INTERNATIONAL

Researchers have many theories about what causes autism, but Ellen Bolte recently advanced one of the most fascinating: that some cases of autism stem from chronic tetanus infections.

Studies show, Bolte says, that "very small amounts of tetanus neurotoxin injected directly into the brains of laboratory animals create a stereotyped behavior syndrome" including repetitive sniffing, gnawing, and run-ning Animals infected with tetanus also show changes in behavior, learning ability, and memory. The same drugs that suppress ste-reotyped behaviors in autistic individuals, Bolte says, also suppress these behaviors in toxin-exposed animals. In addition, she notes, researchers use tetanus neurotoxin to cause epilepsy in animals-and epilepsy is a very common symptom in autism.

Bolte notes that tetanus infection can occur even in immunized individuals. Also, she notes, animal research demonstrates that tetanus infection of the intestinal tract - unlike infections in wounds-can lead to neurological symptoms without causing muscle spasms. Tetanus infection can occur in forms so subtle that many patients (22 percent, in one study) do not have recognizable symp-toms, and chronic tetanus infection has been diagnosed in humans.

Bolte believes that intestinal tetanus infections may occur in children chronically exposed to antibiotics given to treat ear in-fections. She notes that these antibiotics can markedly increase the risk of infection of the intestinal tract by pathogenic bacteria, including the 'cry common ('/os'r1J1u117 (eLini A number of autism's features, Bolte says, could be explained by a sub-acute, chronic tetanus infection. Among them:

· Autism occurs in boys four times as of ten as in girls-a fact believed to indicate genetic influences. But Bolte notes that "tetanus infection is also documented to occur in males four times more often than in females."

· There are "some striking similarities," Bolte says, "in the neuronal damage described in autopsy studies of autistic individuals] and those observed in neurons intoxicated with tetanus neurotoxin." In addition, she notes, inhibitory neurons that release the neurotransmitter GABA are a preferred target for tetanus neurotoxins - and the Purkinje cells of the cerebellum, which often appear highly abnormal in autistic individuals, are inhibitory neurons that release GABA.

· Tetanus infection produces a substance called tetanolysin, which could damage the intestines and increase intestinal permeabil-ity - thus allowing larger-than-normal food molecules to enter the bloodstream, causing immune reactions (and, some researchers speculate, neurological symptoms). Previous research indicates that many autistic individuals have increased intestinal permeability.

Bolte also notes that tetanus infection of the intestines leads to the formation of toxic compounds called phenols, and studies of autistic individuals have detected markedly elevated levels of the phenolic metabolite DHPPA. Several autistic children with high DHPPA levels, Bolte notes, "have shown a significant reduction in stereotyped behaviors when treated with antimicrobials effective against intestinal clostridia" - a genus of bacteria including tetanus. The children became more sociable, spoke more, improved their eye contact, and were less hyperactive and hypersensitive. Bolte adds, "Parents also noted that regression occurred very quickly" after treatment was discontinued.

Given these findings, Bolte says, "Parents, doctors, and researchers must combine efforts to determine if some people diagnosed as autistic are actually suffering from unrecognized forms of subacute tetanus."

"Autism and Clostruidium Tetani," Ellen R.Bolte; Medical Hypotheses, Vol. .51, 1998, pp.133-144. Address: Ellen R Bolte, 705 Misty Creek, Drive, New Lenox, IL 60451.