An empty hospital corridor lit by daylight from a row of windows, with no people present

The Plague Death in Irkutsk: What We Know, What Russia Won’t Say, and Whether Americans Should Worry

On October 6, 2026October 6, 2026 By Dr. Scott RennieIn Infectious DiseaseLeave a comment

Written October 6, 2026. This story is five days old and still moving. Dates and numbers below are what could be verified as of this morning.

A patient put it to me plainly on a video visit: do we have to be worried about a new pandemic with the Russia plague that is in the news?

Fair question. I did not give them a clean yes or no, because five days into something like this, anyone offering a clean yes or no is guessing.

Here is what I can tell you, and more usefully, here is what nobody can tell you yet.

A 28-year-old lab tech, four days, and a death certificate that says pneumonia

Darya Shipilova was 28 years old and worked as a laboratory technician at the Irkutsk Anti-Plague Research Institute in Siberia. On September 25, according to Russian media reporting, she broke a test tube of live bacteria while collecting samples. She was admitted to the hospital on September 29 with what her chart called pneumonia of unknown etiology. She died either October 1 or October 2, depending on which outlet you read, and the fact that we cannot pin down the date a woman died is itself a small piece of information about how much is being released.

Four days from the reported accident to the hospital. Two days from the hospital to the morgue.

Then the response. Roughly 197 people who had contact with her were identified, and 189 of them were hospitalized for observation, 114 at one facility, 63 at another, and 12 sent to the anti-plague institute itself. Contacts were isolated in a center that had been used for COVID patients. FSB officers started escorting the ambulances. By October 4 and 5, City Clinical Hospitals No. 1, No. 3 and No. 10, the Ivano-Matreninskaya Children’s Hospital and at least one maternity hospital in Irkutsk were under three-week quarantine.

That is a plague response. Three weeks is not an arbitrary number, it is roughly what you choose when you want to clear the incubation period of something serious and then clear it again.

The part of this that got reported backward

A lot of the coverage I have seen, and the version most people have in their heads, is that Russia said a test tube broke.

Russia said no such thing. Rospotrebnadzor, the state public health agency, has stated there was no accident involving pathogenic microorganisms at the institute, that no microorganisms associated with her professional work were found in her body, and that the epidemiological situation in Irkutsk and Shelekhov is stable. Her cause of death, officially, is pneumonia of unknown cause.

The broken test tube came from her. It is what she reportedly told the medical staff who admitted her, and it reached the public through Russian media rather than through any official channel.

So the official position is not that there was an accident. The official position is that nothing happened. Hold that next to the children’s hospital being closed for three weeks and you have the actual story of the past week. Plague has still never been publicly lab-confirmed in this case. Meanwhile the governor of Irkutsk Oblast, Igor Kobzev, met with Russia’s chief public health officer about “reports of a suspected case of a particularly dangerous infectious disease,” and the head of neighboring Buryatia said out loud that the death was linked to plague before his statement was quietly amended to something softer.

Two different words that look identical

Worth separating, because it explains some of the panic.

“Plague” means a specific bacterium, Yersinia pestis, which causes bubonic, septicemic and pneumonic disease and which has a known treatment. “Plague” also means, in ordinary English, any catastrophe that sweeps through a population. When a headline says plague in Russia, a sizable fraction of readers are not picturing a gram-negative coccobacillus that responds to doxycycline. They are picturing 1348.

Both meanings are legitimate. Only one of them is a diagnosis.

Could a broken tube really do this?

This is the question I find most interesting clinically, and the honest answer is that it is a stretch.

Simon Clarke, a cellular microbiologist at the University of Reading, put it about as well as it can be put: “an awful lot must have gone wrong for a lab worker to be infected by a broken test tube.” Work with a select agent happens inside layered containment. Biosafety cabinets, directional airflow, respiratory protection, procedures that assume breakage will eventually happen because over enough years it does. A tube hitting the floor inside a functioning cabinet is a cleanup problem, not an exposure. For that breakage to seed a fatal pneumonia, she likely had to be outside containment, or the containment had to be failing, or she inhaled a bolus at close range before anything could capture it.

Which brings up the thing I keep coming back to.

If she broke that tube on September 25 and knew it, she should have been on post-exposure prophylaxis within hours. The CDC’s recommendation is seven days of monotherapy: doxycycline 100 mg every 12 hours, or ciprofloxacin 500 to 750 mg every 12 hours, with levofloxacin and moxifloxacin now also first-line. That is it. Oral pills, generic, sitting in any pharmacy in the world including the one inside an anti-plague institute. Given promptly, the odds she ever became symptomatic drop toward nothing.

She presented on September 29.

I do not know whether she was offered prophylaxis and declined it, or reported the break late, or reported it immediately to someone who decided it did not warrant treating, or was treated and failed. Any of those is possible. What I would say plainly is that the four-day gap, not the bacterium, is the most likely reason a healthy 28-year-old died. Untreated pneumonic plague kills most of the people it infects, and it kills them fast. The treatment window is measured in hours after symptoms start, not days. Once you are four days past an inhalational exposure and presenting with pneumonia, antibiotics are being asked to do something they are not very good at.

That is a boring explanation. It is also the one that requires nothing unusual to be true.

Was it resistant? Was it modified?

Here is where I think the public conversation is making an understandable mistake.

You do not need an engineered organism to explain a fast death. You need a late diagnosis, which we appear to have. Adding a modified pathogen to the story explains something that is already explained.

That said, drug-resistant plague is not hypothetical, and this is the fact I would most want people to walk away with. In 1995 a patient in Madagascar with ordinary bubonic plague yielded an isolate called IP275, the first multidrug-resistant Y. pestis ever found. It carried a self-transmissible plasmid, pIP1202, conferring resistance to at least eight drugs used in plague treatment and prophylaxis, streptomycin and tetracycline and chloramphenicol and the sulfonamides among them. Nobody built it. The plasmid backbone turned out to be nearly identical to resistance plasmids from Salmonella Newport and from a fish pathogen, meaning Y. pestis had picked it up from the enormous reservoir of resistance circulating in agricultural bacteria.

Resistant plague already happened, once, by accident, in a patient in 1995. That is a better reason to pay attention than anything anyone has alleged about Irkutsk. We already live with the mature version of this problem in drug-resistant tuberculosis, and nobody had to engineer that either.

As for whether this particular organism was modified: there is no public evidence of it, and there is one piece of evidence against the scenario people fear most. If this were a highly transmissible engineered strain, those 197 contacts would be the first sign. As of the Rospotrebnadzor statements, they were not showing signs of illness. No secondary cases have surfaced publicly. A pathogen built to spread does not stop at one person.

The institute, and the thing that is actually true about it

The Irkutsk Anti-Plague Research Institute of Siberia and the Far East traces to a plague laboratory set up in Irkutsk in 1923 and was formally established in its current form on June 5, 1934. Its job, for ninety years, has been surveillance and containment of plague and other dangerous infections across Siberia and the Russian Far East. Plague is genuinely endemic in Central Asian rodent populations. An institute like this is the reason outbreaks there stay small.

And yes, the Soviet anti-plague network has a documented connection to Biopreparat, the covert Soviet offensive biological weapons program that weaponized plague, anthrax and tularemia. Igor Domaradskiy, one of Biopreparat’s founders, had previously run the anti-plague institutes at Irkutsk and Rostov-on-Don. That is history, not allegation.

What does not exist is any public evidence that the Irkutsk lab is developing plague as a weapon today, or that this death is connected to an offensive program. A facility with a Cold War lineage working on a pathogen endemic to its own region is not, by itself, a weapons story.

Running the conspiracy theories down

These deserve a real answer rather than a wave of the hand, so here they are, from least to most plausible.

It was deliberately released. No. There is no reason to release a weapon into your own closed city, kill one of your own technicians, and quarantine your own children’s hospital.

It is an engineered superbug and the contacts are already dying in secret. This requires 189 hospitalized people, their families and the staff of five medical facilities to all stay silent. Irkutsk has a population over 600,000 and functioning messaging apps. Containment of information at that scale fails, and it fails fast.

It is not plague at all, it is something worse they will not name. Possible in principle, and it is the theory I can least firmly rule out, because no confirmatory testing has been published. But the response fits plague. The duration of the quarantine fits plague. An institute that works with Y. pestis having a Y. pestis accident is the least exotic available explanation.

There is a much bigger outbreak than they are admitting. Partially plausible, and I would not be shocked. Not because of anything specific to Irkutsk, but because this is a system that denied the test tube ever broke while sealing hospitals. Under-reporting is the house tendency.

An ordinary lab-acquired infection, recognized late, in a bureaucracy whose first instinct is denial. This is almost certainly what happened. Every observed fact fits it: the four-day delay, the speed of death, the aggressive contact tracing, the official denial, the walked-back statement from Buryatia, the pneumonia-of-unknown-cause diagnosis that nobody has updated. Boring, tragic, and entirely consistent.

Can we believe them?

On the specifics, no. On the response, mostly yes.

Watch what a government does rather than what it says. Russia’s words say stable and nothing happened. Russia’s actions say particularly dangerous infection, and they committed real resources to a real containment operation. When those two diverge, believe the resources.

The US State Department’s comment struck me as about right: “Many details have not been confirmed. We encourage Russian authorities to share accurate information quickly and openly,” alongside the observation that plague “is a known disease and is treatable with common antibiotics.” The CDC says it is monitoring. President Trump said his administration is looking at it very strongly and that “anybody that has that kind of a problem, we’re always willing to help,” which, whatever else you think of it, is the correct posture toward an outbreak in a country you are not friendly with.

Clarke’s line about what actually controls an outbreak is the one worth keeping: transparency, rapid diagnosis, effective contact tracing. Russia is doing two of the three.

Is this the next COVID?

No, and I want to be specific about why, because “no” by itself has stopped persuading anyone and I understand why.

A lot of people came out of 2020 believing that COVID began in a laboratory. Whether or not that is what happened, and it remains genuinely unresolved, that belief is the reason a Siberian lab accident in 2026 lands differently than it would have landed in 2015. People are not being irrational. They are pattern-matching to the last five years, and they have been told before that there was nothing to see.

So, the differences that matter.

Yersinia pestis is a bacterium. SARS-CoV-2 is a virus. That distinction is not academic: we have had effective antibiotics against plague since the 1940s, every pharmacy stocks doxycycline, and treatment is cheap and oral. There was no equivalent for COVID in February 2020, which is why the whole fight there moved to vaccination instead of treatment.

Pneumonic plague spreads through respiratory droplets during close, sustained contact. It is not the long-range airborne spreader that COVID turned out to be. It does not do silent asymptomatic transmission for a week before anyone feels sick. It announces itself, violently, within a few days.

And it has never been good at sustained human-to-human chains in the modern era. In the United States, we average about seven plague cases a year, mostly in the rural Southwest from fleas and infected animals. Arizona had a fatal pneumonic case in Coconino County in July 2025, written up in MMWR, the county’s first since 2007. The last documented person-to-person transmission of pneumonic plague in the United States was in 1924, in Los Angeles. A century, with the organism present in our own rodents the entire time.

A pathogen that cannot start a chain cannot start a pandemic.

So should you buy N95s?

No.

Not for this. If you already own a box, you did not waste your money, and if you live where I do, wildfire season is a far better argument for keeping them than Irkutsk is. But buying respirators this week as a response to a plague death 5,000 miles away is spending money and worry on the wrong thing.

If you want a useful response to this story, here is one. Know whether you could get a doctor on the phone within 24 hours of getting sick. That is the variable that killed Darya Shipilova, four days of it, and it is the only variable in this entire story that you personally have any control over. The antibiotics work. Getting to them in time is the whole game.

I say that as someone who practices entirely by video, so treat it as the interested opinion that it is.

The Bottom Line

A 28-year-old technician at a Siberian plague institute broke a tube on September 25, went to the hospital on September 29, and was dead within about two days. Russia says there was no accident and no plague while quarantining five medical facilities and tracking 197 contacts. The most likely explanation needs no engineering and no conspiracy: a laboratory exposure that should have been met with seven days of doxycycline within hours, met instead with four days of delay. Plague remains treatable, remains bad at spreading between people, and has not caused person-to-person transmission in this country since 1924. Watch for confirmatory testing and for secondary cases among the contacts. Those are the two things that would change my read. Skip the N95s.

Sources

Hospitals in Irkutsk impose quarantines after an employee at an anti-plague institute dies. Meduza, October 5, 2026. https://meduza.io/en/feature/2026/10/05/hospitals-in-irkutsk-impose-quarantines-after-an-employee-at-an-anti-plague-institute-dies-russia-s-public-health-agency-says-she-died-of-pneumonia-and-the-epidemiological-situation-remains-stable
Nearly 200 People Under Observation After Irkutsk Lab Worker Dies From Plague. The Moscow Times, October 2, 2026. https://www.themoscowtimes.com/2026/10/02/nearly-200-people-under-observation-after-irkutsk-lab-worker-dies-from-plague-a93857
Siberian Anti-Plague Institute Staff Isolated After Worker’s Death. RFE/RL. https://www.rferl.org/a/russia-plague-warning-siberia-irkutsk-laboratory/33870385.html
Plague outbreak in Russia, expert comment by Dr Simon Clarke. University of Reading, 2026. https://www.reading.ac.uk/news/2026/Expert-Comment/Plague-outbreak-in-Russia-expert-comment
Russia plague: What we know about the suspected case reportedly linked to a lab worker’s death. CNBC, October 5, 2026. https://www.cnbc.com/2026/10/05/russia-plague-suspected-case-irkutsk.html
State Department monitoring reported fatal case of pneumonic plague. ABC News, October 2026. https://abcnews.com/US/state-department-monitoring-reported-fatal-case-pneumonic-plague/story?id=136992734
Russian plague lab researcher dies as nearly 200 monitored: here’s what we know. Forbes, October 5, 2026. https://www.forbes.com/sites/siladityaray/2026/10/05/russian-plague-lab-researcher-dies-as-nearly-200-monitored-heres-what-we-know/
Russian lab worker dies of suspected plague in Siberia; US monitoring case. Al Jazeera, October 5, 2026. https://www.aljazeera.com/news/2026/10/5/russian-lab-worker-dies-of-suspected-plague-in-siberia-us-monitoring-case
Has plague returned to Siberia? Panic in Russia after death of lab worker. Euronews, October 4, 2026. https://www.euronews.com/2026/10/04/has-plague-returned-to-siberia-panic-in-russia-after-death-of-lab-worker
The Siberian lab at the centre of a plague scare: its history, work and what it actually does. ThePrint. https://theprint.in/theprint-essential/the-siberian-lab-at-the-centre-of-a-plague-scare-its-history-work-and-what-it-actually-does/3063082/
Recommended antimicrobial pre- and post-exposure prophylaxis for plague. Centers for Disease Control and Prevention, 2021. https://www.cdc.gov/plague/resources/PlagueProphyTreatmentTable_2021-P.pdf
Nelson CA, et al. Antimicrobial Treatment and Prophylaxis of Plague: Recommendations for Naturally Acquired Infections and Bioterrorism Response. MMWR Recomm Rep, 2021. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8312557/
Welch TJ, et al. Multiple Antimicrobial Resistance in Plague: An Emerging Public Health Risk. PLoS One, 2007. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1819562/
Notes from the Field: Fatal Pneumonic Plague, Coconino County, Arizona, July 2025. MMWR, volume 75. https://www.cdc.gov/mmwr/volumes/75/wr/mm7538a2.htm
Biopreparat, background on the Soviet biological weapons program. https://en.wikipedia.org/wiki/Biopreparat

An amber prescription bottle tipped over on a pale wooden table with pink and white antibiotic capsules spilling out, beside a folded paper card, in bright window light

You Probably Are Not Allergic to Penicillin

On August 31, 2026 By Dr. Scott RennieIn Infectious DiseaseLeave a comment

About one in ten Americans carries a penicillin allergy in their chart (1). When those people are actually tested, the large majority are not allergic.

That gap is one of the most consequential unforced errors in medicine, and almost nobody goes back and checks.

Where the label usually comes from

Most penicillin allergy labels were applied in childhood, by someone who is no longer involved, based on something that happened once.

The classic story is a rash during a course of amoxicillin at age four. Here is the problem with that story. Viral illnesses cause rashes. Children with viral illnesses get prescribed antibiotics. When a rash appears on day three, the antibiotic is the thing everyone is looking at, so the antibiotic gets the blame and the label goes in the chart. It never comes out.

The other common origins are a family member’s allergy transferred onto the patient, and side effects filed as allergy. Nausea is not an allergy. Diarrhea is not an allergy. A yeast infection is not an allergy. They are all reasons to dislike a drug and none of them are reasons to avoid it for life.

Even genuine allergy fades. IgE-mediated penicillin sensitivity wanes over time, and a substantial proportion of people who really were allergic at twenty are not allergic at fifty.

The label is not free

This is the part I want to land, because people assume that avoiding penicillin is the cautious choice and therefore the safe one.

It is not. Blumenthal and colleagues followed 64,141 adults carrying a penicillin allergy label against 237,258 matched comparators for a mean of six years (2). The people with the label had an adjusted hazard ratio of 1.69 for MRSA and 1.26 for Clostridioides difficile.

The mechanism is not mysterious, and the authors show it. Those patients received far more of the alternatives: macrolides at over four times the rate, clindamycin at nearly four times, fluoroquinolones at twice (2). Those drugs do more collateral damage to the gut and select harder for resistance. The excess MRSA and C. difficile were mediated by that substitution.

So the label does not sit there harmlessly. It quietly buys worse antibiotics for the rest of a person’s life.

There is a score for this, and it runs on history alone

The thing that changed my thinking here is that you do not need a skin test to identify most of the people who are low risk. You need four questions.

PEN-FAST was derived and validated by Trubiano and colleagues (3). It scores like this:

Five years or fewer since the reaction: 2 points. Anaphylaxis or angioedema, or a severe cutaneous adverse reaction: 2 points. Treatment required for the episode: 1 point.

A score under 3 means low risk. In the derivation cohort, only 17 of 460 low-risk patients tested positive, giving a negative predictive value of 96.3 percent (3).

Read the criteria again and notice what is not in them. No skin prick. No specific IgE. No blood work at all. Every input is something the patient tells you.

That is why this belongs in a conversation rather than a laboratory, and it is why I think most clinicians could be doing more of this than they are.

What I actually do with this on a video visit

I ask everyone about allergies before I prescribe anything. That part is unremarkable. What is worth describing is what happens next, because it is where most of these labels give themselves away.

When somebody tells me they are allergic to amoxicillin, I ask what the reaction was.

Two answers come back more than any others. The first is that they do not really remember, because they were a baby and their parents told them. The second is some version of “I think I am allergic because my mom is.”

Neither of those is an allergy history. The second one is not even about the patient.

Here is where I part company with the enthusiastic version of this argument. A person who is sick today and needs an antibiotic today is not in a good position to test a theory about their own immune system. If there is any real concern about anaphylaxis in what I am hearing, I do not push it. I pick something else and move on, and I am comfortable with that.

I also do not send people off for an oral challenge as a matter of course. That is a real procedure with a real indication, and routing every vague childhood label into an allergy clinic is not a good use of anyone’s afternoon.

What I do instead is tell them the label is worth reopening properly, and that the time to do it is when they are well rather than in the middle of an infection. It belongs with whoever manages their ongoing care, in a visit where nobody is waiting on a prescription.

The distinction matters. The label deserves to be examined. The examination should not happen while someone is sick and I am trying to treat them.

What a real reaction looks like, and what has changed about treating it

None of the above applies to someone who has had a genuine severe reaction. Anaphylaxis, angioedema, or a severe cutaneous adverse reaction such as Stevens-Johnson syndrome or DRESS means the label stays. Those people are not candidates for de-labeling and should not be challenged.

Worth knowing what has changed on the treatment side. For decades the only option for anaphylaxis outside hospital was an intramuscular auto-injector. There is now an FDA-approved epinephrine nasal spray, neffy, the first intranasal adrenaline product to reach the market (4). Pharmacokinetic studies show plasma concentrations comparable to or exceeding intramuscular injection, and, counterintuitively, nasal congestion does not appear to impair absorption (5).

I mention it because needle avoidance is a real reason people leave their epinephrine at home, and a device you will actually carry beats a better device you will not. If someone genuinely needs to carry epinephrine and the needle is the barrier, that conversation is now worth having.

It does not change the rule that epinephrine is the treatment and antihistamines are not.

For patients

If your penicillin allergy dates from childhood and you cannot remember what happened, it is worth reopening. Ask specifically to be assessed rather than mentioning it in passing, because in passing it stays in the chart.

Before that conversation, work out three things: roughly when it happened, what you or your parents remember seeing, and whether anyone treated it. That is most of the assessment.

Raise it when you are well. A visit for an infection is the wrong moment, because whoever is treating you needs to choose an antibiotic today and will reasonably play it safe. Bring it to a routine appointment instead, when nobody is waiting on a prescription.

If you have taken amoxicillin, Augmentin or any similar antibiotic since the original reaction and were fine, say so early. It is the single most useful thing you can tell your clinician.

And if your reaction involved breathing trouble, swelling of the face or throat, or a blistering rash, the label is real and it stays.

For colleagues

PEN-FAST costs four questions and identifies low-risk labels at the point of care with a negative predictive value of 96.3 percent (3). We are not short of the tool. We are short of anyone taking ownership of the conversation.

Frame it as a safety intervention rather than a convenience one, because it is. The hazard ratios in the Blumenthal cohort are for MRSA and C. difficile, not for inconvenience (2).

And ask the question that costs nothing: has this person taken a penicillin since. A meaningful share of these labels fall over on that answer alone.

The Bottom Line

Roughly ten percent of people carry a penicillin allergy label and most of them are not allergic, usually because a childhood viral rash got blamed on an antibiotic. The label is not harmless. Carrying it is associated with a 69 percent higher risk of MRSA and a 26 percent higher risk of C. difficile, driven by the broader antibiotics used instead. Four questions, scored as PEN-FAST, identify most low-risk labels without any testing at all, which makes this one of the few things in medicine that is fixed by a conversation. If your reaction was anaphylaxis, angioedema or a blistering rash, the label stays and you keep your epinephrine, which now comes as a nasal spray as well as an injector.

Sources

1. Shenoy ES, Macy E, Rowe T, Blumenthal KG. Evaluation and management of penicillin allergy: a review. JAMA. 2019;321(2):188-199. PMID 30644987. https://pubmed.ncbi.nlm.nih.gov/30644987/

2. Blumenthal KG, Lu N, Zhang Y, Li Y, Walensky RP, Choi HK. Risk of meticillin resistant Staphylococcus aureus and Clostridium difficile in patients with a documented penicillin allergy: population based matched cohort study. BMJ. 2018;361:k2400. PMID 29950489. https://pubmed.ncbi.nlm.nih.gov/29950489/

3. Trubiano JA, Vogrin S, Chua KYL, et al. Development and validation of a penicillin allergy clinical decision rule. JAMA Intern Med. 2020;180(5):745-752. PMID 32176248. https://pubmed.ncbi.nlm.nih.gov/32176248/

4. Hernandez-Trujillo V, Tachdjian R, et al. Successful administration of neffy (epinephrine nasal spray) by patients and caregivers. Ann Allergy Asthma Immunol. 2026. PMID 42476303. https://pubmed.ncbi.nlm.nih.gov/42476303/

5. Takahashi K, Yanagida N. Intranasal adrenaline: a new treatment for anaphylaxis. Pediatr Allergy Immunol. 2026;37(3):e70316. PMID 41796069. https://pubmed.ncbi.nlm.nih.gov/41796069/

Unlabeled blister pack of six white oval antibiotic tablets beside a plain paper pharmacy bag on a kitchen table

I hear it almost every day now. “I think I just need a Z-Pak.”

On January 2, 2026September 11, 2026 By Dr. Scott RennieIn Infectious DiseaseLeave a comment

Sometimes it’s phrased as a question. Sometimes it isn’t. In telemedicine especially, many patients request azithromycin by name within the first minute of the visit. The symptoms are familiar. Runny nose. Congestion. Post-nasal drip. Scratchy throat. Maybe a cough that started yesterday. No fever. No shortness of breath. No focal findings anyone could reasonably point to as bacterial.

But they’re convinced the Z-Pak will help them get better faster. They’ve taken it before. It worked last time. Or at least they felt better a few days later and connected the dots.

This didn’t happen by accident.

Azithromycin earned its place in outpatient medicine because it was easier to tolerate than older antibiotics like erythromycin, had fewer drug interactions than clarithromycin, and came packaged in a way that felt efficient. Six pills. Five days. Done. The Z-Pak became a symbol of modern medicine that didn’t slow you down.

Over time, it also became the antibiotic people expected.

In telemedicine, that expectation is even stronger. There’s no exam table. No stethoscope. No labs. No chest X-ray down the hall. The visit is brief by design. When a patient feels sick and wants something tangible, the Z-Pak becomes the path of least resistance. Prescribing it can shorten the encounter. It avoids a long explanation. It reduces the risk of a bad review. It keeps patient satisfaction scores high. It keeps supervisors and clinic managers happy. Everyone moves on to the next visit.

I understand why this happens. I’ve seen it from the inside.

But convenience doesn’t make a treatment safe or appropriate.

Azithromycin does not treat viral infections. It does not help the common cold. It does not clear post-nasal drip. It does not shorten the course of uncomplicated upper respiratory infections. When patients feel better after taking it, they almost always would have improved anyway.

What it does do is expose people to real risk.

Azithromycin can prolong the QT interval. That matters. QT prolongation can predispose patients to dangerous heart rhythms, including torsades de pointes and sudden cardiac death. This risk is higher in people with underlying heart disease, electrolyte abnormalities, or those taking other QT-prolonging medications, but it is not zero in otherwise healthy adults. Large observational studies have shown an increased risk of cardiovascular death during azithromycin treatment compared with other antibiotics or no antibiotics at all.

That risk is invisible to patients. They don’t feel their QT interval getting longer. They just know they want something to help them feel better.

Antibiotics also carry more familiar side effects. Nausea. Diarrhea. Abdominal cramping. Yeast infections. Rashes. Allergic reactions. These are not rare, and they are not trivial when the medication wasn’t needed in the first place.

Then there’s resistance. Every unnecessary antibiotic course applies selective pressure. Azithromycin resistance is already a growing problem in common respiratory pathogens. When we reach for it reflexively, we make it less useful for the patients who actually need it.

The harder part of these visits is the explaining.

It takes longer to walk someone through why their symptoms are viral. Why time, fluids, nasal saline, antihistamines, or intranasal steroids actually help. Why rest matters. Why antibiotics won’t fix inflammation or mucus production. Why feeling miserable does not automatically mean something dangerous is happening.

It’s much faster to send a prescription.

But faster is not better medicine.

I get patients asking for Z-Paks every day that I work in telemedicine. It’s so common that it happens at least once a day, if not three or four times a day. One example sticks with me. A patient requested a Z-Pak for congestion and sinus pressure that had been present for two days. No fever. No facial pain. No worsening course. When I explained why antibiotics wouldn’t help, they were frustrated at first. We talked through what sinus infections actually look like and when antibiotics are appropriate. We discussed symptom control instead. Two days later, they messaged to say they felt better and were glad they didn’t take an antibiotic they didn’t need.

That outcome required time. It required education. It required saying no.

Not every visit goes that smoothly. Some patients remain disappointed. Some leave poor reviews. That pressure is real, especially in high-volume telemedicine environments.

But prescribing antibiotics to keep the peace comes at a cost. It shifts risk onto the patient. It shifts harm into the future. And it reinforces the idea that medicine should always offer a pill, even when the best treatment is patience and support.

Azithromycin became dominant because it was easy. That same ease is why we need to be more careful with it now.

Why Antibiotics Don’t Work for Colds, Flu, or Viruses

On August 10, 2012September 11, 2026 By Dr. Scott RennieIn Infectious DiseaseLeave a comment

I have many patients who come into the clinic with a common cold and request antibiotics. Antibiotics can be harmful to your body in many ways. I think this is very important information from the CDC: Are you aware that colds, flu, most sore throats, and bronchitis are caused by viruses? Did you know that antibiotics do not help fight viruses? It’s true. Plus, taking antibiotics when you have a virus may do more harm than good. Taking antibiotics when they are not needed increases your risk of getting an infection later that resists antibiotic treatment. In addition, antibiotics can cause bloody diarrhea and abdominal pain that can last for weeks, severe life threatening allergic reactions (anaphylaxis) and rashes(hives). Antibiotics can also damage some internal organs such as the liver or kidneys. Improper antibiotic causes prolonged healing time and increased medical costs.

Antibiotics cure bacterial infections, not viral infections such as:
- Colds or flu;
- Most coughs and bronchitis;
- Sore throats not caused by strep; or
- Runny noses.
Taking antibiotics for viral infections, such as a cold, cough, the flu, or most bronchitis, will not:
- Cure the infections;
- Keep other individuals from catching the illness; or
- Help you feel better.

When you use antibiotics appropriately, you do the best for your health, your family’s health, and the health of those around you. “We want Americans to keep their families and communities healthy by getting smart about the proper use of antibiotics,” said Lauri Hicks, D.O., medical director of CDC’s Get Smart campaign.

What To Do

Talk with your healthcare provider about antibiotic resistance.
When you are prescribed an antibiotic,
- Take it exactly as the doctor tells you. Complete the prescribed course even if you are feeling better. If treatment stops too soon, some bacteria may survive and re-infect you.This goes for children, too. Make sure your children take all medication as prescribed, even if they feel better.Throw away any leftover medication once you have completed your prescription

What Not To Do

Antibiotics cure bacteria, not viruses such as:
- Colds or flu;
- Most coughs and bronchitis;
- Sore throats not caused by strep; or
- Runny noses.

Antibiotic Side Effects and Resistance: The Real Cost

On March 18, 2012August 30, 2026 By Dr. Scott RennieIn Infectious DiseaseLeave a comment

This page has carried a warning about antibiotic resistance since 2012. The warning held up. What changed is that we stopped guessing. There are counted deaths now, surveillance from 104 countries, and forecasts out to 2050, and none of it argues for handing antibiotics out more freely.

I practice family medicine and obesity medicine entirely by telemedicine, so antibiotic requests reach me on video and in message threads, usually from someone who feels awful and wants this settled today. The request makes sense from where you sit. The refusal makes sense from where I sit. This post closes that gap with numbers instead of a lecture.

The global count, briefly

In 2021, bacterial antimicrobial resistance was associated with 4.71 million deaths worldwide, and 1.14 million of those were directly attributable to resistant organisms (1)(2). The forecast for 2050 is 1.91 million attributable and 8.22 million associated deaths in that year, with 39.1 million attributable deaths cumulatively between 2025 and 2050 (2).

The shape of the burden shifted in a way that rarely makes headlines. Attributable deaths in children under five fell 60.4% between 1990 and 2021, while deaths in adults 70 and older rose 89.5% (2). Vaccines and better newborn care did the first part. The second is what happens when more people live long enough to pick up a bloodstream infection in a hospital. MRSA alone went from 57,200 attributable deaths in 1990 to 130,000 in 2021 (2).

One in six

WHO’s 2025 surveillance report found that roughly one in six laboratory-confirmed bacterial infections worldwide in 2023 was resistant to the antibiotic meant to treat it (1)(3). Between 2018 and 2023, resistance rose in more than 40% of the pathogen-antibiotic combinations under surveillance, at 5% to 15% a year (3).

Two organisms carry much of that. More than 40% of E. coli and more than 55% of Klebsiella pneumoniae are now resistant to third-generation cephalosporins, which are first-choice treatment for those bloodstream infections (3). In the African Region the Klebsiella figure passes 70% (3). WHO’s 2024 priority list puts carbapenem-resistant Acinetobacter baumannii and carbapenem-resistant Enterobacterales in the critical tier, next to rifampicin-resistant tuberculosis (4).

One caveat. In 2023, 104 countries reported, up from 25 in 2016, and 48% still reported nothing (3). Some of the rise is real. Some of it is us finally looking.

What an antibiotic does to your own bacteria

Here is the part that gets skipped when resistance is framed as a planetary problem. A meta-analysis of 24 studies found that people given an antibiotic in primary care carry resistant bacteria afterward. Among urinary organisms, the pooled odds ratio for resistance was 2.5 within two months and still 1.33 at twelve months. Among respiratory organisms, 2.4 at both points (5).

Your bacteria. Your next urinary tract infection. That is the honest reason a just-in-case prescription is not free, and you are the first person who pays, months later, when the cheap oral drug is likelier to fail. The global statistic is a sum of small personal debts.

If you are the one asking for a Z-Pak

A study of 15.5 million outpatient antibiotic fills in 2016, among 19.2 million privately insured Americans, found azithromycin was the most commonly filled antibiotic in that group, at 19.0% of fills. Only 12.8% of fills were classified as appropriate. Another 23.2% were inappropriate, and 28.5% carried no diagnosis code at all in the three days beforehand (6). Nearly a third of prescriptions, no recorded reason.

Azithromycin is also not a neutral molecule. In a Tennessee Medicaid cohort, a five-day course carried an estimated 47 additional cardiovascular deaths per million courses compared with amoxicillin, rising to 245 per million in the highest decile of cardiovascular risk (7).

When a patient asks me for a Z-Pak and it is not appropriate for what they have, I tell them that plainly. Then we go through the side effects: nausea, diarrhea, a yeast infection, a rash. The last piece is the one worth the time. I explain what azithromycin is actually good for, and what it is not good for, and a sinus infection sits on the second list.

The explanation I lead with, though, is about the differential rather than the drug. A cough can come from a long list of things, and in any given month there is plenty going around: viral pneumonia, bacterial pneumonia, RSV, pertussis, ordinary viral bronchitis. No single antibiotic and no single antiviral covers that list. You have to know what you are dealing with before you can choose the right medication, and choosing one and hoping is how people end up worse rather than better.

So for a cough I cannot account for, what I recommend is an in-person evaluation rather than a prescription. Someone needs to listen to the heart and lungs. Where the findings sit in the chest is a genuine clue to what kind of pathogen is causing it, and sometimes a chest film is what settles it. That is the part a camera cannot do for me.

Notes for clinicians, particularly those of us working by video

Telemedicine earned an early bad reputation here. In 2015 to 2016 claims data, children seen for acute respiratory infection at direct-to-consumer telemedicine visits got antibiotics 52% of the time, against 42% at urgent care and 31% in the primary care office. Guideline-concordant management ran 59% for those video visits and 78% at the office (8).

That finding is seven years old and it has not simply replicated. An Australian study of 2,392 general practice registrars covering 21,384 respiratory infection diagnoses from 2020 to 2023 found telehealth carried lower odds of an antibiotic for sore throat (OR 0.69, 95% CI 0.55 to 0.86) and for upper respiratory infection (OR 0.64, 0.51 to 0.81). Otitis media, 0.47. No difference for bronchitis or sinusitis (9). The authors found no damage to stewardship.

My read is that the modality is not the variable. What matters is whether the visit sits inside a relationship where a callback is possible, and whether you are paid the same for a no as for a prescription. Get those right and video is fine. Leave them broken and a bricks-and-mortar clinic will overprescribe just as fast, with the added problem that the patient drove there and wants something for the trip.

The respiratory complaint I would actually write an antibiotic for is a sinus infection, and the conversation that goes with the prescription is where the cost stops being abstract. I tell the patient what to watch for. Diarrhea, which can turn bloody, and bloody is the one that points at Clostridioides difficile. A yeast infection. Rashes. Swollen lips, which is the allergic signal, the angioedema end of it. And symptoms that get worse, or that simply have not changed, at 48 hours.

That list is the whole argument in miniature. A patient who needed the drug is accepting those risks in exchange for something. A patient who did not need it accepts every one of them in exchange for nothing.

Where the alarm runs ahead of the data

Overselling this teaches patients to discount all of it, so here are the weak spots. Attributable deaths did not explode over three decades. They moved from 1.06 million in 1990 to 1.14 million in 2021, and associated deaths drifted down slightly, from 4.78 million to 4.71 million (2). The 2050 figures are models. The azithromycin cardiac signal looks real in high-risk patients, but a Danish cohort of more than a million treatment episodes in adults aged 18 to 64 found no increase in cardiovascular death against penicillin V (10). ECDC puts the EU and EEA toll above 35,000 deaths a year and ties more than 70% of that health impact to healthcare-associated infections (11), so your outpatient azithromycin is not what drives the worst resistant infections in intensive care.

It still counts, the way a single vote counts, and mostly it counts against you.

The Bottom Line

One in six bacterial infections worldwide already resists the drug meant to treat it (1). Third-generation cephalosporins now fail against more than 40% of E. coli (3). Those figures were assembled out of individual prescriptions, nearly all of which felt reasonable to somebody at the time. When I decline an antibiotic for what is clearly a virus, I am not rationing your care and I am not doubting how bad you feel. I am declining to raise the odds that your own bacteria stop listening, and that bill arrives at your address, not the world’s. Ask me what should happen if you get worse. That answer is worth more than the prescription.

Sources

1. WHO. Antimicrobial resistance fact sheet, updated 16 July 2026. https://www.who.int/news-room/fact-sheets/detail/antimicrobial-resistance

2. GBD 2021 AMR Collaborators. Global burden of bacterial AMR 1990-2021, with forecasts to 2050. Lancet, 2024. https://pmc.ncbi.nlm.nih.gov/articles/PMC11718157/

3. WHO. Warning of widespread resistance to common antibiotics, 13 October 2025. https://www.who.int/news/item/13-10-2025-who-warns-of-widespread-resistance-to-common-antibiotics-worldwide

4. WHO. Bacterial Priority Pathogens List, 17 May 2024. https://www.who.int/news/item/17-05-2024-who-updates-list-of-drug-resistant-bacteria-most-threatening-to-human-health

5. Costelloe C, et al. Antibiotic prescribing in primary care and resistance in individual patients. BMJ, 2010. https://pubmed.ncbi.nlm.nih.gov/20483949/

6. Chua KP, et al. Appropriateness of outpatient antibiotic prescribing, insured US patients. BMJ, 2019. https://pubmed.ncbi.nlm.nih.gov/30651273/

7. Ray WA, et al. Azithromycin and the risk of cardiovascular death. NEJM, 2012. https://pubmed.ncbi.nlm.nih.gov/22591294/

8. Ray KN, et al. Antibiotic prescribing during pediatric direct-to-consumer telemedicine. Pediatrics, 2019. https://pubmed.ncbi.nlm.nih.gov/30962253/

9. Antibiotic prescribing for respiratory infection, telehealth versus face-to-face. J Med Internet Res, 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC11950701/

10. Svanstrom H, et al. Azithromycin and death from cardiovascular causes. NEJM, 2013. https://pubmed.ncbi.nlm.nih.gov/23635050/

11. ECDC. Health burden of antibiotic resistance, key messages. https://antibiotic.ecdc.europa.eu/en/get-informed/key-messages/health-burden-antibiotic-resistance

A 28-year-old lab tech, four days, and a death certificate that says pneumonia

The part of this that got reported backward

Two different words that look identical

Could a broken tube really do this?

Was it resistant? Was it modified?

The institute, and the thing that is actually true about it

Running the conspiracy theories down

Can we believe them?

Is this the next COVID?

So should you buy N95s?

The Bottom Line

Related Reading

Sources

Where the label usually comes from

The label is not free

There is a score for this, and it runs on history alone

What I actually do with this on a video visit

What a real reaction looks like, and what has changed about treating it

For patients

For colleagues

The Bottom Line

Related Reading

Sources

Related Reading

What To Do

What Not To Do

Related Reading

The global count, briefly

One in six

What an antibiotic does to your own bacteria

If you are the one asking for a Z-Pak

Notes for clinicians, particularly those of us working by video

Where the alarm runs ahead of the data

The Bottom Line

Related Reading

Sources