sf_mom

Judy, I am happy to speak with your friend in Northern CA... My son presented with mostly TICS and very mild OCD. I would have missed the OCD if it had not been pointed out to me. There are some fairly good resources for getting help in the Bay Area. You can PM and I'm happy to forward my phone number and e-mail address. -Wendy

I don't know about Dr. Latimer but Dr. Kovacevic has been treating PANDAS for 10 years and is about to publish his findings along side Mayo Clinic and John Hopkins..... Unfortunately, he is not published yet. I found him to be very compassionate, knowledgeable....... I got the feeling he is not stopping until there is a widely accepted treatment.

Wow! I wanted to add something I noticed pre rage in our son.... his pupils seem to be super dilated. Typically, I'll notice his eyes change about 15 minutes to 1/2 hour before the rage. When this occurs, I confirm other individuals in the room under the same light conditions are not as dilated and I know a rage is just around the corner. Thankfully, he has gotten much better.

Faith: Watch the video and I think it will answer some of your questions.

Yes.. I did this independently of any Dr's advice and more from OTHER parents recommendation. I'm only doing it for a short period of time - 14 days in total. When decreasing the antibiotic again and if there is another flair or increase in symptoms I will consult with Dr. K to see if a longer term increase should be considered. I'd say based on your son age and size increasing dose might be a consideration down the road. Give the current Augmentin dose a chance to work 'one month' and if you are seeing improvement I'd think you'd be fine until you see Dr. Latimer to help you make the decision.

There is a great video on-line http://www.tsa-usa.org/People/diagnosed/newly_diagnosed.html Dr. John T. Walkup. In the second or third hour he talks about defiant/oppositional behavior. Its very motivational and gives great suggestions. One important thing I learned watching the video is that a defiant child needs a structured routine that is down to the minute. If you are having difficulties then the routine is wrong. In our house its shower, eat... fully clothed and ready for school - reward is TV until its time to go. Otherwise no TV in the morning. He might get an additional 15 minutes of TV once he is ready for bed but that is all we allow so those couple of minutes are very special to him and he is motivated. I suspect as your daughter gets better the rages will get better but from now until then watch the video. It really helped us. -Wendy

Same here... pale skin and dark circles under his eyes. It was so bad his preschool teacher and an immunologists mentioned it to me. Two other weird symptoms were cradle cap 'dry scalp' at 5 1/2 and chapped lips all the time. ALL symptoms are gone 4 weeks post IVIG. He is on 250 m.g. Azithromycin daily and 45 pounds. I would say try upping his prophylactic dose of azithromycin. Our son complained of a sore throat about 10 days ago and both rapid/cultured strep test were negative. We saw a flair in symptoms and his younger twin brother and sister were sick. We upped his dose and all symptoms disappeared in 48 hours. -Wendy

Welcome and so sorry to hear that your son is so ill but you are definitely heading down the right path to get him proper help!! I would say the first thing you need to do is switch antibiotics to either Augmentin or Azithromycin and potentially up the daily dose depending on current strength. Have his CaM Kinase tested if you haven't already through Madeleine Cunningham. There has been great success with both IVIG and PEX for most children and due to your son's age it should be a consideration. Often anti-anxiety meds are not recommended as PANDAS children often do not respond well. I think others on the forum can speak more directly to this issue as we never pursued that route. Our son is on 250 m.g. Azithromycin per day, he is 5 1/2 years old, 45 Pounds, CaM Kinase 124, Failed 10 of 14 STREP PNEUMOCOCCAL ANTIBODY TITER, 4 weeks post IVIG, currently symptomless and had a sudden on-set June 24th.... we think he was probably sick much longer, approximately 1 1/2 years Hang in there... I'm positive many more will respond this morning.

We see Dr. Lewis on Thursday and I'll be curious as to 'THE STUDY'. I'm also going to send my son's friend to him 'the one who had Scarlet Fever when our kids got sick' and who is also PANDAS. Our son's friend recent Anti-DNase-B was 680, his CaM Kinase was 147, he failed 12 of 14 pnumococcal titers and was exposed to strep 8 days ago (was on 5 day Predisone steroid burst when exposed). As a result, Dr. Lewis is hopefully starting to see similarities between children. I'll let you know what happens. -Wendy Hi EAMom, We saw Dr. E. Richard Stiehm and Dr. Roger Kobayashi at UCLA. They recommended the vaccine to diagnose Specific Antibody Deficiency because my son was within normal limits on all IGs and IGG subclasses. I'm guessing the recommendation to vax and test titers is based on his health history, plus the fact that he failed a number of the Prevnar titers. Also, they see it as a way to possibly protect him from a 7th pneumonia (if the vaccine works). They did the vaccine down at Lucile Packard's pediatric pulmonology/immunology clinic because that's where our pulmonologist, Dr. Milla, is. Dr. Lewis is also getting into the picture now because I made an appointment with him for December when we thought we weren't going to do the vaccine. So he's the one who signed off on the vaccine order (and I found out from the lab tech had extra blood drawn for his "study" which we weren't told about before I asked what the extra vial was for - will be curious to find out what that's all about.)

Dawn, So glad your son is doing better as well. Can't wait to hear how the increased dose of Augmentin works. Seems like it is doing the trick for most. -Wendy Shelly, Hello. I am pretty certain you are the ones across the hall from us when we had our son out in Chicago. I am glad you got a different abx and it's working w/o the tummy troubles and things are improving for your girl. Our first two weeks have been up and down. The first week was pretty rocky; the second week more like waves. The symptoms have waxed & waned, not nearly as intense or as long lived. This morning was pretty rough, but he is doing better. Felt like a one step back day. We emailed Dr. K a couple days ago with our concern that boosting the immune system with IVIG and fighting an resistant strep infection on only 500 mg Augmentin a day at the same time may prove difficult post IVIG. (His titers have been very high & higher He replied immediately and increased the Augmentin to 875mg/2x day for 14 days. Now we're pushing the probiotic a bit harder. Evan has complained of some stomach issues, but I think we're doing better. I know Augmentin can be a tough one for some. I'm anxious to see what this next week brings. Thanks again for treating us to Starbucks! It was great to meet you folks. Dawn

Fantastic News.... My hope of all hopes would never to see a relapse as it feels like we've come so far. BUT, as you said, I now know what to do. I'm glad your daughter is doing better. -Wendy

We are four weeks post IVIG.... We had some post rages but I would say the BIG difference was I had the ability to reason with my son. Prior to IVIG we didn't. Also when he raged after it was mostly about something like 'accidentally dropping/breaking' his Leggo car. His rage was never directed at someone or himself. Each rage has gotten milder, he has become more reasonable and they have become further apart. I witnessed one small mood switching on Friday about accidentally letting a balloon go but otherwise we haven't really witnessed one in well over a week. Hang in there.

Yes! Dr. K pointed out our son had a stomach bug at time pre - IVIG appointment with low grade fever... and, younger son had been in the hospital 5 days and was extremely sick when IVIG was administered. Both my son's rebounded immediately after treatment.

Swedo talks about this type of Chorea on one of the on-line talks she gives. One of the immunologist we saw that knew nothing about PANDAs said our son also had Chorea but it was more in the way he moved his head at peak of symptoms. I would say our son is very close to TIC free...... I'll keep you posted as we are only 4 weeks post IVIG. -W When my daughter holds out her hands, she can't hold her fingers steady, she looks like she is playing a piano. That shows that the basal ganglia is inflamed, and shows that even though the strep titer test was negative,(we do however always culture positive), her brain has been effected by the strep, and it will most likely show up on the Cunningham lab work.

Its unfortunate but 'vigilance' along with IVIG/PEX and prophylactic antibiotics is more likely the cure for now. Is the Dr. in your area a immunologists and have you investigate the underlying issues? If not I would also suggest you start down that path immediately as monthly IVIG might be more of a resolution after initial treatment. BUT, we saw a huge improvement after the initial treatment with Dr. K. We are four weeks post and he is almost symptom free but are not ruling out additional IVIG to boost immune system if required. There is hope... Hang in there.

Specifically http://www.webpediatrics.com/pandasclinicalcases.html at the bottom of the page Dr. K discusses 'Adolescent-Adult Variation of PANDAS is under review!' You can consult with him via e-mail and phone. Primary treatment is IVIG and antibiotics. -Wendy

Part of the other article. Reduced Ability of Penicillin to Eradicate Ingested Group A Streptococci from Epithelial Cells: Clinical and Pathogenetic Implications Edward L. Kaplan,1,a Gursharan S. Chhatwal,2 and Manfred Rohde2 1 Department of Pediatrics, University of Minnesota Medical School, Minneapolis, Minnesota; and 2Department of Microbial Pathogenesis; Helmholtz Centre for Infection Research, Braunschweig, Germany Background. Group A streptococci (Streptococcus pyogenes; GAS) invades human epithelial cell lines. Failure of penicillin to eradicate GAS from the throats of patients, especially those who are GAS “carriers,” has been increasingly reported. However, there has been no comprehensive evaluation of how effectively antibiotics that are used to treat GAS enter upper respiratory tract epithelial cells and kill internalized GAS. We examined the viability of ingested, intracellular GAS after epithelial cell exposure to antibiotics commonly recommended for therapy of GAS infections. Methods. A human laryngeal epithelial cell line (HEp-2) was used. Three techniques were used to study antibiotic (penicillin V, erythromycin, azithromycin, cephalothin, and clindamycin) killing of ingested GAS: ex- amination by electron microscopy of ultrathin sections of ingested GAS, qualitative determination of intra–epithelial cell antibiotic, and special stain evaluation of intracellular GAS viability after epithelial cell exposure to antibiotics. Results. GAS survived intracellularly despite exposure of the GAS-containing epithelial cells to penicillin. In contrast, there was killing of ingested GAS after exposure of epithelial cells to either erythromycin or azithromycin. Electron microscopy confirmed a lack of intracellular GAS fragmentation (cell death) after exposure of epithelial cells to penicillin in contrast to obvious GAS fragmentation after epithelial cell exposure to erythromycin or azithromycin. Cephalothin, a cephalosporin, and clindamycin were more effective in killing ingested GAS than was penicillin, but they were less effective than erythromycin or azithromycin. Conclusions. These observations strongly suggest that if the GAS upper respiratory tract carrier state results from intra–epithelial cell GAS survival, the failure of penicillin to kill ingested GAS may be related to a lack of effective penicillin entry into epithelial cells. These unique observations may have clinical implications for un- derstanding GAS respiratory tract carriers and managing GAS infections.

The article EAMom provided is much more helpful than my theory. 'Amoxicillin failure in strep throat.' A pair of newly detected actions of Group A streptococci may offer clues as to why penicillin and amoxicillin of ten fail to eradicate streptococcal pharyngitis in children and adults, and why cephalosporins or macrolides may be better treatment options. Penicillin failure in eradicating strep throat has been increasingly documented beginning in the 1980s, rising from just 5% in the 1950s to approximately 35% today. My colleague Dr. Janet R. Casey and I have published a series of articles over the years documenting this phenomenon, as have other researchers worldwide. In 2004, Dr. Casey and I conducted two separate meta-analyses demonstrating the clear superiority of cephalosporins--mainly azithromycin and clarithromycin--over penicillin in treating strep throat, both in children (Pediatrics 2004;113:866-82) and adults (Clin. Infect. Dis. 2004;38:1526-34). Traditional antibiotic resistance does not appear to be the reason. In fact, there is absolutely no in vitro resistance of group A streptococci (GAS) to penicillin or amoxicillin (or cephalosporins). Some people have theorized that the inadvertent inclusion of strep carriers in many of the studies explains the eradication failure with penicillin, but that has never made sense to me. Why would such inclusion have increased since the 1950s? In fact, the opposite has happened: Efforts have been made in more recent studies to exclude carriers. Our meta-analyses showed that the failure rate remained pretty much rocksolid at 35%, even when we looked at only the 12 most recent studies that did a fantastic job of excluding carriers. I think the answer lies in considering mechanisms of "resistance" beyond those involving a particular bacterium resisting a particular drug in a test tube. There are two newly appreciated phenomena that I categorize as "in vivo resistance" because they result from a fundamental interaction with the host and can't be measured by a lab test. About 5 years ago, several researchers published studies showing that streptococci were capable of entering and living inside the epithelial cells of the upper respiratory tract, a process dubbed "internalization." Prior to that time, GAS was thought to be a strictly extracellular pathogen. Then, just last year, Dr. Edward L. Kaplan of the University of Minnesota and his associates showed for the first time that internalization was a likely explanation for the treatment failure of penicillin and amoxicillin, which are incapable of penetrating the cell wall. In contrast, erythromycin and azithromycin, which enter cells easily, were the most effective at GAS eradication while the first-generation cephalosporin cephalothin and clindamycin had intermediate efficacy (Clin. Infect. Dis. 2006;43:1398-406). A second mechanism of in vivo resistance, known as "coaggregation," was first described in 2004 by Dr. Eric R. LaFontaine and his associates at the University of Toledo (Ohio). They found that the pathogens Streptococcus pyogenes and Moraxella catarrhalis colonize overlapping regions of the human nasopharynx, and that M. catarrhalis can dramatically increase the adherence of S. pyogenes to human epithelial cells (Infect. Immun. 2004;72:6689-93). Subsequent to that paper, my laboratory group completed a study in which we confirmed Dr. LaFontaine's finding regarding coaggregation of S. pyogenes with M. catarrhalis, and also for the first time demonstrated the same phenomenon with S. pyogenes and Haemophilus influenzae. With coaggregation, the GAS bacteria acquire the ability to attach themselves to the M. catarrhalis or H. influenzae that already colonize the throat at various times during childhood and adulthood (H. influenzae is about 5-6 times more common than M. catarrhalis). While these two organisms have long been known to become pathogenic in certain settings, we are now realizing that they also may serve to enhance the attachment of GAS to throat cells. Indeed, coaggregation is a likely explanation for why some children--such as those more frequently colonized with M. catarrhalis or H. influenzae--are more vulnerable to strep throat than others. Moreover, it also explains our finding that an individual who is colonized with one of those two organisms and then is exposed to streptococcus has a 10-fold increased likelihood of developing strep throat. It also helps explain the differential treatment effect of penicillin/amoxicillin versus other antibiotic classes. Both M. catarrhalis and H. influenzae produce beta-lactamase, which inactivates penicillin and amoxicillin. Cephalosporins, on the other hand, have greater activity in the presence of beta-lactamase, while macrolides such as azithromycin are completely immune to the enzyme. Thus, it appears that beta-lactamase production, a well-described mechanism for in vitro antimicrobial resistance, is being enhanced by this additional coaggregation mechanism. Based on this new information, my practice now uses cephalosporins as first-line treatment for strep throat. Cephalexin is a good option because it's generic, and it's first-generation, so it is not as broad-spectrum. We prescribe it twice daily for 10 days. Second choice would be either a second-or third-generation cephalosporin or azithromycin, depending upon the degree of macrolide resistance in your community. Here in Rochester, where macrolide resistance is about 8%, we normally go with cefprozil, cefdinir, or cefpodoxime. All three are generic, although they're still not cheap--there's currently only one distributor. Cefprozil is the least expensive of the three, and there also is evidence that it eradicates the strep carrier state as well as the active infection (Clin.Ther. 2001;23:1889-900). The Infectious Diseases Society of America is planning to issue new guidelines for the treatment of streptococcal pharyngitis sometime in 2008. Dr. Kaplan is the chairman of the writing committee, and Dr. Casey is a member. The American Academy of Pediatrics" 2006 Red Book still recommends amoxicillin as first-line therapy, but I'm guessing that will not be the case in the next edition, due out in 2009. I have no financial conflicts that are relevant to this article. DR. PICHICHERO, a specialist in pediatric infectious diseases, practices in Rochester, N.Y. He is also professor of microbiology, immunology, pediatrics, and medicine at the University of Rochester. Write to Dr. Pichichero at our editorial offices (pdnews@elsevier.com).

I would also love to hear more about your story..... Our son just completed IVIG about 4 weeks ago and we are trying to figure out the long term plan regarding additional IVIG considering current deficiencies and antibiotics. Our son is 45 pounds and on Azithromycin 250 m.g./per day no problem. Thanks, Wendy

Debbie: I have my own theory and I'm definitely not a Dr. but I believe it is a really difficult strain of strep to eradicate. If you look closely at the information regarding the coccoid strain it is encapsulated making it resistant to certain drugs. Based on conversations with Diana Polhman of PANDAS Network and her visit with Madeleine Cunningham penicillin will just roll right of certain strains of strep in a petri dish. I think azithromycin has the ability to penetrate the encapsulation. 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. Clinical significance of Coccoid Bacteria Important human pathogens caused by coccoid bacteria include staphylococci infections, some types of food poisoning, some urinary tract infections, toxic shock syndrome, gonorrhea, as well as some forms of meningitis, throat infections, pneumonias, and sinusitis.[4]

I would definitely e-mail Diana at PANDASNetwork.org as I think there is a Dr. in the LA area who treats. Dr. Gupta (Not sure if I'm getting the spelling correct)

Copied the whole post and sent it to Diana.

I just sent the information to Diana.

WOW, way to go..... I think you'll see GREAT results as you move forward.

You can always crush pills and put in a small amount of liquid. We did this when our 5 1/2 month old baby needed daily aspirin. I think they sell them at pharmacies... we got ours from the hospital.