Rift Valley Fever: When the Rains Bring Life and Loss

Summary

When the rains return to the Sahel, life blooms — and so do the mosquitoes that carry Rift Valley fever. This year, the virus has swept across southeastern Mauritania and into Senegal, sparking the largest outbreak in years. In this episode, Infectious Dose unpacks how the disease moves between animals, people, and mosquitoes; why the cycle repeats after every rainy season; and what new research from Tanzania reveals about hidden transmission during “quiet” years. It’s a story of science, survival, and the delicate balance between life and loss.

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Full Episode

SETTING THE SCENE

It happens after the rains.

The grass returns, the herds grow fat, and the mosquitoes rise from the floodplains—carrying with them something older than memory.

This year, it began in the goats and camels of southeastern Mauritania. By the time the herders fell ill, the virus had already crossed the border into Senegal.

Hundreds sick. Dozens dead.

And the season isn’t over.

This is Rift Valley Fever: When the Rains Bring Life and Loss

So, here's what's been happening. In late August, goats and camels in southeastern Mauritania began dying—first a few, then dozens. By September, veterinarians in Hodh El Gharbi and Hodh Ech Chargui were sending samples to the lab. The results confirmed what they feared: Rift Valley fever was back.

And by the end of October, the virus had crossed the border into Senegal. Hundreds of people were sick—some bleeding, some blind, some dying—in what has become the largest Rift Valley fever outbreak in years. Between September 20 and October 30, 2025, Mauritania and Senegal together reported more than 400 confirmed human cases—46 in Mauritania and 358 in Senegal—with 42 deaths. And just a few days ago, the first human case of Rift Valley fever was reported in The Gambia.

If you’d like to learn more these outbreaks, the global response and comunity protection, the World Health Organization is hosting a free EPI-WIN webinar today at 1pm CET, which is 7pm EST. And by today I mean the day the episode drops, so November 12th, 2025. The webinar is called “Rift Valley Fever and Community Protection: Gaps, Needs and Priorities,” and it brings together experts from WHO, Senegal, and Rwanda. It should be really informative.

OK, where were we? Oh yes, hundreds of cases and 42 deaths so far. And behind those numbers is a sharp difference in severity. Mauritania’s case fatality rate was about 30 percent, while Senegal’s was closer to eight. The difference partly reflects detection gaps—many mild infections never reach hospitals—but it also highlights the unpredictable nature of this virus.

Let me explain. When you only count the people who are sick enough to end up in a clinic or hospital, it makes the virus look far deadlier than it really is. In places where testing is limited, mild and moderate cases often go unreported, shrinking the total number of “known” infections. That means the fatal cases make up a bigger slice of the pie. In Senegal, where surveillance caught more mild illness, the denominator was larger—and the apparent fatality rate much lower.

But that’s only part of the story. Rift Valley fever itself is notoriously erratic. Even when surveillance is strong, one outbreak might bring mostly mild, flu-like illness, while another leads to blindness, hemorrhage, or death. Differences in viral strain, host health, or even co-infections can all shift the outcome. So Mauritania’s higher fatality rate likely reflects both: fewer detected mild cases, and the virus’s own unpredictable nature—two factors that can work together to shape what we see on paper.

TRANSMISSION

So let's cover some information about this virus. Rift Valley fever, or RVF, is a viral disease that affects livestock—sheep, goats, cattle, and camels. People usually get infected through mosquito bites or by handling animal blood, tissue, or milk. Slaughterhouse workers, farmers, and herders are most at risk.

Rift's primary vectors belong to the Aedes and Culex mosquito genera. A 2022 PLoS Neglected Tropical Diseases systematic review of mechanistic transmission models emphasizes that no single pathway explains every outbreak; instead, RVFV circulates through multiple overlapping routes shaped by rainfall, mosquito ecology, and livestock movement.

Mosquito-borne cycles. Outbreaks typically begin after heavy rains or flooding, when the dry depressions known as dambos fill with water and awaken long-dormant Aedes mosquito eggs. These eggs—laid in the soil during earlier rainy seasons—can survive dry conditions for months or even years, waiting for the next flood to hatch. Some of them already carry Rift Valley fever virus, passed directly from infected mothers to their offspring.

When these infected Aedes emerge, they bite nearby livestock, seeding the virus into herds that quickly develop high levels of virus in their blood. That first wave of infection turns livestock into powerful amplifiers. Soon after, Culex mosquitoes take over. They breed in the new rain-fed pools and feed repeatedly on infected animals, spreading the virus within herds, between villages, and sometimes to people.

In essence, Aedes light the match—releasing the virus from the ground after years of dormancy—while Culex fan the flames, driving the explosive spread that follows. When the rains end and the pools dry up, both species decline, but Aedes eggs left behind in the soil preserve the virus, waiting for the next season of floods and fever. In fact major outbreaks often coincide with El Niño years, as shifting rainfall patterns create ideal conditions for mosquito blooms.

I mentioned vertical transmission so I'd like to clarify that. Vertical transmission in mosquitoes—meaning the virus passes directly from an infected female to her offspring through her eggs—is well documented, but models suggest it cannot, on its own, maintain the virus between epidemics unless unrealistically high transmission rates occur. More likely, low-level vertical transmission, combined with residual virus in small livestock populations and occasional mosquito emergence, sustains the virus during the inter-epidemic years.

Animal and human infections. Humans are usually spillover hosts with Rift, infected by mosquito bites or direct contact with animal blood, tissues, or miscarried material during outbreaks. Mechanistic models consistently identify livestock movement—especially the long-distance trade and nomadic herding systems that link regions—as a dominant driver of spatial spread. A small number of infected animals can seed new outbreaks hundreds of kilometers away, and movement restrictions can sometimes backfire if they delay outbreaks into peak mosquito seasons.

Some wild ungulates carry antibodies to RVFV, suggesting occasional infection, though their role as reservoirs remains unclear. While they’re not considered primary amplifiers like domestic livestock, their exposure points to a broader ecological network that may help the virus persist in certain regions.

Other potential routes. As I mentioned, vertical transmission from mother to fetus has been documented in humans and livestock, but there’s no evidence of sustained human-to-human transmission, and if it occurs at all, it is extremely rare. Ticks have been proposed as possible secondary vectors, but available models and field evidence do not support a major role. For example, ticks have been found to carry viral RNA in some studies, but their competence as vectors for Rift has not been established so they’re not considered major drivers of transmission.

In essence: It’s a complex ecology—mosquitoes, livestock, and weather patterns locked in a shifting balance that makes prediction hard.

THE ANIMAL TOLL

What about in animals? Well, in animals, the virus spreads like wildfire. Miscarriages in livestock are highly variable (Veterinarians call them abortions, but for simplicity I’ll say miscarriages throughout this episode.). Sheep are more affected than goats, and camels are less well studied. But vulnerable pregnant livestock (like sheep) can miscarry en masse, and young animals die within days. In Mauritania, 62 animal outbreaks were confirmed by late October, with 235 positive samples out of 1,106 tested. Seventy-one animals died, mostly goats and camels. The virus moved westward across the country into Brakna, along the Senegal River, where more than 50 livestock deaths were reported.

In Senegal, the picture was similar. Out of more than 1,100 animal samples collected, 160 tested positive, and 640 animal miscarriages were reported across seven regions. The hardest-hit human districts—Richard-Toll, Saint-Louis, Podor, and Dagana—are all clustered along the northern border with Mauritania, tracing the river that links the two countries. This same river valley, rich in farmland and livestock, has long been a hotspot for mosquito-borne outbreaks.

PATHOGENESIS

Inside the Virus

Rift Valley fever virus belongs to the Phenuiviridae family, genus Phlebovirus—a cousin to viruses like Toscana and Heartland. Under the microscope, it’s a tiny sphere wrapped in a lipid envelope, only about 100 nanometers across—nearly a thousand times thinner than a human hair. Its surface bristles with glycoprotein spikes called Gn and Gc, which lock onto host cells and help the virus fuse its membrane with theirs. Inside lie three strands of single-stranded, negative-sense RNA, known simply as L, M, and S—for large, medium, and small. Together they encode the virus’s essential machinery and two notorious nonstructural proteins, NSs and NSm, molecular saboteurs that help Rift Valley fever virus hide, persist, and spread.

Rift Valley fever doesn’t just spread fast—it spreads deep. Once Rift enters the body—most often through a mosquito bite or contact with infected animal blood or tissue, and rarely in occupational settings, through inhaled droplets during slaughter or necropsy—it wastes no time taking over. The incubation period is usually four to six days, just long enough for the virus to quietly multiply in the liver, spleen, and other tissues before the first symptoms hit: fever, headache, back pain, nausea, eyes bloodshot and aching.

For most people, that’s where it ends—a few miserable days of fever and fatigue, then recovery as antibodies rise and the immune system clears the virus from the bloodstream. But for a small number of patients, Rift Valley fever doesn’t stay mild. It turns dark.

Weeks after recovery, some develop confusion, seizures, or even coma as the virus invades the brain—an inflammation called encephalitis. Others lose their sight as lesions scar the retinas, sometimes months after infection. And in the rarest, deadliest cases, the virus brings on hemorrhagic fever: the liver dissolves into necrosis, clotting factors collapse, and the patient begins to bleed internally. Death can come within days.

So what determines who lives and who dies?

Ikegami and Makino’s 2011 review in Viruses traces that question straight to the virus’s genetic core. Of all its molecular weapons, none is more dangerous than NSs, the same stealth protein mentioned earlier. This single protein cripples the host’s defenses—shutting down the interferon response by hijacking the cell’s transcription machinery, silencing key antiviral genes, and even degrading PKR, a protein that would normally halt viral protein synthesis. Without interferon, the virus replicates unchecked, flooding the bloodstream and overwhelming the liver.

Mutant viruses that lack this NSs gene—like the experimental “Clone 13” strain—can’t pull off this sabotage. They trigger immune responses early, lose their lethal edge, and have even become the basis for promising vaccine candidates. One such candidate, Clone 13, along with MP-12, represents a newer generation of vaccines that appear much safer—particularly for pregnant animals—than older options like the live-attenuated Smithburn strain. Smithburn has been used in Africa for decades, but it carries real risks, including fetal malformations and miscarriages if given during pregnancy. Despite their promise, newer vaccines like Clone 13 and MP-12 haven’t yet been widely deployed, due to production limitations, regulatory hurdles, and challenges in reaching remote pastoral communities before outbreaks begin.

Another viral protein, NSm, serves a quieter but insidious purpose: preventing infected cells from dying too soon. By blocking apoptosis, NSm keeps the virus’s factories alive just long enough to maximize viral yield before the immune system catches on.

When the Body Fights Back

But the host matters too. The same virus that devastates one species might barely affect another. In the lab, mice and hamsters die quickly from massive liver necrosis, while gerbils develop mostly encephalitis. Rhesus macaques—the closest model to human disease—sometimes develop hemorrhag` ic fever nearly identical to that seen in humans, but only about one in five do. The rest survive, suggesting that genetics, immune signaling, and perhaps sheer luck all play a role.

The innate immune system—especially type I interferons—is the main line of defense. If that alarm is delayed or muted, Rift Valley fever has time to spread. Too much inflammation, on the other hand—too much IL-6, too little control—and the immune response itself can turn damaging. It’s a fragile balance: too little, and the virus wins; too much, and the host burns.

And though most people recover, some mysteries remain. We now know that Rift Valley fever virus (RVFV) can cross the blood–brain barrier not by rupturing it outright, but by directly infecting endothelial cells, quietly slipping into the nervous system. Evidence also shows that vision loss in later stages may result from direct infection of the retina, optic nerve, or uveal tissue—rather than solely from brain involvement. Yet questions persist: why do only some patients relapse or develop delayed neurological or ocular complications, sometimes weeks after apparent recovery? And what triggers the episodes of thrombosis or clotting that occasionally follow in convalescence? Progress is being made—human models of the blood–brain and blood-retina barriers have advanced our understanding—but the full picture remains elusive.

What’s clear is this: Rift Valley fever isn’t just another mosquito-borne disease. It’s a master of immune evasion, a virus that can go silent or savage depending on the host it meets—and that combination makes it one of the most unpredictable and dangerous of all emerging pathogens.

In Senegal, about 11 percent of confirmed patients had hemorrhagic symptoms, and 20 of those patients died.

Because Rift Valley fever straddles the line between animal and human health, the response has to do the same. Both countries have deployed rapid response teams that bring together doctors, veterinarians, and entomologists in what’s known as a One Health approach. They’re tracing animal movements, testing herds, monitoring mosquito populations, and treating patients, all at once.

ONE HEALTH: The Outbreak No One Saw

(low, steady music — maybe a hum of insects or dry wind under the narration)

Between 2016 and 2018, a team of Tanzanian and international researchers went looking for Rift Valley fever virus in two very different landscapes: the high, dry grasslands of the Ruaha ecosystem, and the low, flood-prone plains of Kilombero. They took a One Health approach — tracking not just people, but their animals, and even the mosquitoes around them.

What they found was unsettling. In people coming to rural clinics with fevers, about eight percent showed antibodies to Rift Valley fever virus — proof they’d been exposed. A few even tested positive for the virus itself. Most thought they just had malaria.

In livestock, nearly one in ten animals carried signs of infection — cows, goats, and sheep, many without any symptoms at all. And in the mosquitoes hovering over those herds? The virus was there too — not just in the classic floodwater Aedes we blame after big rains, but in Culex and Anopheles species feeding quietly around fields and water bodies, season after season.

No one called it an outbreak. But in every sense, it was one — a slow, steady pulse of infection linking humans, animals, and vectors in an invisible chain.

For years, the textbook story has been simple: long quiet periods, then explosive epidemics after heavy rains trigger hatching of infected Aedes mosquitoes. But newer data — including a 2025 Lancet Planetary Health consensus paper — argues that this picture is too simple. Instead of “outbreak versus no outbreak,” Rift Valley fever operates on a spectrum.

On one end are places like Mauritania and Senegal this year: epidemic systems, where specific conditions line up to produce dramatic, visible outbreaks. On the other end are hyperendemic systems, like parts of Tanzania and South Africa, where the virus is circulating almost all the time at lower levels — building up immunity in herds, slipping into human populations — without triggering the kind of die-offs that make headlines.

And here’s the One Health twist: in this newer framework, there is no single secret reservoir animal hiding the virus between storms. The reservoir is the system itself — a maintenance community made up of livestock, wildlife, and diverse mosquito species, shaped by climate, land use, animal movement, and human behavior. Humans are the targets at the edge of that web. When we change grazing patterns, move animals through trade, expand irrigation, or crowd livestock against growing towns, we’re nudging whole regions along that spectrum from quiet circulation toward explosive epidemics, or seeding new hotspots without ever seeing a “start” signal.

(short beat)

Which means if we only look for mass miscarriages in sheep or hemorrhagic human cases, we miss most of the story. In hyperendemic areas, Rift Valley fever can be doing real damage — to livelihoods, to pregnancies, to vision, to health systems — while never being labeled an outbreak at all.

Outbreaks also often trigger livestock trade restrictions that can devastate rural economies dependent on animal sales. Even a few confirmed animal cases can close borders, stall markets, and leave herders with no way to sell or move their animals—especially in pastoral regions where livestock are the backbone of income and food security.

And that mild, low level circulation I mentioned is also a problem for how we detect it. Because if the virus is always moving through this shared human–animal–mosquito environment, then waiting for the spectacular disasters means we’re already too late.

Which brings us to diagnostics — and the challenge of recognizing a virus that hides in plain sight.

DIAGNOSTICS

Rift Valley fever is a tricky one to diagnose. The early symptoms—fever, headache, muscle aches—look just like dozens of other tropical infections. Clinically, there’s no way to tell it apart. So diagnosis depends entirely on lab testing.

In the acute phase, molecular tests like RT-PCR are the gold standard—they can detect viral RNA in blood samples, but only for a few days after symptoms start, because viremia fades fast. Researchers have also developed faster, simpler options like isothermal assays—LAMP and RPA tests that could, in theory, work in the field—but these still need real-world validation before they’re ready for frontline use.

Beyond that short PCR window, serology takes over. IgM and IgG ELISAs are the mainstays for identifying recent or past infection, and newer competitive ELISAs can even screen multiple animal species at once—crucial for livestock surveillance. The virus neutralization test remains the most specific, but it’s labor-intensive and requires high-containment labs.

In practice, the best approach is combined testing—RT-PCR early on, then antibody tests later—to catch both active and recovering cases.

There are also major gaps in diagnostics: most endemic regions still lack BSL-3 lab capacity, there’s no harmonized European diagnostic manual yet, and few commercial human serology kits have been validated. Developing rapid, multiplex, point-of-care tools—the kind that could be used in a rural clinic or a veterinary field lab—remains a top global priority.

In short: when Rift Valley fever strikes, timing is everything—and strong diagnostic systems are the frontline defense that keeps a local outbreak from becoming an international crisis.

THE GLOBAL RESPONSE

Containing Rift Valley fever requires cooperation across sectors. The World Health Organization is coordinating the international response with the Food and Agriculture Organization and the World Organisation for Animal Health. Together they’re training clinicians, veterinary workers, and community leaders to recognize symptoms early. They’re also expanding diagnostic capacity at the district level to reduce the time between infection and confirmation. Supplies of protective equipment, lab reagents, and mosquito control materials are being distributed to affected areas. Public education campaigns are underway to reach those most at risk—herders, butchers, and families who rely on fresh milk or livestock for income.

The advice for the public is straightforward but not easy to practice: avoid contact with animal blood or raw milk, cook all meat thoroughly, wear gloves when handling sick or dead animals, and protect yourself from mosquito bites. These precautions are critical because there’s no human vaccine yet. Livestock vaccination can help prevent outbreaks, but it’s only effective when used before the virus starts circulating—and that window has long since closed for 2025.

For now, WHO considers the outbreak’s public health risk high at the national level, moderate at the regional level, and low globally. The risk to animal health follows the same pattern. The worry is that infected livestock might move across borders, carrying the virus into Mali or deeper into West Africa. Rift Valley fever doesn’t travel easily between people, but animals and mosquitoes don’t respect boundaries.

LESSONS FROM THE VALLEY

At its core, this outbreak is a lesson in ecology. When floods follow droughts, mosquitoes bloom, livestock cluster near standing water, and viruses find their opportunity. The disease is named for Kenya’s Rift Valley, where it was first discovered in the 1930s, but the landscape it represents is global—one where human, animal, and environmental health are inseparable.

For listeners wondering whether this could become the next pandemic, the answer is no. Rift Valley fever doesn’t spread between humans, and it’s not airborne. But that doesn’t make it insignificant. Outbreaks like this are reminders that the line between a local crisis and a global one is often measured in attention, not distance. Each time an endemic virus reemerges, it tests whether the world has learned to see the warning signs early enough to act.

As the rains subside in Mauritania and Senegal, health authorities hope the outbreak will fade. But RVF will be back—it always returns with the next rainy season, carried by mosquitoes and the cycles of climate. The challenge isn’t just to respond, but to anticipate.

Thanks for being here! Come back next week for a conversation in honor of World Antimicrobial Awareness week where I'll explain antimicrobial resistance and why it's a problem. Until next week, stay healthy, stay informed, and spread knowledge not diseases.