Are We Getting Closer to the Treatment of Rabies?

Rodney E Willoughby Jr


Future Virology. 2009;4(6):563-570. 

In This Article


At the time that our initial survivor, aged 15 years, was hospitalized, rabies was 100% fatal and conventional virological therapies had never worked. With limited time to form a strategy, the literature on how to treat rabies was avoided.[26] Instead, the focus was on the virology of wild-type rabies. The lack of the cytopathic effect during wild-type rabies could be paired with observations that rabies was cleared from patients who survived for more than a couple of weeks. If neurotransmitter dysfunction, including dysautonomia, caused brain-assisted suicide, then an anesthesiologist was called upon to sedate the brain long enough in order to allow the natural immune response to clear the infection. Brain-cooling and barbiturate-induced coma were rejected because both inhibit the immune system. Henri Tsiang's group at Institut Pasteur (Paris, France) had earlier despaired of conventional antivirals and vaccines for the treatment of rabies, and turned to investigating neurotransmitters and 'neuroprotectant' drugs. Ketamine, a dissociative anesthetic, demonstrated modest virological effects against rabies. More importantly, the antiviral effect was specific to the rabies virus, worked by a specific mechanism and was consistent with other drugs of the same class, such as MK-801.[27] After vetting by seven consultants and approval by the parents, we initiated ketamine-based sedation to the point of partial burst suppression by electroencephalography. Sedation was withdrawn after a rise in the patients rabies-specific antibodies.[10] The patient survived with almost no permanent sequelae, and is beginning her third year of university studies.[28]