#brain parasites

[powerupcomicstonight]

[tenebris-the-shadow]

What even IS the name for the kink where it’s just entirely for the idea of brainsharing with an alien parasite

‘monsterfucking’ feels too generic. I’m thirsting after the lack of privacy. The violation. The intimacy of it. The potential experience of this entirely alien creature poking and prodding and examining things that are so deeply a core part of a person’s … personhood. The cosmic feeling that they’re doing it from this perspective that, as a human, the only hope you have to sort of make sense of it is to think of it like, he wishes to make you his Wife, but he’s also feeding on you, and he’s also playing with you like a toy. He’s social, and receptive, but in ways you can’t hope to fully understand, even when he’s tongue and balls deep in your brain licking and poking at things he doesn’t really understand but finds fascinating and seeks to learn in an alien way so that he can ‘couple’ to his Wife better. The fact that his Wife’s brain is reading his intrusion as pleasurable, erotic? Well, that’s just a sign to him that he’s found the perfect host, and only serves to make him lick deeper, longer, examining the feelings, the feedback of pleasure so foreign and never before experienced during a … ‘coupling’, when he’s gotten so used to only having unwilling Wives

[kastlestud]

Poor RFK Jr.

He has an actual mind virus, can’t be easy for the poor guy to think too much.

That being said, this mind virus afflicted individual isn’t very good at pretending to be intelligent. In fact every time this thing wearing RFK Jr.’s skin speaks it manages to appear even stupider.

Poor dude.

PS; backhanded insults/malicious pity is an effective way of ticking people like him off. They like to appear strong. Yet they always fail. Reiterate this fact over and over again; demolish their self esteem.

[aita-blorbos]

AITA for my girlfriend a musical singing parasite?

I (31M) was pining after this cute barista (31F) for a long time. I would visit the coffee shop she worked at everyday despite there being a starbucks just across the road.

For context, and, Well, to make a very long story short, a meteor crashed on our small town and infected a bunch of us with a musical parasite. The barista, let’s call her E for simplicity, and I eventually were the last ones alive. I confessed to her, she coughed blood onto me, all that. I went to try and stop the parasite when I was infected too.

We both made it out of our town without her knowing I was infected, so I did what anyone of the hive would do, and spit alien goo into her mouth, infecting her too. Many people seem to think I’m an asshole here but I just did what the hive would have wanted! But now I’m starting to reconsider.

Thanks in advance and may the apotheosis be upon ye!

AITA?

YTA

NTA

JAH

NAH

ESH

INFO

Voting ended onNov 6, 2023

[fuckyeahmedicalstuff]

Brain Parasites: part II.

Taenia solium:

The pork tapeworm, Taenia solium, is the most harmful tapeworm in humans. Taenia solium infection is acquired either from human feces that contains Taenia solium eggs or from uncooked pork which contains larval cysts. If larvae are ingested, they mature into adults in the small intestine. This infection type is called taeniasis and is often asymptomatic. If eggs are ingested, the resulting disease is cysticercosis. It gets its name from larval Taenia solium called cysticercus. Both diseases are common in Africa, Asia, South America and Southern Europe. Taeniasis is rare in Muslim countries since people there do not consume pork.

Taenia solium, as its Latin name suggests, uses pigs as intermediate hosts for its larval stage. A pig gets infected with cysticercosis. If a human eats pork without cooking it, the dormant larva excysts in the bowel. The larva matures into an adult tapeworm which absorbs nutrients from the passing food.

The flat body of an adult Taenia solium consists mostly of segments, proglottids. Pork tapeworm is attached to the intestinal wall of the pig with its head, the scolex. Its head has four suckers and two rows of hooks. It has a neck that produces the segments which grow bigger as they move towards the rectum. They absorb nutrients from the surrounding food. Each segment produces eggs that remain inside it until the segment is passed out in the feces. The segment is less than 1 cm long and 2 cm wide and contains up to 50000 eggs. Taenia solium grows up to 7 meters. A full grown pork tapeworm consists of 1000 segments and sheds six gravid proglottids per day. The segments are detached from the tail.   Sometimes, the cycle gets interrupted. Someone contaminates food with tapeworm eggs bound for a pig's stomach. The tapeworm eggs hatch, but instead of developing into an adult tapeworm in the intestines, they burrow into the bloodstream as would normally occur in a pig. In a human, they often end up in the brain, forming cysts that cause a disease called neurocysticercosis. It can cause seizures, headaches and can lead to death.

Toxoplasma gondii

The single-celled organism Toxoplasma gondii, which can only reproduce in the conditions provided by feline guts, is a master manipulator. When it infects a rat, its makes its host abnormally unafraid of cat urine, upping the rodent's chances of getting eaten by a cat and returning the parasite to its favorite locale. Sadly for humans, humans can also be infected by the sneaky t. gondii. In the U.S., one in four adults has been infected with t. gondii, but only a small number become ill enough to notice, according to Science News. Toxoplasmosis is caused by infection with the protozoan Toxoplasma gondii, an obligate intracellular parasite. The infection produces a wide range of clinical syndromes in humans, land and sea mammals, and various bird species. T gondii has been recovered from locations throughout the world, except Antarctica There are 3 major genotypes (type I, type II, and type III) of T gondii. These genotypes differ in their pathogenicity and prevalence in people. In Europe and the United States, type II genotype is responsible for most cases of congenital toxoplasmosis. T gondii infects a large proportion of the world's population (perhaps one third) but uncommonly causes clinically significant disease.However, certain individuals are at high risk for severe or life-threatening toxoplasmosis. Individuals at risk for toxoplasmosis include fetuses, newborns, and immunologically impaired patients. Congenital toxoplasmosis is usually a subclinical infection. Among immunodeficient individuals, toxoplasmosis most often occurs in those with defects of T-cell–mediated immunity, such as those with hematologic malignancies, bone marrow and solid organ transplants, or acquired immunodeficiency syndrome (AIDS).In most immunocompetent individuals, primary or chronic (latent) T gondii infection is asymptomatic. A small percentage of these patients eventually develop retinochoroiditis, lymphadenitis, or, rarely, myocarditis and polymyositis.  Although latent infection with Toxoplasma gondii is among the most prevalent of human infections, it has been generally assumed that, except for congenital transmission, it is asymptomatic. The demonstration that latent Toxoplasma infections can alter behavior in rodents has led to a reconsideration of this assumption. When infected human adults were compared with uninfected adults on personality questionnaires or on a panel of behavioral tests, several differences were found. Other studies have demonstrated reduced psychomotor performance in affected individuals. Possible mechanisms by which T. gondii may affect human behavior include its effect on dopamine and on testosterone. There's some concern that the parasite slows reaction times and puts people at double the risk of traffic accidents, and a study in JAMA Psychiatry found links between t. gondii and women's risk of self-harm, such as self-mutilation.  Human African Trypanosomiasis 

Two distinct forms of trypanosomiasis exist: Trypanosoma cruzi is responsible for American trypanosomiasis (or Chagas disease), while Trypanosoma brucei subspecies gambiense and rhodesiense cause African trypanosomiasis. CNS infection by Trypanosoma cruziis rare, though more cases have been observed recently due to rising co-infections of HIV in Latin America. On the other hand, CNS infection by Trypanosoma brucei subspecies is far more common, with symptoms that have led many to refer to African trypanosomiasis as “sleeping sickness.” It is very difficult for parasites to become established in the CNS, and so trypanosomiasis hemoflagellates have developed a variety of techniques to invade and persist in the face of the human body’s robust immune response. Upon entry into the bloodstream or mucous membranes by the bite of the Tsetse fly vector, the trypanosomes immediately begin to replicate and invade local tissue. Still non-cerebral, trypanosomes survive the host’s adaptive immune response by cycling expression of a variant surface glycoprotein (VSG), expressing only one at any given time. Host antibodies initially cannot penetrate the shielding created by the VSG, but soon an IgM response specific to the VSG being expressed is launched that successfully destroys most of the trypanosomes in the blood. However, some survive by shedding this coat and subsequently expressing a different VSG than that targeted by the IgM response, and therefore are able to proliferate quickly and cause another wave of parasitemia. Because over 1,000 antigenically distinct VSG genes exist within the trypanosomes, waves of parasitemia can persist for long durations. Trypanosomes also express a surface protein similar to one found in Leishmania, which may protect it from being lysed by complement proteins. Furthermore, infection suppresses normal B cell and T cell immune response, as well as secondary antibody responses other than that of IgM. Trypanosomes are thought to suppress the immune response by triggering prostaglandin E2 and E12 release, lowering cytokine production and perhaps altering sleep patterns (a characteristic symptom of sleeping-sickness). This immunosuppression is why secondary opportunistic infections often occur in patients with trypanosomiasis. While many trypanosomes continue these cycles in the blood, some may successfully infiltrate the CNS.  The mechanism of CNS invasion is not fully understood, but it is hypothesized that trypanosomes penetrate through either the blood-brain barrier or the blood-cerebrospinal fluid barrier. When trypanosomes cause local inflammation at such a barrier, a variety of cytokines, eicosanoids, and neutrophils arrive to mediate the inflammation. Mononuclear cells soon migrate to the site, as well as serum proteins to be transferred to the cerebrospinal fluid. The arrival of this immune response increases permeability of the barrier by a variety of mechanisms. Endothelial cells become more permeable when exposed to cytokines TNF-a, IL-1 and IL-6. Intercellular adhesion molecules ICAM-1 and ICAM-2 within barrier cells that normally assist leukocyte migration also are up-regulated by exposure to IFN-g and IL-1. Furthermore, many of these cytokines induce the expression of inducible nitric oxide synthase, with nitric oxide further enhancing local permeability.  The precise route of penetration is unknown, but independent studies suggest four possibilities. Preferential localization around brain parenchyma protected by the blood-cerebrospinal fluid barrier rather than the blood-brain barrier suggests it may be easier to penetrate the former than the latter. It is possible that trypanosomes enter through the choroids plexus epithelium and into the cerebrospinal fluid, in which it can travel to and infect brain parenchyma. Alternatively, it may pass through brain capillaries and then into cerebrospinal fluid and brain parenchyma. It once was thought that destruction of tight junctions at the blood-brain barrier was necessary for CNS infection, but recent evidence suggests that infection can occur without altering tight junctions. It therefore is believed that trypanosomes may travel alongside or even inside leukocytes, through the aforementioned up-regulation of intercellular adhesion molecules. Once inside the CNS, trypanosomes take advantage of the limited local immune response for their own proliferation and protection.  Late-stage sleeping sickness can have many associated neuropathologies, including “perivascular cuffing, nonspecific lymphoplasmacytic meningoencephalitis, microglial hyperplasia, reactive astrocytes, and infrequent demyelination”. Despite the immunosuppression often found in those infected, hosts often continue to mount an immune response, with MHC class I and MHC class II, B and T cells, and macrophages all being found in inflamed tissue. Animal model studies suggest that many of the symptoms of trypanosomiasis are caused by this pathology and immune response in specific areas of the brain, particularly regions where the blood-brain barrier is relatively weak.   Cerebral Malaria 

Cerebral malaria is an encephalopathy associated with infection by Plasmodium falciparum, and is most often characterized by unarousable coma and high risk of death if left untreated. Only P. falciparum is currently thought to cause cerebral malarial; though rare cases of unarousable coma have been associated with infections of P. malariae and P. vivax, it is suspected that co-infection by P. falciparum was present.Survival in the Liver and BloodOnce a host is inoculated by the bite of a mosquito vector, the injected sporozoites enter the exo-erythrocytic cycle and then the erythrocytic cycle. To avoid the resulting immune response, the parasites use variant surface glycoproteins to shield themselves from host antibodies. Upon each reproductive cycle a new VSG is expressed, preventing the specific response from properly targeting and eliminating the parasites. An important feature of P. falciparum is its cytoadherence characteristic, resulting in the sequestration of mostly parasitized erythrocytes in tissues, particularly in small blood vessels throughout the body. This packing of erythrocytes does not necessarily alter total blood flow, but is associated with local hypoxia. In some vessels this can result in engorgement, hemorrhaging, deformation, and occlusion. The mechanical sequestration of erythrocytes in cerebral capillaries was once thought to be the primary cause of cerebral malaria, but more recent studies have suggested an alternative mechanism involving the host inflammatory response. Alteration of the Inflammatory Response.  Tumor necrosis factor (TNF) is now thought to play a central role in the mechanism of cerebral malaria due to its association with malarial fever and cerebral malaria. It is now believed that schizonts bind to endothelial cells and subsequently rupture. This rupturing and the accompanying release of toxins are thought to be responsible for malarial paroxysm. However, the released toxins also up-regulate TNF production in leukocytes, which stimulates increased expression of intercellular adhesion molecule-1 (ICAM-1) and possibly the cytoadherence receptor E-selectin. Additional parasitized cells can subsequently adhere to endothelium more readily, obstructing small vessels and causing pathology through a purely mechanical mechanism. However, it is now thought that the cytokines produced during a malarial infection (particularly IFN-g and TNF) and possibly toxins released during schizont rupture stimulate macrophages to release high amounts of nitric oxide. Nitric oxide could subsequently pass through the blood-brain barrier and act as a powerful inhibitor of neurotransmitter activity, anesthetizing the patient to the point of unarousable coma. This mechanism is still not fully understood, but may explain why recovery from such comas is so swift and complete.

[powerupcomicstonight]

[aita-blorbos]

AITA for attempting to repay a kindness?

Now, for some well-needed context, I, (erm, I have stopped counting, but I find myself well into adulthood, though my roguish charm does tend to shine through, M), am an author! I am known far and wide for my many manuals and manuscripts of the world I've traveled. And other worlds I've traveled!

Now, in a life such as mine, one ends up picking up certain skills. I'm a bit of a jack of all trades, you see, and I thought I would try my hand at a bit of diplomacy in my attempts to gather details for my latest manuscript.

Rather embarrassingly, however, things went a bit TOO well, and I found myself in the rather unenviable role of a pet pigeon in the very same camp I had attempted to learn from.

Nevertheless, I made a daring escape, assisted slightly by a witness to an attack on a sanctuary I was writing on. They so graciously invited me to join THEIR camp, which I gladly accepted. When I was there, they told me of an affliction I had heard of- although theirs was quite different than the typical cases. After painstaking research, I believed I had the opportunity to assist my new compatriot in ridding themselves of their parasite.

A steady hand and a good bit of misplaced self-confidence does the trick, I always say!

That said, my procedure did involve... an ice pick, a rather unsalvageable eyeball, and a failure to remove the offending parasite. I gave them a shiny new prosthetic eye, free of cost, and I am sure, if they survive this ordeal, a wonderful story for parties.

That said, am I the asshole for repaying my rescuer with an improvisational medical procedure, which I may have slightly fumbled?

AITA?

YTA

NTA

JAH

NAH

ESH

INFO

Voting ended onMar 13, 2024

[aita-blorbos]

AITA for leaving a threat to my friends stranded on an island?

Ok, I know it sounds bad, but my friends and I aren't in the business of taking risks, especially with the whole "threat to planet Earth" kind of thing. So, my friends (15M, 14M, 15M(?), 15F, and 14(Bird)) and I (15F) met this new kid, let's call him D. He actually came across the device we used to gain a special ability, the ability to morph any creature whos DNA he acquired. He was weird, that's for sure, but so were all of us. We had been stretched pretty thin due to the aforementioned threat to Earth in the form of parasitic space slugs, but that isn't relevant at the moment. We come to the conclusion to invite him to our group under the vow of absolute secrecy.

That played out about as well as you would imagine. Soon enough he became absolutely mad, sociopathic even, and went as far as trying to betray and murder my friends.

To keep it short, we had to turn to drastic measures. You see, I work with my parents taking care of different animals for wildlife rehab, and I know the lay of the land pretty well. There was an island pretty close by that was nothing but rats and garbage, so we hatched a plot to uh, leave him there. In the form of a rat. Have I mentioned me and my friends are able to become animals? Not for an unlimited amount of time, though. After two hours? You're stuck, a human mind in an animal body.

Anyway, so that's what we did. We trapped an insane boy in the body of a rat for trying to betray and murder us. I'll admit, I'm kind of the guilty conscience of the group, which I guess is why I'm sending this in the first place.

So, am I the asshole?

AITA?

YTA

NTA

JAH

NAH

ESH

INFO

Voting ended onSep 19, 2023