# Fictional parasites very different from our own

*Note: this is a fictional story. Heavily inspired by SSC’s similar posts on* [*fictional legal systems*](https://slatestarcodex.com/2020/03/30/legal-systems-very-different-from-ours-because-i-just-made-them-up/) *and* [*fictional banned drugs*](https://slatestarcodex.com/2013/10/25/list-of-fictional-drugs-banned-by-the-fda/)*.*

![](https://substackcdn.com/image/fetch/w_1456,c_limit,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F913b2f39-3c76-4fc8-84bd-bdd7c139b056_2040x1144.webp)

Neuroplana temporalis
=====================

Neuroplana temporalis is a flatworm that resides in the cerebrospinal fluid of mammals with a diurnal rhythm. It has a particular affinity for the regions surrounding the [suprachiasmatic nucleus](https://en.wikipedia.org/wiki/Suprachiasmatic_nucleus) — the brain's central pacemaker. From this location, N. temporalis secretes a cocktail of peptides that interact with the host's circadian rhythm regulation.

These peptides modulate the expression of clock genes — [Per1](https://en.wikipedia.org/wiki/Period_circadian_protein_homolog_1), [Per2](https://en.wikipedia.org/wiki/PER2), and [Per3](https://en.wikipedia.org/wiki/PER3) — effectively altering the host's internal perception of time.

Specifically, the primary symptom of N. temporalis infection is a gradual shift in circadian rhythm, overriding typical [zeitgebers](https://en.wikipedia.org/wiki/Zeitgeber) that modulate the host’s internal clock. Infected individuals typically experience extending their perceived day to 27-30 hours, creating a constant misalignment with the Earth's 24-hour cycle. This leads to chronic jet-lag-like symptoms, including sleep disturbances, metabolic irregularities, and cognitive impairments.

Through this disruption of its host’s circadian rhythm, the parasite creates a chronic state of immune fatigue. Infected individuals become increasingly susceptible to opportunistic infections, especially those caused by normally benign microorganisms present in the environment. Common ailments such as upper respiratory infections, skin conditions, and gastrointestinal disturbances become more frequent and severe.

N. temporalis feeds on [cerebrospinal fluid microbes](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8269202/), which thrive due to host immune suppression. Its lifecycle alternates between active feeding periods, where it disrupts the host's circadian rhythm, and dormant phases when the host normalizes. As its food depletes, the parasite reactivates, again releasing peptides to alter the host's rhythm and boost microbial growth, renewing its food source.

This cycle of feeding, dormancy, and reactivation continues indefinitely, creating a long-term pattern of alternating disrupted and normal circadian rhythms in the host. Due to its difficulty of diagnosis and impact on mental health, human hosts often display anxiety, anhedonia, and suicidal ideation.

Given the appearance of the parasite in infants as young as two months, N. temporalis is believed to originate as a parasite within the mother, which ends up infecting a developing embryo. However, it is likely that this infection is unintentional, as N. temporalis is both rare and dies with its host. It is unknown what the original parasite or what its effect on the mother is.

Pulmo extremophilus
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Pulmo extremophilus is a bacterium that primarily inhabits the lungs of humans, with a particular affinity for alveolar spaces. P. extremophilus interacts with the host's respiratory system through a biochemical mechanism that influences gas exchange, respiratory drive, and, in the latest stages, behaviors.

Upon infection, the parasite first secretes a cocktail of compounds that modulate alveolar function and [central chemoreceptor](https://en.wikipedia.org/wiki/Central_chemoreceptors) sensitivity. These secretions include a surfactant-mimicking protein that alters [alveolar surface tension](https://www.ncbi.nlm.nih.gov/books/NBK539825/), alongside a peptide that alters [central chemoreceptor sensitivity to blood gas levels.](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802370/)

The primary effect of P. extremophilus infection is a gradual reduction in alveolar gas exchange efficiency due its impact on alveoli. Infected individuals typically experience a [7% decrease in oxygen uptake,](https://www.verywellhealth.com/oxygen-saturation-914796) creating a chronic state of mild hypoxia. And, as a result of the chemoreceptor alteration, the hypoxia goes largely unnoticed by the host. This eventually causes [natural adaptations amongst red blood cell populations](https://www.nature.com/articles/s41580-020-0227-y), leading to a greater ability to withstand said hypoxia.

Within a few months after initial infection, P. extremophilus further releases a cocktail of chemical compounds that interact with the hosts central nervous system. It is uncharacterized exactly what the neurophysiological impact of these compounds are — likely [NMDA receptor antagonism](https://www.nature.com/articles/npp2015180) — but, following its release, late-stage infected hosts have been observed to frequently engage in a wide variety of high-risk athletic behavior. Amongst the most prevalent ones are free solo climbing, wingsuit flying, and high-altitude climbs.

The initial athletic aptitude afforded to them by the hypoxia adaptations frequently leads to early success in athletic endeavors, reinforcing the host's drive to pursue extreme sports and exploration. In time, the host inevitably suffers a fatal injury for reasons of risks inherent to the sport itself.

Once the parasite senses dangerously low blood oxygen levels, it will release respiratory irritants, causing the host to violently cough, coating their mouth with expelled bacteria. Upon host death, the parasite enters a state of hibernation, only releasing spores when its host body is disturbed. P. extremophilus primary route of infection is oral, so passersby or medical teams who disturb the corpse are typically the next to be infected.

Opticomyces occultans
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Opticomyces occultans is a fungus that colonizes the optic nerve of humans living in rural areas with high amounts of nearby wildlife. The parasite induces blindness to hyper-specific visual stimuli.

Upon initial infection on the outer surface of the optic nerve, typically via nasal spores, the fungus secretes acidic substances to slowly cut its way through the nerve. Over the course of a year, the fungus replaces a segment of the optic nerve with itself. During this period, the host will experience intermittent bouts of mild eye pain and visual noise, but rarely anything more severe.

Once established within the optic nerve, O. occultans acts as a highly selective filter for visual information. The fungus allows most visual signals to pass through unaltered but is also capable of detecting specific distributions of light via stacked [photosensitive proteins](http://photosensitive/). If these sets of proteins are sufficiently activated — typically through [conformational changes](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6697613/) — they will cause downstream signal cascades, rapid alternating the input light signal before re-transmitting it along the optic nerve. This modification process occurs in less than 200 milliseconds, [which is faster than the average human visual reaction time](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4456887/). As a result, the host remains mostly unaware of any manipulation of their visual input.

O. occultans imperfectly alters visual stimuli, but consistently causes infected hosts to misperceive images of large carnivores, often interpreting them as blurs. In areas with high human infection rates, O. occultans spores have been found in the feces of lions, bears, and leopards. This suggests these predators may serve as secondary hosts in the parasite's life cycle. Researchers hypothesize that O. occultans visual alterations in humans aim to increase the likelihood of predation.

Endocrinus empathetica
======================

Endocrinus empathetica is a [protozoon](https://en.wikipedia.org/wiki/Protozoa) which primarily resides in the human gut, feeds on ingested food, and impacts social behavior and emotional processing. It is typically found only in third-world nations with inaccessible medical systems and a lack of sanitization practices.

After several months of infection, the parasite secretes large amounts of oxytocin and vasopressin — hormones crucial for social bonding, trust, and empathetic behaviors. Simultaneously, E. empathetica produces a compound that acts as an antagonist to [glucocorticoid receptors](https://en.wikipedia.org/wiki/Glucocorticoid_receptor), effectively lowering the host's fear response.

The combined effect of increased prosocial hormones and decreased stress response leads to notable behavioral changes in infected individuals. Symptomatically, they typically display increased empathy, improved emotional resilience, and a tendency towards more cooperative behaviors. Amongst the infected, researchers have observed shifts in social structures, with them often assuming leadership or mediator roles within their communities.

In time, the constant release of the aforementioned chemicals eventually leads to host endocrine burnout and depression. Given their status, the host typically receives constant palliative care from rotating members of the community. E. empathetica route of transmission is [fecal-oral](https://en.wikipedia.org/wiki/Fecal%E2%80%93oral_route), and untrained caretakers of the host will frequently accidentally infect themselves while handling the parasite-containing excrement of the host.