Massospora Cicadina: The Zombie Cicada Fungus

Massospora cicadina is a fungal pathogen that consumes a periodical cicada from the inside out, replaces its reproductive organs with a mass of fungal spores, and then manipulates the dying insect’s behavior so it continues to fly around and spread those spores to others. The comparison to zombie fiction is not much of a stretch: infected cicadas walk, sing, and attempt to mate while missing roughly a third of their body, seemingly unaware that their abdomen has been converted into a chalk-white plug of infectious material. What makes Massospora especially strange among parasites is not just the grotesque physical takeover but the chemical and behavioral toolbox the fungus deploys to keep its host useful long after it should be dead.

How Infection Begins

Massospora cicadina’s life cycle is locked to the life cycle of periodical cicadas, the Magicicada species that spend either 13 or 17 years underground as nymphs before emerging en masse to breed. The fungus persists in the soil as thick-walled resting spores, waiting for nymphs to tunnel upward. When cicadas finally dig their way to the surface, they pass through soil laden with these spores, and the spores germinate on contact with the insect’s exoskeleton, penetrating the body wall. Within days, the fungus begins growing through the cicada’s internal tissues.

One of the more surprising findings about these resting spores is that they do not need to wait the full 13 or 17 years between emergences to remain viable. Resting spores collected from a 17-year cicada species in Iowa proved infectious to a 13-year species in Arkansas after only about 10 months of dormancy, raising infection rates in the Arkansas population to roughly 10 percent in treated plots.¹ That means the spores can sit in the ground for a single year or more than a decade and still do their job. This flexibility likely helps the fungus survive in areas where brood emergences are unpredictable or where different broods overlap geographically.

A Body Hollowed Out

Once inside the cicada, Massospora cicadina grows aggressively. The fungus appears in multiple forms as it proliferates, including branching filaments and specialized spore-producing structures. Over the course of several days, it devours and replaces the posterior portion of the abdominal cavity. Histological examination of infected periodical cicadas found that in every specimen studied, the fungal mass had completely displaced the reproductive organs, parts of the digestive tract, fat stores, and even sections of the body wall itself.² What remains of the rear end of the cicada is essentially a chalky, crumbling plug of spores where organs used to be.

The infected cicada, remarkably, keeps moving. It flies, lands on branches, and interacts with other cicadas as though nothing is wrong. Researchers sometimes describe these insects as “flying saltshakers of death” because every movement shakes loose a dusting of spores onto whatever surface the cicada touches. The rear segments of the abdomen slough off, exposing the spore mass directly, and the cicada appears to feel no pain or alarm. This is where Massospora starts looking less like a typical infection and more like a hostile takeover.

Two Stages, Two Strategies

Massospora cicadina uses two distinct stages of spore production, and the difference between them explains a lot about how the fungus spreads. Stage I infections produce conidia, which are actively infective spores designed to spread from one living adult cicada to another through direct contact. Stage II infections produce resting spores, the thick-walled variety that drop to the soil and wait for future generations of nymphs. The two stages are not just different forms of the same spore but represent different transmission strategies, and they trigger different behaviors in the host.

Stage I infected males do something extraordinary: they mimic the wing-flick signals of sexually receptive females. In periodical cicadas, males sing to attract females, and receptive females respond with a precisely timed flick of their wings. Stage I infected males perform this same timed wing-flick when they hear male calls, tricking healthy males into approaching and attempting to mate with them. Every close encounter means more spore transfer.³ In playback experiments spanning multiple years, Stage I infected males consistently responded to recordings of male songs with these female-typical wing-flicks, while no healthy male and no Stage II infected male ever did the same.

Stage II infections, by contrast, do not induce this mimicry behavior. Their job is different: the resting spores need to reach the soil, not another adult cicada. An infected cicada shedding resting spores simply drops them as it moves, depositing future infections into the ground where nymph cicadas will eventually encounter them. The behavioral manipulation is unnecessary for this pathway, and it does not occur.

Psychoactive Compounds Inside the Fungus

In 2018, researchers analyzing the chemical contents of Massospora spore plugs discovered something nobody expected: the fungal tissue contained psychoactive compounds. Massospora cicadina, the species that infects periodical cicadas, produces cathinone, an amphetamine that also occurs naturally in the khat plant. A related species that infects annual cicadas produces psilocybin, the active compound in psychedelic mushrooms.⁴ The cathinone in Massospora cicadina was confirmed through fragmentation analysis against a commercial analytical standard, and it was absent from healthy cicada controls and from the related annual-cicada pathogen.

This discovery raised obvious questions: are the drugs responsible for the zombie-like behavior? The researchers who found these compounds were careful to note that while cathinone might help explain the infected cicadas’ apparent endurance and continued activity despite massive tissue loss, the amphetamine alone does not easily account for the display of female courtship behaviors by males.⁴ An amphetamine could plausibly keep a dying insect active and responsive, but getting a male to perform a specific, precisely timed wing-flick pattern of the opposite sex requires something more targeted. The full mechanism behind the behavioral hijack remains an open question.

The presence of psilocybin in a related Massospora species adds another layer of strangeness. Psilocybin was previously known only from mushrooms in the order Agaricales. Massospora belongs to an entirely different branch of the fungal tree. Whether the fungus independently evolved the ability to produce psilocybin, or acquired the genes through some form of horizontal transfer, is still debated.⁵

Not Just One Fungus

When people say “the zombie cicada fungus,” they usually mean Massospora cicadina specifically, but Massospora is a genus with more than a dozen described species, all of them obligate pathogens of cicadas found across the world.⁶ “Obligate” is the key word here: these fungi cannot survive on any other food source. They can only grow and reproduce inside a living cicada. That extreme specialization has made them almost impossible to grow in the lab, which in turn has made genetic and biochemical study difficult.

Phylogenetic analysis of the genus identified four well-supported lineages within Massospora, suggesting that different species have been evolving alongside different cicada hosts for a very long time.⁶ The relationship is sexually transmitted in a sense that would surprise most people thinking about fungal infections: the primary route of spread among adults is through mating attempts, making it functionally an STI of the insect world. This mode of transmission appears to be shared across the genus, not just in M. cicadina.

Crossing Between Species and Broods

One question that has interested entomologists is whether Massospora cicadina is locked into a single cicada species or can jump between the different Magicicada species. The answer is that it can cross species boundaries with apparent ease. In field experiments, resting spores collected from Magicicada septendecim, a 17-year species, successfully infected Magicicada tredecassini, a 13-year species from a completely different geographic region.¹ This cross-species and cross-brood infectivity means the fungus is not limited to tracking a single host lineage. If different broods emerge in overlapping areas on different schedules, the fungus can potentially use any available periodical cicada as a host.

This flexibility has implications for understanding how the fungus persists over evolutionary time. Periodical cicada emergences are rare and irregular from the perspective of any given patch of soil. A fungus locked to a single species in a single location would need its resting spores to remain viable for exactly 13 or 17 years. The ability to infect whichever Magicicada species comes along, and to germinate after variable dormancy periods, gives Massospora a much wider window of opportunity.

How Much Damage Does It Actually Do

Given the visceral horror of the infection, you might assume Massospora cicadina devastates cicada populations. The reality is more modest. A study of Brood XIX, a 13-year periodical cicada emergence, examined multiple sources of mortality including bird predation, environmental exposure, aging, and fungal infection. The researchers found that fungal infection was not a major source of mortality in the population.⁷

This makes sense when you consider the cicadas’ broader survival strategy. Periodical cicadas rely on predator satiation: they emerge in such staggering numbers that predators (birds, mammals, and even fungi) simply cannot eat or infect them all. The sheer volume of billions of individuals means that even a well-adapted parasite like Massospora can only reach a fraction of the population during any given emergence. Infection rates in natural populations tend to stay in the single digits or low double digits, enough to sustain the fungus across generations but nowhere near enough to threaten the survival of the brood.

This dynamic also means Massospora cicadina is not a viable candidate for biocontrol or pest management. People occasionally ask whether the fungus could be used to reduce cicada populations in areas where emergences cause nuisance damage to young trees. But the infection rates are too low, the fungus is too specialized, and the cicadas’ numbers are too large for this to be practical. The fungus and the cicada have been locked in a long evolutionary arms race, and the cicada’s mass-emergence strategy keeps the fungus in check as effectively as the fungus manipulates individual hosts.

How Zombie-Making Fungi Work More Broadly

Massospora is one member of a broader club of fungi that manipulate insect behavior to aid their own spread. The most famous example is Ophiocordyceps, the “zombie ant fungus” that compels carpenter ants to climb to elevated positions and clamp their jaws onto vegetation before dying, creating ideal conditions for the fungus to release spores from above. Massospora and Ophiocordyceps belong to different fungal orders, but researchers have noted striking parallels in the behavioral outcomes they produce: both fungi induce abnormal activity in dying hosts that positions the insect for maximum spore dispersal.⁸

The mechanisms appear to involve a combination of physical disruption, hijacking of the host’s own chemical signaling pathways, and secreted molecules produced by the fungus itself. Researchers have proposed that convergent evolution accounts for the many similarities in zombie-like behavior across different fungus-insect systems, meaning these parasites arrived at similar solutions to the same problem (how to move spores from host to host) through independent evolutionary paths rather than shared ancestry.⁸ Massospora’s approach is distinct in one important respect: while Ophiocordyceps kills its host and then grows out of the corpse, Massospora keeps its host alive and moving for as long as possible. The cicada’s active flight and social behavior are the dispersal mechanism, so a dead cicada is a useless one.

Why Massospora Remains Hard to Study

Despite its fascinating biology, Massospora cicadina is one of the more frustrating organisms for researchers to work with. Because it is an obligate pathogen of periodical cicadas, it cannot be cultured on any artificial growth medium. You cannot grow it in a petri dish, and you cannot maintain a colony in the lab. Studying it requires access to living, infected cicadas, which means waiting for a brood emergence that may happen only once every 13 or 17 years in a given location. Researchers who work on Massospora plan their field seasons years in advance, coordinating with brood emergence maps to make sure they are in the right place at the right time.

The inability to culture the fungus also limits what can be done with its biochemistry. The discovery of cathinone and psilocybin in spore plugs was made possible by mass spectrometry and metabolomics techniques that can detect compounds in very small samples, but follow-up experiments that would require large quantities of purified fungal tissue are difficult to perform. Nobody can simply grow more Massospora to run additional assays. Each infected cicada provides a tiny amount of material, and there is no way to produce more outside of a natural emergence event.

This constraint is partly why some basic questions remain unanswered. The precise mechanism by which the fungus induces female wing-flick behavior in males is still unknown. Whether the cathinone and psilocybin play a direct role in behavioral manipulation or serve some other function, like suppressing the cicada’s immune response or altering its perception of pain, is speculative. The genetic toolkit the fungus uses to produce these compounds is only beginning to be characterized, and connecting specific genes to specific behavioral outcomes in a host that cannot be experimentally infected in controlled settings is a slow process. For the foreseeable future, Massospora cicadina will remain a parasite understood mostly through field observation during rare windows when its hosts happen to be available.