Desulfovibrio species are potentially important in regressive autism

Autism is a complex disorder with no specific diagnostic test so the disease is defined by its characteristics including cognitive defects, social, communication and behavioral problems, repetitive behaviors, unusual sensitivity to stimuli such as noise, restricted interests, and self stimulation. T...

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Published inMedical hypotheses Vol. 77; no. 2; pp. 270 - 274
Main Author Finegold, Sydney M.
Format Journal Article
LanguageEnglish
Published United States Elsevier Ltd 01.08.2011
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Online AccessGet full text
ISSN0306-9877
1532-2777
1532-2777
DOI10.1016/j.mehy.2011.04.032

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Abstract Autism is a complex disorder with no specific diagnostic test so the disease is defined by its characteristics including cognitive defects, social, communication and behavioral problems, repetitive behaviors, unusual sensitivity to stimuli such as noise, restricted interests, and self stimulation. The incidence of this disease has increased remarkably in recent years and was 110/10,000 children (∼1%) in multiple areas of the US in 2007. The financial burden on families and communities is enormous. In terms of predisposing factors, heredity plays a role in some subjects, but it is clear that environmental factors are also important. Environmental toxins can affect the immune system adversely. Intestinal bacteria are recognized by a few investigators as potentially important and we have proposed that certain antimicrobial drugs may be a key factor in modifying the intestinal bacterial flora adversely, selecting out potentially harmful bacteria that are normally suppressed by an intact normal intestinal flora. We had felt that clostridia in the gut might be involved in autism because they are virulent organisms and spore-formers; spores would resist antibacterial agents so that when antibiotics were discontinued the spores would germinate and by toxin production or another mechanism lead to autism. However, a recent study of ours employing the powerful pyrosequencing technique on stools of subjects with regressive autism showed that Desulfovibrio was more common in autistic subjects than in controls. We subsequently confirmed this with pilot cultural and real-time PCR studies and found siblings of autistic children had counts of Desulfovibrio that were intermediate, suggesting possible spread of the organism in the family environment. Desulfovibrio is an anaerobic bacillus that does not produce spores but is nevertheless resistant to aerobic and other adverse conditions by other mechanisms and is commonly resistant to certain antimicrobial agents (such as cephalosporins) often used to treat ear and other infections that are relatively common in childhood. This bacterium also produces important virulence factors and its physiology and metabolism position it uniquely to account for much of the pathophysiology seen in autism. If these results on Desulfovibrio are confirmed and extended in other studies, including treatment trials with appropriate agents and careful clinical and laboratory studies, this could lead to more reliable classification of autism, a diagnostic test and therapy for regressive autism, development of a vaccine for prevention and treatment of regressive autism, tailored probiotics/prebiotics, and important epidemiologic information.
AbstractList Autism is a complex disorder with no specific diagnostic test so the disease is defined by its characteristics including cognitive defects, social, communication and behavioral problems, repetitive behaviors, unusual sensitivity to stimuli such as noise, restricted interests, and self stimulation. The incidence of this disease has increased remarkably in recent years and was 110/10,000 children (∼1%) in multiple areas of the US in 2007. The financial burden on families and communities is enormous. In terms of predisposing factors, heredity plays a role in some subjects, but it is clear that environmental factors are also important. Environmental toxins can affect the immune system adversely. Intestinal bacteria are recognized by a few investigators as potentially important and we have proposed that certain antimicrobial drugs may be a key factor in modifying the intestinal bacterial flora adversely, selecting out potentially harmful bacteria that are normally suppressed by an intact normal intestinal flora. We had felt that clostridia in the gut might be involved in autism because they are virulent organisms and spore-formers; spores would resist antibacterial agents so that when antibiotics were discontinued the spores would germinate and by toxin production or another mechanism lead to autism. However, a recent study of ours employing the powerful pyrosequencing technique on stools of subjects with regressive autism showed that Desulfovibrio was more common in autistic subjects than in controls. We subsequently confirmed this with pilot cultural and real-time PCR studies and found siblings of autistic children had counts of Desulfovibrio that were intermediate, suggesting possible spread of the organism in the family environment. Desulfovibrio is an anaerobic bacillus that does not produce spores but is nevertheless resistant to aerobic and other adverse conditions by other mechanisms and is commonly resistant to certain antimicrobial agents (such as cephalosporins) often used to treat ear and other infections that are relatively common in childhood. This bacterium also produces important virulence factors and its physiology and metabolism position it uniquely to account for much of the pathophysiology seen in autism. If these results on Desulfovibrio are confirmed and extended in other studies, including treatment trials with appropriate agents and careful clinical and laboratory studies, this could lead to more reliable classification of autism, a diagnostic test and therapy for regressive autism, development of a vaccine for prevention and treatment of regressive autism, tailored probiotics/prebiotics, and important epidemiologic information.Autism is a complex disorder with no specific diagnostic test so the disease is defined by its characteristics including cognitive defects, social, communication and behavioral problems, repetitive behaviors, unusual sensitivity to stimuli such as noise, restricted interests, and self stimulation. The incidence of this disease has increased remarkably in recent years and was 110/10,000 children (∼1%) in multiple areas of the US in 2007. The financial burden on families and communities is enormous. In terms of predisposing factors, heredity plays a role in some subjects, but it is clear that environmental factors are also important. Environmental toxins can affect the immune system adversely. Intestinal bacteria are recognized by a few investigators as potentially important and we have proposed that certain antimicrobial drugs may be a key factor in modifying the intestinal bacterial flora adversely, selecting out potentially harmful bacteria that are normally suppressed by an intact normal intestinal flora. We had felt that clostridia in the gut might be involved in autism because they are virulent organisms and spore-formers; spores would resist antibacterial agents so that when antibiotics were discontinued the spores would germinate and by toxin production or another mechanism lead to autism. However, a recent study of ours employing the powerful pyrosequencing technique on stools of subjects with regressive autism showed that Desulfovibrio was more common in autistic subjects than in controls. We subsequently confirmed this with pilot cultural and real-time PCR studies and found siblings of autistic children had counts of Desulfovibrio that were intermediate, suggesting possible spread of the organism in the family environment. Desulfovibrio is an anaerobic bacillus that does not produce spores but is nevertheless resistant to aerobic and other adverse conditions by other mechanisms and is commonly resistant to certain antimicrobial agents (such as cephalosporins) often used to treat ear and other infections that are relatively common in childhood. This bacterium also produces important virulence factors and its physiology and metabolism position it uniquely to account for much of the pathophysiology seen in autism. If these results on Desulfovibrio are confirmed and extended in other studies, including treatment trials with appropriate agents and careful clinical and laboratory studies, this could lead to more reliable classification of autism, a diagnostic test and therapy for regressive autism, development of a vaccine for prevention and treatment of regressive autism, tailored probiotics/prebiotics, and important epidemiologic information.
Autism is a complex disorder with no specific diagnostic test so the disease is defined by its characteristics including cognitive defects, social, communication and behavioral problems, repetitive behaviors, unusual sensitivity to stimuli such as noise, restricted interests, and self stimulation. The incidence of this disease has increased remarkably in recent years and was 110/10,000 children (∼1%) in multiple areas of the US in 2007. The financial burden on families and communities is enormous. In terms of predisposing factors, heredity plays a role in some subjects, but it is clear that environmental factors are also important. Environmental toxins can affect the immune system adversely. Intestinal bacteria are recognized by a few investigators as potentially important and we have proposed that certain antimicrobial drugs may be a key factor in modifying the intestinal bacterial flora adversely, selecting out potentially harmful bacteria that are normally suppressed by an intact normal intestinal flora. We had felt that clostridia in the gut might be involved in autism because they are virulent organisms and spore-formers; spores would resist antibacterial agents so that when antibiotics were discontinued the spores would germinate and by toxin production or another mechanism lead to autism. However, a recent study of ours employing the powerful pyrosequencing technique on stools of subjects with regressive autism showed that Desulfovibrio was more common in autistic subjects than in controls. We subsequently confirmed this with pilot cultural and real-time PCR studies and found siblings of autistic children had counts of Desulfovibrio that were intermediate, suggesting possible spread of the organism in the family environment. Desulfovibrio is an anaerobic bacillus that does not produce spores but is nevertheless resistant to aerobic and other adverse conditions by other mechanisms and is commonly resistant to certain antimicrobial agents (such as cephalosporins) often used to treat ear and other infections that are relatively common in childhood. This bacterium also produces important virulence factors and its physiology and metabolism position it uniquely to account for much of the pathophysiology seen in autism. If these results on Desulfovibrio are confirmed and extended in other studies, including treatment trials with appropriate agents and careful clinical and laboratory studies, this could lead to more reliable classification of autism, a diagnostic test and therapy for regressive autism, development of a vaccine for prevention and treatment of regressive autism, tailored probiotics/prebiotics, and important epidemiologic information.
Autism is a complex disorder with no specific diagnostic test so the disease is defined by its characteristics including cognitive defects, social, communication and behavioral problems, repetitive behaviors, unusual sensitivity to stimuli such as noise, restricted interests, and self stimulation. The incidence of this disease has increased remarkably in recent years and was 110/10,000 children (∼1%) in multiple areas of the US in 2007. The financial burden on families and communities is enormous. In terms of predisposing factors, heredity plays a role in some subjects, but it is clear that environmental factors are also important. Environmental toxins can affect the immune system adversely. Intestinal bacteria are recognized by a few investigators as potentially important and we have proposed that certain antimicrobial drugs may be a key factor in modifying the intestinal bacterial flora adversely, selecting out potentially harmful bacteria that are normally suppressed by an intact normal intestinal flora. We had felt that clostridia in the gut might be involved in autism because they are virulent organisms and spore-formers; spores would resist antibacterial agents so that when antibiotics were discontinued the spores would germinate and by toxin production or another mechanism lead to autism. However, a recent study of ours employing the powerful pyrosequencing technique on stools of subjects with regressive autism showed that Desulfovibrio was more common in autistic subjects than in controls. We subsequently confirmed this with pilot cultural and real-time PCR studies and found siblings of autistic children had counts of Desulfovibrio that were intermediate, suggesting possible spread of the organism in the family environment. Desulfovibrio is an anaerobic bacillus that does not produce spores but is nevertheless resistant to aerobic and other adverse conditions by other mechanisms and is commonly resistant to certain antimicrobial agents (such as cephalosporins) often used to treat ear and other infections that are relatively common in childhood. This bacterium also produces important virulence factors and its physiology and metabolism position it uniquely to account for much of the pathophysiology seen in autism. If these results on Desulfovibrio are confirmed and extended in other studies, including treatment trials with appropriate agents and careful clinical and laboratory studies, this could lead to more reliable classification of autism, a diagnostic test and therapy for regressive autism, development of a vaccine for prevention and treatment of regressive autism, tailored probiotics/prebiotics, and important epidemiologic information.
Abstract Autism is a complex disorder with no specific diagnostic test so the disease is defined by its characteristics including cognitive defects, social, communication and behavioral problems, repetitive behaviors, unusual sensitivity to stimuli such as noise, restricted interests, and self stimulation. The incidence of this disease has increased remarkably in recent years and was 110/10,000 children (∼1%) in multiple areas of the US in 2007. The financial burden on families and communities is enormous. In terms of predisposing factors, heredity plays a role in some subjects, but it is clear that environmental factors are also important. Environmental toxins can affect the immune system adversely. Intestinal bacteria are recognized by a few investigators as potentially important and we have proposed that certain antimicrobial drugs may be a key factor in modifying the intestinal bacterial flora adversely, selecting out potentially harmful bacteria that are normally suppressed by an intact normal intestinal flora. We had felt that clostridia in the gut might be involved in autism because they are virulent organisms and spore-formers; spores would resist antibacterial agents so that when antibiotics were discontinued the spores would germinate and by toxin production or another mechanism lead to autism. However, a recent study of ours employing the powerful pyrosequencing technique on stools of subjects with regressive autism showed that Desulfovibrio was more common in autistic subjects than in controls. We subsequently confirmed this with pilot cultural and real-time PCR studies and found siblings of autistic children had counts of Desulfovibrio that were intermediate, suggesting possible spread of the organism in the family environment. Desulfovibrio is an anaerobic bacillus that does not produce spores but is nevertheless resistant to aerobic and other adverse conditions by other mechanisms and is commonly resistant to certain antimicrobial agents (such as cephalosporins) often used to treat ear and other infections that are relatively common in childhood. This bacterium also produces important virulence factors and its physiology and metabolism position it uniquely to account for much of the pathophysiology seen in autism. If these results on Desulfovibrio are confirmed and extended in other studies, including treatment trials with appropriate agents and careful clinical and laboratory studies, this could lead to more reliable classification of autism, a diagnostic test and therapy for regressive autism, development of a vaccine for prevention and treatment of regressive autism, tailored probiotics/prebiotics, and important epidemiologic information.
Author Finegold, Sydney M.
Author_xml – sequence: 1
  givenname: Sydney M.
  surname: Finegold
  fullname: Finegold, Sydney M.
  email: sidfinegol@aol.com
  organization: Infectious Diseases Section (111 F), VA Medical Center West Los Angeles, Los Angeles, CA 90073, United States
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Cites_doi 10.1086/341914
10.1099/jmm.0.46101-0
10.1038/nature09146
10.1016/j.neulet.2010.01.033
10.1080/13590840050000861
10.1016/j.anaerobe.2010.06.008
10.1128/AEM.70.11.6459-6465.2004
10.1093/ajcn/80.6.1611
10.1016/j.neuro.2006.03.017
10.1016/j.mehy.2007.07.019
10.1097/00004703-200604002-00010
10.1177/088307380001500701
10.3844/ajbbsp.2008.146.166
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References HSPH. Autism Has High Costs to U.S. Society. Harvard School of Public Health. 2006.
Emanuele, Orsi, Boso, Broglia, Brondino, Barale (b0070) 2010; 471
Finegold, Molitoris, Song, Liu, Väisänen, Bolte (b0035) 2002; 35
Niehus, Lord (b0065) 2006; 27
James, Cutler, Melnyk, Jernigan, Janak, Gaylor (b0075) 2004; 80
Song, Liu, Finegold (b0050) 2004; 70
Sandler, Finegold, Bolte, Buchanan, Maxwell, Vaisanen (b0030) 2000; 15
.
Waring, Klovrza (b0080) 2000; 10
Finegold, Dowd, Gontcharova, Liu, Henley, Wolcott (b0055) 2010; 16
Parracho, Bingham, Gibson, McCartney (b0040) 2005; 54
MacFabe, Rodriguez-Capote, Hoffman, Franklin, Mohammad-Asef, Taylor (b0060) 2008; 4
Centers for Disease Control. Autism and Developmental Disabilities Monitoring (ADDM) Network. Centers for Disease Control. 2008.
Finegold (b0045) 2008; 70
Pinto, Pagnamenta, Klei, Anney, Merico, Regan (b0010) 2010
Herbert, Russo, Yang, Roohi, Blaxill, Kahler (b0015) 2006; 27
Hollander, Anagnostou (b0005) 2008
Waring (10.1016/j.mehy.2011.04.032_b0080) 2000; 10
MacFabe (10.1016/j.mehy.2011.04.032_b0060) 2008; 4
Herbert (10.1016/j.mehy.2011.04.032_b0015) 2006; 27
Pinto (10.1016/j.mehy.2011.04.032_b0010) 2010
Finegold (10.1016/j.mehy.2011.04.032_b0035) 2002; 35
Finegold (10.1016/j.mehy.2011.04.032_b0055) 2010; 16
Song (10.1016/j.mehy.2011.04.032_b0050) 2004; 70
Parracho (10.1016/j.mehy.2011.04.032_b0040) 2005; 54
Niehus (10.1016/j.mehy.2011.04.032_b0065) 2006; 27
Sandler (10.1016/j.mehy.2011.04.032_b0030) 2000; 15
Emanuele (10.1016/j.mehy.2011.04.032_b0070) 2010; 471
10.1016/j.mehy.2011.04.032_b0025
Finegold (10.1016/j.mehy.2011.04.032_b0045) 2008; 70
James (10.1016/j.mehy.2011.04.032_b0075) 2004; 80
10.1016/j.mehy.2011.04.032_b0020
Hollander (10.1016/j.mehy.2011.04.032_b0005) 2008
References_xml – volume: 471
  start-page: 162
  year: 2010
  end-page: 165
  ident: b0070
  article-title: Low-grade endotoxemia in patients with severe autism
  publication-title: Neurosci Lett
– reference: Centers for Disease Control. Autism and Developmental Disabilities Monitoring (ADDM) Network. Centers for Disease Control. 2008. <
– volume: 4
  start-page: 146
  year: 2008
  end-page: 166
  ident: b0060
  article-title: A novel rodent model of autism: intraventricular infusions of propionic acid increase locomotor activity and induce neuroinflammation and oxidative stress in discrete regions of adult rat brain
  publication-title: Am J Biochem Biotechnol
– year: 2008
  ident: b0005
  article-title: Clinical manual for the treatment of autism
– reference: HSPH. Autism Has High Costs to U.S. Society. Harvard School of Public Health. 2006. <
– reference: >.
– volume: 27
  start-page: 671
  year: 2006
  end-page: 684
  ident: b0015
  article-title: Autism and environmental genomics
  publication-title: Neurotoxicology
– volume: 54
  start-page: 987
  year: 2005
  end-page: 991
  ident: b0040
  article-title: Differences between the gut microflora of children with autistic spectrum disorders and that of healthy children
  publication-title: J Med Microbiol
– volume: 15
  start-page: 429
  year: 2000
  end-page: 435
  ident: b0030
  article-title: Short-term benefit from oral vancomycin treatment of regressive-onset autism
  publication-title: J Child Neurol
– volume: 16
  start-page: 444
  year: 2010
  end-page: 453
  ident: b0055
  article-title: Pyrosequencing study of fecal microflora of autistic and control children
  publication-title: Anaerobe
– volume: 10
  start-page: 25
  year: 2000
  end-page: 32
  ident: b0080
  article-title: Sulphur metabolism in autism
  publication-title: J Nutr Environ Med
– volume: 70
  start-page: 508
  year: 2008
  end-page: 511
  ident: b0045
  article-title: Therapy and epidemiology of autism – clostridial spores as key elements
  publication-title: Med Hypotheses
– year: 2010
  ident: b0010
  article-title: Functional impact of global rare copy number variation in autism spectrum disorders
  publication-title: Nature
– volume: 27
  start-page: S120
  year: 2006
  end-page: S127
  ident: b0065
  article-title: Early medical history of children with autism spectrum disorders
  publication-title: Dev Behav Pediatr
– volume: 70
  start-page: 6459
  year: 2004
  end-page: 6465
  ident: b0050
  article-title: Real-time PCR quantitation of clostridia in feces of autistic children
  publication-title: Appl Environ Microbiol
– volume: 80
  start-page: 1611
  year: 2004
  end-page: 1617
  ident: b0075
  article-title: Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism
  publication-title: Am J Clin Nutr
– volume: 35
  start-page: S6
  year: 2002
  end-page: S16
  ident: b0035
  article-title: Gastrointestinal microflora studies in late-onset autism
  publication-title: Clin Infect Dis
– ident: 10.1016/j.mehy.2011.04.032_b0025
– volume: 35
  start-page: S6
  issue: Supp. 1
  year: 2002
  ident: 10.1016/j.mehy.2011.04.032_b0035
  article-title: Gastrointestinal microflora studies in late-onset autism
  publication-title: Clin Infect Dis
  doi: 10.1086/341914
– volume: 54
  start-page: 987
  year: 2005
  ident: 10.1016/j.mehy.2011.04.032_b0040
  article-title: Differences between the gut microflora of children with autistic spectrum disorders and that of healthy children
  publication-title: J Med Microbiol
  doi: 10.1099/jmm.0.46101-0
– year: 2010
  ident: 10.1016/j.mehy.2011.04.032_b0010
  article-title: Functional impact of global rare copy number variation in autism spectrum disorders
  publication-title: Nature
  doi: 10.1038/nature09146
– volume: 471
  start-page: 162
  year: 2010
  ident: 10.1016/j.mehy.2011.04.032_b0070
  article-title: Low-grade endotoxemia in patients with severe autism
  publication-title: Neurosci Lett
  doi: 10.1016/j.neulet.2010.01.033
– year: 2008
  ident: 10.1016/j.mehy.2011.04.032_b0005
– ident: 10.1016/j.mehy.2011.04.032_b0020
– volume: 10
  start-page: 25
  year: 2000
  ident: 10.1016/j.mehy.2011.04.032_b0080
  article-title: Sulphur metabolism in autism
  publication-title: J Nutr Environ Med
  doi: 10.1080/13590840050000861
– volume: 16
  start-page: 444
  year: 2010
  ident: 10.1016/j.mehy.2011.04.032_b0055
  article-title: Pyrosequencing study of fecal microflora of autistic and control children
  publication-title: Anaerobe
  doi: 10.1016/j.anaerobe.2010.06.008
– volume: 70
  start-page: 6459
  year: 2004
  ident: 10.1016/j.mehy.2011.04.032_b0050
  article-title: Real-time PCR quantitation of clostridia in feces of autistic children
  publication-title: Appl Environ Microbiol
  doi: 10.1128/AEM.70.11.6459-6465.2004
– volume: 80
  start-page: 1611
  year: 2004
  ident: 10.1016/j.mehy.2011.04.032_b0075
  article-title: Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism
  publication-title: Am J Clin Nutr
  doi: 10.1093/ajcn/80.6.1611
– volume: 27
  start-page: 671
  year: 2006
  ident: 10.1016/j.mehy.2011.04.032_b0015
  article-title: Autism and environmental genomics
  publication-title: Neurotoxicology
  doi: 10.1016/j.neuro.2006.03.017
– volume: 70
  start-page: 508
  year: 2008
  ident: 10.1016/j.mehy.2011.04.032_b0045
  article-title: Therapy and epidemiology of autism – clostridial spores as key elements
  publication-title: Med Hypotheses
  doi: 10.1016/j.mehy.2007.07.019
– volume: 27
  start-page: S120
  issue: 2
  year: 2006
  ident: 10.1016/j.mehy.2011.04.032_b0065
  article-title: Early medical history of children with autism spectrum disorders
  publication-title: Dev Behav Pediatr
  doi: 10.1097/00004703-200604002-00010
– volume: 15
  start-page: 429
  year: 2000
  ident: 10.1016/j.mehy.2011.04.032_b0030
  article-title: Short-term benefit from oral vancomycin treatment of regressive-onset autism
  publication-title: J Child Neurol
  doi: 10.1177/088307380001500701
– volume: 4
  start-page: 146
  year: 2008
  ident: 10.1016/j.mehy.2011.04.032_b0060
  article-title: A novel rodent model of autism: intraventricular infusions of propionic acid increase locomotor activity and induce neuroinflammation and oxidative stress in discrete regions of adult rat brain
  publication-title: Am J Biochem Biotechnol
  doi: 10.3844/ajbbsp.2008.146.166
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Snippet Autism is a complex disorder with no specific diagnostic test so the disease is defined by its characteristics including cognitive defects, social,...
Abstract Autism is a complex disorder with no specific diagnostic test so the disease is defined by its characteristics including cognitive defects, social,...
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SubjectTerms Autistic Disorder - etiology
Autistic Disorder - microbiology
Desulfovibrio - pathogenicity
Feces - microbiology
Humans
Internal Medicine
Models, Biological
Real-Time Polymerase Chain Reaction
Sequence Analysis, DNA
Title Desulfovibrio species are potentially important in regressive autism
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