The use of antibiotics is ubiquitous among children and adults for bacterial infections, and they are often also prescribed for viral infections. This prolific use is inducing microbial resistance to previously effective antibiotics and rendering them less effective or ineffective against dangerous human pathogens. For example, multidrug-resistant strains of Mycobacterium tuberculosis seriously threaten tuberculosis (TB) control and prevention efforts. Administration of broad-spectrum antibiotics has a profound effect on the normal flora and can result in colonization with antibiotic-resistant organisms. Antibiotic-mediated disruption of the normal flora can lead to fungal infections, such as invasive candidiasis, or to antibiotic-associated colitis caused by Clostridium difficile.
Several neurological or neuropsychiatric conditions, such as autism may have gastrointestinal etiology. Published data lend credence to the notion that an alteration in bowel microflora may be associated with autistic symptoms.
It has been discovered that disruption of gastrointestinal flora or poorly developed gastrointestinal flora in young infants and subsequent pathogenic microbial proliferation in regions of the gastrointestinal tract can mediate disruptions of neurological function. These neurological disruptions are mediated by toxins, or profound metabolic disturbances related to the metabolism of the offending organism (e.g. sulfate metabolism problems related to the utilization of sulfate by Desulfovibrio) which extends to disrupting the protective mucin layer of the GI tract which is made up of sulfated glycoprotein which can result in inflammation and increased permeability of the gut particularly neurotoxins, produced by one or more species of the proliferating microbes. Bacteria of several genera are indicated as the likely causative agents and/or their toxins. The toxins can be potent, non-necrotizing neurotoxins that disrupt neurotransmitter release.
Dr. Sydney M. Finegold of the Department of Veterans Affairs has developed an autism treatment that involves antibiotics to target causative agents followed by repopulating the gastrointestinal tract with normal flora. Specifically, this is a method for treating autism associated with Desulfovibrio overgrowth in the gastrointestinal tract of a patient. The method comprises administering a treatment course of aztreonam and a beta-lactamase inhibitor (clavulanic acid, tazobactam, sulbactam, and LK-157). A gastrointestinal sample is taken from a patient and screened for the presence of the abnormal organism or certain toxic substances. If the agent is of the genus Clostridium or Desulfovibrio the antimicrobial is administered to suppress or eradicate the abnormal organism, then the normal flora is repopulated by the administration of at least one of the normal gut inhabitants.
Additional disorders that can be treated in this manner include attention deficit disorder, depression, bipolar disorder, juvenile diabetes, primary sclerosing cholangitis, Alzheimer’s disease, Parkinson’s disease, Whipple’s disease, Tourette’s syndrome, juvenile rheumatoid arthritis, adult rheumatoid arthritis, multiple sclerosis, Asperger’s syndrome, pervasive development disorder, autism (especially early onset and regressive autism), Rhett’s syndrome, D-lactic acidosis, obesity, atherosclerosis and atherosclerotic heart disease, chronic fatigue syndrome, Gulf War illness, post-traumatic stress disorder and schizophrenia.
Experiments conducted with late-onset autistic children have demonstrated success using methods of this treatment approach. The inventors have recorded significant improvement in the symptoms of children with delayed-onset autism by providing them with antibiotics directed toward common anaerobic intestinal bacteria.
This research is protected by US patents 10,130,614, and 9,707,207.
- Initial data shows significant improvement in the symptoms of children with delayed-onset autism
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