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Leucochloridium cascadia

Leucochloridium cascadia is identical to other parasitic flatworms from the Leucochloridium genus, with members of that genus using snails as their primary and intermediate host, and birds acting as its paratenic host. The most defining trait of the L. cascadia species, however, is that it uses human hosts in the place of snails.

The Leucochloridium flatworms typically utilize aggressive mimicry in the host snail to encourage consumption by insectivorous birds. This is done through the worms sexually maturing inside the snail's eyestalks as swollen broodsacs, giving the appearance of an insect larva such as a caterpillar.

However, because of the absence of tentacular appendages in humans, L. cascadia instead induces abnormal bone growth that emerges from the skin. L. cascadia achieves this by hijacking the host's osteoblasts to form a calcified growth akin to that of bone tumors. It then forms crude blood vessels near the surface. The host's blood can then circulate around the growth at will, giving the pulsating appearance similar to that of snail's broodsacs.

L. cascadia instances begin their life cycle as miracidia, which mature into sporocysts inside the host's blood vessels. The sporocysts asexually produce cercariae, which then directly develop into metacercariae within the sporocyst itself. It is these metacercariae that will reproduce and lay eggs, with the sporocysts acting as the facilitator of their growth.

Such metacercariae then accumulate inside the "bone broodsac" of a host. Upon ingestion by a bird, the metacercariae pass along its alimentary tract and latch themselves onto the bird's cloaca. The metacercariae then fully mature into adult distomes in the cloaca, and are hermaphroditic in nature. Adult distomes then spread themselves by releasing their eggs into the bird's feces.

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• Stage 0 (point of transmission): Upon inhalation of fecal matter from a host bird, L. cascadia eggs utilize their thick mucoid coating to adhere to the throat of a human host. After approximately 3 hours, the internal temperature of the human throat disintegrates the mucoid shell, allowing the eggs to travel further down to the trachea.
  
  
• Stage 1, 1-3 days after transmission: Eggs hatch as miracidia inside the host's trachea, with the host's inhaling motion further pulling the miracidia deep into the lungs. The maturing miracidia may cause irritation in the alveoli, which can cause coughing. The miracidia then use the circulatory system to distribute itself to the entire body of the host. Upon the third day of the infection, The miracidia then matures into sporocysts inside the capillary vessels, near the epidermis. The sporocysts can range in size from approximately 1-1.5mm in diameter. This can cause blockage of blood flow, and ultimately rupture several capillaries, causing bruises in the affected areas.
  
  
• Stage 2, 3-7 days after transmission: Sporocysts begins to release enzymes that hijack the host's osteoblasts, inducing an artificial bone growth similar to that of a bone tumor. If necessary, the sporocysts can also hijack the host's osteoclasts to facilitate growth. The osteoclasts take material from sources near the affected areas, which causes severe degradation of bone structure, and may induce osteoporosis. However, this is only done if there are no other sources of minerals, as in the case where a host is not receiving proper nutritional needs. On the seventh day of the infection, the abnormal bone growth begins to puncture the skin, which may cause bacterial infection.
  
  
• Stage 3, 7-9 days after transmission: Sporocysts forms capillary vessels near the surface of the growths, rapidly transporting blood around and giving it a pulsating appearance. Meanwhile, L. cascadia sporocysts that have latched onto the liver release enzymes that decrease insulin production levels. This increases blood sugar levels and causes the host to secrete glucose-laden blood around open wounds which encourages consumption by birds through its sweet aroma.
  
  
• Stage 4, 9-12 days after transmission: Leftover miracidia travels to the host's brain, latching onto its frontal and occipital lobes. Upon maturity into sporocysts, they stimulates the amygdala and cerebellum whenever it detects ocular stimuli, causing a spike in dopamine production which causes the infected to seek open spaces and bright lights. Sporocysts at this stage has also been observed to propagate in the host's eyes, causing red pulsating broodsacs.
  
  
• Stage 5, 12-15 days after transmission: Sporocysts gains total control of the host's limbic system; hosts loses all voluntary motor functions and instead acts entirely on the stimulation by the sporocysts. L. cascadia also eliminates the function of the brain non-essential to regulating movement, which severely degrades the host's cognitive function. This is considered a last-ditch effort, as a total loss of brain control means loss of the host's perseverance instinct which risks death for both the host and the sporocysts themself. One case of a host surviving 45 days after the point of infection was observed to have severe degradation of the brain, with L. cascadia sporocysts making up 40% of the host's brain volume.

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The origin of L. cascadia remains unclear, with the most widely accepted theory stating that it might have recently evolved from the parasites that infected the snails. This theory is further reinforced as the phylogenetics of L. cascadia distomes indicate that it might have evolved somewhere in Europe in the past 200 years.

However, the Leucochloridium genus of which L. cascadia is a member of, and observations of other species of the same genus (such as L. paradoxum), were seen thriving in the local snail population with no danger of extinction. This contradicts the established wisdom that a species only evolves if met with certain life-threatening situations, such as if the snail population were to rapidly decline.

In addition, DNA sequencing found a DNA strand commonly found in bacteria species, most notably from the Porphyromonas genus. A specific species from the genus, the P. gingivalis, was linked to diseases that exhibit symptoms similar to that of L. cascadia bone growth-inducing trait. This suggests that L. cascadia may be a product of an artificially engineered bioweapon as opposed to a natural form of evolution.