F Rosa Rubicondior: Malevolent Design News - Toxoplasmosis Triumph

Friday 17 July 2020

Malevolent Design News - Toxoplasmosis Triumph

Tachyzoites of Toxoplasma gondii
Credit: Bobbi Pritt, M.D.
Source: PathologyOutlines.com
Toxoplasma at the wheel: Study reveals how a dangerous parasite controls its host cell to spread around the body | Indian University News.

Another example of the length the intelligent [sic] designer is prepared to go to to make people sick (if you believe in the intelligent design hoax).

First, a little bit about Toxoplasma gondii. According to the CDC:

Causal Agent:

Toxoplasma gondii is a protozoan parasite that infects most species of warm-blooded animals, including humans, and causes the disease toxoplasmosis.

Life Cycle


[numbers relate to the image above]
The only known definitive hosts for Toxoplasma gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces[1]. Although oocysts are usually only shed for 1-3 weeks, large numbers may be shed. Oocysts take 1-5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water or plant material contaminated with oocysts[2] . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites[3]. Cats become infected after consuming intermediate hosts harboring tissue cysts[4]. Cats may also become infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment[5]. Humans can become infected by any of several routes:
  • Eating undercooked meat of animals harboring tissue cysts[6].
  • Consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat)[7].
  • Blood transfusion or organ transplantation[8].
  • Transplacentally from mother to fetus[9].
In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens[10]. Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR[11].

People who believe in ID believe this parasite was designed by an intelligent deity who, being omniscient, knew precisely what it was designing, what it would do and why.

Now researchers from Indiana University's Department of Pharmacology and Toxicology have discovered the ingenious way Toxoplasma gondii, which infects up to one third of the human population, gains control of its host's cells.

Christina Griffiths, communications coordinator for Indiana University explains:

“The parasite essentially hijacks these cells, using them as vehicles to get to various organ systems, including the brain,” said Leonardo Augusto, PhD, a postdoctoral fellow in the Department of Pharmacology and Toxicology and lead author on the National Institutes of Health-funded study, which was recently published in mBio. “It’s like the parasite is taking the wheel of its host cell and using it to spread around the body.”

[...]

Toxoplasma gondii infects up to one-third of the world’s population. People typically become infected with it through exposure to cat feces, which is where it goes through its reproductive phases, or consumption of contaminated food and water. The parasite causes life-threatening issues in some patients because of its ability to disseminate to the brain. In the brain and other tissues, the parasite persists as a latent cyst, waiting to reactivate if immunity should wane, such as what happens in HIV/AIDS patients.

“One of the key problems in battling an infection like Toxoplasma is controlling its spread to other parts of the body,” Augusto said. “Upon ingestion of the parasite, it makes its way into immune cells and causes them to move—a behavior called hypermigratory activity. How these parasites cause their infected cells to start migrating is largely unknown.”


This image shows two different Toxoplasma host cells changing their shape to migrate.

The team’s new research is shedding light on this important clinical question, discovering that the parasite trips an alarm system in its host cell that leads to the activation of a protein called IRE1. IRE1 helps the cell cope with stress, which can involve getting it to move to a different location. In cells infected with Toxoplasma, IRE1 connects to the cytoskeleton, a network of structural proteins that gives the cell its shape and coordinates movement. By engaging this network through IRE1, Toxoplasma takes the wheel and causes hypermigration.

“When we infected host cells that were depleted of IRE1, they could no longer move,” Augusto said. “These cells were greatly impaired at disseminating Toxoplasma to the brains of infected mice.”

The results of the research were published open access a few days ago in mBiol

ABSTRACT

Toxoplasma gondii is an intracellular parasite that reconfigures its host cell to promote pathogenesis. One consequence of Toxoplasma parasitism is increased migratory activity of host cells, which facilitates dissemination. Here, we show that Toxoplasma triggers the unfolded protein response (UPR) in host cells through calcium release from the endoplasmic reticulum (ER). We further identify a novel role for the host ER stress sensor protein IRE1 in Toxoplasma pathogenesis. Upon infection, Toxoplasma activates IRE1, engaging its noncanonical role in actin remodeling through the binding of filamin A. By inducing cytoskeletal remodeling via IRE1 oligomerization in host cells, Toxoplasma enhances host cell migration in vitro and dissemination of the parasite to host organs in vivo. Our study has identified novel mechanisms used by Toxoplasma to induce dissemination of infected cells, providing new insights into strategies for treatment of toxoplasmosis.

IMPORTANCE

Cells that are infected with the parasite Toxoplasma gondii exhibit heightened migratory activity, which facilitates dissemination of the infection throughout the body. In this report, we identify a new mechanism used by Toxoplasma to hijack its host cell and increase its mobility. We further show that the ability of Toxoplasma to increase host cell migration involves not the enzymatic activity of IRE1 but rather IRE1 engagement with actin cytoskeletal remodeling. Depletion of IRE1 from infected host cells reduces their migration in vitro and significantly hinders dissemination of Toxoplasma in vivo. Our findings reveal a new mechanism underlying host-pathogen interactions, demonstrating how host cells are co-opted to spread a persistent infection around the body.


So, if you believe in the intelligent [sic] design hoax and believe the Discovery Institute's insistence that ID is a real alternative science which gives a better explanation than the TOE for the diversity of life on earth, you have to be able to explain the appearance of malevolent intent in these sorts of mechanism 'intended' to make the parasite more successful and so make the host sicker and for it to infect more hosts.

From a design perspective, you have to be able to demonstrate a clear purpose for Toxoplasma gondii, other than to make its host sick and explain the intelligence behind creating humans with an immune system to prevent infection with parasitic organisms which were designed for the purpose of parasitism, then designing the parasites to overcome the solution to the problem the immune system was designed for.

You also need to be able to explain the prolific waste involved in making millions of copies of this parasite inside the host just to ensure a few get passed to the next victim and how this approach fits into either intelligence or the principles of good design. But we're not discussing the incompetence of this designer here, but its malevolence.

And you have to explain why evolution is the only explanation for organisms such as Toxoplasma gondii that doesn't leave any designer looking like a malevolent psychopath that hates its creation.

Of course, if you have no regard for the truth or for the morality of your supposed designer, you can continue to believe that this example of stupid design is evidence for intelligence and that the designer who can design these nasty examples of malevolent intent is a benevolent source of morals and a role model for your unfortunate children.

And you can continue to refute the Discovery Institute's lie that ID is genuine science and not Christian fundamentalist Bible literalism disguised in a grubby lab-coat with the intention of deceiving US legislators into allowing fundamentalists to teach Bronze Age superstition at taxpayers expense as a prelude to installing a fundamentalist Taliban-style Christian theocracy in the USA, despite the constitutional prohibition on established religion in government.







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