The onset of illness is typically 5–7 days after the tick bite, although in some cases it may take up to 10 days for symptoms to occur. Symptoms can persist for several days to up to three weeks. Common presenting symptoms include:

Fever
Headache
Muscle aches
Inoculation eschar, which is dead, often black, tissue around a bite site (see photo above)
Eschars may or may not be present. Amblyomma ticks actively attack cattle or humans and can bite more than once. In African tick bite fever, unlike what is typically seen with other Rickettsial spotted fevers when only one eschar is identified, multiple eschars may be seen and are considered pathognomonic. Swollen lymph nodes near the site of the bite
Maculopapular and/or vesicular rash

Complications
Complications are rare and are not life-threatening. No deaths due to African tick bite fever have been reported. Reported complications include:

Prolonged fever > 3 weeks in duration
Reactive arthritis
Moderate to severe headache

Cause
Bacteriology
Rickettsia africae is a gram-negative, obligate intracellular, pleomorphic bacterium. It belongs to the genus Rickettsia, which includes many bacterial species that are transmitted to humans by arthropods. Vectors
Two species of hard ticks, Amblyoma variegatum and Amblyomma hebraeum are the most common vectors of R. africae. Typically, Amblyomma hebraeum transmits the bacteria in South Africa while Amblyoma variegatum carries R. africae throughout West, Central and East Africa and through the French West Indies. Other species of Amblyomma in sub-Saharan Africa can also transmit R. africae and it may be that up to 100% of Amblyomma ticks in sub-Saharan Africa carry R. africae.
Pharmacokinetics
Safinamide is absorbed quickly and nearly completely from the gut and reaches highest blood plasma concentrations after 1.8 to 2.8 hours. There is no relevant first-pass metabolism; total bioavailability is 95%. The substance is bound to plasma proteins to 88–90%.The metabolism is not well understood. The principal step is mediated by amidases which have not been identified, and produces safinamide acid (NW-1153). Other relevant metabolites are O-debenzylated safinamide (NW-1199), the N-dealkylated amine which is then oxidized to a carboxylic acid (NW-1689), and the glucuronide of the latter. In tests with liver microsomes, dealkylation seemed to be mediated by CYP3A4, but other CYP enzymes appear to be involved as well. Safinamide acid binds to the organic anion transporter 3 (OAT3), but this has probably no clinical relevance. Safinamide itself transiently binds to ABCG2. No other transporter affinities have been found in preliminary studies.Safinamide is eliminated, mainly (>90%) in form of its metabolites, via the kidney, with an elimination half-life of 20 to 30 hours. Only 1.5% are found in the stool. History
The compound was originally discovered at Farmitalia-Carlo Erba, which was acquired by Pharmacia in 1993. In 1995, Pharmacia merged with Upjohn. Safinamide was first disclosed in 1998. In the course of a major restructuring in the same year, all rights for safinamide were transferred to the newly formed company Newron Pharmaceuticals, which developed the drug until it was sold to Merck KGaA in 2006.In 2007, a Phase III clinical trial was started, scheduled to run until 2011.