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The Lilakeuma causes Lilac Blood Disease, whose symptoms are akin to leukemia and malaria. Like tetanus, which is both a benign soil bacterium and a severe disease, Lilakeumas can live harmlessly in oceanic silt. However, they are only a minor component of the silt, as they have grown more adapted for life as a disease and occur in much greater numbers within a host.

Hosts typically get Lilakeuma disease when silt containing Lilakeumas gets into bleeding wounds, such as through stirring up silt in a territorial scuffle or when fighting a predator.


The Lilakeuma accumulates within the organ that generates blood cells within Sternobrachians. Lilakeumas "breathe" using the manganese inside the blood cells, and hollow out the cell for the hydrogen compounds it needs. It also gains energy from trace amounts of hydrogen or hydrogen compounds within the blood. As the blood cells do transmit oxygen, it has a higher tolerance for oxygen than its ancestor, and can survive high oxygen levels for about half an hour. Still, its oxygen tolerance is still fairly low, so it normally cannot survive in the higher-oxygen depths of the sunlit zones.

It is very genetically distinct from its relatives, the Tummlix and Mangalix, with big physiological differences. For example, it sports a new kind of “frizz” (extension of its cell membrane it uses to move) that’s thinner; this generally occurs on the tail.

Mutated from that are hairlike structures on its main body, which typically number from five to seven. These somewhat pilli-like structures allow it to pick up genetic code from within its environment. Most extra genes it’s picked up have no clear function, or relate to oxygen tolerance. All these extra genes have lengthened its already big genetic code, resulting in loops that look like “3” or “8” rather than its ancestors’ shapes.

Disease Progression

As Lilakeumas are unable to get past the filtration system in hosts' digestive systems, nor get past their respiratory filters, it can only infect the body through injuries (even a deep enough scratch) that let it infiltrate the host body through its circulatory system. (Although it can grab and hollow out a free-floating blood cell, its weak enzymes make this impractical.) It slithers around arteries until it gets to the blood organ, where it slowly dissolves a hole in a developing cell. It then creeps inside the tiny hole with its amoeba-like body.

Lilakeuma disease, in its late stages, covers the blood-producing organ in a lilac slime. Like leukemia and malaria, symptoms include fatigue and pallor. Weakened blood cell production makes travelling to the lower-oxygen twilight zone risky, which may interrupt daily migration patterns in hosts. Since its hosts lack any defense systems within the blood itself, if left untreated Lilakeuma disease kills its host within one or two weeks.

Lilakeuma disease is not especially contagious: it only spreads if open wounds are in contact with other hosts’ infected areas (wounds in freshly infected hosts or heavily infected blood organs). The most efficient transmission method is a scavenging host devouring the infected blood-producing organ of a dead host while the new host has open wounds in or around its mouth. It can also spread if cannibalistic or territorial hosts nip at the freshly-infected wounds or blood organ of another host, although the chances are lower.

When hosts die, Lilakeumas finish off the blood cells of the organs and blood system, or even rotting muscle tissue, and temporarily become even more abundant as they feed on the hydrogen compounds of decay. (e.g., methane) When the corpse is no longer habitable, they return to the silt.


Lilakeumas, due to their low oxygen tolerance and helplessness against microbe-eaters, don’t survive for long as they float through water. The sunlight zone of the tropics is especially lethal, killing them off within half an hour due to higher oxygen levels, filter-feeder biodiversity, and UV light. (Oddly, at time of evolution no Pathogen-eating Detritis are major predators, since they specialize in Protopathogenan parasites/pathogens.)

Vellicators and insidiators fare better than most Geletaventrians. Due to their habit of nibbling Shevs, they accumulate small levels of toxic heavy metals from the Shevs' shells. In such trace amounts, the heavy metals poison Lilakeumas much more than their hosts, and in sufficient amounts, cure the infection entirely. Since Lilakeumas can only enter hosts' bodies through wounds, it's less likely to infect hosts with tougher skin, quicker-healing skin, or thick skin mucus.