Results for Lyme...

[dga5000]

Just received my results back.. It would seem I tested negative for all the classic lyme disease tests including the SPOT test. I have however tested positive for the following:

Midichloria mitochondrii - Positive
D-lactate 4.74 (0.0 - 1.6)

Has anyone else tested positive for these or know anything about them?

Many Thanks

 

[Ema]

The MM is a pathogen thought to be a part of the ixodes ricinus tick bite. This is a tick more commonly found in Europe and the testing may not be as sensitive as for the more common deer tick (ixodes scapularus).

If you are positive for the MM, I would say that Lyme cannot be ruled out because one without the other would be unlikely. This is why Lyme is still a clinical diagnosis that must be made by a doctor familiar with the limitations of testing and often peculiar presentations of the disease.

D-lactate is often high in ME/CFS and may reflect gut dysbiosis. There are several threads on the form that you can find by searching like this one:

http://forums.phoenixrising.me/inde...-the-same-symptoms-as-d-lactic-acidosis.8159/

 

[Daffodil]

please get the LTT ELISPOT for Borrelia. this is the definitive test for Lyme

 

[dga5000]

Hi Daffodil. I've had LTT ELISPOT for Borrelia and it came back negative. I've now had more than 20 tests for lyme over three rounds of testing, covering differing varieties each time - all negative. Which makes it strange that I've tested positive for Midichloria mitochonardrii.

 

[dga5000]

Any one else tested positive for Midichloria mitochondrii?

 

[dga5000]

The MM is a pathogen thought to be a part of the ixodes ricinus tick bite. This is a tick more commonly found in Europe and the testing may not be as sensitive as for the more common deer tick (ixodes scapularus).

If you are positive for the MM, I would say that Lyme cannot be ruled out because one without the other would be unlikely. This is why Lyme is still a clinical diagnosis that must be made by a doctor familiar with the limitations of testing and often peculiar presentations of the disease.

D-lactate is often high in ME/CFS and may reflect gut dysbiosis. There are several threads on the form that you can find by searching like this one:

http://forums.phoenixrising.me/inde...-the-same-symptoms-as-d-lactic-acidosis.8159/

Thanks so much Ema. Really useful.

 

[Daffodil]

Hi Daffodil. I've had LTT ELISPOT for Borrelia and it came back negative. I've now had more than 20 tests for lyme over three rounds of testing, covering differing varieties each time - all negative. Which makes it strange that I've tested positive for Midichloria mitochonardrii.

wow..negative on the LTT too? dang.

 

[Research 1st]

It increasingly appears the development of chronic disease ME in previously health people is not classical 'Lyme disease', (Borrelia Burgdoferi), caused by nature.

But something else.

 

[Research 1st]

Some research on Midichloria Mitochondrii in insects and humans I wanted to show you all:

An intracellular bacterium with the unique ability to enter mitochondria exists in the European vector of Lyme disease, the hard tick Ixodes ricinus.

'Candidatus M. mitochondrii' is the first bacterium to be identified that resides within animal mitochondria.

Source: Sassera et al, 2006.

Samples of the tick species Rhipicephalus bursa, found positive in the PCR screening, were analysed with transmission electron microscopy, which revealed the presence of bacteria both in the cytoplasm and in the mitochondria of the oocytes. There is thus evidence that bacteria invade mitochondria in at least 2 tick species.

Source: Epis et al, 2008.

‘Candidatus Midichloria mitochondrii’ is a commensural bacterium of invertebrates, already described in ticks. Previous studies showed that it is transmitted transovarially and is prevalent in the female tick. It presents the rare characteristic of being localised in mitochondria. It does not appear to be pathogenic for humans. Complementary investigations are under way in order to better characterize the taxonomic position of this new bed bug bacterium, and to investigate the potential transmission of this agent to humans.

Source: Richard et al, 2009.

We have sequenced the genome of Candidatus Midichloria mitochondrii, a novel and phylogenetically divergent member of the Rickettsiales. We found that it possesses unique gene sets found in no other Rickettsiales, including 26 genes associated with flagellar assembly, and a cbb3-type cytochrome oxidase. Phylogenomic analyses show that these genes were inherited in a vertical fashion from an ancestral a-proteobacterium, and indicate that the FMA possessed a flagellum, and could undergo oxidative phosphorylation under both aerobic and microoxic conditions. These results indicate that the FMA played a more active and potentially parasitic role in eukaryogenesis than currently appreciated and provide an explanation for how the symbiosis could have evolved under low levels of oxygen.

Source: Sassera et al, 2011.

We could then estimate that the seroprevalence for M. mitochondrii was 58.75% in subjects exposed to tick bite (47 out of 80), and 1.18% in the healthy blood donors .

Our work provides strong evidence for the transmission of M. mitochondrii to humans during the blood meal of I. ricinus. Based on the results here reported, we cannot conclude that M. mitochondrii replicates in the human host, determining a true infection. However, should we assume that M. mitochondrii does not replicate into the human host, we would have to conclude that the amount of bacteria (or bacterial antigens) inoculated is by itself sufficient for stimulating an antibody production. Overall, we are more prone to hypothesize that live M. mitochondrii bacteria (and not just proteins/DNA) can be inoculated into the vertebrate host, and that some replication can occur therein.

Source: Mariconti et al, 2012

We used next generation sequencing to detect the bacterium ' Candidatus Midichloria mitochondrii' for the first time in lone star ticks ( Amblyomma americanum) from the eastern United States. 177 individuals and 11 tick pools from seven sites in four states were tested by pyrosequencing with barcoded 16S rRNA gene eubacterial primers targeting variable regions 5-3. Average infection prevalence was 0.15 across all surveyed populations (range 0-0.29) and only the site with the smallest sample size (n = 5) was negative. Three genotypes differing by 2.6-4.1 % in a 271 bp region of 16S rRNA gene were identified. Two variants co-occurred in sites in North Carolina and New York, but were not observed in the same tick at those sites. The third genotype was found only in Georgia. Phylogenetic analysis of this fragment indicated that the three variants are more closely related to ' Candidatus Midichloria mitochondrii' genotypes from other tick species than to each other. This variation suggests that multiple independent introductions occurred in A. americanum which may provide insight into bacterial spread within its ecosystem and parasitism on this tick. Whether the presence of this bacterium affects acquisition or maintenance of other pathogens and symbionts in A. americanum or the survival, biology and evolution of the tick itself is unknown.

Source: Williams-Newkirk et al, 2012

Sequencing of the PCR products showed that the two cell lines gave sequences with 100% similarity to Ca. Midichloria mitochondrii. However, all cell lines, including the two positive cell lines, were negative with the specific primers. Phylogenetic analysis shows that our sequences belong to the subclass α-proteobacteria. They were identical to the sequences amplified from the tick I. ricinus. The results suggest that two cell lines, IRE/CTVM19 and BDE/CTVM14, may contain bacteria closely related to Ca. Midichloria mitochondrii and identical with it in a 350-bp part of the 16S rRNA gene sequence. To our knowledge, this constitutes the first report of the presence of DNA similar to the DNA of Ca. Midichloria mitochondrii in tick cell lines.

Source: Najm et al, 2012

Ticks are important vectors of disease in companion animals and transmit an extensive range of viral, bacterial and protozoan pathogens to dogs and cats. They may also be vectors of zoonotic pathogens which affect the health of in-contact owners. In recent years, babesiosis, and anaplasmosis have all shown signs of increased prevalence and distribution in various parts of Europe. Here, the prevalence of Anaplasma spp. and Babesia spp. pathogens in Ixodes ticks, collected from dogs in the UK in 2009, were evaluated using PCR and sequence analysis of the 16S rDNA or 18S rDNA regions respectively. Species identification was performed by alignment with existing sequences in GenBank. After sequencing, 5 out of 677 tick samples (0.74%) contained rDNA which shared 97-100%% sequence homology with Anaplasma phagocytophilum. Of these, three samples came from Ixodes ricinus and two from Ixodes hexagonus. Sixteen out of 742 ticks (2.4%) were positive for Babesia and of these 11 showed 97-100% homology with B. gibsoni. All of these 11 samples were derived from I. ricinus. One sample, again from I. ricinus, showed 99% homology for B. divergens. Four of the Babesia spp sequences were of the "venatorum" or EU1 type, three of which came from I. ricinus and one from an Ixodes canisuga. This strain has been associated with severe human cases of babeisiosis. A further 246 positive results, which appeared to show the presence of Anaplasma following PCR, were shown by sequence analysis to be derived from the bacterium Candidatus "Midichloria mitochondrii", which to date has been assumed to be non-pathogenic. The results are of interest because the presence of B. gibsoni in the UK further confirms the worldwide distribution of this piroplasm and supports the inference that I. ricinus may act as a vector for Babesia of the gibsoni-complex.

Source: Smith & Wall, 2013.

Here we present two lines of evidence that support the possibility that bacteria from the genus Midichloria are inoculated into vertebrate hosts during a tick bite: (i) a direct evidence, i.e. the detection of circulating DNA from bacteria related with M. mitochondrii, in the blood of vertebrates exposed to tick parasitism; (ii) a further indirect evidence, i.e. the presence of antibodies against an antigen from M. mitochondrii in dogs exposed to the risk of tick bite. It is interesting to note that variability was detected in the Midichloria gene sequences recovered from positive animals, and that some of these sequences were identical to those generated from tick-associated Midichloria. CONCLUSIONS: Based on the results, and on the overall information so far published on the genus Midichloria, we suggest that these bacteria are likely to represent a novel group of vector-borne agents, with the potential of infecting mammalian hosts. Whether inoculation of Midichloria bacteria could cause a true infection and pathological alteration in mammalian hosts is still to be determined.

Source: Bazzocchi et al, 2014.

 

[Research 1st]

Maybe this is related if impaired ATP occurs in the brain.


'CFS' & BRAIN Lactate.(Not Gut D-Lactate).

CFS is associated with significantly raised concentrations of ventricular lactate, potentially consistent with recent evidence of decreased cortical blood flow, secondary mitochondrial dysfunction, and/or oxidative stress abnormalities in the disorder.

Source: Matthew et al, 2009
Ventricular cerebrospinal fluid lactate is increased in chronic fatigue syndrome compared with generalized anxiety disorder: an in vivo 3.0 T (1)H MRS imaging study.

Ventricular CSF lactate was significantly elevated in CFS compared to healthy volunteers, replicating the major result of our previous study. Ventricular lactate measures in MDD did not differ from those in either CFS or healthy volunteers. We found a significant correlation between ventricular CSF lactate and severity of mental fatigue that was specific to the CFS group.

Source: Murrough et al, 2010
Increased ventricular lactate in chronic fatigue syndrome measured by 1H MRS imaging at 3.0 T. II: comparison with major depressive disorder.

Increased ventricular lactate in chronic fatigue syndrome. III. Relationships to cortical glutathione and clinical symptoms implicate oxidative stress in disorder pathophysiology.

Source: Shungu et al, 2012
Increased ventricular lactate in chronic fatigue syndrome. III. Relationships to cortical glutathione and clinical symptoms implicate oxidative stress in disorder pathophysiology.

Prions and Lactate (Non CFS):

PrP regulates release of lactate from astrocytes.

Absence of PrP in PrP-deficient astrocytes dysregulates the transport of lactate and leads to a glutamate-independent increase in lactate transport in vitro. Indication that PrP regulates the release of lactate also in vivo derives from the observation that lactate levels in the CSF of PrP-deficient mice are elevated approximately twofold in comparison with levels observed in the CSF of wild-type mice. Increased lactate levels were also found in the CSF of Creutzfeldt–Jakob-diseased patients (Awerbuch et al., 1988). In animals or humans suffering from prion disease, a conformationally altered PrP leads to a loss of normal PrP function. Because our present results imply that PrP regulates lactate transport by astrocytes, it is tempting to assume that loss of PrP function in astrocytes of prion-diseased brains may result in elevated levels of extracellular lactate and in lactate-induced acidosis and ensuing neuronal damage. Thus, reduction of PrP functions in the homoeostatic network of astrocyte–neuron interactions may play an aggravating role in the stressed or diseased brain and cause deficits in cellular communication as a function of altered cell surface recognition and concomitantly disturbed cellular metabolism.


Source:
Kleene et al, 2007
Prion Protein Regulates Glutamate-Dependent Lactate Transport of Astrocytes.

It's of interest severe ME sufferers appear to have very low or absent PrPC in their blood on an experimental test, with feedback from patients. These people need misfolding assays, but they aren't available.

It's interesting to note increase Lactate in the brain of 'CFS' research, in non severe patients, and D-Lactate elevated in people on this forum, all implying potentially crippling metabolic energy dysfunction would ensue from this. I guess the best treatment for this, is more exercise and CBT. Yes, a brilliant idea!

It would interest me to see who else has Lyme or similar pathogens who have a diagnosis of 'CFS' and have been left to rot in society with horrendous neurological symptoms and signs of autoimmunity and infection/chronic immune activation.

It wouldn't be beyond possibility that severe ME may hide a novel prion disease (loss of PrPC), caused by? That's the 100 million dollar question - perhaps the amount of dollars saved by offering CBT/GE per state., per year as an 'evidenced based' therapy for 'CFS' and turning ME into CFS in the first place and never veering away from the script.

Now how's that 2-day CPET test research evidence for 'CFS' at the IOM/P2P coming along?
The one the CDC rejects outright as useful.....the one that proves mitochondria dysfunction and thus an organic disease is untreated.

 

[dga5000]

Some more info about Midichloria Mitochondrii

Discovery

A couple of years ago, Australian postdoc Nate Lo was working at the University of Milan, looking for human pathogens in the tick species Ixodes ricinus, the main vector for Lyme disease. It was all routine until the day his PCR screening protocol revealed a novel 16S rRNA sequence. When his team took a tick apart to look for the new bug, they found it in the ovaries. And, when they looked closely at electron micrographs of infected ovarian tissues, they could see that the microbes were intracellular - living not in the cytoplasm of tick ova, but within their mitochondria.

http://www.the-scientist.com/?articles.view/articleNo/24528/title/Use-the-force--bacteria/

Where?

"They seem to get in between the inner and outer mitochondrial membranes and eat the mitochondria up. In the end you've just got this empty sack."

http://www.the-scientist.com/?articles.view/articleNo/24528/title/Use-the-force--bacteria/

"It's pretty surprising to see a bacterial species living inside the mitochondrion, which itself was a bacterium," he says. "I think it is significant." Bill Ballard, a mitochondrial specialist from the University of New South Wales, agrees. "This is, as far as I know, the first [bacterium] that actually infects within the mitochondria," he says. "It's a pretty cool paper."

http://www.the-scientist.com/?articles.view/articleNo/24528/title/Use-the-force--bacteria/

Prevalence

Lo moved to his current post at the University of Sydney, and then wrote to scientists across Europe, Russia, North Africa, and the Middle East, asking them to send ticks for him to screen. Sure enough, he found his bugs, nestled into the ovaries of 100% of female ticks.

http://www.the-scientist.com/?articles.view/articleNo/24528/title/Use-the-force--bacteria/

 

[maryb]

@dga5000
which lab did the testing, Infectolab?

 

[Valentijn]

I had blood drawn again today, and one of the co-infections being tested is Midichloria Mitochrondrii. Very interesting stuff, and it sounds like it's been found all over the place, even though the original ticks it was found in were European ones.

I'll try to remember to post here when I get my results.

 

[dga5000]

@dga5000
which lab did the testing, Infectolab?

The MM test was done by GIGA Sequencing at the University of Liege.

 

[Hanna]

I had blood drawn again today, and one of the co-infections being tested is Midichloria Mitochrondrii. Very interesting stuff, and it sounds like it's been found all over the place, even though the original ticks it was found in were European ones.

I'll try to remember to post here when I get my results.

Interesting @Valentijn , and which is the lab that will perform the test ?

 

[Valentijn]

Interesting @Valentijn , and which is the lab that will perform the test ?

Red Laboratories, in Belgium.

 

[Katherine]

I had blood drawn again today, and one of the co-infections being tested is Midichloria Mitochrondrii. Very interesting stuff, and it sounds like it's been found all over the place, even though the original ticks it was found in were European ones.

I'll try to remember to post here when I get my results.

If MM has not been proven to be pathogenic in humans how are they going to interpret those results if positive and what treatment prescribed? Did you ask for the test or was it recommended?

 

[Valentijn]

If MM has not been proven to be pathogenic in humans how are they going to interpret those results if positive and what treatment prescribed? Did you ask for the test or was it recommended?

It was recommended by the doctor. But basically it's a common co-infection (100% of some species of female ticks have it), and it's quite unique in penetrating and hijacking the mitochondria of cells. ME/CFS has a lot in common with mitochondrial diseases, which are typically genetic rather than infectious, so midichloria are a pretty interesting possibility.

I'm not sure what the implication would be for treatment, if proceeding with the assumption that it's causing symptoms.

 

[acer2000]

Have they shown MM can infect humans?

 

[Katherine]

Hi Daffodil. I've had LTT ELISPOT for Borrelia and it came back negative. I've now had more than 20 tests for lyme over three rounds of testing, covering differing varieties each time - all negative. Which makes it strange that I've tested positive for Midichloria mitochonardrii.

It is possible to be bitten by a tick and not have a Borrelia burgdorferi infection but you should probably check out other pathogens that the ticks carry too, such as this one - 'Evidence for Disseminated Mycoplasma fermentans in New Jersey Residents with Antecedent Tick Attachment and Subsequent Musculoskeletal Symptoms'
http://www.ncbi.nlm.nih.gov/pubmed/17041434

I don't know what your symptoms are but the above abstract available in full here http://journals.lww.com/jclinrheum/..._Disseminated_Mycoplasma_fermentans_in.3.aspx is a very interesting read.