Streptococcus Pneumonae

[P_Mom]

Okay...can somebody explain to me what the Prevnar vaccine, and, therefore, the s.pneumonia titer tests have to do with strep A??? I see ALOT of mention on these boards relating s.pneumonia titer response in relation with strep A. In my understanding, they are two completely different microbes...causing different illnesses. I thought that titer response to s. pneumonia (prevnar vaccince) had nothing to do with strep A (PANDAS)??!! What am I missing??????

[peglem]

Okay...can somebody explain to me what the Prevnar vaccine, and, therefore, the s.pneumonia titer tests have to do with strep A??? I see ALOT of mention on these boards relating s.pneumonia titer response in relation with strep A. In my understanding, they are two completely different microbes...causing different illnesses. I thought that titer response to s. pneumonia (prevnar vaccince) had nothing to do with strep A (PANDAS)??!! What am I missing??????

Here's my understanding, completely from memory-

Although S. pneumo and strepA are different bacterias- both are the encapsulated type (what's that capsule called? I can't remember), so the S. pneumo vaccine challenge test is checking for the ability (or inability) of the immune system to respond to encapsulated bacteria.

[AmySLP]

This alone got the diagnosis of Specific immune deficiency. Re-vaccinating will not make a difference in the case of a child with this, as they have already had four vaccines and in my daughter's case, more than 15 + strep infections. There has been plenty of opportunity for the antibodies to be made, apparently her body is unable to mount the immune response to this.

 

Again, I'll take any input on this as I am trying to figure it all out as well,

 

Amy

[saidie10]

So, I met with Diana Polhman yesterday for the first time. We live only a couple of miles apart and she has been helping me tremendously with my son. As most of you know, she met with Dr. Cunningham (STREP EXPERT) last week. It appears and hopefully I'm getting this right..... Dr. Cunningham believes it to be the type of strep. Not typical Streptococcus A but S. pneumoniae which is very difficult to rid the body of infection. Please read the definition below closely. If it is, it would explain why certain antibiotics are not that effective and why repeated IVIG is sometimes required.

 

My child had NEVER been sick until he was exposed to what we now to believe was Scarlet Fever. The first time my son was ever prescribed antibiotics was at 4 1/2...... so, only one year ago. He was healthy, healthy, healthy.

 

What are your thoughts? I hope to have my son tested for S. pneumoniae if possible. I understand its difficult to find someone to test. Plus he is now post IVIG.

 

Taken from Wikipedia

 

Streptococcus pneumoniae, or pneumococcus, is Gram-positive, alpha-hemolytic, bile soluble diplococcus aerotolerant anaerobe and a member of the genus Streptococcus.[1] A significant human pathogenic bacterium, S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century and is the subject of many humoral immunity studies.

Despite the name, the organism causes many types of pneumococcal infection other than pneumonia, including acute sinusitis, otitis media, meningitis, bacteremia, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.

 

S. pneumoniae is the most common cause of bacterial meningitis in adults and children, and is one of the top two isolates found in ear infection, otitis media.[2] Pneumococcal pneumonia is more common in the very young and the very old.

 

S. pneumoniae can be differentiated from other members of Viridans Streptococci, some of which are also alpha hemolytic, using an optochin test, as S. pneumoniae is optochin sensitive. S. pneumoniae can also be distinguished based on its sensitivity to lysis by bile. The encapsulated, gram-positive coccoid bacteria have a distinctive morphology on gram stain, the so-called, "lancet shape." It has a polysaccharide capsule that acts as a virulence factor for the organism; more than 90 different serotypes are known, and these types differ in virulence, prevalence, and extent of drug resistance.

 

Ok so this Strep Pneumoniae is one of two of the typical isolates found in ear infections? Like my boys have both had a gazillion ear infections! Should our kids all be tested for this type of strep too?

[kimballot]

Ok... I guess I got a little excited earlier at the thought that there may be something written about s. pneumoniae since I have been trying to convince people that my son's sinus infections lead to PANDAS symptoms for many years... (fortunately, the PANDAS docs now understand this -though the NIMH website does not list it so regular docs don't get it).

 

My understanding is that group A beta hemolytic strep (GABHS) and Streptococcus pneumoniae are NOT the same thing. GABHS is NOT generally found in the human body, and when it does enter, the body fights it with antibodies. The antibodies have a "memory", so when they see the surface of the group A strep again, they fight it. In the case of our kids, there is thought to be a breach in the blood-brain barrier when there is infection and inflammation, and when antibodies cross over and see the basal ganglia cells they think it is GABHS and start producing lots of antibodies. The antibodies do not destroy the basal ganglia cells, but they do attach to the receptors and make Cam Kinase and dopamine go wild.

 

Strep pneumoniae, on the other hand, IS found in normal sinuses. It generally hangs out there and does not cause much trouble and the body usually has a decent level of antibodies to keep it in check (the s. pneumoniae titers at protective levels). In my son's case, his body did not produce enough s. pneumoniae antibodies, so he was given 2 pneumococcal vaccinations at a young age. A couple of months after the vaccinations his blood work looked like he was mounting a response. However, over time, this protection faded because it was an artificial and temporary boost of his immune system.

 

Currently, he has selective immune deficiency because 10 out of 14 s. pneumoniae titers are below protective levels. In addition, when his allergies flair up or he gets a virus, he has generalize inflammation that results in decreased ability of his sinuses to drain. Once that happens, the warm moist environment in the sinus is a perfect breeding ground for more s. pneumoniae (which his immune system cannot fight), so that is why we believe he (and probably others on this forum) ends up with a sinus infection.

 

Now the question is... why does he get PANDAS symptoms if it is not GABHS? I don't know if he has a GABHS infection somewhere in his body (low ASO, but elevated DNASEB ) and his immune system does not mount enough of a Group A response for an elevated ASO.... or if the problem is just that he has has strep at some time in the past and his antibodies remember what the strep A looked like. Now, when he gets a sinus infection or a virus, he has generalized inflammation that ends up in a breach of the BBB and .... tadaa... those anti strep antibodies spot those basal ganglia cells and start going to work... but they don't actually kill the basal ganglia cells (thankfully)... they just have a little basal ganglia party making lots of Cam Kinase and dopamine to make him act funny and think funny thoughts.

 

Now - if you've stuck with this post this long and you have other ideas about this, please share because my idea about what is going on in his head is certainly open to change and I really want to hear other ideas...

 

Thanks!

Edited June 15, 2010 by kimballot

[sf_mom]

Group B can manifest group A.

 

Group A streptococci are nearly always beta-hemolytic; related Group B can manifest alpha, beta or gamma hemolysis. Most strains of S. pneumoniae are alpha-hemolytic but can cause ß-hemolysis during anaerobic incubation. Most of the oral streptococci and enterococci are non hemolytic. The property of hemolysis is not very reliable for the absolute identification of streptococci, but it is widely used in rapid screens for identification of S. pyogenes and S. pneumoniae.

 

http://www.tjclarkinc.com/bacterial_diseas...us_pyogenes.htm

 

In one article; the claim is made that the S. pyogenes does not create a humoral response in children only cellular... therefore the bacteria proliferates without cross immunity to other more traditional strains of strep. For example: you would need the S. pneumoniae antibodies to potentially fight s. pyogenes.

 

Effect of SpeB and EndoS from Streptococcus Pyogenes on Human Immunoglobulins http://www.ncbi.nlm.nih.gov/pmc/articles/PMC100124/

 

My friend's son who is PANDAS and had RF his S. paneumoniae antibodies dropped drastically over the period of 1 1/2 years until he became deficient during the time we knew he had active strep A infections 'culture positive'. Stanford's Children hospital and others (MC, Kaplan, Bessin inclusive) COULD NOT explain to me why this happened because theoretically they should have gone up if they were fighting an infection.... Maybe it could have been co-infections but my instinct says cross immunity. Something for the GREATER STREP EXPERTS to figure out.

Edited June 15, 2010 by SF Mom

[P_Mom]

Huh???

[kimballot]

Huh???

Was that "huh" for me? Was my post that confusing?? sorry

[justinekno]

Kim,

 

First I have to say that I love your explanation here. It is a nice, basic, easy to understand breakdown of what happens. Thanks!

 

As far as your question about low ASO, but elevated DNASEB, Dr. T. told us (my son has low ASO, but elevated DNASEB) that this likely suggests a non-pharyngeal (rectal, skin perhaps) source. My son gets many rashes (and gut issues) so we are looking at those being the source.

 

My understanding is that group A beta hemolytic strep (GABHS) and Streptococcus pneumoniae are NOT the same thing. GABHS is NOT generally found in the human body, and when it does enter, the body fights it with antibodies. The antibodies have a "memory", so when they see the surface of the group A strep again, they fight it. In the case of our kids, there is thought to be a breach in the blood-brain barrier when there is infection and inflammation, and when antibodies cross over and see the basal ganglia cells they think it is GABHS and start producing lots of antibodies. The antibodies do not destroy the basal ganglia cells, but they do attach to the receptors and make Cam Kinase and dopamine go wild.

 

 

 

 

Now the question is... why does he get PANDAS symptoms if it is not GABHS? I don't know if he has a GABHS infection somewhere in his body (low ASO, but elevated DNASEB ) and his immune system does not mount enough of a Group A response for an elevated ASO.... or if the problem is just that he has has strep at some time in the past and his antibodies remember what the strep A looked like. Now, when he gets a sinus infection or a virus, he has generalized inflammation that ends up in a breach of the BBB and .... tadaa... those anti strep antibodies spot those basal ganglia cells and start going to work... but they don't actually kill the basal ganglia cells (thankfully)... they just have a little basal ganglia party making lots of Cam Kinase and dopamine to make him act funny and think funny thoughts.

 

Now - if you've stuck with this post this long and you have other ideas about this, please share because my idea about what is going on in his head is certainly open to change and I really want to hear other ideas...

 

Thanks!

Edited June 15, 2010 by justinekno

[P_Mom]

No, Kim....for SF Mom. Your post, Kim, I could understand...thanks! No offense, SF Mom!

[sf_mom]

I went back and edited a little so its more understandable. My father-in-law being a Dr. was able to explain the difference between humoral verses cellular immune response and the 'Effect of SpeB and EndoS from Streptococcus Pyogenes on Human Immunoglobulins' to me and why cross immunity would be needed. He has communicated with Dr. K, Dr. Kaplan, MC and Dr Bessin and all concur it is something to be investigated further.

 

For now, what is important..... if your child suffers from strep pneumo titers deficiencies and chronic infections it is likely Dr. B or similar would be able to get your insurance to cover IVIG treatment.

 

-Wendy

[Fixit]

ok ...i think i get kimballots..

Sf mom, would that be your interpratation??

AMyslp, that's for the info also..maybe i can press the ins with that...

thanks all!!!!

[sf_mom]

No, several Dr.'s provided understanding of article to me and validated what it says. See recent post.

[kimballot]

I went back and edited a little so its more understandable. My father-in-law being a Dr. was able to explain the difference between humoral verses cellular immune response and the 'Effect of SpeB and EndoS from Streptococcus Pyogenes on Human Immunoglobulins' to me and why cross immunity would be needed. He has communicated with Dr. K, Dr. Kaplan, MC and Dr Bessin and all concur it is something to be investigated further.

 

For now, what is important..... if your child suffers from strep pneumo titers deficiencies and chronic infections it is likely Dr. B or similar would be able to get your insurance to cover IVIG treatment.

 

-Wendy

 

Thanks, Wendy - I am needing to do more work to understand humeral vs cellular etc... but that is my summer project. In the meantime, I am THRILLED to be among other families who have had similar sinus / PANDAS experiences (not that I wish those experiences on anyone!)... and - yes- Dr. B does seem able to help sort this out.

[lynn]

My DS also has deficiencies of 13 out of 14 of the S. pneumoniae titers. He has normal ASO but elevated anti DNASE. I understand that this will help with insurance for IVIG, but I am curious as to whether there is an actual meaning to this. As far as I know, DS hasn't gotten Prevnar (unless it is one of the standard immunizations?) Does that mean that the titers are irrelevant?