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A new threat from
Lyme-disease ticks

The small, unobtrusive tick called Ixodes scapularis received worldwide medical attention almost 20 years ago, when it was found to play a crucial role in the transmission of Lyme disease. Although the ticks themselves pose no great threat to humans, they carry the disease-causing spirochete Borrelia burgdorferi and provide the route of human infection through their bites.

But their culpability doesn’t end there. In the inaugural issue of the journal Vector Borne and Zoonotic Diseases, Durland Fish, Ph.D., and several colleagues describe a spirochete from I. scapularis that closely resembles B. burgdorferi but does not match it in highly sensitive DNA tests carried out by polymerase chain reaction. The new species of Borrelia was discovered in I. scapularis nymphs that had previously been fed on mice known to be free of B. burgdorferi infection. The yet-unnamed spirochete may infect humans as well, since “all the other organisms that this tick transmits to mice can also infect people,” according to Fish, an associate professor of epidemiology. It is not known what symptoms, if any, such an infection would cause in humans.

“Our sampling of I. scapularis … from the field suggests that this novel Borrelia is widely distributed in nature,” the study’s authors wrote, and its prevalence is “surprisingly high in proportion to the total number of Borrelia species found in these ticks.” They concluded, “These data suggest that a significant proportion of spirochete-positive ticks previously thought to be B. burgdorferi by microscopy is instead this novel Borrelia.” Infection with B. burgdorferi is responsible for more than 15,000 cases of Lyme disease each year. Infection with the new Borrelia organism cannot be found by current Lyme-disease diagnostics—Yale scientists are now working on a specific test—but it might well respond to the same treatments as Lyme disease.

 

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Chronic cocaine use may dull responsiveness to brain signals

In a study measuring the brain’s degree of excitability, the brains of cocaine-dependent people show an abnormally low response to signals in the region responsible for muscle movement, according to a recent article in Biological Psychiatry. The authors, led by Nashatt N. Boutros, M.D., associate professor of psychiatry, reported that cocaine addicts and longtime users require significantly more stimulus to the motor cortex in order to cause the muscles of their fingers and hands to move. The signals in this study were delivered on the scalp in the form of transcranial magnetic stimulation, rapid magnetic pulses from a handheld coil. The motor threshold, the minimum amount of stimulation needed to produce movement, ran at a mean of about 41 percent in normal subjects but about 65 percent in chronic cocaine users.

Cocaine itself is well known as a drug that excites the brain’s signaling pathways rather than impeding them, so one might expect that longtime users of the drug would have the most signal-sensitive brains of all. Boutros and his colleagues offered two possible explanations for the higher motor threshold seen in cocaine-dependent brains. It may reflect either “an adaptation to those effects of cocaine intoxication that promote cortical excitability and seizures,” they said, or else tissue damage that has left this brain region less responsive. In other words, by becoming less sensitive to signals or less well able to respond to them, the brain may be attempting to balance out the dangerous hyperresponsiveness that comes with cocaine use. The next step, said Boutros, will be to replicate these results in additional cocaine-dependent subjects, using several different measures of cortical responsiveness.


Also in Findings:

A new threat from Lyme-disease ticks  |  Chronic cocaine use may dull responsiveness to brain signals 

Chronicle  |  Rounds  |  Et cetera    

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Originally published in Yale Medicine, Summer 2001.
Copyright © 2001 Yale University School of Medicine. All rights reserved.