Background: Recently, it has been suspected that there is a relationship between therapy with some antibiotics and the onset of autism; but even more curious, some children benefited transiently from a subsequent treatment with a different antibiotic. Here, we speculate how aminoglycoside antibiotics might be associated with autism. Presentation: We hypothesize that aminoglycoside antibiotics could a) trigger the autism syndrome in susceptible infants by causing the stop codon readthrough, i.e., a misreading of the
genetic code of a hypothetical critical gene, and/or b) improve autism symptoms by correcting the premature stop codon mutation in a hypothetical polymorphic gene linked to autism. Testing: Investigate, retrospectively, whether a link exists between aminoglycoside use (which is not extensive in children) and the onset of autism symptoms (hypothesis "a"), or between aminoglycoside use and improvement of these symptoms (hypothesis "b"). Whereas a prospective
study to test hypothesis "a" is not ethically justifiable, a study could be designed to test hypothesis "b". Implications: It should be stressed that at this stage no direct evidence supports our speculative hypothesis and that its main purpose is to initiate development of new ideas that, eventually, would improve our understanding of the pathobiology of autism.
Researchers are intrigued by the results of a new study that found treating autistic children with Vancomycin leads to a short-term improvement in symptoms.
First, parents clamored for the hormone secretin in hopes it would help their autistic children. Put to the test, however, secretin is proving disappointing. Now a new theory is triggering desperate parents' interest - and this time the stakes are higher because it could spur misuse of the nation's most precious antibiotic, vancomycin.
Some cases of late-onset (regressive) autism may involve abnormal flora because oral vancomycin, which is poorly absorbed, may lead to significant improvement in these children. Fecal flora of children with regressive autism was compared with that of control children, and clostridial counts were higher. The number of clostridial species found in the stools of children with autism was greater than in the stools of control children. Children with autism had 9 species of Clostridium not found in controls, whereas controls yielded only 3 species not found in children with autism. In all, there were 25 different clostridial species found. In gastric and duodenal specimens, the most striking finding was total absence of non-spore-forming anaerobes and microaerophilic bacteria from control children and significant numbers of such bacteria from children with autism. These studies demonstrate significant alterations in the upper and lower intestinal flora of children with late-onset autism and may provide insights into the nature of this disorder.
The scientists replaced a single atom from the molecular structure of vancomycin aglycon, a glycopeptide antibiotic that attacks the bacteria by inhibiting cell wall synthesis, significantly increasing the drug's spectrum of activity. In recent years, a number of the most common strains of enterococci have become resistant to vancomycin and use of the antibiotic has been under scrutiny. This re-engineering effort could help make the drug more effective in treating infections produced by vancomycin resistance enterococci (VRE), a serious and growing problem in the nation's hospitals.
Vancomycin is a macrolide glycopeptide class of antibiotic. It interacts with many drugs and may cause kidney, hearing, or balance dysfunction. Its adverse effects also include the following: skin rash, red neck, flushing, drug fever, low white blood cell count, increased eosinophil count in blood, allergic shock, low blood pressure, wheezing, and skin eruptions. Most of these reactions are seen only during injectable treatment. Vancomycin is one of our main-stays against multi-drug resistant life threatening infection with Staphylococcus aureas or antibiotic induced large gut infection. If it is misused by indiscriminate oral therapy as above, then the bacteria may become resistant to vancomycin also, and we will have lost another important battle against drug resistant bacteria. This is why doctors are still hesitant to prescribe vancomycin for autism till we have more conclusive data.