Jump to content
ACN Latitudes Forums

PANDAS update


Recommended Posts

Alison,

 

I quickly googled azithromycin+half life. Found this article near the top.

 

http://www.answers.com/topic/azithromycin

 

Metabolism

 

Following a single 500mg dose, plasma concentrations of azithromycin declined in a polyphrasic pattern with a mean apparent plasma clearance of 630mL/min and a terminal elimination half-life of 68 hours. The prolonged terminal half-life is thought to be due to extensive uptake and subsequent release of drug from tissues.

 

Also worth noting (although I'm sure you are used to taking this into consideration when taking antibiotics)

 

Drug Interactions: Unlike erythromycin and clarithromycin, azithromycin is generally considered free of interactions with most other medicines. It is recommended that azithromycin not be taken at the same time as aluminum- or magnesium- based antacids, such as Mylanta or Maalox because antacids will bind the azithromycin and prevent it from being absorbed from the intestine.

 

So this drug is extensivley absorbed into the tissue, and released from there over an extended period of time.

 

The 68 hour half life, would be the part that is bothering you, considering this is the only dose for a week, right?

 

 

Kim

Link to comment
Share on other sites

  • Replies 35
  • Created
  • Last Reply

Top Posters In This Topic

Alison (part two)

 

I have been reading a little on immunology when I get some free time, and this site has been really helpful, in case you want to check it out.

 

http://www.ncbi.nlm.nih.gov/entrez/query.f...optcmdl=TOCView

 

 

I was trying to find a something that would give a description on the ASO and anti-DNase tests. This gave a little overview. This was just for my benefit, in trying to understand how much information these tests give and how they work.

 

http://www.healthatoz.com/healthatoz/Atoz/...ibody_tests.jsp

 

Antistreptolysin O titer (ASO)

 

The ASO titer is used to demonstrate the body's reaction to an infection caused by group A beta-hemolytic streptococci. Group A streptococci produce the enzyme streptolysin O, which can destroy (lyse) red blood cells. Because streptolysin O is antigenic (contains a protein foreign to the body), the body reacts by producing antistreptolysin O (ASO), which is a neutralizing antibody. ASO appears in the blood serum one week to one month after the onset of a strep infection. A high titer (high levels of ASO) is not specific for any type of poststreptococcal disease, but it does indicate if a streptococcal infection is or has been present.

 

Serial (several given in a row) ASO testing is often performed to determine the difference between an acute or convalescent blood sample. The diagnosis of a previous strep infection is confirmed when serial titers of ASO rise over a period of weeks, then fall slowly. ASO titers peak during the third week after the onset of acute symptoms of a streptococcal disease; at six months after onset, approximately 30% of patients exhibit abnormal titers.

Antideoxyribonuclease-B titer (anti-DNase B, or ADB)

 

Anti-DNase-B, or ADB, also detects antigens produced by group A strep, and is elevated in most patients with rheumatic fever and poststreptococcal glomerulonephritis. This test is often done concurrently with the ASO titer, and subsequent testing is usually performed to detect differences in the acute and convalescent blood samples. When ASO and ADB are performed concurrently, 95% of previous strep infections are detected. If both are repeatedly negative, the likelihood is that the patient's symptoms are not caused by a poststreptococcal disease.

* * * * * * *

This is a surprise to me :blink:

The way I read this, is that these tests are good indicators of strep having been present, but don't give a whole lot of info beyond that.

 

So ASO simply tells that your body has produced antistreptolysin O, to neutralize streptolysin O. produced by the strep, and anti-Dnase detects antigens produced, again, by the strep.

 

This was not the picture I had in mind of "high titers."

 

Interesting!

 

Now I'm wondering which antibodies that you were referring to at the bottom of your post, that you wondered if the antibiotic is interacting with, as opposed to the step? Has your son had another test, other than the two I was looking at here?

 

Kim

Link to comment
Share on other sites

Hi Kim,

 

Thank you so much for the info! You continue to amaze me.

 

I had found the info on the 68 hour half life, I have also read 63 hour. I am assuming a full life is not always double the half life - but even so, 68 hours x 2 is really just 5 days. Ronna has advised she found her son symptomatic waiting the full 7 days. I think I will start at the 5 day prophylactic dose and see how he does and maybe increase after a few weeks by one day. I have a tremendous fear of him deteriorating as he has done so many times when he goes off or lowers the dose of antibiotics, then it seems adding back in the antibiotic that had been working, they no longer work. It feels like we are creating some sort of super bug in him.

He is doing really well right now - at the point where no one would notice anything. Big change from a once a second vocal tic.

 

Regarding the titers, my concern is that with PANDAS the idea is the strep antibodies react with the basal ganglia - and if they are still elevated than any insult on the immune system will kick them into actions. The bucket theory. My son's remain at about 600 - normal on the test he did was under 65 although I have seen normal as under 200 as well. I am thinking, since he has these antibodies that are not going down, then anytime his immune system is bothered they are ready to attack the brain. If they were down to a normal level - then we would not see tics emerge from pizza lunch etc.

 

He has been on prophylactic antibiotics for almost 2 years - why are these antibodies not going down? I wrote to NIMH to ask and got a reply that consisted of some research papers - ultimately saying they can stay elevated for up to 6 months - but this is 2 years later.

 

We are going to be going back to the infectious disease clinic so I will ask them about these titers.

 

Thanks so much for the time you spent finding the info - you are a pro. It took me several nights to finally figure our the half life info!

 

I am so thrilled with how well he is doing right now, and thank you all for your support - and for Ronna and Mustang Carole for pointing me in the right direction in recent weeks. I am so fortunate that we live in times when we can learn from others through the internet.

Link to comment
Share on other sites

Alison,

 

I can't tell you how glad I am to help in any way possible, even if it's only to bumble through places that others have been, and explained much better than I can.

 

Your question, and the studies that I read last night have been on my mind all day( If obsessive compulsive has crossed anyones mind, I would NOT be insulted) . The fact that your sons titers remain highly elevated, seem most likely to be caused by one of two things (?). The strep is never fully eradicated, or he has a high re-exposure rate.

 

I was wondering if strep ( I have read about strep something or other... found in the gastro tract, when reading about probiotics), could morph, something like yeast, to become infectous, instead of living harmlessly, like other bacterias can within us. I was wondering if your son could be reinfecting himself.

 

A little more hunting tonite, turned these up, which I though you may be interested in reading. I know there is other info. on the Yaskow site about strep, as in what blood types may be most susceptible to problems with molecular mimicky, but this was the first time I read this one. I promise it's not as complicated as the immunology site, that I posted last nite :( That one's a killer. I practically have to make myself a quiz on every paragraph to retain any of it!

 

This article talks mostly about problems women have with yeast, but it did relate a bit to what I was thinking about. BTW, I do know that you're using probiotics.

 

http://www.womentowomen.com/digestionandgihealth/probiotics.asp

 

Of the trillions of microbes in your system, researchers have identified some — but by no means all — of the friendly flora species. Categorized through a complex process of culturing and DNA isolation, essential players include Escherichia, Lactobacillus, and Bifidobacterium. Other common inhabitants include Bacteroides, Clostridium, Fusobacterium, Eubacterium, Streptococcus and certain yeast (Candida) strains.

 

AND

 

Other good bacteria produce natural antibiotics and antifungals; for instance, Streptococcus salivarius manufactures an antiseptic that neutralizes the sulfur compounds responsible for bad breath (halitosis). Friendly flora also keep unfriendly bacteria in check by depriving them of nutrients and secreting acids (acetic, lactic, and formic) that create a hostile environment for pathogens.

 

Then this..hang in there until you get about 2/3 of the way down the page.

 

http://www.autismanswer.com/articles/yasko/autism_virus_thimerosal.html

 

I believe that it is likely that the streptococcus permanently resides as part of the bacteria or flora in the nasopharyngeal cavity of these children who are highly susceptible to streptococci. The mucous system in our nasal passages flushes bacteria and viruses into our stomach. It is easy to see how under "compromised conditions", streptococci could survive the stomach and make its way to the intestinal tract. Gastric reflux has been implicated as a factor in ear infections.26 It is not surprising then, to note that in addition to its role in ear infections and strep throat, streptococcus has been implicated in leaky gut.27

 

Gut flora changes play a major role in causing the increased intestinal membrane permeability that is seen with leaky gut. Depletion of glutathione is a common occurrence in leaky gut. Streptococcal infection, or the presence of chronic or recent infection, depletes glutathione levels.28 High glutamate levels also result in the depletion of glutathione.29 Streptococcal infection is also more likely to be an issue in individuals with high glutamate levels, as glutamate is related to virulence in streptococci. Streptococcus flourishes in a high glutamate, low glutathione environment.30,31 Thus, the combined effects of changes in gut flora and depleted glutathione lay the groundwork for leaky gut.

 

The info here about zinc and strep caught my eye too.

 

Forgive me if this is all just old news to you. :blink: I know you have addressed many of the things talked about in this article.

 

BTW, I think you are right at the top of the list of super mom's and pretty amazing too! I'm sure everyone here is very appreciative of the details you share. I feel like our kids are so amazing, it's wonderful to see so many people working together to try to help them (and affected adults too!) become healthier.

 

Kim

Link to comment
Share on other sites

Alison,

 

If you have a little spare time today (lol) you might want to read through these too.

 

I think I have a pretty good idea now of how your son's titers could remain elevated, and why a particular antibiotic could be effective at reducing symptoms, and then lose it effectiveness.

 

Let me know what you think!

 

I tried to condense things as much as possible, but reading the whole articles may be necessary to get out of it, what I did.

 

 

http://en.wikipedia.org/wiki/Streptococcus_pyogenes

 

Streptococcus pyogenes is a Gram-positive bacterium that grows in long chains depending on the culture method.[1] S. pyogenes displays group A antigen on its cell wall and beta-hemolysis when cultured on blood agar plate. S. pyogenes typically produces large zones of beta-hemolysis, the complete disruption of erythrocytes and the release of hemoglobin, and it is therefore called Group A (beta-hemolytic) Streptococcus (abbreviated GAS).

 

S. pyogenes has several attributes that make it more virulent.[2] A carbohydrate capsule surrounds the bacterium, protecting it from attack by macrophages (part of the immune system). Further, there are proteins, lipoteichoic acids, embedded within the capsule (M protein) that also increase virulence by facilitating attachment to host cells.[3] M protein inhibits a branch of the immune system called the complement system, which binds to and destroys invading bacteria. However, the M protein is also the weakest point in this organism's defense as this is what antibodies produced by the immune system use to recognize the bacterium. M proteins are unique to each strain and identification can be used clinically to confirm the strain causing an infection.

 

http://textbookofbacteriology.net/antiimmuno.html (brilliant here, took a while to figure out Ag=antigen)

 

Tolerance is a property of the host in which there is an immunologically-specific reduction in the immune response to a given Ag. Tolerance to a bacterial Ag does not involve a general failure in the immune response but a particular deficiency in relation to the specific antigen(s) of a given bacterium. If there is a depressed immune response to relevant antigens of a parasite, the process of infection is facilitated. Tolerance can involve either AMI or CMI or both arms of the immunological response.

 

Tolerance to an Ag can arise in a number of ways, but three are possibly relevant to bacterial infections.

 

Fetal exposure to Ag. If a fetus is infected at certain stages of immunological development, the microbial Ag may be seen as "self", thus inducing tolerance to the Ag which may persist even after birth.

 

2. High persistent doses of circulating Ag. Tolerance to a bacterium or one of its products might arise when large amounts of bacterial antigens are circulating in the blood.

 

3. Molecular mimicry. If a bacterial Ag is very similar to normal host "antigens", the immune responses to this Ag may be weak giving a degree of tolerance. Resemblance between bacterial Ag and host Ag is referred to as molecular mimicry. In this case the antigenic determinants of the bacterium are so closely related chemically to host "self" components that the immunological cells cannot distinguish between the two and an immune response cannot be raised. Some bacterial capsules are composed of polysaccharides (hyaluronic acid, sialic acid) so similar to host tissue polysaccharides that they are not immunogenic.

 

Antigenic Variation

 

One way bacteria can avoid forces of the immune response is to periodically changing antigens, i.e., to undergo antigenic variation. Some bacteria avoid the host antibody response by changing from one type of fimbriae to another, or by switching fimbrial tips. This makes the original AMI response obsolete by using new fimbriae that do not bind the previous antibodies. Pathogenic bacteria can vary (change) other surface proteins, especially outer membrane proteins, that are the targets of antibodies.

 

Antigens may vary or change within the host during the course of an infection, or alternatively antigens may vary among multiple strains (antigenic types) of a parasite in the population. Antigenic variation is an important mechanism used by pathogenic microorganisms for escaping the neutralizing activities of antibodies. Antigenic variation usually results from site-specific inversions or gene conversions or gene rearrangements in the DNA of the microorganisms.

 

Many pathogenic bacteria exist in nature as multiple antigenic types or serotypes, meaning that they are variant strains of the same pathogenic species. For example, there are multiple serotypes of Salmonella typhimurium based on differences in cell wall (O) antigens or flagellar (H) antigens. There are 80 different antigenic types of Streptococcus pyogenes based on M-proteins on the cell surface. There are over one hundred strains of Streptococcus pneumoniae depending on their capsular polysaccharide antigens. Based on minor differences in surface structure chemistry there are multiple serotypes of Vibrio cholerae, Staphylococcus aureus, Escherichia coli, Neisseria gonorrhoeae and an assortment of other bacterial pathogens. Antigenic variation is prevalent among pathogenic viruses as well.

 

If the immune response is the main defense against a pathogen, then being able to shed old antigens and present new ones to the immune system might allow infection or continued invasion by the pathogen to occur. Furthermore, the infected host would seem to be the ideal selective environment for the emergence of new antigenic variants of bacteria. Perhaps this explains why many bacteria exist in a great variety of antigenic types.

 

http://www.mndaily.com/daily/2000/12/12/news/new5/

 

University researchers and Pennsylvania-based Wyeth-Ayerst laboratories, a division of American Home Products, are focusing on a protein on the strep bacteria which suppresses the immune response needed to combat disease. The protein is common in several different diseases.

 

Normally, when a bacteria invades the body a signal is sent for disease-fighting cells to surround, engulf and digest the microorganism.

 

"In simple terms, when strep bacteria in the throat starts a fire (the disease-fighting cells) dampen the fire," said University microbiologist Patrick Cleary, developer of the vaccine.

 

This particular protein prevents the signal from being sent, allowing the bacteria to invade the mucus-lined surfaces of the body, including the throat and nose, resulting in illness. A course of antibiotics controls the bacteria.

 

The few of these I scanned, talk about the danger of this type of vaccine inteferring with heart tissue. What about BRAIN tissue in a particular segment of the population. Some scary stuff here, as I have found with most vaccine research.

 

Protein M and strep vaccine development

 

http://www.google.com/search?hl=en&ie=ISO-...G=Google+Search

Link to comment
Share on other sites

Thanks Kim - I will have to read read the last post a few more times until I fully understand it.

 

Your post from last night hit the nail on the head - the two things I am concerned about in light of his titers is that we never fully eradicate the strep - or he is re-infected from exposure- which is why when my youngest tested positive for strep with no symptoms we thought he might be a carrier. We have now swabbed him twice since the antibiotics and he was negative both times - so the doctor says he is not a carrier - I do remember your comment at the time that your son would be positive a few months later so I will re-test again in a couple of months.

 

I am sure you understand the info you have posted for me far better than I do - any advise for me???

Does the info you have provided mean ultimately all antibiotics could stop working and then we are out of luck?

 

I am going to re-read it all once the kids are in bed.

Link to comment
Share on other sites

Alison,

 

Have the Dr.s ever said how many kids they have seen with this type of problem? Have you discussed the usual outcome? Do they out grow it?

 

Do they think that there is a chance of creating a "super bug"?

 

From the segment: Antigenic variation

 

Pathogenic bacteria can vary (change) other surface proteins, especially outer membrane proteins, that are the targets of antibodies.

 

There are 80 different antigenic types of Streptococcus pyogenes based on M-proteins on the cell surface.

 

M proteins are unique to each strain and identification can be used clinically to confirm the strain causing an infection.

 

One way bacteria can avoid forces of the immune response is by periodically changing antigens, i.e., to undergo antigenic variation

 

If the immune response is the main defense against a pathogen, then being able to shed old antigens and present new ones to the immune system might allow infection or continued invasion by the pathogen to occur. Furthermore, the infected host would seem to be the ideal selective environment for the emergence of new antigenic variants of bacteria.

 

Has your sons strain been identified?

 

Has it remained consistent?

 

Is it possible that rotating antibiotics could be helpful? Sort of, hit it with different antibiotics, more frequently before it has a chance to make the changes that could be protecting it?

 

Just a thought :)

 

Kim

Link to comment
Share on other sites

Thanks Kim,

 

I am hoping to get some answers from the infectious disease clinic and rheumatology - I am really hoping they do some immunology panels so we can better understand what is going on. All we know is he has had high ASO titers.

He is not doing as well today as yesterday - he started to decline last night after playing outside - not sure if it was fatigue, allergies, or the antibiotic not working as well. We are still on the full dose, we added in a few extra days - I had tried to get in touch with the doctor for approval of this but did not hear back so went ahead - now I am scared to go to the prophylactic dose even more. I have had an upset stomach as did my husband so the increase could also be a viral thing as he was not very hungry over the last few days. I have to say that today I went out back to school shopping with him and he almost seemed better on the drive home than the drive there - I hate this... I added in allergy medication incase the increase was from something outside yesterday - my husbands allergies have been bad recently.

I met with his teacher today and she seemed like she will be fine with the floresent lights being off and me bringing in the tv etc.

Thanks you again for the time you have taken replying to my posts.

 

I will keep you posted...

 

Just wanted to add...regarding PANDAS - it is thought to be something that these kids will outgrow - it is a pediatric illness. My fear is any possible permanent damage being done to the basal ganglia. My doctor has a few patients who have PANDAS - different treatments have worked for different kids. Some choose meds to deal with the symptoms. That would be my last resort - but never say never.

Link to comment
Share on other sites

Hi,

 

I haven't posted in a while... but I've been somewhat following along.

 

ad_ccl, your experience with your son sounds very similar to mine. My son has had elevated titers for over a year, whether he is on antibiotics or not, and is constantly swabbing negative on his throat cultures. We did try to experiment and take him off of medication for a few months here and there, but ultimately his symptoms eventually reappear.

 

I still can't seem to determine the one medication that works for him. I just finished a week of Augmentin, with no results - moved on to Ceclor (which worked very well last month) and don't see any improvement yet - it's day number four today. BTW, my pediatrician highly recommended Zithromax specifically for PANDAS. We tried it for a few months and had no success with it, but she claims that many of her patients with PANDAS have had huge success with Zithromax.

 

At this point I am so sick of all the medication - my son has had chronic diarrhea for almost a year already. This began when we were trying so many different antibiotics.

 

I finally went ahead with a new Doctor - I'm not sure if she is what you would call a DAN doctor, but her approach is basically the route that many of the posters on this forum have been following. First find out if there are any food allergies, yeast, parasites, bacteria in the intestinal tract...etc., and then use many supplements and even medication if necessary to eliminate the problems.

 

I don't think I ever would have gone ahead with her if not for this forum and all of the information that I picked up from everybody here. I'm really more the "if your sick, take medicine" type, but after reading this forum for over a year, I became so much less skeptical and more open-minded to the alternative approaches out there. Thanks everyone!!

 

Well, we just did an extensive gluten and casein (dairy) test with Entero Labs which is done by testing the stool - not a blood test for celiac like my original pediatrician did a few months ago, and lo and behold - he is sensitive to both gluten and casein.

 

His original blood test for celiac had come back normal, so I was hoping that he wouldn't be allergic, but deep down inside I really had this gnawing feeling that this was a large part of his problem, especially when he developed this little rash a few months ago. They look like little mosquito bite scabs - he has it pretty mild, but they are there on his legs and bottom/back area. I read online about a rash called Dermatitis herpetiformis that sounded like what he has - which is a rash that mostly celiacs have.

 

I am still waiting for the rest of his test results but am a bit numb due to the gluten/casein result. I am so worried about what he's going to eat (he's SOOOO skinny!) and how he's going to react...We have't told him yet - we are waiting for the rest of the results to be in before we begin his new diet. I will do my very best to make it easy for him, and hope to be have the strength to be able to tackle this.

 

The truth is, it's really good news - I now know in black and white - that this has been causing his diarrhea, and most probably his PANDAS as well, being that celiac can cause different autoimmune diseases. Hopefully, once we begin his new diet, we will see positive results..I'll keep you all posted.

 

Thanks for all of your support and for being the greatest soundboard! (Sorry if I've rambled...)

Link to comment
Share on other sites

Hi Allison,

 

I have meant to reply to your question re: titers for awhile and today's discussion reminded me and I thought I would post the info here as it may help others in understanding titer levels.

 

Ok, so when you see the doctor the most likely response to your question as to why your son's titers remain high will be...and I know that this sounds overly simple... when you are looking at "normal" levels...well you have to take into account individual variabilities. Some children do have chronically elevated titer levels which is normal for them.

 

I have posted in the past and will do so again...the most significant part when looking at titer levels for strep is whether the levels are climbing (indicates more recent infection) or declining (recovery). If the titer levels are staying relatively stable regardless of the number then you can assume there has been no infection.

 

A quote from the NIMH...

 

[b]It is important to note that some grade-school aged children have chronically “elevated” titers. These may actually be in the normal range for that child, as there is a lot of individual variability in titer values. Because of this variability, doctors will often draw a titer when the child is sick, or shortly thereafter, and then draw another titer several weeks later to see if the titer is “rising” ? if so, this is strong evidence that the illness was due to strep. (Of course, a less expensive way to make this determination is to take a throat culture at the time that the child is ill.) [/b]

 

In our own situation we can certainly look back and be fairly certain when my son had strep and the resulting PANDAS symptoms. However, once the immune system is primed to over react it will, for example one of my son's biggest set backs over the last few years was with the chicken pox. As well, even this summer we all had a viral illness and for Kurt he did have tics with the illness, the first we had seen or heard in awhile and they disappeared as the illness passed.

 

However, as you know Kurt is on prophylactic azithromycin and doing well with this. It is my feeling that although viral illnesses etc do cause an increase in symptoms it is nothing compared to him getting another strep infection which we really want to prevent if possible.

 

I hope this makes sense as I seem to be chronically tired lately and to sum things up...I would not get caught up in the actual numbers but look at their pattern instead.

 

Ronna

Link to comment
Share on other sites

Ronna,

 

I had actually read some Pub Med studies (one in particular) that seemed to be saying exactly what you did in your post. I started thinking that maybe Alison's son's titer levels were not necessarily abnormal for him. Then, I started to wonder why he seemed to react favorably to the introduction of a different antibiotic, or negatively when the dose of a current one was lowered. It seems to be distinctly correlated most of the time, from what I gather.

 

[

b]It is important to note that some grade-school aged children have chronically “elevated” titers. These may actually be in the normal range for that child, as there is a lot of individual variability in titer values

 

This sounds like the same language in one of the studies.

 

However, once the immune system is primed to over react it will, for example one of my son's biggest set backs over the last few years was with the chicken pox.

 

This makes sense too. It will be interesting to see if Alison sees a relationship to what would be a suspected strep flair, which I'm assuming would be a more distinct reaction, or possibly a different "bug," maybe viral (?), in which case the antibiotic would not be a big factor in worsening or improvement in symptoms.

 

Evie's post kind of fits into this pattern too. A secondary condition (gluten and casein sensitivities) in addition to a PANDAS problem, which would go back to your statement about "being primed to overreact."

 

Alison's post gave me a boost to try to get a little more educated on this subject since both of my boys have a history of strep, and tics and I have always wondered how so many things can be overlapping, but never what I would call an over night exacerbation.

 

I did learn a lot, but some of the lines defining this as two separate syndromes still remain a bit fuzzy for me.

 

Thanks for your informative post, as always.

 

Hope you get some rest!

 

Kim

Link to comment
Share on other sites

Hi everyone,

 

Just a short response - I am soooo tired, eyes stinging kind of tired. This has taken a toll on me - can't sleep at night, up in the middle of the night searching for answers on the computer. Anyway- just wanted to give a quick update - things are amazing - he is doing so well. The doctor gave the go ahead for a longer run on the azithromycin - I think I may add on another couple days to get us to the first day of school, then may slowly move to the prophylactic dose - not waiting a full 5 days the first time. He is so happy, he went skating today for about a half hour - I had forgotten how he sounded when he laughed, I did not realize how little he has laughed in recent weeks - it is like he has come alive again. Not just lethargic - I am sure all the antibiotics did a number on his system. The vocal tic is at a minimum - no one would notice it at all, it was always worst when he ate, I often had to leave the room it made me so nuts, I think he made one noise through all of dinner tonight - and at that it was soft. He was hiding on me this evening in his room - I could not hear a thing - silence. He has been doing a little eye stuff, very subtle looking down - no one would notice - and I am not caring about that - compared to the once a second loud squeak - this is nothing.

 

I will re-read your posts as I know I have wanted to reply to specific things in them, but have been too tired to start a response - but am reading everything. Thank you all so much for all of the support you have shown me.

Link to comment
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now

×
×
  • Create New...