Transmission between humans is extremely rare. A few cases have been recorded through transplant surgery. After a typical human infection by bite, the virus enters the peripheral nervous system. It then travels along the nerves towards the central nervous system. During this phase, the virus cannot be easily detected within the host and vaccination may still confer cell-mediated immunity to prevent symptomatic rabies.
Once the virus reaches the brain, it rapidly causes encephalitis. This is called the “prodromal” phase, and is the beginning of the symptoms. Once it reaches this point and symptoms show, there is no treatment and death is certain. Rabies may also inflame the spinal cord producing transverse myelitis.
Almost every infected case with rabies resulted in death until a vaccine was developed by Louis Pasteur and Emile Roux in 1885. Their original vaccine was harvested from infected rabbits, from which the nerve-tissue was weakened by allowing to dry for five to ten days. Similar nerve tissue-derived vaccines are still used in some countries, as they are much cheaper than modern cell culture vaccines.
The human diploid cell rabies vaccine (HDCV) was started in 1967, however, a new and less expensive purified chicken embryo cell vaccine and purified vero cell rabies vaccine are now available. A recombinant vaccine called V-RG has been successfully used in the field of Belgium, France, Germany and the United States to prevent outbreaks of rabies in wildlife. Currently pre-exposure immunisation has been used in both human and non-human populations, whereas in many jurisdictions domesticated animals are required to be vaccinated.
In the US, since the widespread vaccination of domestic dogs and cats and the development of effective human vaccines and immunoglobulin treatments, the number of recorded deaths from rabies has dropped from one hundred or more annually in the early twentieth century, to 1–2 per year, mostly caused by bat bites, which may go unnoticed by the victim and hence untreated.