wed, 16 Oct 2024 00:00:00 GMT

The Section on Infectious Diseases and the Atrium Health Division of Infectious Diseases attended IDWeek 2024 in Los Angeles, CA and made a strong showing. Presentations and posters were presented by a variety of members including infectious diseases pharmacists, pharmacy residents, medical residents,infectious disease fellows, and infectious disease physicians.

Poster Presentations

Impact of a preoperative in-person assessment (PIPA) on Hip and Knee Replacement Surgical Site Infections (SSI) (Presenter: Anupama Neelakanta)
Exploring the association between penicillin allergy labels (PAL), beta-lactam utilization and surgical site infections (Presenter: Rupal Jaffa)
No targets, no problem: evaluation of patients with bloodstream infections without a molecular target detected by a rapid diagnostic assay (Presenter: Julie Williamson)
Differential impact of a penicillin allergy assessment tool on orthopedic surgical patients from areas of high social vulnerability (Presenter: Katie Passaretti)
Back to School! Improving Pharyngitis Care for School Students (Presenter: Lisa Davidson)
Evaluating the Impact of a Pharmacy Technician in an Antimicrobial Stewardship Program (Presenter: Lisa Davidson)
Shorter versus Longer Duration of Antibiotic Therapy for Gram-Negative Bacteremia (GNB) in Immunocompromised Patients (Presenter: Nicole Slain)
Antibiotic Inertia Occurs Frequently in Patients Admitted from the Emergency Department on Guideline Non-Concordant Therapy (Presenter: Adrianna Elashker)
Impact of Rapid Methicillin-Resistant Staphylococcus aureus (MRSA) Nasal Polymerase Chain Reaction (PCR) Screening on Duration of Vancomycin Therapy for Suspected Pneumonia (PNA) in Adult Patients Admitted to the Trauma Intensive Care (Presenter: Alex D. Taylor)
Real-World Efficacy of Fosfomycin for Treatment of Cystitis Caused by E. coli Versus Non-E. coli Bacteria With High Rates of FosA (Presenter: Ryan C. McCormick)
Palliative medicine consultation does not reduce antimicrobial use during end-of-life care (Presenter: Hanna Akula)
Monocyte Distribution Width (MDW) as a Biomarker to Distinguish Septic Shock with Bacteremia from Cardiogenic Shock (Presenter: Kaylie Goldner)

Oral Presentations

Three days of antibiotics for uncomplicated CAP: Ready for Prime Time? (Lisa Davidson)
Impact of Universal Nasal Decolonization with an Alcohol-Based Nasal Antiseptic (ABNA) Versus Mupirocin on Infection Rates and Antimicrobial Utilization in Patients (Pts) Admitted to the Burn Service (Alex D. Taylor)
Evaluation of Fecal Pharmacokinetics and Metagenomic Changes Following the Administration of Intravenous Omadacycline to Healthy Patients (Co-author: John C. Williamson)

Pre-meeting workshops

Exapnding your influence to Improve Antibiotic Use in Outpatient settings (Lisa Davidson)

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@online{e._dewitt2024,
  author = {E. DeWitt, Michael},
  title = {IDWeek 2024},
  date = {2024-10-16},
  url = {https://wakeforestid.com/posts/2024-10-16-idweek2024/},
  doi = {10.59350/kygvg-kc478},
  langid = {en}
}

For attribution, please cite this work as:

E. DeWitt, Michael. 2024. “IDWeek 2024.” October 16. https://doi.org/10.59350/kygvg-kc478.

International Field Epidemiology and Tropical Medicine in Peru

Michael DeWitt — Sun, 30 Jun 2024 00:00:00 GMT

Michael DeWitt attended the 2024 International Field Epidemiology and Tropical Medicine course in Peru hosted by the Universidad Peruana Cayetano Heredia and the EMERGE group(Unidad de Investigación en Enfermedades Emergentes y Cambio Climático) along with students and faculty from the University of Texas Medical Branch.

Members of the 2024 International Field Epidemiology and Tropical Medicine course in Peru

As part of this 10 day field experience, the group received training in epidemiology, entomology, diagnostics, field logistics, tropical medicine, and field epidemiology in Lima Peru. Then on the second day of the course, the group flew to Tumbes, Peru to continue their training. While in Tumbes, the group was introduced to the local public health infrastructure. Additionally, they conducted epidemiological investigations into a Dengue outbreak with the local health authorities. They also received training in many aspects into conducting a field investigation of an emerging pathogen including practical experience in:

Setting mosquitto traps and identification of mosquito species
Approaches to capture ticks and identification
Approaches to capture, indentify, and test rodents include bats
Setting up a field laboratory and data collection
Geospatial analysis of outbreak data

Collecting Sherman traps in a rice field in Tumbes, Peru

Identification of ticks under a microscope

Setting different types of mosquito traps

Setting mosquitos traps near a stream

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@online{dewitt2024,
  author = {DeWitt, Michael},
  title = {International {Field} {Epidemiology} and {Tropical}
    {Medicine} in {Peru}},
  date = {2024-06-30},
  url = {https://wakeforestid.com/posts/2024-06-30-international-field-epidemiology/},
  doi = {10.59350/h6nf1-8ww98},
  langid = {en}
}

For attribution, please cite this work as:

DeWitt, Michael. 2024. “International Field Epidemiology and Tropical Medicine in Peru.” June 30. https://doi.org/10.59350/h6nf1-8ww98.

Truly Trading One Drug for Another”

Erin Barnes — Fri, 05 May 2023 00:00:00 GMT

Truly Trading One Drug for Another

‘You are just trading one drug for another’ is a common refrain in the world of substance use disorders. And frequently there is truth to it. Let’s take a look at what and why this is.

First, remember that addiction is not defined by WHAT you use but HOW you use and what the use does to your life and the life of your loved ones. Some persons come to realize that they have a problem with a certain substance- maybe an opioid, maybe alcohol, maybe cocaine. Somehow it has gone from being something they enjoyed and felt in control of to something that just keeps pulling them away from the person they want to be, life they want to have, and their loved ones.

Figure 1

So a sneaky thought appears: what if we stop using THIS thing and try to use this OTHER thing, which we DON’T have a problem with, INSTEAD? Won’t that fix the problem?

This makes sense at first glance- it is someone trying to regain control by moving from something they recognize as a problem to something that they perceive to be less dangerous and less addictive. But there are problems with this approach. First, remember, addiction is a biopsychosocial disease. A person’s biology, psychology, and environment are all likely the same when they move from one substance to another. Biology DEFINITELY is. By virtue of already having one substance use disorder they clearly have the genes that predispose to addiction. And while SOME genes seem to make persons more inclined to have issues for a SPECIFIC substance, a LOT of the genes seem to make one prone to addiction to ANY of the substances—all the different substance share the same common addiction problem genes¹. In addition all the drugs of abuse have a common end pathway: they give that dopamine rush.

Figure 2

So all we are doing is getting to the same ends by a different means; what we still want, NEED, is that dopamine. The brain of one with a substance use disorder now processes rewards and negative consequences in a way that keeps the substance use and craving going. So: same person, same situation, same genes, now already have a brain wired to let something get out of control…this does not sound like it will go well. I tend think of this as having built a racetrack in your brain and now it doesn’t care what kind of horse is brought in to run on it: it is going to let it RUN.

Along with all that biology and brain wiring, we have also had a lot of time using a drug to manage our emotions and moods. The more severe an addiction becomes, the more an automatic loop develops:

That behavioral loop has now become wired into our brain pathways as well. It is automatic- it happens without even having to think about, faster than the speed of conscious thought, and sometimes without even realizing it. You just all of a sudden notice you are craving more. So now even if we change what the substance is we are reaching for, we are still going to end up reaching for it to fill the same holes the old substance filled. The substance is still being used as the main coping strategy. It is how we feel better after a hard day, how we celebrate good things, how we feel/share connection with people in our social circle. It is still filling an outsized role in our life.
And it is preventing us from doing the work to figure out what healthy behaviors and relationships could be used to fill those gaps instead.

Because of all of these things, the new substance becomes a problem over time-it tends to escalate. Even worse, its use increases the chances that we fall back to the OLD substance…and now we have problems with that old substance AND this new substance! After all, mood altering substance like meth, cocaine, opioids, and alcohol all tend to lower a person’s inhibitions and prevent making clear/rational choices. They make that little voice shouting ‘No! Stop! Don’t Use That! You Know it Doesn’t Go Well!’ quieter and the voice saying ‘Just this once it is ok’ to get louder.

I frequently see persons who have tried to switch from heroin/fentanyl to the stimulants meth/cocaine. They believe these drugs will be safer and won’t be a problem for them since it is a different drug type. Other people switch from the drug cocaine to meth. Or stop all drugs but then notice they seem to be drinking more (or gambling more or online shopping more or binge eating sugar more-dopamine is dopamine). The intentions can be good. The realization and admitting a certain substance is a problem is good. It is just that trying to trade one dangerous and addictive substance for another dangerous and highly addictive substance is doomed to fail. Cross addiction is sort of wanting to have your cake and eat it too: we want to continue to be able to use a substance to help us cope, not seek care, not have to change our friends/living situations/way of thinking about the world, not have to face some hard truths and harder choices…but we want to be back in control. It just doesn’t work.

This cross addiction concept explains the interesting fact that persons who continue to smoke are more likely to relapse back to things like heroin!!!!!²

Those things seem on the surface to have _nothing to do with each other. BUT. The nicotine molecule is keeping some of those addictive brain circuits open and active while also providing extra slugs of dopamine. Let’s also think about when people smoke- when it is a certain time of day or event (like mealtimes or morning coffee) or when they are stressed out or when others around them smoke. The link of increased craving and reaching for a cigarette automatically when certain things/situations/feelings occur- using a chemical to control our emotions and selves- is the same behavioral link to ‘worse’ substances. It is a little toe sticking into a door we are trying to slam shut.

Historically, and still in some clinics, this understanding of how cross addiction sabotages people and its dangers is why persons would be kicked out of treatment for having urine tests positive for anything (including marijuana). This was done even if someone was engaging in and improving in care and/or staying away from the substance that originally brought them to treatment. It was done because of this understanding that one drug changes to another which places you at risk to fall back to the original drug AND the new drug. The medical field has increasingly moved away from this punitive type of treatment as we come to better realize that being engaged in care and helping people take small steps towards health on their own timeline is a better strategy to improve lives and health than suddenly cutting people off from care and leaving them on their own.

Please read the previous blog posts (here and here) about how prescribed addiction treatment medications affect the brain differently than these other substances of abuse and occur in a different environment than substances of abuse and thus are NOT the same as cross addiction.

In summary it is easy to accidentally or intentionally start using more of one substance when trying to stop using a DIFFERENT substance to which one is addicted. In the end, though, it doesn’t work and can frequently make things worse. Staying vigilant against slipping into cross addiction is important at all stages of recovery.

Footnotes

Hatoum, A.S., Colbert, S.M.C., Johnson, E.C. et al. Multivariate genome-wide association meta-analysis of over 1 million subjects identifies loci underlying multiple substance use disorders. Nat. Mental Health 1, 210–223 (2023). https://doi.org/10.1038/s44220-023-00034-y↩︎
NIDA. 2018, May 31. Cigarette Smoking Increases the Likelihood of Drug Use Relapse. Retrieved from http://nida.nih.gov/news-events/nida-notes/2018/05/cigarette-smoking-increases-likelihood-drug-use-relapse on 2023, April 5↩︎

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@online{barnes2023,
  author = {Barnes, Erin},
  title = {Truly {Trading} {One} {Drug} for {Another”}},
  date = {2023-05-05},
  url = {https://wakeforestid.com/posts/2023-04-05-cross-addiction/},
  doi = {10.59350/s9xha-k8q95},
  langid = {en}
}

For attribution, please cite this work as:

Barnes, Erin. 2023. “Truly Trading One Drug for Another”.” May 5. https://doi.org/10.59350/s9xha-k8q95.

Why Medication for Opioid Use Disorder Is Not “Trading One Drug For Another: Part 2”

Erin Barnes — Fri, 13 Jan 2023 00:00:00 GMT

What is happening when an addictive substance is used in the brain?

Figure 1

Every addictive substance acts on a chemical in the brain called dopamine. Those drugs that release a LOT of dopamine and act VERY quickly tend to be more addictive. This is because dopamine helps our brains decide what gives us pleasure, what is rewarding, and what we should be paying attention to in the world. It is what causes feelings of satisfaction and pleasure when we connect with friends, do an activity we enjoy, achieve a goal, eat, or love someone. These things feel good and so we want to do them more. This is beneficial to humans as these things are essential to human survival: building communities with others, seeking out food, and forming families helped the human race survive. BUT. The amount of dopamine released by the drug is WAAAAAYYYY more than what is released by these other activities. Our brain interprets this to mean this drug must be WAAAAAYYY better and more important than all those other things. If the drug continues to be present, over time the brain literally re-wires itself. This ability for brains to change over time is called ‘brain plasticity’. Now the brain is constantly seeking signs of the drug and figuring out how to get the drug and thinking about the drug. Additional changes that affect rational thinking, make one more impulsive, and cause chronic stress also happen. The longer the drug is used and the more of it that is used, the more these circuits strengthen. And those other, normal things no longer really cause the same level of pleasure response anymore. You can’t feel the drop of water when you are drowning in the ocean.

Figure 2

When someone addiction to opioids suddenly stops using the drug then problems develop. The brain has literally changed itself to accommodate this drug being present all the time. It has now become so changed that the person feels unwell, ill, anxious, and depressed when the drug is not there. In the later stages of addiction the drug no longer really even results in a ‘high’ when used; persons at this stage are instead using just to feel somewhat normal and not sick. The first few days or weeks the after abruptly stopping use will result in days to a couple weeks of feeling very physically ill with nausea, vomiting, severe aching pains, restlessness, feelings of skin sensations, and more. This is the acute withdrawal period. However, even once this period recedes, it takes months to years for the brain to re-wire itself. The feelings of anxiety, depression, lack of motivation, and altered sleep last weeks and months and more. The brain also still is trying to think about and search for the drug so cravings can remain; it takes a lot of time for this to fade. This is why persons with severe addiction relapse weeks and months or even years after a ‘detox’ when physical withdrawal has ended.

And that is where the medicines come in. The goal of the medicines is to help stabilize the changes in the brain circuits that have occurred with moderate to severe addiction so that the person is better able to feel, think, and function normally. It then allows them to participate in counseling, develop new coping strategies, get jobs, and heal relationships. All of those things help the brain to change itself back into a healthy brain. The three medications used to treat moderate to severe opioid use disorder are methadone, buprenorphine, and naltrexone.

First let’s look at Naltrexone. Naltrexone works by blocking the opioid receptor. An opioid has to bind to the receptor for any changes or effects to happen. If it now cannot get to the receptor, nothing will happen when one takes an opioid! Knowing this up front makes persons less likely to try to use a drug and even if they suffered a lapse they would be unlikely to feel much. This medication is not addictive and so there is no withdrawal if one suddenly stops taking it. It is not a controlled substance and so can be given in almost any location. It comes as a month long injection which can be helpful in sticking to the treatment plan since you don’t have to remember or commit to taking a pill every day.

And that is where the medicines come in. The goal of the medicines is to help stabilize the changes in the brain circuits that have occurred with moderate to severe addiction so that the person is better able to feel, think, and function normally. It then allows them to participate in counseling, develop new coping strategies, get jobs, and heal relationships. All of those things help the brain to change itself back into a healthy brain. The three medications used to treat moderate to severe opioid use disorder are methadone, buprenorphine, and naltrexone.

First let’s look at Naltrexone. Naltrexone works by blocking the opioid receptor. An opioid has to bind to the receptor for any changes or effects to happen. If it now cannot get to the receptor, nothing will happen when one takes an opioid! Knowing this up front makes persons less likely to try to use a drug and even if they suffered a lapse they would be unlikely to feel much. This medication is not addictive and so there is no withdrawal if one suddenly stops taking it. It is not a controlled substance and so can be given in almost any location. It comes as a month long injection which can be helpful in sticking to the treatment plan since you don’t have to remember or commit to taking a pill every day.

There are downsides, however. If one was to be in an accident or break a leg it would be very difficult to treat that pain because the naltrexone is blocking all those opioid receptors. You must carry a medical alert bracelet or medical alert card so that in such a situation the doctors would know they had to treat your pain differently. Also because of this, this medication does not work as well for those with chronic pain in addition to addiction. Most importantly, this medication is essentially the same as Naloxone (Narcan) which is used in overdose reversal. It pushes any opioid present in the system off the opioid receptor and takes its place. This results in withdrawal. This means you have to be AT LEAST 7 days without any opioids AT ALL in your system before you take this shot or it will push you into severe and irreversible withdrawal. Persons with severe addiction can have a hard time getting that 7 days or more with zero use.

Methadone can fully activate the opioid receptor just like heroin, oxycodone, and other opioids. The very key difference is that it takes a loooooooonnnngggg time for the methadone to kick in fully- well over 24 hours- and it lasts in the system for days. This means persons do not really get a rush or high when they take it for treatment. It can also be more helpful for those with both chronic pain and addiction; it is used in those without addiction as a treatment for severe chronic pain. Imagine the opioid receptor as a radio with a volume dial. Heroin turns the volume up all the way to 100% VERY quickly. Methadone turns the volume up to 100% as well but it does it verrrrryyyy sloooowwwwllly.

The downsides to methadone reflect the dangers of other opioids: you withdraw from it if you suddenly stop taking it and if you take too much it could stop your breathing, cause an overdose, or alter your heart rhythm. For that reason methadone is very tightly controlled to keep people safe. It can only be dispensed by regulated methadone clinics for the treatment of addiction. One generally has to go daily to this clinic to receive the medication; this can make it difficult for those who lack transportation or live in rural areas far from a clinic. Public methadone clinics may cost as little as 6 dollars a day, however, and usually have staff to help with psychiatric diseases and difficulties with housing, joblessness, and more which still make them one of the most effective treatment options for those with severe substance use disorders.

Buprenorphine is in between methadone and naltrexone. It can turn the opioid receptor on half-way. This means it has enough activity to stabilize the brain but it has a ‘ceiling effect’. This ceiling makes it very unlikely someone with a substance use disorder using it for treatment would be able to overdose or have their breathing stopped by this medication. Those cases where overdoses have been reported in such persons have found other sedating substances were mixed with the buprenorphine like alcohol, gabapentin, and benzodiazepines. Because it is safer than methadone, buprenorphine can be prescribed in regular doctors’ clinics which makes it easier for people to access. Buprenorphine also is very effective for pain and is used in general medicine separately as a pain treatment medication. It is a controlled substance, however, and addictive so you would withdraw from it if you suddenly stopped using the medication.

Figure 3

One of the main downsides of buprenorphine is it can be tricky to get started on the medication. Though buprenorphine is only turning the receptor on half-way, it binds the receptor tighter than any other opioid. This means that if another opioid is present like heroin, the buprenorphine will come in, push the heroin off the receptor, and take its place. Since the buprenorphine doesn’t turn the receptor on as much as the heroin, this will cause withdrawal symptoms. This means that persons have to wait a certain amount of time after their last dose of a regular opioid to start the buprenorphine medication. They must be feeling at least some moderate withdrawal before they take the first dose of buprenorphine or they will feel WORSE rather than better. The positive side of this is that if someone takes a regular opioid after taking their buprenorphine, they will not feel that other opioid they took nearly as strong. It blunts the high of that drug similar to how naltrexone does which prevents the person from having positive feedback from the drug.

Imagine the opioid receptor as a radio again: Buprenorphine turns the volume up only half-way to 50% unlike methadone and heroin which turned the dial up all the way to 100%. Now imagine that you have three hands going to adjust the volume of the radio: heroin, methadone, and buprenorphine. Buprenorphine will always slap those other hands out of the way and grab the dial, turn it to 50%, and then it will NOT let go. If the heroin hand was already there holding the dial at 100% volume, buprenorphine will push its hand out of the way, grab the volume dial, and turn it down to 50%. That sudden drop from 100% to 50% causes withdrawal.

No one is identical. The right medication and the dose of the medication will depend on the person, their situation, their use history, and more. These medications all have extensive evidence showing that they are more effective than counseling alone at keeping those with moderate to severe substance use disorder in treatment and in better health.

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@online{barnes2023,
  author = {Barnes, Erin},
  title = {Why {Medication} for {Opioid} {Use} {Disorder} {Is} {Not}
    “{Trading} {One} {Drug} {For} {Another:} {Part} 2”},
  date = {2023-01-13},
  url = {https://wakeforestid.com/posts/2023-01-13-medication-for-opioid-2/},
  doi = {10.59350/g7dhw-37s72},
  langid = {en}
}

For attribution, please cite this work as:

Barnes, Erin. 2023. “Why Medication for Opioid Use Disorder Is Not ‘Trading One Drug For Another: Part 2’.” January 13. https://doi.org/10.59350/g7dhw-37s72.

Why Medication for Opioid Use Disorder Is Not “Trading One Drug For Another”

Erin Barnes — Thu, 05 Jan 2023 00:00:00 GMT

Part 1: Defining Addiction

A 22 year old male is sitting in bed, pale and mildly short of breath. He is recovering from a surgery on his heart valve which was badly damaged by infection he developed from injecting drugs intravenously. His pain is being treated with a combination of medications including buprenorphine. He feels it is working well and he is not having any withdrawal which he considers a small miracle. However in discussing his ongoing healthcare, he notes that he does not want to continue on buprenorphine after this hospital stay because ‘he does not want to trade one drug for another’. He intends to stop his use because he has now had a wakeup call and does not believe he needs anything else. He has tried to stop in the past without success….but now he feels absolutely sure…he’s got this.

Figure 1

The above is a fictional example of real conversations I have had with innumerable patients. This phrase of ‘replacing one drug with another’ is a common refrain echoed by groups as variable as Uncle Joe at Thanksgiving, politicians, the NA meeting counselor in recovery, and those in active addiction seeking treatment. It is even uttered by physicians. And repetition of this inaccurate statement is deeply damaging. It prevents those seeking recovery from utilizing all of the tools available to them in their recovery…the very tools shown over and over again to be the most effective. And it makes my eye twitch with anger.

In order to understand why medications like methadone and buprenorphine used for the treatment of addiction are NOT just trading one drug for another, we must look closely at what addiction is and what the medications do.
Medical professionals use sets of symptoms to help diagnose substance use disorders. The most recent criteria are in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (aka the DSM-5) which came out in 2013. There are different entries for each substance including alcohol but if you look at the criteria for each substance…you will see that the criteria are essentially the same for each one. And that right there is our first clue that the drug alone is not what defines a substance use disorder. ‘Dependence’ alone is not what makes a substance use disorder.

To better understand, let’s look at some vocabulary:

Hazardous use: Using a drug (or drinking alcohol) in a pattern which increases the risk for health problems Harmful Use: The drug or drinking IS or HAS caused health problems Substance Use Disorder: Ranges from mild to severe based on how many of the symptoms (criteria) the person has. In simplified language the criteria are that in the last 12 months the individual has:

Figure 2

Used more of the drug or used over a longer period than was intended
Wants to or has tried to cut down/stop the drug and just can’t seem to
Spends a lot of time getting, using, or recovering from the drug
Craved the drug
Been unable to do what needs to be done at home, at work, and/or at school
Keeps using even when it keeps causing problems in relationships
Given up or lessened hobbies or social/job roles because of the drug use
Continued using the drug in hazardous situations
Continued using despite knowing of a health problem caused or worsened by the drug use 10.* Physical tolerance is present meaning more drug must be taken over time to get the same effect 11.* Withdrawal is present if one suddenly stops taking the drug

If you have 2-3 of these criteria it is consistent with mild opioid use disorder, 4-5 with moderate disorder, and 6 or more is consistent with severe opioid use disorder. Symptoms number 10 and 11 are sometimes referred to colloquially as ‘dependence’ but this term is no longer recommended. More importantly, symptoms number 10 and 11 don’t even COUNT for opioids if you are taking them under appropriate medical supervision and as prescribed. This is because even an 80 year old man taking 10mg of oxycodone a day for his arthritis pain who never misuses it, has no cravings, no signs of an addiction, will still likely need medication increases one day as the medication becomes less effective (Criteria 10) and will become suddenly ill and go into withdrawal if the medication is suddenly stopped (Criteria 11). Withdrawal IS NOT THE SAME AS ADDICTION.

The Opposite.

Part 2: How Opioid Treatment Medications Do not Meet Criteria for Addiction

So…. What if you are receiving a medication like buprenorphine or methadone from a physician and using it as intended for treatment of your opioid use disorder? How are we doing now on meeting those criteria above? Well you WILL experience withdrawal if you suddenly stop taking this medication (Criteria 11)… but as we just noted, tolerance and withdrawal don’t count when taking a medication as prescribed. So that’s out. Cravings for other drugs may be present but usually fade over time and generally it is not these medications that are craved but the heroin or opioids that originally caused the use disorder. And I guess if we wanted to be SUPER technical we could say some people might still fight with loved ones over using this medication…but now these fights are often because the loved ones question if the person ‘really needs’ the medication and says they are ‘just trading one drug for another’.

Figure 3

What about those other criteria. What we see that what people on these medications are doing is working on developing new and healthy coping skills. They reach back out to friends and family to repair relationships. They seek work and get jobs. They go back to school. They go to doctors’ visits and counseling visits and get healthier. THEY. STAY. ALIVE. The drugs being used in addiction take a person away from their interests, away from their values, away from their loved ones, away from themselves. The medications in treatment and recovery are helping to stabilize the changes in the brain so that they can return to these things, return to these people, return to themselves. THIS IS LITERALLY THE OPPOSITE OF ADDICTION.

Figure 4

These medications are not panaceas. They alone do not solve substance use disorders. But the evidence is VERY clear that for more severe addiction the medications are SIGNIFICANTLY more likely to keep someone in recovery, engaged in care, and alive. So our theoretical patient absolutely can decide he wants to stick with counseling and social programs alone. But if he decides not to be on medication it should be because he truly understands the risks and benefits of it and has decided it is not consistent with his goals, needs, or abilities…not because of a snappy catchphrase and fear of judgement from others.

Note to readers: A future post on cross-addiction (truly trading one drug for another) will eventually be coming

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@online{barnes2023,
  author = {Barnes, Erin},
  title = {Why {Medication} for {Opioid} {Use} {Disorder} {Is} {Not}
    “{Trading} {One} {Drug} {For} {Another}”},
  date = {2023-01-05},
  url = {https://wakeforestid.com/posts/2023-01-4-medication-for-opioid-use-disorder/},
  doi = {10.59350/s9xha-k8q95},
  langid = {en}
}

For attribution, please cite this work as:

Barnes, Erin. 2023. “Why Medication for Opioid Use Disorder Is Not ‘Trading One Drug For Another’.” January 5. https://doi.org/10.59350/s9xha-k8q95.

Addiction As a Biopsychosocial Disease

Erin Barnes — Sat, 05 Nov 2022 00:00:00 GMT

There are many arguments in academic circles about how to frame and think about addiction. In my personal experience, I find one of the most helpful ways to think of addiction is the classic framework that views addiction as a ‘biopsychosocial’ disease. I like this framework because it helps us identify and then examine all of the key ingredients that go into forming and maintaining a substance use disorder. That then provides us with multiple different paths to treatment.

Bio

Figure 1

Addiction is a biologic disease. Studies show that genetics explain 30-50% of an individual’s addiction. This is because we have found that there are MANY genes that influence how the brain releases the chemicals that drive addiction and how our brain responds to those chemicals. All of these changes combine together to make a person’s risk of developing a substance use disorder more or less likely. Not only does biology affect the likelihood that one would develop addiction, it also plays a role in reinforcing addiction…the likelihood that an addiction will continue to grow and worsen. The brain and body progressively change their structure and pathways to adapt to having the substance around. This leads to physical dependence, tolerance, withdrawal, and cravings which can then lead to increased use.

Psych

Figure 2

Addiction is a psychologic disease. Decades of evidence show that those with other mental health disorders are more likely to develop substance use disorders. This includes mood disorders like depression and anxiety to disorders that involve impulsivity such as ADD to conditions which can impact how persons perceive and respond to the world such as PTSD and schizophrenia. For some the substance becomes a way to escape from the stress and negative feelings that come with these conditions. These conditions may also contribute to characteristics that make substance use more likely to occur like a tendency to be impulsive, adrenaline/novelty seeking, etc. As substance use continues, the drug use itself causes mood changes such as anxiety and depression and impulsivity. Severe use can increase the risk of traumatic experiences with resulting PTSD. We now have the original psychiatric condition compounded by substance induced psychiatric conditions and this can lead to a spiral as the person tries to use more to cope with an increasing amount of negative feelings and emotions.

How do we use this knowledge?

We can now see how there are factors at the biologic, psychologic, and societal level that can make someone more or less likely to develop a substance use disorder. Each of these factors is then in itself influenced by the ongoing use of the substance. And each of these factors is related to the other. Biology and environment influence the development of psychologic disorders. Your psychology and mental health will impact those around you and your environment. Environmental/sociologic conditions change a person’s genes and DNA through epigenetics. None of these 3 factors can be isolated from the other.

Figure 4

This means that the most effective treatments will be those that address all three realms together: medications for the biologic aspects, medications and counseling for the psychologic aspects, and strong community programs and supports for the sociologic aspects. We also can use now understand why what works for one person may not work for another. Some persons with severe addiction may be able to stop ‘cold turkey’ while others cannot. Perhaps their genes were different. Or their psychology was different. Or their social environments were different. Maybe ALL of it was different.

Addiction is a disease that ranges from factors as small as a strand of DNA to as large as the cities and states in which we live. Each individual with a substance use disorder will be their own unique mixture of factors. We must continue the work to bring together treatments that can meet this range of needs and ensure that all persons have equal access to the medication, counseling, and social investments that best treat substance use disorders. Unfortunately, most US treatment sites can only treat one facet at a time and few to none can treat all three. It is why if you google ‘addiction treatment’ you may find tons of places pop up. But how many are only group counseling? How many can prescribe medications? How many can prescribe medications to you even if you have no insurance and are poor? How many have case managers helping file forms for low income housing, food stamps or can link you to GED programs? Until we stop trying to piecemeal the treatment and move forward together, we are all going to continue to fail those who need our help the most.

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@online{barnes2022,
  author = {Barnes, Erin},
  title = {Addiction {As} a {Biopsychosocial} {Disease}},
  date = {2022-11-05},
  url = {https://wakeforestid.com/posts/2022-11-05-addiction-as-a-biopsychosocial-disease/},
  doi = {10.59350/8tjrv-psh93},
  langid = {en}
}

For attribution, please cite this work as:

Barnes, Erin. 2022. “Addiction As a Biopsychosocial Disease.” November 5. https://doi.org/10.59350/8tjrv-psh93.

A Case Series of Serratia Marcescens in Persons Who Inject Drugs

Erin Barnes — Fri, 04 Nov 2022 00:00:00 GMT

Our second year Infectious Diseases fellow Dr. Cook presented this work on serratia endocarditis at 2022 IDWeek in Washington DC! Here at AHWFB Health we have been seeing an increasing number of infections of the heart due to the bacteria Serratia marcescens in persons who inject drugs. This is a reddish-orange bacteria commonly found in soil and water that is not a usual cause of serious infections. The biggest series of cases of heart infections caused by this organism published in the literature in California in the 1970s but few reports have followed since. This bacteria belongs to a family of bacteria (the Gram Negative bacteria) that are less likely to cause heart infections than bacteria such as Staphylococcus aureus or Streptococci (the Gram Positive bacteria) which are skin and mouth. These latter bacteria are still the most common cause of heart infections in both persons who do and do not inject drugs. We do not know what has caused this increase in Serratia heart infections but we believe that other centers in the Southeast are seeing similar increases. We look forward to collaborating with our infectious colleagues across the nation to unravel how and why these infections are occurring and how best to treat them!

Image credit: https://en.wikipedia.org/wiki/Serratia_marcescens#/media/File:Serratia_marcescens.jpg

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@inproceedings{cook2022,
  author = {Cook, Julia and B. Anderson, Matthew and Barnes, Erin},
  title = {A {Case} {Series} of {Serratia} {Marcescens} in {Persons}
    {Who} {Inject} {Drugs}},
  booktitle = {IDWeek2022},
  date = {2022-11-04},
  url = {https://wakeforestid.com/posts/2022-11-04-serratia/},
  doi = {10.5281/zenodo.7277381},
  langid = {en}
}

For attribution, please cite this work as:

Cook, Julia, Matthew B. Anderson, and Erin Barnes. 2022. “A Case Series of Serratia Marcescens in Persons Who Inject Drugs.” IDWeek2022, accepted, November 4. https://doi.org/10.5281/zenodo.7277381.

An Introduction to the Intersection of Infectious Diseases and Addiction

Erin Barnes — Fri, 12 Aug 2022 00:00:00 GMT

Infectious diseases and addiction

One of the most frequent questions I am asked is, “What does infectious diseases have to do with addiction!? How did you get into this?” I began my fellowship in infectious diseases at AHWFB in Winston Salem, NC in 2014. At this time prescription opioid prescribing was still near its peak. The first person I saw was a 22 year old male who died of injection drug use associated infection of the heart (endocarditis). And from that day on my service was FULL of very young people suffering from infections of the heart and bones due to injection drug use. I had just completed my internal medicine training in Richmond VA only 4 hours away, but I had never seen anything like this. At this time, the majority were injecting a substance called oxymorphone, which was also new to me- this prescription opioid was not as widely prescribed as some comparators and its illicit use was much more regionally variable. That is a good thing because it was found that an ingredient in the 2012 tamper-resistant version of oxymorphone resulted in Very Bad Things if injected. It caused a condition that destroyed the kidneys and the platelets that help blood to clot in addition to the person being sick from the infection.

Not only was the number of these cases shockingly higher than they had been in my previous location, these patients were SICK. What I had generally been taught in my medical training could be distilled as ‘this type of endocarditis is not nearly as bad as ‘regular’ endocarditis and they should mostly do fine’. The medical reports and studies of previous cases also taught that racial minorities, males, and urban settings would have the highest rates of this otherwise rare infection.

So I was confused. None of this matched what I was seeing. My patients were predominately White and I had as many females as males. Winston Salem was more rural than my previous center but I saw much more injection drug use here. And these patients were definitely NOT fine. Many of them died. Many of them stayed in the hospital for weeks at a time receiving intravenous antibiotics but we had no addiction medicine care. We then sent them back to rural and under-resourced areas where relapse to substance use and subsequent infection were common. And then I watched more of them die.

These experiences changed the direction of my vocation and life. I became interested in learning more. What had changed that this disease was now so much more common and looked so very different? At this time the reports on the rising rates of substance use disorder associated were just beginning to be published so for all I knew this was unique to my location or maybe even the oxymorphone. I pursued additional training in research methods to better understand how to ask and answer questions about this population. But even more than curiosity I felt frustration. I was spending weeks treating an infection while doing nothing to impact the root cause. The number one rule of infectious diseases treatment is that source control is the most important thing!

This population tends to be uninsured, have limited access to transportation, and has multiple socioeconomic barriers. This limited their ability to enter substance use treatment even before they became sick. And now that they had such severe physical illnesses, many existing substance use treatment programs were not equipped to handle their complex needs. Some of these patients had not wanted to stop their use until this happened. I now had persons in a unique window of time where someone was vulnerable and truly seeking help…and I did not know how to give it!

And so…I decided to try. Despite being afraid to do something I had not been systematically taught in medical school or seen other physicians model first, I embraced the thought that surely I couldn’t be worse than nothing and became waivered to prescribe buprenorphine. At this same time Dr. Ernesto Aranda completed his infectious diseases fellowship and became the first addiction medicine fellow at AHWFB. Together we began a combined clinic which sought to capitalize on this time of crisis and potential change. Our goal was to catch these patients on discharge from the hospital to continue care for their infectious diseases, provide basic primary care services, and administer medication assisted treatment with buprenorphine for opioid use disorder. We were joined by Dr. Kelsie Pierre 2 years later who did an additional year of addiction medicine training following completion of her infectious disease fellowship.

We screen for sexually transmitted infections, hepatitis, and HIV. We treat sexually transmitted infections and hepatitis C. We vaccinate against hepatitis A and B and more. We provide care for members of our HIV clinic population who also suffer from opioid use disorder. Since this clinic endeavor started we have suffered heartbreak, self-doubt, innumerable logistical challenges, ethical and moral dilemmas, and joyful celebration of victories large and small. It is the most simultaneously challenging and rewarding aspect of medicine I have ever experienced.

The overlap between the care of infectious diseases and addiction medicine is startling large and is expanding all the time. The same work force of physicians who rallied to treat the disease of HIV when it was complex, ostracized, and misunderstood is uniquely placed to join the fight against substance use disorder. I look forward to exploring these intersections, challenges, and unresolved questions with you in coming posts.

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@online{barnes2022,
  author = {Barnes, Erin},
  title = {An {Introduction} to the {Intersection} of {Infectious}
    {Diseases} and {Addiction}},
  date = {2022-08-12},
  url = {https://wakeforestid.com/posts/2022-08-11-an-introduction-to-the-intersection-of-infectious-diseases-and-addiction/},
  doi = {10.59350/jzfmb-a1w05},
  langid = {en}
}

For attribution, please cite this work as:

Barnes, Erin. 2022. “An Introduction to the Intersection of Infectious Diseases and Addiction.” August 12. https://doi.org/10.59350/jzfmb-a1w05.

Estimated Monkeypox Susceptible MSM Population in North Carolina Review

Michael DeWitt — Thu, 11 Aug 2022 00:00:00 GMT

How many vaccines do we need?

The 2022 global outbreak of monkeypox virus has been predominantly in gay, bisexual, and other men who have sex with men (MSM). A group of researchers in the Section on Infectious Diseases and the Division of Infectious diseases sought to answer the question of how many MSM could be in the state of North Carolina as well as estimate the proportion of those who had more than one sexual partner in the last year, individuals who represent the highest risk for infection and onward transmission of monkeypox. Understanding these figures will aid in the public understanding of how many vaccines are needed and how to prioritize the limited supply of vaccines.

Key findings

Researchers found that at a minimum roughly 15,700 sexually active MSM in North Carolina should be offered vaccines to reduce the risk of monkeypox infection and to blunt transmission chains, which is unfortunately far greater than the current vaccine supply in North Carolina. Additionally, about 49,400 vaccines should be offered to other members of the MSM community in North Carolina to reduce their risk of infection. These estimates do not include other occupations where there is a high risk for monkeypox exposure including laboratory personnel and front-line healthcare workers with dedicated public health response roles where exposure could rapidly increase with increasing prevalence. Monkeypox is an infectious disease and can infect anyone.

Study limitations

The basis for estimating sexual activity and practice relies on the accuracy of responses to the NHANES survey. Because of violence and stigma against MSM, respondents may not be inclined to answer questions about sexual practices, thus these estimates could underestimate the true number of MSM or the number of persons exposed to monkeypox.
The NHANES survey is a national level so inferences at the subnational level may have much larger error due. These limitations are more likely to underestimate the eligible population for vaccination, suggesting significant expansion of vaccine supply will be needed in order to contain the current monkeypox outbreak.

Read the full report

The full pre-print is available on medRxiv.

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BibTeX citation:

@online{dewitt2022,
  author = {DeWitt, Michael},
  title = {Estimated {Monkeypox} {Susceptible} {MSM} {Population} in
    {North} {Carolina} {Review}},
  date = {2022-08-11},
  url = {https://wakeforestid.com/posts/2022-08-11-estimated-monkeypox-susceptible-msm-population-in-north-carolina/},
  doi = {10.59350/pj19b-p0w43},
  langid = {en}
}

For attribution, please cite this work as:

DeWitt, Michael. 2022. “Estimated Monkeypox Susceptible MSM Population in North Carolina Review.” August 11. https://doi.org/10.59350/pj19b-p0w43.

Tracking Monkeypox Cases in North Carolina

Michael DeWitt — Wed, 27 Jul 2022 00:00:00 GMT

Tracking the Outbreak

Learning lessons from the emergence of SARS-CoV-2 and the COVID-19 pandemic, we have launched a new website tracking the reported number of Monkeypox cases in North Carolina using data reported by the North Carolina Department of Health and Human Services (NCDHHS) as well as across the United States using data provided by the Centers for Disease Control and Prevention (CDC). Monkeypox virus (MPX), a double stranded DNA virus belonging to the orthopoxvirus genus,is endemic in West and Central Africa. In May 2022, reports emerged of growing cases of MPX in Europe and North America with the World Health Organization declaring MPX a Public Health Emergency of International Concern on July 23, 2022.

You can visit the website at https://mpx.wakeforestid.com.

Next Steps

We will be calculating relevant epidemiological metrics such as the effective reproduction number and the doubling time of cases. We anticipate that this website will continue to evolve as our understanding of the current outbreak unfolds.

Reported MPX Cases in North Carolina

We provide an interactive longitudinal view of all states using the CDC data.

Interactive View of Reported MPX Cases by State

Questions?

Please reach out to your provider if you have any questions regarding monkeypox infections.

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@online{dewitt2022,
  author = {DeWitt, Michael},
  title = {Tracking {Monkeypox} {Cases} in {North} {Carolina}},
  date = {2022-07-27},
  url = {https://wakeforestid.com/posts/2022-07-27-tracking-monkeypox-cases-in-north-carolina/},
  doi = {10.59350/gk4v5-pv624},
  langid = {en}
}

For attribution, please cite this work as:

DeWitt, Michael. 2022. “Tracking Monkeypox Cases in North Carolina.” July 27. https://doi.org/10.59350/gk4v5-pv624.

Wake Forest School of Medicine Section on Infectious Diseases

Why Dog Rabies Persists—and What It Takes to Eliminate It

References

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Why Is Getting on Buprenorphine So HARD These Days?! : Part 2

Option 1: Go Inpatient

Option 2: Methadone

Option 3: High Dose Induction: Pedal to the Metal

Option 4: A Variation on the Old Way

Option 5: The Long-Acting Shot

Footnotes

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Why Is Getting on Buprenorphine So HARD These Days?! : Part 1

The Rise of Fentanyl

How We Used To Do It

Fentanyl Gumming Up The Works

Stimulants and Xylazine

Footnotes

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Farewell to Dr. Phil Lackey

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In the news: Wake Forest faculty discusses H5N1 and ongoing research

References

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Antimicrobial Awareness Week 2024

Antimicrobial Awareness Week 2024

Educational Materials

How does antimicrobial resistance spread?

What is one thing you wish more people knew about antimicrobial resistance?

How do animals contribute to antimicrobial resistance?

How can AMR awareness be included in medical student interactions with patients?

What are things in my everyday life to combat antimicrobial resistance?

How do we make smart decisions about antimicrobial use in resource-limited settings?

What are some of the things being done internationally to combat antimicrobial resistance?

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Collabathon on Estimating Real-Time Epidemic Growth Rates

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Medical Student 2024

CDC’s STI Conference

International Conference on Emerging Infectious Diseases

Medical Student Research Program

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IDWeek 2024

Poster Presentations

Oral Presentations

Pre-meeting workshops

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International Field Epidemiology and Tropical Medicine in Peru

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Truly Trading One Drug for Another”

Truly Trading One Drug for Another

Footnotes

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Why Medication for Opioid Use Disorder Is Not “Trading One Drug For Another: Part 2”

What is happening when an addictive substance is used in the brain?

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Why Medication for Opioid Use Disorder Is Not “Trading One Drug For Another”

Part 1: Defining Addiction

Part 2: How Opioid Treatment Medications Do not Meet Criteria for Addiction

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Addiction As a Biopsychosocial Disease

Bio

Psych

Social

How do we use this knowledge?

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