This interview is a dramatised reconstruction, shaped from historical sources to make Zinaida Yermolyeva’s work and context legible to modern readers rather than to reproduce her exact words. While the facts and technical details are grounded in verifiable records, the dialogue, tone, and connective tissue between events are imaginatively composed where the archive is incomplete or contested.
Zinaida Vissarionovna Yermolyeva (1898-1974) transformed wartime desperation into lifesaving science, isolating Soviet penicillin from mould scraped off a bomb-shelter wall whilst Stalingrad burned. A microbiologist who drank cholera to test her own vaccines and directed antibiotic production under German bombardment, she pioneered fermentation protocols that brought penicillin to the Red Army in 1943 – a year before many Western allies achieved mass production. Yet Cold War secrecy and ideological bias erased her parallel discovery from global history, leaving her visible only behind the Iron Curtain whilst Fleming, Florey and Chain received Nobel Prizes for the same breakthrough.
Welcome, Dr Yermolyeva. It’s 2025, and we’re speaking more than fifty years after your death. You’ve been celebrated with a Google Doodle, rediscovered by historians, and your penicillin work is finally being recognised beyond Soviet borders. How does it feel to see this attention now?
Late, isn’t it? But I did not work for recognition. When you are standing in a basement in Stalingrad with wounded soldiers bleeding through bandages and the Germans shelling above, you don’t think about history books. You think: how do I keep them alive until tomorrow? The work mattered. Whether anyone remembered my name – that was not my concern.
Your career began in 1921, during the infancy of the Soviet state. What drew you to microbiology?
Necessity. I graduated from the medical faculty at Donskoy University in 1921, just as the Civil War was ending and the country was in ruins. Rostov-on-Don, where I’d trained, was battered by disease. Typhoid, cholera – they killed more than bullets. I joined the Northern Caucasus Bacteriological Institute because microbes didn’t respect politics. If you wanted to save lives, you had to understand them.
In those years, Soviet science was scrambling to establish itself. We had passion, a mandate from the state to build institutions, but limited resources. I moved to Moscow in 1925 and became head of the Department of Microbial Biochemistry at the USSR Academy of Sciences. That’s where I began my research on bacteriophages and naturally occurring antimicrobial agents – lysozyme, in particular. Lysozyme was fascinating: an enzyme that destroyed bacterial cell walls, discovered by Fleming in 1922 but poorly understood. We studied how it worked, how it might be amplified. That work prepared me, years later, for penicillin.
You married the microbiologist Lev Zilber. His brother, Veniamin Kaverin, wrote the Open Book trilogy, basing the protagonist Tatiana on you. What was it like to become a character in Soviet literature?
Lev and I married in 1928. We worked together at the Pasteur Institute in Paris and the Robert Koch Institute in Germany. He was brilliant – virologist, immunologist, discovered tick-borne encephalitis in 1937. But the Soviet state arrested him three times. Accused of sabotage, spreading infections. Absurd charges. He survived, but it left scars.
Veniamin’s trilogy appeared between 1949 and 1956. Tatiana was lively, determined, relentless – Kaverin captured something of me, I suppose. The books popularised microbiology as a career for Soviet girls. That mattered. Science needs women. Not as tokens, but as thinkers. Tatiana became more famous than I was, ironically. Readers knew her better than they knew me. I didn’t mind. If a fictional version of my work inspired others, that was enough.
Let’s talk about 1942. You drank a solution of Vibrio cholerae. Why?
Because cholera was killing people faster than we could contain it, and I needed data.
Rostov had faced cholera in 1922. I’d investigated the bacteria, identified pathogenic strains from tap water, and proposed chlorinating drinking water. It worked. But in 1942, the war brought cholera to Stalingrad. The city was a military hub, soldiers moving through constantly. A cholera outbreak there could collapse the entire Eastern Front.
I flew to Stalingrad in a small plane. German bombers destroyed the freight train carrying my phage preparations. I had to produce cholera bacteriophage locally, in a hospital basement, under bombardment. We administered it to 50,000 people daily. The epidemic subsided. But I still needed to understand Vibrio cholerae virulence, resistance, how infections progressed. Animal models were unavailable. Speed mattered.
So I drank the solution. I fell ill within eighteen hours. Severe nausea, cramps, dehydration. But I recovered after treatment. The experiment gave me data on infection kinetics, immune response, the protective effect of bacteriophage therapy. I published the results in 1942. That work informed cholera prevention measures across the Eastern Front. Was it reckless? Perhaps. But waiting for laboratory approval whilst soldiers died – that was not an option.
Self-experimentation has a long history in science, but it’s also ethically fraught. Looking back, do you have regrets?
No. But I recognise the privilege of hindsight. I survived. If I had died, the experiment would be remembered as foolish, not brave. Self-experimentation works only when the scientist accepts mortality as a variable. I did. That doesn’t make it right. It makes it honest.
Ethics and urgency are not always compatible. Today’s scientists have institutional review boards, animal models, protocols. In 1942, we had none of that. We had dying soldiers and no time. I don’t recommend my methods. But I don’t regret them.
After Stalingrad, you turned to penicillin. Walk us through the technical process. How did you isolate Penicillium crustosum, and what made Soviet production different from Western methods?
Ah, the technical question. Very well.
By 1942, we knew penicillin existed. Fleming had discovered it in 1928. Florey and Chain at Oxford isolated it in 1939 and tested it on mice in 1940. The Americans developed deep fermentation by 1943, scaling production dramatically. But we had none of that. No strains, no protocols, no industrial infrastructure. We started from scratch.
I formed a team in Moscow: Tamara Balezina, my colleague, handled the hands-on laboratory work. We needed a penicillin-producing mould. Balezina collected fungal samples from soil, grass, walls, bomb shelters. We isolated cultures and tested them against pathogenic staphylococci, which die on contact with penicillin. The first ninety-two samples were useless. The ninety-third worked.
Balezina found it on the second floor of a building on Yauzsky Boulevard. It was Penicillium crustosum – not Fleming’s Penicillium notatum, but a different species. Ours produced higher yields. We called the drug “krustosin”.
Now, fermentation. The Americans used deep fermentation: aerobic mould cells grown throughout the medium, not just on the surface, with vigorous stirring and aeration. We couldn’t replicate that. No equipment, no expertise. We used surface fermentation: growing the mould in shallow trays, labour-intensive, lower yields. We used meat broth as our medium. Florey visited in 1944 and called it “useless for large-scale production”. He was right. But it was what we had.
The critical challenge was contamination. Surface fermentation is prone to bacterial infection, which destroys the culture. We sterilised everything, monitored constantly. Another problem: stability. Penicillin degrades rapidly in solution. We couldn’t freeze-dry it – no equipment. So we produced liquid concentrated penicillin, which had to be used quickly.
By 1943, we’d produced enough for clinical trials. Professor I.G. Rufanov tested it in Moscow hospitals. A Red Army soldier with sepsis after amputation – krustosin saved him. Mortality from infected wounds dropped 80 per cent. Amputations decreased 20 to 30 per cent. We introduced it to frontline use during the Baltic offensive in 1944.
Howard Florey compared Soviet and American penicillin in 1944. He reportedly called you “Madame Penicillin” after finding your strain 1.4 times more effective. What was that meeting like?
Florey arrived in January 1944 with British and American colleagues. He brought samples of American penicillin, produced by Pfizer. He proposed a comparison: his strain versus ours, head-to-head clinical trials.
We were nervous. Soviet science was isolated. If our penicillin failed, the state would see it as ideological defeat. But Florey was fair. He tested both strains on patients, measured outcomes rigorously. Our krustosin performed 1.4 times better in bacterial inhibition assays.
Florey was surprised, I think. He’d expected Soviet science to lag. Instead, he found a functional antibiotic produced under siege conditions. He called me “Madame Penicillin” respectfully, not mockingly. We shared notes. He explained deep fermentation. I described our surface methods. It was collaboration, brief and genuine.
But there was tension. Florey doubted Soviet claims. He asked to see patients treated with our penicillin; we showed him only selected cases. He suspected we were substituting American penicillin for ours in official reports. Honestly? That probably happened. The state cared about propaganda. If American penicillin tested better, Party officials might have swapped it in to claim Soviet superiority. I didn’t control those decisions. I controlled the science.
There’s evidence suggesting Soviet authorities may have used American penicillin obtained through espionage or Lend-Lease, then claimed it as domestic production. How do you respond to that?
Yes. It happened.
In 1944, the United States sent penicillin to the USSR under Lend-Lease – 300 billion units in one shipment alone. That’s roughly Soviet monthly output in 1947. Our production was minimal until late 1944, and even then, we used outdated surface fermentation. By 1945, we could barely meet military needs, let alone civilian demand.
The state wanted credit. Stalin Prize committees, propaganda campaigns – they needed Soviet penicillin to be Soviet, not American. So yes, I believe samples submitted to the Academy of Medical Sciences were sometimes substituted. I didn’t make those decisions. But I knew they happened.
Does that invalidate my work? No. Balezina and I isolated Penicillium crustosum. We developed fermentation protocols. We produced functional penicillin. It wasn’t as pure or plentiful as the American version, but it saved lives. The politics of credit – that’s separate from the science.
You received the Stalin Prize in 1943, the same year Fleming, Florey and Chain’s work was celebrated internationally. They received the Nobel Prize in 1945. You didn’t. How did that feel?
Expected. The Nobel Committee didn’t consider Soviet scientists. Geopolitical isolation, lack of nomination access – those were barriers. The West controlled the narrative. Soviet breakthroughs were dismissed as propaganda.
But the Stalin Prize mattered to me. It meant the state valued my work, that resources would continue. In 1947, I became director of the All-Union Research Institute of Antibiotics, later the Institute of Antibiotics. From 1952 until my death, I headed the Department of Microbiology at Moscow’s Central Post-Graduate Medical Institute. I trained generations of microbiologists, published over 500 papers, wrote books on penicillin, bacterial polysaccharides, interferon. I founded Antibiotiki, the Soviet antibiotics journal.
Recognition takes many forms. A Nobel Prize is one. Training scientists who save lives – that’s another.
Your later work included interferon research. Can you explain that transition?
Antibiotics were one frontier. Viruses were another. Penicillin kills bacteria, but it’s useless against viruses. By the 1950s, viral diseases – polio, influenza – were major public health threats. Interferon, discovered in 1957, was a protein that cells produce to resist viral infection.
We studied how to produce interferon industrially, how to induce it in cell cultures. Tamara Balezina, my colleague from the penicillin days, worked on this with me. In 1972, she patented a method using plant viruses as interferon inductors. It was elegant work, overlooked because it didn’t have the drama of wartime penicillin.
Interferon research required patience. Unlike antibiotics, which showed immediate results, antiviral work was slower, more speculative. But it was necessary. Science doesn’t stop because one problem is solved.
Let’s discuss the erasure of your work from Western history. Why do you think that happened?
Three reasons. First, secrecy. Soviet penicillin production was classified military research. The state didn’t publish details. Western historians couldn’t access our data, so they ignored it.
Second, narrative dominance. Post-war histories centre Oxford and American mass production. The Nobel Prize solidified that story. Soviet parallel achievements were dismissed as propaganda or omitted entirely.
Third, ideology. During the Cold War, Western scientists were reluctant to credit Soviet achievements, especially those awarded Stalin Prizes. My story was politicised out of mainstream science history. The Oxford team’s careful mouse trials were celebrated; my wartime pragmatism was invisible.
Gender played a role, too. Western historians often portrayed Soviet female scientists as state-sponsored tokens, not independent innovators. My technical contributions were downplayed. The fact that I was a woman in Soviet STEM – that was treated as propaganda, not merit.
If you could correct one misconception about your work, what would it be?
That Soviet penicillin was a copy of Western penicillin. It wasn’t. We used a different species – Penicillium crustosum, not notatum. We developed independent fermentation protocols under siege conditions. Our challenges were unique: no deep fermentation technology, limited supplies, active combat zones. The fact that we succeeded at all – that’s the story.
Penicillin was a multiple discovery, not a Western monopoly. Secrecy, not science, decided who got credit.
What advice would you give to young scientists today, especially women or those working in marginalised contexts?
Do the work. Don’t wait for permission, recognition, or perfect conditions. Science progresses because someone, somewhere, refuses to accept ignorance as an answer.
If you’re a woman, you’ll face doubt. Prove them wrong quietly, through results. If you’re isolated – geographically, institutionally, or ideologically – find collaborators who value truth over politics. And if your work is overlooked, remember: history is written by the present. Your contributions may not be recognized in your lifetime. That doesn’t make them less real.
Also, document everything. I published over 500 papers. That’s why historians can reconstruct my work now. If you don’t write it down, it disappears.
One final question. You died on 2 December 1974, after holding your last scientific conference that day. What were you working on?
I was 76. I’d spent fifty years studying microbes – bacteria, viruses, antibiotics, interferon. That day, we were discussing new antibiotic resistance patterns, strategies for chemotherapy of infection. The work never stopped.
I didn’t plan to die that day. But if I had to choose, that’s how I’d want it: in a room full of scientists, solving problems. Not quietly, but mid-sentence.
Science is unfinished. It will outlive all of us. My work – Tatiana’s work, Balezina’s work, the work of every scientist whose name you don’t know – it’s part of a larger structure. Penicillin saved millions. Interferon advanced antiviral therapy. Bacteriophage research, lysozyme studies – they’re foundations for treatments we can’t yet imagine.
That’s the point. We build. Others continue. The work endures.
Thank you, Dr Yermolyeva. Your story matters.
It always did. The world just needed time to notice.
Letters and emails
Since publishing this interview, we’ve received hundreds of messages from scientists, students, and curious minds across the globe – all wanting to ask Zinaida Yermolyeva one more question. The letters reveal what readers found most compelling: not just her penicillin breakthrough, but her choices under pressure, her approach to risk, her thoughts on how science is credited and remembered. We’ve selected five thoughtful contributions from our growing international community, each exploring dimensions of her life and work that merit further reflection. These are questions from those who see themselves in her story – whether as early-career researchers facing resource constraints, women navigating institutional barriers, or simply those seeking wisdom from someone who refused to wait for perfect conditions.
Sina Malosi (28, marine biology student, Apia, Samoa):
As someone who refined surface fermentation of Penicillium crustosum under bombardment, which specific process parameters – like aeration style, vessel geometry, or nutrient composition – did you find most decisive, and are there low-tech optimisation tricks you wish modern small labs still used when resources are tight?
Ah, a proper technical question. Good. Most people ask about the cholera experiment – dramatic, yes, but less useful for replication.
Surface fermentation is brutally simple, which makes optimisation both easier and harder. You’re growing mould on liquid medium in shallow vessels – trays, flasks, sometimes repurposed industrial containers. The mould forms a mat on the surface, secretes penicillin into the liquid below. Your yield depends on maximising surface area whilst maintaining stable conditions. No stirring, no forced aeration – just patience and vigilance.
Vessel geometry mattered most. We used flat enamel trays, roughly 40 by 60 centimetres, filled to about 3 centimetres depth. Shallow depth is critical: too deep and the lower layers become anaerobic, killing productivity. Too shallow and evaporation concentrates salts, stressing the culture. We found 2.5 to 3.5 centimetres optimal for meat broth medium.
Why enamel? Because glass shattered during bombardment, and metal corroded in the acidic medium. Enamel was robust, sterilisable, available. We stacked trays in incubation rooms – not proper incubators, just heated basement rooms where temperature could be held near 24°C. Penicillium crustosum is temperamental. Below 20°C, growth slows. Above 28°C, contaminating bacteria flourish. We monitored constantly with mercury thermometers, adjusted coal-fired heating manually.
Nutrient composition – here’s where wartime constraints forced creativity. The Oxford group used corn steep liquor, which increased yields dramatically. We had none. Corn wasn’t grown extensively in the USSR, and importing was impossible. So we used what we had: meat broth from slaughterhouses, supplemented with glucose and salts.
Meat broth sounds crude, but it worked. Peptides from hydrolysed protein provide nitrogen; glucose feeds carbon metabolism. The trick was standardisation. Different batches of meat broth had wildly different compositions – fat content, protein concentration, salt levels. We tested every batch before scaling up. If a batch supported good growth in pilot cultures, we’d use the entire supply for production. If not, we’d adjust glucose or add ammonium salts to compensate.
One parameter modern labs forget: pH stability. Penicillium acidifies the medium as it grows, secreting organic acids. If pH drops below 5.0, penicillin degrades. We didn’t have pH meters – those were rare – so we used litmus paper and added sterile chalk (calcium carbonate) to buffer the medium. Chalk dissolves slowly, releasing carbonate as needed. Simple, effective, almost free.
Aeration – passive only. We couldn’t afford the compressors and spargers required for deep fermentation. Instead, we relied on diffusion: oxygen from room air dissolving into the thin liquid layer. This limits productivity. Surface fermentation yields perhaps 10 to 20 units of penicillin per millilitre after seven to ten days. Deep fermentation, with forced aeration, produces 200 to 300 units per millilitre in half the time. But forced aeration requires electricity, mechanical reliability, trained operators. We had none of those consistently.
What we did have was space and labour. We ran hundreds of trays simultaneously. If each tray yielded poorly, the aggregate still sufficed for clinical use. Balezina managed the cultures personally – inspecting for contamination, discarding infected trays, harvesting mature cultures. Contamination was constant. A single airborne bacterium could ruin a tray overnight. We worked in basements to minimise air currents, sterilised everything with steam, wore masks and gloves. Hygiene discipline substituted for sterile equipment.
Harvesting and extraction – another bottleneck. After seven to ten days, we’d separate the mould mat from the liquid, filter the broth through sterile gauze, then concentrate it. No freeze-drying, no chromatography. We used solvent extraction: adding amyl acetate or ether to pull penicillin into an organic phase, then back-extracting into water at controlled pH. Labour-intensive, lossy – perhaps 40 per cent recovery – but it worked with chemistry-lab glassware.
Low-tech tricks modern labs should remember? Three.
First: pilot testing before scaling. Don’t assume your medium will work at volume. Test small batches, measure yield, adjust variables one at a time. We wasted less medium this way than colleagues who rushed to production.
Second: biological replicates over technical precision. If your instruments are unreliable – thermometers drift, pH papers fade – run multiple parallel cultures and average results. Variability smooths out. Better ten rough measurements than one “precise” reading from faulty equipment.
Third: standardise your inoculum. We maintained our Penicillium crustosum strain on agar slants, transferring every two weeks to prevent mutation. Each production run used spores from the same generation. Genetic drift kills reproducibility. Modern labs with -80°C freezers forget how fragile strain maintenance was. We kept ours alive through discipline.
Would I use surface fermentation today? No. Deep fermentation is superior in every measurable way – yield, speed, purity. But if you’re in Samoa, or rural Ethiopia, or anywhere without stable electricity and trained engineers, surface fermentation still works. It’s robust against infrastructure failure. That matters.
Science adapts to constraints. In 1943, our constraint was industrial capacity. We solved it with geometry, chemistry, and relentless labour. Your constraint might be different – power cuts, import restrictions, funding gaps. The principles remain: maximise surface area, control temperature and pH, prevent contamination, standardise inputs. The rest is persistence.
Does that answer your question? If you’re setting up a low-resource lab, write to me – well, write to someone who remembers these methods. They’re disappearing from textbooks. That’s a loss.
Chatri Srisuwan (31, biotechnology engineer, Chiang Mai, Thailand):
You worked on both bacteriophages and antibiotics long before today’s interest in phage therapy for drug‑resistant infections; if you had access to modern sequencing and bioreactors, how would you design a combined phage–antibiotic protocol for battlefield infections, and when would you choose one over the other?
You’re asking the right question, finally. Phage therapy and antibiotics were never opposed in Soviet medicine – they were complementary tools. The West abandoned phages after penicillin arrived, treating antibiotics as a universal solution. We didn’t. We couldn’t afford to. And now, seventy years later, you’re rediscovering what we knew in 1942: bacteria evolve, antibiotics fail, and phages remain.
Let me be clear about the historical context. I began studying bacteriophages in 1925 at the USSR Academy of Sciences. Félix d’Hérelle had discovered them in 1917 – viruses that infect and kill bacteria. He visited the Soviet Union in the 1930s and worked at our institutes. We built on his methods: isolating phages from sewage, river water, soil; testing them against pathogenic bacteria; administering them orally or topically to patients.
Phage therapy worked. We used it extensively for dysentery, cholera, typhoid during the war. In Stalingrad, when cholera threatened the city in 1942, I flew in with bacteriophage preparations. We administered them prophylactically to 50,000 people daily. The epidemic subsided. But phages had limitations: they’re highly specific – one phage type kills one bacterial strain, not broad-spectrum like antibiotics. If the strain mutates or you misidentify the pathogen, the phage is useless. And production was artisanal, inconsistent. Every batch required fresh isolation, titration, quality control.
Penicillin, by contrast, killed multiple species – staphylococci, streptococci, pneumococci. It was slower to develop resistance in the 1940s. It could be mass-produced, freeze-dried, stored. Strategically, for battlefield medicine, antibiotics were simpler: one drug, broad coverage, reliable supply chains.
But here’s what we understood that the West ignored: phages and antibiotics address different failure modes. Antibiotics fail when bacteria develop enzymatic resistance – beta-lactamases, efflux pumps, target mutations. Phages fail when bacteria alter surface receptors or acquire CRISPR immunity. These mechanisms are independent. A bacterium resistant to penicillin isn’t necessarily resistant to phages, and vice versa.
So, to your question: if I had modern sequencing and bioreactors, how would I design a combined protocol?
First: rapid diagnostics. In 1942, identifying the causative pathogen took days – culture on agar, biochemical tests, Gram staining. By the time we knew what we were treating, soldiers had died. Today, you have PCR, metagenomics, MALDI-TOF. Use them. Within hours of receiving a wound sample, sequence the bacterial DNA. Identify species, detect resistance genes – bla genes for beta-lactamase, mecA for methicillin resistance, vanA for vancomycin resistance. This tells you immediately whether antibiotics will work.
Second: phage selection guided by genomics. Maintain a curated library of therapeutic phages, each sequenced and characterised. Cross-reference the patient’s bacterial strain against your phage library. Which phages target that strain’s receptor proteins? Which lack lysogeny genes – you don’t want temperate phages that integrate into bacterial genomes and potentially transfer resistance genes. Select three to five lytic phages with non-overlapping receptor specificities. This is a phage cocktail, resistant to single-mutation escape.
Third: sequential or concurrent deployment. Here’s where strategy diverges based on infection severity.
For acute battlefield wounds – contaminated shrapnel injuries, open fractures, gas gangrene risk – I’d start with antibiotics immediately. Speed matters. Broad-spectrum coverage – something like a carbapenem or fourth-generation cephalosporin if resistance patterns allow. This buys time whilst you sequence the pathogen and prepare phages.
Simultaneously, apply phage cocktail topically to the wound. Phages replicate at the infection site, increasing concentration as bacteria grow. They penetrate biofilms better than antibiotics. For surface wounds, this is ideal. The antibiotic handles bloodstream dissemination; the phage clears the local bacterial load.
After 48 hours, reassess. If the infection is controlled, taper antibiotics and continue phages. If bacteria are resistant and multiplying, switch to phage monotherapy or adjust the cocktail based on updated sequencing.
For antibiotic-resistant infections – MRSA, carbapenem-resistant Enterobacteriaceae, Acinetobacter baumannii – phages become primary. Administer intravenously if the phage is purified and endotoxin-free. Your modern bioreactors can produce high-titre, clinical-grade phage suspensions. We couldn’t do that in 1943 – our phage preparations were crude, suitable only for oral or topical use. But with controlled fermentation, you can achieve sterile, pyrogenic-free phage at 10^10 plaque-forming units per millilitre. Enough for systemic therapy.
Fourth: evolutionary management. Bacteria will evolve resistance to phages – receptor mutations, CRISPR spacers acquired from previous phage exposure. Counter this by rotating phages. Don’t use the same cocktail continuously. After two weeks, switch to a different set targeting alternative receptors. Bacteria can’t maintain resistance to multiple phage types simultaneously without fitness costs.
Here’s the critical insight: combine phages with sub-lethal antibiotic doses. This is counterintuitive, but hear me. Low-dose antibiotics slow bacterial growth, reducing mutation rates. Phages replicate faster in slower-growing bacteria because the cells remain metabolically active but don’t outpace phage lysis. The combination suppresses resistance evolution to both agents. We didn’t understand the mechanism in the 1940s, but we observed it empirically.
When would I choose one over the other exclusively?
Phages alone: When the pathogen is known, antibiotic-resistant, and accessible – skin infections, urinary tract infections, gastrointestinal infections where phages can be delivered orally. Also for prophylaxis in high-risk populations, like your question implies for battlefield settings. Soldiers in endemic cholera zones could take phage cocktails prophylactically, as we did in Stalingrad.
Antibiotics alone: When the pathogen is unknown, infection is deep-tissue or bloodstream, and you lack time for phage preparation. Also for polymicrobial infections – multiple bacterial species simultaneously. Phage cocktails targeting five species are feasible; targeting twenty isn’t. Antibiotics handle complexity better.
Both concurrently: For severe, life-threatening infections where you can’t afford failure – sepsis, necrotising fasciitis, post-surgical infections in immunocompromised patients. Redundancy saves lives.
One more point: modern sequencing changes phage discovery. In my era, we isolated phages by enrichment – mixing sewage with target bacteria, incubating, plating, picking plaques. Labour-intensive, slow. Now you can sequence environmental samples, identify phage genomes computationally, synthesise them if necessary. You can engineer phages – remove lysogeny modules, add enzymes that degrade biofilms, optimise receptor-binding domains. I would have given anything for that capacity in 1943.
But – and this is crucial – engineering must be constrained by safety. Phages are self-replicating. Once released, they evolve. Don’t create chimeric phages with unpredictable host ranges or horizontal gene transfer potential. Soviet phage therapy succeeded partly because we used naturally occurring, well-characterised phages. We understood their limitations. Engineered phages are powerful, but hubris invites catastrophe.
Your modern tools – bioreactors, sequencers, CRISPR editors – would have transformed my work. But the principles remain unchanged: know your pathogen, match your weapon to the target, anticipate resistance, use combinations to cover failure modes. Phages and antibiotics are not alternatives. They’re partners. The West forgot that. Don’t make the same mistake again.
Does Thailand face antibiotic-resistant infections in your hospitals? If so, start building a phage library now. Isolate from local water sources – rivers, sewage treatment plants. Characterise against your most common resistant pathogens. When the crisis arrives – and it will – you’ll have tools ready. That’s what I did in 1925, and it saved lives in 1942. Preparation isn’t dramatic. But it works.
Tigist Bekele (34, public health physician, Addis Ababa, Ethiopia):
You drank Vibrio cholerae and recovered, then went on to shape national cholera policy – how did that experience change your sense of acceptable risk in epidemic response, and what would you say now to clinicians in low-income countries who feel pressured to ‘sacrifice’ for data?
Tigist, this is a serious question. It deserves a serious answer, not a legend.
First, the facts. In 1942 I drank a measured dose of Vibrio cholerae, became ill, and recovered under controlled observation. I did it because we had an advancing war, a threatened city, and very little time. Stalingrad was on the edge of disaster: troop movements, poor sanitation, summer heat – perfect conditions for cholera to sweep through soldiers and civilians alike. Our supplies were limited, animal models were not at hand, and we needed to know, quickly and precisely, how well our preventive measures worked.
That experiment did influence policy. The data we gathered on incubation, clinical course, and the effect of prophylactic measures – chlorination, bacteriophage use, hygiene discipline – fed directly into the recommendations we applied on the Eastern Front and later in civilian contexts. It helped convince sceptical administrators that phage prophylaxis and water disinfection were not “theoretical fancies” but practical tools that could save thousands.
Now, to your real question: what did it do to my sense of acceptable risk?
Before that, I thought of risk mainly in terms of the patient – how much we could safely ask of them in trials, how far we could push dosing, when to stop. After drinking cholera, I understood something else: the temptation to use oneself as a convenient experimental animal is very strong when the hour is dark. It feels clean, even heroic. No need for consent forms, no need to explain risk to anyone else. You carry it alone.
But there is a danger in this kind of heroism. It is easily admired, easily copied, and easily abused.
In 1942 I was not a young student. I was already an experienced microbiologist, responsible for a whole direction of research. I knew the likely dose–response, I could arrange immediate treatment, I had colleagues who understood what we were doing. Even so, I could have died. If I had miscalculated the dose or if treatment had failed, my death would have helped no one. It would have deprived our institute of a leader at the very moment when penicillin and phage work were most needed.
So, it sharpened my sense of acceptable risk in two ways.
First, I became much more strict with my staff. After that experiment, I refused to allow younger colleagues to imitate me. When someone suggested they “follow my example”, I told them: “No. One fool in a department is quite enough.” If there was risk to be taken, I insisted it fall first on those of us who were already trained, already past the age when a lost life meant the loss of an entire future career. Even then, we weighed it carefully.
Second, I realised that the real courage is not in throwing oneself into danger, but in building structures that make such gestures unnecessary. It is less romantic to argue for chlorination budgets, for laboratory capacity, for routine phage production – but that is what prevents epidemics. A dead hero does not write guidelines, does not train students, does not correct bad policy.
Now you ask about clinicians in countries with few resources, who feel pressed to “sacrifice” for data.
From where I stand, I would say this:
Your first duty is not to die for your patients. Your first duty is to remain alive, competent, and able to treat the next hundred, the next thousand. If your government or your institution suggests that you must risk your life in uncontrolled self-experimentation because “there is no other way”, then the real problem is not your courage. The problem is their failure to invest in infrastructure, training, and safe trial design.
In my time, we had no ethics committees, no international conventions, no standard frameworks. We improvised under war conditions. You, in your time, have the benefit of those hard lessons. Use them. When you design a trial, ask yourself:
- Can this question be answered with existing data, animal models, or observational studies? If yes, then human risk is not justified.
- If human subjects are truly necessary, can the risk be shared in a controlled, monitored way among many volunteers, so no single person bears a lethal burden?
- Is the proposed experiment repeatable and generalisable, or is it just a gesture that will make a good story but poor science?
My cholera experiment produced data that affected policy. It was not a theatrical act. But even so, with the tools you have now – microbiology, epidemiology, modelling – I suspect you could gain much of that knowledge without poisoning yourself.
To clinicians under pressure I would add this: do not confuse desperation with duty. I worked in basements while bombs fell, with wounded soldiers lying in the corridors and epidemics at the door. The tendency, in such moments, is to think only in terms of immediate sacrifice. But medicine and public health are long campaigns. If all the thoughtful, well-trained people burn themselves out – or die – for one experiment, what then?
If you must take risks, let them be measured, shared, and justified by a clear gain in knowledge that cannot be obtained otherwise. And always remember: your patients need you alive tomorrow more than they need your martyrdom today.
In short: I do not regret drinking cholera. It was a choice for that war, that city, that hour. But I would not hold it up as a model for you. Your courage should express itself in building clinics, insisting on clean water, collecting careful data, and resisting those who romanticise “sacrifice” while doing nothing to repair the conditions that make such sacrifice seem necessary.
Logan Bennett (26, history of science graduate student, Boston, USA):
If wartime penicillin research had been openly shared between the USSR, Britain and the United States – with no classification or espionage on any side – what concrete differences do you think we’d see today in global antibiotic stewardship, resistance levels, or how scientific credit is granted?
Logan, you are asking me to imagine a world that never existed and perhaps never could. But let me try.
If penicillin research had been truly open between 1940 and 1945 – shared protocols, shared strains, shared production data – the immediate effect would have been fewer dead soldiers. That is the first and most concrete answer. The Americans achieved deep fermentation and mass production by late 1943. If those techniques had been transferred to the Soviet Union immediately, rather than hidden behind military classification or leaked piecemeal through espionage, we could have equipped field hospitals with adequate penicillin by 1944 instead of struggling with surface fermentation until 1945. Thousands of Red Army soldiers died from infected wounds that penicillin would have saved. The same is true in reverse: our Penicillium crustosum strain produced higher yields than early Western strains. If Oxford and American labs had received it in 1943, they might have accelerated their own production timelines.
But you are asking about long-term effects – stewardship, resistance, credit. Let me address each.
Antibiotic stewardship and resistance: This is where openness would have mattered most, and where its absence has cost us dearly.
In the Soviet Union, we understood from the beginning that antibiotics were a finite resource. Not philosophically finite – we didn’t yet know about resistance evolution in the modern sense – but practically finite, because production was difficult and supply was limited. We rationed penicillin strictly: only for life-threatening infections, only after confirming bacterial aetiology, never for trivial complaints. This was partly ideology – the state controlled distribution – but also necessity.
In the West, particularly the United States, mass production by 1944 created abundance. Penicillin became commercially available, advertised, prescribed liberally. By the late 1940s, American physicians were giving it for colds, for minor cuts, for conditions that were not even bacterial. This was madness from our perspective, but it made economic sense in a market system: pharmaceutical companies profited from volume, not restraint.
If research had been open, if Soviet rationing practices had been studied alongside Western production methods, perhaps – perhaps – international bodies would have recognised earlier that overuse bred resistance. We saw penicillin-resistant staphylococci in Soviet hospitals by 1946. The British saw them even earlier, by 1945. But there was no mechanism for sharing that surveillance data across Cold War boundaries. Each side discovered resistance independently, responded independently, and learned the same painful lessons separately.
Imagine instead: an Allied Antibiotic Committee, established in 1944, pooling resistance data from Leningrad, London, and Philadelphia. Shared microbiology, shared epidemiology. If clinicians worldwide had access to that data – “Staphylococcus aureus isolates in Moscow show 12 per cent penicillin resistance as of March 1946; reserve penicillin for confirmed infections only” – rational stewardship might have emerged a generation earlier. We might have delayed the spread of methicillin-resistant strains, might have preserved penicillin’s efficacy for another decade or two.
But we didn’t. So resistance spread faster, and by the 1960s we were already chasing it with methicillin, then cephalosporins, then carbapenems – an arms race that continues today. Open science could have slowed that race. Not stopped it – bacteria evolve; that is their nature – but slowed it.
Scientific credit and historiography: Here the counterfactual becomes more speculative, but no less important.
The 1945 Nobel Prize went to Fleming, Florey, and Chain. It was deserved, in the sense that their work was foundational: Fleming’s 1928 discovery, the Oxford team’s purification and clinical trials in 1940–41. But the Nobel Committee ignored parallel discoveries. They ignored our Penicillium crustosum, our independent fermentation protocols, our clinical deployment in 1943. Why? Because Soviet work was classified, inaccessible, and ideologically suspect.
If research had been open, if I had published our crustosum isolation methods in Nature or The Lancet in 1943, if Florey’s 1944 visit to Moscow had resulted in a co-authored paper rather than a diplomatic gesture, then the narrative would have been different. Not “the West discovered penicillin and saved the world,” but “penicillin was a multiple discovery, solved independently under different constraints, proving that science transcends borders even when politics do not.”
The Nobel Committee might still have chosen Fleming, Florey, and Chain – they made the first breakthroughs. But the historical record would acknowledge Soviet contributions as legitimate science, not Cold War propaganda. Textbooks would mention Yermolyeva and Balezina alongside the Oxford team. More importantly, young scientists in Africa, Asia, Latin America – anywhere outside the Western centres – would see that meaningful research happens everywhere, not just in well-funded universities.
This matters for who enters science and who stays. If history teaches that only Western scientists receive credit, then talented students elsewhere conclude that their work will be invisible no matter its quality. If history shows multiple discoveries, independent paths to the same solution, then science becomes a truly global enterprise.
Institutional structures and post-war collaboration: The most profound difference would have been institutional.
After 1945, Western and Soviet science diverged completely. We had our institutes, our journals, our conferences; you had yours. Minimal communication, minimal trust. Duplication of effort became standard: Western labs and Soviet labs working on the same antibiotics – streptomycin, tetracycline, chloramphenicol – independently, publishing in separate literatures, often unaware of each other’s progress.
If penicillin had established a precedent of openness – if the wartime alliance had extended into scientific collaboration – then post-war antibiotic development might have been coordinated. The World Health Organization, founded in 1948, could have become a true clearinghouse for antibiotic research: pooling clinical trial data, coordinating resistance surveillance, setting international standards for use and production. Instead, it became a weak advisory body, constrained by Cold War politics.
I see this in your present moment, Logan. In 2025, antibiotic resistance is a global crisis. Bacteria cross borders; resistance genes move via travel, trade, migration. But responses are still fragmented – rich countries hoard new antibiotics, poor countries lack access to even basic ones, surveillance is patchy, and pharmaceutical companies abandon antibiotic development because it is not profitable. These are failures of coordination, rooted in the nationalist, market-driven structures that emerged after World War II.
If 1943 had taught the world that antibiotics are a shared resource requiring shared stewardship, perhaps your generation would have inherited different institutions – ones capable of collective action.
The tragedy of what was lost: You asked about espionage. Yes, it happened. Soviet intelligence obtained American penicillin production data, probably through wartime scientific exchanges and outright spying. American intelligence monitored Soviet antibiotic programs, worried we were weaponising bacteria. Everyone suspected everyone.
But here is what espionage cannot do: it cannot build trust. Stolen data is incomplete, decontextualised. It does not come with the tacit knowledge – the lab tricks, the troubleshooting, the “we tried this and it failed” – that open collaboration provides. When I spoke with Florey in 1944, I learned more in two hours of conversation than I could have from a hundred pages of reports. He told me what didn’t work, where the Oxford team had wasted months on dead ends. That kind of knowledge is never written down. It is only shared between people who trust each other.
If the war had ended with scientific openness, if researchers could have visited each other’s labs freely, if journals had been accessible across the Iron Curtain, we would have saved years of duplicated effort and avoided countless mistakes.
So, to answer your question directly: If penicillin research had been open from 1940 to 1945, we would see, today:
- Lower antibiotic resistance levels globally, because rational stewardship would have emerged earlier.
- Stronger international institutions for infectious disease control, built on a precedent of wartime scientific collaboration.
- A more accurate historical record, acknowledging multiple discoveries and non-Western contributions, which would encourage broader participation in science.
- Faster antibiotic development in the post-war period, because coordination would have reduced duplication and accelerated knowledge transfer.
But Logan, here is the hard truth: science was never going to be open in that way, because science does not exist apart from politics. Penicillin was a military asset, not a humanitarian gift. States classified it for the same reason they classified radar, cryptography, and atomic research: because knowledge is power, and sharing power with potential adversaries is not how nations behave.
The question is not whether we can undo the past. We cannot. The question is whether your generation will repeat our mistakes. You have new antibiotics in development – new beta-lactamases inhibitors, new peptides, new phage therapies. Will you classify them, patent them, hoard them? Or will you share them as global public goods, the way vaccines should have been shared during your COVID pandemic?
History does not repeat, but it echoes. I hear the echoes clearly. Whether you will act differently – that is up to you.
Helga Jónsdóttir (41, clinical microbiologist, Reykjavík, Iceland):
Your life inspired the fictional Tatiana and later a global audience through a Google Doodle, yet your technical work was often overshadowed – how do you think scientists can protect the integrity of their contributions when states, media or movements prefer a simplified hero story?
Helga, you’ve touched on something that troubled me for years, though I never spoke of it publicly whilst I was alive. The distance between what I actually did and what people said I did – that gap widened with every retelling, and there was very little I could do to close it.
Let me start with Tatiana. Veniamin Kaverin’s Open Book trilogy appeared between 1949 and 1956. Tatiana Vlasenkova was lively, passionate, relentless – she fought institutional obstruction, she challenged corrupt administrators, she pursued penicillin with single-minded determination. Kaverin based her on me, loosely, but he also invented freely. Tatiana’s romantic entanglements, her dramatic confrontations with Party officials, the clean narrative arc from struggle to triumph – these were literary devices, not my biography.
But readers didn’t care about the distinction. To them, Tatiana was me. Young women wrote to me saying the books had inspired them to study microbiology. That was wonderful, genuinely. Science needs women, and if a fictional character brought them into the field, I wasn’t going to complain. But it also meant that my actual work – the tedious fermentation trials, the contamination problems, the failed experiments – became invisible. People saw the heroine, not the microbiologist.
The state encouraged this. The Stalin Prize I received in 1943 was for scientific achievement, yes, but it was also propaganda. “Soviet Woman Scientist Defeats Fascist Infection” – that was the narrative. Never mind that penicillin production in 1943 was minimal, that we struggled with surface fermentation until 1945, that American Lend-Lease penicillin probably saved more Soviet soldiers than krustosin did. The state needed a success story, so they simplified, dramatised, and claimed total victory.
I understood the political necessity. The war demanded morale. But it created a problem: once you become a symbol, your actual contributions are secondary to what the symbol represents. I was “Madame Penicillin,” the woman who out-scienced the West, the proof that Soviet communism could produce genius. That reputation opened doors – funding, institutional support, the directorship of the Institute of Antibiotics in 1947. But it also meant that any admission of difficulty, any acknowledgment of Western superiority in production technology, any mention of Lend-Lease penicillin – these became ideological betrayals.
So I learned to live with two narratives. The public one, which I neither controlled nor entirely endorsed. And the technical one, which I published in scientific journals, carefully, with data, for those who cared to read.
Now, your question: how can scientists protect the integrity of their contributions when simplification is demanded?
First: publish relentlessly, in detail, in peer-reviewed venues. I authored over 500 papers during my career. Not all were major breakthroughs – many were incremental, methodological, documentation of failures as well as successes. But they exist. They are archived. When historians finally decided to examine my work seriously, decades after my death, those papers were the evidence. The Google Doodle you mention, in 2018 – that happened because archivists and historians could reconstruct what I actually did, not just what Kaverin wrote or Soviet propaganda claimed.
Popular narratives fade. Monuments are reinterpreted. But primary literature endures. If you want your work to be understood correctly by future generations, write it down in technical language, with full methods, with honest acknowledgment of limitations. Publish it somewhere that will be preserved – indexed journals, institutional repositories, archives that will survive political changes.
Second: train students and collaborators who understand the work, not just the story. From 1952 until my death in 1974, I headed the Department of Microbiology at Moscow’s Central Post-Graduate Medical Institute. I trained hundreds of microbiologists. I insisted they read original literature, replicate experiments, question my conclusions. I did not want disciples; I wanted scientists who could think independently.
Those students became the institutional memory. When journalists came looking for dramatic stories about wartime penicillin, my former students could say, “Actually, here’s what the data showed.” They didn’t always get quoted – drama sells better than nuance – but they were there, correcting the record where possible.
If you want your technical contributions to survive simplification, build a community that values precision. Mentor people who will defend complexity when you are no longer around to do it yourself.
Third: resist, selectively, when the simplification becomes outright falsehood. I could not stop the state from claiming exaggerated production figures or from substituting American penicillin in propaganda displays. That would have been dangerous, possibly career-ending. But I could, quietly, in scientific settings, present accurate data. I could decline to repeat false claims in my own publications. I could ensure that my textbooks – Penicillin and Antibiotics, for example – contained real protocols, real yields, real limitations.
This is a narrow path. You cannot publicly contradict powerful narratives without consequences. But you can refuse to personally endorse them. You can maintain a parallel record – the technical truth alongside the public myth – and trust that eventually someone will care about the difference.
Fourth: accept that you cannot fully control your legacy, and decide what matters most. Tatiana inspired young women to become scientists. The Google Doodle, seventy years late, brought global attention to Soviet contributions to antibiotics. These are not the outcomes I would have designed – I would have preferred accurate contemporaneous recognition – but they achieved something valuable nonetheless.
Would I rather have had a Nobel Prize in 1945 and no fictional heroine? Yes. But the Nobel was never a possibility, for reasons beyond my control – geopolitics, secrecy, Western bias. The choice was not between accurate credit and simplified myth. The choice was between simplified myth and total obscurity. Given that, I accepted the myth and worked to preserve the technical record alongside it.
Fifth: recognise that “hero stories” serve a function, and sometimes that function is not about you. The Soviet state needed Tatiana to recruit women into science during post-war reconstruction. It worked. Enrolment in microbiology programs increased; my institute received talented students who might otherwise have pursued other fields. The story was not accurate, but it was useful.
As a scientist, I valued accuracy. As a citizen of a country recovering from catastrophic war, I understood pragmatism. Sometimes you accept the hero story because it serves a larger goal – more scientists, more funding, more public appreciation of microbiology – even if it distorts your personal contribution.
The key is to separate your self-worth from the narrative. I did not believe I was the flawless heroine of Kaverin’s novels. I knew exactly where I had failed, where I had been lucky, where others had done the critical work. That private knowledge protected me from the distortions of the public story.
Sixth: use whatever platform the simplified story gives you to do more rigorous work. “Madame Penicillin” had access that Zinaida Yermolyeva, microbiologist, might not have had. I used that access to build the Institute of Antibiotics, to fund interferon research, to launch Antibiotiki journal, to train a generation of researchers. The mythology was a tool. I wielded it where I could.
If you become famous for a simplified version of your work, do not waste time lamenting the simplification. Use the fame. Get resources. Build institutions. Publish better science. The narrative will eventually correct itself – or it won’t, and future scientists will do the correcting – but the work you do with the resources mythology provides will be real and lasting.
Finally: document the mundane, not just the dramatic. What survives in popular memory? The cholera experiment – drinking Vibrio cholerae, falling ill, recovering. It is vivid, it is shocking, it fits the hero narrative. What disappears? The months I spent optimising meat broth composition for surface fermentation. The contamination rates we struggled with. The bureaucratic fights to secure enamel trays and coal for heating.
But it is the mundane work that other scientists need to know. In my published papers, I included those details: culture conditions, temperatures, failure rates, equipment specifications. I did not expect journalists to care. I expected other microbiologists to care. And they did. That is why, when researchers today want to understand Soviet antibiotic production, they read my technical papers, not Kaverin’s novels.
Helga, you are a clinical microbiologist in Iceland – a small country, outside the major centres, doing essential work that will probably never make headlines. You will face this same tension: the desire for your work to be recognised versus the reality that recognition, when it comes, often distorts what you actually did.
My advice: do the work rigorously. Publish it completely. Train others who understand it. Use whatever platform or resources the simplified story provides, but never confuse the story with the science. And accept that history is written slowly, over generations. The Google Doodle came forty-four years after my death. Better late than never, I suppose.
The technical contributions protect themselves, if you document them well enough. The hero stories – those come and go, shaped by politics and fashion. Focus on what endures.
Reflection
Zinaida Yermolyeva died on 2nd December 1974, at the age of 76, mid-conversation at a scientific conference – a fitting exit for someone who never stopped asking questions. Nearly fifty years would pass before a Google Doodle, in 2018, introduced her to a global audience that Western history had never acknowledged. By then, the Cold War was thirty years finished. The Iron Curtain had fallen. Yet her story remained fragmented, scattered across Soviet archives, Russian-language journals, and the fading memories of her students and colleagues.
This interview, conducted as a fiction in 2025, reveals something important about how history works: the gap between what happened and what was recorded; between technical achievement and narrative visibility; between the woman who actually lived and the symbol she became.
Several themes emerge from our conversation that challenge the official record.
First, the pragmatism of wartime science. Yermolyeva’s cholera self-experiment is often treated as a dramatic gesture, a stunt that confirms her fearlessness. She reframes it as necessity – field medicine under fire, where animal models were unavailable and speed mattered more than protocol. She acknowledges the element of recklessness, but places it within the constraints of 1942, not as a timeless model for ethical conduct. This distinction matters. It suggests that history has simplified her motivations, turning survival into romance.
Second, the ambiguity of Soviet credit. When pressed on whether American Lend-Lease penicillin was substituted for Soviet krustosin in official propaganda, Yermolyeva admits it “probably happened”. She does not defend the practice, but neither does she disown her work because it was politicised. This honesty – this refusal to either fully claim or fully renounce the myths built around her – is rarely captured in historical accounts. The recorded narrative tends toward either uncritical celebration of Soviet achievement or dismissal of Soviet claims as propaganda. Yermolyeva’s actual position sits between these poles: her work was real, but its credit was contested and compromised by state interests.
Third, the overlooked institutional work. Whilst her penicillin breakthrough dominates memory, Yermolyeva emphasises her later work on bacteriophages, interferon, and bacterial polysaccharides. She directed the Institute of Antibiotics from 1947 onwards and headed the Department of Microbiology at Moscow’s Central Post-Graduate Medical Institute from 1952 until her death. She founded and edited Antibiotiki, shaping the entire direction of Soviet antibiotic research for decades. Yet these contributions – the slow, unglamorous work of institution-building, training, editorial stewardship – receive minimal attention in popular accounts. Her legacy is reduced to a single wartime achievement, when in fact her career was a half-century of continuous innovation and mentorship.
Fourth, the gendered nature of erasure. Yermolyeva was explicit: Western histories dismissed Soviet female scientists as “state-sponsored tokens rather than independent innovators”. Her work was treated as ideological propaganda partly because it was Soviet, partly because it was achieved by a woman, and partly because these two facts combined made her scientifically inconvenient to Western narratives. The 1945 Nobel Prize went to Fleming, Florey, and Chain – all men, all Western. Yermolyeva received the Stalin Prize the same year, which recognised equal achievement but carried the liability of Cold War politics. Neither award fully acknowledged the multiple, parallel discoveries that characterised penicillin research.
Gaps and uncertainties in the historical record persist. How much of Soviet penicillin production in 1943–1945 was genuinely Soviet versus American Lend-Lease supplies repackaged or relabelled? The archival evidence remains contested, partly because Soviet records were classified. What were the actual yields of Yermolyeva’s surface fermentation compared to Western deep fermentation? Publications exist, but they are scattered across Soviet journals with limited international circulation. How directly did Tamara Balezina contribute to the Penicillium crustosum isolation, and why has she been almost entirely erased from popular memory? The interviews suggest Balezina’s role was central, yet Western histories mention her barely, if at all.
Rediscovery and influence. Yermolyeva’s work lay dormant in Western consciousness for decades after her death. Interest revived in the 1980s and 1990s as Cold War tensions eased and historians began examining Soviet scientific achievement without ideological bias. Scholars like Luba Vikhanski have pieced together her biography from Russian-language sources. The 2018 Google Doodle marked a turning point – a moment when global recognition, however brief, acknowledged her contributions. Contemporary microbiologists studying antibiotic resistance, bacteriophage therapy, and fermentation technology are now citing her papers, recognising that her wartime protocols and post-war research on interferon and bacterial polysaccharides contain ideas still relevant to modern challenges.
Connections to today’s challenges. Yermolyeva’s story illuminates three contemporary crises. First, antibiotic resistance: her warnings about overuse and her advocacy for rational stewardship went unheeded during the post-war pharmaceutical boom, contributing to the resistance crisis now confronting medicine. Had open scientific collaboration existed between East and West after 1945, surveillance networks might have detected and slowed resistance evolution. Second, the recovery of non-Western science: as biomedical research becomes increasingly global, the rediscovery of Soviet, Chinese, Indian, and African scientific contributions challenges the Western-centric histories that long dominated. Yermolyeva’s erasure was not unique; it was systematic across non-Western science. Third, women’s visibility in STEM: whilst Yermolyeva achieved institutional leadership, trained generations of scientists, and authored over 500 papers, she remains less known than male contemporaries with comparable contributions. Young women today encounter similar pressures – to accept simplified narratives of their work, to have their contributions attributed to male supervisors or institutions, to choose between technical depth and public recognition.
For women pursuing science today. Yermolyeva offers an unconventional model. She did not fight for individual recognition in real time; she built institutions, published rigorously, trained others, and trusted that future historians would find the evidence. This is both inspiring and cautionary. It acknowledges that some recognition may come late or come not at all, but it insists that the work itself – the rigorous, documented, peer-reviewed work – is sufficient justification. Her advice to clinicians under pressure to sacrifice themselves for data is particularly important: institutional change and adequate resources are more important than individual heroism. And her counsel to Helga about protecting technical integrity whilst accepting simplified narratives suggests a mature approach to the gap between how science is lived and how it is remembered.
The unfinished archive. What remains unknown about Yermolyeva? Her personal correspondence, if it survived Soviet purges and Cold War secrecy, likely contains technical details and personal reflections lost in formal publications. Her relationship with Lev Zilber, her husband – how did their partnership shape her work, and how did his arrests affect her career? What conversations occurred during Florey’s 1944 visit to Moscow, and what was actually agreed versus what was later claimed? How much of her later work on interferon and bacteriophage therapy represents genuinely novel research versus responses to political pressure to produce new discoveries? These questions remain open, awaiting historians with access to Russian archives and the linguistic fluency to interpret them.
A spark for the present moment. Yermolyeva’s life argues that science is never separate from politics, that institutional power matters as much as individual brilliance, and that the work of building communities and training the next generation is as important as making discoveries. For women in science – and for all scientists from outside the dominant Western centres – her example offers something better than a hero myth: it offers a pathway. Document your work thoroughly. Publish in venues that will endure. Train others who understand it. Use whatever resources and platforms come your way, but never mistake the simplified narrative for the complex reality. And persist. Persist through bombardment, bureaucracy, and erasure, because fifty years later, historians will find your papers in the archive, and your students will remember what you taught them, and your methods will still solve problems that the present generation faces.
The Google Doodle, seventy years after her death, was late. But it was not nothing. It was the beginning of remembering – not Madame Penicillin, the Soviet heroine, but Zinaida Yermolyeva, the microbiologist who mastered mould, who drank cholera, who directed institutes, who published relentlessly, and who built the foundations upon which modern antibiotic science stands. That remembering continues. The archive is unfinished. And the most important pages – the ones that will reshape how future scientists understand antibiotic stewardship, phage therapy, and the role of non-Western research – have yet to be written by those who read her work now and build upon it with the urgency and rigour she modelled.
Editorial
This interview is a work of historical fiction – a dramatised reconstruction based on extensive archival research, peer-reviewed literature, declassified documents, and published biographical accounts. Every factual claim, technical detail, and historical reference derives from verifiable sources, including Soviet-era scientific journals, wartime records, post-war intelligence reports, and contemporary scholarship. The conversation itself, however, is imagined: a narrative device designed to bring coherence to fragmented evidence and to render accessible the complex, often contested legacy of Zinaida Yermolyeva.
Methodology and Sources
The reconstruction draws upon primary sources including Yermolyeva’s own publications (over 500 scientific papers and several monographs), Soviet medical archives, CIA intelligence reports on Soviet penicillin production (1943–1947), and the diary of Howard Florey’s 1944 Moscow visit. Secondary sources include biographical articles from UNESCO, the Russian Academy of Sciences, and Western historians of Soviet science. Technical details of fermentation protocols, penicillin yields, and bacteriophage therapy practices are taken from contemporaneous Soviet microbiology journals and post-war comparative studies.
Interpretive Choices and Limitations
Where archival evidence is incomplete or contradictory, the narrative reflects the most plausible interpretation supported by available documentation. For example, the extent of Soviet substitution of American Lend-Lease penicillin for domestic production remains disputed; Yermolyeva’s acknowledgment of this possibility reflects documented intelligence assessments rather than definitive proof. Similarly, her precise motivations for the 1942 cholera self-experiment are inferred from her published methodology and wartime context, as no private correspondence describing that decision has been located.
The voice attributed to Yermolyeva is constructed from her writing style – direct, technically precise, unsentimental – and from memoirs of colleagues who described her as disciplined, pragmatic, and disinclined toward self-promotion. Era-appropriate speech patterns and Soviet scientific terminology are employed to maintain historical texture, though some anachronisms are unavoidable when addressing modern readers.
What Is Documented vs. What Is Speculative
All technical descriptions – surface fermentation parameters, phage cocktail design, interferon research, institutional leadership roles – are documented in Yermolyeva’s publications and in Soviet scientific archives. The cholera experiment, Stalin Prize, Florey visit, and founding of Antibiotiki are well-established facts. Speculative elements include the precise wording of private conversations, internal motivations not recorded in writing, and hypothetical scenarios (such as the consequences of open scientific collaboration between Allied powers). These are clearly signposted as counterfactuals within the narrative.
Reader Guidance
Approach this reconstruction as an interpretive portrait, not a verbatim transcript. The aim is to illuminate Yermolyeva’s scientific reasoning, ethical reasoning, and personal resilience while acknowledging the gaps, biases, and political constraints that shaped the historical record. For those seeking strictly factual accounts, the primary sources cited throughout provide the documentary foundation; for those seeking to understand the human experience behind the data, this dramatisation offers a plausible, evidence-based window into a life that official histories have too often simplified or erased.
The work of historical recovery is ongoing. New archives may surface, new interpretations may emerge. This reconstruction represents our best understanding as of December 2025, informed by the sources available and the conviction that science, like memory, belongs to everyone willing to do the work of remembering accurately.
Who have we missed?
This series is all about recovering the voices history left behind – and I’d love your help finding the next one. If there’s a woman in STEM you think deserves to be interviewed in this way – whether a forgotten inventor, unsung technician, or overlooked researcher – please share her story.
Email me at voxmeditantis@gmail.com or leave a comment below with your suggestion – even just a name is a great start. Let’s keep uncovering the women who shaped science and innovation, one conversation at a time.
Bob Lynn | © 2025 Vox Meditantis. All rights reserved.
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