In 1873, Otto Obermeier first described the disease-causing ability and mechanisms of spirochetes, but was unable to reproduce the disease in inoculated test subjects and thereby unable to fulfill Kochs postulates. The disease was not  successfully produced in an inoculated subject until 1874. In 1904 and 1905, a series of papers outlined the cause of relapsing fever and its relationship with ticks. Both Joseph Everett Dutton and John Lancelot Todd contracted relapsing fever by performing autopsies while working in the eastern region of the Congo Free State. Dutton died there on February 27, 1905. The cause of tick-borne relapsing fever across central Africa was named Spirillum duttoni. In 1984, it was renamed Borrelia duttoni. The first time relapsing fever was described in North America was in 1915 in Jefferson County, Colorado.Sir William MacArthur suggested that relapsing fever was the cause of the yellow plague, variously called pestis flava, pestis ictericia, buidhe chonaill, or cron chonnaill, which struck early Medieval Britain and Ireland, and of epidemics which struck modern Ireland in the famine. This is consistent with the description of the symptoms experienced by King Maelgwn of Gwynedd as recorded in words attributed to Taliesin and with the "great mortality in Britain" in 548 CE noted in the Annales Cambriae. See also
Lyme disease
Typhus
Continuous fever
Intermittent fever
Remittent fever

References
External links
CDC: Relapsing Fever
The active metabolite of progesterone has been found to enhance the binding of benzodiazepines to the benzodiazepine binding sites on the GABAA receptor. The cross-tolerance between GABAA receptor positive modulators, including benzodiazepines, occurs because of the similar mechanism of action and the subunit changes that occur from chronic use from one or more of these compounds in expressed receptor isoforms. Abrupt withdrawal from any of these compounds, e.g., barbiturates, benzodiazepines, alcohol, corticosteroids, neuroactive steroids, and nonbenzodiazepines, precipitate similar withdrawal effects characterized by central nervous system hyper-excitability, resulting in symptoms such as increased seizure susceptibility and anxiety. While many of the neuroactive steroids do not produce full tolerance to their therapeutic effects, cross-tolerance to benzodiazepines still occurs as had been demonstrated between the neuroactive steroid ganaxolone and diazepam. Alterations of levels of neuroactive steroids in the body during the menstrual cycle, menopause, pregnancy, and stressful circumstances can lead to a reduction in the effectiveness of benzodiazepines and a reduced therapeutic effect. During withdrawal of neuroactive steroids, benzodiazepines become less effective. Physiology of withdrawal
Withdrawal symptoms are a normal response in individuals having chronically used benzodiazepines, and an adverse effect and result of drug tolerance. Symptoms typically emerge when dosage of the drug is reduced. GABA is the second-most-common neurotransmitter in the central nervous system (the most common being glutamate) and by far the most abundant inhibitory neurotransmitter; roughly one-quarter to one-third of synapses use GABA.