Post by roadvirus91 on Nov 3, 2016 4:21:43 GMT
Hey monarchs, today I'd like to talk about something that scares the shit out of me, and fascinates me, too. I don't think enough people even know that this brain parasite even exists -- or how much damage it could do (or be doing) to our civilization. I'll start with the basics, before I get into the really scary shit in the posts that will follow. I'll probably get 2 or 3 good posts in tonight, and try to do the same tomorrow.
I'm no scientist, but I've done my research, and you'll see my sources as numbers in brackets, with bibliography below.
Toxoplasma gondii (T gondii or TG for short) is a protozoan and an obligate intracellular parasite. A protozoan is a single-celled microbe that differs from bacteria or fungi; the best-known protozoan would likely be amoebas. However, Toxoplasma gondii belongs to the Apicomplexans, which are a large group (phyla) of parasitic protozoa containing such well-respected members as Cryptosporidium and Malaria (1). TG is an obligate parasite because it has no choice but to use its host organism to reproduce, and it's intracellular (rather than inter) because it gathers its nutrients from outside host cells. It has been linked most strongly to rodents and cats as the intermediate hosts before we get the privelege of taking the title of definitive (or final) host. However, it has repeatedly shown incredible adaptivity to new hosts and environments.The most commonly accepted life cycle (2) for T Gondii is a straightforward pathway from rodents to cats to humans.
First, unsporulated TG oocytes (free-living "eggs" that resemble bacterium, sometimes called sporozoites) are injected by rats or mice. Rodents instinctively fear the scent of cat urine, however TG is able to influence the rodent's thought patterns so the smell of cat urine produces a response similar to sexual arousal (3). This makes them easy prey for cats, who distribute oocytes in their feces. Cat's rarely suffer any symptoms or apparent neurological changes, but they can suffer and die from toxoplasmosis just like us.
As the definitive host, a human will then come into contact with the now-sporulated oocytes. Upon entering the preferred host (usually through ingestion), they rapidly mature to tachyzoites (also called endozoites), and begin rapidly moving towards the central nervous sytem -- usually headed for the brain. In this form, a tachyzoite can rapidly enter a cell, gut it, then cover itself with a membrane composed of parts of itself and it's victim. This renders it invisible, giving it time to reproduce until the membrane explodes and the process continues. At some point, the tachyzoite transforms into the slower bradyzoite, which forms cysts. These cysts can form anywhere at any time and place great stress upon the immune system. Conversion between any three forms can happen at any time -- an unusual trait and one that speaks to the adaptability of this organism.
It is generally believed all currently existing strains of TG descended from a single lineage approximately 10 000 years ago, and was first recognized in 1908 (4). The general hypothesis is that we became a normal carrier for this organism around the time agriculture overtook hunting/gathering as our major form of sustenance. Or, more specifically, when domesticated meat became our primary protein source -- domestication likely placed us at a much higher risk of acquiring the parasite. There are some arguments that the feline - human transfer may have already existed beforehand... but that we were more likely to be eaten by said cat, making the feline the definitive host.
It has been hypothesized that the continuing survival of Toxoplasma requires the continued existence of cats, because felines are the only hosts observed in which sexual reproduction was able to occur (5). This is based on the rationale that sexual reproduction is essential to the continued genetic diversity of a species. However, T gondii can reproduce asexually, and often does in ecosystems where a feline host is not readily available (6). Amazingly, the genetic diversity of these "wild-type" T gondii strains have shown HIGHER genetic diversity, which is a result of this species' ability to ALTER IT'S OWN DNA AND RNA with snippets gleaned from host cells -- and even from "novel sources." (7) (8)
Usually, one acquires TG from consuming undercooked contaminated meat, or by coming into close contact with oocytes (eggs) deposited from the fecal matter of felines. Other disease vectors include secondary contact with items that may be contaminated with oocytes or tachyzoites (unwashed fruits and vegetables, water, cutlery, etc.). At least some strains of TG are excellent and crossing the placental barrier in pregnant females and infecting unborn child (congenital or prenatal toxoplasmosis). (9) Additionally, there is some evidence TG can be sexually transmitted -- as seen in experiments using sheep and dogs (10) (11).
Those at risk to are generally stated to be those with compromised immune systems, or the young or elderly. It's estimated 10-20% of afflicted will acquire symptoms such as fatigue, aching muscles, a fever, body pains, and sore muscles. These wonderfully vague flu-like symptoms, if they go unchecked, can lead to major cyst formations, brain damage, blindness, and death.(12)
Another major risk factor is unborn children, who will generally be born asymptomatic, and gradually, throughout their lives, begin suffering symptoms such as eye lesions, deformed spines and skulls, and severe mental retardation. (13).
The majority of the time, a healthy adult who has contracted Toxoplasmosis will have what is commonly known as latent, or asymptomatic TG. However, there has been emerging evidence that latent toxicoplasmosis can have impacts on our brains, psychological disorders, and cultural development. As late as 2006 (a century after the disease was discovered) "much is still unknown about host reactions to its chronic presence." (14)
But, ultimately, the most frightening aspect of Toxoplasma gondii's increasing presence in the world, is our lack of knowledge. This disease is often -- a level of successful spread that has never been documented before. In warm countries with dense populations and contaminated drinking water (3 of T gondii's favorite things), we see seroprevalence (infection rates as determined by blood samples) as high as 98% (15). It is often estimated between a third and half of the world population (between 2 to 3 billion people) are carrying some form of the disease (16).
And yet very few people seem to even know this disease exists! The information that interests people is the sensational or the odd -- such as the inundation of blogs and newspapers fr,m 2015-2016 feeling the need to tell us our cats are zombies, or we're zombies. And, although we sit having mapped this organism's genome over 10 years ago, it continues to hold nothing but surprises for us.
I'm no scientist, but I've done my research, and you'll see my sources as numbers in brackets, with bibliography below.
Toxoplasma gondii (T gondii or TG for short) is a protozoan and an obligate intracellular parasite. A protozoan is a single-celled microbe that differs from bacteria or fungi; the best-known protozoan would likely be amoebas. However, Toxoplasma gondii belongs to the Apicomplexans, which are a large group (phyla) of parasitic protozoa containing such well-respected members as Cryptosporidium and Malaria (1). TG is an obligate parasite because it has no choice but to use its host organism to reproduce, and it's intracellular (rather than inter) because it gathers its nutrients from outside host cells. It has been linked most strongly to rodents and cats as the intermediate hosts before we get the privelege of taking the title of definitive (or final) host. However, it has repeatedly shown incredible adaptivity to new hosts and environments.The most commonly accepted life cycle (2) for T Gondii is a straightforward pathway from rodents to cats to humans.
First, unsporulated TG oocytes (free-living "eggs" that resemble bacterium, sometimes called sporozoites) are injected by rats or mice. Rodents instinctively fear the scent of cat urine, however TG is able to influence the rodent's thought patterns so the smell of cat urine produces a response similar to sexual arousal (3). This makes them easy prey for cats, who distribute oocytes in their feces. Cat's rarely suffer any symptoms or apparent neurological changes, but they can suffer and die from toxoplasmosis just like us.
As the definitive host, a human will then come into contact with the now-sporulated oocytes. Upon entering the preferred host (usually through ingestion), they rapidly mature to tachyzoites (also called endozoites), and begin rapidly moving towards the central nervous sytem -- usually headed for the brain. In this form, a tachyzoite can rapidly enter a cell, gut it, then cover itself with a membrane composed of parts of itself and it's victim. This renders it invisible, giving it time to reproduce until the membrane explodes and the process continues. At some point, the tachyzoite transforms into the slower bradyzoite, which forms cysts. These cysts can form anywhere at any time and place great stress upon the immune system. Conversion between any three forms can happen at any time -- an unusual trait and one that speaks to the adaptability of this organism.
It is generally believed all currently existing strains of TG descended from a single lineage approximately 10 000 years ago, and was first recognized in 1908 (4). The general hypothesis is that we became a normal carrier for this organism around the time agriculture overtook hunting/gathering as our major form of sustenance. Or, more specifically, when domesticated meat became our primary protein source -- domestication likely placed us at a much higher risk of acquiring the parasite. There are some arguments that the feline - human transfer may have already existed beforehand... but that we were more likely to be eaten by said cat, making the feline the definitive host.
It has been hypothesized that the continuing survival of Toxoplasma requires the continued existence of cats, because felines are the only hosts observed in which sexual reproduction was able to occur (5). This is based on the rationale that sexual reproduction is essential to the continued genetic diversity of a species. However, T gondii can reproduce asexually, and often does in ecosystems where a feline host is not readily available (6). Amazingly, the genetic diversity of these "wild-type" T gondii strains have shown HIGHER genetic diversity, which is a result of this species' ability to ALTER IT'S OWN DNA AND RNA with snippets gleaned from host cells -- and even from "novel sources." (7) (8)
Usually, one acquires TG from consuming undercooked contaminated meat, or by coming into close contact with oocytes (eggs) deposited from the fecal matter of felines. Other disease vectors include secondary contact with items that may be contaminated with oocytes or tachyzoites (unwashed fruits and vegetables, water, cutlery, etc.). At least some strains of TG are excellent and crossing the placental barrier in pregnant females and infecting unborn child (congenital or prenatal toxoplasmosis). (9) Additionally, there is some evidence TG can be sexually transmitted -- as seen in experiments using sheep and dogs (10) (11).
Those at risk to are generally stated to be those with compromised immune systems, or the young or elderly. It's estimated 10-20% of afflicted will acquire symptoms such as fatigue, aching muscles, a fever, body pains, and sore muscles. These wonderfully vague flu-like symptoms, if they go unchecked, can lead to major cyst formations, brain damage, blindness, and death.(12)
Another major risk factor is unborn children, who will generally be born asymptomatic, and gradually, throughout their lives, begin suffering symptoms such as eye lesions, deformed spines and skulls, and severe mental retardation. (13).
The majority of the time, a healthy adult who has contracted Toxoplasmosis will have what is commonly known as latent, or asymptomatic TG. However, there has been emerging evidence that latent toxicoplasmosis can have impacts on our brains, psychological disorders, and cultural development. As late as 2006 (a century after the disease was discovered) "much is still unknown about host reactions to its chronic presence." (14)
But, ultimately, the most frightening aspect of Toxoplasma gondii's increasing presence in the world, is our lack of knowledge. This disease is often -- a level of successful spread that has never been documented before. In warm countries with dense populations and contaminated drinking water (3 of T gondii's favorite things), we see seroprevalence (infection rates as determined by blood samples) as high as 98% (15). It is often estimated between a third and half of the world population (between 2 to 3 billion people) are carrying some form of the disease (16).
And yet very few people seem to even know this disease exists! The information that interests people is the sensational or the odd -- such as the inundation of blogs and newspapers fr,m 2015-2016 feeling the need to tell us our cats are zombies, or we're zombies. And, although we sit having mapped this organism's genome over 10 years ago, it continues to hold nothing but surprises for us.
