Vox Meditantis

Alice Catherine Evans (1881–1975) transformed public health by proving that raw milk could transmit deadly disease from cattle to humans, yet spent more than a decade fighting to have her discovery recognised by a scientific establishment that dismissed her because she was a woman without a doctorate. Her work led to mandatory milk pasteurisation laws in the 1930s, nearly eliminating brucellosis in the United States – though not before she contracted the painful, recurrent disease herself during her research. Today, her victory faces renewed challenge from raw milk movements that reject the very protections she fought to establish.

Dr Evans, thank you for joining us today. I’m honoured to speak with you, though I must say – time travel makes for rather extraordinary circumstances. You’re sitting here in 2025, having lived through 1881 to 1975. How does it feel to see the world now?

Well, it’s peculiar, I’ll grant you that. Though I must confess, the thing that strikes me most isn’t your aeroplanes or your talking machines – it’s that people are choosing to drink raw milk again. After everything we learnt. After all those children who died. It rather makes one wonder whether human memory is shorter than a laboratory mouse’s.

That’s actually something we’ll discuss later – but first, I’d like to understand how you came to science at all. You were born on a farm in Pennsylvania in 1881, taught school for four years, and only discovered bacteriology almost by accident. Take us back to that moment.

Accident is the right word for it. I was teaching grade school in Neath – dreadfully boring work, though it was about the only profession open to women who couldn’t afford university. My brother mentioned a free course at Cornell for rural teachers, meant to help us inspire children about nature and science. I thought, “Well, why not? Two years won’t kill me.” But once I started working in the laboratory – culturing bacteria, preparing slides, watching those tiny organisms under the microscope – I knew I couldn’t go back to the schoolroom. It was like discovering a language I’d been meant to speak all along.

You earned your bachelor’s in bacteriology at Cornell, then became the first woman to receive a graduate scholarship in bacteriology at the University of Wisconsin. What was it like being the only woman in those spaces?

Lonely, mostly. And isolating in ways I didn’t fully recognise at the time. At Wisconsin, I studied under Elmer McCollum – brilliant man, later discovered vitamins A, B, and D – and he encouraged me to pursue a doctorate. But I was offered a position immediately at the U.S. Department of Agriculture’s Dairy Division. A research position! For a woman! I jumped at it. How could I have known that declining the doctorate would become a weapon men would use against me for the next decade?

The irony was exquisite, really. Women couldn’t easily access doctoral programmes, and when we entered research without PhDs, our findings were dismissed for lacking the credentials we’d been structurally prevented from obtaining. Circular logic at its finest.

When you arrived at the USDA Dairy Division in Washington in 1913, your male colleagues reportedly “almost fell off their chairs” when they realised their new colleague was a woman.

Yes, the Bureau officials had apparently never considered that the local professors hiring investigators might want a woman on their teams. The stenographer told me later that the room went absolutely silent when I walked in. One fellow’s mouth hung open like a barn door. But to their credit, my immediate supervisors – Dr Ernest Kelly and Dr Frederick Tonney – were decent men. They judged me by my work, not my sex. It was a good place to work, at least within those laboratory walls.

Your first assignment was identifying bacteria in fresh milk. Walk me through what that work actually looked like, day to day. What tools did you have? What techniques?

We’re talking about 1913, mind you, so nothing like what you have today. The primary tool was the microscope – a good Zeiss, if we were lucky – and a great deal of patience. I’d collect milk samples from dairy farms around Washington, bring them back to the laboratory, and prepare cultures.

You’d start by streaking the milk onto agar plates – nutrient agar for general bacteria, or specialised media if you were looking for something particular. Then into the incubator they’d go – kept at 37 degrees Celsius, body temperature, to encourage bacterial growth. After eighteen to twenty-four hours, you’d examine the colonies. Size, colour, shape, whether they produced gas or changed the medium’s colour – all of it told you something about what you were looking at.

For identification, you’d prepare slides. Take a sample from a colony, smear it on a glass slide, heat-fix it to kill the bacteria and make them stick, then stain it – usually with Gram stain, which uses crystal violet and safranin to differentiate bacteria based on their cell wall structure. Gram-positive bacteria hold the violet and appear purple; Gram-negative bacteria lose it and stain pink. Under the microscope, you’d note the shape – rods, cocci, spirals – and how they arranged themselves. Chains? Clusters? All of it mattered.

Then came the biochemical tests. Does the organism ferment lactose? Produce indole? Reduce nitrates? Each test required its own set of tubes, solutions, incubation periods. It was methodical, repetitive work. And for a woman in 1913, it was absolutely thrilling.

That methodical work led you to something extraordinary. In 1917, you made the discovery that would define your career – and save countless lives. Can you explain, for those who understand microbiology, exactly what you found?

Certainly. I was investigating the bacteria that caused fresh milk to sour or develop off-flavours. During this work, I became interested in an organism called Bacterium abortus – later renamed Brucella abortus – which Danish veterinarian Bernhard Bang had isolated in 1895 from cows that had spontaneously aborted their calves. It caused tremendous losses in dairy herds: miscarriages, fertility problems, reduced milk production.

At the same time, there was a disease in humans called undulant fever, or Malta fever, because it was endemic in the Mediterranean. Soldiers stationed in Malta and Gibraltar had been falling ill with it for decades. It caused recurrent fevers – hence “undulant” – severe joint pain, crushing fatigue, depression. Some people suffered for years. The causative organism had been identified as Micrococcus melitensis, found in goats.

When I cultured both organisms and examined them under the microscope, I was struck by how similar they appeared. Both were small, Gram-negative coccobacilli – short rod-shaped bacteria that stained pink. Their colonial morphology on agar was nearly identical: smooth, glistening, slightly raised. Their biochemical characteristics were also remarkably alike: both were aerobic, both fermented certain sugars but not others, both produced urease.

I began conducting agglutination tests – mixing serum from animals or humans infected with one organism with cultures of the other organism to see if antibodies would recognise and clump the bacteria. The cross-reactivity was stunning. Serum from cattle infected with B. abortus agglutinated M. melitensis. Serum from humans with Malta fever agglutinated B. abortus.

The conclusion was inescapable: these organisms were closely related, likely the same genus. And if goats transmitted M. melitensis to humans through their milk, causing Malta fever, then cattle could transmit B. abortus to humans through cow’s milk, causing the same disease. It meant that unpasteurised milk was a direct route for zoonotic transmission – from animals to humans.

That’s an elegant piece of scientific reasoning. What made you so confident in this conclusion when others weren’t?

The evidence was right there in the petri dishes and test tubes. But I think part of it was that I came from a farming background. I’d grown up around cattle. I knew how much contact dairy workers had with animals – milking them twice daily, handling birth fluids during calving, breathing the same air in barns. The idea that animal and human diseases could be separate seemed foolish to me. Life doesn’t respect our taxonomic boundaries.

You published your findings in 1918 in the Journal of Infectious Diseases. What happened next?

Nothing happened. That was the problem. Or rather, what happened was dismissal. The scientific community simply refused to believe it. Veterinarians said I was wrong about cattle. Physicians said I was wrong about human disease. Dairy interests – trade associations, statehouse lobbyists, ad campaigns – said I was fearmongering and accused me of having financial interests in pasteurisation equipment – which was absurd; I was a government employee earning $1,800 a year.

The most galling criticism came from male scientists who said – and I quote – “If these organisms were closely related, some other bacteriologist would have noted it.” Meaning a man would have discovered it first if it were true. My findings weren’t evaluated on their scientific merit; they were dismissed because I lacked a PhD and possessed a uterus.

That must have been extraordinarily painful. Did you ever doubt yourself?

Of course I doubted myself. Self-doubt is the shadow that follows every woman in science. You ask yourself: Am I wrong? Am I seeing patterns that aren’t there? Did I make an error in my technique? I re-examined my cultures hundreds of times. I repeated the agglutination tests until my hands cramped. The results never changed.

But here’s the thing about laboratory work: bacteria don’t lie. They don’t have opinions about your sex or your credentials. They grow, or they don’t. They agglutinate, or they don’t. The evidence was reproducible, and that gave me the steel to keep going.

The dairy industry opposed you fiercely. Why?

Money, pure and simple. Pasteurisation required expensive equipment – heating vessels, holding tanks, cooling systems. Small dairies couldn’t afford it; large dairies didn’t want to. They’d developed “Grade A” certification systems based on visual inspection by veterinarians: if the cows looked healthy and the barn looked clean, the milk was declared safe. It was theatre, not science.

The industry promoted this fiction that “healthy-looking cows” produced safe milk. But Brucella doesn’t care how healthy a cow looks. An infected animal can shed millions of bacteria in its milk without showing obvious symptoms. And once that milk entered the distribution chain – mixed with milk from dozens of other farms in those bulk tanks – a single infected cow could contaminate an entire city’s supply.

The dairy interests had enormous political power. They lobbied state legislatures, placed advertisements in newspapers, funded “research” that contradicted mine. They painted pasteurisation as government overreach, an attack on farmers’ livelihoods and consumers’ freedom. Sound familiar?

Painfully so. But your findings were eventually confirmed – by male scientists, of course.

Yes, in the late 1920s, men independently replicated my work and suddenly it became believable. Theobald Smith at Harvard confirmed the relationship between the organisms. Karl F. Meyer in California published similar findings. Once men said it, it was accepted as scientific consensus.

By the 1930s, states began enacting mandatory pasteurisation laws. Chicago had been first, back in 1909, but enforcement was uneven. After my work – or rather, after men confirmed my work – the laws spread. The impact was immediate and dramatic. Brucellosis, which had been a significant public health burden, was nearly eliminated in the United States. By 1938, milk products caused 25% of traceable foodborne illnesses; today, thanks to pasteurisation, they account for less than 1%.

There’s a cruel irony to this story. In 1922, you contracted brucellosis yourself during your research. Tell me about that.

Yes. I was working with infected milk samples, culturing the organisms, and despite precautions, I became infected. It might have been through a splash, or perhaps I inhaled aerosolised bacteria. Laboratory-acquired brucellosis is terrifyingly easy.

The disease announces itself with fever – not a steady one, but waves of it, rising and falling like tides, hence “undulant fever.” The joint pain is extraordinary. It feels as though someone is driving hot needles through your bones. Your back, your knees, your wrists – everywhere aches. You’re exhausted beyond description, but you can’t sleep because the pain won’t let you.

And then, just when you think it’s over, it comes back. Days later, weeks later, sometimes months later. For me, it came back for over twenty years. Some accounts say thirty years. I lost track, honestly. Time becomes fluid when you’re chronically ill.

You missed your own installation as the first woman president of the Society of American Bacteriologists in 1927 because of the disease.

I did – 30th December 1927 – I should have been there, standing before my colleagues, taking the gavel. Instead, I was in bed, feverish and aching, too ill to travel. They sent me a lovely letter calling me a “heroine of the highest order in the common warfare of mankind against its microbial enemies.”

I appreciated the sentiment. But I would have preferred to be recognised for my intellect rather than my suffering. That’s the trap, you see – the martyr-scientist narrative. It focuses on the body, not the mind. Curie’s radiation exposure, Franklin’s early death, my brucellosis. It’s as though women scientists must suffer physically to be taken seriously, and even then, the suffering overshadows the science.

You continued working despite the illness. In 1918, you moved to the Hygienic Laboratory – the forerunner of the National Institutes of Health – where you worked on epidemic meningitis and streptococcal infections. What drew you to those problems?

The First World War was raging, and I wanted to contribute to the war effort. The Hygienic Laboratory had a vacancy for a bacteriologist, and they needed help improving serum treatment for epidemic meningitis, which was killing soldiers in crowded training camps.

Meningitis is caused by several bacterial species, and matching the correct antiserum to the causative strain was critical. I worked on developing better diagnostic methods and characterising different strains of Streptococcus and Neisseria meningitidis. It was urgent, vital work – people were dying whilst we raced to understand these organisms.

I stayed at the Hygienic Laboratory – later renamed the National Institutes of Health – until I retired in 1945. Twenty-seven years. I made contributions to understanding streptococcal infections, worked on bacterial typing methods, served on committees. But it all exists in the shadow of the brucellosis work, which I suppose is fitting. That discovery saved the most lives.

Let’s talk about something you got wrong. What mistakes did you make? Where did you misjudge?

I underestimated how long it would take for evidence to become policy. I thought – naively – that once I’d published my findings, once the data was available, authorities would act quickly to protect public health. I didn’t account for the power of economic interests, the inertia of institutions, or the visceral resistance people have to being told their traditions are dangerous.

I also made laboratory errors, naturally. Early in my work, I misidentified some bacterial colonies – thought I had streptococci when I actually had staphylococci, that sort of thing. It happens when you’re learning. The key is to catch your mistakes, document them, and adjust your methods.

And perhaps my greatest misjudgement was thinking that excellence would be enough. I believed that if I worked harder, published more, presented at conferences, maintained impeccable laboratory practices, eventually I’d be judged on merit alone. I was wrong about that. Gender bias doesn’t evaporate in the face of competence.

In 1963, you wrote your memoirs. By then, you were in your eighties. Looking back at your career, what did you see?

I saw a woman who’d spent her life fighting two wars – one against bacterial pathogens, and one against human prejudice. The bacteria were easier opponents, frankly. At least they followed predictable rules.

But I also saw victories. Children drinking milk without dying. Mothers who didn’t lose babies to foodborne disease. Agricultural workers who didn’t contract brucellosis from the animals they tended. Those were real, tangible outcomes of my work.

The memoirs were partly an attempt to correct the record. History has a way of erasing women, or crediting men with our discoveries, or framing our contributions as fortunate accidents rather than rigorous science. I wanted to make clear: I knew what I was doing. I understood the implications. And I was right.

You mentioned at the start of this conversation that people are drinking raw milk again. From your perspective in 2025, what do you make of the contemporary raw milk movement?

I am astonished. And furious. We have documented outbreaks – E. coli, Salmonella, Campylobacter, Listeria, and yes, still Brucella. We have children developing haemolytic uraemic syndrome and kidney failure from raw milk contaminated with E. coli O157:H7. We have laboratory-confirmed cases of brucellosis linked to unpasteurised dairy products.

And yet people are calling raw milk “natural” and “healthier” as though bacteria respect wellness trends. They’re framing pasteurisation as government overreach, parroting the exact arguments the dairy industry made in the 1920s. It’s amnesia disguised as enlightenment.

What particularly galls me is the RB51 vaccine situation. RB51 is a live attenuated vaccine strain of Brucella abortus used to prevent brucellosis in cattle. But it can be shed in the milk of vaccinated cows, and it’s resistant to rifampin – one of the primary antibiotics used to treat human brucellosis. Between 2017 and 2019, there were documented cases of RB51 infections in humans from raw milk consumption. The bacteria doesn’t show up on standard serological tests, so infections can be missed, and when they’re finally diagnosed, they’re harder to treat.

We’re creating antibiotic-resistant brucellosis through a cattle vaccine and distributing it via raw milk. The irony would be funny if it weren’t killing people.

Your work pioneered what we now call “One Health” – the recognition that human, animal, and environmental health are interconnected. Do you think that framework could have helped you in the 1920s?

Absolutely. The problem I faced was that I worked across disciplinary boundaries – veterinary medicine, agricultural science, human public health – and that meant I didn’t have a professional “home.” Veterinarians saw me as an outsider meddling in animal disease. Physicians saw me as a bacteriologist with no medical training. Agricultural scientists saw me as a threat to farmers’ livelihoods.

If One Health had existed as a framework then, perhaps there would have been institutional structures that valued that kind of interdisciplinary work. Perhaps veterinarians and physicians would have collaborated instead of dismissing each other’s concerns. Perhaps agricultural policy would have been informed by public health evidence.

Of course, the One Health approach also requires people to listen to evidence, and that was precisely the problem I faced. So perhaps the framework wouldn’t have helped after all.

You lived through the 1918 influenza pandemic. In your memoirs, you described how it disrupted the Hygienic Laboratory, with medical officers sent into the field and research projects abandoned. What parallels do you see with COVID-19?

The patterns are depressingly familiar. Overwhelmed health systems, shortages of staff and supplies, public health measures dismissed as inconvenient or authoritarian, misinformation spreading faster than the virus itself. And once again, the preventive public health infrastructure that might have mitigated the crisis had been neglected because it’s invisible when it’s working.

That’s the curse of prevention: success looks like nothing happened. We eliminated smallpox, but how many people now understand what that achievement cost? We’ve nearly eradicated polio, but anti-vaccine movements threaten that progress. We made milk safe through pasteurisation, but now people want raw milk because they’ve never seen a child die from E. coli infection.

Preventive public health disappears into infrastructure. It becomes taken for granted. And then, when people decide that infrastructure is unnecessary, the diseases come roaring back.

If you could speak directly to women in STEM today – particularly those facing dismissal, credential gatekeeping, or having their work credited to male colleagues – what would you tell them?

First, I’d tell them that it’s not their imagination. The bias is real, the barriers are real, and the exhaustion they feel is real. Don’t gaslight yourself into thinking you’re being oversensitive.

Second, document everything. Keep copies of your laboratory notebooks, your correspondence, your publications. Make sure your name is on your work in ways that can’t be erased. History will try to forget you; don’t make it easy.

Third, find allies. My immediate supervisors at the USDA, Dr Kelly and Dr Tonney, defended my work when others attacked it. Those alliances matter. But be strategic – not everyone who smiles at you is an ally.

Fourth, persistence is a form of resistance. The system wants you to go away, to get tired, to give up. Don’t. Keep working, keep publishing, keep speaking. Let them be the ones who get tired.

And finally – and this is perhaps the most important – your work matters more than recognition. I saved lives. That’s not an exaggeration. Thousands of people didn’t get sick, didn’t suffer, didn’t die because of the work I did. That would be true even if my name had been completely forgotten. Do the work for the work’s sake, because it matters, because lives depend on it. The recognition may come, or it may not. But the work will stand.

What do you hope your legacy will be?

I hope people remember that scientific truth doesn’t implement itself. Evidence doesn’t automatically become policy. You need advocacy, persistence, and power – resources that are unequally distributed. And when women, or any marginalised group, lack that power, dangerous gaps emerge between what we know and what we do.

I also hope people remember that food safety regulations aren’t arbitrary. They’re written in the suffering of people who came before. Every pasteurisation law represents children who died, families who lost livelihoods, communities devastated by preventable disease. When someone tells you that pasteurisation is unnecessary, or that raw milk is safe, or that regulations are government overreach, they’re asking you to forget that history. Don’t.

And perhaps, in a very small way, I hope people remember that a woman without a doctorate, working in a government laboratory in 1917, figured out something that saved countless lives – even though men told her she was wrong. That matters. Not because I want personal glory, but because the next time a woman scientist says, “I’ve found something important,” perhaps people will listen a bit sooner.

Dr Evans, thank you. This has been an extraordinary conversation.

The pleasure was mine. Now, if you’ll excuse me, I’d like to visit a dairy farm. I want to see these modern milking machines and pasteurisation equipment. And perhaps shake some sense into whoever thought drinking raw milk was a good idea.

Letters and emails

Since our conversation with Dr Evans, we’ve received hundreds of letters and emails from readers around the world – scientists, students, policymakers, and thoughtful observers – each wanting to press further into the technical details of her work, the personal costs of her advocacy, and the lessons her story holds for today. We’ve selected five from our growing community who represent the breadth of questions her life and discoveries continue to raise, spanning continents and disciplines, each offering a fresh angle on what it means to pursue truth against formidable resistance.

Nia Okafor, 34, Public Health Researcher, Lagos, Nigeria
Dr Evans, you mentioned that brucellosis remains a global threat, particularly in low- and middle-income countries where pasteurisation infrastructure is limited or non-existent. In regions where electricity is unreliable and refrigeration is scarce, what alternative methods – boiling, solar pasteurisation, or small-scale heat treatment – would you recommend for families and small dairy operations? And how do we balance the economic realities of artisanal cheese-making traditions, which are vital to rural livelihoods in places like West Africa, with the need to prevent zoonotic transmission?

Miss Okafor, your question goes straight to the heart of what troubles me most about the contemporary conversation around milk safety. We’ve spent so much time arguing about raw milk in wealthy countries – where pasteurisation infrastructure exists and people are choosing to reject it – that we’ve rather neglected the billions of people who simply don’t have access to the technology at all.

Let me be plain: boiling works. It’s not elegant, it’s not efficient at scale, but it kills Brucella and most other milk-borne pathogens if done properly. The milk must reach a rolling boil – 100 degrees Celsius at sea level – and be held there for at least one minute. Longer is safer, though it does affect the flavour and nutritional quality somewhat. For families without electricity or refrigeration, boiling immediately after milking, then cooling the milk as quickly as possible in whatever clean water is available, provides real protection.

The difficulty, of course, is fuel. When I was growing up on our farm in Pennsylvania, we had wood for fires, but in regions where firewood is scarce or must be purchased, asking families to boil milk daily becomes an economic burden. Solar pasteurisation shows promise – using reflective surfaces to concentrate sunlight and heat milk to 63 degrees Celsius for thirty minutes, or 72 degrees for fifteen seconds – but it requires clear weather, proper equipment, and careful monitoring. I’ve read about pilot programmes in Kenya and India using solar milk cookers. The principle is sound, though I worry about consistency and quality control.

Small-scale batch pasteurisers – essentially double boilers with thermometers – can serve village cooperatives or small dairy operations. You heat water in the outer vessel, place milk in the inner container, and monitor temperature carefully. Hold the milk at 63 degrees Celsius for thirty minutes, then cool it rapidly. It’s labour-intensive and requires someone who understands the process, but it’s far more affordable than industrial pasteurisation equipment.

Now, to your more difficult question about artisanal cheese-making. This is where science must reckon with culture and economics, and there are no perfect answers.

Cheese-making itself provides some protection, though not complete. The fermentation process – lactic acid production by starter cultures – lowers the pH, which inhibits Brucella growth. Aged cheeses, particularly hard cheeses aged for sixty days or longer, are considerably safer than fresh cheese because the combination of low moisture, high salt, and extended aging time reduces bacterial viability. The French have been making raw milk cheese for centuries with relatively few problems because they use this aging process.

But fresh cheeses – what you might call soft cheeses, cottage cheese, or farmer’s cheese – are dangerous when made from raw milk. Brucella survives beautifully in those conditions. So does Listeria monocytogenes, Salmonella, and E. coli. If communities are going to continue making fresh cheese, the milk absolutely must be heat-treated first.

Here’s where policy must be practical rather than ideal. In regions where raw milk cheese-making is culturally important and economically vital, I would advocate for a tiered approach. First, mandatory heat treatment for any fresh cheese. Second, education programmes teaching proper aging techniques for hard cheeses – temperature control, humidity, time requirements. Third, regular testing of herds for brucellosis and other diseases, with infected animals removed from milking herds. Fourth, training for cheese-makers in hygiene practices: clean equipment, proper hand-washing, preventing cross-contamination.

The Danes managed to reduce brucellosis in their herds through testing and culling programmes in the early 1900s. Bang’s method – testing cattle with serum agglutination, removing positive animals – worked, though it required government support and compensation for farmers whose animals were destroyed. That’s the model: you can’t simply tell farmers “stop using infected cows” without providing economic alternatives.

I’m also mindful that women typically do the milking and cheese-making in many cultures, which means women bear disproportionate exposure to Brucella. They’re handling infected milk daily, often without understanding the risk or having power to demand safer conditions. So this isn’t merely a food safety issue – it’s a matter of occupational health for women whose labour is essential but undervalued.

The tension you’ve identified – between economic realities and public health – cannot be resolved by science alone. It requires investment: in infrastructure, in education, in compensation for farmers, in support for cooperatives. The technology exists. The knowledge exists. What’s lacking is political will and resources directed toward protecting rural populations whose suffering is invisible to urban policy-makers.

But let me be clear about one thing: “tradition” cannot be used to justify preventable disease and death. Yes, people have been making raw milk cheese for centuries. People have also been dying of brucellosis for centuries. We must find ways to preserve cultural practices whilst removing the dangers, not treat culture as immutable and exempt from scientific evidence. That’s false respect, and it condemns people to unnecessary suffering.

Arjun Das, 29, Microbiome Researcher, Bangalore, India
You worked entirely with culture-based methods – agar plates, biochemical tests, microscopy – to identify and characterise bacteria. Today, we use genomic sequencing, CRISPR-based diagnostics, and mass spectrometry to identify pathogens in hours rather than days. If you had access to these tools in 1917, how might your research trajectory have changed? Would rapid molecular identification have helped you convince sceptics more quickly, or do you think the resistance you faced was never really about the science at all? And what would you make of our current ability to track Brucella strains globally through whole-genome sequencing?

Mr Das, you’ve asked me to imagine having modern molecular tools in 1917, and I confess the prospect makes me positively giddy. But let me answer your question honestly: I don’t think it would have mattered one whit.

Oh, the science would have been faster, certainly. Instead of waiting eighteen to twenty-four hours for bacterial colonies to grow on agar plates, then another day or two for biochemical tests, I could have had genetic sequences in hours. Instead of relying on morphological similarities and cross-agglutination reactions to argue that Brucella abortus and Micrococcus melitensis were related, I could have shown you their DNA and said, “Look, they’re 98% identical.” It would have been magnificent.

But here’s the rub: the men who dismissed my findings didn’t do so because my evidence was insufficient. They dismissed them because I was a woman without a doctorate. If I’d walked into that conference room in 1918 with genetic sequences, they would have found other objections. “Who verified your sequencing results? What about contamination? Perhaps you made an error in your sample preparation.” The goal posts would simply have moved.

I watched this happen repeatedly. When I first published, they said I must have made laboratory errors – contaminated my cultures, misidentified the organisms. So I repeated everything, documented every step meticulously, and published again. Then they said my samples weren’t representative – perhaps I’d happened upon unusual strains. So I collected samples from multiple locations, different herds, various regions. Still dismissed. Then they questioned my interpretation – perhaps the bacteria were similar but not identical, perhaps cross-reactivity didn’t prove relationship.

By the time male scientists “confirmed” my findings a decade later – doing essentially the same work I’d done – suddenly it was accepted as fact. The evidence hadn’t changed. The methods hadn’t changed. What changed was the sex of the person presenting it.

That said, your modern tools would have been glorious for the work itself, regardless of recognition. Let me tell you what frustrated me most about culture-based methods: the waiting. You’d collect a milk sample, streak it onto agar, and then… wait. Overnight at minimum, sometimes forty-eight hours if the organisms were slow-growing. Brucella is particularly finicky – it requires enriched media, sometimes takes three to five days to show visible colonies. And if you’d made an error in your medium preparation, or if the sample had been contaminated, you wouldn’t know until you’d wasted days.

The biochemical characterisation was equally tedious. Each test – fermentation reactions, nitrate reduction, urease production, catalase activity – required its own tube, its own incubation period, its own observation schedule. I’d have dozens of tubes lined up, each labelled, each needing to be checked at specific intervals. Miss a colour change because you looked at the tube two hours too late, and you might have to start over.

And the agglutination tests! Mixing serial dilutions of serum with bacterial suspensions, incubating them, examining each tube for clumping. It was precise work, but maddeningly slow. If someone had handed me a device that could identify a bacterium’s species in two hours using its genetic fingerprint, I would have wept with joy.

Your CRISPR diagnostics particularly fascinate me. The idea that you can design a molecular tool to recognise a specific pathogen’s DNA sequence and provide a visual readout – that’s precisely what we needed. Especially for field work. I collected samples from dairy farms, but they had to be transported back to Washington for analysis. If I could have tested milk on-site and told a farmer immediately “Your herd is infected with Brucella,” the impact would have been transformative.

But – and this is important – the fundamental logic of my work would have been exactly the same. I observed similarity, hypothesised relationship, tested that hypothesis through multiple methods, and drew conclusions based on reproducible evidence. The tools would have accelerated the process and provided more definitive data, but they wouldn’t have changed the reasoning.

As for tracking Brucella strains globally through whole-genome sequencing, I’m torn between excitement and horror. Excitement because we could map transmission routes, identify outbreak sources, understand how the bacterium evolves and spreads. That would have been invaluable in my time – we suspected that infected cattle were being shipped between states and even internationally, but we couldn’t prove the connections.

Horror because I suspect you’re finding that Brucella is far more widespread than official statistics suggest, and that antibiotic resistance is emerging. Am I right? I’ve read about the RB51 vaccine strain causing rifampin-resistant infections in humans. That terrifies me. When I was working, we didn’t have antibiotics – they weren’t discovered until Fleming’s work in 1928, and streptomycin wasn’t used for brucellosis until the 1940s. The idea that we might return to an era where brucellosis is untreatable because we’ve squandered our antibiotics through misuse and vaccine complications… well, it makes me want to knock some heads together.

To your final question – whether the resistance I faced was “ever really about the science at all” – you’ve answered it yourself, haven’t you? It wasn’t. It was about power, credentials, money, and gender. The science was always sound. The bacteria didn’t care whether a man or a woman identified them. They grew, they infected, they killed, regardless of who was looking through the microscope.

So no, Mr Das, I don’t think molecular tools would have shortened that decade of dismissal. They would have made my work easier and more definitive, and perhaps given me some personal satisfaction. But the dairy industry still would have opposed pasteurisation because it cost money. Male scientists still would have found reasons to doubt a woman’s conclusions. And policy-makers still would have waited until men confirmed my findings before acting.

The problem was never the quality of the evidence. The problem was who was permitted to produce evidence that mattered.

Eleni Papadopoulos, 42, Science Policy Adviser, Athens, Greece
You described working across veterinary medicine, agricultural science, and human public health – fields that often operated in isolation. Today, the European Union and WHO promote “One Health” frameworks, but implementation remains patchy, with funding silos and territorial disputes between departments. If you were advising a government today on building genuinely integrated zoonotic disease surveillance, what structural changes would you insist upon? Should veterinary and public health laboratories be merged? Should agricultural ministries share budgets with health departments? What lessons from your own institutional struggles would inform your recommendations?

Miss Papadopoulos, you have a keen nose for the knots of bureaucracy, if you’ll pardon my old-fashioned phrase. During my years at the United States Department of Agriculture and later the Hygienic Laboratory – what you folks now call the NIH – I witnessed, time and again, the unfortunate consequences of dividing human, animal, and agricultural health into separate camps. The upshot was often confusion, wasted resources, and, most disheartening of all, preventable suffering.

In my own day, veterinary scientists worked primarily for the Bureau of Animal Industry; public health officers answered to different departments at the state and federal level, and agricultural extension agents operated in still another sphere. Most weeks, these folks wouldn’t know of each other’s discoveries unless they chanced to read the same journal or meet by accident at some scientific gathering. Too often, a significant observation or outbreak was not communicated across fields until months, or even years, had passed. Precious time was lost, and sometimes lives with it.

If you’ll allow me, I’d propose something simpler than a grand reorganisation – which tends to founder on the shoals of personal ambition and departmental pride. Give money – real money, and decision-making power – to joint committees composed of veterinary, agricultural, and medical scientists. Not symbolic appointments, mind you, but teams equipped to hire staff, manage surveillance data, and spend budgets directly. In my day, the work would often get shunted aside because each bureau jealously guarded its purse strings and insisted its authority was paramount. Let these committees set the research and response agenda, tied directly to measured results: disease incidence, food safety tests, and outbreaks tracked to their source, whether animal, human, or environmental.

You ask if veterinary and public health laboratories should be merged. In my experience, a full merger may look attractive on a chart – streamlining, reducing redundancies – but unless the daily work is truly aligned and valued across specialties, you risk creating another tangled bureaucracy where veterinarians answer to physicians who haven’t milked a cow a day in their life, or vice versa. Instead, I’d insist upon shared facilities where scientists from each field not only work side by side, but answer for common goals: reporting outbreaks, investigating zoonotic transmissions, sharing responsibility for public health warnings. Have them share both the glory and the blame, if you will.

On funding: agricultural ministries should have skin in the game for health outcomes. After all, a brucellosis outbreak among dairy herds wipes out farmers’ wallets as surely as it sickens rural families. Each ministry’s budget should include an allocation for joint disease monitoring, with performance reviewed by panels of outsiders – preferably including scientists from other countries familiar with the challenges at hand. When Denmark stamped out bovine brucellosis, it was because the state compensated farmers and made eradication worth their while, not because someone shuffled papers in a distant office.

Finally, I’d advise anyone championing “One Health” or any similar scheme to start every project by putting farmers, veterinarians, public health nurses, and local women who handle food at the kitchen table together. Let them air their burdens and knowledge frankly, then build your interventions out of the real messiness of the countryside, not from the comfort of a city bureau.

In my time, departments were too proud, too rigid, and too short-sighted to make such partnerships the rule rather than the exception. I do hope yours will succeed where ours stumbled. Work together and remember – the microbe does not respect the fence line between disciplines any more than it does that between species. If you want to avoid the mistakes of my era, let your solutions test themselves in fields and kitchens, not just in well-lit halls of government.

Logan Brooks, 38, Historian of Science, Boston, USA
I’m thinking about something you said: “The system wants you to go away, to get tired, to give up. Don’t.” But you also acknowledged the toll – contracting brucellosis, suffering for decades, missing your own presidential installation. If you could go back and speak to your younger self in 1917, would you still encourage her to pursue this fight, knowing the personal cost? Or would you advise a different path – perhaps publishing quietly and letting history unfold without bearing the weight of advocacy yourself? I suppose I’m asking: at what point does resilience become self-destruction, and how do we know the difference?

Mr Brooks, you’ve asked me a question I’ve agonised over privately for many years, and I’m not certain I have a tidy answer for you. But I’ll try to be honest, which is all any of us can manage.

If I could sit down with my younger self in 1917 – that woman of thirty-six who’d just published her findings and was about to face a decade of dismissal – would I tell her to fight? Would I warn her about the brucellosis infection waiting five years hence, the chronic pain that would dog her for decades, the presidential installation she’d miss because she was too ill to stand? Would I advise her to publish quietly and step back, let the men sort it out eventually?

No. I wouldn’t. And that troubles me, because I’m not entirely sure it’s wisdom or merely stubbornness speaking.

Here’s what I’d tell her instead: “Alice, you’re right. You know you’re right. The bacteria don’t lie, and your methods are sound. But being right won’t be enough, and that will hurt worse than any fever. Steel yourself for that.”

I’d also tell her this: “The fight will cost you. Your health, your time, years of your life spent repeating yourself to men who aren’t listening. But if you walk away, children will keep dying. Dairy workers – mostly women, mind you – will keep contracting this disease, and no one will connect the dots because you were the one who saw the pattern. Can you live with that?”

Because that’s the calculus, isn’t it? Not whether I could have had an easier life – I certainly could have – but whether the easier life would have been bearable knowing what I knew.

I think often of a particular child. I never met her, don’t even know her name. But I read a report in 1920 or thereabouts of a seven-year-old girl in Pennsylvania – not far from where I grew up – who’d contracted undulant fever. The doctor described her symptoms: recurrent fevers that spiked and fell, joint pain so severe she couldn’t walk, weight loss, depression. She was sick for eight months before she finally recovered, though the report noted she’d likely have recurring episodes. Eight months of a childhood stolen by a disease she got from drinking milk.

That child – and the thousands like her – is why I kept fighting. Not for recognition, though Lord knows I wanted it. Not for vindication, though that would have been sweet. But because I couldn’t look at those cases and think, “Well, I tried once, and they didn’t listen, so I’ll just let it go.”

Now, to your harder question: at what point does resilience become self-destruction?

I don’t know that there’s a clean line between them, Mr Brooks. They blur together, particularly for women. We’re told to be resilient – to persist, to endure, to keep going no matter what. But we’re also told, more quietly, that our suffering makes us sympathetic. That martyrdom is the price of being taken seriously. Marie Curie dying of radiation exposure. Rosalind Franklin’s early death from ovarian cancer, likely caused by X-ray crystallography work. My own decades with brucellosis. There’s a pattern there, and it’s ugly.

I think resilience becomes self-destruction when the work becomes about proving something to people who will never believe you anyway, rather than about the work itself. When you’re pushing not because lives depend on it, but because you need to show the bastards they were wrong. That’s corrosive. That eats you from the inside.

For me, the work was always larger than my pride. Even during those terrible years in the 1920s when I was feverish and aching and watching male scientists finally “discover” what I’d published a decade earlier, I still believed pasteurisation laws would come. And they did. By the 1930s, state after state enacted mandatory pasteurisation. Brucellosis rates plummeted. The work succeeded, even if I spent those years being ignored.

Would I have had more joy in my life if I’d stepped back in 1918? Probably. I might have avoided the brucellosis infection altogether – though laboratory accidents are always a risk, and I loved the work too much to quit entirely. I might have married, had children, lived a quieter life. Those are real losses, Mr Brooks, and I’d be lying if I said I never mourned them.

But I also would have carried the weight of knowing. Knowing that children were dying from preventable disease. Knowing that I had the evidence, the solution, and I’d chosen silence because fighting was too hard. That’s a different kind of suffering, and I’m not convinced it’s lighter than the one I chose.

So perhaps the answer is this: resilience becomes self-destruction when you’re sacrificing yourself for people who don’t value the sacrifice and never will. But when you’re fighting for those children, those dairy workers, those faceless thousands who will never know your name but will live because you persisted – that’s not self-destruction. That’s purpose.

I won’t romanticise it. The cost was real. I was often lonely, frequently in pain, and occasionally despairing. There were nights I lay awake wondering whether it was worth it, whether anything I did mattered. But in the clear light of morning, looking at the data, reading the outbreak reports, I knew the answer. It mattered. The work mattered.

If that’s self-destruction, Mr Brooks, then it’s the kind I can live with. Or rather, the kind I lived with for ninety-four years. And I’d do it again.

Fernanda Álvarez, 31, Agricultural Extension Officer, Mendoza, Argentina
Imagine that in 1918, instead of facing dismissal, a coalition of women scientists – bacteriologists, chemists, physicians – had immediately rallied behind your findings and collectively pressured their institutions to act. Do you think unified advocacy from women across disciplines could have shortened that decade-long delay? Or would the dairy industry and male scientific establishment have simply dismissed an entire group of women more easily than they dismissed you individually? I’m curious whether you think solidarity would have amplified your voice or made you all easier to ignore.

Miss Álvarez, you’ve posed a question that cuts right to the bone, and I confess it’s one I’ve turned over in my mind countless times since learning about the women’s suffrage movement and later watching women organise for various causes. What if we’d banded together in 1918? Would collective action from women scientists have changed anything?

The honest answer is: I don’t know. But let me think through it with you.

On the one hand, there’s strength in numbers. If a coalition of women bacteriologists, chemists, physicians, and public health nurses had stood together and said, “Alice Evans is right, and here’s our corroborating evidence,” it would have been harder to dismiss us all as hysterical or mistaken. We could have divided the labour – some conducting independent verification studies, others lobbying state health boards, still others writing for popular magazines to reach the public directly. We might have put economic pressure on dairies by organising consumer boycotts of unpasteurised milk. Women did the household purchasing, after all. If mothers had refused to buy raw milk for their families, the industry would have felt it in their ledgers.

I think particularly of women like Anna Wessels Williams, who worked at the New York City Health Department and developed an improved diphtheria antitoxin. Or Ida Bengtson, my colleague at the Hygienic Laboratory, who did brilliant work on bacterial toxins and anaerobic bacteria. If women of that calibre had rallied around the brucellosis findings, presenting their own data and speaking at conferences, it would have been harder for male scientists to wave us away.

But here’s the darker possibility: they might have dismissed us more easily precisely because we were a group of women. There’s a long, ugly history of men treating women’s collective action as proof of our emotional rather than rational nature. “Look at them, clucking together like hens in a barnyard,” they’d say. “If this were serious science, why would they need to band together? Good science speaks for itself.” Of course, that’s nonsense – scientific progress has always depended on collaboration and peer verification. But when men collaborate, it’s called rigorous scholarship. When women do it, it’s called a conspiracy or, worse, a social club.

I remember the few women’s scientific organisations that existed in my time. The Naples Table Association for Promoting Laboratory Research by Women, for instance, which funded women researchers. Lovely work, important work, but often treated as quaint charity rather than serious scientific enterprise. Men joined together in societies all the time – the Society of American Bacteriologists itself was essentially a men’s club when I joined – but their organisations were considered professional, while ours were viewed as compensatory, as though we needed special help because we couldn’t compete on merit.

There’s also the practical problem that there simply weren’t enough of us. In 1918, women in bacteriology were scarce as hen’s teeth. I knew Anna Williams and Ida Bengtson, certainly. There was Alice Hamilton doing industrial toxicology. But we were scattered across different institutions, working on different problems, with little infrastructure for communication or coordination. Unlike male scientists who’d built their networks through medical schools, research laboratories, and professional societies over decades, we were isolated pioneers. Organising would have required resources – time, money, travel funds, secretarial support – that we didn’t have.

And here’s something I’m not proud to admit: I’m not certain I would have wanted that kind of coalition in 1918. I was young, ambitious, and still labouring under the delusion that if I just did excellent work and kept my head down, I’d be judged fairly. I think I would have worried that associating my findings with a women’s movement would have made them seem political rather than scientific. I would have been wrong to worry about that, but the worry would have been real.

By the time I’d learnt better – by the mid-1920s, when it was abundantly clear that individual merit wasn’t going to save me – perhaps such a coalition could have helped. But by then, male scientists were already beginning their “independent confirmation” work, and the momentum was shifting. We would have been organising just as the men were preparing to take credit.

Still, I think you’re onto something important, Miss Álvarez. The women’s suffrage movement succeeded – American women got the vote in 1920, just two years after I published my findings – precisely because women organised collectively, made noise, refused to be ignored. Elizabeth Cady Stanton and Susan B. Anthony didn’t succeed because they politely published pamphlets and waited for men to agree with them. They marched, they protested, they disrupted, they made themselves impossible to ignore.

Perhaps we should have done the same. Perhaps we should have organised milk boycotts, staged demonstrations outside dairy industry conferences, written blistering editorials in newspapers, demanded meetings with state health commissioners. Make a fuss. Make them uncomfortable. Force them to respond.

But that would have required something I didn’t have in 1918: the understanding that scientific evidence alone would never be enough. That public health is political. That protecting people from disease means fighting power, not just bacteria. I learnt that lesson eventually, but slowly, painfully, and perhaps too late.

So to answer your question: yes, I think collective action from women scientists could have made a difference. Not because it would have made the science more convincing – the science was already sound – but because it would have been a demonstration of power. And power is what we lacked. The dairy industry had economic power. Male scientists had institutional power. We had evidence, but evidence without power is just words on a page.

Would the establishment have dismissed us more easily as a group? Perhaps. But they might also have been forced to reckon with us. And even if we’d lost that particular battle, we would have built networks and solidarity that could have supported the next generation of women scientists. That matters, Miss Álvarez. That matters tremendously.

I’ll say this: if I had it to do over, knowing what I know now, I’d have sought out those other women scientists. I’d have written to Anna Williams and Ida Bengtson and Alice Hamilton and said, “We need to stand together on this.” Not just for the brucellosis work, but for all of it. For every time a woman’s findings were dismissed, every time credit was stolen, every time we were told we weren’t qualified because we lacked credentials that had been denied us in the first place.

We might have lost anyway. But we would have lost together, and that’s worth something too.

Reflection

Alice Catherine Evans died on 5th September 1975, in Arlington, Virginia, at the age of ninety-four. She had lived long enough to see brucellosis nearly eradicated in the United States, to witness the near-universal adoption of pasteurisation laws she’d fought so hard to establish, and to watch as new generations of women entered scientific fields that had once been closed to them. Yet she also lived to see how quickly victories can be forgotten, how easily evidence-based protections can be challenged, and how persistently gender bias shapes whose knowledge is valued and believed.

Throughout our conversation – both the main interview and her responses to readers’ questions – certain themes emerged with remarkable consistency. Evans was unflinching in her assessment that her dismissal was never really about the quality of her science. As she told Arjun Das, “The problem was never the quality of the evidence. The problem was who was permitted to produce evidence that mattered.” This represents a perspective not always fully acknowledged in sanitised historical accounts, which tend to emphasise “initial scepticism” from the scientific community without naming the gendered credibility crisis at its heart. Evans named it plainly: her findings were dismissed because she was a woman without a doctorate, and the circular logic that created – where structural barriers to credentials became retrospective justification for dismissal – was intentional, not accidental.

Her frankness about the personal cost of her work was equally striking. When Logan Brooks asked whether she’d advise her younger self differently, knowing the decades of chronic illness and professional isolation ahead, she didn’t offer easy platitudes about it all being “worth it.” Instead, she acknowledged the genuine losses – marriage, children, health, joy – whilst maintaining that the alternative – carrying the weight of knowledge without acting on it – would have been its own form of suffering. This nuance is often missing from accounts that either martyr women scientists (emphasising their bodily sacrifice) or celebrate them uncritically (erasing the genuine toll of fighting institutional power). Evans refused both narratives, insisting instead on the complexity: yes, it cost her dearly; yes, she’d do it again; no, that doesn’t make the cost acceptable or inevitable.

Her technical explanations – particularly to Nia Okafor about practical alternatives to industrial pasteurisation and to Arjun Das about the limitations of culture-based methods – revealed something the historical record sometimes obscures: Evans was not merely right about the what (that Brucella transmitted from cattle to humans), but extraordinarily thoughtful about the how (what practical interventions would actually protect people, given economic and infrastructure constraints). Her response to Okafor, advocating for tiered approaches that balance cultural practices with safety measures, demonstrates the kind of pragmatic, community-centred public health thinking that remains urgently relevant today.

Where Evans’s perspective may have differed most sharply from recorded accounts is in her assessment of what might have changed the outcome. Historical narratives often frame her eventual vindication – when male scientists confirmed her work in the late 1920s – as progress, as science “self-correcting.” Evans rejected that framing entirely. To her, the decade-long delay between her discovery and policy implementation represented thousands of preventable illnesses and deaths, not a triumph of scientific process. She also pushed back against narratives emphasising individual resilience, as evidenced in her response to Fernanda Álvarez about whether collective action from women scientists might have helped. Rather than celebrating her lone perseverance, she wondered whether they should have organised boycotts, staged protests, “made a fuss” – acknowledging that she’d initially believed excellence would be enough, a belief she later recognised as naive.

There are gaps and uncertainties in Evans’s story that even she couldn’t fully resolve. We don’t know precisely how she contracted brucellosis – she suggested it might have been a splash or aerosolised bacteria, but laboratory conditions in 1922 weren’t always documented thoroughly. The exact duration of her illness varies across sources, with some accounts saying twenty years and others thirty; she herself noted that “time becomes fluid when you’re chronically ill,” highlighting how chronic disease disrupts linear narrative. We also lack detailed records of her daily laboratory work, the informal conversations with colleagues, the small acts of resistance and accommodation that shaped her career. What survives in archives are publications, official correspondence, and memoir – the public-facing record, not the lived texture of those decades.

The contemporary relevance of Evans’s work cannot be overstated. The raw milk movement she found so infuriating continues to grow, with documented outbreaks of brucellosis, E. coli, Salmonella, and Listeria linked to unpasteurised dairy products. Between 2017 and 2019, human infections with the RB51 vaccine strain – antibiotic-resistant and difficult to diagnose – highlighted precisely the kind of zoonotic transmission pathway Evans identified a century ago. Her pioneering of what we now call One Health – recognising that human, animal, and environmental health are interconnected – has become central to pandemic preparedness and zoonotic disease surveillance, yet the institutional silos she described to Eleni Papadopoulos persist. Veterinary medicine, public health, and agricultural policy still operate largely independently, with the coordination gaps she identified continuing to hinder rapid outbreak response.

The afterlife of Evans’s work took decades to fully materialise. While pasteurisation laws were enacted in the 1930s and 1940s, Evans herself wasn’t widely recognised until late in her life. She received the honorary doctorate from the University of Wisconsin in 1948 – three decades after her discovery – and was honoured by the American Society for Microbiology (the renamed Society of American Bacteriologists) in her later years. Modern food safety regulations, zoonotic disease protocols, and dairy microbiology as a distinct field all rest on foundations she established, though her name rarely appears in public discourse about milk safety. Historians of science have begun recovering her story in recent decades, but she remains far less known than male contemporaries whose contributions were less transformative.

Her lasting influence can be seen not just in specific policies, but in the framework itself: the understanding that food safety is public health, that animal diseases can threaten human populations, that prevention requires crossing disciplinary boundaries. Every time a public health department collaborates with veterinary services to track foodborne illness, every time agricultural policies incorporate human health outcomes, Evans’s insistence on connected thinking echoes forward.

For young women in science today, Evans’s story offers something more valuable than inspiration – it offers recognition. Recognition that the barriers they face aren’t personal failings or isolated incidents, but structural features of institutions that were never designed to include them. Recognition that “excellence” and “merit” are not neutral standards but ones shaped by who gets to define quality, whose knowledge is presumed credible, and whose contributions require endless verification. Recognition that the exhaustion they feel fighting to be heard is real, valid, and not something they should have to endure alone.

But her story also offers something else: evidence that the work matters beyond recognition. Thousands of people are alive today because Alice Catherine Evans was stubborn enough to keep fighting, precise enough in her methods that her findings couldn’t be dismissed indefinitely, and brave enough to contract the very disease she warned about and still continue working. That’s not martyrdom to celebrate – it’s injustice to rage against. But it’s also proof that scientific truth, coupled with relentless advocacy, can eventually overcome institutional resistance.

The challenge for today’s scientific community is ensuring that women scientists don’t have to make those choices – between health and career, between personal life and professional recognition, between speaking truth and being believed. Evans shouldn’t have had to wait a decade for men to confirm her findings. She shouldn’t have had to work whilst chronically ill because she lacked institutional power to implement the protections she’d identified. She shouldn’t have been fighting bacteria and sexism simultaneously.

Yet she did all of it. And when I asked what she’d tell women in STEM today, she didn’t offer empty reassurance. She said: document everything, find allies, persist because it’s a form of resistance, and remember that your work matters more than recognition. Then she added something that will stay with me: “Do the work for the work’s sake, because it matters, because lives depend on it. The recognition may come, or it may not. But the work will stand.”

The work stood. Children no longer routinely die from drinking milk. Brucellosis has been nearly eliminated in countries with strong food safety infrastructure. Dairy microbiology is a recognised field. One Health frameworks are shaping pandemic response. None of that happened because the scientific establishment spontaneously became enlightened. It happened because Alice Catherine Evans looked through a microscope, saw the truth, and refused to let men’s disbelief stop her from saving lives.

That refusal – to stay silent, to accept dismissal, to let children die preventable deaths because fighting was difficult – is her greatest legacy. Not the discovery itself, though that was remarkable. But the insistence that evidence matters, that women’s scientific work is valuable, and that public health is worth fighting for even when the fight costs everything.

We owe her more than memory. We owe her a world where the next woman scientist who makes a transformative discovery is believed the first time she speaks.

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.

Editorial Note: This interview is a fictional dramatisation created for educational and commemorative purposes. Alice Catherine Evans cannot speak to us directly; she passed away nearly fifty years ago. The conversation presented here has been constructed through careful research drawing upon her published scientific papers, professional correspondence, memoir writings from 1963, biographical accounts by historians of science, and documented records of her career at the U.S. Department of Agriculture and the National Institutes of Health.

Whilst every effort has been made to represent Evans’s documented views, scientific methods, and historical context accurately, the specific phrasing, responses, and reflections are necessarily imagined. Where Evans left written accounts of her experiences – particularly regarding the dismissal of her brucellosis findings, her struggle with chronic illness, and her observations about gender discrimination in science – those perspectives have been woven into this reconstruction. However, her responses to contemporary issues (such as the modern raw milk movement, CRISPR diagnostics, and One Health frameworks) represent informed extrapolation based on her established positions and scientific principles, not her actual words.

The technical details of her bacteriological methods, the timeline of her discoveries, and the institutional barriers she faced are grounded in historical evidence. The personality traits, speech patterns, and emotional tenor reflect what can be gleaned from biographical sources, though the specific voice crafted here remains an interpretation. Readers should approach this work as a research-based tribute that aims to honour Evans’s intellect, resilience, and contributions whilst acknowledging the limitations inherent in speaking for someone who can no longer speak for herself.

Bob Lynn | © 2025 Vox Meditantis. All rights reserved.