Quorum sensing and "hive" behavior in microbes.

I am writing based on my own experience with this. I know there is a whole science that is based on pleomorphism, but I have been seeing something, I think is unique.
I have covered quite a bit of ground with my own parasite, and have "almost" established, that it belongs to the family of apicomplexia. This is based on stages I have extrapolated by isolation, growth and observation [DNA analysis pending].

I recently observed blood sample of 'subject' who has multiple symptoms including neurological and digestive issues.
Upon first observation of blood on slide [week-old, but sealed] there was evidence of "spore" like objects in the [1-2 micrometer range dark field] sample.
The neutrophils were releasing granules, [granule proteins abundant] and I think there MAY have been NK cells present. I did not see macrophages, other than the neutro-leukocytes. The leukocytes were loaded up with these spores. It is obvious from this, that an immunotolerance has been established to a certain point. The housekeeping cells, however, are in full force trying to control extracellular infiltration of these spores. There were a few bacteria present, but I could not be sure of contamination.

The 'subject' is chronically affected, but still maintains relative health.
This person had western blot for Lyme disease, and was positive for a few bands, which I reviewed, and decided was not enough for solid positive. It did show many elements of bacterial antigens.
I would have like to seen results for protozoan antigens--------and this is where I am going.
I cultivated the blood in saline solution, at body temp. This activated the spores, which turned out to be small short-rod bacteria. They created aggregates or "clusters" which had a very interesting pattern, shown by spectral rings in dark field. Many were independent, and there was an increase of very small proteins. This could have been host proteins, but many more spores were developing.
As these clusters increased, I started to notice [after a few days] yeast-like cells growing in chains of 4. There were singlets, triplets, quins, and more, but the vast majority were quads.
These cells would eventually migrate together, and create a larger unit, something like the smaller bacterial looking things were doing.
This reminded me of the behavior I had observed with my oocysts! I therefore believe these are indeed oocysts. But the morphology is remarkably phenotypic of yeast cells.
The sample does not grow on plate nutrient with sugar, and microbes are temperature sensitive, going into dormancy outside 37 C.
I am speculating, there is a fungal quality to these microbes, as well as protozoan. The small microbes, look and behave like my own 'zoites.
I will be analyzing the spectral rings, and comparing them to my 'zoites with special equipment soon.
I think we have another example of these mystery apicomplexan-like parasites.
More tests are now being conducted, and I will post more on this later.

Proteasome and it's role in immunity

It is one direction scientists are taking to review some of the aspects of disease.
One very important mechanism of antigen presentation, is the digestion of said antigen, into small [8-10kDa] peptides which fit well within the Class 1 MHC receptor pocket.
Since everyone has different genes that code for MHC receptor, there is a significant polymorphism that exists here. This is how nature ensures greater diversity among same species, so odds of survival are increased in the face of danger from disease.
If one person cannot handle a solid presentation of antigen because of poor binding properties of antigen, another person may do this extremely well. This individual will have best chance at eliminating dangerous antigens [virus, intracellular disease etc].

The proteasome is a little molecular machine in all eukaryotic cells which digest proteins within the cell for recycling, antigen presentation, or elimination.

I have to make a personal comment on this process. Why can't we grow cells in culture, of people who have ability to digest certain antigens, isolate them, and serve them to a person who has poor ability to digest this particular antigen.
It would stand to reason, the individuals t-cells will pick-up these pre-digested antigens, and have far better chance of making a successful presentation.
Why could we not experiment with the proteasomes of certain frogs or other exotic life forms to evaluate the antigen digestion abilities of their proteasomes, and keep a data base of these records?

Potential for creating unique vaccinations seems promising using this direction.
That was just a personal observation, and maybe it's old news. I have not researched it very far, yet.

Can protozoa or apicomplexia shift to fungi forms?

This is something of interest to me. I have no evidence of it, except the fact that if it did happen, and if it only happened within specific host or primary host, it would be missed by observation. Because these microbes carry such complex gene-line variation, it can be hard to recognize mutations, and related phenotypes.
Plus, what about gene sharing? Some microbes are known for this, and some share plasmids which can offer extended genetic characteristics to the microbe.
I will be posting more on this later..........

Medical experiment

I am taking an immunological approach, strategically designed to prompt neurotransmitter shifts in the body, directed at disrupting mast cell stimulation.
This will be attempted by ingesting 120 mg of pseudoephedrine hydrochloride and 7200 mg of ascorbic acid at once before bed.
This is only a preparatory experiment to record physiologic affects.
Pathways of interest are those involve with alpha melanocyte hormone regulation, numerous cytokines and other regulators.
Chemical competition for mast cell receptors is a key goal in this experiment.

By disrupting the status of chronic stimulation of mast cells, I hope to damage the equilibrium, infecting {apicomplexia} parasites are creating with immune functions. I am assuming the parasite is deliberately sequestering the mast cells to control mediators governing other immune factors.
The protocol may not be effective, but observations could be useful.

This is March 15 2009
Day after the experimental drug\vitamin C cocktail;
My symptomolgy dropped by close to 80%! This was completely unexpected, but confirms the hypothesis that mast cells are the central area of concern. This places the disease in awkward direction.
It has been proven the parasitic 'zoites infect these cells in vitro, so elevation of activity with these cells is no surprise. The consequences of sustained amplitude in cell activity and differentiation, is physiologic toxicity. This is now an established fact based on solid scientific evidence.
The next hypothesis is; does the parasite deliberately create a system of survival by using the mast cells and\or other highly specific immune processes to it's advantage?

The fact these parasites cannot live among lactobacteria in vitro, and my digestive system is almost devoid of these types, suggest the mast cell activity kills these bacteria which could be advantageous to the parasite. The epithelial cells are very active producing cryptocidins as well, which might also play a part. It seems these molecules in high abundance, help growth of parasite in vitro. It also has antibiotic effect.
I have noticed high defensin activity in prostatic fluid, and cysts have been observe there [I have seen other unidentified objects of microbial interest there as well].

The next phase of this experiment, is to triple the dosages{per day}, add charcoal and chorophyll to the protocol, and dramatically increase probiotics, and yeast to diet.
I will do prostatic fluid exam in one week. Stool exams will be on going to observe changes in microbiota.
WARNING Do not attempt this experiment. There are dangers associated with cardiac functions in some people.

Date March 17\2009
The experiment has been successful in making a dynamic shift in my overall physiology, symptomology. The symptoms which have been undeviating for many months have shifted.
I think the ascorbic acid has interacted with the pseudoephedrine hydrochloride more than I had expected.
There has been changes in sleeping patterns, and big changes in digestion.
Mood changes are in good territory, indicating hormonal\neurotransmitter adjustment.
These are not subtle changes, and are related to the protocol. Further investigation of these chemical interactions must be elucidated.
Note: I have reduced the pseudoephedrine to 60 mg and ascorbic acid to 500 mg once a day. I have added bentonite and chlorophyll to the protocol as well.

March 18 2009'
The reduced dosage of pseudoephedrine hydrocholide, has allowed homeostasis functions of the body to become stable, and therefore effects of anti-inflammation to wear off. The ascorcic acid, also speeds the metabolic processes of the pseudoephedrine hydrochloride, through the body, and reduces affect.

The impact of infection was not affected, and symptoms are very quick to return.
Therefore, it would seem decreases in mediators from mast cells were either not strong enough to cause differential impact on parasitic factors, or parasite has no intimate reliance on mast cells specifically.
Antigen stimulation, at sub-levels of immune activation are what probably keep symptoms and parasitic infection in balance. ---end of study-----

Can parasites manipulate thoughts?

Parasite-induced modification of animal behavior, is one of the least understood phenomenon of parasite\host relationships.
There are plenty of clinical studies, many focusing on animals and insects in the natural environment.
There have been studies on domestic animals, and on humans. Plenty of scientific data exists on the subject, but it still remains a shadowy area of research especially where human behavior is concerned.

Toxoplasma gondii has been characterized as a parasite capable of inducing behavioral modifications of intermediate hosts. The exact mechanics of this process is still being evaluated.
Many larger parasites like worms, [which are animals] have rudimentary nervous systems, and therefore can secrete hormones, neurotransmitters, and many other biologically active soluble proteins. The potential for direct, or indirect physiological and psychological affects on the host are obvious. The wastes produced by these organisms further add to the complexity of this interconnectedness.

In many cases, host behavior modification by parasites have been seen as an adaptive response to benefit the parasite by increasing it's probability for successful transmission.
It would seem an evolutionary process is active within the host, for purposes of survival.
In order to reason with the mechanics involved in host manipulation, one must first examine the biological parameters confronting the parasite.

First, the energy spent on manipulation of host, will cause a deficit of energies spent on other functions such as growth.

A theory that governs parasitic manipulation effort on host behavior goes something like this:

1) typical same species population size decreases
2) prevalence increases
3) longevity of parasitism within host decreases
4) passive transmission decreases
5) potential reproductive capacity decreases

To access some of the some of the physiological responses associated with parasitism, clinical studies have focused on some of the following areas: neurology, endocrinology, neuromodulatory and immunomodulatory components and cognitive studies.

There are many intriguing examples in nature, that highlight the incredible evolutionary sparing between parasite\host dynamics which can determine and alter destinies of species populations.
These are important observations to consider, when evaluating the circumstances of human pathology.

In my next blog, I will focus on some clinical examples of host manipulation from a cross-section of human parasites.