The DRC Ebola Outbreak: A Predictable Diagnostic Failure

The outbreak of Bundibugyo ebolavirus in the Democratic Republic of the Congo is not, primarily, a story about a deadly and scary virus. It is a story about systemic failure — in diagnostics, in institutional capacity, and in countermeasure preparedness — that my colleagues and I have been warning about for years.

By the time you read this, the official case count is approaching 1000. The real number is higher. That gap isn’t a mystery — it’s the direct consequence of a diagnostic delay that gave the virus a several week head start. Bundibugyo is a rare species of Ebola, having caused just two prior outbreaks, and initial testing, targeted to the far more common Zaire species, missed it. By the time anyone knew what they were dealing with, untraced transmission chains were already in motion. Typical Ebola outbreaks get flagged when there are 20 or 30 cases, beginning containment when cases are in the triple digits with significant momentum is a different containment problem entirely.

This is exactly the kind of failure I testified about before the House Foreign Affairs Subcommittee in 2021. I argued then that we have a “biological dark matter” problem — undiagnosed clinical syndromes circulating everywhere, containing early signals we’re not catching because our diagnostic infrastructure isn’t looking for them. Far too many unknown infectious syndromes — from Pittsburgh to Bunia — go without a specific microbiologic diagnosis. The 20,000+ case West African Ebola epidemic of 2013–2016 offered the same lesson: Ebola had been circulating for over a decade mixed in with (and likely mistaken for) Lassa Fever cases. Guinea took three months to realize it was dealing with an Ebola outbreak and not cholera. The trajectory of the current DRC outbreak echoes the past.

What made this outbreak worse is that the US surveillance infrastructure that would have sounded the alarm earlier has been dismantled. USAID, which operated in the DRC, was impacted by DOGE program. In addition, the director-less and RFK Jr-beholden CDC has lost over 700 people from its emerging-disease activities — employees and contractors — including the head of the high-consequence infectious disease group directly responsible for Ebola response. The storied agency that was once first on the ground, first to brief the world, now can’t even participate directly with the WHO without asking permission.

A major aspect of the US response to all this has been a travel ban — on DRC, Uganda, and South Sudan. It is the wrong move, for the same reasons it has always been the wrong move. Travel bans, though a favorite tool of politicians who want to appear as if doing something, impede the flow of personnel and resources intooutbreak zones. Healthcare workers who might volunteer to fight this outbreak will now have to contemplate being corralled by the policy. Other countries follow suit with cascading bans. As such, the International Health Regulations oppose travel bans. They are not evidence-based and objectively harmful. Targeted travel screening is what works. Blanket restrictions have the very real potential to postpone the extinguishing of outbreaks at their source. Critically, the US has 13 NETEC biocontainment treatment centers built precisely for this, and we should be vigilant and proactive without being rattled.

There is also a countermeasure reality to face: there are no approved vaccines or specific treatments for Bundibugyo ebolavirus. The drugs that worked so well in the DRC’s 2018–2020 outbreak are specific to Zaire ebolavirus. They don’t reliably cross-protect against Bundibugyo. BARDA is advancing a monoclonal antibody that targets Ebola Sudan and may have some cross-reactivity (it is likely the treatment that Dr. Stafford has received in Germany), and Oxford and the Serum Institute of India are working on a vaccine using the AstraZeneca COVID platform that might be field-deployable within months.

This countermeasure gap extends to other filoviruses as well. Neither Ebola Sudan nor Marburg, both of which have causes recent outbreaks, have countermeasures as well. These are filoviruses with case fatality rates that routinely exceed 50 percent, and we have had no licensed tools against them. We built countermeasures for Zaire ebolavirus in response to its potential use as a bioweapon and the magnitude of the outbreak 2014. We have not applied the same urgency to the rest of the family, and every outbreak of Sudan virus or Marburg is a reminder of why a viral family approach is desperately needed.

The post-COVID media continually wants to know if this outbreak is “the next COVID” (as they did for hantavirus). The answer is no — Ebola spreads through blood and body fluids, not the respiratory route. Its transmission is constrained. Ebola is a virus that spreads through direct contact with the bodily fluids of the sick and the dead — it finds exactly what it needs in overwhelmed clinics with no PPE and burial traditions that involve touching the body, but the moment it lands somewhere with isolation rooms and infection control, it is quickly stopped in its tracks. They also mention The World Cup. Mass gathering events are perfect venues for crowd diseases such as those caused by a respiratory or gastrointestinal virus — measles, influenza, COVID, norovirus — diseases that spread through the air and via causal contact requiring little more than proximity. Ebola requires you to be in direct contact with someone who is visibly, severely ill and is not a crowd disease.

The real worry isn’t what Bundibugyo will do to the American public. It’s what our hollowed-out response infrastructure will do when the US inevitably faces a true pandemic threat.

Germ Theory is Not a Narrative

Multiple times in recent weeks, people have posted some version of the same claim on my social media accounts: viruses don't exist. The comments usually arrive with a set of caveats — cell culture techniques don't count as evidence, electron microscopy is interpreted too liberally, the photographs are artifacts. This is a total absurdity.

The evidence for the existence of viruses is incontrovertible and manifold. In 1892, a Russian botanist named Dmitri Ivanovsky passed the sap from diseased tobacco plants through a Chamberland filter — a porcelain filter fine enough to trap every known bacterium — and the filtrate still caused disease. Something was passing through that no bacterium could. That was the first documented encounter with what we now call a virus. Over the following century, the evidence compounded and converged: electron microscopy visualized viral particles directly beginning in the 1930s; fluorescence microscopy tracked their movement through living cells in real time; cytopathic effect — the characteristic pattern of cell destruction that differs systematically by pathogen — became a diagnostic standard that clinicians use today. These are not interpretations. They are observations, replicated independently on every continent, across 130 years.

The reason scientific evidence is inadmissible in these discussions is not because it is weak. It is because the people making these arguments have pre-rejected the epistemological framework which includes the scientific method. In their wicked egalitarianism, no one's standpoint is closer to reality than anyone else's — a virologist peering through an electron microscope has no more claim to truth than the person who watched a YouTube video about it. To even call this an argument gives it too much respect. It is the complete flattening and destruction of the concept of expertise.

That philosophical infrastructure underlies what is now US health policy. RFK Jr., the current Secretary of Health and Human Services, overtly questions germ theory in favor of what he calls terrain theory — the claim that what we label infectious disease results not from external pathogens but from an unhealthy internal "terrain." This is not a new idea. It is miasma theory, the discredited framework that predates Pasteur's epoch-making development of germ theory. Sanitation does matter — it reduced infant mortality meaningfully, and no one disputes that. But sanitation explains declining death rates from cholera and typhoid. It does not explain the elimination of smallpox, the near-eradication of polio, why pediatric wards are no longer filled with children with Hib meningitis, the survival of children who would otherwise have died of Hib meningitis. Vaccines and antibiotics explain those. The terrain model cannot account for what Fleming found growing on that contaminated petri dish, or what Jenner observed when the milkmaid who'd had cowpox didn't contract smallpox.

For many adherents of this worldview, infectious disease expertise (even when discussing a non-communicable disease) is inseparable from social control. Public health becomes not a response to pathogens but a mechanism of coercion. In this framing, outbreaks justify restrictions, experts become instruments of (bio)power, and skepticism itself becomes a form of resistance. The field of infectious disease medicine has been recast as a psyop designed to implement an agenda of social control. They respond with what the philosopher Foucault called counter-conduct: not just rejecting medical authority but appropriating its language — informed consent, bodily autonomy, "do your own research" — while treating ivermectin as a tribal symbol and any pathogen as a pretext for political theater.

I wonder whether they would have discouraged Jenner, Pasteur, Koch, and Fleming from trying to solve the human problems that infectious diseases posed. These were not agents of control. They were scientists who looked at people dying of preventable diseases and refused to accept it as the natural order of things.

D.A. Henderson's smallpox eradication campaign was not an act of biopower. It was an act of human reason applied to a significant and deadly human problem. That is what infectious disease medicine is — and has always been. Germ theory is not a narrative. It is a description of reality. As an infectious disease physician, I have treated patients with illnesses whose course changed because germ theory was true: bacterial infections halted by antibiotics, opportunistic infections prevented with antimicrobials, diseases made rare by vaccines. My field has always fought for civilization by trying to master an inhospitable natural world (as it always has) — it now faces an anti-human attack wielded by an army of postmodern nihilists who have been granted government power.

Vaccination is Liberation

Every summer for most of human history, parents watched their children with dread. Not because summer was dangerous in the way we mean today — it was something more specific and more terrible. Pools were closed. Crowded places were avoided. A child who woke up with a fever and leg pain was a child who might never walk again. Polio was seasonal. Parents knew this. They planned around it. They feared it the way you fear something that doesn't announce itself before it takes.

That was the normal condition of human life before vaccines. Not the exception. The norm.

In the 20th century alone, smallpox killed an estimated 300 million people — more than all the wars of that century combined. Before Edward Jenner developed the smallpox vaccine in 1796, the disease killed roughly one in three of those it infected and blinded many of those it didn't. In 18th century Russia, every seventh child born died from smallpox. It was not an anomaly to dread. It was a tax that nature collected on the act of being born.

We ended it. With a vaccine. In 1980, the WHO certified smallpox eradicated — the only human disease ever fully extinguished. That is one of the most extraordinary achievements in the history of our species and was led by DA Henderson, a mentor to me and larger than life Homeric hero.

What vaccines actually are

We haven't properly understood what vaccines are. They are liberation technology. They are what happens when human beings refuse to accept nature's terms.

Energy expert Alex Epstein has a concept he calls "climate mastery." His core argument is that the right question about climate isn't how to minimize our footprint — it's how to build the technological capacity to master climate dangers. Humans don't just "adapt" to storms, drought, and extreme temperatures; we build levees, irrigation systems, and weather-forecasting networks. The result: climate-related deaths have fallen roughly 98% over the last century, even as the human population more than tripled.

The same principle, applied to the microbial world, is what I'd call infection mastery. Nature has never been on our side. Viruses and bacteria do not intend harm — they have no intentions at all. They replicate, mutate, and spread because that is what selection pressure optimized them to do. Infectious disease has always been the price of living on a planet that was microbial long before it was human. For most of history, that price was paid in full — with paralyzed limbs, blind eyes, dead children, and shortened lives. There have been 10,000 generations of humans and it’s only the last 4 that humans have been able to master some infectious diseases.

Vaccines are infection mastery in concentrated form. They don't ask us to accept the disease burden nature imposes. They allow us to build immunity without paying the cost of the disease itself — to take the lesson without the punishment. The result: polio, which paralyzed tens of thousands of American children per year in the 1950s, has been eliminated from the Western hemisphere. Measles, which killed 2.6 million people per year before the vaccine, is now eminently preventable — when we bother to use it. The HPV vaccine prevents cervical cancer. The flu vaccine reduces heart attacks. The shingles vaccine cuts stroke risk. These tools don't just stop infections; they reshape the entire downstream arc of a life.

The misunderstanding that keeps getting people killed

Some people frame vaccination as humans "interfering" with nature, as if nature had a preference worth respecting. But this gets the relationship exactly backward. The human immune system, the human brain, the capacity for abstract reasoning that lets a scientist synthesize an mRNA vaccine in a year — all of that is nature. It evolved. When we make a vaccine, we aren't defying natural selection. We are what natural selection produced: a species capable of turning reason outward onto a hostile world and making it less lethal. On my first trip to the Galápagos, where Darwin amassed the observational data needed to formulate the theory of evolution via natural selection, a naturalist guide told me humans shouldn't interfere with how infectious disease shapes our species. My answer then is what it is now: building tools to master infection is the most natural thing we do. It is natural selection completing itself through us.

This is why the current erosion of vaccine confidence isn't just a public health problem. It is a civilizational one. Measles is spreading across American states not because we lack the tools to stop it, but because we have chosen to walk away from them — to voluntarily return to a world our grandparents spent their lives escaping. The West Texas outbreak, the Florida cases, exposures at Lincoln Center, and South Carolina— these aren't bad luck. They are the predictable result of surrendering infection mastery to ideology.

If a 98% reduction in climate deaths counts as mastery, what do we call the eradication of smallpox? What do we call a world where your child doesn't spend August in fear of a limp? We call it what it is: a triumph of human reason over nature's indifference. And it is ours to lose.

Hantavirus Panic and the Media’s Outbreak Attention Problem

Hantavirus is having a media moment again. First came the death of Betsy Arakawa, wife of actor Gene Hackman, from hantavirus pulmonary syndrome. That was soon forgotten. Then came intense coverage of a suspected cluster aboard a cruise ship traveling from Argentina toward Cape Verde. Suddenly, headlines and cable segments began treating hantavirus as if it were poised to become the next major global infectious threat.

As someone who has spent the last several days doing television, radio, podcast, and print interviews on hantavirus, I’ve repeatedly found myself trying to inject proportionality into the conversation. The challenge has not been convincing journalists that hantavirus is serious — it can be — but rather helping audiences understand what kind of threat it actually represents, and what kind it does not.

Because this reaction says more about how modern media ecosystems process infectious disease stories than it does about the actual public health risk posed by hantavirus.

Hantaviruses are real, serious pathogens. In the Americas, they can cause hantavirus pulmonary syndrome, a severe respiratory illness with a high case fatality rate. However, they are also exceedingly rare. Since surveillance began in 1993, the United States has documented fewer than 1,000 total cases. Most cases occur after direct or indirect exposure to rodent droppings in rural environments — cabins, sheds, barns, crawl spaces, and other enclosed settings where deer mice live.

That epidemiology matters.

Unlike influenza, measles, SARS-CoV-2, or norovirus, hantavirus is not efficiently transmitted person-to-person in the United States. It lacks the characteristics that allow respiratory viruses to sustain large outbreaks in human populations. Even in South America, where limited human-to-human transmission has occasionally been documented with the Andes strain, spread is uncommon and typically requires close contact.

Yet the media response often strips away that nuance. Rare diseases with dramatic clinical presentations tend to generate disproportionate attention because they satisfy several conditions modern news systems reward: novelty, mystery, severity, and emotional salience. A virus with a 30–40% fatality rate sounds terrifying, even if the average person’s probability of exposure is extraordinarily low.

The same pattern occurs with public health response language. During outbreak investigations, media reports will often breathlessly note that the CDC has activated at “Level 3,” without explaining what that actually means. To many readers, “Level 3 activation” sounds ominous — as though the agency is escalating toward emergency footing. In reality, CDC emergency activations are inverted from how most people intuitively think about them: Level 1 is the highest, most serious activation, while Level 3 is the lowest level of activation and often reflects a relatively modest operational response. Omitting that context can unintentionally magnify public fear and create the impression that officials view the situation as far more dangerous than they actually do. There are different levels of public health emergencies and not all constitute epidemic —let alone pandemic — threats

This dynamic is amplified by the post-COVID information environment. Both journalists and the public are now primed to interpret any unusual infectious disease event almost exclusively through a pandemic lens. A cruise ship cluster becomes framed less as an epidemiologic investigation and more as a possible origin story for “the next pandemic.” That framing may drive clicks and engagement, but it can distort public understanding of risk.

The irony is that many much larger infectious disease threats struggle to command sustained attention. Seasonal influenza kills thousands annually. Drug-resistant bacterial infections steadily expand. Measles outbreaks are re-emerging because of declining vaccination rates. Tick-borne illnesses continue to rise across the United States. These problems are epidemiologically far more important to the average person than hantavirus.

Part of the issue is that public perception of risk is not calibrated by statistical probability. It is calibrated by imagery, narrative, and fear. Rodent-borne viruses on remote cruise ships feel cinematic. Endemic respiratory viruses do not.

None of this means hantavirus should be ignored. Clinicians should recognize it. Public health officials should investigate clusters aggressively. Situations like the cruise ship outbreak require adept epidemiologic investigation, careful risk communication, and thoughtful operational management in order to protect passengers while avoiding unnecessary panic. Rodent control and environmental hygiene matter. But proportionality matters too.

One of the most important functions infectious disease experts can serve in media appearances is not simply explaining pathogens, but calibrating risk. Sometimes that means sounding alarms. Other times it means lowering the temperature. In the case of hantavirus, the latter is often what is needed most.

One of the central challenges in infectious disease communication is helping people distinguish between a dangerous pathogen and a civilization-altering one. The question is not simply whether a pathogen is dangerous. The question is when to worry — and why.

Infectious disease reporting works best when it informs rather than startles — when it contextualizes risk instead of merely amplifying anxiety. Hantavirus is a fascinating virus and an important pathogen. It is not, however, civilization’s next existential microbial threat.

Hantavirus on a Cruise Ship: What You Need to Know

When you think about viruses spreading on cruise ships, hantavirus is probably not what comes to mind. Norovirus, sure. Influenza, absolutely. COVID, of course. But hantavirus? That one is unusual enough to warrant a closer look.

That is exactly what happened in May 2026, when a cluster of cases emerged aboard a ship that had traveled from Argentina to Antarctica and onward toward the Cape Verde Islands. People got sick. Some died. And a lot of people were left asking a very reasonable question: how does hantavirus end up on a cruise ship?

The answer begins with a simple but critical point: hantavirus doesn’t spread the way people think. This is not a contagious respiratory outbreak. It is a problem of environmental exposure.

A Rodent Virus With a Long History

Hantaviruses are a family of viruses found worldwide, and they are fundamentally viruses of rodents. Mice, rats, and other small mammals carry them. Humans are incidental hosts—we are not part of the natural transmission cycle.

These infections have been recognized for decades. During the Korean War, soldiers developed illnesses later understood to be caused by hantaviruses circulating among rodents in the region. Those infections often involved kidney damage and sometimes hemorrhagic complications, a syndrome now known as hemorrhagic fever with renal syndrome, or HFRS. These “Old World” hantaviruses circulate in Europe and Asia and primarily affect the kidneys.

Globally, most hantavirus infections actually present in this form.

The Four Corners Outbreak and the Lung Disease Form

In the early 1990s, a very different hantavirus story unfolded in the United States. A cluster of cases appeared in the Four Corners region, where New Mexico, Arizona, Colorado, and Utah meet. Young, otherwise healthy individuals developed what initially looked like a flu-like illness. Then, in some cases, their lungs filled with fluid and they rapidly deteriorated.

The cause was a previously unrecognized hantavirus—Sin Nombre virus—and the disease it produced became known as hantavirus pulmonary syndrome.

This is the form most familiar in the United States, and it can be severe. The virus damages the small blood vessels in the lungs, causing them to leak fluid into the airspaces. There is no specific antiviral treatment and no widely available vaccine. Because early symptoms are nonspecific—fever, fatigue, muscle aches—diagnosis often comes late, when patients are already critically ill. When severe disease develops, case fatality rates can be high.

How Transmission Actually Occurs

Here is the single most important fact to know when alarming headlines appear: hantavirus is not a contagious respiratory virus.

It does not spread efficiently from person to person. Instead, infection occurs when humans intersect with a contaminated environment—typically one involving rodents.

The classic scenario is someone cleaning an enclosed space—a shed, a barn, a cabin—where rodents have been present. Dried droppings or urine are disturbed, particles become airborne, and the virus is inhaled. After an incubation period of roughly one to two weeks, symptoms begin.

This is not about proximity to other people. It is about proximity to contaminated environments.

In the United States, only a few dozen cases are reported each year. A recent fatal case in New Mexico involving the wife of actor Gene Hackman brought renewed attention to the disease—a reminder that hantavirus has not gone anywhere, even if it remains rare. Last week, a case was reported in the Carson City area.

A Note on Andes Virus

There is one exception worth noting. A hantavirus called the Andes virus, found in parts of South America, has demonstrated limited person-to-person transmission.

But even in those cases, spread is inefficient and requires close, prolonged contact. It does not behave like a typical respiratory pathogen, and it is not capable of driving widespread outbreaks in the way viruses like influenza or SARS-CoV-2 can. The genomic investigation of the virus isolated from cruise ship patients will be important to determine which version of hantavirus is responsible since there is an epidemiological link with Argentina, where Andes virus is found.

Why Outbreaks Follow Bountiful Years

One of the more interesting aspects of hantavirus ecology is how closely it tracks environmental conditions.

In years with heavy rainfall—often associated with El Niño cycles—vegetation flourishes. Food sources for rodents increase. Rodent populations expand. And as rodent populations grow, so does the likelihood of human exposure.

This pattern was recognized long before modern epidemiology. Indigenous communities in the American Southwest had oral traditions describing illnesses that followed years of abundance. Modern research has confirmed the biological basis of those observations.

The disease follows the rodents, and the rodents follow the food supply.

Back to the Cruise Ship

With that background, the cruise ship cluster becomes easier to interpret, even if key details are still being investigated.

The ship departed from southern Argentina, a region where multiple hantavirus strains circulate. The central epidemiologic question is straightforward: where did the exposure occur?

There are two main possibilities.

In the first, passengers were exposed before boarding or during excursions—through contact with rodent-contaminated environments on land. The virus incubated during the voyage, and symptoms appeared days to weeks later.

In the second, rodents were present on the ship itself, creating an ongoing source of exposure.

The distinction matters enormously. If exposure occurred prior to boarding or during excursions, the risk is largely over. If the source is onboard, new exposures could continue until the problem is identified and controlled.

Epidemiologically, a shared exposure event—rather than ongoing transmission aboard the ship—is more consistent with how hantavirus behaves.

The cruise ship is where the cases were recognized, not necessarily where the exposure occurred.

Keeping the Headlines in Perspective

A cruise ship, a deadly virus, and passengers stranded at sea: it is the kind of story that naturally generates alarm.

But context matters.

Hantavirus can be severe, particularly in its pulmonary form. The absence of a specific treatment or vaccine makes it a serious infection when it occurs. At the same time, its inability to spread efficiently between people means it does not have the capacity to become a self-sustaining epidemic.

The risk is real—but it is bounded.

For most people, the relevant risk is not sitting next to someone on a ship. It is disturbing a rodent-contaminated environment without proper precautions.

Rodents have traveled on ships for centuries, and the diseases they carry have followed them. What makes this case unusual is not the biology, but the setting. A cruise ship is not where we expect to see hantavirus, and that contrast amplifies concern.

But the public health logic remains straightforward: identify the source, eliminate it, and protect those who may have been exposed.

That is what investigators are working to do now.