Re: Re: Stan this research matches your statement that only 30% benefit from Valtrex/

[Guest guest]

Stan,

In your post you mentioned two times "if it's done right". Can I ask what you mean by this? Is there a right/wrong way to give Valtrex?

Sheryl

Re: Stan this research matches your statement that only 30% benefit from Valtrex/

You know, I wish I had time right now to catch up on the posts, but this one was on top and happened to catch my eye.I believe MORE than 30% of the children will improve with this therapy if it's done right and I think it's beyond the typical herpes connection. I don't believe we can test for all the herpes strain viruses and I believe that there may be a non-herpes connection to this therapy for some children.It seems to me that about half of the people who try this therapy end up with good results (if they do it right). Obviously we'll need to track that data to see if I'm right.I'll see you soon. Stan> > > >> > > > Journal of Neuroscience Research> > > >> > > >> > > > Evidence for Mycoplasma ssp., Chlamydia pneunomiae and Human > > Herpes> > > > Virus-6 Co-Infections in the Blood of Patients with Autistic > > Spectrum> > > > Disorders> > > > Garth L. Nicolson1 Gan1 L. Nicolson1 and > > Joerg> > > > Haier1,2> > > >> > > >> > > >> > > >> > > > 1The Institute for Molecular Medicine, Huntington Beach, > > California,> > > > USA,, 2Department of Surgery, University Hospital, Munster, > > Germany> > > >> > > >> > > >> > > >> > > >> > > >> > > >> > > >> > > >> > > > Correspondence: Prof. Garth L. Nicolson, Office of the > > President, The> > > > Institute for Molecular Medicine, 16371 Gothard Street H, > > Huntington> > > > Beach, California 92647. Tel: ; Fax: 714-596-> > 3791; Email:> > > > gnicolson@ <mailto:gnicolson@ ; Website:> > > > www.immed.org> > > >> > > >> > > >> > > >> > > >> > > > Running Title: Infections in Autistic Spectrum Disorders> > > >> > > >> > > > ABSTRACT. We examined the blood of 48 patients from Central > > and> > > > Southern California diagnosed with Autistic Spectrum > Disorders > > (ASD)> > > > using forensic polymerase chain reaction and found that a > > large subset> > > > (28/48 or 58.3%) of patients showed evidence of Mycoplasma > spp.> > > > infections compared to two of 45 (4.7%) age-matched control > > subjects> > > > (Odds Ratio=13.8, p<0.001). Since ASD patients have a high > > prevalence> > > of> > > > one or more Mycoplasma species and sometimes show evidence of> > > infections> > > > with Chlamydia pneumoniae, we examined ASD patients for other> > > > infections. Also, the presence of one or more systemic > > infections may> > > > predispose ASD patients to other infections, thus we > examined > > the> > > > prevalence of C. pneumoniae (4/48 or 8.3% positive, Odds > > Ratio=5.6,> > > > p<0.01) and Human Herpes Virus-6 (HHV-6, 14/48 or 29.2%, Odds> > > Ratio=4.5,> > > > p<0.01) co-infections in ASD patients. We found that> > > > Mycoplasma-positive and -negative ASD patients had similar> > > > percentages of C. pneumoniae and HHV-6 infections, > suggesting > > that> > > such> > > > infections occur independently in ASD patients. Control > > subjects also> > > > had low rates of C. pneumoniae (1/48 or 2.1%) and HHV-6 > (4/48 > > or 8.3%)> > > > infections, and there were no co-infections in control > > subjects. The> > > > results indicate that a large subset of ASD patients show > > evidence of> > > > bacterial and/or viral infections (Odds Ratio=16.5, > p<0.001). > > The> > > > significance of these infections in ASD is discussed in > terms > > of> > > > appropriate treatment.> > > >> > > >> > > >> > > > Key Words: Autism, Infection, HHV-6 virus, Chlamydia > > pneumoniae,> > > > Mycoplasma species,> > > >> > > >> > > > INTRODUCTION Autism was first identified in 1943 (Kanner, > > 1943), and> > > > these patients generally suffer from an inability to properly> > > > communicate, form relationships with others and respond > > appropriately> > > to> > > > their environments. Autism patients often display > repetitive > > actions> > > > and develop troublesome fixations with specific objects, and > > they are> > > > often sensitive to certain sounds, tastes and smells. > Autism > > patients> > > > do not all share the same signs and symptoms but tend to > share > > certain> > > > social, communication, motor and sensory problems that > affect > > their> > > > behavior in predictable ways (Berney, 2000). Autism and > > related> > > > disorders have been recently placed into a multi-disorder > > category> > > > called Autistic Spectrum Disorders (ASD), which includes > > autism,> > > > Attention Deficit Disorder (ADD) Attention Deficit > > Hyperactivity> > > > Disorder (ADHD) and other disorders (Keen and Ward, 2004). > The> > > criteria> > > > for diagnosis of ASD are, in general terms, the presence of > a > > triad of> > > > impairments in social interaction, communication and > > imagination (Wing> > > > et al., 2002). These signs and symptoms are thought to be > due > > to> > > > abnormalities in brain function or structure and are thought > > to have a> > > > genetic basis (Folstein and Rosen-Sheidley, 2001; Weenstra-> > Vanderweele> > > > et al., 2003). The incidence of ASD is currently estimated > at > > 1 in> > > > 1,000 children, and in genetically predisposed families the > > disorder> > > is> > > > ~100-times higher in incidence than in the general population> > > (Folstein> > > > and Rosen-Sheidley, 2002). The concordance rate in > > monozygotic twins> > > is> > > > 70-90%, whereas in dizygotic twins the rate is close to 0%, > > suggesting> > > a> > > > strong genetic component (Weenstra-Vanderweele et al., > > 2003). In> > > some> > > > patients there are also a number of other less specific > > chronic signs> > > > and symptoms. Among these are fatigue, headaches, > > gastrointestinal and> > > > vision problems and occasional intermittent low-grade fevers > > and other> > > > signs and symptoms that are generally excluded in the > > diagnosis of> > > ASD.> > > > These suggest that a subset of ASD patients may suffer from > > bacterial> > > or> > > > viral infections (Takahashi et al., 2001). There are > several > > reasons> > > > for this, including the nonrandom or clustered appearance of > > ASD,> > > > sometimes in immediate family members or particular regions, > > the> > > > presence of certain signs and symptoms associated with > > infection, the> > > > cyclic course of the illness and in some cases its response > to> > > > anti-microbial therapies. Although no single underlying > cause > > has> > > been> > > > established for ASD, there is growing awareness that ASD can > > have an> > > > infectious nature that may be a cofactor for the illness or > > appears as> > > > an opportunistic infection(s) that can aggravate patient > > morbidity> > > > (Takahashi et al., 2001; Libbey et al., 2005; Yamashita et > > al., 2003).> > > > Identifying systemic infections, such as those produced by > > Mycoplasma> > > > species (Huang et al., 1998; Nicolson et al., 2000; 2003a,b. > > 2005;> > > Nijs> > > > et al., 2002) Chlamydia pneumoniae (Chia and Chia, 1999; > > Nicolson et> > > > al., 2003a, and Human Herpes Virus-6 (HHV-6) (Braun et > al., > > 1997;> > > > Campadelli-Fiume et al., 1999; Nicolson et al., 2003a,, is > > likely to> > > > be important in determining the treatment strategies for > many > > ASD> > > > patients. These infections can penetrate the CNS and are > > associated> > > > with other neurological diseases (Nicolson et al., 2002). In> > > addition,> > > > heavy metal, chemical and environmental exposures also > appear > > to be> > > > important in ASD (Colborn, 2004; son et al., 2004; > > Eppright et> > > al.,> > > > 1996). Here we examined ASD patients to see if a subset of > > patients> > > show> > > > evidence of infection with Mycoplasma spp., C. pneumoniae or > > HHV-6.> > > > Since these infections can cause neurological signs and > > symptoms> > > > (Baseman and Tully, 1997; Nasralla et al., 1999; 2000; > > Nicolson et> > > al.,> > > > 2003a), they may be important in ASD. Previously we found > that> > > children> > > > of Mycoplasma-positive Gulf War veterans were over 18-times > > more> > > likely> > > > to come down with Mycoplasma fermentans than the general > > population,> > > and> > > > there was a high incidence of ASD in their children > (Nicolson > > et al.,> > > > 2003c). In addition, examination of a group of autism > > patients from> > > > civilian families revealed that there was a high incidence of> > > > mycoplasmal infections, including M. fermentans, M. > pneumoniae > > and M.> > > > hominis (Nicolson et al., 2005b). Since mycoplasmal > > infections can> > > > often be found as co-infections with C. pneumoniae or HHV-6 > > (Nicolson> > > et> > > > al., 2003a,b, 2005a), we examined ASD patients to see if > they > > had> > > > evidence of co-infections of Mycoplasma spp., C. pneumoniae > > and HHV-6.> > > >> > > > MATERIALS AND METHODS> > > >> > > > Patients> > > > All ASD patients (N=48) were from families in contact with > > patient> > > > support groups and were referred from Central and Southern > > California> > > > physicians after diagnosis with ASD according to the > > International> > > > Classification of Diseases (ICD-10) and the Diagnostic and > > Statistical> > > > Manual of Mental Disorders (DSM-IV). All patients were > > assessed by> > > the> > > > Autism Diagnostic Interview-Revised (ADI-R) (Lord et al., > > 1997) and> > > > Childhood Autism Rating Scale (CARS) (Van Bourgondien et > al., > > 1992;> > > > Pilowsky et al., 1998). Patients also underwent a medical > > history,> > > > completed a sign/symptom illness survey and had routine > > laboratory> > > > tests. Additionally, all parents were questioned about > > medication use> > > > during the three months prior to the study, and patients had > > to be> > > free> > > > of antibiotic treatment for two months prior to blood > > collection. Of> > > > the 48 patients, 42 were diagnosed with autism and six with > > Attention> > > > Deficit Disorder. Control subjects were from families > > recruited for> > > > unrelated studies (N=45), and they had to be free of any > > disease for> > > at> > > > least three months prior to data collection, and free of > > antibiotic> > > > treatment for three months prior to blood collection.> > > >> > > >> > > > Blood Collection> > > > Blood was collected in EDTA-containing tubes and immediately > > brought> > > to> > > > ice bath temperature as described previously (Nicolson et > al.,> > > > 2003a,b,c, 2005a; Nijs et al., 2002). Samples were shipped > > with wet> > > ice> > > > by overnight air courier to the Institute for Molecular > > Medicine for> > > > analysis. All blood samples were blinded. Whole blood (50 > > ml) was> > > used> > > > for preparation of DNA using Chelex (Biorad, Hercules, USA) > as> > > follows.> > > > Blood cells were lysed with nano-pure water (1.3 ml) at room> > > temperature> > > > for 30 min. After centrifugation at 13 000 x g for 2 min, > the> > > > supernatants were discarded. Chelex solution (200 ml) was > > added, and> > > > the samples were incubated at 56°C and at 100°C for 15 > minutes> > > > each. Aliquots from the centrifuged samples were used > > immediately for> > > > Polymerase Chain Reaction (PCR) or flash frozen and stored at> > > > -70°C until use. Multiple aliquots were used for experiments> > > on> > > > all patient samples.> > > >> > > >> > > >> > > > Detection of Mycoplasma by Forensic PCR.> > > >> > > > Amplification of the target gene sequences was performed in > a > > total> > > > volume of 50 ml PCR buffer (10 mM Tris-HCl, 50 mM KCl, pH 9)> > > containing> > > > 0.1% Triton X-100, 200 mm each of dATP, dTTP, dGTP, dCTP, > 100 > > pmol of> > > > each primer, and 0.5-1 mg of chromosomal DNA. Purified > > mycoplasmal DNA> > > > (0.5-1 ng of DNA) was used as a positive control for > > amplification.> > > > Additional primer sets were used to confirm the species > > specificity of> > > > the reaction (Nicolson et al., 2003a,b,c, 2005a). The > > amplification> > > was> > > > carried out for 40 cycles with denaturing at 94°C and > > annealing at> > > > 60°C (genus-specific primers and M. penetrans) or 55°C (M.> > > > pneumoniae, M. hominis, M. fermentans). Extension > temperature > > was> > > > 72°C in all cases. Finally, product extension was performed > at> > > > 72°C for 10 min. Negative and positive controls were present > in> > > each> > > > experiment. The amplified samples were run on a 1% agarose > gel> > > > containing 5 ml/100 ml of ethidium bromide in TAE buffer > (0.04 > > M> > > > Tris-Acetate, 0.001 M EDTA, pH 8.0). After denaturing and> > > > neutralization, Southern blotting was performed as described > > below.> > > >> > > >> > > >> > > > Chlamydia pneumoniae Detection by Forensic PCR.> > > >> > > > PCR detection of Chlamydia (Chlamydophila) pneumoniae was > done > > as> > > > described above for various Mycoplasma species, except that > the> > > > conditions and primers differ (Nicolson et al., 2003a,b, > > 2005a). PCR> > > > was carried out using the C. pneumoniae-specific primers:> > > >> > > > 5'-TGACAACGTTAGAAATACAGC-3' (upstream) and downstream> > > > 5'-CGCCTCTCTCTCCTATAAAT-3'. Additional primer sets were used > to> > > > confirm the species specificity of the reaction. The DNA was> > > amplified> > > > for 30 cycles using standard cycle parameters, and the > product> > > evaluated> > > > by agarose-gel electrophoresis. The efficiency of the PCR > > process was> > > > monitored by amplification of b-actin mRNA. The presence of> > > > amplifications inhibitors were evaluated by spiking negative > > samples.> > > > C. pneumoniae-specific oligonucleotides in the PCR product > were> > > > identified by Southern Blot and dot-blot hybridization using > a > > 21-mer> > > > internal probe:> > > >> > > > (5'-CGTTGAGTCAACGACTTAAGG-3') 3' end-labelled with> > > > digoxigenin-UTP or 32P-labeled probe.> > > >> > > >> > > >> > > > HHV-6 Detection by Forensic PCR> > > >> > > > PCR detection of HHV-6A was done as described above, except > > that the> > > > conditions and primers differ and plasma was used for > > polynucleotide> > > > isolation to detect active infections (Nicolson et al., > > 2003a,. PCR> > > > reactions were carried out using the following HHV-6A-> specific> > > primers:> > > >> > > > 5'-GCGTTTTCAGTGTGTAGTTCGGCAG-3' (upstream) and downstream> > > >> > > > 5'-TGGCCGCATTTCGTACAGATACGGAGG-3'. The nucleotides were> > > > amplified for 30 cycles using standard cycle parameters, and > > the> > > product> > > > evaluated by agarose-gel electrophoresis. The efficiency of > > the PCR> > > > process was monitored by amplification of b-actin mRNA. The > > efficiency> > > > of the PCR process was monitored by amplification of b-actin > > mRNA. The> > > > presence of amplification inhibitors were evaluated by > spiking> > > negative> > > > samples. HHV-6A-specific oligonucleotides in the PCR > product > > were> > > > identified by Southern Blot and dot-blot hybridization using > a > > 21-mer> > > > internal probe: (5'-ATCCGAAACAACTGTCTGACTGGCA-3') 3'> > > > end-labelled with digoxigenin-UTP or 32P-labeled probe.> > > >> > > >> > > > Southern Blot Confirmation> > > > The amplified samples were run on a 1% agarose gel in TAE > > buffer (0.04> > > M> > > > Tris-Acetate, 0.001 M EDTA, pH 8.0). After denaturating and> > > > neutralization, Southern blotting was performed as follows. > > The PCR> > > > product was transferred to a Nytran membrane. After > transfer, > > UV> > > > cross-linking was performed (Nasralla et al., 1999). > > Membranes were> > > > pre-hybridized with hybridization buffer consisting of 1x > > Denhardt's> > > > solution and 1 mg/ml salmon sperm DNA as blocking reagent. > > Membranes> > > > were then hybridized with digoxigenin-UTP or 32P-labeled > > internal> > > > probe (107 cpm per bag). After hybrization and washing to > > remove> > > > unbounded probe, the membranes were examined (digoxigenin-> UTP-> > labeled> > > > probe) or exposed to autoradiography film (32P-labeled > probe) > > for> > > 0.5-2> > > > days at -70°C (Nicolson et al., 2003a,b, 2005).> > > >> > > > The sensitivity and specificity of the PCR method for > > detection were> > > > determined by examining serial dilutions of purified DNA > from > > the> > > > microorganisms themselves in blood samples. Control DNA > > samples were> > > > provided by the American Type Culture Collection (Manasses, > > VA). The> > > > primers produced the expected amplification product size in > > all test> > > > species, which was confirmed by hybridization using the > > appropriate> > > > 32P-labeled internal probe (Nasralla et al., 1999). Amounts > as > > low as> > > a> > > > few fg of purified DNA were detectable for all species with > the> > > specific> > > > internal probes. There was no cross-reactivity between the > > internal> > > > probes of one species and the PCR product from another > species> > > (Nasralla> > > > et al., 2000; Nicolson et al., 2003a,b,c). The techniques > > used have> > > > been validated in various studies (for example, Berg et al., > > 1996;> > > > Bernet et al., 1995).> > > >> > > >> > > >> > > >> > > > Statistics> > > > Subjects' demographic characteristics were assessed using> > > > descriptive statistics and students' t-tests (independent > > samples> > > > test, t-test for equality of means, 2-tailed). The 95% > > confidence> > > > interval was chosen for minimal significance. Odds Ratios > were> > > > calculated using logistic regression (Logit method) > Statistica > > 5.5> > > > (Statsoft, Tulsa, OK). In some cases Pearson Chi-Square > test > > was> > > > performed to compare prevalence data between patients and > > control> > > > subjects.> > > >> > > >> > > > RESULTS> > > >> > > >> > > > Patients and Control Subjects> > > >> > > > ASD patients and control subjects were approximately similar > > in age> > > > (control subjects mean age = 8.4; ASD patients: mean age = > > 7.9). ASD> > > > patients differed significantly according to sex > distribution > > (p<> > > 0.05);> > > > 75% of the patients were male, whereas 25% of the patients > were> > > female.> > > > Similarly, 62.2% of control subjects were male, while 37.8% > > were> > > female.> > > > Patients were from Central and Southern California and > resided > > in> > > > approximately equally in rural and urban environments (Table > > 1).> > > >> > > >> > > >> > > > Bacterial and Viral Infections in ASD Patients> > > >> > > > Using PCR we examined ASD patients' blood for the presence of> > > > bacterial and viral infections. Evidence for Mycoplasma > spp.> > > > infections was found in 28/48 or 58.3% of ASD patients and > > 2/45 (4.7%)> > > > age-matched control subjects (Odds Ratio=13.8, p<0.001). C.> > > pneumoniae> > > > infections were found in 4/48 or 8.3% of ASD patients and in > > 1/45 or> > > > 2.1% of control subjects (Odds Ratio=5.6, p< 0.01). We also > > examined> > > > the incidence of HHV-6 infections in ASD patients and found > > that 14/48> > > > or 29.2% of ASD patients were positive compared to 4/45 > (8.8%)> > > positives> > > > in age-matched control subjects (Odds Ratio=4.5, p<0.01). > We > > did not> > > > find any multiple co-infections in control subjects (Table > > 2). The> > > rate> > > > of positive results in control subjects was similar to > previous> > > studies> > > > (Nasralla et al., 2000; Nicolson et al., 2003a,b,c, 2005). > The> > > > differences between infections in ASD patients and control > > subjects> > > were> > > > highly significant (Odds Ratio=16.5, p< 0.001). Significant> > > differences> > > > were not found in the prevalence of infections in urban and > > rural> > > > patients, in male or female patients or between autism and > > other ASD> > > > diagnoses.> > > >> > > >> > > >> > > > Multiple Co-Infections in ASD Patients> > > >> > > > We studied multiple infections in patients by examining > whether> > > patients> > > > who were positive (or negative) for one type of infection > also > > tested> > > > positive for other infections. Eight of 14 patients with > HHV-6> > > positive> > > > results (57.1%) were also positive for mycoplasmal > infections, > > whereas> > > > of the 6 out of 14 HHV-6-negative patients 50% were> > > mycoplasma-positive.> > > > C. pneumoniae infections were observed in two of four> > > > mycoplasma-positive ASD patients and two of four mycoplasma-> > negative> > > > patients. Thus we did not find a preference for particular > > multiple> > > > infections. Multiple mycoplasmal infections were found in > 12 > > of 48 or> > > > 25% of ASD patients; only M. fermentans plus other species > > were found.> > > > We examined 45 control subjects who did not show clinical > > signs and> > > > symptoms and found that only two were positive for a single > > mycoplasma> > > > species (Mycoplasma pneumoniae) (Table 2). Differences > > between ASD> > > > patients and control subjects were highly significant (Table > > 2).> > > >> > > >> > > >> > > > DISCUSSION> > > >> > > >> > > >> > > > Previously we found that chronic infections in Gulf War > > veterans> > > > diagnosed with Gulf War Illness could also be found in > > symptomatic> > > > family members, including their children (Nicolson et al., > > 2003c). In> > > > the families chosen for study chronic illnesses were not > > reported> > > until> > > > after the veteran in the family returned from the Gulf War.> > > > Interestingly, common diagnoses of illness in the children > of > > Gulf War> > > > veterans with mycoplasmal infections included ASD-like > > illnesses,> > > among> > > > others, and we found the same infection, primarily M. > > fermentans, in> > > > both the sick adults and children in these families. This > > suggested> > > > that the M. fermentans was likely passed from the veterans > to > > their> > > > children (Nicolson et al., 2003c). Although preliminary and > > not> > > > carefully analyzed or studied further, this result suggested > > that> > > > infections might be present in ASD patients. Therefore, we > > examined a> > > > small group of ASD patients (28 autism patients, age range 3-> > 12) in> > > > Central California for evidence of mycoplasmal infections, > and > > we> > > found> > > > that slightly over one-half were positive for one of four > > species of> > > > Mycoplasma (Nicolson et al., 2005b). In contrast to the > > children in> > > > military families where primarily one species of Mycoplasma > > was found> > > > (usually M. fermentans), the majority of ASD patients in > > Central> > > > California were found to have single or multiple mycoplasmal> > > infections> > > > involving M. pneumoniae, M. fermentans, M. hominis or M. > > genitalium.> > > We> > > > found similar results in the present study, but in addition > to> > > > infections with Mycoplasma spp., we also examined two other > > commonly> > > > found infections in chronically ill patients, C. pneumoniae > > and HHV-6> > > > (Nicolson et al., 2003a,. The results suggested that > > infections are> > > a> > > > common feature in ASD. Consistent with this hypothesis is > the > > finding> > > > that autism occurs at greater prevalence during periods of > more> > > frequent> > > > hospitalizations for bronchitis or pneumonia (Tanoue et al., > > 1988),> > > and> > > > maternal viral infections during the second trimester of > > pregnancy are> > > > associated with increased risk of autism in their offspring> > > (Ciaranello> > > > and Ciaranello, 1995; Wilkerson et al., 2002). Infections > are > > thought> > > > to play important roles in a variety of neurodevelopmental > > diseases,> > > > including ASD (Horning et al., 1999; Libbey et al., 2005; > > Nicolson et> > > > al., 2002). Such infections could be involved in the > etiology > > of the> > > > disease, or more likely they could cause co-morbid states > > (Nicolson et> > > > al., 2003a,b, 2005).> > > >> > > > We found higher prevalence of Mycoplasma spp. (Odds > > Ratio=13.8), C.> > > > pneumoniae (Odds Ratio=5.6) and HHV-6 (Odds Ratio=4.5) among > > children> > > > diagnosed with ASD compared to age-matched control subjects. > > The PCR> > > > techniques used in the present study have been validated in > > other> > > > studies (Nicolson et al., 2003a,b,c, 2005). There are some> > > similarities> > > > between the environmental exposures of Gulf War veterans and > > children> > > > with ASD. Both groups were given multiple vaccines prior to > > their> > > > illnesses, and heavy metals and chemicals have been found in > > both> > > groups> > > > (Boyd, 2004; Buttram, 2004; son et al., 2004; Eppright > et > > al.,> > > > 1996; Geier and Geier, 2004), but these findings are not > > universal> > > > ( and Garrod, 1978). There are reports of clinical > > improvement> > > > with treatment for these environmental exposures (reviewed > by > > Kidd,> > > > 2002).> > > >> > > > There were some limitations in the present study, including > > sample> > > size.> > > > Although all of the patients in the study were ASD patients, > > almost> > > all> > > > (42/48) had a diagnosis of autism. Removal of the other six > > patients> > > > from the analysis, however, did not change the results or > > conclusions.> > > > Other factors, such as geography, family socioeconomic > status,> > > > vaccination records and educational level were not analyzed.> > > >> > > > The infections found in ASD patients in the present and > > previous> > > studies> > > > (Libbey et al., 2003; Nicolson et al., 2003c; 2005; > Takahashi > > et al.,> > > > 2001; Yamashita et al., 2003) could have originated from > > vaccines or> > > > from opportunistic infections in immune suppressed children.> > > Bacterial> > > > contamination has been found in commercial vaccines, and in > > one study> > > 6%> > > > of commercial vaccines were contaminated with mycoplasmas > > (Thornton,> > > > 1986). Thus the appearance of infections in children > > diagnosed with> > > ASD> > > > may eventually be linked to the multiple vaccines received > > during> > > > childhood either as a source or from opportunistic > infections > > in> > > immune> > > > suppressed recipients of multiple vaccines. Although the > > etiology of> > > > ASD is currently unknown and thought to involve both genetic > > and> > > > environmental factors (Libbey et al., 2005; Lipkin and > Hornig, > > 2003),> > > > the infections found in ASD patients should be considered > > along with> > > > other factors in the management of these disorders (Kidd, > > 2002).> > > >> > > >> > > >> > > >> > > >> > > >> > > > REFERENCES> > > >> > > >> > > >> > > > Baseman J, Tully J. 1997. Mycoplasmas: sophisticated, > > reemerging, and> > > > burdened by their notoriety. Emerg Infect Dis 3:21-32.> > > >> > > > Berg S, Lueneberg E, Frosch M. 1996. 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Patient demographic data.> > > >> > > >> > > >> > > >> > > >> > > > N> > > >> > > > Mean age (SD)> > > >> > > > Range> > > >> > > > Males (%)> > > >> > > > Females> > > >> > > > (%)> > > >> > > > Patients> > > >> > > > 48> > > >> > > > 8.4 (2.8)> > > >> > > > 3-14> > > >> > > > 36 (75)> > > >> > > > 12 (25)> > > >> > > > Controls> > > >> > > > 45> > > >> > > > 7.9 (3.3)> > > >> > > > 4-11> > > >> > > > 28 (62.2)> > > >> > > > 17 (37.8)> > > >> > > > Rural patients> > > >> > > > 18> > > >> > > > 8.1 (2.9)> > > >> > > > 3-14> > > >> > > > 14 (77.7)> > > >> > > > 4 (22.3)> > > >> > > > Urban patients> > > >> > > > 30> > > >> > > > 8.6 (3.2)> > > >> > > > 4-14> > > >> > > > 22 (73.3)> > > >> > > > 8 (26.7)> > > >> > > >> > > >> > > >> > > >> > > >> > > > TABLE 2. Prevalence and Odds Ratio analysis of infections in > > ADS> > > > patients and control> > > >> > > > subjects.> > > >> > > > Type of infection> > > >> > > > ASD Patients> > > >> > > > N = 48 (%)> > > >> > > > Control Subjects> > > >> > > > N = 45 (%)> > > >> > > > Odds Ratio, p or Chi2> > > >> > > > HHV-6> > > >> > > > 14 (29.2)> > > >> > > > 4 (8.3)> > > >> > > > 4.5, p< 0.01> > > >> > > > C. Pneumoniae> > > >> > > > 4 (8.3)> > > >> > > > 1 (2.1)> > > >> > > > 5.6, p< 0.01> > > >> > > > Mycoplasma spp.> > > >> > > > 28 (58.3)> > > >> > > > 2 (4.7)> > > >> > > > 13.8, p< 0.001> > > > M. pneumoniae> > > > 16> > > >> > > > 2> > > >> > > > 9.2, p< 0.001> > > >> > > > M. fermentans> > > >> > > > 17> > > >> > > > 0> > > >> > > > 14.8, p< 0.001> > > >> > > > M. hominis> > > >> > > > 5> > > >> > > > 0> > > >> > > > 11.8, p< 0.01> > > >> > > > M. penetrans> > > >> > > > 1> > > >> > > > 0> > > >> > > > 6.6, p< 0.01> > > >> > > > Single mycoplasmal infection> > > >> > > > 16 (33.3)> > > >> > > > 2 (4.7)> > > >> > > > 13.8, p< 0.001> > > >> > > > Multiple mycoplasmal infections> > > >> > > > 12 (25.0)> > > >> > > > 0 (0)> > > >> > > > Chi2 = 11.7, p< 0.001> > > >> > > > M. fermentans +M. pneumoniae> > > >> > > > 7> > > >> > > > 0> > > >> > > > Chi2 = 4.7, p< 0.01> > > > M. fermentans +M. hominis> > > > 2> > > >> > > > 0> > > >> > > > Chi2 = 1.9, p< 0.3> > > >> > > > M. pneumoniae +M. hominis> > > >> > > > 1> > > >> > > > 0> > > >> > > > Chi2 = 1.4, p< 0.2> > > >> > > > M. fermentans +M. hominis + M. pneumoniae> > > >> > > > 2> > > >> > > > 0> > > >> > > > Chi2 = 1.9, p<0.2> > > >> > > > Mycoplasma + HHV-6> > > >> > > > 8 (16.7)> > > >> > > > 0 (0)> > > >> > > > Chi2 = 4.4, p< 0.01> > > >> > > > Mycoplasma + C. pneumoniae> > > >> > > > 2 (4.2)> > > >> > > > 0 (0)> > > >> > > > Chi2 = 2.1, p< 0.19> > > >> > > > C. pneumoniae + HHV-6> > > >> > > > 1 (2.1)> > > >> > > > 0 (0)> > > >> > > > Chi2 = 1.6, p< 0.3> > > >> > > > > > WOW THAT IS A LOT OF INFO AND I JUST CAME ACCROSS A LINK TO THE > PNNEUMONIAES AND ASTHMA AND TREATING THIS UNDERLYING VIRAL HAS CURED > COMPLETELY CURED ASTHMA FOR SOME PEOPLE. THEY ARE RECCOMENDING > ZITHROMAX ANTIBIOTIC, MAYBE IT HAS SOME USE FOR THOSE NOT RESPONDING > TO VALTREX PLUS I HAVE READ AUTISTIC KIDS SEEM BETTER ON > ANTIBIOTICS? I AM UNSURE TO ALL THE VIRUSES VALTREX TREATS BUT MAYBE > IT MISSES THE CHLAMYDIA AND MYCOPLASMA PNEUMONIAES, MAYBE SOMETHING > TO BE TESTING FOR REGARDLESS. THE SITE LINKING TO ASTHMA IS > ASTHMASTORY.COM AND YOU CAN LINK UP TO A FORUM THERE ALSO. I SUSPECT > IF ASTHMA RUNS IN A FAMILY IT MAY BE THAT THE VIRUSES WERE PASSED ON > FROM PERSON TO PERSON AND WHY SOME GET ASTHMA AND OTHERS DONT(AS OF > YET MAY BE THAT IT LAYS DORMANT AND MAY MANIFEST AS OTHER AUTOIMMUNE > DISORDERS LATER ON) IS A BIG QUESTION!!! PERHAPS ALSO SOME > TODDLERS/BABIES WHO COME IN CONTACT OR PASSED ON THROUGH MOTHERS > WOULD BE SUSEPTABLE TO ASTHMA/ALLERGIES/ EVEN AUTISM???? IT WOULD BE > INTERESTING TO TEST A MAJORITY OF OUR KIDS FOR THIS AND SEE, COULD > IT POSSIBLY BE A COMMON LINK???? SUPOSEDLY THIS AIRBORN VIRUS IS > VERY EASILY TRANSMITTED AS MUCH AS THE COLD VIRUS... > > > > > > > > > > > > > > > > > > -----------------------------------------------------------------> --> > ---------> > > --> > > > > >> > > > > > > > > -----------------------------------------------------------------> --> > ---------> > > --> > >> > > > > > > > > > > > > >