Complement deficiency?

[kim]

I think that I've seen a couple of posts here regarding Complement testing (immune deficiencies).

 

I'm wondering if anyone has had a immuno Dr. discuss anything relating to this statement with them?

 

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

 

Deficiencies of the terminal pathway predispose to both autoimmune disease and infections (particularly Neisseria meningitidis, due to the role that the membrane attack complex plays in attacking Gram-negative bacteria).

 

http://www.els.net/WileyCDA/ElsArticle/refId-a0000511.html

 

Terminal pathway of complement refers to the sequence of interactions between components C5b, C6, C7, C8 and C9 that leads to the production of a ‘membrane attack complex’ possessing the ability to disrupt cell membranes.

 

In light of the recent discussion on another thread (vaccine discussion) I'm wondering if a known deficiency would be a case where vaccination would be highly indicated, or if it would be ineffective anyway because of the deficiency? Does anyone have any knowledge here?

 

excerpt from the National Vaccine Information Center

http://www.nvic.org/Vaccines-and-Diseases/Meningitis.aspx

 

Meningitis associated with Neisseria meningitidis is most often encountered in children and young adults. In 2005, a meningococcal vaccine was recommended by the CDC for 11 year olds and college students, especially freshman living in dorms on campuses. In 2010, the CDC expanded meningococcal vaccine recommendations to include a booster dose of meningococcal vaccine for all 16 year olds in addition to the first dose given to all 11-12 year olds.

[LNN]

Way over my head. You're going to have to put this into Linda Blair Syndrome and S on Toast analogies for me.

 

The only complement testing we've done has been on C3a, C3d and C4a.

[kim]

Way over my head. You're going to have to put this into Linda Blair Syndrome and S on Toast analogies for me.

 

The only complement testing we've done has been on C3a, C3d and C4a.

 

 

LLM,

 

Read just the wiki page and you'll see why I can't possibly put this on toast, not even a whole loaf! Complement is one complicated issue

http://en.wikipedia....mplement_system

 

Were any of the levels abnormal?

[LNN]

I've tried to understand the complement system for 2 years. I always get off the laptop feeling like i just got off one of those puke-inducing rides at Six Flags.

 

DS had elevated C3d that went from 25 to 50 during the first 2 yrs of disease (maybe because of undiagnosed lyme?). It was 53 pre-IVIG and 52 ten weeks post-IVIG. I asked the immunologist "if IVIG worked, shouldn't the compliment be much lower now?" and he thought probably yes, unless there was still an underlying infection. That, plus an Igenex test with 5 positive or IND bands, led us to lyme land. When we last tested it about a year ago, 7 months into lyme treatment, it was in the 20s. At the same time, his C3a was normal but C4a was elevated, suggesting a problem with ongoing mold exposure or long term lyme. Haven't tested it lately.

 

DD had elevated C3d when we first suspected PANS two yrs ago. Over her first year of being on the radar but not treated, C3d went from 20s to 50s to 90s. When it was in the 90s, we also did Cunningham test and got CamK 179 and anti-lysoganliosides >1200 which is the highest bracket. Other Cunningham results were borderline normal. When we last tested C3d last summer, 8 months into treatment with combo abx, it had fallen into the 20s. Her C3a was elevated but her C4a was normal. She is a high histamine kid with wicked seasonal allergies and allergies to penicillin, cephalosporins and any natural supplement derived from a weed (andrographis, oregano, resveratrol). But her IgE levels, eosinophils etc are normal.

 

Like I said, I can only stare at the research for just so long before I get dizzy. What are you wondering about complexes? I'm not sure I understood your question.

[kim]

I always get off the laptop feeling like i just got off one of those puke-inducing rides at Six Flags.

 

Thanks for your response LLM. Btwn you and Nancy, It's nice to get a chuckle here and there.

 

I'll explain why I was asking, then maybe I can ask you a couple of things that relate to your kids results specifically?

 

Ok, my original intention was to go back to the thread where we were discussing vaccines and post some review of the Meningococcal vaccine because there were a few comments there about that being one that parents worried about in particular (I do too). When one of my sons was horribly ill and hospitalized with EBV, the ped asked about vaccinations and I told him when we quit and what my son was not up to date on. He didn't really bat an eye, except for the "meningitis vaccine." I nearly hyperventilated in the wee morning hours thinking that I had signed a consent to treat form, and wondered if they could vaccinate him when I wasn't there. We were discussing that at the nurses station the next day and one said that she would have if a Dr. would have ordered it and one said that she would have waited for me to sign a seperate consent form. Anyway, this son tested negative on 3 seperate mono spot tests and EBV was only declared positive with additional antibody testing ordered by infectous disease Dr. I so wish that I would have asked the ID doc if there was any immune system red flags since he was negative on the mono spot.

 

It looks like deficiencies are the worrisome factor, not elevations in regards to meningitis? When discussing vaccines, it's important to remember that meningitis is a condition brought on by invasion of a bacteria. HIB, S pneumoniae, Neisseria meningitidis (meningococcus..the vaccine that most parents think of for their teen or college age kids) along with viral infections (usually a more mild disease) are all capable of causing meningitis. You are vaccinating against the bacteria, not really the "condition."

I'm finding Pubmed info easier to decipher relating to complement and meningitis.

 

http://www.ncbi.nlm.nih.gov/pubmed/1588179

The role of complement in the host's defense against Haemophilus influenzae.

 

http://www.ncbi.nlm.nih.gov/pubmed/20930072

Infections of people with complement deficiencies and patients who have undergone splenectomy.

 

Since there are many on this forum that have children that have some form of immune dysfunction or suspected immune dysfunction, it seems like a basic understanding of the statement in my original post might be important so that parents with good immuno Dr.s, can discuss it with them. If it's deficiency only, and most who have had testing show elevation, that would be good to know. By the same token, if a child has a deficiency in a complement component and could be more prone to a complication, well, that is something I would certainly consider in relationship to a vaccine decision.

Does that make more sense?

Edited March 7, 2012 by kim

[LNN]

So let me see if I have this right...

If you have a deficient complement system (and I understand that is a gross oversimplification, but I am dizzy fro reading your links and this is all I can manage), you are at greater risk for contracting both the 3 bacterial infections that cause meningitis and meningitis itself.

 

Deficiencies of the alternative and terminal complement pathways result in an almost exclusive predisposition to invasive meningococcal disease.

 

So you are the exact group most in need of vaccination against these bacteria, according to the PubMed article (whether we would agree and also whether the other ingredients of a vaccine are safe is a different matter). Most of our kids have probably been vaccinated against two of the three culprits

Three pathogens(organisms) are associated with 80%of cases of bacterial meningitis: Hemophilus influenza type b, Streptococcus pneumoniae (pneumococcus) and Neisseria meningitidis (meningococcus).

 

 

Haemophilus influenzae type b was the most commonly diagnosed bacterial meningitis in the United States in the 20th century and nearly all cases occur in children under age six. The H. influenzae type b (HIB) vaccine was introduced in 1988 for toddlers and, in 1991, for infants and is recommended by the CDC for children at two, four, six and 12-15 months.

 

Pneumococcal meningitis caused by Streptococcus pneumoniae is most frequently observed in adults over the age of 30 years but also can affect children. 84 different serotypes of S. pneumonia have been identified that are associated with bacterial pneumonia, pneumococcal meningitis, endocarditis, otitis media (middle ear infection), mastoiditis, sinusitis and conjunctivitis.

 

A pneumococcal vaccine containing 23 strains of pneumococcal is recommended by the CDC for adults over age 65. A pneumococcal vaccine containing 7 strains of pneumococcal was introduced in 2000 and recommended by the CDC for children at two, four, six and 12-15 months. A new version containing 13 pneumococcal strains was introduced in 2010.

 

Meningitis associated with Neisseria meningitidis is most often encountered in children and young adults. In 2005, a meningococcal vaccine was recommended by the CDC for 11 year olds and college students, especially freshman living in dorms on campuses. In 2010, the CDC expanded meningococcal vaccine recommendations to include a booster dose of meningococcal vaccine for all 16 year olds in addition to the first dose given to all 11-12 year olds.

 

If you have a complement deficiency, the risks of not getting vaccinated may be as great as not getting vaccinated - is that your point? (tho the efficacy of the vaccine is also a consideration - at least the menactra brand

Menactra protects against serotypes A, C, Y and W-135. However, the vaccine does not contain serotype B, which causes about one-third of all cases of meningococcal disease in the US. and more than 50 percent of cases in young infants. Therefore, in terms of preventing meningococcal disease in America, Menactra is ineffective 30 to 50 percent of the time, depending upon age.

Or do I have your point backward? I told you I was feeling nauseous...

 

After reading, my next questions are:

1. how do you test for a complement deficiency? Does having elevated C3d et al suggest there is no deficiency or do you need to look at C3b or some other complement measurement?

2. My bigger concern is how do you test for a CCP (complement control protein) deficiency, which seems to carry a greater risk for autoimmune problems

from Wiki

The complement system has the potential to be extremely damaging to host tissues, meaning its activation must be tightly regulated. The complement system is regulated by complement control proteins, which are present at a higher concentration in the blood plasma than the complement proteins themselves. Some complement control proteins are present on the membranes of self-cells preventing them from being targeted by complement. One example is CD59, also known as protectin, which inhibits C9 polymerisation during the formation of the membrane attack complex. The classical pathway is inhibited by C1-inhibitor, which binds to C1 to prevent its activation.

 

Ok...I need to wobble away for a bit.

[kim]

LLM,

 

I typed you a line by line reply last night, hit send and the whole thing disappeared (the heading was God Bless You LLM).

 

I think you and I were understanding things basically the same way though.

 

If you have a complement deficiency, the risks of not getting vaccinated may be as great as not getting vaccinated - is that your point? (tho the efficacy of the vaccine is also a consideration - at least the menactra brand

 

I think what you meant to say was that the risk of not getting vaccinated may be greater than getting vaccinated? If that was what you meant, I think I would agree. I would want to discuss it with a good Immun Dr. and find out what the odds were that protective antibodies would be formed with vaccination. One thing that I read looked like prop. antibiotics would be in order (vaccine wasn't mentioned) one, it was. So???

 

One thing that I do know, if my child had an inherited deficiency and there was a vaccine that could protect them from something deadly, I would be one grateful Mom. As many before me have said, it's not about being "anti vaccine," it's about being "pro informed choice," that parents are fighting for. This attitude of "do it or else," once a vaccine is formally added to the schedule is what's not acceptable IMO. Informed choice does require some time, but once you get into it a little, well, it seems it's time very well spent.

 

After reading, my next questions are:

1. how do you test for a complement deficiency? Does having elevated C3d et al suggest there is no deficiency or do you need to look at C3b or some other complement measurement?

2. My bigger concern is how do you test for a CCP (complement control protein) deficiency, which seems to carry a greater risk for autoimmune problems

from Wiki

 

#2 was what I was referring too, when I said something about "your kids results," in above post. I'm sure you have seen this page

http://labtestsonline.org/understanding/analytes/complement-levels/tab/test

 

C3 and C4 levels are the most frequently ordered, but others, such as C1 inhibitor, may be ordered when other deficiencies are suspected.

 

It seems they can test the C1 hibitor to see if it's deficient?

Once the wobblies stabilized did you find anything else?

[LNN]

I think what you meant to say was that the risk of not getting vaccinated may be greater than getting vaccinated? If that was what you meant, I think I would agree.

 

As many before me have said, it's not about being "anti vaccine," it's about being "pro informed choice," that parents are fighting for. This attitude of "do it or else," once a vaccine is formally added to the schedule is what's not acceptable IMO.

 

 

Yes, I meant to say that maybe this group of kids would be well served by the meningitis vaccine, despite it's risks. And you're right, getting tested for a complement deficiency would be a good idea. No, our immunologist never tested. (unless it's accurate to assume that if you mount high C3d you don't have an overall deficiency, but that's not what I get from trying to understand this stuff - it seems the problem isn't a lack of complement response, it's a lack of an "off" button to control the response.)

 

It would seem from my own kids' experiences that they are low on complement inhibitor proteins - thus the cytokine storms that wreck havoc in our lives. No problem getting complement to act like little Rambos attacking infection. Just lots of problems getting them back into the barracks.

 

I am not anti-vaccine either - just anti being mandated and anti accepting unnecessary risks from what's put into the vaccine to give it a longer shelf life. Make a vaccine that's in the body's best interest, not what maximizes the corporation's profits. Suck up a logistical inconvenience or cost and remove the dangerous preservatives and "inconvenience" of having to see a doctor for three separate shots instead of a more dangerous combo shot.

 

But let's say you did have a CCP deficiency but yet you still had a chronic infection to deal with (in my case, lyme).

1.if you did have a CCP deficiency, does a vaccination, intended to stimulate an immune response, make things worse? Which is the greater risk? Vaccinating and creating an unregulated storm or not vaccinating and being at risk for a serious/deadly infection?

2. What do you do to correct a CCP deficiency?

Edited March 9, 2012 by LLM

[JAG10]

Quote

 

Three pathogens(organisms) are associated with 80%of cases of bacterial meningitis: Hemophilus influenza type b, Streptococcus pneumoniae (pneumococcus) and Neisseria meningitidis (meningococcus).

 

 

Haemophilus influenzae type b was the most commonly diagnosed bacterial meningitis in the United States in the 20th century and nearly all cases occur in children under age six. The H. influenzae type b (HIB) vaccine was introduced in 1988 for toddlers and, in 1991, for infants and is recommended by the CDC for children at two, four, six and 12-15 months.

 

Pneumococcal meningitis caused by Streptococcus pneumoniae is most frequently observed in adults over the age of 30 years but also can affect children. 84 different serotypes of S. pneumonia have been identified that are associated with bacterial pneumonia, pneumococcal meningitis, endocarditis, otitis media (middle ear infection), mastoiditis, sinusitis and conjunctivitis.

 

A pneumococcal vaccine containing 23 strains of pneumococcal is recommended by the CDC for adults over age 65. A pneumococcal vaccine containing 7 strains of pneumococcal was introduced in 2000 and recommended by the CDC for children at two, four, six and 12-15 months. A new version containing 13 pneumococcal strains was introduced in 2010.

 

Meningitis associated with Neisseria meningitidis is most often encountered in children and young adults. In 2005, a meningococcal vaccine was recommended by the CDC for 11 year olds and college students, especially freshman living in dorms on campuses. In 2010, the CDC expanded meningococcal vaccine recommendations to include a booster dose of meningococcal vaccine for all 16 year olds in addition to the first dose given to all 11-12 year olds.

[JAG10]

1331376391[/url]' post='134281']

Quote

 

Three pathogens(organisms) are associated with 80%of cases of bacterial meningitis: Hemophilus influenza type b, Streptococcus pneumoniae (pneumococcus) and Neisseria meningitidis (meningococcus).

 

 

Haemophilus influenzae type b was the most commonly diagnosed bacterial meningitis in the United States in the 20th century and nearly all cases occur in children under age six. The H. influenzae type b (HIB) vaccine was introduced in 1988 for toddlers and, in 1991, for infants and is recommended by the CDC for children at two, four, six and 12-15 months.

 

Pneumococcal meningitis caused by Streptococcus pneumoniae is most frequently observed in adults over the age of 30 years but also can affect children. 84 different serotypes of S. pneumonia have been identified that are associated with bacterial pneumonia, pneumococcal meningitis, endocarditis, otitis media (middle ear infection), mastoiditis, sinusitis and conjunctivitis.

 

A pneumococcal vaccine containing 23 strains of pneumococcal is recommended by the CDC for adults over age 65. A pneumococcal vaccine containing 7 strains of pneumococcal was introduced in 2000 and recommended by the CDC for children at two, four, six and 12-15 months. A new version containing 13 pneumococcal strains was introduced in 2010.

 

Meningitis associated with Neisseria meningitidis is most often encountered in children and young adults. In 2005, a meningococcal vaccine was recommended by the CDC for 11 year olds and college students, especially freshman living in dorms on campuses. In 2010, the CDC expanded meningococcal vaccine recommendations to include a booster dose of meningococcal vaccine for all 16 year olds in addition to the first dose given to all 11-12 year olds.

 

I was one of the parents concerned about the meningitis conjugate vaccine. My girls are not protected from 2/3 because even though they were vaccinated, they failed to have an adequate response to all 14 serotypes as well as the Hib vaccine. Why would I think the meningococcus vaccine would even work for them? Both of my girls have C3D in the upper twenties, which is slightly elevated. The lab reference range used to have an upper limit of 8 the first time we tested, dd was 25. Retesting over a year later, she is still 25, but the reference range upper limit is now 25..... So I don't know how to qualify improvement?

If you follow Dr Jory Goodman's blog, he is a big T & A removal advocate. He had a patient with very elevated anti-DNAse B. Post surgery, the tonsils were tested to find no strep, but positive for Hib. ???? After the surgery, the DNAseB dropped indicating it was the Hib infection elevating the titer. I thought an Hib infection would put a kid in the hospital??? Does anybody who is just showing behavioral signs of illness test for Hib? Why are these titer tests that are supposed to be specific cross reacting?

[JAG10]

Here is a copy of Dr. Jory Goodman's reply I referred to in last post:

 

Hi Anonymous,

Jgoodman has commented on: "EVIL PANDAS: A Scourge on the Brain"

Subject: Good Info

Hi. This is the dat we need. I've had a boy with severe PANDAS (tics,Tourette's) and ADHD, Very high anti-DNAase B antibody. Only H. Flu intonsils. Complete remission and titre dropped to normal after surgery. Meansseveral things:

1. PANDAS is caused by many things other than strep (see my most recent postshere and on my own blog);

2. The antibody IS NOT specific for strep and may rise secondary to otherinfectious agents

3. Research obsessively focused on strep is too narrow and will miss manythings.

4. Another illustration that removal of T & A definitely benefits manypatients.

 

Happy to know your child is doing better. Thanks, Dr. G

 

You can view the comment at the following urlhttp://www.psychologytoday.com/comment_redirect/216712

 

 

Edited March 10, 2012 by JAG10

[kim]

LLM,

 

DD had elevated C3d when we first suspected PANS two yrs ago. Over her first year of being on the radar but not treated, C3d went from 20s to 50s to 90s.

"

 

Is there a "normal" range for this or do you gauge infection by a rising trend?

 

So you are the exact group most in need of vaccination against these bacteria, according to the PubMed article (whether we would agree and also whether the other ingredients of a vaccine are safe is a different matter). Most of our kids have probably been vaccinated against two of the three culprits

 

I know that you are most interested in the inhibitory aspect right now, but in regards to trying to figure out the risk/reward of the vaccine with no known deficiency, this is just a thought. Our kids get these vaccines in series. With each vaccine a more robust immune response is mounted (supposedly). What is considered a "protective," level is not achieved until the series is complete. If there was a problem here, especially an inherited deficiency, seems there would be a history of illness with these types of menningtis? S pneumonia infections, yes, but I don't think I know of a single case of a parent reporting a case of N.meningitis, either here or on the TS forum.

 

Anyway, these are a few excerpts from a CDC pdf. titled

 

Persons at Highest Risk of

Meningococcal Disease or

Suboptimal Vaccine Response

 

bolding mine

 

http://www2.erie.gov/wnypac/sites/www2.erie.gov.wnypac/files/uploads/pdfs/presentationchild.pdf

 

Very high antibody titer required to

compensate for complement deficiency

 

Serologic data are now available from the

manufacturer that show significant decline

in antibody 3-5 years after vaccination

although few breakthrough cases have

been reported

 

Ok, back to a deficiency in an inhibitory response. I know that I read recently that the antibody levels created by the HPV vaccine is higher than would be mounted in a natural response. Also, when I discussed the fact that my kids only received one varicella vaccine with their Dr. He suggeted titer testing and said if they didn't show immunity (from the 1 that they did get), that we might want to jump right to the shingles vaccine. No thank you. If I were going to do the 2nd one, I would want the lesser amt. of antigen in the reg varicella vax, because of just what you are thinking about. That was just instinct, I knew nothing about the immune system and still know very little.

 

In a perfect world, our children would be evaluated and there would be some information available to us, but that would be too costly and time consuming, so they recommend them and those who seem to benefit, great...those who end up injured or damaged, oh well. The greater good, ya know.

 

2. What do you do to correct a CCP deficiency?

 

No idea. Have you found anything?

Edited March 11, 2012 by kim

[kim]

Hi Anonymous,

Jgoodman has commented on: "EVIL PANDAS: A Scourge on the Brain"

Subject: Good Info

Hi. This is the dat we need. I've had a boy with severe PANDAS (tics,Tourette's) and ADHD, Very high anti-DNAase B antibody. Only H. Flu intonsils. Complete remission and titre dropped to normal after surgery. Meansseveral things:

1. PANDAS is caused by many things other than strep (see my most recent postshere and on my own blog);

2. The antibody IS NOT specific for strep and may rise secondary to otherinfectious agents

3. Research obsessively focused on strep is too narrow and will miss manythings.

4. Another illustration that removal of T & A definitely benefits manypatients.

 

 

Jag,

 

I'm confused about what he's saying here. I don't think many here would have a hard time believing that neuro symptoms can be caused from many things other than strep. "Epitope spreading," can be a factor too, another concept that I have very limited understanding of. Under #2 though, is he saying that anti-DNase B anitbody rose from H influenza and dropped post T&A????

As a side note, H influenza is not type B or HIB. Other strains of H. Influenza were known to increase with the introduction of the HIB vaccine. There are types a-f which are polysaccharide encapsulated and nonencapsulated strains that are referred to as non typeable/ NTHi.

 

edit...I should have read all of your posts Jag. I see now that you were basically asking the same questions.

Edited March 11, 2012 by kim

[kim]

There are two responses prior to this one. I'm just coming back as time permits.

 

Jag,

 

My girls are not protected from 2/3 because even though they were vaccinated, they failed to have an adequate response to all 14 serotypes as well as the Hib vaccine

 

I don't know how long ago your girls received the HIB vaccine, but I can't find anything that shows what titers would look like long term. There is something here about 1/2 way down.

 

http://cvi.asm.org/content/17/10/1639.full#ref-28

 

excerpt

 

However, this study showed that, despite the high reported Hib vaccination coverage in Mexico, there is a significant reduction of vaccine-induced seroprotection against Hib in the group aged 24 to 59 months, particularly among those children 30 to 47 months of age. This reduction in seroprotective titers suggests the potential need for providing one booster dose to prevent the threat of reemergence of Hib in children from 2 to 5 years of age, as has occurred elsewhere (5, 6, 8, 19, 23-25). The risk of Hib invasive disease occurs mostly during the first 2 years of life, but the risk remains for those between the ages of 24 and 59 months (9). Our findings support reports demonstrating decreased vaccine effectiveness associated with waning protective titers against Hib (20). The increasing use of Hib-CV and the removal of opportunities for natural boosting mean that maintaining long-lived immunity to Hib remains a significant challenge. These were some of the reasons behind the 2005 recommendation from the National Vaccination Council in Mexico to move from a three-dose regimen to a 4th-dose Hib schedule through an acellular pentavalent vaccine (DTaP-IPV/Hib), starting its implementation in 2007 (21).

 

If a significant reduction was shown btwm 24 and 59 months (after 3 vaccines), what would levels look like from a child say 5-10 years later, especially without a challenge by revaccination? Maybe there are better stats and I just didn't look hard enough, but I would really like to know if "failure," is really indicative an an immune problem.

 

Good info on HIB and H influenza here

 

http://emedicine.medscape.com/article/218271-overview#a0199

 

I think this is on the 2nd page

 

The Hib conjugate vaccine does not provide protection against NTHi strains. Since the widespread use of the Hib conjugate vaccine, NTHi has become more of a pathogen.

 

The NTHi strains colonize the nasopharynx in up to 80% of individuals. The spread of bacteria by direct extension to the eustachian tubes causes otitis media. Spread to the sinuses leads to sinusitis. Spread down the respiratory tract results in bronchitis and pneumonia. Eustachian tube dysfunction, antecedent viral upper respiratory tract infection (URTI), foreign bodies, and mucosal irritants, including smoking, can promote infection.

Edited March 12, 2012 by kim

[JAG10]

That's a good question about the Hib titers as children age. The lab reference range on her report indicates her level should be greater than 1.0 mcg/mL and my dd's was reported as 0.48 L (low)

 

Just a side note here.....one thing I've noticed in comparing my girls' labs from year to year (since late 2009 to present) is that the reference ranges are moving around quite a bit and all within Quest Laboratories. As mentioned above, the normal range for C3D used to have an upper limit of 8, now it is 25. Anti-DNAse B used to have an upper limit of 187 and now it is 376. I checked to make sure this was not happening due to their ages; it is not.

 

Regarding Goodman's comment regarding anti-DNAse B, yes...that is what he is intimating...that anti-DNAse B can rise from something other than strep. I have no idea was "epitope spreading" is, but I did read something about liver issues interfering with accurate results? I haven't been able to find much about anti-DNAse B that isn't related to strep though. Who would know about that? Someone with an expertise in strep??